SURGERY

OF THE
THIRD VENTRICLE
EDITED BY

Michael L. J. Apuzzo, M.D.

Professor
Department of Neurological Surgery
University of Southern California School of Medicine
Los Angeles, California

WILLIAMS & WILKINS

Baltimore • London • Los Angeles •
Sydney
Foreword

The third ventricle lying at the center of the cerebral hemispheres surrounded by brain, exquisite
both in terms of complexity and function, has enticed neurosurgeons for as long as the depths of
brain have entered their ken. The ventricle and its neural surround also have interested
neuroanatomists, neurophysiologists, endocrinologists, psychiatrists, and psychologists attempting
to decipher the anatomical and functional relationships of the area. These functions are as basic as
reproduction and emotion and extend to maturation and differentiation of the entire organism. The
relationships of this area to cerebral function and differentiation of the organism have resisted study
with an almost overwhelming tenacity, in part because of the complexities involved, in part because
of the anatomical position of the neural neighborhood, and in part because the techniques used for
the studies have, in themselves, altered the functional milieu being investigated.
The background of almost unlimited questions, anatomical position, and altered function when
the area has been approached, has also caused problems in diagnosing and treating lesions of the
third ventricle, as well as being an attraction to basic and clinical neuroscientists. Studies, both basic
and clinical, have, however, slowly assembled a matrix of information that allows, at this time, the
formation of concepts and hypotheses that can be evaluated and supported or disproved. Not the
least of the supporting structures for building the matrix have been changes in diagnostic imaging,
surgical techniques, anesthesia, and control of vital functions of the body during surgery that have
allowed the clinician both to treat and study problems in the area.
As a clinician, I am more aware of the changes in clinical approaches to malfunction of areas
adjacent to the third ventricle, particularly neoplasms adjacent to and within the ventricle and how
the information gained from this has influenced the study of this central neural area. This
manuscript fills a void that has been present in assembling what is known about this area; what
experimental approaches are available, what they have revealed, and how modern diagnostic
imaging, neuroan-atomical techniques, neurosurgical techniques, endocrine studies and
psychological methods have contributed to an understanding of the functional relationships of the
neural. The sum of this information is greater than its parts and cannot be appreciated without this
collation.

When I started in medical school, or even at the time when I finished neurosurgical training, a
volume such as this would have been short, inaccurate, and mainly of value in demonstrating what
damage was done with surgical approaches, what pathology was found, and perhaps suggesting that
other methods of treatment of conditions in this area must evolve. The manuscripts constituting this
volume, in contrast, not only summarize what has been accomplished, but also rather than pointing
to an area that on the basis of previous work appears fruitful or should be studied, defines those
areas and those directions. Lesions in this area are not common in the average physician's practice,
are relatively uncommon even in a neurosurgeon's practice, but they are important. Their diagnosis
and treatment not only adds to the well-being of the individual suffering from such conditions but
also allows investigative clinicians, treating such patients, to add to the general knowledge of the
nervous system and neurosurgery. This book defines the bases for such investigations and, in
addition, offers the neurosurgeon an up-to-date evaluation and summary of the multiple therapeutic
options for treating lesions in and around the third ventricle.

William F. Collins, Jr. New Haven, Connecticut

 Preface

It has been more than 50 years since the publication of Walter Dandy's monograph, Benign
Tumors in the Third Ventricle of the Brain, an important work detailing his concepts of pathology
and surgery and his experience with the management of tumors affecting the third ventricular
chamber. Since that time progress in aspects of surgical techniques, radiological imaging, scientific
methodologies related to neurological anesthesia, and comprehension of neurophysiological
parameters has developed at a striking pace. As no text or atlas has singularly addressed the topic of
third ventricular surgery for over a half century, it seems that a work (text/atlas) focusing on issues
attendant to this challenging region is in order.
In the development of this project an effort has been made to provide commentary on pertinent
topics from recognized authoritative neurologists, neurosurgeons, neuroradiologists, and
neuroscientists with special interest in the topic and to develop a broad and practical perspective.
The book is particularly addressed to the general neurological surgeon who encounters lesions
involving this region infrequently.
The work has been arranged in two major portions. The first provides an intellectual substrate
related to issues of anatomy, embryology, physiology, pathology, and radiology that is the essential
basis for substantive approaches to issues of therapy. The second section focuses upon surgical
technique and strategy with a detailed account of the methodology attendant to the multiple surgical
corridors applicable for access to the region. Matters associated with intraoperative anatomy,
techniques, and decision-making are approached. Issues of preoperative and intraoperative strategies
are discussed and developed in detail. To expand perspective, innovative and challenging
methodologies are also presented.
Considering the number of contributors, each with a wealth of experience in dealing with specific
surgical issues, no effort has been made to provide a rigidly unified surgical attitude, and certain
elements of controversy related to the individual prejudices of the authors are presented within the
work. However, effort has been expended to provide the logic involved in the development of each
perspective.
Finally, commentary is offered on the role of and expectations for adjuvant therapy (radiotherapy
and chemotherapy) for neoplastic lesions in the region.
The primary objective of this text/atlas is to provide neurosurgeons, neurologists, and
neuroscientists with a single reference that will offer current, substantive, and practical guidance in
the comprehension and management of lesions affecting the third ventricular chamber.

Michael L. J. Apuzzo Los Angeles

 Acknowledgments

Special gratitude must be expressed to Carolyn Soter, who provided a major force in bringing this
project to completion. Over a 3-year period she gave attentive and tireless energy to all aspects of
the general organization, solicitation of manuscripts, and physical preparation of this work.
Janice Jones energetically attended to the complex task of bibliography retrieval and the
procurement of resource materials, invaluably contributing to the substance and credibility of the
manuscripts.
The Department of Photography at the Los Angeles County-University of Southern California
Medical Center provided careful attention to the reproduction and generation of many of the
illustrations in this volume. In particular Andy Gero, R.B.P., Chief Medical Photographer, Frank
Park, Michael Gail, and Tom Meichelbock should be recognized for their patience and care in
producing illustrations of the highest quality.
The Williams & Wilkins staff has been a flexible, valuable, and understanding partner during the
development of this complex work. In particular, Carol-Lynn Brown must be recognized for her
guidance, patience, prudence, and support during the evolution of the scope of the volume.
Finally, it is most important to recognize our teachers, patients, and predecessors in neurosurgery
who have provided the events, stimulation, and experiences generating the intellectual substrate that
made this work possible.
Contributors

Diane Abeloff, M.A., A.M.I. W. Kemp Clark, M.D.

Medical Illustrator, Baltimore, Maryland Professor, Department of Neurological Surgery, The
Michael L. J. Apuzzo, M.D. University of Texas Southwestern Medical School, Dallas,
Professor, Department of Neurological Surgery, University Texas
of Southern California School of Medicine, Los Angeles, William F. Collins, Jr., M.D.
California Harvey and Kate Cushing Professor, Division of
Erik-Olof Backlund, M.D. Neurological Surgery, and Chairman, Department of
Professor and Chairman, Department of Neurological Surgery, Yale University School of Medicine, New Haven,
Surgery, University of Bergen, School of Medicine, Connecticut
Bergen, Norway Eric R. Cosman, Ph.D.
Gilbert A. Block, M.D. Professor, Department of Physics, Massachusetts Institute
Instructor, Department of Neurology, Cornell University of Technology, Cambridge, Massachusetts
Hospital, New York, New York Antonio R. Damasio, M.D., Ph.D.
Joseph E. Bogen, M.D. Professor and Chief, Division of Behavioral Neurology,
Clinical Professor of Neurological Surgery, University of The University of Iowa Hospitals and Clinics, Iowa City,
Southern California School of Medicine, and Adjunct Iowa
Professor, Department of Psychology, University of Richard L. Davis, M.D.
California at Los Angeles, Los Angeles, California Professor of Pathology, Department of Pathology,
Adam Borit, M.D. University of California Medical Center, San Francisco,
Professor of Pathology, Department of Pathology, The California
University of Texas System Cancer Center, Houston, Michael S. B. Edwards, M.D.
Texas Associate Professor, Department of Neurosurgery,
Robert E. Breeze. M.D. University of California Medical Center, San Francisco,
Clinical Instructor, Department of Neurological Surgery, California
University of Southern California School of Medicine, Los Bruce Ehni, M.D.
Angeles, California Clinical Instructor, University of Texas Medical
Parakrama T. Chandrasoma, M.D. School, Houston, Texas
Assistant Professor, Department of Pathology, University George Ehni, M.D.
of Southern California School of Medicine, Los Angeles, Professor, Neurological Surgery, University of
California Texas Medical School, Houston, Texas
Ivan S. Ciric, M.D. Craig A. Fredericks, M.D.
Professor of Clinical Surgery (Neurosurgery), Clinical Instructor, Department of Neurological Surgery,
Northwestern University Medical School, Chicago, University of Southern California School of Medicine, Los
Illinois Angeles, California
Henry D. Garretson, M.D., Ph.D.
Professor and Director, Division of Neurosurgery,
University of Louisville School of Medicine, Louisville,
Kentucky
Steven L. Giannotta, M.D.
Associate Professor, Department of Neurological Surgery,
University of Southern California School of Medicine, Los
Angeles, California
Philip H. Gutin, M.D.
Associate Professor, Department of Neurosurgery,
University of California Medical Center, San Francisco,
California
M. Peter Heilbrun, M.D.
Professor and Chairman, Division of Neurosurgery,
University of Utah Medical Center, Salt Lake City, Utah
Harold J. Hoffman, M.D., F.R.C.S.(C)
Professor, Division of Neurological Surgery, University of
Toronto School of Medicine, Toronto, Ontario, Canada
Kazuhiro Hongo, M.D.
Clinical and Research Fellow, Department of
Neurosurgery, Shinshu University, School of Medicine,
Matsumoto, Japan
Patrick J. Kelly, M.D.
Associate Professor, Department of Neurosurgery, Mayo
School of Medicine, Rochester, Minnesota
E. Leon Kier, M.D.
Professor and Chief, Division of Neuroradiology, Yale
University School of Medicine, New Haven, Connecticut
Alexander N. Konovalov, M.D.
Professor and Director, N. N. Burdenko Neuro-
surgical Institute, Moscow, U.S.S.R.
Eddie Kwan, M.D.
Assistant Professor, Department of Radiology, Tufts
University School of Medicine, Boston, Massachusetts
Claude Lapras, M.D.
Professeur a la Faculte, Neurochirurgien des Hopitaux,
Lyon, France
Michael H. Lavyne, M.D.
Associate Professor of Surgery, Division of Neurological
Surgery, Cornell University Medical Center, New York,
New York
Victor A. Levin, M.D.
Professor, Department of Neurosurgery, University of
California Medical Center, San Francisco, California
F. Miles Little, M.D.
Assistant Professor, Department of Neurosurgery,
University of Southern California School of Medicine, Los
Angeles, California
Masao Matsutani, M.D.
Assistant Professor, Department of Neurosurgery, Tokyo
University, Tokyo, Japan
J. Gordon McComb, M.D.
Professor, Department of Neurological Surgery, University
of Southern California School of Medicine, Los Angeles,
California
Michael T. Modic, M.D.
Professor, Department of Radiology, University Hospital,
Case Western Reserve School of Medicine, Cleveland,
Ohio
Robert B. Page, M.D.
Professor, Division of Neurosurgery, Department of
Anatomy, Hershey Medical Center, Hershey, Pennsylvania
J. D. Patet, M.D.
Neurochirurgien des Hopitaux, Lyon, France
Russel H. Patterson, Jr., M.D.
Professor and Chairman, Department of Neurological
Surgery, Cornell University Medical Center, New York,
New York
Jerome B. Posner, M.D.
Professor and Chairman, Department of Neurology,
Cornell University Hospital, New York, New York
Albert L. Rhoton, Jr., M.D.
R. D. Keene Family Professor and Chairman, Department
of Neurosurgery, University of Florida College of
Medicine, Gainesville, Florida
Peter Roth
Scientific Artist, Neurosurgical Department, University
Hospital, Zurich, Switzerland
Madjid Samii, Prof. Dr. med.
Neurochirugische Klinik, Krankaenhaus Nor-stadt,
Hannover, West Germany
Robert A. Sanford, M.D.
Associate Professor, Department of Neurosurgery,
University of Tennessee, Memphis, Tennessee
Keiji Sano, M.D., D.M.Sc., F.A.C.S.(hon.)
Professor and Director, Department of Neurosurgery,
Teikyo University Hospital, Tokyo, Japan
Henry H. Schmidek, M.D.
Professor of Neurosurgery, Department of Neu-robiology,
Harvard Medical School, Boston, Massachusetts
William Shucart, M.D.
Professor and Chairman, Department of Neurosurgery,
New England Medical Center, Boston, Massachusetts
Robert R. Smith, M.D.
Professor and Chairman, Department of Neurological
Surgery, University of Mississippi Medical Center,
Jackson, Mississippi
Steven P. Smith, M.D.
Fellow, Neuroradiology, New England Medical Center,
Boston, Massachusetts
Bennett M. Stein, M.D.
Byron Stookey Professor of Neurosurgery, Neurological
Institute, New York, New York
Kenichiro Sugita, M.D.
Professor and Chairman, Department of Neurosurgery,
Shinshu University, Matsumoto, Japan
Jiro Suzuki, M.D.
Professor and Chairman, Department of Neurosurgery,
Tohoku University, Sendai, Japan
Kintomo Takakura, M.D.
Professor and Chairman, Department of Neurosurgery,
Tokyo University, Tokyo, Japan
Peter J. Teddy, D.Phil, F.R.C.S.
Consultant Neurosurgeon, Department of Neurological
Surgery, Oxforshire Area Health Authority, The Radcliffe
Infirmary, Oxford, England
George T. Tindall, M.D.
Professor of Surgery, Chief, Division of Neurosurgery,
The Emory University School of Medicine, Atlanta,
Georgia
Suzie C. Tindall, M.D.
Assistant Professor of Surgery, Division of Neurosurgery,
The Emory University School of Medicine, Atlanta,
Georgia
Gary W. Van Hoesen, Ph.D.
Professor, Anatomy and Neurology, Department of
Anatomy, The University of Iowa Hospitals and Clinics,
Iowa City, Iowa
Roger I. von Hanwehr, M.D.
Clinical Instructor, Department of Neurological Surgery,
University of Southern California School of Medicine,
Los Angeles, California
Steven L. Wald, M.D.
Assistant Professor of Neurosurgery, Division of
Neurosurgery, University of Vermont College of Medicine,
Burlington, Vermont
William M. Wara, M.D.
Professor and Vice Chairman, Department of Radiation
Oncology, University of California, San Francisco, San
Francisco, California
Martin H. Weiss, M.D.
Professor and Chairman, Department of Neurological
Surgery, University of Southern California School of
Medicine, Los Angeles, California
Trent H. Wells, Jr.
President, Trentwells, Inc., South Gate, California
Robert H. Wilkins, M.D.
Professor and Chief, Division of Neurological Surgery,
Duke University Medical Center, Durham, North Carolina
Samuel M. Wolpert, M.B., B.Ch.
Professor of Radiology and Neurology, Tufts University
School of Medicine, and Chief, Neuroradiology, New
England Medical Center, Boston, Massachusetts
M. Gazi Yasargil, Prof. Dr. med.
Director der Neurochirurg, Universitatsklinik Zurich,
Zurich, Switzerland
Chi-Shing Zee, M.D.
Assistant Professor, Department of Radiology, University
of Southern California School of Medicine, Los Angeles,
California
Vladimir Zelman, M.D., Ph.D.
Associate Professor, Department of Anesthesiol-ogy and
Department of Neurosurgery, University of Southern
California School of Medicine, Los Angeles, California
Contents обложка

Foreword .................................................................................................................. vii

Preface ................................................................................................................... ix
Acknowledgments ................................................................................................. xi
Contributors ............................................................................................................. xiii

I. HISTORICAL PERSPECTIVE _____________________________________

1 . History of Surgery of the Third Ventricular Region. Robert

H. Wilkins, M.D ....................................................................................................... 3

II. FUNDAMENTAL CONSIDERATIONS ______________________________

2. Comparative Anatomy of the Third Ventricular Region.

E. Leon Kier, M.D.................................................................................................... 37
3. Microsurgical Anatomy of the Third Ventricular Region.
Albert L. Rhoton, Jr., M.D ....................................................................................... 92
4. Surgery of the Third Ventricle: Regional Embryology.
Ivan S. Ciric, M.D .................................................................................................... 167
5. Physiological Consequences of Complete or Partial
Commissural Section. Joseph E. Bogen, M.D 175
6. Pathological Correlates of Amnesia and the Anatomical
Basis of Memory. Antonio R. Damasio, M.D., Ph.D., and
Gary W. Van Hoesen, Ph.D 195
Commentary A. Memory in Man: A Neurosurgeon's
Perspective. Henry D. Garretson, M.D., Ph.D 209
7. Anatomy and Physiology of Consciousness: Syndromes of
Altered Consciousness Related to Third Ventricular Surgery.
Gilbert A. Block, M.D., and Jerome B. Posner, M.D 213
8. Deep Veins. Robert R. Smith, M.D., Robert A. Sanford, M.D.,
and Henry H. Schmidek, M.D 224
9. Pathological Lesions of the Third Ventricle and Adjacent
Structures. Richard L. Davis, M.D 235
10. Tumor Markers in Third Ventricular Neoplasms. Henry H.
Schmidek, M.D., Adam Borit, M.D., and Steven L. Wald, M.D. . . 253
1 1 . Radiology of Third Ventricular Lesions. Eddie Kwan,
M.D., Samuel M. Wolpert, M.B., B.Ch., Steven P. Smith, M.D.,
and Michael T. Modic, M.D 262

III. SURGICAL APPROACHES, TECHNIQUES, AND STRATEGIES

ANTERIOR APPROACHES
12. Anterior Transcallosal and Transcortical Approaches.
William Shucart, M.D 303
13. Considerations in Transforaminal Entry. George Ehni,
M.D., and Bruce Ehni, M.D 326
14. Transcallosal Interforniceal Approach. Michael L. J.
Apuzzo, M.D., and Steven L. Giannotta, M.D 354
15. Subchoroidal Trans-Velum Interpositum Approach.
Michael H. Lavyne, M.D., and Russel H. Patterson, Jr., M.D. . . . 381
16. Subfrontal Transsphenoidal and Trans-Lamina Terminalis
Approaches. Russel H. Patterson, Jr., M.D 398
17. Bifrontal Anterior Interhemispheric Approach. Jiro
Suzuki, M.D 413
18. Pterional Approach. George T. Tindall, M.D., and Suzie C.
Tindall, M.D 440
19. Combined Approaches. M. Gazi Yasargil, Prof. Dr. med.,
Peter J. Teddy, D. Phil., F.R.C.S., and Peter Roth 462
20. Transnasal Transsphenoidal Approach. Martin H. Weiss,
M.D 476
21. Anterior and Mid-Third Ventricular Lesions: A Surgical
Overview. Michael L. J. Apuzzo, M.D., Chi-Shing Zee, M.D., and
Robert E. Breeze, M.D 495
Commentary B. Technique and Strategies of Direct Surgical
Management of Craniopharyngioma. Alexander N. Konovalov,
M.D 542
Commentary C. Diencephalic Structures at Risk in Third
Ventricular Surgery. Robert B. Page, M.D 553

POSTERIOR APPROACHES
22. Posterior Transcortical Approach. Kenichiro Sugita, M.D.,
and Kazuhiro Hongo, M.D 557
23. Infratentorial Supracerebellar Approach. Bennett M.
Stein, M.D 570
24. Occipital Transtentorial Approach. W. Kemp Clark, M.D. 591
25. Posterior Intrahemispheric Retrocallosal and Transcallosal
Approaches. J. Gordon McComb, M.D., and Michael L. J.
Apuzzo, M.D 611
Commentary D. Operative Management of Malformations of
the Vein of Galen. J. Gordon McComb, M.D., and Michael L. J.
Apuzzo, M.D 641
26. Controversies, Techniques, and Strategies for Pineal Tumor Surgery. Claude Lapras,
M.D., and J. D. Patet, M.D. . . . 649
27. Pineal Region and Posterior Third Ventricular Tumors: A Surgical Overview. Keiji
Sano, M.D., D.M.Sc., F.A.C.S.(hon.) . . . 663

SPECIALIZED ISSUES
28. Technical Aspects of Excision of Giant Basal Tumors with Third Ventricular
Involvement. Madjid Samii, Prof. Dr. med. . . 684
29. Cerebrospinal Fluid Diversion. J. Gordon McComb, M.D.,
and F. Miles Little, M.D 699
30. Considerations and Techniques in the Pediatric Age
Group. Harold J. Hoffman, M.D., F.R.C.S.(C) 727
31. Applications of Computerized Tomographic Guidance
Stereotaxis. Michael L. J. Apuzzo, M.D., Parakrama T.
Chandrasoma, M.D., Vladimir Zelman, M.D., Roger I. von
Hanwehr, M.D., and Craig A. Fredericks, M.D 751
Commentary E. Contemporary European Contributions to
Neurosurgical Stereotaxy. Roger I. von Hanwehr, M.D 793
Commentary F. Role of Stereotaxis in the Management of
Midline Cerebral Lesions. Erik-Olof Backlund, M.D., Ph.D 802
Commentary G. Magnetic Resonance Stereotaxy.
Eric R. Cosman, Ph.D., M. Peter Heibrun, M.D., and Trent H.
Wells, Jr 806
32. Computer-assisted Stereotaxic Laser Microsurgery.
Patrick J. Kelly, M.D 811

IV. ADJUVANT THERAPIES

33. Radiotherapy of Pineal and Suprasellar Tumors.
William M. Wara, M.D., and Philip H. Gutin, M.D 831
34. Chemotherapy of Tumors of the Third Ventricular Region.
Michael S. B. Edwards, M.D., and Victor A. Levin, M.D 838
35. Therapeutic Modality Selection in Management of Germ Cell
Tumors. Kintomo Takakura, M.D., and Masao Matsutani, M.D. 843
1
History of Surgery of the Third Ventricular Region
Robert H.Wilkins,M.D.
This chapter deals with the history of surgery of the
third ventricular region. I have arbitrarily limited my
considerations to the surgical treatment of abnormalities of
or in the third ventricle itself, of lesions of the roof of the
third ventricle, and of tumors in the region of the pineal
gland. I have not included the treatment of sellar or su-
prasellar lesions (even those that invaginate the floor of the
third ventricle), of arteriovenous malformations draining
into the vein of Galen, or of tumors of the thalamus,
hypothalamus, or brain stem.
I have tried to avoid undue emphasis on the
establishment of priority because some uncertainty always
exists about who was the first to describe a pathological
entity or an approach to treatment. As Palmer has noted,
"... an author can never tell how many cases . . . have
previously been reported: no amount of library research
will permit more than a rough guess" (106). The reason for
this is that even after a thorough search in a medical
library, the author will have missed unindexed cases
reported in sources such as textbooks and monographs,
governmental reports, doctoral theses, and the letters to the
editor section of many journals. Furthermore, "... the
author also must understand that, as important as the entity
seems to him, others who have dealt with similar cases
[may not] . . . have bothered to write them up" (106).
With that caveat in mind, I focus attention in this
chapter on the contributions of Walter Dandy, who had a
unique interest in third ven-
tricular lesions and an unprecedented experience in dealing
with them (36, 55, 62). I begin each section of this chapter
with an account of his work and then consider the other
historical developments, most of which came after Dandy's
pioneering efforts.
Cerebrospinal Fluid and the Ventricular System;
Hydrocephalus
During his senior year and then after his graduation from
medical school in 1910, Walter Dandy worked in the
Hunterian Laboratory of Experimental Medicine of Johns
Hopkins University, where he studied the blood supply and
nerve supply of the pituitary gland (24, 46). Subsequently,
in association with Kenneth Black-fan, he performed a
series of animal experiments and human investigations that
clarified where cerebrospinal fluid (CSF) is produced, how
it circulates, where it is absorbed, and what types of
hydrocephalus result from the various abnormalities that
alter its production, circulation, and absorption (43-45).
Then during his last year of residency (1918) and first year
of practice (1919), Dandy introduced ventriculography and
pneu-moencephalography (26, 28), thus permitting vi-
sualization of the third ventricle for diagnostic purposes.
Based on these early investigations, Dandy maintained
for the rest of his career an interest in hydrocephalus and
its treatment and in the diagnosis and treatment of tumors
and other
lesions in and around the third ventricle (36, 55, 62, 158).
He introduced the operations of choroid plexectomy (27,
39), cannulation of the aqueduct of Sylvius (29), and third
ventriculostomy (33, 41) to treat hydrocephalus and
ventriculoscopy (32) for inspection of the ventricular
system and as an aid to choroid plexectomy.
In his 1918 paper on extirpation of the choroid plexus of
the lateral ventricles for treatment of communicating
hydrocephalus, Dandy wrote, "A remarkable exposure is
obtained during the operation in the ventricle. One can see
the third and opposite lateral ventricle and the septum
lucidum which is frequently perforated in many places
owing to pressure atrophy" (27). In a report in 1922 on
ventriculoscopy, he stated,
On two occasions, it has seemed advisable to inspect a
lateral ventricle. This was done in one instance through a
small cystoscope and in a second an attempt was made
with the help of a small operating ventriculoscope to
remove and fulgurate the
choroid plexus. ... It was possible to see practically the
entire extent of the lateral ventricle, the foramen of
Monro, the septum lucidum with numerous perforations
in it, and the entire extent of the choroid plexus. . . (32).
The procedure of excision of the choroid plexus had a
high mortality rate and was abandoned early (59, 113, 131,
132). However, endoscopic cauterization of the choroid
plexus, which apparently had also been tried by Lespinasse
in 1910 (95), was developed and used by Dandy (39) (Fig.
1.1), Putnam (115), Scarff (129, 132), Feld (57, 58), and
others for 30 to 40 years, when the combination of the
equivocal results of this procedure and the introduction of
successful valved shunt systems led to its abandonment as
well (113). Likewise, direct cannulation of the aqueduct of
Sylvius was tried by Dandy (29) (Fig. 1.2), and
subsequently by Leksell (94), Norlen (104), Elvidge (53),
and a few other neurosurgeons (145, 148), but the
procedure did not prove to be of value.

Figure 1.1. Composite drawing. Center. Sites at which the choroid plexus is cauterized
and removed. A and a. The glomus of the choroid plexus on each side. В and b. The
choroid plexus in the posterior cranial fossa. С, с, and c'. The choroid plexus from the
body of each lateral ventricle. (From Dandy WE: The operative treatment of
communicating hydrocephalus. Ann Surg 108:194-202, 1938.)
 Figure 1.2. Sagittal view of the brain showing a shunt tube in position in the aqueduct of
Sylvius. (From Dandy WE: The diagnosis and treatment of hydro-cephalus resulting
from strictures of the aqueduct of Sylvius. Surg Gynecol Obstet 31:340-358, 1920.)

In contrast, neurosurgeons have maintained some
interest in third ventriculostomy over the years because of
its promise of relieving hydro-cephalus without the
insertion of a shunt system (59, 113, 131). In 1922, Dandy
wrote,
Strictures of the aqueduct of Sylvius recur after any
attempt to restore the lumen. For this reason, if
treatment is to be successful, the fluid must be
sidetracked into its normal channels. With this in mind,
a procedure which apparently is anatomically correct
has been devised, to supersede any direct attack on the
aqueduct. This consists in removing the floor of the
third ventricle. A small opening is made in the skull and
dura in the frontal region, the frontal lobe is elevated
until the bulging third ventricle is well exposed. . . . This
opening in the floor of the third ventricle affords an exit
from the dilated ventricles, so that the fluid can now
pass directly into the cisterna chiasmatis and
interpeduncu-laris—the normal distributing centers for
cerebro-spinal fluid.. . . The ventricular wall is a very
thin membrane and offers a minimum of glia tissue to
repair the defect. This procedure is by no means
analogous to making an opening in the roof of the third
ventricle. The latter can have no beneficial result
because the fluid escapes into the subdural
space where the absorption is slightly, if at all, greater
than in the ventricles. Moreover, the opening is through
cerebral tissue which proliferates and closes it, unless a
good deal of the brain has been destroyed. We have
employed this method 6 times. No claim is made for its
success. Time alone will decide . . . (33).
When the pathogenesis of obstructive hydro-
cephalus was fully appreciated, operations to reroute the
ventricular fluid were devised. Perhaps, the forerunner
of these was the "Balkenstich" operation of Anton and
von Bramann [ ], which consisted of passing a brain
cannula through a midline frontal trephine opening,
along the falx through the corpus callosum and into the
... ventricle. It was presumed that the ventricular fluid
would pass through the fenestrated corpus callosum to
the cal-losal subarachnoid pathways, but the procedure
lost its popularity when it was found that the passageway
did not remain open (59).
As mentioned, Dandy thought that ventriculostomy
through the floor of the third ventricle held advantages
over ventriculostomy through its roof. His initial subfrontal
approach to third ventriculostomy involved the sectioning
of one optic
nerve to gain exposure (33), but in 1932 he reported on a
lateral (transtemporal) third ven-triculostomy that did not
require division of the optic nerve (36). The steps in this
procedure, as listed by Dandy, were:
1 . A plaster cast was molded to the infant's
head (Fig. 1.3). A defect was made in the tem
poral region of the side to be operated upon.
2. Small curved skin and muscle incisions were
made in the temporal region (Fig. 1.3).
3. A small area of bone was removed above the
base of the skull and a dural flap was reflected
toward the base.
4. The head was lowered about 50° and the
temporal horn of the lateral ventricle was tapped,
with the evacuation of 60 to 80 ml of CSF. A
short flanged ventricular needle was left in place
during the operation.
5. The temporal lobe was retracted to expose
the lateral wall of the interpeduncular cistern
and this wall was opened behind the oculomotor
nerve or between the carotid artery and the ocu
lomotor nerve (Fig. 1.4).
6. The bulging floor of the third ventricle was
then identified and opened, with the opening
preferably being made just posterior to the hy-
pophyseal stalk (Fig. 1.5).
7. The ventricles were then filled with the pre
viously aspirated CSF or with an isotonic solution
and the wound was closed in layers (Fig. 1.5).
In 1945, Dandy reported 92 patients that he had treated
in this fashion, with a 12% mortality rate and with arrest of
the hydrocephalus in 50% of the patients for periods
averaging more than 7 years (Table 1.1) (131). Reoperation
had been necessary in 7 of the 92 patients.
After Dandy's 1922 report of subfrontal third
ventriculostomy, several surgeons pursued the idea of
venting the third ventricle into an adjacent subarachnoid
cistern. The following year, Mixter reported treating an
infant with obstructive hydrocephalus by approaching the
floor of the third ventricle with a urethroscope inserted
through the lateral ventricle and foramen of Monro and
then using a flexible sound to puncture an opening into the
interpeduncular cistern (102). Scarff subsequently
performed a similar procedure, which he reported in 1936
(129).
In 1936, Stookey and Scarff described a subfrontal
approach with puncturing of the lamina terminalis and then
the floor of the third ventricle (130, 141) (Fig. 1.6). In
1963, Scarff gave the results in 527 hydrocephalic patients
treated by 12 surgical groups by puncture of the lamina
terminalis alone or combined with puncture of the floor of
the third ventricle, and/or by
puncture of the lateral wall of the hypothalamus (131). The
patients were followed for an average of 5 years. The
operative mortality was approximately 15% and the initial
success rate was about 70%.
Various surgeons have pursued the operation of anterior,
inferior, lateral, or superoposterior third ventriculostomy
by direct or indirect techniques, as detailed in the excellent
publications of Scarff (131) and of Pudenz (113). The
procedure has been aided by the development of ster-
eotaxic techniques and positive contrast ventric-ulography
(Fig. 1.7) (74, 80, 128). In 1980, Hoffman et al.
summarized the results of third ventriculostomy by the
open technique that had been performed by 13 surgical
groups (80). There were 569 patients; the operative
mortality was 10.3% and the success rate was 53.6%
(Table 1.2). These authors also showed the results of third
ventriculostomy by the percutaneous technique as
performed by 12 groups of surgeons. The success rate was
approximately the same (53%), but the operative mortality
was lower (3.5%) (Table 1.3).
During the period when the procedures of cauterization
of the choroid plexus and of third ventriculostomy were
being tried, the techniques of ventriculoscopy and
ventriculography were also being developed.
Ventriculoscopy was of some help in these operations
initially, but despite clever technical advances such as
flexibility, fiberoptic lighting, and video attachments, ven-
triculoscopy never has become an important diagnostic or
therapeutic tool (32, 36, 39, 56-58, 64, 65, 75, 80, 95, 102,
115, 129, 132, 144, 155, 156).
In comparison, after their introduction in 1918 (26) and
1919 (28), pneumoventriculography and
pneumoencephalography rapidly became the keys to the
diagnosis of third ventricular lesions and subsequently to
the performance of stereo-taxic operations adjacent to the
third ventricle. This has changed only in recent years
because of the advent of computerized tomographic (CT)
scanning and magnetic resonance imaging.
For the contrast media, Dandy used ordinary room air.
Bingel ... suggested the use of carbon dioxide in 1922,
because it was absorbed rapidly. In the same year,
Jungling . . . recommended the use of oxygen. . . .
Although gaseous media demonstrated the lateral
ventricles clearly, the third and fourth were often not
well visualized even with special positioning techniques.
To obtain better contrast various other media were tried.
After the introduction of lipiodol, . . . Jacobaeus and
Nord ... in 1924 experimented with it for
ventriculography. The following year Schuster . . . used
it. About the same
Figure 1.3. Dandy's operative approach for third ventriculostomy. (From Dandy WE:
The brain. In Lewis D (ed): Practice of Surgery. Hagerstown, MD, WF Prior, 1932, pp
1-682.)

Figure 1.4. The bulging third ventricle exposed through the lateral wall of the
interpeduncular cistern between the carotid artery and the oculomotor nerve. (From
Dandy WE: The brain. In Lewis D (ed): Practice of Surgery. Hagerstown, MD, WF
Prior, 1932, pp 1-682.)
 a
From Scarff JE: Treatment of hydrocephalus: An
historical and critical review of methods and results. J
Neurol Neurosurg Psychiatry 26:1-26, 1963.

time Balado, Morea and Donovan ... in the Argentine

Figure 1.5. The upper composite drawing indicates all of
the steps in Dandy's third ventriculostomy. The lower
drawing shows the method of filling the ventricles before
closure. (From Dandy WE: Diagnosis and treatment of
strictures of the aqueduct of Sylvius [causing
hydrocephalus]. Arch Sarg 51:1-14, 1945.)
tested the oil in the ventricles of experimental animals
and finding no untoward reactions began using it
routinely, particularly for demonstration of the third and
fourth ventricles (157).
The use of lipiodol waned, and trials of other positive
contrast agents were performed (124, 157). These included
thorium dioxide, diiodoty-rosine-gelatin, and abrodil.
Then, when ethyl iodophenylundecylate was introduced as
a mye-lographic agent, it found use in ventriculography as
well. More recent attempts to use water-soluble contrast
media for ventriculography did not meet with much
success until the introduction of metrizamide, and this has
been combined with CT scanning to give excellent
visualization of the cisterns and ventricles (49).

Table 1.2.
Summary of Experiences with Third Ventriculostomy by Open Operationa

No. Operative Success

Author Year Cases Mortality Rate
(%) (%)
Wertheimer & Mansuy 1938 3 33 66
Pennybacker 1940 5 20 80
White & Michelsen 1942 11 18 46
Dandy 1945 92 17 39
Tolosa 1948 26 25 50
Guillaume & Mazars 1950 230 3.4 54
Krayenbuhl et al. 1950 17 17 60
Fasiani 1951 72 20 70
Scarff 1951 34 15 56
Morello & Migliavacca 1959 28 3 75
Volkel & Voris 1966 12 0 33
Patterson & Bergland 1968 29 6 34
Brocklehurst 1974 10 0 70
Summary 569 10.3 53.6
a
From Hoffman HJ, Harwood-Nash D, Gilday DL: Percutaneous third ventriculostomy
in the management of noncommunicating hydrocephalus. Neurosargery 7:313-321, 1980.
 Table 1.3.
Summary of Experiences with Third Ventriculostomy by Percutaneous
Techniquea

No. Operative Success

Author Year Cases Mortality Rate
(%) (%)
McNickle 1947 7 0 71
Forjaz et al. 1968 15 20 67
Perlman 1968 1 0 100
Raimondi 1972 3 0 0
Guiot 1973 14 0 64
Plerre-Kahn et al. 1975 44 7 64
Poblete & Zamboni 1975 10 0 70
Hoffman 1976 11 0 27b
Sayers & Kosnick 1976 46 4 89
des Plantes & Crezee 1978 61 0 15
Vries 1978 5 0 20
Hoffman et al. 1980 22 0 45
Summary 228 3.5 53
a
From Hoffman HJ, Harwood-Nash D, Gilday DL: Percutaneous third
ventriculostomy in the management of noncommunicating hydrocephalus. Neurosurgery
7:313-321, 1980.
b
Originally reported as 64%; subsequent obstruction largely due to shunt placement
has reduced this success rate to 27%.

Figure 1.6. Third ventriculostomy by the subfrontal route, with puncture of both the
lamina termlnalis and the floor of the third ventricle. (From Scarff JE: Treatment of
obstructive hydrocephalus by puncture of the lamina terminalis and floor of the third
ventricle. J Neurosurg 8:204-213, 1951.)

Figure 1.7. Diagrammatic sketch of a percutaneous method
of third ventriculostomy. (From Hoffman HJ, Harwood-
Nash D, Gilday DL: Percutaneous third ventriculostomy in
the management of noncommunicat-ing hydrocephalus.
Neurosurgery 7:313-321, 1980.)
Lesions of the Roof of the Third Ventricle
In 1931, Walter Dandy published an unusual paper
entitled, "Congenital Cerebral Cysts of the Cavum Septi
Pellucidi (Fifth Ventricle) and Ca-vum Vergae (Sixth
Ventricle): Diagnosis and Treatment" (35). He began the
paper as follows: "In the midline of the brain and within
the confines of the corpus callosum either or both of the
cavum septi pellucidi and cavum vergae are not
infrequently found. Neither cavity has excited much
interest either anatomically or clinically. The two cases
here reported are, I believe, the first instances in which a
diagnosis of these spaces, dilated in abnormal degree, has
been made during life, the first in which the lesion has
been found at or treated by operation and the first in which
clinical symptoms are shown to be related to the lesions
(35).
After discussing the anatomy, occurrence, and
contents of the fifth and sixth ventricles, Dandy then
presented two patients with symptomatic cysts of these
structures (Fig. 1.8) that he had treated by a transcallosal
exposure and fenestra-tion of the cyst into the lateral
ventricles (Fig. 1.9). He ended his paper as follows:
1 . Two cases of cysts of the cavum septi pellucidi
and cavum vergae are reported. In each case the two
cavities were continuous.
2. The cysts acted as tumors and caused
compression of the motor tracts on both sides. Men
tal symptoms were decided in both cases. One pa
tient had peculiar epileptic attacks.... Suggestive
evidence of intermittent intracranial pressure ex
isted in both instances. . . .
4. The diagnosis is easily made by ventriculog-
raphy. . . .
5. An operation is offered for cysts of this char
acter (35).
In 1967, Kempe and Busch reported a symptomatic cyst
of the cavum septum interpositum that had caused head
enlargement during the first 4 months of life (90). This cyst
was exposed through the corpus callosum and psalterium,
and a communication was established with the cis-terna
venae magnae Galeni and ambiens. The patient then
developed normally over the follow-up period of 4 years.
Symptomatic cysts of this sort have been very rare
(152), as have neuroepithelial (colloid) cysts of the septum
pellucidum (18) and diencephalic cysts that extend up from
the third ventricle through the corpus callosum (11).
Somewhat less rare are meningiomas arising from the
velum interpositum and confined predominantly to the
third ventricle and pineal region (without dural attachment)
(111, 123). Among 16 cases of this nature reviewed by
Rozario et al. in 1979, 8 were located in the
pineal/posterior third ventricular region, whereas only 3
were located in the anterior third ventricle (123). Various
surgical approaches were used for the removal of these tu-
mors. Most were operated upon via a transcorti-cal or
occipital approach before the advent of the operating
microscope. In 50%, total removal was achieved. The
operative mortality was 37% (before 1970 it was 60% and
after 1970 it was 0%).
Figure 1.8. Position of a congenital cyst of the cavum septi pellucidi and cavum vergae
in relationship to the ventricular system. (From Dandy WE: Congenital cerebral cysts of
the cavum septi pellucidi [fifth ventricle] and cavum vergae [sixth ventricle): Diagnosis
and treatment. Arch Neurol Psychiatry 25:44-66, 1931.)
 Figure 1.9. Dandy's method of producing an opening between each lateral ventricle and
the cyst of the cavum septi pellucidi. (From Dandy WE: Congenital cerebral cysts of the
cavum septi pellucidi [fifth ventricle] and cavum vergae [sixth ventricle]: Diagnosis and
treatment. Arch Neurol Psychiatry 25:44-66, 1931.)

Third Ventricular Tumors pneumography localization of the tumor and con-

In 1922, Walter Dandy published the following brief
account in the Johns Hopkins Hospital Bulletin:
In one patient, a woman 24 years of age, the only
symptoms were those referable to intracranial pressure.
By cerebral pneumography, it was determined that each
lateral ventricle was greatly enlarged, but there was no
communication between them. Hence we concluded that
there must be a tumor in the third ventricle and
occluding each foramen of Monro; that the tumor must
be small because neither ventricle was dislocated away
from it. A large bone flap was turned down as in a pineal
approach, and the corpus callosum split posteriorly for
about 5 to 6 cm. The right lateral ventricle was then
opened through the mesial wall at the septum lucidum.
No tumor could be seen; the right foramen of Monro
seemed normal on inspection from this lateral ventricle,
but a probe would not pass through it, an obstruction
being encountered in the third ventricle. The foramen of
Monro was then widened and a small encapsulated,
spherical tumor, about 1 cm. in diameter, easily shelled
out in toto. The tumor was of ependymal origin. The
patient recovered. Without cerebral
sequently its removal would have been impossible (31).
Then in a monograph published 11 years later, Walter
Dandy summarized his experience with the diagnosis and
treatment of benign third ventricular tumors (37). He
purposely omitted from this work a consideration of
cerebral gliomas, pineal tumors, "hypophyseal duct
tumors," and large pituitary tumors with upward extension
into the third ventricle. The tumors in his 21 patients
included 5 colloid cysts, 5 "ependymal gliomata," 1
choroid plexus papilloma, 1 epider-moid tumor, and 1
"dermoid." The other 8 tumors were more difficult to
classify.
In addition to his own 21 cases, Dandy also considered
in his discussion "all cases of similar character that could
be assembled from the literature" (37). These latter tumors
were from autopsy material, "... there being no instance of
a tumor having been disclosed at operation" (37). This last
statement by Dandy is of interest be-
cause Harvey Cushing had removed a third ventricular
meningioma from one patient in 1927 and from another in
1931 (23, 123) and had resected an astroblastoma of the
third ventricle at the first meeting of the Harvey Cushing
Society in 1932 (66). The operation for astroblastoma was
memorable. At 10 a.m. on May 6, 1932, Dr. Cushing
welcomed the members of the newly formed organization
that had adopted his name. "He then operated in the large
amphitheater before the entire group, exposing a third-
ventricle tumor through a transcortical incision and re-
moving a large part of it. [The patient, who was shown at
the evening clinic the day of her operation turned out to
have a most favorable tumor. . . . She was married a short
time later and is still living and well, with a family of two
children (Nov. 1945).]" (66). In Dandy's defense, Cushing
did not publish the first two cases until 1938 (23), and
Dandy was not a member of the Harvey Cushing Society.
Dandy began his monograph as follows:
A most interesting and important group of tumors
lying within the third ventricle has, until the past few
years, remained without the fields of diagnosis and
treatment. Of benign type, slow growth and
Figure 1.10. Diagram to show how air injected into a
dilated lateral ventricle fails to fill the third ventricle,
which is occupied by tumor, and the opposite lateral
ventricle (unless there are f enestrations in the septum
pellucidum). (From Dandy WE: Benign Tumors in the
Third Ventricle of the Brain: Diagnosis and Treatment.
Springfield, IL, Charles С Thomas, 1933.)
small size, their removal by surgical treatment is
relatively simple and affords a permanent cure if only a
correct diagnosis and localization can be made. They
produce fulminating signs and symptoms of intracranial
pressure owing to their strategic position along the
channels through which cerebro-spinal fluid must leave
the brain, and yet localization of the tumors by
neurological signs and symptoms is almost impossible.
The advent of ventricu-lography has, however, by its
mechanical evidence made the diagnosis and localization
one of the greatest accuracy and certainty, and has,
therefore, provided the precision that is an absolute
prerequisite for their surgical attack (37).
Dandy then went on to present his 21 cases individually
and then to summarize the various aspects of these cases
plus similar ones from the literature. He pointed out the
characteristic ven-triculographic findings of third
ventricular tumors (Fig. 1.10) and described various
operative techniques for their removal (Figs. 1.11 to 1.15).
Concerning these operative approaches, Dandy stated:
Four operative attacks are used to expose and remove
tumors of the third ventricle: (1) Posterior (pineal)
approach . . . ; (2) Anterior (a) Frontal (hy-pophyseal)
approach with removal of a round or oval area of the
frontal lobe (usually right); (b) Frontal (hypophyseal)
with transection of the frontal lobe (usually right); (c)
Mid-sagittal approach through corpus callosum (used
only for cysts of the septum pellucidum). .. .
Since tumors within the third ventricle are quite
Figure 1.11. Sketches concerning a posterior trans-callosal
operation for the removal of a colloid cyst of the third
ventricle. (From Dandy WE: Benign Tumors in the Third
Ventricle of the Brain: Diagnosis and Treatment.
Springfield, IL, Charles С Thomas, 1933.)
Figure 1.12. Another posterior transcallosal operation for
the removal of a colloid cyst, showing the method of
incising the roof of the ventricle to expose the tumor.
(From Dandy WE: Benign Tumors in the Third Ventricle of
the Brain: Diagnosis and Treatment. Springfield, IL,
Charles С Thomas, 1933.)
Figure 1.13. Transfrontal operation for the removal of a
colloid cyst of the third ventricle. These drawings show the
approach. (From Dandy WE: Benign Tumors in the Third
Ventricle of the Brain: Diagnosis and Treatment.
Springfield, IL, Charles С Thomas, 1933.)
Figure 1.14. Transfrontal operation for the removal of a
colloid cyst of the third ventricle. These drawings show the
intraventricular exposure and removal of the cyst. (From
Dandy WE: Benign Tumors in the Third Ventricle of the
Brain: Diagnosis and Treatment. Springfield, IL, Charles
С Thomas, 1933.)
Figure 1.15. A posterior transcallosal operation for the
removal of a posterior third ventricular tumor. (From
Dandy WE: Benign Tumors in the Third Ventricle of the
Brain: Diagnosis and Treatment. Springfield, IL, Charles
С Thomas, 1933.)
small when compared with other intracranial tumors, it
might seem that any approach that exposes the growth
would be satisfactory. On the contrary, the
determination of the approach is a matter of the utmost
importance. The choice of methods is almost entirely
dependent upon the ventriculographic information
concerning the third ventricle. As previously noted, it
is, therefore, necessary to fill with air and
roentgenographically disclose, as far as possible, every
part of the third ventricle that is not actually filled by
tumor.
The choice between either anterior and the posterior
(pineal) approach is decided entirely upon the position
of the tumor, i.e., whether it lies in the anterior or
posterior part of the third ventricle. If the tumor
occupies only the posterior part of the third ventricle the
pineal approach is absolutely necessary. If the tumor
occupies only the anterior part of the third ventricle the
frontal (hypophyseal) approach is much superior,
although the pineal approach is very satisfactory. The
greatest diagnostic difficulty lies in separating the small
tumors which occupy only the anterior part of the third
ventricle from the larger growths that occupy the entire
ventricle. Obviously the only instances in which this
differential diagnosis can be made by ventriculog-raphy
are afforded by tumors causing only a partial block and
allowing a small amount of air to fill the small posterior
remains of the third ventricle. . .. When the tumor is
known to block the foramina of Monro and no
information is obtainable, either by ventriculographic or
neurological findings, of the posterior extent of the
tumor, the choice of approach is difficult. Formerly I
used the pineal approach exclusively, but more recently
the frontal approach in increasing numbers, because of
the possibility of encountering tumors that are not
primary in the third ventricle but have grown into the
ventricle from without. Then too the colloid cysts
which usually give signs of complete obstruction of the
foramina of Monro are much easier to remove by the
anterior approach. Other things being equal, I prefer the
frontal approach with oval resection or transverse
section of the frontal lobe to the pineal approach. It is
perhaps less dangerous and there is a much better
exposure of the tumor area. The danger is less because
the attack upon the tumor is at a distance from the veins
of Galen. On the other hand, if the growth extends back
to the great vein of Galen, the danger is greater by the
frontal route, for the tumor must be blindly separated
from the venous trunks.
There is practically no risk in either type of section
of the frontal lobe and no loss of function, mental or
physical. One may ask why it is not possible to remove
such tumors through a speculum introduced into the
anterior horn of the lateral ventricle. Such a procedure
is indeed possible with some of the simpler tumors, but
should the operator encounter bleeding, he would be
greatly handicapped for room and might well lose the
patient through the effects of trauma and hemorrhage,
when it is too late to provide the adequate exposure
except through a heroic effort. There is little to lose
and everything to gain in safety of life and function by
providing an adequate exposure through the
preliminary removal of cerebral tissue. There is, of
course, always the
thought in mind that epilepsy may follow in the wake of
the cerebral defects created for the purpose of exposing
the tumor. As yet no patients so treated have had
convulsions following the operation, if they were absent
before.
It is not always certain that the tumor is confined
entirely to the third ventricle. For example, in Case 8,
Group II, the tumor had passed through the foramen of
Monro and the extension in the lateral ventricle was
much larger than the tumor in the third ventricle. For the
removal of such a growth, the pineal approach would be
very embarrassing, perhaps impossible. In this instance
the filling defect in the lateral ventricle left no doubt of
the exact location of the tumor and of the character of
the operative approach.
For the anterior approach either the right or left side
may be chosen. Although there is little difference in the
choice, the right side is chosen in right-handed
individuals, and the left side in those who are left-
handed, unless there are reasons to believe that the
tumor may have extended to one side as in the above
case. If the tumor is suspected or known to have
extended to one side, the operative approach is made
upon that side. . . .
The size of the lateral ventricle is another very
important factor in determining the site of the operative
approach. In all of our cases there have been very large
lateral ventricles, such as would be expected with tumors
obstructing either the foramina of Monro or the aqueduct
of Sylvius. Large ventricles are absolutely essential to a
posterior (pineal) approach because room for the
operative attack is provided only by releasing fluid from
one or both lateral ventricles. It is conceivable that in the
early stages of primary tumors of the third ventricle the
lateral ventricles might not yet be sufficiently enlarged
to permit of this approach, but in the present state of our
diagnostic ability it is most unlikely that such an early
diagnosis would be made. But in the event that a tumor
should be diagnosed when the ventricles are small, the
anterior approach with resection of the frontal lobe
would afford ample room.
The larger tumors in the region of the third ventricle
and filling it secondarily usually show small lateral
ventricles and, therefore, practically preclude the
posterior approach, except perhaps to explore a tumor
along the falx. At first glance the statement that in the
larger tumors the lateral ventricles are smaller may
appear paradoxical. Although they cause the same
ventricular obstruction and should, therefore, produce
the same degree of hydrocephalus, the ventricles are
actually smaller because the bulk of the tumor
encroaches upon and fills or obliterates both lateral
ventricles. The primary tumors of the third ventricle are
usually so small that their actual volume is of little or no
importance in the creation of intracranial pressure,
which is due solely to the obstruction to the channels of
exit of the cerebrospinal fluid. Small ventricles with a
tumor of the third ventricle, therefore, strongly suggest a
large tumor and one arising presumably outside the third
ventricle. Moreover, such tumors-usually gliomata—are
much more common than the primary tumors in the third
ventricle. In the treatment of such large growths the
anterior approach, with cerebral resection, is necessary
(37).
 Dandy ended his monograph with the following
statement: "The mortality from the entire series of
extirpations, covering a period of eleven years, has been
33.3 per cent. However, in the past two and one-half years
fourteen of these tumors have been removed with a
mortality of 14.3 per cent. Except for occasional minor
effects, these patients make almost perfect recovery of all
functions (37).
After the publication of Dandy's book, the direct
operative removal of colloid cysts of the third ventricle
became the standard approach to the treatment of these
lesions (3) until the development of CT scanning and of
stereotaxic and ven-triculoscopic techniques offered other
possibilities for management (depending upon symptoms
and ventricular size), such as simply following the patient
with serial CT scans, shunting the lateral ventricle(s),
shunting the cyst, aspirating the cyst percutaneously, or
aspirating or removing the cyst endoscopically (10, 76,
112, 121). Direct operative excision also became the pre-
ferred treatment of other types of benign tumors of the
third ventricle such as epidermoid and dermoid cysts,
meningiomas (23, 111, 123), symptomatic
xanthogranulomas (68, 125), cho-roid plexus papillomas
(70), intraventricular craniopharyngiomas (69, 91, 96, 97,
99, 107, 137, 143, 149), and the subependymal giant cell
astrocytomas of tuberous sclerosis (12, 20, 86).
However, the removal of such tumors sometimes proved
difficult, especially when they were located primarily in
the posterior portion of the third ventricle or were adherent
to the hypothal-amus. It was found that operative injury to
the hypothalamus might result in diabetes insipidus.
(Incidentally, another condition studied by Walter Dandy
during his career was diabetes insipidus (40, 117)).
Problems of this sort were especially true before the
development of microsurgery and prompted Torkildsen in
1948 to publish a paper entitled, "Should Extirpation be
Attempted in Cases of Neoplasm in or near the Third
Ventricle of the Brain? Experiences with a Palliative
Method" (146). Torkildsen concluded as follows:
Attempts at the removal of neoplasms in regions of
the pineal gland and the 3rd ventricle of the brain are
associated with such a grave mortality rate that, if
possible, such operations should be avoided.
It is possible to treat patients with such lesions by
ventriculocisternostomy, with satisfactory results. I have
performed the operation in 8 cases of tumor in the pineal
region, with 1 postoperative death, and in 11 cases of
tumor in or near the 3rd ventricle outside the pineal
region, with 2 fatalities.
The above results show that the mortality rate by
this operation is far below that following attempts at
surgical extirpation of the tumors.
The fate of the patients depends primarily on the
malignancy of the neoplasm. Tumors of high expanding
energy infiltrating this region of the brain will in any
case cause the death of the patient within limited time. In
such cases no other operation can possibly save the life
of the patient.
Most of the tumors, however, are of very slow
growth, and the patients may live comfortably with the
neoplasm if the symptoms due to the obstruction of the
flow of the cerebrospinal fluid can be relieved. In my
series there are several cases in which no visible growth
of the neoplasm has taken place after intervals of 7 or 8
years.
In any case of tumor in the pineal region, neoplasm in
or near the 3rd ventricle, craniopharyn-gioma, and
stenosis of the Sylvian aqueduct whether due to
neoplasm or not, ventriculocisternostomy should be
carried out before any other surgical procedures are
undertaken (146).
Most neurosurgeons at that time took a similar approach
to third ventricular masses, namely, diagnosis by air study
and (unless a colloid cyst, choroid plexus papilloma,
epidermoid or dermoid cyst, meningioma,
craniopharyngioma, or subependymal giant cell
astrocytoma was suspected) treatment by radiation therapy
from an external source. Significant hydrocephalus was
treated by ventriculocisternostomy. Yet without a tissue di-
agnosis the neurosurgeon took the chance that the lesion
was benign and the radiation therapy inappropriate.
With the advent of microneurosurgery, the pendulum
then swung toward open operative exposure of the tumor
for diagnosis and, frequently, resection. Stein stated, "In
our experience with 46 patients encompassing all types of
third ventricular tumors, the surgical mortality has been
under 5% and approximately 30% of the tumors have been
benign, encapsulated, and resectable" (139). But with such
a direct approach the surgeon did add to the patient's im-
mediate morbidity and mortality risks and took the chance
of opening up a tumor that would be more appropriately
treated with radiotherapy or chemotherapy.
Fortunately, the subsequent development of CT-guided
stereotaxic biopsy techniques (5, 87, 109, 118), the
discovery of tumor markers (126, 134), and the
improvement of CSF cytodiagnosis (9) have provided the
neurosurgeon the means of being relatively certain of the
diagnosis before the decision is made about definitive
treatment. In addition, if surgical resection is chosen, the
neurosurgeon of today has more tools than ever before to
accomplish this goal, such as micro-surgical instruments,
the ultrasonic aspirator,
and various surgical lasers. Kelly and his colleagues are
currently perfecting a CT-guided stereotaxic system that
uses a computer to direct and monitor tumor removal by
laser energy (88, 89).
Cysticercosis of the Third Ventricle
Cysticercosis can involve the central nervous system in
various ways (54, 98, 100, 140). One of these is by the
development of cysticercus cysts within the ventricular
system. The larval forms pass through the choroid plexus,
develop in the ventricles as cysts, and migrate caudally
through the ventricular system. When these cysts are
within the ventricles, they usually do not incite an
inflammatory response, but when they reach the basilar
cisterns they usually evoke a significant adhesive basilar
arachnoiditis. Thus, over the years, emphasis has been
placed on the surgical removal of such cysts while they
are still within the ventricular system.
The cysts are ordinarily diagnosed by positive contast
ventriculography, now with CT imaging. They frequently
are multiple, and the exact route of operative attack is
determined by their locations and sizes. When such cysts
have been discovered within the third ventricle, the same
surgical approaches have been used as for third
ventricular tumors.
Ventriculoscopy and cyst removal have been de-
scribed, but the latter has been reported to be associated
with breakage of the cyst with intraventric-ular
spillage, which can evoke ventricular inflammation.
Exposure . . . permits gradual removal of the lesion into
the aperture and complete delivery of the cysts... . The
lesions seem to conform to the surgical egress route but
may need to be assisted in their delivery by the use of
hydraulic dissection, a mild Valsalva maneuver by the
anesthesiologist, and gentle teasing with nonpenetrating
instruments. When the cysts are approached surgically
in the lateral and third ventricles, the use of a slender
Pasteur pipette with gentle suction is reported to extract
the lesions effectively. . . . Patients are best treated
intraoperatively by corticosteroid medication. Under
these circumstances, rupture has not excited adverse
reactions. . . . Results in the management of exclusively
intraventricular cysts are excellent, especially when
these are isolated or solitary. The surgical management
of the other forms appears to be primarily palliative
(140).
Pineal Tumors
In 1915, Walter Dandy published a paper, "Extirpation
of the Pineal Body," that dealt with pinealectomy in the
dog (25). Dandy concluded:
1. Following the removal of the pineal I have
observed no sexual precocity or indolence, no adi-
oposity or emaciation, no somatic or mental precocity or
retardation.
2. Our experiments seem to have yielded nothing
to sustain the view that the pineal gland has an
active endocrine function of importance either in
the very young or adult dogs.
3. The pineal is apparently not essential to life
and seems to have no influence upon the animal's
well being. [25]
Of more importance to the subsequent development of
the surgical exposure and resection of pineal tumors in
humans, Dandy noted, in comparing his new method to his
previous methods:
To be of practical value the pineal body must be more
easily reached and removed with greater certainty and
less mortality. Consequently a new and simple method of
attack has been evolved. Though more delicate and
requiring more painstaking care, it can be done almost as
easily as a canine hypoph-ysectomy. The new operation
can be done in less than one hour. It differs from the
preceding operation in that the pineal is reached from in
front through the third ventricle rather than from behind.
In this way the extensive bleeding consequent to
liberation of the vein of Galen is obviated, sidetracked as
it were, and the operation can be performed almost
bloodlessly. This is accomplished by dividing the
splenium of the corpus callosum in the midline for a
distance of about 2 cm. from its posterior terminus. This
exposes the transparent roof of the third ventricle which
is distended by the contained cerebrospinal fluid. A large
anemic area is visible in the midline of the roof of the
ventricle, between the two small veins of Galen. This is
perforated and the opening enlarged backward to the
origin of the vena Galena magna by releasing the blades
of the forceps. The entire third ventricle is thus brought
in full view and the pineal body is readily seen under the
origin of this vein, in the median quadrigeminal groove.
The pineal body can easily be grasped in the jaws of the
cupped biting forceps and completely removed (Figs.
1.16 and 1.17) (25).
Six years later, in 1921, Dandy published an account
entitled, "An Operation for the Removal of Pineal Tumors"
(30), a subject to which he returned in 1929 (34) and again
in 1936 (38). He began his 1921 paper in this way:
"Tumors of the pineal body have rarely been diagnosed and
substantiated. The total number of authenticated pineal
tumors is less than one hundred and almost all have been
accidental findings at necropsy" (30).
In his thorough review of the history of the surgery of
pineal lesions, Pendl (110) gives credit to Victor Horsley
(81, 82) as being the first to attempt to remove a pineal
tumor by direct surgical attack. Two such procedures (in
1905 and 1909), done through an infratentorial approach,
were unsatisfactory, prompting Horsley in 1910
 Figure 1.16. Canine pinealectomy. The upper drawing demonstrates the sple-nium
divided, exposing the roof of the third ventricle with its veins. The lower drawing shows
the method of perforation of the roof between the internal cerebral veins. (From Dandy
WE: Extirpation of the pineal body. J Exp Med 22:237-247, 1915.)

to recommend a supratentorial exposure with splitting of
the tentorium (81). Others also reported operations for
palliation of pineal tumors in 1908, 1910, and 1911 (110). *
According to Pendl (110), Ludwig Pussep (114) in 1910
was probably the first to reach a pineal tumor by a direct
surgical approach. Pussep exposed the cystic tumor of a 10-
year-old boy through an occipital approach by transecting
the transverse sinus and splitting the tentorium. He was able
to remove parts of the tumor, but the child died on the third
postoperative day.
In his neurosurgical textbook, Fedor Krause (92) "...
suggested in 1911 an infratentorial and supracerebellar
route for surgical exploration of the upper vermis and
quadrigeminal region. In 1913 he presented a 10-year-old
boy to the Medical Society in Berlin, from whom, 6 weeks
prior, he had resected a 4 cm pineal tumor. This was
achieved in the sitting position using an inf raten-torial-
supracerebellar approach. ... As was pointed out by Zulch. .
., this was the first report
of a successful extirpation of a tumor from the pineal
region" (110).
Pendl further reports that Brunner unsuccessfully
explored the posterior fossa of a patient with a
quadrigeminal tumor in 1911 and then the following year
decided to approach a pineal tumor in a cousin of the first
patient by a transcallosal route. "Because of severe venous
hemorrhage and difficulties in exposure, the tumor was not
reached and the operation abandoned" (110). Other
operations were proposed or attempted by various
surgeons, but without success (110).
Thus, the stage was set for Dandy's 1921 report of his
method of posterior transcallosal exposure of a pineal
tumor (Figs. 1.18 to 1.22):
The operation has been performed on three patients.
In the first instance a silent cerebellar tumor had
secondarily involved the region of the pineal body and
the corpora quadrigemina; after exposure of the tumor,
no attempt was made to remove it, because of its
infiltrating character. This case, how-
 Figure 1.17. Canine pinealectomy. The upper drawing shows that, after the defect in the
roof of the third ventricle is opened and widened, the pineal gland is well exposed. The
lower drawing illustrates the way the pineal gland is grasped with the biting forceps, the
jaws of which are also shown separately. (From Dandy WE: Extirpation of the pineal
body. J Exp Med 22:237-247, 1915.)

ever, showed that a good exposure of this region is
possible. On two subsequent occasions, tumors of the
pineal body have been completely removed. In one
case an encapsulated tubercle of the pineal body was
extirpated, the patient recovering only to die 8 months
later, presumably of the effects of other tubercles of the
brain. . . . The results of this case demonstrated not
only the feasibility of the removal of tumors of the
pineal body but also the absence (in this case at least)
of any injurious mental or physical effects due to the
operation.
The extirpation of the second pineal tumor was very
much more difficult. The tumor was much larger and
since the vena Galena magna and both small veins of
Galen passed directly through the tumor and could not
be dissected from it, the removal of practically all of
these veins was a prerequisite to enucleation of the
tumor. . . . The patient lived 48 hours, dying
presumably of the shock due to the magnitude of the
operation. His vitality was doubtless impaired by a
cerebellar operation which was performed 10 days
previously and at which the
tumor was found; but it was entirely inaccessible for
removal by this approach. . . . One must also consider
whether the complete removal of all the main trunks of
the intracranial venous system— the large vein of Galen
and both small veins of Galen—would be compatible
with life. I know of no previous instance in which these
veins have been removed or even ligated. In dogs I have
ligated the vena Galena magna without effect when the
ligation is distally placed but when proximally placed a
mild grade of hydrocephalus has resulted. . . . Whether
the collateral venous system in the human brain could be
developed to compensate for this tremendous loss can
only be surmised; it does seem doubtful, but there was
no alternative to the removal of these veins with the
tumor. [30]
In 1928, Otfrid Foerster published his experience with
the exposure of the quadrigeminal plate and pineal area in
three patients (60, 61).
A large occipital craniotomy, close to the superior
 Figure 1.18. Cross sectional diagram showing the various steps in the transcal-losal
removal of a pineal tumor. (From Dandy WE: An operation for the removal of pineal
tumors. Surg Gynecol Obstet 33:113-119, 1921.)
longitudinal sinus and the right transverse sinus, exposed
the occipital lobe; the dura was opened and reflected as
well over the sagittal and transverse sinuses; the
bridging veins were ligated and transected. The posterior
horn of the lateral ventricle was punctured by a cannula
with sufficient decompression to allow retraction of the
occipital lobe from the falx and tentorium. The splenium
corporis callosi was thus exposed. For better access to
the quadrigeminal area, the tentorium along the sinus
rectus could be cut and reflected laterally, and a few
centimeters of the splenium split. If the tumor on the left
was not sufficiently exposed, the falx could be incised to
better visualize the opposite side.
Foerster's first case, a 25-year-old man, was operated
on in 1927 with a total removal of a glioma and
subsequent full recovery. The second reported case,
operated on initially in 1923 with only a partial
evacuation of a cystic tumor, required a second ap-
proach. However, the well-exposed tumor could not be
removed from dense adhesions to the midbrain and the
patient died on the second postoperative day. In the third
case, the clinical signs indicated a pineal tumor; the
whole quadrigeminal area was exposed, but no tumor
and also no pineal gland was found (110).
In 1931, William Van Wagenen introduced an entirely
different approach to pineal tumor sur-
gery (150). He had exposed the tumor in his patient
through the dilated right lateral ventricle. The lateral
cortical incision had extended superiorly and posteriorly
from the posterior end of the superior temporal gyrus, and
the ventricle had been entered at the atrium. The
spongioblas-tic tumor had then been exposed through the
thinned medial ventricular wall and had been almost
completely removed.
Harris and Cairns in 1932 reported an unsuccessful
attempt to remove a pineal tumor through a suboccipital
exposure in 1930 (77). Six months after the initial attempt,
the tumor was successfully removed through a right
parietooccipital transcallosal approach.
In his 1932 monograph on intracranial tumors, Cushing
wrote:
"Personally I have never succeeded in exposing a pineal
tumour sufficiently well to justify an attempt to remove it.
Encouraging reports of such procedures, however, have
been made by W. E. Dandy of Baltimore (1921), by Otrid
Foers-ter of Breslau (1928), and I have personal knowl-
edge of two highly successful operations per-
 Figure 1.19. Exposure of the medial cerebral cortex before exposure of the corpus
callosum. A ventricular needle has been inserted to drain CSF from the lateral ventricle.
(From Dandy WE: An operation for the removal of pineal tumors. Surg Gynecol Obstet
33:113-119, 1921.)
formed by my former assistants, Dr. W. P. Van Wagenen
of Rochester, New York, and Mr. Hugh Cairns of
London" (22).
Pendl cites various sources to indicate that Ernest
Sachs removed a large cystic tumor from the pineal
region in 1926 and Max Peet removed a pineal tumor
through a right parietooccipital transcallosal approach in
1927 (110). By 1936, Dandy was able to comment on 10
personal cases (Figs. 1.23 to 1.25) (38), but he was
pessimistic:
Although an operative approach to the pineal region
was proposed by me in 1921 [30], it was not until a
decade later (1931) that the first pineal tumor was
successfully extirpated [37]. A disastrous toll of seven
fatal issues during this long period seemed almost to
indicate the futility of further efforts. Yet the same
approach was used successfully in a number of cases of
tumor of the third ventricle in which, though the lesion
was in the same general region, less serious difficulties
were offered. In addition to the aforementioned case,
successful extirpation has since been performed in two
others, thus indicating that the lesion is not entirely
hopeless, although it remains one of the most
dangerous of all intracra-nial growths. This seeming
success, however, is still further tempered by the fact
that in two of these
cases the tumor has since recurred, in one after two and
one-half years and in the other after three months. Only
the last of the three patients remains well, and the period
after operation has been only four months. Since the
growth in the first case was solid and encapsulated and
was extirpated intact, I expected a permanent cure.
However, the growth was teratomatous, containing, in
addition to the pineal element, ciliated columnar cells of
ependymal origin, cartilage and tissue resembling the
salivary gland. The tumor in the second case was much
larger; it was so soft and cellular and its capsule so thin
that it could not be shelled out intact but had to be
removed in fragments. The patient died at her home
three months later, but permission for necropsy was not
obtained. It is, perhaps, more conceivable that
cicatrization at the mouth of the aqueduct caused her
death than that such rapid recurrence was responsible.
The tumor of the third patient was a pure pinealoma and
was perfectly encapsulated. It is unbelievable that it can
recur, although I felt equally secure in such a prediction
for the first case. In that instance, however, the tumor
was a teratoma, whereas in this case the growth was a
pure pinealoma.
Reports of three cases of pineal tumor in which the
patient survived the operation are appended. Particularly
of interest are the remarkable transient postoperative
sequelae and the absence of recognizable effects arising
from the removal of part or all
Figure 1.20. After the bridging veins have been ligated and divided, the cerebral
hemisphere is retracted to expose the falx and the corpus callosum. (From Dandy WE:
An operation for the removal of pineal tumors. Sura Gynecol Obstet 33-113-119, 1921.)
Figure 1.21. The inferior longitudinal sinus has been clipped and the falx has been
divided inferiorly. The corpus callosum has been split longitudinally to expose the
pineal tumor, the internal cerebral veins, and the vein of Galen. (From Dandy WE: An
operation for the removal of pineal tumors. Surg Gynecol Obstet 33:113-119, 1921.)
Figure 1.22. After removal of the pineal tumor, the intact roof of the third ventricle is
seen. (From Dandy WE: An operation for the removal of pineal tumors. Surg Gynecol
Obstet 33:113-119, 1921.)
Figure 1.23. Drawings showing the operative procedure in the removal of a teratoma
from the pineal region. (From Dandy WE: Operative experience in cases of pineal
tumor. Arch Surg 33:19-46, 1936.)
Figure 1.24. Drawings illustrating the method of producing more adequate exposure of a
large tumor in the pineal region by resecting the occipital lobe and, when necessary, the
lower part of the falx, parts of the right and left sides of the tentorium, the vein of Galen,
and the straight sinus. (From Dandy WE: Operative experience in cases of pineal tumor.
Arch Surg 33:19-46, 1936.)
 Figure 1.25. Operative sketches of the removal of a pineal tumor, showing that the right
internal cerebral vein had to be divided. (From Dandy WE: Operative experience in
cases of pineal tumor. Arch Surg 33:19-46, 1936.)

of the main trunks of the internal venous system of the
brain (38).
Many other surgeons have been involved in the
development of the surgical treatment of pineal tumors
since 1930, as mentioned in the publications of Thomson
(145), Schmidek (133), Zulch (162), Sano (126), and
Pendl (110). As with tumors of the third ventricle, the
high operative morbidity and mortality of direct exposure
and resection of pineal tumors led most neurosur-geons
for the next 40 years to use the more conservative course
of CSF shunting and radiation therapy (1, 48, 52, 79, 116,
146). This ap-
proach to treatment was strengthened by the development
of better techniques of CSF shunting and of radiotherapy
(7, 59, 113, 131). Then, after the advent of
microneurosurgery, interest in direct surgical treatment
began to return (122, 138, 153, 160). However, the need
for operative exposure and resection of these lesions has
been modified by the development of CT-guided ster-
eotaxic biopsy techniques, the increase in reliance on
biochemical tumor markers and CSF cytology for the
diagnosis of pineal tumors, and a revival of interest in the
implantation of radiation sources for the treatment of
intracranial neoplasms (5, 9, 63, 85, 103, 109, 118, 126,
134).
Operative Approaches to the Third Ventricle
As noted previously, Dandy exposed the third ventricle
for ventriculostomy by a subfrontal and later by a
transtemporal approach. For anterior third ventricular
tumors, he preferred a frontal transcortical route, and for
posterior third ventricular and pineal tumors, a
parietooccipital transcallosal approach. Dandy thought that
no neurological deficit occurred as a result of either
approach (37, 71). However, "if the splenium of the corpus
callosum is completely sectioned, appropriate testing will
reveal that most postoperative patients cannot read in their
left visual fields, even when all other neurological
functions have returned to normal. This phenomenon, ap-
propriately called hemialexia, was first reported by
Trescher and Ford in 1937 [147]. Their patient had the
posterior corpus callosum split by Walter Dandy for
removal of a colloid cyst of the 3rd ventricle. . . . Since that
time the reality of the deficit has been proven repeatedly. .
." (71).
These and various other operative approaches to the
region of the third ventricle have been developed, primarily
since Dandy's time. Many of these have been discussed by
Rhoton and Yamamoto (Fig. 1.26) (119, 120, 161) and by
Antunes et al. (4), as well as at a recent international
symposium organized by Madjid Samii and held in
Hannover, West Germany (83).
The transsphenoidal and certain subfrontal (i.e.,
subfrontal subchiasmatic or subfrontal transsphenoidal)
approaches permit access to the sella turcica and
chiasmatic area but do not ordinarily permit visualization
within the third ventricle. The same is true of the more
lateral subfrontal and subtemporal approaches. Tumors can
be drawn down from the third ventricle but entry into the
ventricle is quite limited by the angle of entry and the
important structures that are interposed (optic nerves,
chiasm, and tracts; arteries of the circle of Willis and their
branches; hypothalamus; pituitary stalk and gland; etc.).
The occipital transtentorial and infratentorial
supracerebellar approaches have been used pri-

Figure 1.26. A midsagittal view of the head, showing the basic operative approaches to
the third ventricle. (From Rhoton AL Jr, Yamamoto I, Peace DA: Microsurgery of the
third ventricle: Part 2. Operative approaches. Neurosurgery 8:357-373, 1981.)
marily to expose tumors in the region of the pineal gland.
The early history of these approaches has been
considered, and the reader is referred to the publications
of Thomson (145), Schmidek (133), Zulch (162), Sano
(126), and Pendl (110) for details about the subsequent
development of these procedures.
Among the subf rental approaches, the one that has
been somewhat helpful in dealing with low anterior third
ventricular tumors has been the one that involves entry
into the ventricle through the lamina terminalis. Such
entry was used for third ventriculostomy, as previously
discussed. King (91) and Suzuki et al. (142) have outlined
the history of its use for tumors such as intra-ventricular
craniopharyngiomas.
The posterior transventricular approach has been of
limited value. However, the anterior transventricular route
through a dilated lateral ventricle to high anterior third
ventricular tumors such as colloid cysts has remained
useful (52).
Transcallosal operations were done occasionally after
Dandy developed the posterior transcallosal approach (16,
17, 50-52, 72, 73, 108, 151), but it was not until the
introduction of microsurgical techniques (101) that the
transcallosal route became popular (52, 96, 97, 136). The
anterior transcallosal approach has become a preferred
method of access to the third ventricle (Sano even uses it
for pineal region neoplasms (126, 127)), especially since
it has been found that anterior or middle transcallosal
operations may not cause behavioral or neurological
abnormalities (67, 159). The emphasis in recent years has
been on the refinement of techniques for opening the roof
of the third ventricle (4, 6, 13, 21,47,78,83,93, 154).
Concluding Remarks
The central location of the third ventricle and the pineal
gland within the brain have lent them a certain mystery.
Descartes thought of the pineal gland as "the seat of the
soul" (19). Surgeons dealing with lesions of the third
ventricle have noted that such lesions (or injuries
resulting from the attempts to remove them) may cause
alterations in consciousness (14, 15, 42). In fact, Walter
Dandy's last paper, published 3 months after his death,
contained his speculations about the location of the
"conscious center" in the brain, based on a study of 10 of
his patients, 2 of whom were rendered unconscious by
the removal of tumors from the third ventricle (42).
The mysteries surrounding lesions of the third
ventricular region are slowly being solved. The pioneering
work of Walter Dandy and others has laid the foundation
for our present methods of diagnosing and treating these
conditions. These current methods and the future
advancements they may permit are detailed in the rest of
this book.
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2
Comparative Anatomy of the Third
Ventricular Region
E.Leon Kier,M.D.
What is often more condensed or more concealed in one species Nature displays more clearly and openly in
another.
De Graaf (1664) quoted by Cole (1944)

Lateral Walls Commissures

Hypothalamus Limbic System
Thalamus (Massa Intermedia) Lamina Terminalis
Intraventricular Foramen (Monro) Anterior Commissure
Floor Paraterminal Body
Optic Chiasm Septal Area
Optic Recess Hippocampal Commissure
Infundibular Hippocampus
Recess Saccus Fornix
Vasculosus Tuber Corpus Callosum
Cinereum Subiculum
Hypophyseal Indusium Griseum
Recess Longitudinal striae
Hypophysis Septum Pellucidum
Mammillary Bodies Cavum Septi Pellucidi
Premamillary Arteries
Recess Principles of Cerebral Vascular
Postmamillary Development
Recess Midbrain Delivering Arteries
Roof and Posterior Wall End Arteries
Paraphysis Recurrent Artery of Heubner
Velum Transversum Perforating end arteries of Hypothalamus
Dorsal Sac (Saccus Dorsalis) and Thalamus
Suprapineal Recess Arterial Circle (Willis)
Parencephalon Anterior Cerebral
Habenulae Anterior Choroidal
Pineal (epiphysis) Posterior Cerebral
Parietal Eye Posterior Choroidal
Pineal Recess Veins
Parapineal
Posterior Commissure
Tela choroidea (Velum
Interpositum)
Optic Lobes (Corpora Bigemina)
Auditory Lobes
Superior Colliculi
Inferior Colliculi
Quadrigeminal Plate (Corpora
Quadrigemina)
Mesencephalic Ventricle
Optic Ventricle
Aqueduct
Aqueductal Ampulla
 Comparative anatomical knowledge can enhance and
enliven the study of neuroanatomy and neuroradiological
anatomy (11). The study of developmental and adult
neuroanatomy is thus transformed from memorizing a large
number of anatomical structures to a meaningful under-
standing of many features of the human brain (32, 33).
This meaningful understanding is based on the slowly
evolving needs of different vertebrates manifested in
various evolutionary modifications of the central nervous
system.
The study of comparative anatomy permits a relatively
slow longitudinal study of the developing human central
nervous system. This slower pace is not available in human
embryos that "recapitulate" many stages very quickly and
transiently (13).
In addition, many congenital, metabolic, toxic, and Figure 2.2. Midsagittal section of the third ventricle. The
degenerative disorders may be viewed through the floor extends from the optic chiasm to the aqueduct. The
anterior wall extends from the optic chiasm to the foramen
perspective of evolution (67). Certain disorders such as of Monro (interventricular foramen). The roof extends
developmental hypoplasias involve new phylogenetic from the foramen of Monro to the suprapineal recess. The
structures while sparing the older phylogenetic section of posterior wall extends from the suprapineal recess to the
the nervous aqueduct. (From Yama-moto I, Rhoton AL, Pierce RA:
Microsurgery of the third ventricle: Part 1. Microsurgical
anatomy. Neu-rosurgery 8:333-356, 1981.)

Figure 2.1. Diagram of the medial aspect of the left cerebral hemisphere demonstrating
the majority of the structures of the limbic system. Note that many of these complex
structures are part of the anatomy of the third ventricular region. From Warwick R,
Williams PL (eds): Gray's Anatomy. Philadelphia, WB Saunders Co, 1980, British ed 36.
system. In contrast, anomalies of the central nervous
system such as holoprosencephaly and Dandy-Walker
selectively affect the oldest phy-logenetic structures while
sparing the newer ones.
The merit of a comparative anatomical study is
particularly apparent in the elucidation of the complex
anatomy of the commissures in the region of the third
ventricle (Fig. 2.1). In addition the various forms of corpus
callosum dysgenesis are clarified by the knowledge of its
evolutionary changes.
In this chapter an effort was made to group the various
structures according to the usual anatomical and
neurosurgical landmarks of the third ventricle (83, 89)
(Fig. 2.2). However, the roof and posterior wall structures
are grouped together because in many vertebrates the
posterior wall cannot be defined as a separate structure.
The complex evolution of the commissures and cer-
tain principles governing vascular evolutionary changes are
described in separate sections.
Lateral Walls
Phylogenetically the hypothalamus is probably the
oldest cerebral structure with remarkably similar nuclear
differentiation and fiber connections in all vertebrates (67).
Evidence of neurose-cretory activity is present even in the
simplest invertebrates. In certain worms the entire brain
could be considered to be a form of the hypothalamus.
Internal neurosecretory control preceded the evolution of
special sensory and locomotor systems relating the
organism to the outside world. Thus the phylogenetic
variability of the evolving hypothalamus is manifested in
the variability of the floor of the third ventricle.
The evolving thalamus affects the topography of the
phylogenetically changing lateral ventricles and
commissures (33). In addition, the evolv-

Figure 2.3. Ventrodorsal roentgenograms of a shark (A) and a frog (B) and the brain of
an iguana (C), rabbit (D), dog (E), and monkey (F) with barium-cast ventricles. Except
the shark, all other specimens demonstrate a small interven-tricular foramen. The wider
thalamic part is superimposed on the narrower hypothalamic part of the third ventricle.
In the shark and the frog the lateral ventricles are anterior to the interventricular
foramen. In the iguana the posterior pole of the lateral ventricle is now posterior to the
interventricular foramen (arrow). In the rabbit the major part of the lateral ventricle is
posterior to the interventricular foramen. From Kier EL: The cerebral ventricles: a
phylogenetic and ontogenetic study. In Newton TH, Potts DG (eds): Radiology of the
Skull and Brain, vol. 3, Anatomy and Pathology, St. Louis, The CV Mosby Co, 1977, pp
2787-2914.
ing thalamus and lateral geniculate body contribute to the
phylogenetic changes involving the anterior and posterior
choroidal arteries (32). The interthalamic adhesion (massa
intermedia) varies in size, and the hypothalamus and
thalamus create minor differences in the lateral walls of the
third ventricle. Except for the frog and iguana, the
vertebrates studied demonstrate that the hypothalamic part
of the third ventricle is narrower than the thalamic part
(Fig. 2.3). In addition, the evolution of the cerebrum
changes the topographic relationship of the lateral ven-
tricles and the intraventricular foramen (Fig. 2.3).
In the shark and the frog the lateral ventricles are
anterior to the intraventricular foramen. In the iguana the
posterior pole of the lateral ventricle is posterior to the
intraventricular foramen. In the rabbit the major part of the
lateral ventricle is posterior to the intraventricular foramen.
The comparative study demonstrated that all specimens
except the shark had small interven-ticular foramina (Fig.
2.3). It seems that the corpus striatum is the major structure
reducing the size of the interventricular foramen and not
the evolving fornix and thalamus. The latter structures are
not present in the frog or iguana.
Floor
An optic chiasm is present in the floor of the
diencephalon of all vertebrates except bony fish. In the
latter the decussation of the optic nerves is between the
eyes and the diencephalon (25). The optic chiasm is a
major modifier of the floor of the third ventricle because
its size and location affect the size and configuration of
the optic and infundibular recesses (Figs. 2.4 to 2.11).
The number of optic nerve fibers, the extent of mye-
linization, and the degree of decussation in the optic
chiasm vary among the different vertebrates (59, 67). The
following examples demonstrate the extensive variability
that exists in the number of optic nerve fibers present and
the importance and development of the visual system:
lamprey, 5,217; frog, 29,000; turtle and alligator,
105,000; shark, 113,000; cat, 119,000; dog, 154,000;
rabbit, 265,000; sheep, 649,000. In some primates and
birds in which sight is the dominant sense, the number of
optic nerve fibers reaches or exceeds 1 million. In the less
developed vertebrates the optic nerve fibers are poorly
myelinated. In advanced teleosts, birds, and most
terrestrial vertebrates the majority of fibers are heavily
myelinated. The presence of myelin seems to be associated
with improved visual function.
Nearly all optic nerve fibers in nonmammalian
vertebrates and in some lower vertebrates decussate in the
optic chiasm. The crossing of the optic fibers at a
primoridal chiasm was an early evolutionary development.
The presence of axons that crossed between the epithelium
of the primitive photoreceptor—the precursor of the eye—
and the effector system of the opposite side of the body
permitted the primitive prevertebrate to move away from a
threatening photic stimulus. The evolution of the two eyes
in the non-mammalian vertebrates, each with its own mo-
nocular field of vision, is postulated to have necessitated
the decussation of the optic fibers. Without the decussation
the segments of a visualized object would be incompatibly
recombined in the brain. In mammals the number of
crossing optic nerve fibers is reduced progressively. This
reduction is associated with the changing axis of vision and
the development of binocular fields of view. In rodents,
with laterally placed eyes and
 Figure 2.4. Sagittal section of the brain of a shark with barium-cast ventricles. The roof
of the third ventricle and its recesses are not covered by the cerebrum. The anterior
commissure is present. The dorsal sac is the homologue of the suprapineal recess in the
human. The infundibular recess in the shark is the ventricular extension into the inferior
lobes of the hypothalamus. Note the large optic ventricle. Only the proximal end of the
pineal recess is seen.

minimal overlapping of the monocular fields of vision,
only a small number of fibers do not decussate. At least
one-third of the fibers are nondecussating in carnivores and
primates, with frontally placed eyes and overlapping fields
of view. In primates nearly half the fibers do not decussate.
This degree of nondecussation is one of the important
factors that allow two identical retinal images to be
transferred to the brain, producing the highly evolved
stereoscopic vision of primates.
All of these factors affect the size and shape of the optic
chiasm and result in variation of the optic and infundibular
recess. The optic recess seems to be a residual space on the
floor of the
third ventricle whose formation, shape, and size are the
result of the varying indentation of the ventricular floor by
the chiasm (Figs. 2.5, 2.7 to 2.10, and 2.13 to 2.17).
The infundibular recess, however, is a true extension of
the third ventricle that undergoes evolutionary
modifications, ranging from that seen in the shark to that
seen in mammals. The infundibular recess is a funnel-
shaped extension of the third ventricle extending through
the hypothalamus to end in the hypophysis. The infun-
dibular portion of the hypothalamus and its lumen, the
infundibular recess, vary greatly among the different
vertebrates (Figs. 2.4 to 2.20).
In the lamprey, which is without an infun-
Figure 2.5. Sagittal section of the brain of a frog with barium-cast ventricles. The roof of
the third ventricle and its recesses are not covered by the cerebrum. The anterior and
hippocampal commissures have developed in the paraterminal body. The infundibular
recess is incompletely filled, and its full extent is seen in Figure 2.13. The
mesencephalic and optic ventricles are no longer a single large cavity.

Figure 2.6. Sagittal section of the brain of an iguana with barium-cast ventricles. The
posterior pole of the cerebrum overlaps the roof of the third ventricle except for the
dorsal sac—the homologue of the suprapineal recess. As a result the paraphysis, velum
transversum, and dorsal sac are angled posteriorly before reaching the dorsal surface of
the brain. The pineal body is large. Note the hippocampal commissure dorsal to the
anterior commissure. The cast of the large infundibular recess was partially damaged
during dissection. It extended to fill the area outlined by the arrows.

45
 Figure 2.7. Sagittal section of the brain of a rabbit with barium-cast ventricles. The
enlarged cerebrum covers the entire third ventricle and superior col-liculus. A new
commissure, the corpus callosum, is present. Note the junctional zone (crossed arrow)
where the posterior margin of the corpus blends into the subiculum dorsal to the
hippocampus. The septum pellucidum area is still small. The large suprapineal recess
was damaged during dissection. The direction of the long axis of the suprapineal recess
changes from the iguana to the rabbit. Note the recesses of the superior and inferior
colliculi, the remnants of the optic ventricle.

dibulum, the homologue of the neural lobe of the
hypophysis is a simple plate of tissue that lies on the floor
of the diencephalon (64). In the various fishes the
hypothalamus is highly developed and extends ventrally to
the midbrain to form two distinct structures, the inferior
lobes of the hypothalamus (Fig. 2.21). The prominent
inferior lobes of the hypothalamus in the shark surround a
large ependymal-linked infundibular recess (Figs. 2.4 and
2.12).
An additional unique structure in fishes is the saccus
vasculosus, a highly vascularized vesicle with
neurosensory cells whose lumen is continuous with the
infundibular recess (Figs. 2.4 and 2.12). The saccus is
largest in deep sea fishes,
small in shallow water fishes, and absent in amphibians
and other terrestrial vertebrates. Its function probably
relates to perception of the pressure of intraventricular
fluid relative to the depth of water and influences the size
of the swim bladder (67).
In amphibians and reptiles the hypothalamus is a
relatively small structure consisting largely of the tuber
cinereum (55) (Figs. 2.22 and 2.23). The small size is a
result of the absence of the saccus vasculosus and the
limited development of gustatory impulses (30). The
largest hypothalamus is present in teleosts and mammals.
In mammals the tuber cinereum may be divided into
median and lateral eminences. Of note is
 Figure 2.8. Sagittal section of the brain of a cat with barium-cast ventricles. The corpus
callosum is further developed, especially posteriorly, where the sple-nium overlaps the
suprapineal recess. Note the anteroposterior axis of the supra-pineal recess and its
curvature around the splenium (arrouj). The fornix is elongated and arched under the
corpus callosum. The corpus callosum is thin. The presence of the premamillary and
postmamillary recesses relates to the variable development of the mamillary bodies.

the prominent size of the infundibular recess in many
nonhuman vertebrates (Figs. 2.4 to 2.7). The
hypophyseal recess in the cat (Fig. 2.16) is of interest
because it represents the residual cavity of the
infundibular recess within the developing
neurohypophysis. The hypophyseal recess has been
observed by Levinger and Edery (42) and apparently is a
frequent finding in adult cats (35). Only two cases of
persistence of the infundibular recess in the adult human
have been reported (10, 35). The varied appearance of
the mammalian infundibular recess and the presence of
premamillary and postmamillary recesses are
manifestations of the varied development of the
components of the hypophysis and the size of the
mamillary bodies (Fig. 2.9). In the cat and the dog the
pars distalis of the hypo-
physis, originating from Rathke's pouch, extends much
more caudally around the pars neur-alis than in the human
(56). The pars intermedia, which in the human is limited to
the rostral aspect, surrounds the pars neuralis completely in
the dog and cat.
The mamillary body is probably premordial in teleosts
and amphibians. It can be identified in reptiles, birds, and
mammals. In the rat it is a band of gray matter continuous
in the midline. In humans the mamillary body is relatively
larger than in other primates. The posterior inferior
recess—demonstrated by Westergaard (84) in the guinea
pig, the hamster (85), and the rat (86)—seems to be a
manifestation of the previously mentioned varied
development of the hypophysis and mamillary body.
Figure 2.9. Sagittal section of the brain of a dog with barium-cast ventricles. The corpus
callosum is larger. Note the hippocampus, which is present ventral to the splenium and
fornix. The suprapineal recess, the pineal body, and the colliculi are in a more ventral
position.
Figure 2.10. Sagittal section of brain of a monkey with barium-cast ventricles. The
corpus callosum is increased in size. The septum pellucidum is enlarged. The cavum
septi pellucidi is partially filled with barium. The pineal body is wedged between the
splenium and the corpora quadrigemina. The smaller suprapineal recess is associated
with the larger splenium. The optic chiasm is large.
Figure 2.11. Sagittal section of the brain of adult human. The corpus callosum is
markedly enlarged and arched. The splenium is posterior to the thalamus. Note the
relative reduction in the size of the quadrigeminal plate.
Figure 2.12. Lateral roentgenograms of a shark (A) and of the brain of a shark (B) with
barium-cast ventricles. The ventricular system has a linear arrangement. The
intraventricular foramen is large. Contrast (arrow) has leaked into the ventral aspect of
the medulla.
Figure 2.13. Lateral roentgenograms of a frog (A) and of the brain of a frog (B) with
barium-cast ventricles. The ventricular system is still linear with the entire lateral
ventricle anterior to the interventricular foramen, which is small.
Figure 2.14. Lateral roentgenograms of an iguana (A) and of the brain of an iguana (B)
with barium-cast ventricles. The linearity of the ventricular system is no longer present
and the lateral ventricles are dorsal to the third ventricle. Note the molding of the lateral
ventricle with the presence of frontal and temporal horns.
 Figure 2.15. Lateral roentgenograms of a rabbit (A) and of the brain of a rabbit (B) with
barium-cast ventricles. Note the large suprapineal recess and massa intermedia.

In the midbrain of the shark, an acoustico-lateral line oped than in bony fish. In reptiles, midbrain structures are
and trigeminal fibers, nuclei of the trochlear nerve, and a demonstrated, suggestive of mammalian differentiation.
few fiber tracts are present. In amphibians the midbrain is The reticular formation in reptiles has changed to a nuclear
less devel- mass that
Figure 2.16. Lateral roentgenograms of a cat (A) and of the brain of a cat (B) with
barium-cast ventricles. The suprapineal recess is in a more caudal position as a result of
enlargement of the splenium of the corpus callosum. The central cavity of the
hypophysis is filled via the infundibular recess.
Figure 2.17. Lateral tomographic roentgenogram of a monkey (A) and a roent-genogram
of the brain of a monkey (B) with barium-cast ventricles. Note the small size and caudal
position of the suprapineal recess. The optic recess is very small because of the large
chiasm and was visualized only by tomography.
Figure 2.18. Ventral views of the brains of shark (A), frog (B), rabbit (C), cat (D), and
sheep (£) demonstrating evolutionary modifications in the relationship of the chiasm,
hypothalamus, and hypophysis. The hypothalamus is no longer visible in the cat and
sheep.
 constitutes a primordial red nucleus. In mammals the red
nucleus becomes a prominent structure. The cerebral
peduncles increase progressively as the corticopontine,
corticobulbar, and corticospinal tracts enlarge during
cerebral evolution. The substantia nigra also enlarges pro-
gressively in mammals. The foregoing evolutionary
changes are mani-
Figure 2.20. Diagram of the third ventricle and neighboring
structures of a lizard to show the various structures of the

Figure 2.19. Schema to show probable evolutionary

changes in the vertebrate pituitary gland. Arrow extending
from the median eminence to the pars distalis represents
the hypophyseal portal system. CAU, caudal division of
the avian interior lobe; CEP, cephalic division of the
same; PPD, proximal pars distalis; RPD, rostral pars
distalis; VL, ventral lobe of the elasmo-branch pituitary; roof including the dorsal (parietal) eye. (From Romer AS:
SV, saccus vasculosus. (From Romer AS: The Vertebrate The Vertebrate Body. Philadelphia, WB Saunders Co,
Body. Philadelphia, WB Saunders Co, 1970, ed 4.) 1970, ed 4).

Figure 2.21. Lateral view of the brain of a shark demonstrates the major subdivisions of
the brain. The roof of the diencephalon is visible and is interlaced by a prominent venous
plexus.
 Figure 2.22. Lateral view of the brain of a frog shows the linearity of the major
subdivisions of the brain. The forebrain (cerebrum) demonstrates a small cerebral
hemisphere (arrow), which begins to overlap the diencephalon. The relatively small
hypothalami of the amphibians and reptiles consist largely of the tuber cinereum.

Figure 2.23. Lateral view of the brain of an iguana. The linear arrangement of the
subdivisions of the brain is no longer present. The forebrain (cerebrum) is increased in
size and dorsally overlaps the diencephalon. Only the ventral hypo-thalamus and
hypophysis are still visible.

fested in the increased size of the midbrain ventral to the
mesencephalic ventricle and aqueduct. In the shark and the
frog the floor of the midbrain is sagittally smaller than
either the optic lobes or the spinal cord (Figs. 2.4 and 2.5).
In the iguana
the floor of the midbrain is enlarged and is greater than the
optic lobes in sagittal height (Fig. 2.6). The mammalian
midbrain is greatly increased in size and is even larger
sagittally than the spinal cord (Figs. 2.7 to 2.11).
Roof and Posterior Wall
In the shark (Figs. 2.4 and 2.12) the following structures
are identifiable: paraphysis, velum transversum, dorsal
sac, pineal recess, and ha-benular and posterior
commissures. The paraphysis and velum transversum are
choroid plexus structures (73).
The paraphysis is an extraventricular choroid plexus. In
the shark it is a dorsal evagination with origin in the
anterior end of the roof of the third ventricle (Fig. 2.4).
The paraphysis curves around the posterior pole of the
cerebral hemisphere and its cavity communicates freely
with the third ventricle (Fig. 2.4 and 2.12).
The velum transversum is a modified choroid plexus
that originates in the roof of the third ventricle, projects
into the ventricle, and serves as an arbitrary border
between the diencephalon and the telencephalon (Fig.
2.4).
In the frog the paraphysis is a prominent ex-
traventricular structure (Fig. 2.5). It is cone-shaped and
protrudes dorsally from the anterior end of the roof of the
third ventricle (73). The numerous villi of the
intraventricular choroid plexus are attached to the roof of
the third ventricle around the narrow orifice of the pa-
raphysis. These villi are seen as filling defects in casts of
the ventricles (Figs. 2.5 and 2.13). A distinct velum
transversum does not exist in the frog (28).
The dorsal sac (saccus dorsalis) is the thin-walled roof
of the third ventricle in front of the habenulae. It is also
called the parencephalon (30). Whether the term
parencephalon includes the velum transversum and
paraphysis is not clear. The dorsal sac is a large,
distensible structure in the shark (Figs. 2.4 and 2.12).
The present investigation did not reveal a dorsal sac in
the frog. This absence may relate to the relatively thick
roof of the third ventricle, which seems to be secondary
to the habenular commissure. Herrick (24) demonstrated
the habenular commissure as forming the roof of the third
ventricle between the paraphysis and the posterior
commissure.
Comparative investigation suggested that the dorsal sac
in the shark is the homologue of the human suprapineal
recess (33). The pineal and the dorsal sac—suprapineal
recess—maintain their adjacent relation from the shark to
the human. What does change is the direction of the long
axis of these two structures because of overlapping of the
third ventricle by the cerebrum and corpus callosum. In
the shark the dorsal sac has a ventrodorsal axis (Fig. 2.4).
In the iguana
the proximal end of the dorsal sac is angled posteriorly by
the posterior pole of the enlarged cerebrum (Fig. 2.6). The
axis of the large supra-pineal recess in the rabbit is more
posteriorly directed (Fig. 2.7 and 2.15). In the cat and the
dog, because of the great enlargement of the corpus
callosum, the long axis of the suprapineal recess has an
anteroposterior direction (Figs. 2.8, 2.9, and 2.16).
The shape and size of the suprapineal recess are related
to the size of the corpus callosum. The increasing size of
the splenium, as seen from the cat to the monkey, is
associated with a concomitant reduction of the suprapineal
recess (Figs. 2.8 to 2.10, 2.16, and 2.17).
The habenulae are relatively large, paired structures in
vertebrates with a small forebrain (67). The habenulae are
especially developed in vertebrates that rely heavily on
olfaction, such as sharks and bloodhounds. In humans,
because of the development of the neocortex and the rel-
ative unimportance of olf action, the habenulae are the
smallest. The habenulae may have an important function in
neonatal feeding reactions. An unusual feature in the
central nervous system is the asymmetry of the habenulae.
In sharks and frogs the left habenula is larger. In birds and
mammals, habenular symmetry is variable.
The pineal gland in the shark is a long and slender
structure whose distal end is situated in a depression in the
cartilaginous brain case (Fig. 2.4).
In the frog the pineal is a long slender nerve structure
extending from the roof of the diencephalon through the
parietal foramen in the roof of the skull. It terminates in the
frontal organ, situated under the calvarial skin (80). The
frontal organ in the frog is a poorly differentiated parietal
eye (67). Jolie (28) and van de Kamer (80) demonstrated a
small pineal cavity situated within the diencephalon of the
frog. This location may explain why the pineal recess was
not seen in the studied specimens.
In the iguana the striking evolutionary changes of the
reptilian brain are demonstrated. The cerebrum has
increased to such a degree that it completely overlaps the
roof of the third ventricle (Figs. 2.6, 2.24, and 2.25). Only
the distal end of the dorsal sac and the dorsal tip of the
pineal gland remain visible on the dorsal aspect of the
brain. In the shark the paraphysis curves anteriorly and the
dorsal sac has a straight dorsal course (Fig. 2.4). In the
iguana these two structures are angled posteriorly around
the posterior
 Figure 2.24. Lateral view of the brain of a rabbit. In the rabbit the neopallium of the
cerebrum has enlarged to such a degree that it dorsally overlaps the diencephalon and
mesencephalon. None of the diencephalic structures are visible.

pole of the cerebral hemisphere (Fig. 2.6). Of note is the
massive size of the pineal.
The pineal undergoes complex evolutionary changes
closely related to changes of the parietal eye (also called
the median or dorsal eye). A median eye situated on the
forehead and directed dorsally was apparently present in
ancestral bony fishes, amphibians, and reptiles (64) (Fig.
2.20). Some of these ancestral forms may have had two
median eyes. In modern vertebrates the parietal eye is
present in the lamprey, some fishes and lizards, and the
sphenodon (a surviving Mesozoic lizard) (64). Although a
miniature cornea and retina may be present, the parietal
eye—covered by connective tissue and epithelium—is
capable of little except detection of light. Romer postulated
that the ancestral vertebrates were presumably bottom-
dwelling mud strainers in which the parietal eye provided
vital protective information (64). Vertical vision lost its
importance for the more active modern vertebrates. It also
has been theorized that the parietal eye-pineal complex was
associated with thermoregulation (63).
The parietal eye, when present, develops from the distal
end of the pineal body. Since the pineal originates as an
evagination from the roof of the diencephalon, the parietal
eye, like the lateral eyes, is essentially a structure of the
brain. Occasionally the parietal eye develops from another
vesicular structure adjacent and similar to the pineal, the
parapineal organ.
In the sphenodon and modern lizards the parapineal
organ is the functional eye. In the lamprey both the pineal
and the parapineal form parietal eyes, of which the pineal
eye is dominant.
The complex and controversial anatomy and
terminology of the pineal and parapineal bodies and the
parietal eye are reviewed by Oksche (50). The lumen of the
pineal gland, the pineal recess, becomes progressively
reduced in the ascending vertebrate series. This reduction
results from cellular proliferation and leads to the compact
glandlike structure in mammals. In some bony fish and
turtles the lumen of the pineal does not communicate with
the third ventricle. The pineal is absent in certain
vertebrates, including the
 Figure 2.25. Dorsal views of brains demonstrate evolutionary changes at the roof of the
third ventricle. A. Shark. The highly vascular roof of the third ventricle (diencephalon) is
uncovered. Note that the veins of the cerebrum are anterior to the diencephalic veins.

crocodile and some whales and dolphins. The external
form of the pineal body varies greatly among the
different mammals (30, 50, 63, 81, 82). It is elongated in
guinea pigs, club-shaped in rabbits, round in goats,
conical in carnivores, and pear-shaped in cattle and
humans (Figs. 2.6 to 2.10).
The mechanism of formation of the double-layered tela
choroidea (velum interpositum) in the human (7, 17) is
diagrammed in Figure 2.26. This process is clarified
when considered in evolutionary terms, as demonstrated
by the shark, frog, iguana, and rabbit (Figs. 2.21 to 2.25).
In the shark the linear arrangement of the
major subdivisions of the brain is demonstrated (Fig. 2.21).
The cerebrum is anterior to the diencephalon. The entire
roof of the diencephalon is visible and is comprised of a
single layer of pia mater (Figs. 2.21 and 2.25A). The linear
arrangement of the brain is still present in the frog (Figs.
2.22 and 2.25B). A rudimentary cerebral hemisphere,
however, is beginning to overlap the diencephalon (Fig.
2.22). The pronounced changes of the reptilian brain are
shown in Figure 2.23. The linear arrangement of the subdi-
vision of the brain is no longer present. The cerebrum has
increased to such a degree that it overlaps the
diencephalon, which is no longer
 Figure 2.25B. Frog. The roof of the third ventricle is still uncovered.
visible (Figs. 2.23 and 2.25C). In the rabbit the cerebrum
overlaps the diencephalon and mes-encephalon (Fig. 2.24).
This overlapping produces a double-layered tela
choroidea. The human embryological changes that result in
the formation of a double-layered tela choroidea are an
ontogenic "recapitulation" of the phylogenetic process
previously described.
In their anatomical and radiographic studies, Larroche
(36), Larroche and Baudey (37), and Baudey-Pasquier and
Larroche (6) considered the
cavum vergae, which is situated below the corpus callosum
and above the fornix, as the posterior continuation of the
cavum septi pellucidi.
In the material of Larroche, a cavum vergae was never
present without a cavum septi pellucidi (6, 37). The cavum
vergae seemed to develop ontogenetically later than and
disappeared before the cavum septi pellucidi. The
disappearance of the cavum vergae by the time of birth
may be explained by several factors demonstrated in a
comparative study (33). The progressive enlargement of
the splenium as seen in the
 Figure 2.25C. Iguana. The forebrain (cerebrum) is increased in size and overlaps the roof
of third ventricle, which is no longer visible. The only diencephalic structures visible are
the distal ends of the dorsal sac and pineal gland.

rabbit, cat, dog, and monkey (Figs. 2.7 to 2.10) is
"recapitulated" in the human fetus (Fig. 2.27). Kappers et
al. (30) also noted that the posterior thalamus enlarges
progressively in the ascending phylogenetic series. The
thalamic enlargement increases the dorsal arching of the
fornix. All of these factors would contribute to the
obliteration of the cavum vergae in the older human fetus
while the cavum septi pellucidi is maintained.
A comparative study demonstrated that the human
aqueduct is a residual cavity that results from phylogenetic
modifications of the walls surrounding the ventricular
system of the midbrain (33).
The roof (tectum) of the midbrain is the primary visual
center in nonmammalian vertebrates. The presence of the
visual center in the tectum would seem to have been the
reason for the evolution of this region into a major associa-
 Figure 2.25D. Rabbit. The cerebrum covers both the diencephalon and mesen-cephalon.
tion center (64). The tectum in fishes and amphibians is the
dominant brain center; it associates visual, olfactory, lateral
line, and other somatic sensory stimuli with the motor
columns of the brain stem and cord.
In the lamprey the nerve structures of the eye are
developed and the optic tract ends in a discernible tectum.
Although the tectum is still partly ependymal, it already
has enlarged into a pair of recognizable optic lobes. The
two optic lobes (corpora bigemina) are the homologues of
the superior colliculi.
In the shark and the frog the optic lobes are prominent
structures (Figs. 2.4, 2.5, 2.21, and 2.22). In the iguana the
cerebrum is beginning to
become the dominant structure and the optic lobes are
relatively reduced in size (Figs. 2.6 and 2.23). In some
reptiles a pair of auditory lobes, the homologues of the
inferior colliculi, are present caudal to the optic lobes. The
auditory lobes, which receive fibers from the cochlea, are
not present in fishes that lack a cochlea. In amphibians the
cochlea is small and the auditory center is not large enough
to form a bulge on the surface of the mesencephalon (31).
At some critical evolutionary stage a supraseg-mental
area, more elaborate than the optic lobes, became
necessary for the integration of refined visual perceptions
(79). The evolution of the cerebrum provided a more
elaborate suprasegmen-

Figure 2.26. Diagram to demonstrate the formation of the
double layer of the tela choroidea (velum inter-positum) in
the human. 1. The developing neural tube includes the
forebrain (FB), which is surrounded by primitive pia
mater (broken line). 2 and 3. The expanding vesicle of the
cerebral hemisphere (HV) carries its own pia mater (b),
which overlaps the pia mater (a) of the third ventricle. IF,
interventricular foramen. 4. A double layer of pia is
interposed between the two cerebral vesicles and the roof
of the third ventricle (3V). E, ependyma. 5. The two layers
of pia (b, a) over the roof of the third ventricle persist after
connection of the hemispheres by the commissures. This
process "recapitulates" the phylogenetic overlapping of
the diencephalon by the cerebrum demonstrated in Figures
2.12 to 2.17 and 2.21 to 2.25. (From Brash JC (ed):
Cunningham's Textbook of Anatomy. New York, Oxford
University Press, 1951, ed 9. Modified from Frazer JE: A
Manual of Embryology. New York, William Wood & Co,
1932.)
tal region capable of integrating refined visual
perceptions such as color, form, size, and detection of
motion and distance. In mammals most of the visual,
auditory, and other somatic sensations—instead of being
integrated in the mid-brain—are relayed via the thalamus
to the cerebral hemispheres. The thalamus in nonmam-
malian vertebrates is a smaller anterior extension of the
sensory association area of the mid-brain. It reaches its
maximal development in mammals as a result of its
function as a relay center to the association centers in the
cerebral hemispheres.
In mammals the optic lobes differentiate into the
superior and inferior colliculi (corpora quadrigemina).
The cephalic shift in mammals is demonstrated in the
inverse relationship in the sizes of the cerebrum and
corpora quadrigemina. The increase in the size of the
cerebrum from the rabbit to the human is associated with
a relative reduction in the size of the corpora quad-
rigemina (Figs. 2.7 to 2.11).
Furthermore, the relative sizes of the superior and
inferior colliculi also change. In the rabbit the superior
colliculi are much larger than the
inferior colliculi (Fig. 2.7), in the cat the difference
between collicular sizes is diminished (Fig. 2.8), and in the
dog and monkey the superior and inferior colliculi are of
approximately equal size. Previously the superior colliculi
were considered to be exclusively an optic structure and
thus the homologue of the optic lobes. The inferior colliculi
were considered to be auditory centers that developed as a
result of the evolution of the hearing function of the ear.
This interpretation of collicular function has been modified
as other connections than purely visual and auditory have
been demonstrated in the colliculi (83).
The human fetus demonstrates a "recapitulation" of the
interrelationship in the sizes of the tectum and cerebrum
(Fig. 2.27). As the cerebrum enlarges, particularly the
occipital lobe, the large tectum is transformed into the
relatively smaller corpora quadrigemina.
The ventricular system of the midbrain, from the fish to
the primate, undergoes a pronounced transformation. In the
shark the walls of each optic lobe surround a large optic
ventricle, a dorsal expansion of the mesencephalic ventricle
(Figs. 2.4 and 2.12). The mesencephalic and optic
ventricles form a large continuous cavity.
In the frog the ventricular system of the mid-brain is
smaller as a result of increased thickness of the midbrain
walls (tegmentum) (Figs. 2.5 and 2.13). A constricted
communication demarcates the dorsolateral optic ventricles
from the mesencephalic ventricle. In the iguana, as a result
of the enlarged tegmentum and peduncles, the mes-
encephalic ventricle joins the third ventricle at a more
acute angle than in the frog (Figs. 2.6 and 2.14).
In the rabbit the mesencephalic ventricle demonstrates
some of the features of the definitive aqueduct. As a result
of the enlargement of the tegmentum and peduncles, the
floor assumes a dorsally convex curve. The rostral end of
the ventricle, molded by the superior colliculis and
tegmentum, has the configuration of the anterior part of the
aqueduct (Figs. 2.7 and 2.15). The recesses of the superior
and inferior colliculi are the remnants of the optic
ventricles. The definitive aqueductal configuration may be
seen in the cat (Figs. 2.8 and 2.16). The aqueductal am-
pulla, the widest segment of the mammalian aqueduct, is
the remnant of the mesencephalic and optic ventricles.
Further minor modifications in the contours of the
mammalian aqueduct are the result of enlargement of the
cerebellum, tegmentum, and peduncles associated with re-
duction in size of the corpora quadrigemina and increased
angulation of the brain (46).
Figure 2.27. Sagittal sections of human fetal heads demonstrate the "recapitulating"
change in the relative size of the midbrain tectum and cerebrum. As the cerebrum
enlarges, particularly the occipital lobe, the large tectum is transformed into the
relatively smaller corpora quadrigemina. Also note the enlarging corpus callosum. A. 11
weeks. The posterior margin of the thin occipital lobe does not extend posteriorly to the
relatively large midbrain. Note the size of the tectum relative to cerebellar size. From
Kier EL: The cerebral ventricles: A phylogenetic and ontogenetic study. In Newton TH,
Potts DG (eds): Radiology of the Skull and Brain, Vol. 3, Anatomy and Pathology. St.
Louis, The CV Mosby Co, 1977, pp 2787-2914.

Figure 2.27B. 15 weeks. The occipital pole of the cerebrum extends posteriorly between
the tectum and the skull. The tectum is still larger than the cerebellum.
Figure 2.27C. 24 weeks. The occipital pole is behind the cerebellum, which is now larger
than the tectum.
 Figure 2.27D. 30 weeks. Note the relatively small corpora quadrigemina. The splenium
is well developed. A cavum vergae is present between the corpus callosum and the
fornix.
Commissures
The literature dealing with the evolution of the
commissures is not always easy to understand.
Occasionally the descriptions and terminology are
conflicting. In this section, I describe aspects relevant to
the third ventricle.
The commissures are part of the limbic system (lobe).
Many of the structures of the limbic system (Fig. 2.1) are
phylogenetically old and are topographically interposed
between the dien-cephalon and the neocortex of the
cerebral hemispheres (83).
The fibers of the anterior commissure in the human
connect with the olfactory tracts and the piriform,
prepiriform, and amygdaloid bodies. The fornix is the
efferent fiber system of the hippocampi, and the corpus
callosum joins the neopallial regions of the cerebral
hemispheres.
The location, size, and interrelation of the anterior
commissure, fornix, and corpus callosum are understood
best in light of the evolutionary modifications of the
cerebrum.
The cerebrum first evolved as an olfactory organ. In the
lamprey the primordia of the cerebral hemispheres,
manifested by the presence of bilateral vesicular
outpouchings of the forebrain, are united by the lamina
terminalis. Cells from the two adjacent medial portions of
the olfactory lobes invaded the lamina terminalis. Thus the
two olfactory nuclei were connected by a thickened lamina
terminalis through which passed the anterior commissure
(27). The term para-terminal body was introduced by
Smith (75) to include the septal area and the medial
olfactory ganglionic mass. The septal area consists mainly
of nuclear masses of gray matter anterior and superior to
the lamina terminalis and anterior commissure (83). The
septal area superior to the anterior commissure
(supracommissural) corresponds to the area of the septum
pelluci-dum.
During the evolutionary growth of the cerebrum, the
hippocampal formation (archipallium) and the neopallium
evolved dorsal to the olfactory cortex (Fig. 2.5). At the
same time the fornix
(the commissures of the hippocampus) and corpus
callosum evolved dorsal to the anterior commissure (Figs.
2.6 and 2.7).
In the lamprey the lamina terminalis delineates the
anterior end of the brain. An anterior commissure
connecting the striatal areas and a primordial
hippocampus are already present (26). The rudimentary
hippocampus is situated above the interventricular
foramen and receives second order olfactory fibers and
ascending fibers from the hypothalamus. The entrance of
these fiber tracts into the rudimentary hippocampus
establishes it as a correlating center for olfactory and
visceral impulses. In the shark the primordial
hippocampus is larger, occupies the roof of the lateral
ventricle, and extends along the upper border of the wall
of the third ventricle (Fig. 2.4). According to Johnston
(26), the fiber tracts, homologous to the fornix, descend
from the primordial hippocampus through the medio-
rostral and ventral wall of the cerebrum and pass between
the lateral ventricles to the hypothalamus.
In the frog the primordial hippocampus forms the entire
length of the dorsomedial wall of the cerebral hemisphere
(23). Johnston (26) and Her-rick (24) described a
hippocampal commissure, dorsal to the anterior
commissure, that projected into the floor of the third
ventricle of the amphibian salamander (Fig. 2.5). The
hippocampal commissure is the homologue of the fornix
and in the amphibian passes behind the interventricular
foramen.
In reptiles most of the primordial hippocampus has been
transformed into a specialized cerebral cortex that occupies
the dorsomedial aspect of the entire cerebral hemisphere
(23, 26, 27). Within the hippocampus, fibers arise to form a
tract on its ventricular surface. This tract, the homologue of
the mammalian fornix, passes rostral to the interventricular
foramen and forms a commissure that crosses the lamina
terminalis dorsal to the anterior commissure (Fig. 2.6).
In monotremes such as the platypus and spiny anteater,
which belong to the lowest subclass of mammals, the
hippocampus is still large and

Figure 2.28. Midsagittal sections of the head of a rabbit (A), dog (B), and monkey (C)
demonstrating the relationship between the increasing size of the cerebrum and corpus
callosum. The genu and splenium are present in the dog and are increased in size in the
monkey. Note the changing facial-neurocranium ratio from the rabbit to the monkey.
Compare with the predominant neurocranium in the human fetus (Fig. 2.27).
Figure 2.28B

Figure 2.28C
assumes the elongated and arched contours of the cerebral
hemisphere.
In the platypus the posterior limb of the fornix assumes
the curved shape of the hippocampus (74). In the spiny
anteater the posterior limb of the fornix is better developed
and corresponds to the larger temporal segment of the
hippocampus. Thus already in monotremes the fornix
extends from the temporal lobe to the mamillary body and
is curved by the large mammalian thalamus. The arch of
the fornix increases in the ascending mammalian scale as a
result of the progressive enlargement of the thalamus.
A major transformation of the mammalian brain is the
progressive enlargement of the cerebrum. The increase in
size of the mammalian cortical neopallium in placental
mammals is accompanied by a new commissure, the
corpus callosum (Figs. 2.7 to 2.11). Nieto et al. (48)
demonstrated a linear correlation between surface area of
the corpus callosum and the brain weight of different
animals (Fig. 2.28). The only exception was in the
dolphin. In this mammal the corpus callosum is
comparatively small in spite of relatively massive
development of the cerebral hemispheres. They postulated
that the lack of extremities in cetaceans may account for
the relative smallness of their corpus callosum.
The appearance of the corpus callosum first in placental
mammals may relate to expansion of the associated areas
of the neocortex (67). Smith (74), Johnston (27), and
Abbie (4) demonstrated that the evolutionary increase of
the corpus is associated with a concomitant decrease of
the hippocampal formation in the roof and medial wall of
the lateral ventricle (Fig. 2.29).
To state that the corpus callosum replaces the
hippocampus in the roof of the body of the lateral
ventricle is not strictly accurate. The concept of
replacement, substitution, or suppression, however,
facilitates understanding of the topographic relation of the
corpus callosum, fornix, and hippocampus. An example
of the "replacement" is seen in the rabbit, where the
posterior margin of the evolving corpus blends with the
anterior margin of the remaining hippocampus (Fig. 2.7).
Smith (75) stated that, "in all mammals the cerebral
cortex is fringed with some structure representing a
hippocampal formation along the whole extent of its
mesial edge—from the olfactory peduncle in front to the
region of the uncus behind and below" (Fig. 2.30). Smith
thought that the indusium griseum and the longitudinal
striae were vestigial hippocampal structures. Kappers et
al. (30) further elaborated this theory. Abbie (4)
demonstrated that the indusium gri-
seum is not a remnant of the hippocampus but is formed by
eversion of a lip of the subiculum. The subiculum is
transitional (mesocortex) cerebral tissue at the junction of
the hippocampus and the neocortex (3).
The evolution of the corpus callosum was divided by
Abbie (4) into the following stages (Fig. 2.29): (a)
reduction in the size of the hippocampal segment adjacent
the lamina terminalis, (b) piercing of the subiculum
adjacent to the lamina terminalis by fibers of the corpus
callosum, (c) enlargement of the corpus callosum adjacent
to the lamina terminalis, (d) formation of the sple-nium by
linear caudal expansion, and (e) formation of the genu and
septum pellucidum by frontal arciform expansion. These
stages are diagrammed in Figure 2.29 and are demonstrated
in dissected specimens in Figures 2.7 to 2.10.
In monotremes, such as the platypus and the spiny
anteater, the paraterminal body contains the lamina
terminalis, a large anterior commissure, and dorsal to it a
smaller round hippocampal commissure. In the marsupial a
large hippocampus on the medial aspect of the cerebral
hemisphere extends anterior to the lamina terminalis
(precommissural hippocampus) and posteriorly
(postcommissural hippocampus) into the temporal lobe
(Fig. 2.29A). The anterior commissure is still a large
structure. The commissure of the fornix (inferior fornix)
has a primordial elongated shape.
A postulated intermediate phase demonstrates the first
stage in the formation of the corpus callosum (Fig. 2.29B).
The hippocampus adjacent to the lamina terminalis is
reduced in size secondary to infolding.
The hippocampal infolding results in approximation of
the subiculum and lamina terminalis. The broken line in
the subiculum indicates the point at which the fibers of the
corpus callosum pierce the subiculum.
In the hedgehog and the bat the fibers of the corpus
callosum break through the subiculum (Fig. 2.29C). With
the appearance of the corpus callosum, the hippocampus
disappears almost completely from the region dorsal to the
commissures in the lamina terminalis. The anterior com-
missure is reduced, the inferior fornix is enlarged, and a
new hippocampal fiber tract (the superior fornix) appears
in the region of the lamina terminalis.
In the rat the corpus callosum is enlarged dorsal to the
lamina terminalis (Fig. 2.29D). This enlargement is
associated with a further reduction of the precommissural
and postcommissural hippocampi, which are ventral to the
corpus cal-
Figure 2.29. Diagram of the medial aspect of a cerebral hemisphere to demonstrate the evolution of
the corpus callosum and septum pellucidum. A, marsupial; B, postulated intermediate phase; C,
hedgehog and bat; D, rat; E, rodent; F, primate. Expansion of the corpus callosum (c.c.) is associated
with concomitant reduction in size of the hippocamus (hi.). Elongation of the superior (f.s.) and
inferior (fi.) fibers of the fornix is related to growth of the splenium (s.) of the corpus callosum. The
septum pellucidum (si.) results from thinning of the lamina terminalis (lt.) secondary to the arched
expansion of the genu of the corpus callosum; ca., anterior commissure; pt. b., paraterminal body;
hi. p., precommis-sural hippocampus; r., rostrum; su., subiculum. (From Abbie AA: J Comp Neural
70:9-44, 1939.)

Figure 2.30. Diagrammatic across sections of the left
cerebral hemisphere show the evolutionary changes in the
position of the hippocampus. A. In the primitive stage the
cerebrum is essentially an olfactory lobe composed only
of the paleopallium. The hippocampus (archipallium) is
not present. B. In the amphibian the hippocampus forms
the medial wall of the hemisphere. С and D. In early and
late reptilian stages the hippocampus is medial and
superior to the lateral ventricle. In the late reptilian stage
(D), the neopallium is still rudimentary. E. In the primitive
mamallian stage, the neopallium has expanded and the
hippocampus is rolled in on the medial surface of the
hemisphere, adjacent to the lateral ventricles. F. In the
higher mammals the neopallium has markedly expanded.
The rolled-in hippocampus is separated from the ventricle
by the corpus callosum. a, archipallium (hippocampus); b,
basal nuclei; cc, corpus callosum; n, neopallium; p,
paleopallium; v, ventricle. (From Romer AS: The
Vertebrate Body. Philadelphia, WB Saunders Co, 1970, ed
4.)
losum. The inferior and superior fornices are elongated.
Similar changes are seen in the rabbit (Fig. 2.7).
In another rodent the stage of caudal expansion of the
corpus callosum is demonstrated (Fig. 2.29E). This
expansion leads to formation of the splenium. The caudal
expansion of the corpus callosum is a simple linear
extension and carries with it the fibers of the fornix,
which become increasingly elongated. Both the splenium
and the commissure of the fornix remain dorsal to
the hippocampus. These changes are demonstrated in the
cat and dog (Figs. 2.8 and 2.9).
The last stage of development of the corpus callosum
involves the region of the genu. Progressive expansion of
the genu associated with formation of a septum pellucidum
is seen in the cat and the dog (Figs. 2.8 and 2.9). The
frontal expansion of the corpus callosum reaches its
maximal size in primates (Figs. 2.10 and 2.11). The
development of large frontal lobes in primates is associated
with the development of the large arched genu and a large
septum pellucidum (Figs. 2.29F).
Thompson (78) reviewed the controversial literature
dealing with the presence of a cavum septi pellucidi and its
open status in a large number of mammals such as
ungulates, carnivores, and primates. Johnston (27)
postulated that the cavum septi pellucidi was the result of
trapping and roofing by the genu of a cavum formed by
lamina of the paraterminal body and open dorsally into the
superior longitudinal fissure (Fig. 2.31). Abbie (4) pointed
out that a cavum opening dorsally into the superior longi-
tudinal fissure has never been demonstrated in vertebrates
without a corpus callosum. Abbie (4) attributed the
formation of the septum pellucidum to the arched
expansion of the genu (Fig. 2.31). The upward expansion of
the genu draws up the lamina terminalis and the superior
fornix into the concavity of the arch, thus forming the
septum pellucidum. In the cat the septum is still solid. The
tension produced by further arched expansion of the genu
results in condensation of the septum into two laminae with
a cavum between them. Abbie (4) postulated that similar
upward expansion in the region of the splenium cannot take
place because of the restraining fibers of the columns of the
fornix (62).
According to Sarnat and Netsky (67) the leaves of the
septum pellucidum are composed of neural tissues and the
cavum septi pellucidum is an ependyma-linked cavity
deriving from the lamina terminalis. Rakic and Yakovlev
(62) considered the cavum septi pellucidi as a dorsally
open pocket that is open at birth. Later it is sealed by the
rostrum of the corpus callosum. The pocket stays open in
rodents, carnivores, and monkeys (rhesus). Loeser and
Alvord (43, 44), Probst (60, 61), and Lemire et al. (41)
reviewed the contro-versial development of the human
septum pellucidum.
 Figure 2.31. Diagrams of the brain of the rat to illustrate two different theories of the
formation of the septum pellucidum, the indusium griseum, and the longitudinal striae.
A. Johnston demonstrates a hippocampal remnant above the corpus callosum (c.c.). The
septum pellucidum is formed within the hippocampal primordium (spindle-shaped
spots). The paraterminal body is shaded with horizontal lines. c. h., hippocampal
commissure; c.a., anterior commissure. B. Abbie demonstrates no hippocampal (black)
tissue above the corpus callosum (c.c.). Instead, the subiculum (su), a mesocortical
tissue, lies above the corpus callosum. The septum pellucidum area is formed by the
drawing up of the lamina terminalis (l.t.).f.s., superior fornix;f.i., inferior fornix; hi.p.,
precommissural hippocampus; c.a., anterior commissure;f.l. (f.s.), long fornix; pt.b.,
paraterminal body; ol.t., olfactory tubercle. (A. From Johnston; J Comp Neurol 23:371-
478, 1913.) (B. From Abbie: J Comp Neurol 70:9-44, 1939.)
study of the general principles that govern the
vascularization of the brain and of certain evolutionary
Arteries modifications of the arterial system is helpful in
Neuroradiologists and neurosurgeons are constantly understanding the vascular variability of the arteries
aware of the marked variability in angio-graphic and supplying the hypothalamus and the thalamus (32).
neurosurgical vascular anatomy. A Streeter (76, 77) pointed out the following important
principles of cerebrovascular develop-
ment. (a) The development of the cerebrovascu-lar system
is not an independent phenomenon. (b) The vascular
system constantly adapts to the changing brain.
In comparative anatomical studies Shellshear (69-72)
repeatedly stressed the unity of the brain and its vascular
supply. He expressed the belief that earlier workers had
been misled by overemphasis on the variation of the larger
vessels. Because the size of the arteries served as an index
of their importance, the fundamental characteristic of
arterial distribution was overlooked. An analysis of
arteries, in terms of their final areas of supply, showed a
remarkable constancy. Shellshear divided the cerebral
arteries into two major divisions: the end arteries and the
blood vessels that lead to the end arteries (32).
Abbie (1, 2), in studies of the comparative anatomy of
the circulation of the brain, confirmed the postulates of
Shellshear in regard to constancy of the cerebral arteries
in their terminal supply. In his studies he reemphasized
the concept that the brain and its blood supply are not
independent and that both evolve simultaneously. Abbie,
as well as Shellshear, pointed out that the variation in the
origin and course of the vascular trunks leading to the
functional end arteries is of secondary importance. This
variation depends on the evolutionary direction of growth
of an organ and on hemodynamic factors such as the
closeness, economy of distribution, and convenience of
the source of blood (Fig. 2.38). This last concept was
alluded to by Evans (15), who stated, "The larger vessels
are to be considered in the light of servants of the capil-
laries, for which they are but the delivering and draining
pipes."
Roofe (65), in his comprehensive study of the
endocranial circulation of the salamander, emphasized the
great variability in the supply of various territories of the
brain. Areas of the brain that are well defined
morphologically and functionally are supplied by
delivering arteries whose course varies greatly.
The terms nutrient, applied by Gillilan (19) to the end
arteries, and conducting, applied to the major trunks that
lead to the end arteries, convey the physiological aspects
of the cerebral circulation.
The end arteries supply a constant functional territory.
This constancy is mediated through elements of the
sympathetic nerves that accompany the vessels. These
end arteries develop synchronously with the structures
that they supply, and their evolution parallels the
evolutionary changes of their territories of supply.
The central artery of the retina is the best example of an
end artery. The cerebral perforating arteries of the brain
communicate with each other only through the capillary
bed and from a practical point of view are end arteries (83).
Neuroangiography and microneurosurgery visualize
only the variable "delivering (conducting) pipes" of the
hypothalamus and thalamus. These are the circle of Willis
and the anterior cerebral, anterior communicating, internal
carotid, posterior cerebral, posterior communicating, and
anterior and posterior choroidal arteries (38, 89). The
perforating branches of these arteries are the end arteries
supplying fairly specific territories in the third ventricular
region (Fig. 2.32) (18, 34, 39, 40, 57, 58, 66). Although the
hypo-thalamic branches of the superior hypophyseal artery
are end arteries, the branches supplying the hypophysis and
its stalk are not end arteries (47).
Padget (51, 52), in her studies of the early fetal arterial
system, noted that, in accordance with the five stages of
cerebral blood vessel development of Streeter (77), the
early process of vascular development involves changes in
certain channels of the primitive vascular plexus. These
changes depend on the specific needs of areas to be
supplied. The needs may be permanent or transitory and
result in the elaboration of permanent or transitory arteries.
The great variability in the region of the anterior
communicating artery is a function of these factors (38).
The recurrent artery of Heubner is an example of
evolutionary change of source of supply for reasons of
economy of blood distribution (2). Because of the bending
of the rhinal fissure, the anterior cerebral artery takes over
some of the territory previously supplied by the middle
cerebral artery. This territory includes a segment of the
basal ganglia. The terminal arterioles of Heubner's artery
never change their territory of supply; rather the
conducting arteries to these arterioles are changed (32).
Earlier in the evolutionary phase, the terminal arterioles of
Heub-ner's artery are supplied by the middle cerebral
artery. In primates they are supplied by a new conducting
artery, which, because of its origin from the anterior
cerebral artery, must pass laterally to reach its arterioles.
The great variability in the origin of the artery of Heubner
depends on the particular anastomotic channel that
becomes the stem of the artery (Fig. 2.33).
Other examples of variability in the vascular trunks
supplying the same end arterioles are the inverse
relationship between the size of the anterior and posterior
choroidal arteries and the
Figure 2.32. Diagrams of the arterial territories in the third ventricular region. A. Sagittal:
1, anterial cerebral; 2, posterior cerebral; 3, anterior and posterior choroidal; 4, posterior
communicating; 5, internal carotid. B. Floor: 1, anterior cerebral; 2, posterior cerebral; 3,
posterior communicating; 4, internal carotid. С and D. Transverse and coronal: 1,
anterior cerebral; 2, middle cerebral; 3, posterior cerebral; 4, anterior choroidal; 5,
posterior choroidal; 6, posterior communicating. (From Krayenbuhl HA, Yasargil MG:
Cerebral Angiography. Philadelphia, JB Lippincott, 1968. After Lazorthes G:
Vascularisation et Circulation Cere-brales. Paris, Masson & Cie, 1961.)
 Figure 2.33. Dissected human fetal arteries: 16-week fetus (A); 24-week fetus (B). Note
the variability in the origin, size, and course of the recurrent arteries of Heubner. From
Kier EL: The fetal cerebral arteries: a phylogenetic and ontogenetic study. In Newton
TH, Potts DG (eds): Radiology of the Skull and Brain, Vol. 2, Book 1, Angiography. St.
Louis, The CV Mosby Co, 1974.

large anterior inferior cerebellar artery supplying the
territory of the posterior inferior cerebellar artery or the
reverse anomaly.
The human circle of Willis is but one of many cerebral
arterial circles that evolved in the various vertebrate
groups to assure an adequate supply of blood to the brain
(87). An additional possible explanation of its function in
the evolve-ment of the cerebral arterial circle is to assure
equal pressure in the three major cerebral arteries (88).
In fish, amphibians, reptiles, and birds, the internal
carotid arteries are the sole source of blood to the brain
(14). In these four classes of vertebrates, the internal
carotid arteries divide into cranial and caudal divisions.
The caudal division unites to form the basilar artery in all
four classes. The cranial divisions remain separate in fish,
amphibians, and birds. In most rep-
tiles the cranial division unites to form a single artery that
passes anteriorly to supply the olfactory lobes. Thus in fish,
amphibians, and birds the arterial circle is open anteriorly,
whereas in the majority of reptiles it is completely closed.
Occasionally an anterior communicating artery may exist
in certain amphibians (14).
The monotremes possess definite mammalian features,
such as the presence of an internal capsule and a crus
cerebri and pons (22). The cerebral arterial circle of
monotremes is the earliest true homologue of the human
circle of Willis, for it unites the carotid and vertebral
circulations and is completely closed. The term circle of
Willis should be limited to the human cerebral arterial
circle (22).
The cerebral arterial circle of the different mammals
varies greatly and can be grouped into three fundamental
groups (14). These groups are
distinguished by the relative contribution of the carotid and
vertebral arteries to the arterial circle.
Group I
The carotid and vertebral circulations participate in
approximately equal manner. To this group belong
humans, anthropoid apes, monkeys, insectivores (shrew,
mole, hedgehog), and certain carnivores, rodents, and
toothless mammals.
Group II
The carotid arteries are the major source of supply to the
cerebral arterial circle. In this group the vertebral and
basilar arteries are greatly attenuated. The monotremes,
marsupials, whales, odd-toed ungulates (horse, zebra),
even-toed ungulates (cattle, deer, camel, giraffe), and many
land and marine (seal, sea lion, walrus) carnivores belong
to this group.
Group III
The vertebral and basilar arteries are the major source of
supply to the arterial circle. The inter-
nal carotid arteries are attenuated. To this group belong
many rodents and some lemurs, bats, and toothless
mammals.
According to Nilges (49) the arterial circle of the guinea
pig is derived entirely from the vertebral arteries. The
internal carotid artery leaves the cranial cavity as the
ophthalmic artery without participating in the formation of
the cerebral arterial circle.
In some ruminants (ox, goat, sheep, pig) and in the cat,
the internal carotid artery has been replaced by a vascular
plexus—the rete mirabile— which connects the cerebral
arterial circle with branches of the external carotid artery
(12, 16, 20).
The fish brain is supplied entirely by the internal carotid
artery. The internal carotid artery divides into two
branches, a rostral and a caudal division, whose sizes relate
to the functional preponderance of the various brain
components. The rostral branch is small and divides into a
medial and a lateral olfactory artery. The medial olfactory
artery supplies the medial aspect of the primitive forebrain,
the septal region, and the medial part of the primordial
hippocampi. It is
Figure 2.34. Diagrams demonstrating the variable evolutionary origin of the posterior
cerebral artery. A. In the chicken the posterior cerebral artery (a. cer. post.) originates
from the rostral branch (r. rost.) of the internal carotid artery. B. In the marsupial the
origin of the posterior cerebral artery is now more posterior, originating from the basilar
artery. (A. From Gillilan LA: J Comp Neurol 130:175-196, 1967. B. From Abbie AA: J
Anat 67:491-521, 1933.)
the homologue of the anterior cerebral artery of the higher
forms. The lateral olfactory artery supplies the region of
the primordia of the hy-popallium, piriform lobe, most of
the hippocampus, and the paleostriatum. The caudal branch
is larger, and its branches supply the dien-cephalon, optic
lobes, cerebellum, and medullary centers.
In amphibians the internal carotid artery divides into a
cranial and a caudal division of approximately equal
calibers. The medial olfactory artery of amphibians is
similar to that of the fish in its course and territory of
supply and is the homologue of the anterior cerebral artery.
The anterior cerebral artery of reptiles is the homologue
of the medial olfactory artery of fish and amphibians. In
reptiles the main stream of blood has been deflected to the
medial wall of the telencephalic hemisphere, probably in
response to the increased demands of the new reptilian
cortex.
The anterior cerebral artery in birds contributes little to
the supply of the forebrain. A few small branches to the
medial and central aspect of the forebrain originate from
the anterior cerebral artery before this vessel leaves the
cranial cavity to become the ethmoidal artery.
The original course of the anterior cerebral artery
homologue in the lower forms is indicated in humans by a
few small branches that run forward toward the olfactory
bulb.
The homologue of the anterior choroldal artery first
appears as an entity in the reptilian class. This vessel
supplies branches to the optic tract, lateral geniculate body,
and amygdaloid.
In marsupials the anterior choroidal artery has evolved
into a complete homologue of the primate anterior
choroidal artery. It arises from the internal carotid artery,
courses posteriorly along the optic tract and lateral
geniculate body, and terminates in the posterior cerebral
artery. Along its course it sends a few small branches that
reach the choroid plexus through the choroid fissure.
In the sheep the course of the artery is similar to that in
marsupials. The choroidal branches in the sheep, however,
are much more prominent than in the lower forms. The
branches of the anterior choroidal artery that supply the
choroid plexus in the ape equal the size of those that supply
the optic tract and lateral geniculate body.
From reptiles to humans, the anterior choroidal artery
maintains a close topographic relation with the optic tract
and lateral geniculate body. The artery undergoes a
functional change, however. From mainly a visual function
in the
reptiles, its contribution to the choroid plexus becomes
greater as the cerebrum progressively enlarges in the
ascending evolutionary scale.
The posterior cerebral artery and its homo-logues
undergo significant evolutionary changes in their origin,
course, and territory of supply. The diencephalic and tectal
arteries of fish and amphibians (21) are homologues of the
posterior cerebral artery of higher forms. They arise from
the caudal division of the internal carotid artery and supply
the optic lobes and the dorsomedial aspect of the primitive
forebrain.
The reptilian posterior cerebral artery is the true
forerunner of that artery in mammals. In the various
reptiles it may arise as a branch of either the cranial
division of the internal carotid artery (21) or the caudal
division (8); it may also arise at the bifurcation of the
internal carotid artery (9), or it may represent the entire
caudal division of lower forms (2).
In the mammalian class the origin or source of blood for
the posterior cerebral artery shifts from the carotid to the
basilar artery. As the cerebral hemisphere enlarges in the
ascending mammalian series, the cerebral territory supplied
by the posterior cerebral artery is gradually shifted more
posteriorly and overhangs the midbrain. The distance
between the origin of the posterior cerebral artery and the
final areas of supply is increased. For economy of
distribution, the posterior cerebral artery shifts its stem
progressively posteriorly (Fig. 2.34). Successive posterior
anastomotic channels enlarge to convey the main stream of
blood to the posterior cerebral artery. These anastomotic
channels, which successively enlarge to form the stem of
the posterior cerebral artery, revert to their original small
size when their need as the main conduit of blood to the
posterior cerebral artery disappears. In its evolutionary
course posteriorly the main trunk of the posterior cerebral
artery incorporates the territory of the various vessels that
have become its temporary or permanent stem. In the
higher mammals the posterior cerebral artery uses the
anterior midbrain channels as a stem. These channels are
supplied by a greatly enlarged basilar artery; eventually the
posterior cerebral artery seems to arise directly from the
basilar artery.
The posterior choroldal arteries join the anterior
choroidal artery in a rich network that supplies the optic
tract, lateral geniculate body, and choroid plexus of the
third ventricle.
The posterior choroidal vessels increase in number and
complexity in the ascending phylo-genetic scale.
According to Abbie (1) the variabil-
Figure 2.35. Lateral view of arterially injected brain of an iguana. The posterior cerebral
artery is seen on the surface of the brain supplying the optic lobe. Note the artery
supplying the chiasm and hypophysis (arrow).

Figure 2.36. Lateral view of a dissected brain of a rabbit. The posterior cerebral artery
can only be demonstrated by dissection because of the marked expansion of the
neopallium. Note the relatively large size of the superior colliculus and the large
homologues of the medial and lateral posterior choroidal arteries. The posterior
pericallosal artery is curving around the corpus callosum to supply the roof of the third
ventricle.
Figure 2.37. Lateral view of dissected brain of a cat. The colliculi and posterior
choroidal arteries are relatively reduced in size. The enlarged occipital lobe is supplied
by a large branch of the posterior cerebral artery (crossed arrow).

Figure 2.38. Dorsal view of the roof of the third ventricle of a dissected 24-week human
fetus. Note the large posterior pericallosal artery curving around the rudimentary
splenium of the corpus callosum.
ity of the major posterior choroidal branches is a function
of the rich vascular network that supplies the choroid
plexus. The functional end arteries of the posterior
choroidal arteries remain constant; only their larger
conducting trunks vary. The constancy of the end arteries
is manifested in the precise correlation of their distribution
in the various laminae of the lateral ge-niculate body and
in the areas of the functional representation of the retina.
In the iguana the posterior cerebral artery supplies the
optic lobe (Fig. 2.35). In the rabbit significant evolutionary
change has occurred. The posterior cerebral artery supplies
not only the optic lobe but the new visual centers, the ge-
niculate body and pulvinar. The homologues of the medial
and lateral posterior choroidal arteries can be seen only by
dissection because of the marked enlargement of the
cerebrum (Fig. 2.36).
In the cat there are further changes. The optic lobe is
reduced in relative size. A large posterior cerebral artery
branch to the occopital lobe is seen (Fig. 2.37). In higher
vertebrates the choroidal branches will relatively diminish
in size, while the cortical branches increase in size.
The posterior growth of the cerebrum and corpus
callosum elongates the course of the anterior cerebral
artery to the roof of the third ventricle. This long course
results in the inconsistent presence of the posterior
pericallosal artery in the human adult. The medial
posterior choroidal artery has a shorter course to the roof
of the third ventricle and is rarely absent (Fig. 2.38).
Veins
There are few studies dealing with the cerebral veins in
nonhuman vertebrates. In the shark the forebrain veins are
anterior to the diencephalic veins of the uncovered roof of
the third ventricle (Fig. 2.25A). In the salamander (65) the
veins of the brain are superficial and their course is ex-
ceedingly variable. The veins of the choroid plexus are
wide sinusoidal channels that drain into a rete of the nodus
vasculoses that permeates the paraphysis and dorsal sac.
The dorsal hemispheric veins are pial and also drain into
the nodus vasculoses. In the turtle (68) the venous
channels are situated on the superior surface of the brain.
The largest one is a median dorsal longitudinal vein that
commences anteriorly near the interventricular foramen
and passes posteriorly on the surface of the brain to exit
from the skull near the fourth ventricle. There are no
venous channels within the brain.
In the dog the great cerebral vein is the main vessel of
the velum interpositum. It passes ven-
tral to the corpus callosum (5). Review of their Figure 5
demonstrates a straight great cerebral vein secondary to the
small splenium in the dog. A diagram of the
intraventricular venous drainage of the capuchin monkey
also demonstrates a straight great cerebral vein (45).
These features seem to be "recapitulated" in the human
embryo (29, 54). In the 40-mm embryo (21/2 months) the
arterial circle of Willis and its branches are clearly defined.
However, the deep venous system is still rudimentary, con-
sisting of the primitive great cerebral vein (Galen), which
leaves the membranous diencephalic roof near the pineal
primordium (53). The primitive internal cerebral vein is
still extracer-ebral, lying in dorsal contact with the dience-
phalic roof. The internal cerebral vein will become
enclosed within the two leaves of the tela choroidea of the
third ventricle during further growth of the cerebrum. The
great cerebral vein derived its curvature during the growth
of the splenium of the corpus callosum.
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3
Microsurgical Anatomy of the Third Ventricular Region
Albert L. Rhoton, Jr., M.D.
The third ventricle is located in the center of the head,
below the corpus callosum and the body of the lateral
ventricle; above the sella turcica, pituitary gland, and
midbrain; and between the cerebral hemispheres, thalami,
and the walls of the hypothalamus. It is intimately related
to the circle of Willis and its branches and the vein of
Galen and its tributaries. Selecting an operative approach
to a lesion involving the third ventricle requires an
understanding of the anatomy of the sella turcica, sphenoid
sinus, lateral ventricles, and basal cisterns.
This chapter is divided into four sections. The first three
sections deal with the neural, arterial, and venous
relationships around the third ventricle. The fourth section
on the sellar region deals with the structures in the cranial
base that are important in performing the subcranial op-
erative approaches to lesions around the third ventricle.
The section on neural relationships includes a review of the
anatomy of the lateral ventricles and the cisterns
surrounding the ten-torium incisura because many lesions
involving the third ventricle are approached through these
spaces (8, 25, 26, 43, 55).
Neural Relationships
Third Ventricle
The third ventricle is a narrow, funnel-shaped,
unilocular, midline cavity. It communicates at its
anterosuperior margin with each lateral ventricle through
the foramen of Monro and posteriorly with the fourth
ventricle through the aqueduct
of Sylvius. It has a roof, a floor, and an anterior, posterior,
and two lateral walls (Fig. 3.1).
Roof
The roof of the third ventricle forms a gentle upward
arch, extending from the foramen of Monro anteriorly to
the suprapineal recess posteriorly. The roof has four layers:
one neural layer formed by the fornix, two thin
membranous layers of tela choroidea, and a layer of blood
vessels between the sheets of tela choroidea (Figs. 3.2 to
3.4).
The upper, or neural, layer is formed by the fornix. The
fornix is formed by axons that arise in the floor of the
temporal horns from the hippocampi and extend around the
thalami to reach the mamillary bodies. The fornix is
composed of a body, two anterior limbs called columns,
two posterior limbs called crura, and two inferior limbs
called fimbria (Fig. 3.2). The initial part of the fornix, the
fimbria, arises in the floor of the temporal horn on the
ventricular surface of the hippocampal formation and
passes posteriorly to become the crus of the fornix. The
crus wraps around the posterior surface of the pulvinar of
the thalamus and arches superomedial toward the lower
surface of the splenium of the corpus callosum. At the
junction of the atrium and the body of the lateral ventricle,
the paired crura meet to form the body of the fornix, which
runs forward along the superomedial border of the thalami
in the medial wall of the body of the lateral ventricle. The
body forms a gentle arch located between the roof of the
third ventricle
Figure 3.1. Midsagittal section of the third ventricle. The floor extends from the optic
chiasm (O.Ch.) to the aqueduct of Sylvius and includes the lower surface of the optic
chiasm, the infundibulum (Infund.), the infundibular recess (Infund. Recess), the pituitary
gland (Pit. Gland), the tuber cinereum (Tuber Cin.), the mamillary bodies (Mam. В.), the
posterior perforated substance (Post. Perf. Subst.), and the part of the midbrain anterior to
the aqueduct. The anterior wall extends from the optic chiasm to the foramen of Monro
(F. Monro) and includes the upper surface of the optic chiasm, the optic recess (O.
Recess), the lamina terminalis (Lam. Ter.), the anterior commissure (Ant. Comm.), and
the foramen of Monro. The roof extends from the foramen of Monro to the suprapineal
recess and is formed by the fornix and the layers of the tela choroidea (Tela), between
which course the internal cerebral vein and the medial posterior choroidal artery. The
hippocampal commissure (Hippo. Comm.), corpus callosum (Corp. Call.), and septum
pellucidum (Sept. Pel.) are above the roof. The posterior wall extends from the
suprapineal recess to the aqueduct and includes the habenular commissure (Hab.
Comm.), pineal gland, pineal recess, and posterior commissure (Post. Comm.). The
oculomotor nerve (HI) exits from the midbrain. The hypothalamic sulcus (Hypothal.
Sulc.) forms a groove between the thalamic and hypothalamic (Hypothal.) surfaces of the
third ventricle. (From Yamamoto I, Rhoton AL Jr, Peace DA: Microsurgery of the third
ventricle: Part 1. Microsurgical anatomy. Neurosurgery 8:334-356, 1981.)
and the floor of the body of each lateral ventricle. The positum above the pineal body to enter the quadrigeminal
body of the fornix splits into two columns at the anterior cistern and join the great vein.
margin of the opening of each foramen of Monro into The lateral margin of the roof is formed by the cleft
the ipsilateral lateral ventricle. The columns terminate in between the lateral edge of the fornix and the superomedial
the mamillary bodies. The crura, just posterior to where surface of the thalamus (Fig. 3.2). This narrow cleft
they join to form the body of the fornix, are intercon- between the fornix and the thalamus, which in its entirety is
nected by a sheet of white matter called the hippocampal C-shaped, is called the choroidal fissure. The choroid
commissure. plexus of the lateral ventricle is attached along this fissure.
The upper layer of the anterior part of the roof of the The fornix forms the outer margin of the C-shaped fissure,
third ventricle is formed by the body of the fornix, and and the thalamus forms the inner margin. The choroidal
the posterior part of the roof is formed by the crura and fissure is limited in the body of the ventricle by the body of
the hippocampal commissure. The septum pellucidum is the fornix superiorly and by the thalamus inferiorly, in the
attached to the upper surface of the body of the fornix. atrium by the crus of the fornix posteriorly and the pulvinar
The septum pellucidum is tallest anteriorly and shortest anteriorly, and in the inferior horn by the fimbria of the
posteriorly, disappearing near the junction of the body fornix below and the striae terminalis and the thalamus
and crura of the fornix. In our studies, the above. The tela cho-roidea forming the pedicle of the
anteroposterior length of the septum pellucidum varied choroid plexus of the third ventricle is continuous through
from 28 to 50 mm (55). At the posterior end of the the choroidal fissure with the choroid plexus in the lateral
septum pellucidum, the crura and hippocampal ventricle.
commissure fuse with the lower surface of the corpus
callosum.
The tela choroidea forms two of the three layers in the
roof below the layer formed by the fornix (Fig. 3.3). The
tela choroidea consists of two thin, semiopaque
membranes derived from pia mater, which are
interconnected by loosely organized trabeculae. The
final layer in the roof is a vascular layer located between
the two layers of tela choroidea. The vascular layer
consists of the medial posterior choroidal arteries and
their branches and the internal cerebral veins and their
tributaries. Parallel strands of choroid plexus project
downward on each side of the midline from the inferior
layer of tela choroidea into the superior part of the third
ventricle.
The velum interpositum is the space between the two
layers of the tela choroidea in the roof of the third
ventricle. The velum interpositum is usually a closed
space that tapers to a narrow apex just behind the
foramen of Monro, but it
may infrequently have an opening situated between the
splenium and the pineal body that communicates with
the quadrigeminal cistern to form the cisterna velum
interpositum. The upper layer of tela choroidea is
attached to the lower surface of the fornix and the
hippocampal commissure (Figs. 3.2 and 3.3). The
anterior part of the lower wall is attached to the teniae
thalami, small ridges on the free edge of a fiber tract, the
striae medullaris thalami, which extends along the
superomedial border of the thalamus from the foramen
of Monro to the habenular commissure. The posterior
part of the lower wall is attached to the superior surface
of the pineal body. The internal cerebral veins arise in
the anterior part of the velum interpositum, just behind
the foramen of Monro, and they exit the velum inter-
Figure 3.2. A-D. Neural relationships. A. Superior view. The upper part of the cerebral
hemispheres has been removed to expose the lateral ventricles. The frontal horn (Front.
Horn) extends into the frontal lobe (Front. Lobe) anterior to the foramen of Monro (For.
Monro). The body of the lateral ventricle (Body Lat. Vent.) is behind the foramen of
Monro and above the thalamus. The atrium is located posterior to the thalamus deep to
the parietal lobe (Par. Lobe). The occipital horn (Occip. Horn) extends backward from
the atrium into the occipital lobe (Occip. Lobe). The temporal horn extends forward from
the atrium into the temporal lobe (Temp. Lobe). The lateral wall of the frontal horn is
formed by the head of the caudate nucleus (Caudate Nucl. Head); the floor medial to the
caudate nucleus is formed by the rostrum of the corpus callosum; the medial wall is
formed by the septum pellucidum (Sept. Pell.); the anterior wall is formed by the forceps
minor, a bundle composed of fibers crossing in the genu of the corpus callosum; and the
roof is formed by the anterior part of the body and the posterior part of the genu of the
corpus callosum. The lateral wall of the body of the lateral ventricle is formed by the
body of the caudate nucleus: the floor is formed by the superior surface of the thalamus;
the roof is formed by the body of the corpus callosum; and the medial wall is formed by
the septum pellucidum above and the body of the fornix below. The fornix passes along
and is separated from the superomedial margin of the thalamus by a narrow cleft, the
choroidal fissure (Chor. Fiss.), along which the choroid plexus (Chor. Plex.) is attached.
The choroid plexus has been removed along the posterior part of the choroidal fissure on
the right side. The atrium and occipital horn have the same structures in their walls. The
lateral part of the anterior wall of the atrium is formed by the pulvinar, and the medial
part is formed by the cms of the fornix. The superior part of the medial wall is formed by
a large fiber tract from the splenium, the forceps major, which interconnects the occipital
lobes and produces a prominent bulge in the medial wall called the bulb of the corpus
callosum. The inferior part of the medial wall is formed by the calcar avis, a prominence
overlying the depths of the calcarine sulcus. The medial part of the floor of the atrium is
formed by the posterior part of the hippocampus, the smooth prominence overlying the
hippocampal formation, and the lateral part of the floor is formed by the collateral
trigone (Collat. Trig.), a prominence that overlies the collateral sulcus on the inferior
surface of the temporal lobe. The lateral wall just posterior to the pulvinar is formed by
the tail of the caudate nucleus as it wraps around the lateral edge of the pulvinar, and the
part behind the caudate nucleus is formed by the tapetum of the corpus callosum, a fiber
tract from the body and splenium that passes around the lateral margin of the atrium and
the temporal horn. The parietooccipital sulcus (Par. Occip. Sufc.) extends deeply into the
medial surface of the hemisphere above the cuneus. The superior sagittal sinus (Sup.
Sag. Sinus) courses in the outer periphery of the falx. B. Enlarged view of the region of
the foramen of Monro. The choroid plexus has been removed from its attachment along
the choroidal fissure on the right side. The anterior thalamic tubercle (Ant. Thal. Tuber.),
which overlies the anterior nucleus of the thalamus, bulges upward at the posterior
margin of the foramen of Monro. The columns of the fornix pass anterior and superior to
the foramen of Monro. The striothalamic sulcus (Str. Thal. Sufc.) separates the caudate
nucleus and the thalamus. C. The level of the cross section has been extended deeper into
the right cerebral hemisphere through the caudate nucleus and the thalamus. The
posterior part of the body and the superior part of the crus of the fornix have been
removed on the right side to expose the tela choroidea (Tela) in the roof of the third
ventricle. The anterior limb of the internal capsule (Int. Cap. Ant. Limb) is located
between the head of the caudate nucleus and the lentiform nuclei (Lent. Nucl.). The
posterior limb of the internal capsule (Int. Cap. Post. Limb) is located between the
thalamus and the lentiform nucleus. The genu of the internal capsule (Genu Int. Cap.)
touches the lateral wall of the ventricle between the caudate nucleus and the thalamus.
The calcar avis and the bulb of the corpus callosum (Bulb Corp. Call.) bulge into the
medial wall of the atrium and the occipital horn. The collateral trigone bulges in the floor
of the atrium. The glomus, a large tuft of choroid plexus, is attached in the atrium
between the fornix and the pulvinar. D. The fornix has been divided at the junction of its
body and the columns above the foramen of Monro and reflected backward to expose the
velum interpositum (Vel. Interpos.) located between the layers of tela choroidea in the
roof of the third ventricle. The medial part of the floor of the temporal horn (Temp.
Horn) is formed by the hippocampus, the smooth prominence overlying the hippocampal
formation, and the lateral part of the floor is formed by the collateral eminence (Coff.
Eminence), which overlies the deep part of the collateral sulcus. The pes hippocampus
(Pes Hipp.) is the bulbous, digitated anterior part of the hippocampal formation. The
hippocampal commissure (Hipp. Comm.) interconnects the medial margins of the crura
of the fornix.
Figure 3.2. E-H. Neural relationships (continued). E. The body and anterior part of the
crura of the fornix have been removed to expose the third ventricle (3 Vent.) and the
quadrigeminal plate and pineal regions. The massa intermedia (Massa Inter.) extends
into the third ventricle anteriorly, and the habenular (Hab. Comm.) and posterior (Post.
Comm.) commissures cross the posterior part of the third ventricle. The habenular
commissure is connected anteriorly with the habenular trigones (Hab. Trig.) and the
striae medullaris thalami (Str. Med. Thal.). The pineal body projects posteriorly above
the superior (Sup. Coll.) and inferior colliculi (Inf. Coll.). The subiculum, the rounded
medial edge of the parahippocampal gyrus, is exposed lateral to the colliculi. The inferior
sagittal sinus (Inf. Sag. Sinus) courses in the inferior margin of the falx and joins the
straight sinus at the tentorial apex (Apex. Tent.). F. Right superolateral view. The frontal
and parietal operculae have been removed to expose the sylvian fissure (Sylvian Fiss.)
and the transverse temporal gyri (Transv. Temp. Gyr.). G. Further removal of deep
cerebral tissue exposes the hippocampal formation and the collateral eminence in the
floor of the temporal horn. The collateral eminence is continuous posteriorly with the
collateral trigone in the floor of the atrium. H. Enlarged view to show structures in the
medial wall of the atrium and the floor of the temporal horn. The fimbria of the fornix
arises on the surface of the hippocampus and is continuous posteriorly with the crus of
the fornix. (From Ono M, Rhoton AL Jr, Peace DA, Rodriguez R: Microsurgical
anatomy of the deep venous system of the brain. Neurosurgery 15:621-657, 1984.)
Figure 3.3. Superior view of stepwise dissection of layers in the roof of the third
ventricle. A. Superior part of cerebral hemispheres, with the corpus callosum (Corp.
Call.) including a part of the splenium removed to expose the choroid plexus (Ch. PL) of
the lateral ventricle. A superior choroidal vein (S. Ch. V.) passes along the free edge of
the choroid plexus. The glomus of the choroid plexus projects into the atrium. The
caudate nucleus projects into the anterior horn and body of the lateral ventricle. The
septum pellucidum (Sept. Pel.) forms the medial walls of the lateral ventricles. The
bodies of the fornix are medial to the choroid plexus in the bodies of the lateral ventricle.
B. The body of the fornix and septum pellucidum are divided and lifted up to expose the
tela choroidea (Tela) in the roof of the third ventricle. C. The body of the fornix removed
at the junction with the columns of the fornix (Columns). The medial posterior choroidal
arteries (M. P. Ch. A., broken line) course between the upper and lower layers of the tela
choroidea. D. The tela choroidea was removed to expose the parallel strands of choroid
plexus in the roof of the third ventricle (Ch. PI.-3V) and the interior third ventricle (3V).
Part of the splenium of the corpus callosum was removed to show the pineal body. Right
and left thalami form the lateral walls of the third ventricle. (From Fujii K, Lenkey C,
Rhoton AL Jr: Microsurgical anatomy of the choroidal arteries: Lateral and third
ventricles. J Neurosurg 52:165-188, 1980.)
Figure 3.4. Inferior views of the roof of the third ventricle. A. The portion of the third
ventricle and cerebral hemispheres below the roof of the third ventricle has been
removed to provide an inferior view of the roof. The choroid plexus (Ch. Pl.) hangs
downward from the tela choroidea into the superior part of the third ventricle. The
internal cerebral veins (Int. Сет. V) and the medial posterior choroidal arteries (Med.
Post. Ch. A.) course below the fornix and between the two halves of the thalamus. The
choroid plexus in the roof of the third ventricle is continuous through the foramen of
Monro (F. Monro) with the choroid plexus in the lateral ventricle. The body of the
fornix splits into two columns at the anterior margin of the foramen of Monro. The
anterior commissure (Ant. Comm.) is anterior to the columns of the fornix. The massa
intermedia (Massa Inter.) projects into the upper partof the third ventricle. The
internal cerebral veins join to form the vein of Galen (V. Galen) in the posterior part
of the roof. B. The medial edges of the thalamus on each side have been removed to
provide a wider view of the body and crura of the fornix, the medial posterior
choroidal arteries, and the internal cerebral veins. The crura of the fornix pass
posteriorly below the sple-nium of the corpus callosum (Splenium). The internal
cerebral veins pass posteriorly above the pineal gland (Pineal) and join to form the
vein of Galen. The choroidal fissure (Chor. Fiss.) is a groove on each side between the
fornix and the thalamus. The upper part of the stalk of the pineal gland formed by the
habenular commissure (Hab. Comm.) has been preserved. C. The choroidal fissure on
each side has been opened wider by the removal of more of the medial surface of the
thalamus. The lateral ventricles (Lat. Vent.) are seen through the enlarged choroidal
fissures. The choroid plexus of the lateral ventricles is exposed and branches of the
lateral posterior choroidal arteries (Lat. Post. Ch. A.) and the superior choroidal veins
(Sup. Ch. V.) are seen on the surface of the choroid plexus. The hippocampal
commissure (Hippo. Comm.) interconnects the medial margins of the crura of the
fornix above the pineal gland. The pineal gland is below the splenium and the
hippocampal commissure. The posterior part of the crura of the fornix and the
hippocampal commissure are adherent to the lower margin of the splenium of the
corpus callosum. (From Yamamoto I, Rhoton AL Jr, Peace DA: Microsurgery of the
third ventricle: Part 1. Microsurgical anatomy. Neurosurgery 8:334-356, 1981.)
Floor
The floor extends from the optic chiasm anteriorly to the
orifice of the aqueduct of Sylvius posteriorly (Figs. 3.1 and
3.5). The anterior half of the floor is formed by
diencephalic structures and the posterior half is formed by
mesence-phalic structures.
When viewed from inferiorly, the structures forming the
floor from anterior to posterior include the optic chiasm,
the infundibulum of the hypothalamus, the tuber cinereum,
the mamil-lary bodies, the posterior perforated substance,
and (most posteriorly) the part of the tegmentum of the
midbrain located above the medial aspect of the cerebral
peduncles. The optic chiasm is located at the junction of
the floor and the anterior wall of the third ventricle. The
chiasm slopes posteriorly and superiorly from its junction
with the optic nerves. The inferior surface of the chiasm
forms the anterior part of the floor and the superior surface
forms the lower part of the anterior wall. The optic tracts
arise from the posterolateral margin of the chiasm and
course obliquely away from the floor toward the lateral
margin of the midbrain. The infundibulum, tuber cinereum,
mamillary bodies, and posterior perforated substance are
located in the space limited anteriorly and laterally by the
optic chiasm and tracts and posteriorly by the cerebral
peduncles.
The infundibulum of the hypothalamus is a hollow,
funnel-shaped structure located between the optic chiasm
and the tuber cinereum. The pituitary gland (hypophysis) is
attached to the infundibulum, and the axons in the
infundibulum extend to the posterior lobe of the hypo-
physis. The tuber cinereum is a prominent mass of
hypothlamic gray matter located anterior to the mamillary
bodies. The tuber cinereum merges anteriorly into the
infundibulum. The tuber cinereum around the base of the
infundibulum is raised to form a prominence called the
median eminence. The mamillary bodies form paired,
round prominences posterior to the tuber cinereum. The
posterior perforated substance is a depressed, punctuated
area of gray matter located in the interval between the
mamillary bodies anteriorly and the medial surface of the
cerebral peduncles posteriorly. The posterior part of the
floor extends posterior and superior to the medial part of
the cerebral peduncles and superior to the tegmentum of
the midbrain.
When viewed from above and inside the third ventricle,
the optic chiasm forms a prominence at the anterior margin
of the floor (Fig. 3.5). The infundibular recess extends into
the infundibu-lum behind the optic chiasm. The mamillary
bodies form paired prominences on the inner surface of the
floor posterior to the infundibular recess. The part of the
floor between the mamillary bodies and the aqueduct of
Sylvius has a smooth surface, which is concave from side
to side. This smooth surface lies above the posterior perfo-
rated substance anteriorly and the medial part of the
cerebral peduncles and the tegmentum of the midbrain
posteriorly.
Anterior Wall
The anterior margin of the third ventricle extends from
the foramina of Monro above to the optic chiasm below
(Figs. 3.1, 3.5, and 3.6). Only the lower two-thirds of the
anterior surface is seen on the external surface of the brain;
the upper one-third is hidden posterior to the rostrum of the
corpus callosum. The part of the anterior wall visible on
the surface is formed by the optic chiasm and the lamina
terminalis. The lamina terminalis is a thin sheet of gray
matter and pia mater that attaches to the upper surface of
the chiasm and stretches upward to fill the interval between
the optic chiasm and the rostrum of the corpus callosum.
When viewed from within, the boundaries of the anterior
wall from superiorly to inferiorly are formed by the
columns of the fornix, foramina of Monro, anterior
commissure, lamina terminalis, optic recess, and optic
chiasm. The foramen of Monro on each side is located at
the junction of the roof and the anterior wall (Figs. 3.1 and
3.5). The foramen is a ductlike canal that opens between
the fornix and the thalamus into the lateral ventricle and
extends inf eriorly below the fornix into the third ventricle
as a single channel. The foramen of Monro is bounded
anteriorly by the junction of the body and the columns of
the fornix and posteriorly by the anterior pole of the
thalamus (Figs. 3.1, 3.2, and 3.5). The size and shape of the
foramina of Monro depend on the size of the ventricles: if
the ventricles are small, each foramen is a crescent-shaped
opening bounded anteriorly by the concave curve of the
fornix and posteriorly by the convex anterior tubercle of the
thalamus. As the ventricles enlarge, the foramen on each
side becomes rounder. The structures that pass through the
foramen are the choroid plexus, the distal branches of the
medial posterior choroidal arteries, and the internal
cerebral, thalamostriate, superior choroidal, and septal
veins.
The anterior commissure is a compact bundle of
myelinated nerve fibers that cross the midline in front of
the columns of the fornix. The anter-oposterior diameter of
the anterior commissure varies from 1.5 to 6.0 mm (55).
The distance from the posterior end of the anterior
commissure to the anterior border of the foramen of Monro
ranges from 1.0 to 3.5 mm (average, 2.2 mm). The distance
from the upper edge of the optic chiasm to the anterior
border of the anterior commissure ranges from 8 to 12 mm
(average, 10 mm). The lamina terminalis fills the interval
between the anterior commissure and the optic chiasm
(Fig. 3.1). The lamina attaches to the midportion of the
superior surface of the chiasm, leaving a small cleft
between the upper half of the chiasm and the lamina, called
the optic recess.
Figure 3.5. Anterosuperior views of the third ventricle. A. Part of the anterior wall of the third ventricle and the
anterior part of the cerebral hemispheres have been removed. The septum pellucidum (Sept. Pel.) is attached to the
upper margin of the fornix. The optic chiasm (O. Ch.) and nerves (O. N.) are at the lower margin of the anterior
wall, and the optic tracts (O. Tr.) extend laterally below the floor of the third ventricle (3V). The choroid plexus (Ch.
Pi.) is attached over the surface of the thalamus on each side. The thalamostriate vein on each side (Thal. Sir. V.)
courses forward between the caudate nucleus (Caudate Nucl.) and the thalamus. The infundibular recess (Infund.
Recess) extends downward posterior to the optic chiasm and anterior to the mamillary bodies (Mam. В.). The
midportion of the anterior commissure (Ant. Comm.) has been removed to expose the columns of the fornix anterior
to the foramina of Monro. The body and columns of the fornix join anterior to the foramina of Monro. The corpus
callosum (Corp. Call.) is above the lateral ventricles. B. The septum pellucidum and the medial part of the body of
the fornix have been removed to expose each foramen of Monro (F. Monro) and the full length of the floor of the
third ventricle. The floor extends from the aqueduct of Sylvius (Aqueduct) posteriorly to the optic chiasm anteriorly.
The habenular commissure (Hab. Comm.) forms the upper margin of the stalk of the pineal gland (Pineal), and the
posterior commissure (Post. Comm.) forms the lower stalk of the pineal gland. The pineal recess is between the two
commissures. A branch of the medial posterior choroidal artery (Med. Post. Ch. A.) passes under the fornix to join
the choroid plexus. The superior choroidal veins (Sup. Ch. V.) course on the surface of the choroid plexus. The crus
of the fornix is above the pineal gland. The optic recess (O. Recess) extends anterior to the upper one-half of the
optic chiasm. C. The body of the fornix has been removed to show the internal cerebral veins (Int. Сет. V.) and the
medial posterior choroidal arteries in the roof of the third ventricle. A ventricular vein drains into the internal
cerebral vein. The internal cerebral veins join to form the vein of Galen (V. Galen). D. Enlarged view shows the
habenular commissure above the posterior commissure below the pineal recess. The internal cerebral veins and the
medial posterior choroidal arteries pass forward and intermingle along the superolateral margin of the pineal gland.
The columns of the fornix are anterior to the foramen of Monro. The crura of the fornix are above the pineal gland
and below the splenium (Splenium) of the corpus callosum. (From Yamamoto I, Rhoton AL Jr, Peace DA:
Microsurgery of the third ventricle: Part 1. Microsurgical anatomy. Neurosurgery 8:334-356, 1981.)
Figure 3.6. Neural relationships. Posterior and midsagittal views. A. Posterior view with
orientation as shown in the insert. The right occipital lobe (Occip. Lobe) has been
retracted away from the tentorium (Tent.) and the straight (Str. Sinus) and inferior sagittal
(Inf. Sag. Sinus) sinuses to expose the tentorial apex (Apex Tent.). The tentorium behind
its free edge (Tent. Edge) has been opened to expose the superior surface of the
cerebellum. The pineal body projects backward above the superior colliculi (Sup. Coll.).
The habenular commissure (Hab. Comm.) crosses the posterior end of the third ventricle.
The suprapineal recess (Sup. Pineal Recess) of the third ventricle extends posteriorly
between the superior surface of the pineal body and the tela choroidea (Tela) in the roof
of the third ventricle. The isthmus of the cingulate gyrus (Isthmus) is a narrow cortical
bridge between the cingulate (Cing. Gyr.) and parahippocampal (Parahippo. Gyr.) gyri.
The medial geniculate body (Med. Gen. Body) and brachium of the inferior colliculus
(Brach. Inf. Coll.) are posterior to the cerebral peduncle (Ped.). B. Posterior view. The
posterior part of the cerebral hemispheres has been removed to expose the posterior part
of the third ventricle (3rd Vent.) and the pineal region, where the deep veins converge on
the vein of Galen. The atria and the bodies of the lateral ventricles (Body Lat. Vent.) are
deep within the parietal lobe (Par. Lobe), below the corpus callosum (Corp. Call.). The
caudate nuclei (Caudate Nucl.) are lateral to the thalami. The crura of the fornix pass
around the pulvinar. Choroid plexus (Chor. Plex.) is attached along the choroidal fissure,
the cleft between the fornix and the thalamus. The subiculum is the rounded medial edge
of the parahippocampal gyrus of the temporal lobe (Temp. Lobe). The collateral sulcus
(Coll. Sulc.) is lateral to the parahippocampal gyrus. C. Posterior view below the
tentorium. The cerebellum was removed by dividing the superior (Sup. Cer. Ped.),
middle (Mid. Cer. Ped.), and inferior (Inf. Сет. Ped.) cerebellar peduncles just dorsal to
the floor of the fourth ventricle (4 Vent.}. The structures just above the posterior part of
the incisura include the splenium, the crura of the fornix, the pineal body, and the
superior and inferior colliculi (Inf. Coll.). The trochlear nerves (V) arise below the inferior
colliculi and pass around the brain stem. The superior medullary velum (Sup. Med.
Velum) forms the medial part of the roof of the fourth ventricle. The flocculus and the
rhomboid lip border the lateral recess (Lat. Recess) of the fourth ventricle and extend
laterally above the glossopharyngeal (IX), vagus (X), and accessory (XI) nerves. The
hippocampal commissure (Hippo. Comm.) is a fiber tract connecting the medial margins
of the crura of the fornix. D. Midsagittal section. The rostrum of the corpus callosum is
continuous below the anterior commissure (Ant. Comm.) with the lamina termin-alis
(Lam. Term.). The massa intermedia (Massa Inter.) protrudes into the central part of the
third ventricle. The pineal body is attached to the posterior part of the third ventricle by a
stalk composed of the habenular and posterior commissures (Post. Comm.). The striae
medullaris thalami (Str. Med. Thal.) course on the medial surface of the thalamus from
the foramen of Monro to the habenular commissure. The septum pellucidum and the part
of the fornix above the thalamus have been removed. The choroid plexus is attached
along the choroidal fissure (Chor. Fiss.), the cleft between the fornix and thalamus. The
caudate nucleus (Caudate Nucl.) is exposed in the far wall of the frontal horn (Front.
Horn) and the body of the right lateral ventricle. The cms of the fornix is fused for a short
distance to the lower surface of the splenium. The brain stem has been sectioned at the
level of the cerebral peduncle. The dentate gyrus (Dentate Gyr.) forms a beaded
longitudinal cortical strip above the parahippocampal gyrus. The hippocampal sulcus
(Hippo. Sulc.) separates the dentate and parahippocampal gyri. The fimbria of the fornix
arises on the surface of the hippocampal formation in the floor of the temporal horn and
forms a longitudinal strip that is separated from the dentate gyrus by the fimbriodentate
sulcus (Fimb. Dentate Sulc.). The fimbria is continuous posteriorly with the crus of the
fornix. The column of the fornix passes anterior and superior to the foramen of Monro
(For. Monro) to terminate in the mamillary bodies (Mam. Body). The lateral geniculate
body (Lat. Gen. Body) protrudes from the inferior surface of the thalamus. The
infundibular recess (Infund. Recess) extends inferiorly into the base of the infundibulum.
The hypothalamic sulcus (Hypothal. Sulc.) separates the thalamus and hypothalamus.
(From Ono M, Rhoton AL Jr, Peace DA, Rodriguez R: Micro-surgical anatomy of the
deep venous system of the brain. Neurosurgery 15:621-657, 1984.)
Figure 3.7. A-D. Tentorial incisura: stepwise dissection, anterior-superior view. A. The
anterior part of the frontal lobe has been removed to expose the anterior incisural space.
The section of the frontal lobe passes adjacent to the septum pellucidum (Sept. Pell.) and
through the rostrum and genu of the corpus callosum (Corp. Call.), the caudate nucleus
(Caudate Nucl.), the putamen, and the frontal horn of the lateral ventricle (Lat. Vent.).
The choroid plexus (Chor. Plex.) extends through the foramen of Monro (For. Monro).
The anterior incisural space is located anterior to the midbrain and extends upward
around the optic chiasm, lamina terminalis (Lam. Term.), and anterior part of the third
ventricle (3 Vent). The optic tract (Optic Tr.) extends posteriorly above the oculomotor
nerve (HI). The infundibulum (Infund.) of the pituitary gland passes through the
diaphragma sellae (Diaph.). The carotid artery (Car. A.) has been divided below the optic
nerve (Optic N.). The cingulate gyri (Cing. Gyr.) lie above the corpus callosum. A septal
vein (Septal V.) courses on the septum pellucidum. The paraterminal (Paraterm. Gyr.)
and paraolfactory gyri (Paraolf. Gyr.) are above the gyrus rectus (Gyr. Rectus). The
semilunar (Semilunar Gyr.) and ambient gyri (Ambient Gyr.) are on the superior surface
of the temporal lobe bordering the sylvian fissure (Sylvian Fiss.). The anterior limb of the
internal capsule (Int. Cap. Ant. Limb) is situated between the caudate nucleus and the
putamen. The oculomotor nerve enters the dura mater posterior to the anterior clinoid
process (Ant. Ciinoid). B. The transverse section has been extended behind the foramen
of Monro to include part of the cerebral peduncle (Ped.). The posterior part of the right
optic nerve and the right half of the optic chiasm have been removed to expose the
posterior part of the anterior incisural space. The substantia nigra (Subst. Nigra) and red
nucleus (Red. NucL) are at the level of the transection of the midbrain. The thalamus and
internal capsule are located directly above the cerebral peduncle. The middle incisural
space is between the uncus and the midbrain. The parahippocampal gyrus (Parahippo.
Gyr.) and uncus protrude medial to the tentorial edge (Tent. Edge). The caudate nucleus
extends from the lateral part of the frontal horn around the atrium into the roof of the
temporal horn (Temp. Horn), where the tail of the caudate nucleus is located. The
lentiform nucleus formed by the globus pallidus (Globus Pall.) and the putamen are
lateral to the internal capsule. The collateral sulcus (Coll. Sulc.) extends into the temporal
lobe near the lateral part of the temporal horn. The anterior hippocampal sulcus (Ant.
Hippo. Sulc.) separates the uncus and parahippocampal gyrus. The anterior commissure
(Ant. Comm.) is in the anterior, the mamillary bodies (Mam. Body) are in the inferior,
and the massa intermedia (Massa Int.) is in the central part of the third ventricle. The
choroid plexus is attached in the lateral and third ventricle along the choroidal fissure
(Chor. Fiss.) located between the fornix and the thalamus. The callosal sulcus (Call.
Sulc.) separates the corpus callosum and the cingulate gyrus. C. Enlarged view. The
anterior choroidal (Ant. Chor. A.) and posterior cerebral arteries (P. C. A.) pass around
the cerebral peduncle medial to the uncus and the parahippocampal gyrus. The tela
choroidea and choroid plexus in the temporal horn are attached to the tenia choroidea and
the tenia fimbriae along the choroidal fissure in the medial part of the temporal horn. The
pontomesencephalic sulcus (Pon. Mes. Sulc.) marks the junction of the midbrain and
pons. The oculomotor nerve enters the dura lateral to the posterior clinoid process (Post.
Clinoid). The trochlear nerve (IV) passes below the uncus. D. The coronal section
extends just behind the posterior (Post. Comm.) and habenular (Hab. Comm.)
commissures into the base of the pineal body (Pineal). The internal cerebral veins (Int.
Cer. V.) course in the velum interpositum located between the two layers of the tela
choroidea (Tela) in the roof of the third ventricle. The upper layer of tela is attached to
the lower surface of the fornix. The mesial temporal structures that form the lateral wall
of the middle incisural space include the subiculum, the rounded medial surface of the
parahippocampal gyrus, which blends into the Ammon's horn (a curled horn-shaped
collection of gray matter in the hippocampal formation), the dentate gyrus (Dentate
Gyr.), a strip of cortex located above the subiculum, and the fimbria of the fornix, a fiber
tract that arises in the floor of the temporal horn on the surface of the hippocampal
formation. The pineal body projects into the posterior incisural space below the
suprapineal recess and the internal cerebral veins. The medial (Med. Gen. Body) and
lateral geniculate bodies (Lat. Gen. Body) are dorsolateral to the cerebral peduncle.
 midbrain anteriorly, the splenium above, and the cer-
ebellum below. The vein of Galen (V. of Galen) enters the
straight sinus. The trochlear nerve arises below the inferior
colliculus (Inf. Coll.) and passes forward in the
cerebellomesencephalic fissure (Cer. Mes. Fiss.) situated
between the cerebellum and midbrain. The paraterminal
and paraolfactory gyri, the gyrus rectus, and the anterior
(Ant. Paraolf. Sulc.) and posterior paraolfactory (Post.
Paraolf. Sulc.) sulci are below the rostrum. The optic
recess extends inferiorly between the optic chiasm and the
lamina terminalis, and the infundibular recess (Infund.
Recess) extends into the infundibulum behind the chiasm.
The layer of tela choroidea that forms the upper wall of the
velum interpositum is adherent to the lower margin of the
body and cms of the fornix. The layer of tela choroidea that
forms the lower wall of the velum interpositum is attached
anteriorly to the striae medullaris thalami (Str. Med. Thal.)
and posteriorly it adheres to the superior margin of the
pineal body. The striae medullaris thalami extend forward
from the habenular commissure along the superomedial
margin of the thalamus. The lateral mesencephalic sulcus
(Lat. Mes. Sulc.) extends along the posterior edge of the
cerebral peduncle, and the interpeduncular fossa (Interped.
Fossa) is between the cerebral peduncles. G. Enlarged
view. The tela choroidea and the deep veins have been
removed. The choroidal fissure is located between the
fornix and the thalamus. The isthmus of the cingulate gyrus
(Isthmus) is a cortical bridge between the parahippocampal
and cingulate gyri. The fasciolar gyrus and the gyri
Andreae Retzii form a beaded collection of gray matter that
is continuous below with the dentate gyrus and above with
the indusium griseum, a thin layer of gray matter on the
surface of the corpus callosum. The quadrangular lobule
(Quad. Lobule) of the cerebellum is behind the colliculi.
(From Ono M, Ono M, Rhoton AL Jr, Barry M:
Microsurgical anatomy of the region of the tentorial
incisura. J Neurosurg 60:365-399, 1984.)

Figure 3.7. E-G. Tentorial incisura (continued). E. The

level of the section has been extended behind the pineal
body to expose the posterior incisural space and the vein of
Galen. The pineal body projects into the posterior incisural
space. The parahippocampal gyrus overlies the free edge
and forms part of the lateral wall of the posterior incisural
space. The fibers arising on the surface of the hippocampal
formation pass through the fimbria to the crus of the fornix,
which extends upward toward the splenium. The parahip-
pocampal gyrus is separated from the dentate gyrus by the
hippocampal sulcus (Hipp. Sulc.), and the fornix is
separated from the dentate gyrus by the fim-briodentate
sulcus (Fimb. Dent. Sulc.). F. The right cerebral
hemisphere has been removed to expose all of the posterior
incisural space located between the apex of the tentorium
(Apex. Tent.) posteriorly, the

Posterior Wall
The posterior wall of the third ventricle extends from the
suprapineal recess above to the aqueduct of Sylvius below
(Figs. 3.1, 3.5, and 3.6). When viewed from anteriorly and
within the third ventricle, it consists, from above to below,
of the suprapineal recess, the habenular commissure, the
pineal body and its recess, the posterior commissure, and
the aqueduct of Sylvius (Fig. 3.5). The suprapineal recess
projects posteriorly between the upper surface of the pineal
gland and the lower layer of tela choroidea in the roof. The
pineal gland extends posteriorly into the quadrigeminal
cistern from its stalk. The stalk of the pineal gland has a
cranial and a caudal lamina. The habenular commissure,
which interconnects the habenulae, crosses the midline in
the cranial lamina, and the posterior commissure crosses in
the caudal lamina. The pineal recess projects posteriorly
into the pineal body between the two laminae. The shape of
the orifice of the aqueduct of Sylvius is triangular: the base
of the triangle is on the posterior commissure and the other
two limbs are formed by the central gray matter of the
midbrain.
When viewed from posteriorly, the only structure in the
posterior wall is the pineal body (Fig. 3.6). The pineal
gland projects posteriorly into the quadrigeminal cisterns
and is concealed by the splenium of the corpus callosum
above, the thalamus laterally, and the quadrigeminal plate
and the vermis of the cerebellum inferiorly.
Lateral Wall
The lateral walls are not visible on the external surface
of the brain, but are hidden between the cerebral
hemispheres (Figs. 3.1, 3.6, and 3.7). They are formed by
the hypothalamus inferiorly and the thalamus superiorly.
The lateral walls have an outline like the lateral silhouette
of a bird's head with an open beak. The head is formed by
the oval medial surface of the thalamus; the open beaks,
which project anteriorly and inferiorly, are represented by
the recesses in the hypothalamus: the pointed upper beak is
formed by the optic recess and the lower beak is formed by
the infundibular recess. The hypo-thalamic and thalamic
surfaces are separated by the hypothalamic sulcus, a
groove that is often
ill-defined and extends from the foramen of Monro to the
aqueduct of Sylvius. The superior limit of the thalamic
surfaces of the third ventricle is marked by narrow, raised
ridges, known as the striae medullaris thalami. These striae
extend forward from the habenulae along the su-
peromedial surface of the thalamus at the site of the
attachment of the lower layer of the tela choroidea. The
habenulae are small eminences on the dorsomedial surfaces
of the thalamus just in front of the pineal gland. The
habenulae are connected across the midline in the rostral
half of the stalk of the pineal gland by the habenular
commissure.
The massa intermedia projects into the upper one-half of
the third ventricle and often connects the opposing surfaces
of the thalamus. The massa intermedia was present in 76%
of the brains examined and was located 2.5 to 6.0 mm
(average, 3.9 mm) posterior to the foramen of Monro (55).
The columns of the fornix form distinct prominences in the
lateral walls of the third ventricle just below the foramen of
Monro, but inferiorly they sink below the surface.
Lateral Ventricles
An understanding of the anatomy of the lateral ventricles
is important because third ventricular tumors are
commonly approached through the lateral ventricles. Each
of the paired lateral ventricles is a C-shaped cavity that
wraps around the thalamus and is situated deep within the
cerebrum (Figs. 3.2, 3.3, and 3.7). Each ventricle has five
parts: the frontal, temporal, and occipital horns and the
body and atrium. Each of these five parts has medial and
lateral walls, a roof, and a floor; in addition, the frontal and
temporal horns and the atrium have anterior walls. These
walls are formed predominantly by the thalamus, septum
pellucidum, deep cerebral white matter, corpus callosum,
and two C-shaped structures, the caudate nucleus and
fornix, which wrap around the thalamus.
The thalamus is located in the center of the lateral
ventricle. Each lateral ventricle wraps around the superior,
inferior, and posterior surfaces of the thalamus. The body
of the lateral ventricle is above the thalamus, the atrium
and occipital horn are posterior to the thalamus, and the
temporal horn is inferior to the thalamus. The superior
surface of the thalamus forms the floor of the body, the
posterior surface of the thalamus forms the anterior wall of
the atrium, and the inferior surface of the thalamus forms
the medial part of the roof of the temporal horn.
The caudate nucleus is an arched, C-shaped,
 cellular mass that wraps around the thalamus and
constitutes an important part of the wall of the lateral
ventricle. It has a head, body, and tail. The head bulges into
the lateral wall of the frontal horn and the body of the
lateral ventricle. Its body forms part of the lateral wall of
the atrium, and its tail extends from the atrium into the roof
of the temporal horn and is continuous with the amygdaloid
nucleus near the tip of the temporal horn. In the body of the
lateral ventricle, the caudate nucleus is superolateral to the
thalamus; in the atrium, it is posterolateral to the thalamus;
and, in the temporal horn, it is inferolateral to the thalamus.
The striae terminalis, a fiber tract that runs parallel and
deep to the thalamostriate vein, arises in the amygdaloid
nucleus and courses along the border between the caudate
nucleus and the thalamus in the wall of the lateral ventricle.
The fornix is another C-shaped structure that wraps
around the thalamus in the wall of the ventricle. The fornix
has four parts (the fimbria, crus, body, and columns) and
extends from the floor of the temporal horn around the
thalamus to the mamillary bodies. In the body of the lateral
ventricle, the body of the fornix is in the lower part of the
medial wall; in the atrium, the crus of the fornix is in the
medial part of the anterior wall; and, in the temporal horn,
the fimbria of the fornix is in the medial part of the floor.
The corpus callosum, which forms the largest part of the
ventricular walls, contributes to the wall of each of the five
parts of the lateral ventricle. The corpus callosum has two
anterior parts, the rostrum and genu; a central part, the
body; and a posterior part, the splenium. The rostrum is
situated below and forms the floor of the frontal horn. The
genu gives rise to a large fiber tract, the forceps minor,
which forms the anterior wall of the frontal horn as it
sweeps obliquely forward and lateral to connect the frontal
lobes. The genu and the body of the corpus callosum form
the roof of both the frontal horn and the body of the lateral
ventricle. The splenium gives rise to a large tract, the
forceps major, which forms a prominence, the bulb, in the
upper medial wall of the atrium and the occipital horn as it
sweeps posteriorly to connect the occipital lobes. Another
fiber tract, the tapetum, which arises in the posterior part of
the body of the corpus callosum, sweeps laterally and
inferiorly to form the roof and lateral walls of the atrium
and the temporal and occipital horns.
The septum pellucidum, which is composed of paired
laminae, separates the frontal horns and bodies of the
lateral ventricles in the midline. In
the frontal horn, the septum pellucidum is attached to the
rostrum of the corpus callosum below, the genu anteriorly,
and the body above. In the body of the lateral ventricle, the
septum is attached to the body of the corpus callosum
above and the body of the fornix below. The septum
pellucidum disappears posteriorly where the body of the
fornix meets the splenium. There may be a cavity, the
cavum septum pellucidum, in the midline between the
laminae of the septum pellucidum.
The choroid plexus in the lateral ventricle has a C-
shaped configuration that parallels the fornix (Figs. 3.1 to
3.3) (8). It is attached along the choroidal fissure, a narrow
cleft between the fornix and the thalamus, in the medial
part of the body, atrium, and temporal horn. The choroid
plexus extends through the foramen of Monro into the roof
of the third ventricle. In the atrium, the choroid plexus has
a prominent triangular tuft called the glomus. The edges of
the thalamus and fornix bordering this fissure have small
ridges, the teniae, along which the tela choroidea, the
membrane in which the choroid plexus arises, is attached.
The choroidal fissure extends from the foramen of Monro
along the medial wall of the body, atrium, and temporal
horn to its inferior termination, the inferior choroidal point,
located just behind the tip of the temporal lobe and uncus.
The veins coursing in the walls of the ventricles exit the
ventricles by passing, in a subependymal location, through
the margin of this fissure to reach the internal cerebral,
basal, or great veins.
The frontal horn, the part of the lateral ventricle located
anterior to the foramen of Monro, has a medial wall formed
by the septum pellucidum, an anterior wall formed by the
genu of the corpus callosum, a lateral wall composed of the
head of the caudate nucleus, and a narrow floor formed by
the rostrum of the corpus callosum (Fig. 3.2). The columns
of the fornix, as they pass anterior to the foramen of
Monro, are in the posteroinfer-ior part of the medial wall.
The body of the lateral ventricle extends from the
posterior edge of the foramen of Monro to the point where
the septum pellucidum disappears and the corpus callosum
and fornix meet. The roof is formed by the body of the
corpus callosum, the medial wall by the septum pellucidum
above and the body of the fornix below, the lateral wall by
the body of the caudate nucleus, and the floor by the
thalamus (Fig. 3.2).
The atrium and occipital horn together form a roughly
triangular cavity, with the apex posteriorly in the occipital
lobe and the base anteriorly
on the pulvinar (Figs. 3.2, 3.6, and 3.7). The atrium opens
anteriorly above the thalamus into the body, anteriorly
below the thalamus into the temporal horn, and posteriorly
into the occipital horn. The roof of the atrium is formed by
the body and tapetum of the corpus callosum. The medial
wall has an upper part formed by the bulb of the corpus
callosum and a lower part formed by the calcar avis, a
prominence overlying the deepest part of the calcarine
sulcus. The lateral wall has an anterior part formed by the
caudate nucleus as it wraps around the lateral margin of
the pulvinar and a posterior part formed by the fibers of
the tapetum as they sweep anteroinfer-iorly along the
lateral margin of the ventricle. The anterior wall has a
medial part composed of the crus of the fornix as it wraps
around the posterior part of the pulvinar and a lateral part
formed by the pulvinar of the thalamus. The floor has a
medial part composed of the posterior part of the
hippocampus, the prominence overlying the hippocampal
formation, and a lateral part formed by the collateral
trigone, the triangular prominence deep to the posterior
end of the collateral sulcus. In the atrium, the choroid
plexus has a prominent tuft called the glomus. The oc-
cipital horn extends posteriorly into the occipital lobe from
the atrium. Its medial wall is composed of the bulb and the
calcar avis, the roof and lateral wall are formed by the
tapetum, and the floor is formed by the collateral trigone.
The temporal horn extends forward from the atrium
below the pulvinar into the medial part of the temporal
lobe and ends blindly in the anterior wall situated
immediately behind the amygdaloid nucleus (Figs. 3.2
and 3.7). The floor of the temporal horn is formed
medially by the hippocampus and laterally by the smooth
white prominence overlying the collateral sulcus. The
roof is formed medially by the inferior surface of the
thalamus and the tail of the caudate nucleus, which are
separated by the striothalamic sulcus, and laterally by the
tapetum of the corpus callosum, which also sweeps
inferiorly to form the lateral wall of the temporal horn.
The medial wall is little more than a narrow cleft, the cho-
roidal fissure, between the inferolateral part of the
thalamus and the fimbria of the fornix. The inferior end of
the choroid fissure, the inferior choroidal point, is located
just behind the amygdaloid nucleus and the uncus.
Basal Cisterns in Tentorial Incisura
The third ventricle is commonly approached through
the cisterns surrounding the tentorial incisura (25). These
cisterns, which are inti-
mately related to the third ventricle, contain the bifurcation
of the carotid and basilar arteries, the circle of Willis, the
convergence of the deep intracranial venous system on the
great vein, and parts of the first six cranial nerves.
The tentorial incisura is a triangular space situated
between the dorsum sellae and the free edges of the
tentorium. Its apex is dorsal to the midbrain, just posterior
to the pineal gland. The upper brain stem sits in the center
of the incisura. The area between the brain stem and the
free edges is divided into: (a) an anterior incisural space
located in front of the brain stem; (b) paired middle
incisural spaces situated lateral to the brain stem; and (c) a
posterior incisural space located behind the brain stem
(Figs. 3.7 to 3.9).
Anterior Incisural Space
The anterior incisural space is located anterior to the
midbrain. It extends obliquely forward and upward around
the optic chiasm to the subcal-losal area. It opens laterally
into the medial part of the sylvian fissure and posteriorly
between the uncus and the brain stem into the middle
incisural space (Figs. 3.7 to 3.9).
The part of the anterior incisural space located below the
optic chiasm has posterolateral and posterior walls. The
posterolateral wall is formed by the anterior one-third of
the uncus, which hangs over the free edge above the
oculomotor trigone. The posterior wall is formed by the
cerebral peduncles. The infundibulum of the pituitary gland
crosses the anterior incisural space to reach the opening in
the diaphragma sellae. The part of the anterior incisural
space situated above the optic chiasm is limited superiorly
by the rostrum of the corpus callosum, posteriorly by the
lamina terminalis, and laterally by the part of the medial
surfaces of the frontal lobes located below the rostrum.
The anterior incisural space opens laterally into the part
of the sylvian fissure situated below the anterior perforated
substance. The anterior limb of the internal capsule, the
head of the caudate nucleus, and the anterior part of the
lentiform nucleus are located above the anterior perforated
substance.
The interpeduncular cistern, which sits in the posterior
part of the anterior incisural space between the cerebral
peduncles and the dorsum sellae, communicates laterally
with the sylvian cistern below the anterior perforated
substance and anteriorly with the chiasmatic cistern located
below the optic chiasm. The interpeduncular and
chiasmatic cisterns are separated by Liliequist's membrane,
an arachnoidal sheet ex-
Figure 3.8. A-C. Tentorium and inclsura: stepwise dissection. A. Right super-olateral
view. The right cerebral hemisphere has been removed to expose the tentorium (Tent.),
falx, and medial surface of the right cerebral hemisphere. The tentorial edge (Tent. Edge)
slopes downward from the apex (Apex Tent.) along the side of the brain stem to the area
lateral to the dorsum sellae (Dorsum). The third ventricle (3 Vent.) has been divided in
the midline and the right half of the upper midbrain has been divided transversely to
expose the cerebral peduncle (Ped.), red nucleus (Red Nucl.), substantia nigra (Subst.
Nigra), and inferior colliculi (Inf. Coll.). The midbrain is in the center of the incisura. The
anterior incisural space is located anterior to the midbrain and extends downward
between the dorsum sellae and brain stem and upward around the optic chiasm to the area
anterior to the lamina terminalis (Lam. Term.). The optic nerves (Optic N.), carotid
arteries (Car. A.), and infundibulum (Infund.) of the pituitary gland cross the anterior
incisural space. The middle incisural space is located lateral to the midbrain. It extends
into the supratentorial area between the temporal lobe and the midbrain and into the
infratentorial area between the cerebellum and the brain stem. The posterior incisural
space is located between the apex of the tentorium posteriorly, the midbrain anteriorly,
the splenium above, and the cerebellum below. The corpus callosum (Corp. Call.),
septum pellucidum (Sept. Pell.), and fornix are located above the third ventricle. The
cingulate gyrus (Cing. Gyr.) wraps around the corpus callosum and has the cingulate
sulcus (Cing. Sulc.) and medial frontal gyrus (Med. Front. Gyr.) on its outer margin. The
tentorium is attached anteriorly to the petrous ridge and temporal bone and posteriorly to
the occipital bone. The posterior part of the falx has been removed to expose the medial
surface of the parietal and occipital lobes, including the precuneus and cuneus, the
parietooccipital (Par. Occip. Sulc.), and calcarine (Calc. Sulc.) sulci and the lingual gyrus
(Lingual Gyr.). The olfactory tract (Olf. Tr.) passes posteriorly along the lateral margin of
the gyrus rectus (Gyr. Rectus). The oculomotor nerve (III) arises on the medial surface of
the cerebral peduncle and enters the dura mater lateral to the posterior clinoid process.
The trochlear nerve (IV) arises below the inferior colliculus and passes forward in the
cerebellomesencephalic fissure (Cer. Mes. Fiss.) between the cerebellum and midbrain.
B. Superior view. The falx and the dura covering the left hemisphere have been removed.
The left insula has been exposed by removing the operculum of the frontal lobe (Front.
Lobe). The central sulcus separates the precentral and postcentral gyri and the frontal
(Front. Lobe) and parietal (Par. Lobe) lobes. The straight sinus (Str. Sinus) passes
backward between the occipital lobes (Occip. Lobe). The cerebellum forms the floor of
the posterior incisural space. The trochlear nerve enters the anterior part of the free edge.
The oculomotor nerve enters the roof of the cavernous sinus. The trigeminal nerve (V)
arises in the infratentorial part of the middle incisural space. The frontal sinus (Front
Sinus) is anterior to the frontal lobe and the floor of the anterior cranial fossa (Ant.
Fossa). C. The superior part of the left cerebral hemisphere has been removed to expose
the lateral ventricle (Lat. Vent.). The thalamus and the body of the lateral ventricle (Body)
are located above the central part of the incisura; the frontal horn (Front. Horn) is above
the anterior incisural space; and the atrium is above the posterior incisural space. The
culmen and the quadrangular lobule (Quad. Lobule) of the cerebellum form the floor of
the posterior incisural space. The forceps major, a bundle of white matter emanating from
the splenium of the corpus callosum, sweeps posteriorly in the medial wall of the atrium
and occipital horn (Occip. Horn) deep to the parietooccipital sulcus. The forceps minor,
another bundle of white matter, radiates from the genu of the corpus callosum along the
medial margin of the frontal horn. The caudate nucleus (Caudate Nucl.) and corona
radiata are lateral to the frontal horn and body of the lateral ventricle. The choroid plexus
(Chor. Plex.) is attached along the choroidal fissure, the cleft between the fornix and
thalamus. The oculomotor nerve enters the roof of the cavernous sinus through the
oculomotor trigone (Oculomotor Trig.), which is situated between three dural folds: the
interclinoid fold (Interclin. Fold), which extends from the posterior (Post. Clinoid) to the
anterior (Ant. Ca'noid) clinoid process, forms the medial margin; the anterior petroclinoid
fold (Ant. Petroclin. Fold), which extends from the petrous apex to the anterior clinoid
process, forms the lateral margin; and the posterior petroclinoid fold (Post. Petroclin.
Fold), which extends from the petrous apex to the posterior clinoid process, forms the
posterior margin. The septum pellucidum is in the medial wall of the lateral ventricle. The
infundibulum passes through the diaphragma sellae (Diaph.).
 Figure 3.8. D and E. Tentorium and incisura (continued). D. Another layer of the left
cerebral hemisphere has been removed. The anterior limb (Ant. Limb) of the internal
capsule (Int. Cap.) is between the head of the caudate nucleus and the putamen, and the
posterior limb (Post. Limb) is between the thalamus and the putamen. The thalamostriate
vein (Thal. Str. V.) courses between the caudate nucleus and the thalamus. The column of
the fornix passes anterior to the foramen of Monro (For. Monro). Structures in the
anterior wall of the atrium include the crus of the fornix, the pulvinar of the thalamus,
and the tail of the caudate nucleus. The choroid plexus in the atrium is attached between
the thalamus and the fornix. E. Deeper section through the left cerebral hemisphere. The
caudate and lentiform nuclei, the thalamus, the internal capsule, and the body, frontal
horn, and atrium of the lateral ventricle are above the tentorial incisura. The junction of
the anterior and posterior limbs of the internal capsule abuts on the wall of the lateral
ventricle between the caudate nucleus and thalamus in the area lateral to the foramen of
Monro. The thalamus lies directly above the midbrain and the central part of the incisura.
The head of the caudate nucleus, the anterior limb of the internal capsule, and the
anterior part of the lentiform nucleus, formed by the putamen and globus pallidus
(Globus Pall.), are above the anterior incisural space. The posterior limb of the internal
capsule and the posterior part of the lentiform nucleus are above the middle incisural
space. The atrium and splenium are directly above the posterior incisural space. (From
Ono M, Ono M, Rhoton AL Jr, Barry M: Microsurgical anatomy of the region of the
tentorial incisura. J Neurosurg 60:365-399, 1984.)

tending from the dorsurn sellae to the anterior edge of the
mamillary bodies. The chiasmatic cistern communicates
around the optic chiasm with the cisterna laminae
terminalis, which lies anterior to the lamina terminalis.
The optic and oculomotor nerves and the posterior part
of the olfactory tracts pass through the anterior incisural
space (Figs. 3.7 to 3.9). Each olfactory tract runs
posteriorly and splits just above the anterior clinoid process
to form the medial and the lateral olfactory striae, which
course along the anterior margin of the anterior perforated
substance.
The optic nerves and chiasm and the anterior part of the
optic tracts cross the anterior incisural space. The optic
nerves emerge from the optic canal medial to the
attachment of the free edge to the anterior clinoid processes
and are directed posterior, superior, and medial toward
the optic chiasm. From the chiasm, the optic tract continues
in a posterolateral direction around the cerebral peduncle to
enter the middle incisural space. The optic nerve proximal
to its entrance into the optic canal is covered by a reflected
leaf of dura mater, the falciform process, which extends
medially from the anterior clinoid process across the top of
the optic nerve (36). The length of nerve covered by dura
only at the intracranial end of the optic canal may vary
from less than 1 mm to as great as 1 cm. Coagulation of the
dura above the optic nerve just proximal to the optic canal
on the assumption that bone separates the dura mater from
the nerve could lead to nerve injury. Compression of the
optic nerves against the sharp edge of the falciform process
may result in a visual field deficit even if the compressing
lesion does not damage the nerve enough to cause visual
loss.
The ophthalmic artery is found inferolateral to the optic
nerve when the periosteum lining the optic canal is opened.
Normally the optic nerve is separated medially from the
sphenoid sinus by a thin plate of bone, but in a few cases
this bone is absent and the optic nerves may protrude di-
rectly into the sphenoid sinus, separated from the sinus by
only mucosa and the dural sheath of the nerve (7, 36).
The relationship of the chiasm to the sella (Fig. 3.10) is
an important determinant of the ease with which the
pituitary fossa may be exposed by the transfrontal surgical
route. The normal chiasm overlies the diaphragma sellae
and the pituitary, the prefixed chiasm overlies the tu-
berculum sellae, and the postfixed chiasm overlies the
dorsum sellae. In approximately 70% of cases the chiasm
is in the normal position. Of the remaining 30%, about half
are "prefixed" and half "postfixed" (36).
A prominent tuberculum sellae may restrict access to the
sellae even in the presence of a normal chiasm. The
tuberculum may vary from being almost flat to protruding
upward as much as 3 mm, and it may project posteriorly to
the margin of a normal chiasm (36).
The limited transfrontal approach exposure provided by
a prefixed chiasm, a normal chiasm with a small area
between the tuberculum and the chiasm, and a superior
protruding tuberculum sellae may be enlarged by using the
trans-frontal-transsphenoidal approach advocated by Rand
(35). In this approach, access is obtained by opening into
the sphenoid sinus from above by drilling through the
tuberculum and planum sphenoidale, thus converting the
approach to a "transfrontal-transsphenoidal" one. If the
chiasm is normal or "postfixed," a subchiasmatic approach
below the chiasm is possible. If the chiasm is prefixed and
the tumor is seen through a thin, stretched anterior wall of
the third ventricle, the lamina terminalis may be opened to
expose the tumor. If the space between the carotid artery
and the optic nerve has been enlarged (e.g., by a lateral or
parasellar extension of tumor), the tumor may removed
through this space (43). If more space is needed in the
interval between the carotid artery and optic nerve, the
carotid artery, rather than the optic nerve, may be gently
retracted.
An understanding of the relationship of the carotid
artery, optic nerve, and anterior clinoid process is
fundamental to all surgical approaches to the sellar and
parasellar areas (Fig. 3.11). The carotid artery and the
optic nerve are medial to the anterior clinoid process. The
artery exits the
cavernous sinus beneath and slightly lateral to the optic
nerve. The optic nerve pursues a pos-teromedial course
toward the chiasm and the carotid artery pursues a
posterolateral course toward its bifurcation into the anterior
and middle cerebral arteries.
The oculomotor nerve emerges from the mid-brain on
the medial surface of the cerebral peduncle. It crosses the
anterior incisural space between the posterior cerebral and
the superior cerebellar arteries and passes inferomedial to
the uncus to enter the roof of the cavernous sinus.
Middle Incisural Space
The middle incisural space is located lateral to the brain
stem (Figs. 3.6 to 3.9). This narrow space, which extends
upward between the temporal lobe and the midbrain, has
medial and lateral walls and a roof.
The medial wall is formed by the lateral surface of the
midbrain. This surface of the midbrain is divided into a
larger anterior part formed by the cerebral peduncle and a
smaller posterior part formed by the tegmental surface. The
tegmental surface is formed by the lemniscal trigone, a
triangular area situated just posterior to the peduncle, and
by the brachium of the inferior col-liculus, a prominence
posterior to the lemniscal triangle that is directed upward
from the inferior colliculus toward the medial geniculate
body.
The roof of the middle incisural space has a narrow
anterior part formed by the posterior part of the optic tract,
which is flattened between the cerebral peduncle and the
uncus, and a wider posterior part formed by the inferior
surface of the pulvinar. The lateral geniculate body pro-
trudes from the inferior surface of the pulvinar just lateral
to the posterior edge of the cerebral peduncle. The medial
geniculate body bulges into the roof posteromedial to the
lateral geniculate body just behind the lateral
mesencephalic sul-cus.
The lateral wall of the supratentorial part of the middle
incisural space is composed of the hippocampal formation
on the medial surface of the temporal lobe. The uncus and
parahippocam-pal gyri, the most inferior structures in this
part of the lateral wall, form a curved border around the
middle incisural space. The uncus bulges medially at the
anterior end of the parahippo-campal gyrus.
Posterior to the uncus, the surface of the temporal lobe
facing the middle incisural space is formed by three
longitudinal strips of neural tissue, one located above the
other, which are interlocked with the hippocampal
formation to
Figure 3.9. A-C. Neural relationships. A. Lateral view. The temporal lobe (Temp. Lobe)
has been elevated from the tentorium (Tent.) and the floor of the middle cranial fossa.
The free edge (Tent. Edge) has grooved (Tent. Groove) the lower surface of the uncus.
The rhinal (Rhinal Sulc.) and collateral (Coll. Sulc.) sulci separate the occipitotemporal
(Occip. Temp. Gyr.) and the parahippocampal (Parahippo. Gyr.) gyri. The gyrus rectus
(Gyr. Rectus) is medial and the orbital gyri (Orb. Gyr.) are lateral to the olfactory tract
(Off. Tr.). The anterior perforated substance (Ant. Perf. Subst.) extends into the medial
part of the sylvian fissure (Sylvian Fiss.). The calcarine sulcus (Calc. Sulc.) divides the
medial surface of the occipital lobe. The optic tract (Optic Tr.) passes backward between
the uncus and the cerebral peduncle (Ped.). The brachium of the inferior colliculus
(Brach. Inf. Coll.) extends from the inferior colliculus (Inf. Coll.) along the side of the
superior colliculus (Sup. Coll.) toward the medial geniculate body (Med. Gen. Body).
The lemniscal trigone (Lemniscal Trig.) is located between the brachium of the inferior
colliculus and the lateral mesencephalic sulcus (Lat. Mes. Sulc.). The oculomotor nerve
(III) arises below the mamillary bodies (Mam. Body) just above the pontomesencephalic
sulcus (Pon. Mes. Sulc.). B. Enlarged view. The temporal lobe has been elevated further
to show the lower surface of the pulvinar and the termination of the optic tract in the
lateral geniculate body (Lat. Gen. Body). The optic nerve (Optic N.) passes above the
divided end of the carotid artery (Car. A.). The anterior hippocampal sulcus (Ant. Hippo.
Sulc.) separates the uncus and the parahippocampal gyrus. The calcarine sulcus separates
the lingual gyrus (Lingual Gyr.) and the cuneus. C. The anteromedial part of the temporal
lobe has been removed to expose the temporal horn (Temp. Horn). The removal crosses
the amygdaloid nucleus (Amygd. Nucl.), which lies deep to the uncus. The choroid
plexus (Chor. Plex.) is attached along the choroidal fissure (Chor. Fiss.), a cleft between
the temporal lobe and pulvinar. The olfactory tract splits into the medial (Med. Olf. Stria)
and lateral olfactory striae (Lat. Olf. Stria).
Figure 3.9. D and E. Neural relationships (continued). D. Inferior view of basal structures
surrounding the course of the basal vein. The cerebrum was removed by dividing the
midbrain at the level of the red nucleus (Red Nad), substantia nigra (Subst. Nigra), and
posterior perforated substance (Post. Perf. Subst.). The infundibulum (Infund.) arises
from the tuber cinereum (Tuber). The uncus extends medial to and is grooved by the
tentorial edge in the area anterolateral to the cerebral peduncle. The subiculum, the
rounded medial edge of the parahip-pocampal gyrus, has been retracted to expose the
dentate gyrus (Dentate Gyr.) and the fimbria of the fornix on the medial surface of the
temporal lobe. The fimbria and dentate gyrus are separated by the fimbriodentate sulcus
(Fimb. Dentate Sulc.), and the dentate gyrus and the subiculum are separated by the
hippocampal sulcus (Hippo. Sulc.). The choroidal fissure opens into the temporal horn
between the pulvinar and fimbria. The fibers in the fimbria are continuous with those in
the crus of the fornix. The dentate gyrus is continuous posteriorly with the fasciolar
gyrus (Fasciolar Gyr.), located below the splenium. E. The temporal tip has been
retracted to expose the anterior perforated substance, which is bounded anteriorly by the
medial and lateral olfactory striae, medially by the optic tract, posteriorly by the temporal
lobe, and laterally by the limen insula. The semilunar (Semilunar Gyr.) and ambient
(Ambient Gyr.) gyri, which are continuous posteriorly with the uncus, are on the superior
surface of the temporal tip immediately posterior to the anterior perforated substance.
(From Ono M, Rhoton AL Jr, Peace DA, Rodriguez R: Microsurgical anatomy of the
deep venous system of the brain. Neurosurgery 15:621-657, 1984.)

Figure 3.10. Three sagittal sections of the sellar region showing neural structures,
chiasm, posterior lobe pituitary and hypothalamus, anterior lobe pituitary, dura, and
intracavernous venous connections. Prefixed chiasm above tuberculum (left), normal
chiasm above diaphragma (center), and postfixed chiasm above dorsum (right). (From
Rhoton AL Jr, Maniscalco J: Microsurgery of the sellar region. Neuroophthalmology
9:106-127, 1977.)

Figure 3.11. Right anterior and lateral views of the
suprasellar area. A. Right anterolateral view. Anterior
clinoid process (Ant. Clinoid), lateral to optic nerve (O.N.)
and carotid artery (C.A.). Perforating arteries pass from the
carotid to terminate in the optic chiasm and tract (O.Tr.)
arid the hypothalamus anterior to the mamillary body
(Mam. В.). Right posterior communicating artery (P.Co.A.)
is medial to the carotid artery. Anterior choroidal artery
(A.Ch.A.) arises from the carotid and passes above the
posterior cerebral artery (P.C.A.). The third nerve (HI) lies
below the right posterior cerebral artery. The right
recurrent artery of Huebner (Rec. A.) arises from the
anterior cerebral artery (A.C.A.) proximal to the anterior
communicating artery (A.Co.A.). M.C.A., middle cerebral
artery; A-2, anterior cerebral artery distal to the anterior
communicating artery. B. Right lateral view with temporal
lobe removed. Anterior clinoid (din.) is lateral to the
carotid artery. Premamillary (Premam. A.) arises from the
posterior communicating artery. Thalamoperfor-ating
arteries (Th. Pe. A.) arise from the proximal posterior
cerebral artery. The optic tract passes around the peduncle
to the lateral geniculate body. Arterioles pass from the
carotid artery to the optic nerve. The basilar artery (B.A.) is
medial to the third and fourth (IV) cranial nerves. The
trigeminal nerve (V) is below the superior cerebellar artery
(S.C.A.). (From Saiki N, Rhoton AL Jr: Microsurgical
anatomy of the upper basilar artery and the posterior circle
of Willis. J Neu-rosurg 46:563-577, 1977.)
make an important part of the limbic system (Figs. 3.7 and
3.9). The most inferior strip is formed by the subiculum,
the rounded medial edge of the parahippocampal gyrus; the
middle strip is formed by the dentate gyrus, a serrated or
beaded strip of gray matter located on the medial surface of
the hippocampal formation; and the superior strip is formed
by the fimbria of the fornix, a white band formed by the
fibers emanating from the hippocampal formation that are
directed posteriorly into the crus of the fornix.
The choroidal fissure, the cleft along which the choroid
plexus of the temporal horn is attached, is situated at the
junction of the roof and lateral wall of the middle incisural
space between the fimbria below and the pulvinar above.
The inferior choroidal point, at the inferior end of the
choroidal fissure, is located immediately lateral to the
lateral geniculate body.
The supratentorial part of the middle incisural space
contains the crural and ambient cisterns. The crural cistern,
located between the cerebral peduncle and the uncus, is a
posterolateral extension of the interpeduncular cistern. The
crural cistern opens posteriorly into the ambient cistern, a
narrow communicating channel demarcated medially by
the midbrain, above by the pulvinar, and laterally by the
subiculum, dentate gyrus, and fimbria of the fornix. The
ambient cistern is continuous posteriorly with the quad-
rigeminal cistern.
The trochlear nerve is related predominatly to the middle
incisural space and is the cranial nerve most intimately
related to the free edge. The trochlear nerve arises below
the inferior colliculus in the posterior incisural space and
passes forward through the middle incisural space between
the posterior cerebral and superior cerebellar arteries. Its
initial course around the midbrain is medial to the free edge
in the space between the tectum and cerebellum. It reaches
the lower margin of the free edge at the posterior edge of
the cerebral peduncle. It pierces the anterior part of the free
edge before entering the cavernous sinus.
Posterior Incisural Space
The posterior incisural space lies posterior to the
midbrain and corresponds to the pineal region (Figs. 3.6 to
3.8). It has a roof, floor, and anterior and lateral walls and
extends backward to the level of the apex of the tentorium.
The quadrigeminal plate is located at the center of the
anterior wall. The anterior wall rostral to
the colliculi is formed by the pineal body and the
habenular trigones and commissure. The habenular
trigones overlie the habenular nuclei on the posteromedial
surface of the pulvinar and are connected across the
midline by the habenular commissure. The habenular
trigones are continuous anteriorly with the striae
medullaris thai-ami, which course along the medial surface
of the thalamus. The habenular commissure forms the
upper half and the posterior commissure forms the lower
half of the attachment of the pineal body to the posterior
part of the third ventricle. The part of the anterior wall
below the colliculi is formed in the midline by the lingula
of the vermis and laterally by the superior cere-bellar
peduncles as they ascend beside the lingula.
The roof of the posterior incisural space is formed by
the lower surface of the splenium, the terminal part of the
crura of the fornix, and the hippocampal commissure.
The floor of the posterior incisural space is formed by
the anterior superior part of the cerebellum. This space
extends inferiorly into the cerebellomesencephalic fissure,
the cleft opening inferiorly between the anterior superior
part of the vermis and the colliculi. The anterior wall of
the fissure is formed by the lingula and superior cerebellar
peduncles, and the posterior wall is formed by the
cerebellum.
Each lateral wall is formed by the pulvinar, crus of the
fornix, and medial surface of the cerebral hemisphere.
The anterior part of the lateral wall is formed by the part
of the pulvinar located just lateral to the pineal body. The
lateral wall, posterior to the pulvinar, is formed by the
segment of the crus of the fornix that wraps around the
posterior margin of the pulvinar. The posterior part of the
lateral walls is formed by the cortical areas located below
the splenium on the medial surface of the hemisphere.
These areas include the posterior part of the parahip-
pocampal and dentate gyri and several small nodular
collections of gray matter, the fasciolar gyri and Retzius'
gyri, which are located at the posterior end of the dentate
gyrus (Fig. 3.7).
The quadrigeminal cistern, situated posterior to the
quadrigeminal plate, is the major cistern in the posterior
incisural space. It has also been referred to as the cisterna
venae magnae cerebri because the vein of Galen passes
through it. The quadrigeminal cistern communicates
above with the posterior pericallosal cistern, which
extends around the splenium between the cerebral hem-
ispheres; inferiorly into the cerebellomesencephalic
cistern, also called the precentral cerebel-
lar cistern, which extends into the cerebellomesencephalic
fissure; inferolaterally into the posterior part of the ambient
cistern located between the midbrain and the
parahippocampal gyrus; and laterally into the retrothalamic
cistern, which curves around the posterior margin of the
pulvinar medial to the crus of the fornix. The
quadrigeminal cistern may communicate with the velum
interpositum. Another cavity, the cavum vergae, is located
just above the velum interpositum between the
hippocampal commissure and the splenium: its roof is
formed by the lower surface of the splenium, its floor is
formed by the hippocampal commissure, and the lateral
walls are formed by the crura. Substances instilled in the
subarachnoid space only infrequently enter a cavum
vergae.
Arterial Relationships
Each wall of the third ventricle has surgically important
arterial relationships: the posterior part of the circle of
Willis and the apex of the basilar artery are below the floor;
the anterior part of the circle of Willis and the anterior
cerebral and anterior communicating arteries are intimately
related to the anterior wall; the posterior cerebral,
pericallosal, superior cerebellar, and posterior choroidal
arteries pass adjacent to the posterior wall; both the anterior
and posterior cerebral arteries send branches into the roof;
and the internal carotid, anterior choroidal, anterior and
posterior cerebral, and anterior and posterior
communicating arteries give rise to perforating branches
that reach the walls of the third ventricle. All arterial
components of the circle of Willis and the adjacent carotid
and basilar artery and their perforating branches may
become stretched around third ventricular and selar tumors.
The arterial relationships in the anterior incisural space are
among the most complex in the brain because it contains all
the components of the circle of Willis (Figs. 3.11 to 3.13).
Internal Carotid Artery
The internal carotid artery exits the cavernous sinus
along the medial surface of the anterior clinoid process to
reach the anterior incisural space. After entering this space
it courses posterior, superior, and lateral to reach the site of
its bifurcation below the anterior perforated substance. It is
first below and then lateral to the optic nerve and chiasm
(Figs. 3.11, 3.13, and 3.14). It sends perforating branches
to the optic nerve, chiasm, and tract and to the floor of the
third ventricle. These branches pass across the interval
between the internal carotid artery and

Figure 3.12. Arterial relationships of the third ventricle. A
and С are inferior views of the floor of the third ventricle,
and В and D are midsagittal sections through the third
ventricle. A and В show the relationship of the main trunks
and perforating branches of the following arteries to the
third ventricle: internal carotid (C.A.), anterior choroidal
(A.Ch.A.}, basilar apex (B.A.), posterior cerebral (P.C.A.),
medial posterior choroidal (Med.Post.Ch.A.), lateral
posterior choroidal (Lat.Post.Ch.A.), thalamoperforating
(Thal. Perf.A.), and thalamogeniculate (Thal.Gen.A.) arter-
ies. С and D show the relationships of the main trunks and
perforating branches of the following arteries to the third
ventricle: anterior cerebral (A.C.A.), anterior
communicating (A..Co.A.), and posterior communicating
arteries. The olfactory (Olf.N.) and optic (O.N.) nerves are
anterior to the floor of the third ventricle. The structures in
the floor are the optic chiasm (O.Ch.), optic tracts (O.Tr.),
infundibulum (Infund.), tuber ci-nereum (Tuber Cin.), and
mamillary bodies (Mam. В.). The midbrain and cerebral
peduncles (Ped.) are inferior to the posterior half of the
floor. The anterior perforated substance (Ant. Perf. Subst.)
is lateral to the optic tracts. The lateral geniculate (Lat. Gen.
B.) and medial geniculate (Med. Gen. B.) bodies are at-
tached to the lower margin of the thalamus near the
pulvinar (Pulv.}, lateral to the midbrain. The structures in
the anterior wall of the third ventricle are the anterior
commissure (Ant. Comm.), lamina terminalis (Lam. Теr.),
and optic chiasm. The corpus callosum (Corp. Call.) and
septum pellucidum (Sept. Pel.) are above the roof of the
third ventricle. The roof is formed of the two layers of tela
choroidea (Tela), the fornix, and a vascular layer composed
of the internal cerebral veins and the medial posterior
choroidal arteries. The oculomotor nerve (HI) exits from
the midbrain. (From Yamamoto I, Rhoton AL Jr, Peace
DA: Microsurgery of the third ventricle: Part 1.
Microsurgical anatomy. Neurosurgery 8:334-356, 1981.)
the optic nerve and may serve as an obstacle to the
operative approaches directed through the triangular space
between the internal carotid artery, the optic nerve, and the
anterior cerebral artery. The internal carotid artery also
gives off the superior hypophyseal artery, which runs me-
dially below the floor of the third ventricle to reach the
tuber cinereum and joins its mate of the opposite side to
form a ring around the infundibulum (10).
The supraclinoid (C4) portion of the internal carotid
artery is divided into three segments based on the origin of
its major branches: the ophthalmic segment extends from
the origin of the ophthalmic artery to the origin of the
posterior communicating artery; the communicating
segment extends from the origin of the posterior
communicating artery to the origin of the anterior choroidal
artery; and the choroidal segment extends from the origin
of the anterior choroidal artery to the bifurcation (Figs. 3.15
to 3.17) (10). Each segment gives off a series of perforating
branches with a relatively constant site of termination. The
branches arising from the ophthalmic segment pass to the
optic nerve and chiasm, infundibulum, and the floor of the
third ventricle. The branches arising from the com-
municating segment pass to the optic tract and the floor of
the third ventricle. The branches arising from the choroidal
segment pass upward and enter the brain through the
anterior perforated substance.
Ophthalmic Artery
The ophthalmic artery is the first branch of the internal
carotid artery above the cavernous sinus (Figs. 3.14 and
3.16). Its origin and proximal segment may be visible
below the optic nerve without retracting the nerve,
although elevation of the optic nerve away from the carotid
artery is usually required to see the segment proximal to the
optic foramen. The artery arises from the supraclinoid
segment at the carotid artery in most cases, but it may also
arise within the cavernous sinus or be absent in a few cases
(14, 36).
The ophthalmic artery origin has a variable relationship
to the tip of the anterior clinoid process. Its origin may vary
from as far as 5 mm anterior to 7 mm posterior to the
clinoid tip and 2 to 10 mm medial to the clinoid process
(14). Most arise anterior and approximately 5 mm medial
to the tip. In our studies, 14% of ophthalmic arteries exited
from the carotid artery and immediately entered the optic
canal; in the remaining 86% the maximal preforaminal
length was 7 mm and the mean was 3 mm (14).
 Posterior Communicating Artery
The posterior communicating artery arises from the
posterior wall of the internal carotid artery and courses
posteromedially below the optic tracts and the floor of the
third ventricle to join the posterior cerebral artery (Figs.
3.11 to 3.19). Its branches penetrate the floor between the
optic chiasm and the cerebral peduncle and reach the
thalamus, hypothalamus, subthala-mus, and internal
capsule. Its posterior course varies depending on whether
the artery provides the major supply to the distal posterior
cerebral artery. If it is normal, with the posterior cerebral
artery arising predominantly from the basilar artery, it is
directed posteromedially above the oculomotor nerve
toward the interpeduncular fossa. If the posterior cerebral
artery has a fetal type configuration in which it arises from
the carotid artery, the posterior communicating artery is
directed posterolaterally below the optic tract. The
oculomotor nerve pierces the dura mater of the roof of the
cavernous sinus 2 to 7 mm (average, 5 mm) posterior to
the initial supracli-noid segment of the carotid artery (14,
42).
Anterior Choroidal Artery
The anterior choroidal artery arises from the posterior
surface of the internal carotid artery 0.1 to 3.0 mm above
the origin of the posterior communicating artery (Figs.
3.11 to 3.20). It is directed posterolaterally below the optic
tract between the uncus and cerebral peduncle. It passes
through the choroidal fissure near the inferior choroidal
point to supply the choroid plexus in the temporal horn. It
sends branches into the optic tract and posterior part of the
floor that reach the optic radiations, globus pallidus, inter-
nal capsule, midbrain, and thalamus (8, 38).
Anterior Cerebral and Anterior
Communicating Arteries
The anterior cerebral artery arises from the internal
carotid artery below the anterior perforated substance and
courses anteromedially above the optic nerve and chiasm
to reach the interhemispheric fissure, where it is joined to
the opposite anterior cerebral artery by the anterior
communicating artery (Figs. 3.11 to 3.20) (30, 31, 37).
The junction of the anterior communicating artery with the
right and left A1 segments is usually above the chiasm
rather than above the optic nerves. In our studies 70%
were above the chiasm and 30% were in a prefixed
position above the optic nerves (Fig. 3.21). The shorter A1
segments are stretched tightly over the chiasm, and the
longer ones pass anteriorly over the nerves. The arteries
with a more forward course are often tortuous and
elongated, and some may course forward and rest on the
tuberculum sellae or planum sphenoidale (Fig. 3.21). The
anterior cerebral artery ascends in front of the lamina
terminalis and the anterior wall of the third ventricle and
passes around the corpus callosum. It gives off the
orbitofrontal artery before reaching the corpus callosum.
Often the anterior cerebral artery on one side sends
branches across the interhemispheric fissure to supply the
medial part of the opposite cerebral hemisphere (31). The
distal part of the anterior cerebral artery may be exposed
not only above, but also below the corpus callosum because
the terminal branch of the pericallosal artery may pass
around the splenium and course forward in the roof of the
third ventricle, reaching as far anterior as the foramen of
Monro (31).
The anterior cerebral and anterior communicating
arteries give rise to perforating branches that terminate in
the whole anterior wall of the third ventricle and reach the
adjacent parts of the hypothalamus, fornix, septum
pellucidum, and striatum (Figs. 3.22 and 3.23). A
precallosal artery may originate from the anterior cerebral
or the anterior communicating artery, run upward across
the lamina terminalis, and send branches into the anterior
wall (Fig. 3.22D).
The pericallosal arteries send short and long callosal
arteries into the corpus callosum. The short callosal arteries
pass directly into the corpus callosum. The long callosal
arteries course parallel to the pericallosal arteries, between
them and the corpus callosum. The callosal arteries send
branches into the corpus callosum that reach the septum
pellucidum and the fornix.
The recurrent branch of the anterior cerebral artery,
which is referred to as the recurrent artery of Heubner, is
encountered frequently in approaches to the anterior part of
the third ventricle (Figs. 3.11, 3.22, and 3.23). It arises
from the anterior cerebral artery in the region of the
anterior communicating artery, courses laterally above the
bifurcation of the internal carotid artery, and enters the
anterior perforated substance (30). The recurrent artery
courses anterior to the A1 segment of the anterior cerebral
artery and would have been seen when elevating the frontal
lobe before visualizing the A1 segment in about two-thirds
of cases. Of the remaining one-third, most coursed superior
to A1 Some of its branches reach the anterior limb and
genu of the internal capsule.
Middle Cerebral Artery
The middle cerebral artery courses laterally from its
origin below the anterior perforated substance (Figs. 3.11,
3.13, 3.15, 3.18, and 3.19) (9). The major bifurcation of
the middle cerebral artery is usually located in the lateral
part of the anterior incisural space.
The middle cerebral artery has been divided into four
segments, M1 through M4 (9). The M1 segment begins at the
origin of the middle cerebral artery lateral to the optic
chiasm, at the medial end of the sylvian fissure, and
extends laterally below the anterior perforated substance,
toward the insula. The M1 segment terminates at the limen
insulae, the site of a 90° turn, the genu, where the artery
curves sharply posterosuperior to form the M2 segment,
composed of the trunks coursing over the insula. The M1
segment is subdivided into a prebifurcation and a
postbifurcation part. The major division of the artery is a
bifurcation in 86% of hemispheres and a trifurcation in the
remaining 14% of hemispheres (9). The bifurcation occurs
proximal to the genu in most hemispheres.
The middle cerebral artery branches to the anterior
perforated substance are called the len-ticulostriate arteries
(44). The lenticulostriate arteries are divided into medial,
intermediate, and lateral groups, each of which has a
unique origin, composition, morphology, and characteristic
distribution in the anterior perforated substance. The
medial group of lenticulostriate arteries arises on the
medial part of the M1 segment near the carotid bifurcation
and pursues a relatively direct course to enter the anterior
perforated substance. The intermediate lenticulostriate
arteries form a complex array of branches resembling a
candelabra before entering the anterior perforated
substance between the medial and lateral lenticulostriate
arteries. The lateral lenticulostriate arteries originate
predominantly on the lateral part of the M1 portion, pursue
an S-shaped course, and enter the lateral part of the anterior
perforated substance. They arise from the parent trunks,
travel medially with the parent trunks, then loop sharply
posterior, lateral, and superior, and finally turn
posteromedial just before penetrating the anterior
perforated substance.

Figure 3.13. A and B. Superior view of the arteries in the suprasellar area. A. The
posterior part of the optic chiasm is split at the junction with the optic tracts (O. Tr.) to
give this view. The proximal portions of the anterior cerebral arteries (A-1) arise from
the carotid arteries (C.A.) and pass above the optic nerves (O. N.) and chiasm; the
anterior third ventricle lies above the mamillary bodies (Mam. В.). The
thalamoperforating arteries (Th.Pe.A.) terminate in the retromamillary area and the
interpeduncular fossa. The right posterior choroidal artery (P.Ch.A.) originates from the
posterior cerebral artery (P.C.A.). Small branches arise from the posterior cerebral artery
and terminate in the peduncle. The left third nerve (III) courses medial to the posterior
communicating artery (P.Co.A.). The right posterior communicating artery joins the
posterior cerebral artery medial to the third nerve. The left anterior choroidal artery
(A.Ch.A.) passes to the peduncle and optic tract. Trigeminal nerves (V) are lateral to the
carotid artery. M.C.A., middle cerebral artery. B. Inferior view of the circle of Willis.
Fetal type of left posterior cerebral artery. The left third nerve courses under the
posterior cerebral artery distal to its junction with the posterior communicating artery
and the right nerve courses under the part proximal to the communicating artery. The left
thalamoperforating and the posterior choroidal (P.Ch.A.) arteries originate from the
proximal part of the posterior cerebral artery. The right premamillary artery (Premam.
A.) emerges from the anterior and the left from the middle third of the posterior
communicating artery. Small posterior communicating branches course superiorly and
medially, terminating in the premamillary area. The left thalamoperforating and right
premamillary arteries are well developed in spite of the small trunk of origin. The
superior cerebellar artery (S. C. A.) arises below the posterior cerebral artery. No
branches arise on the anterior surface of the basilar artery (B.A.) A-2, distal part of the
anterior cerebral artery. C. Superior view of the suprasellar area. Arterial branches
stretch around the superior extension of a pituitary tumor. Anterior cerebral arteries send
branches to the superior surface of the optic nerves and chiasm. The posterior
communicating, internal carotid, and posterior cerebral arteries send branches into the
area below and behind the chiasm. Recurrent arteries (Rec. A.) arise just distal to the
anterior communicating artery. IV, trochlear nerve. (From Saeki N, Rhoton AL Jr:
Microsurgical anatomy of the upper basilar artery and the posterior circle of Willis. J
Neurosurg 46:563-577, 1977.)

Figure 3.14. Inferior views of the perforating branches of
the supraclinoid portion of the internal carotid artery (ICA).
A. The supraclinoid portion of the ICA gives rise to the
ophthalmic (Ophth. A.), posterior communicating
(P.Co.A.), and anterior choroidal (A.Ch.A.) arteries. The
supraclinoid portion of the artery is divided into three
segments based on the site of origin of these three
branches: the ophthalmic segment (C4-Op.) extends from
the origin of the ophthalmic artery to the Origin of the
PCoA; the communicating segment (C4-Co.) extends from
the origin of the PCoA to the origin of the AChA; and the
choroidal segment (C4-Ch.) extends from the origin of the
AChA to the bifurcation of the carotid artery into the
anterior and middle cerebral arteries. The optic nerves
(O.N.) are above the ophthalmic arteries. The optic chiasm
and optic tracts (O.Tr.) are above the anterior (Ant.Lobe)
and posterior (Post. Lobe) lobes of the pituitary gland. The
tuber cinereum (Tuber Cin.) is anterior to the apex of the
basilar artery (B.A.). The posterior cerebral arteries (P.C.A.)
pass around the cerebral peduncles (Cer. Ped.) above the
oculomotor nerves (III). The perforating branches arising
from the ophthalmic segment pass superior to the anterior
lobe to the optic nerve and chiasm and to the anterior part
of the tuber cinereum. A single perforating branch arises
from the communicating segment on each side and passes
upward to the optic tract and the floor of the third ventricle.
B. The anterior lobe of the pituitary gland has been
reflected backward to show the superior hypophyseal
arteries (Sup. Hyp. A.) passing from the ophthalmic
segment to the infundibulum (Infund.). The anterior
cerebral (A.C.A.) and the anterior communicating (A.Co.A.)
arteries are seen above the optic chiasm (O.Ch.). (From
Gibo H, Lenkey C, Rhoton AL
Posterior Cerebral Artery
The bifurcation of the basilar artery into the posterior
cerebral arteries is located in the posterior part of the
anterior incisural space below the posterior half of the floor
of the third ventricle (Figs. 3.11 to 3.20) (45, 57). A high
basilar bifurcation may indent the floor. The posterior
cerebral artery encircles the mesencephalon to reach the
posterior incisural space and the quad-rigeminal cistern. It
courses laterally around the cerebral peduncle, above the
oculomotor nerve, and exits the anterior and enters the
middle incisural space by coursing between the uncus and
the cerebral peduncle. It enters the posterior incisural space
from anteriorly and courses through the lateral part of the
posterior incisural space. It bifurcates into the
parietooccipital and calcarine arteries as it crosses above
the free edge of the tentorium. It sends cortical branches to
the temporal, occipital, and parietal lobes and callosal
branches to the splenium of the corpus callosum. Its
callosal branch, the posterior peri-callosal artery, may
anastomose with the callosal branches of the anterior
cerebral artery. Its branches reach the floor, roof, and
posterior and lateral walls of the third ventricle.
The thalamogeniculate and the thalamoperfor-ating
arteries are two of the larger perforating branches (Figs.
3.13 and 3.19). The thalamoper-forating arteries arise from
the proximal part of the posterior cerebral arteries and the
posterior part of the posterior communicating arteries, enter
the brain through the posterior part of the floor and the
lateral walls. The thalamogeniculate arteries arise from the
posterior cerebral arteries in the ambient cisterns below the
pulvi-nar and course superiorly through the geniculate
bodies to reach the adjacent parts of the thala-mus and
internal capsule.
The medial posterior choroidal arteries arise from the
proximal portions of the posterior cerebral arteries in the
anterior incisural space and course around the midbrain in
the middle incisural space to reach the quadrigeminal
cistern in the posterior incisural space (Figs. 3.12 and 3.18
to 3.20) (8, 38). They turn forward at the side of the pineal
body and pass above the habenular trigone, course between
the layers of the tela choroidea in the velum interpositum,
and supply the choroid plexus in the roof of the third
ventricle and the body of the lateral ventricle. The
Jr: Microsurgical anatomy of the supraclinoid portion of
the internal carotid artery. J Neurosurg 55:560-574, 1981.)

Figure 3.15. Inferior views of the perforating branches of
the supraclinoid portion of the internal carotid artery
(ICA). A. The supraclinoid portion of the artery gives rise
to the posterior communicating (P.Co.A.), anterior
choroidal (A.Ch.A.), middle cerebral (M.C.A.), and
anterior cerebral arteries (A.C.A.). The supraclinoid
portion of the artery is divided into three segments based
on the site of origin of these branches. An ophthalmic
segment (C4-Op.) that extends from the origin of the
ophthalmic artery (not shown because the ICA was
divided above the level of origin of the ophthalmic artery)
to the origin of the PCoA; a communicating segment (C4-
Co.) that extends from the origin of the PCoA to the
origin of the AChA; and a choroidal segment (C4-Ch.)
that extends from the origin of the AChA to the level of
the bifurcation of the ICA into the anterior cerebral and
middle cerebral arteries. The ophthalmic segment sends
perforating branches to the optic nerves (O.N.), optic
chiasm (O.Ch.), and tuber cinereum (Tuber Cin.). The
superior hypophyseal arteries (Sup. Hyp. A.) pass to the
infundibulum of the hypophysis (Infund.). The communi-
cating segment sends one perforating branch on each side
to the optic tracts (O.Tr.) and the region around the
mamillary bodies (Mam. Body). The choroidal segment
sends its perforating branches into the anterior perforated
substance (Anr. Perf. Subst.). The posterior cerebral
arteries (P.C.A.) arise from the basilar artery (B.A.) and
pass laterally around the cerebral peduncles (Cer. Ped.).
The temporal lobe (Temp. Lobe) is lateral to the carotid
artery. The middle cerebral arteries pass laterally into the
sylvian fissure below the anterior perforated substance.
The frontal lobes (Fr. Lobe), gyrus rectus (Gyr. Rectus),
and olfactory nerves (Olf. N.) are above the optic nerves.
The thalamoperforating
lateral posterior choroidal arteries arise from each posterior
cerebral artery in the area lateral to the midbrain and pass
superolaterally through the choroidal fissure and around
the pulvinar to supply the choroid plexus in the temporal
horn and atrium. The posterior choroidal arteries send
small branches to the surface of the thalamus along their
course.
The perforating branches of the posterior cerebral and
superior cerebellar arteries and the medial posterior
choroidal arteries supply the walls of the posterior incisural
space. The posterior cerebral arteries supply the structures
above the level of the lower margin of the superior
colliculi, and the superior cerebellar arteries supply the
structures below the upper margin of the inferior colliculus.
There are numerous anastomoses between the two arteries
over the surface of the colliculi. The pineal gland and the
habenula are supplied by the branches of the medial
posterior choroidal arteries.
Superior Cerebellar Artery
This artery arises from the basilar artery in the posterior
part of the anterior incisural space, encircles the midbrain
below the posterior cerebral artery, and passes through the
quadri-geminal cistern to reach the superior surface of the
cerebellum (Figs. 3.18 and 3.19) (13). It dips below the
tentorium to reach the superior surface of the cerebellum at
the junction of the anterior and middle incisural spaces. It
bifurcates into a rostral trunk that supplies the vermis and a
caudal trunk that supplies the cerebellar hemisphere as it
passes around the lateral margin of the cerebral peduncle to
enter the middle incisural spaces.
The segment of the artery in the quadrigeminal cistern is
exposed in the supra- and infratento-rial operative
approaches to the posterior part of the third ventricle, and
its cortical branches are exposed in the infratentorial
approaches. Perforating branches arising in the
quadrigeminal region supply the inferior colliculi.
arteries (Thal. Perf. A.) pass posteriorly between the
oculomotor nerves (Ш). B. Inferior view of another
specimen. The ophthalmic segment gives rise to per-
forating branches that pass to the optic nerves, chiasm, and
tracts and to the infundibulum and tuber cinereum. No
perforating branches arise from the communicating
segment on either side in this specimen. The perforating
branches from the choroidal segment pass into the anterior
perforated substance. (From Gibo H, Lenkey C, Rhoton
AL Jr: Microsurgical anatomy of the supraclinoid portion
of the internal carotid artery. J Neurosurg 55:560-574,
1981.)
Figure 3.16. Anterior and anteroinferior views of the supraclinoid portion of the internal
carotid artery (ICA). A. Anterior view. The optic nerves (O.N.) enter the optic canals
medial to the anterior clinoid processes (Ant Clinoid). The infundi-bulum (Infand.)
passes inferiorly below the optic chiasm (O.Ch.) to the pituitary gland. The carotid
arteries (C.A.) are posterior to the optic nerves. The planum sphenoidale (Planum) is
anterior to the chiasmatic sulcus (Ch. Sulc.) and the tuberculum sellae (Tuberculum). The
perforating branches of the carotid artery pass medially in the subchiasmatic space. The
superior hypophyseal arteries (Sup. Hyp. A.) arise from the carotid artery and pass to the
infundibulum. The falciform process (Falc. Process) is a fold of dura mater that passes
above the optic nerve proximal to the optic foramen. B. The right optic nerve has been
divided at the optic foramen and elevated to show the perforating branches of the
supraclinoid portion of the carotid arteries. The right anterior cerebral artery (A.C.A.)
was divided at its origin so that the optic nerve and chiasm could be elevated. The carotid
artery gives rise to multiple perforating branches as well as the ophthalmic (Ophth. A.),
posterior communicating (P.Co.A.), anterior choroidal (A.Ch.A.), and middle cerebral
arteries (M.C.A.). The supraclinoid portion of the ICA is divided into three segments
based on the origin of its major branches: the ophthalmic segment (C4-Op.) extends from
the origin of the ophthalmic artery to the origin of the PCoA, the communicating segment
(C4-Co.) extends from the origin of the PCoA to the origin of the AChA, and the
choroidal segment (C4-Ch.) extends from the origin of the AChA to the bifurcation of the
carotid artery. The perforating branches arising from the ophthalmic segment pass to the
optic nerve, chiasm, infundibulum, and floor of the third ventricle. The perforating
branches arising from the communicating segment pass to the optic tract and the floor of
the third ventricle. The perforating branches arising from the choroidal segment pass
upward and enter the brain through the anterior perforated substance (Ant. Perf. Subst.)
The diaphragma sellae (Diaph.) surrounds the infundibulum above the pituitary gland.
The temporal lobe (Temp. Lobe) is below the middle cerebral artery. C. The left optic
nerve has been divided at the optic foramen and the anterior cerebral artery has been
divided near its origin so that both optic nerves and the chiasm and tract could be
elevated to show the perforating branches of the carotid artery. The Liliequist membrane
(Lilieq. Memb.) is posterior to the infundibulum and hides the basilar artery but not the
posterior cerebral artery (P.C.A.). The perforating branches of the ophthalmic segment
pass upward to the infundibulum and the optic nerve, chiasm, and tract. D. Both optic
nerves and both anterior cerebral arteries and the infundibulum have been divided to
permit the optic nerves and chiasm to be elevated with a forceps for this view under the
optic chiasm and across the diaphragma sellae and dorsum to the upper part of the basilar
artery (B.A.) and the oculomotor nerves (III). The oculomotor nerves pass forward below
the posterior cerebral arteries. The perforating branches of the supraclinoid segment of
the carotid artery pass upward to supply the infundibulum, the optic chiasm and tracts,
and the floor of the third ventricle; some enter the brain through the anterior perforated
substance. The right AChA is very large. (From Gibo H, Lenkey C, Rhoton AL Jr:
Microsurgical anatomy of the supraclinoid portion of the internal carotid artery. J
Neurosurg 55:560-574, 1981.1
Figure 3.17. Posterior views of the perforating branches of
the supraclinoid portion of the internal carotid artery (ICA).
A. The basilar artery (B.A.) and brain stem have been
divided and the floor of the third ventricle has been elevated
to provide this posterior view of the supraclinoid portion of
the ICA. The optic nerves (O.N.) can be followed back to
the optic chiasm and the optic tracts (O.Tr.). The
infundibulum of the pituitary gland (Infund.) arises from the
tuber ciner-eum (Tuber Cin.). The mamillary bodies (Mam.
Bodies) lie posterior to the tuber cinereum. The
supraclinoid portion of the ICA gives rise to the posterior
communicating (P.CO.A.), anterior choroidal (A.Ch.A.),
middle cerebral (M.C.A.), and anterior cerebral (A.C.A.)
arteries. The PCoA can be followed backward to its
junction with its posterior cerebral arteries (P.C.A.). The
supraclinoid portion of the ICA is divided into three
segments on the basis of the origin of its major branches:
the ophthalmic segment (C4-Op.) extends from the origin
of the ophthalmic artery to the origin of the PCoA, the
communicating segment (Cr-Co.) extends from the origin
of the PCoA to the origin of the AChA, and the choroidal
segment (C4-Ch.) extends from the origin of the AChA to
the bifurcation into the anterior and middle cerebral
arteries. The perforating branches arising from the
ophthalmic segment in this specimen enter the optic tract,
the floor of the third ventricle, and the infundibulum. The
superior hypoph-yseal arteries (Sup. Hyp. A.) pass to the
infundibulum. A single perforating artery arises from the
communicating segment on each side. The posterior wall of
the choroidal segment is the source of numerous perforating
branches. The pituitary stalk passes through the diaphragma
sellae (Diaph.) anterior to the dorsum sel-lae (Dorsum). B.
The right half of the dorsum sellae and the right posterior
clinoid process (Post. Clinoid) have been removed to
expose the pituitary gland and its anterior (Ant. Lobe) and
posterior (Post. Lobe) lobes. The infraclinoid segment of
the carotid artery (C.A.) is exposed to the right of the
pituitary gland. The apex of the basilar artery and the
proximal parts of the posterior cerebral and the superior
cerebellar (S.C.A.) arteries have been elevated to expose
the pituitary stalk and floor of the third ventricle. The
intracavernous portion of the carotid artery gives rise to the
inferior hypophyseal (Inf. Hyp. A.) and the tentorial (Tent.
A.) arteries. The posterior half of the right PCoA is dupli-
cated. The ophthalmic segments give rise to the superior
hypophyseal arteries. The left carotid artery has been
divided just distal to the origin of the PCoA. C. Posterior
views of the anterior part of the circle of Willis. The optic
chiasm has been divided posterior to its junction with the
optic nerves and anterior to where the infundibulum arises
from the floor of the third ventricle. The superior
hypophyseal arteries pass medially from the carotid artery
to the infundibulum and also give rise to branches coursing
to the lower surface of the optic chiasm. The
communicating segment gives rise to one perforating
branch on the right and two on the left. The choroidal
segment gives rise to more perforating branches than the
other segments, but they have been divided near their
origin. The anterior cerebral artery gives rise to perforating
branches coursing to the upper surface of the optic chiasm
and nerves. The anterior communicating artery (A.Co.A.) is
seen above the optic chiasm. (From Gibo H, Lenkey C,
Rhoton AL Jr: Microsurgical anatomy of the supraclinoid
portion of the internal carotid artery. J Neuro-surg 55:560-
574, 1981.)
Figure 3.18. Arterial relationships. A. Right lateral view.
The temporal lobe (Temp. Lobe) has been retracted to
expose the upper surface of the tentorium (Tent.) and the
tentorial edge (Tent. Edge). The uncus, when not retracted,
hangs over the free edge antero-lateral to the cerebral
peduncle (Ped.). The collateral (Coll. Sulc.) and rhinal sulci
(Rhinal Sulc.) separate the parahippocampal (Parahipp.
Gyr.) and occipito-temporal gyri (Occip. Temp. Gyr.). The
carotid artery (Car. A.) bifurcates below the anterior
perforated substance (Ant. Perf. Subst.). The middle
cerebral artery (M. C. A.) courses in the sylvian fissure
(Sylvian Fiss.) between the temporal and frontal lobes
(Front Lobe) and anterior cerebral artery (A.C.A.), which
passes between the optic nerve (Optic N.) and olfactory
tract (Olf. Tr.). The posterior communicating artery (Post
Comm. A.) lies above the oculomotor nerve (III). The
anterior choroidal artery (Ant Chor. A.) courses below the
optic tract (Optic Tr.). The basilar artery (Bas. A.) gives off
the superior cerebellar (S.C.A.) and posterior cerebral
arteries (P.C.A.) in the anterior incisural space. The PCA
gives off long (Long Circ. A.) and short circumflex (Short
Circ. A.) arteries, anterior (Ant Temp. A.), middle (Mid.
Temp. A.), and posterior temporal (Ant Temp. A.) middle
(Mid. Temp. A.), and posterior temporal (Post Temp. A.)
arteries, and medial posterior choroidal (Med. Post. Chor.
A.) and cal-carine (Calc. A.) arteries. The SCA bifurcates
into rostral (Ro. Tr.) and caudal trunks (Ca. Tr.). The su-
perior (Sup. Coll.) and interior (Inf. Coll.) colliculi are
supplied by branches of the SCA and PCA. The lateral
mesencephalic sulcus (Lat Mes. Sulc.) separates the
peduncular and tegmental parts of the midbrain. The
pontomesencephalic sulcus (Pon. Mes. Sulc.) separates the
midbrain and pons. B. Enlarged view. The carotid and
basilar bifurcations are in the anterior incisural space. The
anterior clinoid process (Ant Cli-noid) is lateral to the
carotid artery. The lenticulos-triate branches (Lent. Str. A.)
arise from the proximal part of the MCA. The anterior
choroidal artery passes posteriorly below the optic tract to
enter the middle incisural space. The oculomotor nerve
enters the dura lateral to the posterior clinoid process (Post
Clinoid). C. The temporal lobe has been removed to expose
the choroid plexus (Chor. Plex.) within the temporal horn.
The mamillary bodies (Mam. Body) lie above the basilar
bifurcation. The recurrent artery (Rec. A.) arises from the
АСА. (From Ono M, Ono M, Rhoton AL Jr, Barry M:
Microsurgical anatomy of the region of the tentorial
incisura. J Neurosurg 60:365-99, 1984.)
Figure 3.19. Tentorial incisura: arterial relationships. A. Anterior view. The anterior part
of the left frontal lobe (Front. Lobe) has been removed to expose the anterior incisural
space, which extends upward around the optic nerves (Optic N.) and chiasm and laterally
along the sylvian fissure (Sylvian Fiss.). The internal capsule (Int. Cap.) is located above
the anterior incisural space between the caudate nucleus (Caudate Nucl.) and the
putamen. The rostrum, genu, and body of the corpus callosum (Corp. Call.) surround the
anterior part of the lateral ventricle (Lat. Vent). The fornix extends along the lower
margin of the septum
pellucidum (Sept. Pell.) and forms the anterior and superior margin of the foramen of
Monro (For. Monro). The middle cerebral artery (M.C.A.) passes laterally in the sylvian
fissure above the temporal lobe (Temp. Lobe) and gives rise to the lenticulostriate arteries
(Lent. Str. A.). The anterior cerebral artery (A.C.A.) gives rise to the frontopolar (Front.
Pol. A.), pericallosal (Pericall. A.), and recurrent (Rec. A.) arteries. Perforating branches
(Perf. A.) from the АСА reach the lamina terminalis (Lam. Term.). The olfactory tract
(Olf. Tr.) has been divided. The oculomotor nerve (Ш) is exposed behind the carotid
artery (Car.A.). Choroid plexus (Chor.Plex.) is attached along the choroidal fissue
(Chor.Fiss.) situated between the fornix and thalamus. B. Lateral view. The inferior part
of the temporal lobe has been removed. The choroid plexus in the temporal horn (Temp.
Horn) has been preserved. The branches of the MCA pass over the insula and loop
around the frontal operculum (Front. Operc.). The posterior communicating artery (Post.
Comm. A.) passes lateral to the infundibulum (Infiind.) and joins the proximal part of the
posterior cerebral artery (P.C.A.). The anterior choroidal artery (Ant. Chor. A.) enters the
choroid plexus in the temporal horn. The PCA arises at the bifurcation of the basilar
artery (Bas. A.), passes posteriorly around the cerebral peduncle (Ped.), and gives rise to
long (Long Circ. A.) and short circumflex (Short Circ. A.) arteries, lateral (Lat. Post.
Chor. A.) and medial posterior choroidal (Med. Post. Chor. A.) arteries, and posterior
pericallosal (Post. Pericall. A.), posterior temporal (Post. Temp. A.), calcarine (Calc. A.),
and parietoocciptal (Par. Occip. A.) arteries. The superior cerebellar artery (S.C.A.) arises
from the basilar artery and dips below the tentorial edge (Tent. Edge). The vein of Galen
passes above the superior (Sup. Coll.) and inferior colliculi (Inf. Coll.). The lateral
mesencephalic sulcus (Lat. Mes. Sulc.) is dorsal to the cerebral peduncle. C.
Superolateral view. All of the tentorium except the free edge and the attachment along
the petrous ridge has been removed. The basilar artery bifurcates in the anterior incisural
space. The trochlear nerve (IV) encircles the brain stem between the PCA and SCA. The
abducent nerve (VI) passes above the anterior inferior cerebellar artery (A.I.C.A.). The
SCA bifurcates into a rostral (Ro. Tr.) and a caudal trunk (Ca. Tr.) above the trigeminal
nerve (V). A bridging vein (Bridg. V.) enters the lateral wall of the cavernous sinus. The
oculomotor nerve enters the dura lateral to the posterior clinoid process (Post. Clinoid).
D. Another specimen with the temporal horn exposed, lateral view. The anterior
choroidal artery gives rise to peduncular perforating branches (Ped. Perf. A.) before
entering the temporal horn. The lateral posterior choroidal arteries pass through the
choroidal f issue between the f imbria and pulvinar to enter the choroid plexus. The
thalamogeniculate arteries (Thal. Gen. A.) enter the medial (Med. Gen. Body) and lateral
(Lat. Gen. Body) geniculate bodies and the thalamus. The hippocampal formation on the
medial surface of the temporal lobe includes the subiculum of the parahippocampal gyrus
(Para-hipp. Gyr.), the dentate gyrus (Dentate Gyr.), and the fimbria. The amygdaloid
nucleus (Amygd. Nucl.) is in the anteromedial margin of the temporal horn. E. Posterior
incisural space, posterior-superior view. The occipital lobe, splenium, and the posterior
part of the fornix have been removed to expose the SCA and PCA and their branches in
the posterior incisural space. The SCA gives rise to vermian arteries (Ve. A.), which pass
over the culmen just below the tentorial apex. The lateral posterior choroidal arteries pass
around the pulvinar to reach the temporal horn and atrium. The medial posterior
choroidal arteries encircle the brain stem to enter the roof of the third ventricle. The
choroid plexus in the lateral ventricle is attached along the choroidal fissure. The striae
terminalis (Str. Term.) courses along the groove between the caudate nucleus and the
thalamus. The posterior part of the hippocampal formation (Hippocamp.) is exposed in
the floor of the atrium. The tela choroidea (Tela), forming the upper wall of the velum
interpositum (Vel. Interpos.), has been removed, but the lower layer, which is attached to
the medial surface of the thalamus along the striae medullaris thalami, has been
preserved. The suprapineal recess is located between the pineal body and the lower layer
of the tela. F. The tentorium, except for the free edge and the strip along the straight sinus
(Str. Sinus), and the tela choroidea in the roof of the third ventricle (3 Vent.) have been
removed. The lateral posterior choroidal arteries ascend to reach the glomus of the
choroid plexus. The medial posterior choroidal arteries pass forward in the roof of the
third ventricle above the habenula and the massa intermedia (Massa Inter.). The SCA
gives rise to the vermian and hemispheric arteries (He. A.) in the posterior incisural
space. The quadrigeminal branches (Quad. A.) of the PCA and SCA pass to the colliculi.
(From Ono M, Ono M, Rhoton AL Jr, Barry M: Microsurgical anatomy of the region of
the tentorial incisura. J Neurosurg 60:365-399, 1984.)
 Figure 3.21. Superior views of the sellar region. A. Carotid
arteries are lateral to the optic nerves, anterior cerebral
arteries are stretched across the superior surface of the
optic chiasm, and the right optic nerve is shorter than the
left. B. Long, tortuous anterior cerebral arteries are above
the optic chiasm. The A1 segment of the right anterior
cerebral artery loops in a complete circle between its origin
from the carotid artery and its junction with its mate from
the opposite side at the anterior communicating artery. A
tortuous left anterior cerebral artery rests against the
tubercu-lum sellae covering the prechiasmatic space.
(From Renn WH, Rhoton AL Jr: Microsurgical anatomy of
the sellar region. J Neurosurg 43:288-298, 1975.)

Figure 3.20. Inferior views with part of the temporal lobes

removed to show the choroidal arteries supplying the
choroid plexus of the inferior horn and atrium. A. The
anterior choroidal arteries (A.Ch.A.) arise from the carotid
arteries (C.A.), course posteriorly below the optic tracts
(O.Tr.), and pass through the choroidal fissure to enter the
choroid plexus (Ch. PL) of the temporal horn (Temp.
Horn). The medial posterior choroidal arteries (M.P.Ch.A.) A.), parietooccipital (P-O.A.), and posterior temporal
arise from the proximal or P1 segment (P-1) of the posterior arteries (P.T.A.) arise from the PCAs. The cut end of the
cerebral artery (PCA), encircle the brain stem, and pass basilar artery (B. A.) is between the cerebral peduncles
forward beside the pineal body and below the splenium of (Ped.). B. Inferior view of temporal horn and atrium of
the corpus callosum to enter the choroid plexus in the roof right lateral ventricle. Enlarged view of the AChA,
of the third ventricle. The lateral posterior choroidal LPChA, and MPChA, showing their relationship to the
arteries (L.P.Ch.A.) arise from the P2 segment of the PCA optic tract, cerebral peduncles, brain stem, and pulvinar.
(P-2) and course below the pulvinar of the thala-mus The glomus of the choroid plexus projects into the atrium
(Pulv.) and lateral geniculate bodies (L. Gen. Bo.) to enter of the ventricle. The lenticulos-triate arteries (Len. Str. A.)
the choroid plexus in the temporal horn and atrium. The arise from the middle cerebral artery (M.C.A.), and the
carotid arteries are lateral to the optic nerves (O.N.) and anterior cerebral arteries (A.C.A.) pass above the optic
optic chiasm (O.Ch.). The superior hypophyseal arteries (S. chiasm. (From Fujii K, Lenkey C, Rhoton AL Jr:
Ну. A.) pass medially from the carotid artery below the Microsurgical anatomy of the choroidal arteries: Lateral
optic chiasm to the pituitary stalk (Pit. Stalk). The and third ventricles. J Neurosurg 52:165-188, 1980.)
premamillary artery (Pre-mam. A.) arises from the
posterior communicating artery (P.Co.A.) and enters the
hypothalamus anterior to the mamillary bodies (Мат. В.).
The calcarine (Cal.
Figure 3.22. Anterosuperior view of the perforating arteries entering the anterior wall of
the third ventricle. A. The optic nerves (O.N.), chiasm (O.Ch.), and tracts (O.Tr.) are
medial to the carotid arteries (C.A.) and below the anterior cerebral (A.C.A.) and
anterior communicating (A.Co.A.) arteries. The frontal lobes (Fr. Lobe) and anterior
perforated substance (Ant. Perf. Subst.) are above the anterior cerebral arteries. The
anterior cerebral arteries give rise to a group of perforating arteries that enter the
suprachiasmatic area and the upper surface of the optic chiasm. The recurrent artery
(Rec. A.) arises from the anterior cerebral artery near the level of the anterior
communicating artery. The olfactory nerves (Olf.N.) are above the anterior cerebral
arteries. B. The anterior communicating artery gives rise to a series of perforating
arteries (Perf. A.) that enter the area around the lamina terminalis (Lam. Теr.). С. A
probe elevates the anterior communicating artery to expose two perforating arteries that
pass through the lamina terminalis to enter the walls of the third ventricle (3V). The left
recurrent artery arises from the anterior communicating artery in a common trunk with a
branch to the frontal lobe (Fr. Br.). D. A precallosal artery (Pre.Cal.A.) arises from the
anterior communicating artery and passes upward in front of the lamina terminalis to
supply the rostrum (Rostrum) of the corpus callosum. (From Yamamoto I, Rhoton AL
Jr, Peace DA: Microsurgery of the third ventricle: Part 1. Microsurgical anatomy.
Neurosurgery 8:334-356, 1981.)

Figure 3.23. Anterosuperior view of the lamina ter-
minalis. A. The optic nerves (O.N.), chiasm (O.Ch.), and
tracts (O.Tr.) are below the lamina terminalis (Lam. Теr.).
The carotid arteries (C.A.) pass laterally below the optic
nerves. The anterior cerebral (A.C.A.) and anterior
communicating (A.Co.A.) arteries are above the optic
chiasm. The recurrent arteries (Rec. A.) arise at the level of
the anterior communicating artery. The olfactory nerves
(Olf. N.) have been divided near their junction with the
brain. B. The lamina terminalis has been opened along the
dotted line shown in A to expose the cavity of the third
ventricle (3V). The optic recess (O. Recess) extends
downward between the lamina terminalis and the superior
surface of the optic chiasm. The right anterior cerebral
artery is hypoplastic, and the left anterior cerebral artery
gives rise to both distal segments of the anterior cerebral
artery. (From Yamamoto I, Rhoton AL Jr, Peace DA:
Microsurgery of the third ventricle: Part 1. Microsurgical
anatomy. Neurosurgery 8:334-356, 1981.)
Venous Relationships
The deep cerebral venous system is intimately related to
the walls of the third ventricle (Figs. 3.24 to 3.26) (25, 26).
It represents a formidable obstacle to the operative
approaches to the third ventricle, especially in the region of
the pineal gland, where the internal cerebral vein and the
basal vein on each side converge on the great vein.
Internal Cerebral Vein
The paired internal cerebral veins originate just behind
the foramen of Monro and course posteriorly within the
velum interpositum (Figs. 3.24, 3.26, and 3.27). Initially,
they follow the gentle convex upward curve of the striae
medul-laris thalami and, further distally, as they course
along the superolateral surface of the pineal body, they
follow the concave upward curve of the inferior surface of
the splenium. The union of the paired veins to form the
great vein may be located above or posterior to the pineal
body and inferior or posterior to the splenium. The length
of the internal cerebral vein varies from 19 to 35 mm
(average, 30.2) (26).
Great Vein and Straight Sinus
The great vein, after being formed by the union of the
internal cerebral veins, curves posteriorly and superiorly
around the splenium to join the straight sinus at the anterior
end of the junction of the falx and tentorium (Figs. 3.24,
3.26, and 3.28). The straight sinus courses posteroinfer-
iorly along the falcotentorial junction to the tor-cular. The
junction of the great vein with the straight sinus varies from
being nearly flat if the tentorial apex is located below the
splenium to forming a sharp angle if the apex is located
above the splenium, so that the great vein must turn sharply
upward to reach the straight sinus at the apex. The average
length of the great vein is 12 mm (range, 8 to 25 mm) (26).
The major tributaries of the great vein are the internal
cerebral and basal veins, but it also receives blood from nu-
merous other veins in the region. The convergence of
multiple veins at the great vein results in a high density of
veins in the area.
Basal Vein
The basal vein is formed below the anterior perforated
substance in the anterior incisural space by the union of
veins draining the walls of this space. It proceeds
posteriorly between the midbrain and the temporal lobe to
drain the walls of the middle incisural space before
emptying into the internal cerebral or great vein (Figs. 3.24,
3.26, 3.28, and 3.29). The basal vein is divided into
anterior, middle, and posterior segments that correspond to
the parts of the vein coursing within the anterior, middle,
and posterior incisural regions. The anterior and middle
incisural regions are drained, almost totally, by tributaries
of the basal vein. The veins in the posterior incisural region
join the internal cerebral and great veins, as well as the
basal vein.

Figure 3.24. Schematic drawing of the ventricular veins.
Lateral (top), anterior (middle), and superior (lower) views.
The ventricular veins are divided into a medial and a lateral
group. The ventricular veins drain into the internal cerebral
(Int. Cer. V.}, basal (Basal V.), and great (V. Galen) veins.
The lateral group consists of the anterior caudate vein (Ant.
Caud. V.) in the frontal horn; the thalamostriate (Thal. Str.
V.), posterior caudate (Post. Caud. V.), and thalamocau-
date (Thal. Caud. V.) veins in the body; the lateral atrial
vein (Lat. Atr. V.) in the atrium; and the inferior ventricular
(Inf. Vent. V.) and amygdalar veins (Amygd. V.) in the
temporal horn. The medial group is formed by the anterior
septal vein (Ant. Sept. V.) in the frontal horn, the posterior
septal veins (Post. Sept. V.) in the body, the medial atrial
vein (Med. Atr. V.) in the atrium, and the transverse
hippocampal veins (Trans. Hippo. V.) in the temporal horn.
The transverse hippocampal veins drain into the anterior
(Ant. Long. Hippo. V.) and posterior longitudinal
hippocampal (Post. Long. Hippo. V.) veins. The superior
cho-roidal veins (Sup. Chor. V.) drain into the thalamo-
striate and internal cerebral veins, and the inferior
choroidal vein (Inf. Chor. V.) drains into the inferior
Tributaries of the Deep Veins
The tributaries of the internal cerebral, basal, and great
veins drain the walls of the lateral and third ventricles, the
periventricular white and gray matter, the corpus callosum,
the thalamus, the septum pellucidum, the upper midbrain,
the choroid plexus of the lateral and third ventricles, and
the superior part of the cerebellum.
Ventricular Drainage
The veins draining the deep gray and white matter of the
cerebrum converge on the large veins coursing in and near
the walls of the third ventricle (Figs. 3.24 to 3.29) (26). The
veins from the frontal horn, the body of the lateral ventricle,
and the surrounding gray and white matter drain into the
internal cerebral vein; the veins from the temporal horn and
the adjacent periventricular structures drain into the basal
veins; and those draining the atrium and adjacent parts of
the brain drain into the basal, internal cerebral, and great
veins. The veins collecting blood from the periventricular
white and gray matter join to form subepedymal channels
in the walls of the lateral ventricles. These subependymal
channels in the walls of the ventricle are divided into a
medial and a lateral group. Both the lateral and the medial
group pass through or adjacent to the choroidal fissure to
reach the internal cerebral, basal, or great vein. The medial
group consists of those veins that traverse the medial wall
and roof of the frontal horn and body, the medial wall of
the atrium, and the hippocompal surface of the floor of the
temporal horn. The lateral group consists of those veins that
traverse the lateral wall and floor of the frontal horn and
body, the lateral wall of the atrium, and the roof of the
temporal horn. In the temporal horn, the roof corresponds
to the lateral group and the floor corresponds to the medial
group.
In the frontal horn, the medial group is formed by the
anterior septal veins, which cross the septum pellucidum
and fornix to join the internal cerebral vein, and the lateral
group is formed by the anterior caudate veins, which cross
the ventricular surface of the caudate nucleus and ter-
ventricular vein. The vein of Galen drains into the straight
sinus (Str. Sinus). The anterior (Ant. Cer. V.) and deep
middle cerebral (Deep. Mid. Cer. V.) veins join to form the
basal vein. (From Ono M, Rhoton AL Jr, Peace D,
Rodriguez R: Microsurgical anatomy of the deep venous
system of the brain. Neurosurgery 15:621-657, 1984.)
Figure 3.25. A and B. Ventricular veins. A. Anterior view (along the arrow in the insert)
into the frontal horn (Front. Horn) and body of the lateral ventricle (Body Lat. Vent). The
frontal horn is located anterior to the foramen of Monro (For. Monro) and has the septum
pellucidum (Sept Pell.) in the medial wall, the genu and body of the corpus callosum
(Corp. Call.) in the roof, the caudate nucleus (Caudate Nucl.) in the lateral wall, the genu
of the corpus callosum in the anterior wall, and the rostrum of the corpus callosum in the
floor. The body of the lateral ventricle has the thalamus in its floor, the caudate nucleus
in the lateral wall, the body of the fornix and septum pellucidum in the medial wall, and
the corpus
minate in the thalamostriate or internal cerebral vein. In the
body, the medial group is formed by the posterior septal
veins, and the lateral group is formed by the thalamostriate,
thalamocau-date, and posterior caudate veins. The
thalamostriate vein is the largest tributary of the internal
cerebral vein. It courses anteriorly and medially in the
groove between the caudate nucleus and the thalamus
beneath the striae terminalis. At the level of the foramen of
Monro, it curves around the anterior tubercle of the
thalamus and joins the internal cerebral vein. The
thalamocau-date originates at the lateral angle of the body
of the lateral ventricle and runs across the caudate nucleus
and thalamus to join the internal cerebral vein more
posteriorly than does the thalamostriate vein. The posterior
caudate veins cross the lateral wall of the body of the
ventricle and empty into the thalamostriate or
thalamocaudate vein. The posterior septal veins cross the
posterior part of the septum pellucidum and pass around
the fornix to enter the internal cerebral vein. In the atrium,
the medial group is formed by the medial atrial veins, and
the lateral group is formed by the lateral atrial veins. The
atrial veins pass through the choroidal fissure to enter the
basal, internal cerebral, or great vein. In the temporal horn,
the veins draining the roof correspond to the lateral group,
and the veins draining the floor correspond to the medial
group. The medial group is formed from the transverse hip-
pocampal veins that run in the floor on the sur-
face of the hippocampus and drain into the basal vein. The
lateral group is formed by the inferior ventricular vein. It
runs in the roof of the temporal horn and passes through the
choroidal fissure to join the basal vein.
Incisural and Cisternal Veins
The main venous trunk related to the anterior incisural
space is the basal vein (Figs. 3.28 to 3.30) (25, 26). The
veins joining below the anterior perforated substance to
form the basal vein include the olfactory vein, which runs
posteriorly in the olfactory sulcus; the frontoorbital vein,
which courses along the orbital surface of the frontal lobe;
the deep middle cerebral vein, which receives the veins
from the insula and passes medially across the limen
insulae; the uncal veins, which course medially from the
uncus; and the anterior cerebral vein, which descends on
the lamina terminalis and crosses the optic chiasm to reach
the basal vein. The paired anterior cerebral veins are joined
across the midline above the optic chiasm by the anterior
communicating vein and receive the paraterminal vein from
the paraterminal and parolfactory gyri and the anterior
pericallosal veins from the rostrum and genu of the corpus
callosum.
The veins on the surface of the brain stem that form the
posterior wall of the anterior incisural space are divided
into transversely or vertically oriented groups (21, 22, 25,
26). The transverse veins are the peduncular vein, which
passes hor-

callosum in the roof. The choroid plexus (Chor. Plex.) is attached along the choroidal
fissure (Chor. Fiss.), the cleft between the fornix and thalamus. The anterior septal veins
(Ant. Sept. V.) cross the roof and medial wall of the frontal horn and pass posteriorly
toward the foramen of Monro, where they join the anterior end of the internal cerebral
veins. The anterior caudate veins (Ant. Caud. V.) cross the lateral wall of the frontal horn
and join the thalamostriate vein (Thal. Str. V.), which passes through the foramen of
Monro. The superior choroidal vein (Sup. Chor. V.) courses on the choroid plexus in the
body. The posterior septal veins (Post. Sept. V.) cross the roof and medial wall of the
body and pass through the margin of the choroidal fissure. The posterior caudate veins
cross the lateral wall of the body and join the thalamostriate vein, which courses along
the striothalamic sulcus (Str. Thal. Sulc.). Anterior (Ant. Superf.. Thal. V.) and superior
(Sup. Superf. Thal. V.) superficial thalamic veins cross the surface of the thalamus. The
anterior thalamic vein (Ant. Thal. V.) drains the nuclei in the anterior-superior part of the
thalamus. B. Anterior-superior view (along the arrow in the insert) into the body, atrium,
and occiptal horn (Occip. Horn) of the lateral ventricle. The calcar avis and bulb of the
corpus callosum (Bulb Corp. Call.) form the medial wall of the atrium and occipital horn.
The floor of the atrium is formed by the collateral trigone (Coll. Trig.). The roof and
posterior part of the lateral walls are formed by the tapetum of the corpus callosum. The
caudate nucleus is in the anterior part of the lateral wall of the atrium. The medial (Med.
Atr. V.) and lateral (Lat. Atr. V.) atrial veins pass forward on the medial and lateral walls
of the atrium toward the choroidal fissure. A thalamocaudate vein (Thal. Caud. V.)
crosses the lateral wall posterior to the thalamostriate vein. The superior choroidal vein
courses toward the foramen of Monro.
Figure 3.25. С and D. Ventricular veins (continued). C. Posterior view (along the arrow
in the insert) into the atrium and temporal horn. The atrium has the tapetum of the corpus
callosum in the roof, the bulb of the corpus callosum and the calcar avis in its medial
wall, the hippocampal formation and the collateral trigone (Coll. Trig.) in the floor, the
caudate nucleus and tapetum in the lateral wall, and the crus of the fornix and the
pulvinar and choroid plexus in the anterior wall. The floor of the temporal horn (Temp.
Horn) is formed by the hippocampus and collateral eminence (Coll. Eminence). The
inferior choroidal vein (Inf. Chor. V.) courses on the choroid plexus in the temporal horn.
The lateral atrial veins
izontally around the anterior surface of the cerebral
peduncle and terminates in the basal vein at the junction
of the anterior and middle inci-sural spaces, and the vein
of the pontomesence-phalic sulcus, which courses below
the peduncular vein in the pontomesencephalic sulcus.
The vertically oriented veins on the posterior wall of the
anterior incisural space are the median anterior
pontomesencephalic vein, which courses in the midline
and connects the peduncular veins above with the pontine
veins below, and the lateral anterior pontomesencephalic
veins, which course on the anterolateral surface of the
cerebral peduncle and the pons and join the basal vein
superiorly and the vein of the pontomesencephalic sulcus
or a transverse pontine vein inferiorly.
The venous relationshps in the middle incisural space
are relatively simple (Figs. 3.28 to 3.30). The basal vein
courses along the upper part of the cerebral peduncle and
below the pul-vinar to reach the posterior incisural space.
It may infrequently terminate in a tentorial sinus in the
free edge at this level. The veins draining the medial wall,
from anterior to posterior, are the lateral
pontomesencephalic vein, which runs vertically on the
lateral surface of the cerebral peduncle and pons and
terminates in the basal vein superiorly and the vein of the
pontomesencephalic sulcus inferiorly, and the lateral mes-
encephalic vein, which runs vertically along the
lateral mesencephalic sulcus and terminates above in the
basal vein near the medial genicu-late body and below in a
petrosal vein.
Numerous veins from the lateral wall of the middle
incisural space converge on the basal vein near the inferior
choroidal point. These veins are the anterior hippocampal
vein, which courses posteriorly from the anterior
hippocampal sulcus; the uncal veins, which drain the
medial surface of the uncus; and the anterior longitudinal
hippocampal vein, which courses anteriorly along the
dentate gyrus.
The venous relationships in the posterior incisural space
are the most complex in the cranium because the internal
cerebral and basal veins and many of their tributaries
converge on the great vein within this area (Figs. 3.38 to
3.30). The internal cerebral veins exit the velum
interpositum and the basal veins exit the ambient cistern to
reach the posterior incisural space, where they empty into
the great vein. The great vein passes below the splenium to
enter the straight sinus at the tentorial apex. Other veins
converging on this area include the posterior pericallosal
veins, which course posteriorly around the splenium to
terminate in the great vein or the internal occipital vein; the
lateral atrial veins, which drain the lateral wall and roof of
the atrium and course medially through the choroidal
fissure to terminate in the basal, internal cerebral, or great
vein either directly or after

arise on the lateral wall and cross the tail of the caudate nucleus and the pulvinar to pass
through the choroidal fissure. The medial atrial veins pass forward and penetrate the crus
of the fornix near the choroidal fissure to reach the quadri-geminal cistern. Some of the
medial atrial veins also drain the roof and floor. Transverse hippocampal veins (Transv.
Hippo. V.) cross the floor of the atrium and temporal horn. Posterior superficial thalamic
veins (Post. Superf. Thal. V.) cross the atrial surface of the thalamus. D. Anterior view
(along the arrow in the insert) into the temporal horn. The floor of the temporal horn is
formed by the collateral eminence and the hippocampal formation. The roof and lateral
wall, from medial to lateral, are formed by the thalamus, the tail of the caudate nucleus,
and the tapetum of the corpus callosum. The medial wall is little more than the cleft
between the inferior surface of the thalamus and the fimbria. The amygdaloid nucleus
(Amygd. Nucl.) bulges into the anteromedial part of the temporal horn. The pes
hippocampus (Pes Hipp.), the bulbous digitated anterior end of the hippocampal
formation, is in the anterior part of the floor. The fimbria of the fornix arises on the
surface of the hippocampal formation and passes posteriorly to become the crus of the
fornix. The choroid plexus is attached along the choroidal fissure. The inferior ventricular
vein (Inf. Vent. V.) drains the roof of the temporal horn and receives the amygdalar vein
(Amygd. V.) from the ventricular surface of the amygdaloid nucleus. The inferior
choroidal vein joins the inferior ventricular vein. The transverse hippocampal veins
draining the floor of the temporal horn pass medially through the choroidal fissure to
enter the basal vein or its tributaries. (From Ono M, Rhoton AL Jr, Peace D, Rodiguez R:
Microsurgical anatomy of the deep venous system of the brain. Neurosurgery 15:621-
657, 1984.)

Figure 3.26. Midsagittal sections. A. The brain stem has
been sectioned at the level of the midbrain. The
parahippocampal gyrus (Parahippo. Gyr.) has been
depressed to expose the basal vein (Basal V.) between the
uncus and the cerebral peduncle (Ped.) and the choroidal
fissure (Chor. Fiss.), the cleft between the fimbria and the
pulvinar. The anterior septal vein (Ant. Sept. V.) passes
posteriorly on the septum pel-lucidum (Sep. Pell.) toward
the foramen of Monro (For. Monro) and joins the internal
cerebral vein (Int. Cer. V.) in the roof of the third ventricle
(3rd Vent). The internal cerebral vein passes posteriorly
above the massa intermedia (Massa Inter.) and the choroid
plexus (Chor. Plex.) in the roof of the third ventricle and
exits the velum interpositum (Vel. Interpos.), situated
between the layers of the tela choroidea (Tela) in the roof of
the third ventricle, by passing below the splenium to join
the vein of Galen (V. of Galen). The basal vein passes
below the lateral geniculate body (Lat. Gen. Body) and
pulvinar. The anterior longitudinal hippocampal vein (Ant.
Long. Hippo. V.) joins the anterior end of the basal vein.
The posterior longitudinal hippocampal (Post. Long. Hippo.
V.), internal occipital (Int. Occip. V.), and lateral atrial (Lat.
Atr. V.) veins join the posterior end of the basal vein. The
posterior pericallosal vein (Post. Pericall. V.) passes around
the splenium to join the great vein. The paraterminal vein
(Paraterm. V.) passes in front of the lamina terminalis
(Lam. Ter.) and anterior commissure (Ant. Comm.) on the
paraterminal gyrus (Paraterm. Gyr.) and courses toward the
anterior end of the basal vein. The habenular (Hab. Comm.)
and posterior (Post. Comm.) commissures form the stalk of
the pineal body. The fornix fuses to the lower surface of the
splenium posteriorly and passes superior and anterior to the
foramen of Monro anteriorly. The cin-gulate gyrus (Cing.
Gyr.) is above the corpus callosum (Corp. Call.). The
calcarine sulcus (Calc. Sulc.) divides the medial surface of
the occipital lobe above the lingual gyrus (Lingual Gyr.).
The infundibular (Infund.) and mamillary (Mam. Body)
bodies are in the floor of the third ventricle. B. Enlarged
view of the inferior part of the choroidal fissure. The veins
exiting the temporal horn pass through the choroidal fissure,
the cleft between the fimbria of the fornix and the pulvinar.
The inferior end of the choroidal fissure, called the inferior
choroidal point (Inf. Chor. Point), is located just behind the
uncus. The basal vein passes below the medial (Med. Gen.
Body) and lateral geniculate bodies. The anterior
longitudinal hippocampal vein passes forward and the
posterior longitudinal hippocampal vein passes backward
on the dentate gyrus. The hippocampal sulcus (Hippo.
Sulc.) separates the dentate and parahippocampal gyri, and
the fimbriod-entate sulcus (Fimb. Dentate Sulc.) separates
the fimbria and the dentate gyrus. The section of the brain
stem crosses the red nucleus (Red. Nucl.). C. Enlarged
view. The septum pellucidum and body of the fornix have
been removed to expose the right lateral ventricle (Lat.
Vent). The thalamostriate vein (Thal. Str. V.) passes forward
between the caudate nucleus (Caudate Nucl.) and the
thalamus and enters the internal cerebral vein. The anterior
septal vein passes through the posterior margin of the
foramen of Monro and enters the internal cerebral vein in
the posterior part of the roof of the third ventricle. The stria
medullaris thalami (Str. Med. Thal.) passes posteriorly in
the wall of the third ventricle toward the habenular
commissure. A superior choroidal vein (Sup. Chor. V.)
courses on the surface of the choroid plexus. (From Ono M,
Rhoton AL Jr, Peace D, Rodriguez R: Microsurgical
anatomy of the deep venous system of the brain.
Neurosurgery 15:621-657, 1984.)
forming a common stem with the medial atrial veins; the
medial atrial veins, which drain the medial wall and roof
of the atrium and occipital horn and course anteromedially
through the cho-roidal fissure before terminating in the
internal cerebral vein; the posterior longitudinal hippo-
campal vein, which courses posteriorly along the dentate
gyrus and terminates in the internal cerebral, basal, or
great vein or one of the atrial veins; and the internal
occipital veins, which originate in the calcarine and
parietooccipital sulci and course anteromedially along the
calcarine sulcus to terminate in the great vein.
The largest vein from the infratentorial part of the
posterior incisural space is the vein of the
cerebellomesencephalic fissure, which is also called the
precentral cerebellar vein (Figs. 3.28 and 3.30). It
originates from the union of the paired veins of the
superior cerebellular peduncle and courses
anterosuperiorly through the cerebellomesencephalic
fissure to terminate with the superior vermain vein in the
great vein (21, 26). The veins of the superior cerebellular
peduncle arise below the inferior colliculi on the external
surface of the superior cerebellar peduncles. The superior
vermian and the superior hemispheric veins from the
anterosuperior part of the cerebellum arise from the
infratentorial part of the posterior incisural space and pass
forward under the free edge of the tentorium to empty into
the great vein either directly or after joining with the vein
of the cerebellomesencephalic fissure.
Smaller thalamic, epithalamic, and tectal veins emerge
from the walls of the posterior incisural space and
terminate in the internal cerebral, basal, or great veins or
the vein of the cerebellomesencephalic fissure.
Choroidal Veins
Two other veins that course near the walls of the third
ventricle are the superior and inferior choroidal veins
(26). Both lie within the choroid plexus of the lateral
ventricles and are covered by ependyma (Figs. 3.24, 3.25,
and 3.27 to 3.29). The superior choroidal vein runs in the
choroid plexus of the atrium and body of the lateral ven-
tricle. It terminates in either the thalamostriate
or the internal cerebral vein near the foramen of Monro.
The inferior choroidal vein drains the choroid plexus of the
temporal horn and atrium. It courses downward and
forward in the roof of the temporal horn and joins the
inferior ventricular vein near where the latter passes
through the choroidal fissure or passes directly to the basal
vein.
Bridging Veins
The veins coursing from the surface of the brain to the
venous sinuses in the dura mater that are encountered in
retracting the brain to reach the walls of the third ventricle
include the superficial superior cerebral veins that cross
from the superior margin of the cerebrum to the superior
sagittal sinus; the cingulate and callosal veins that drain the
cingulate gyrus and upper surface of the corpus callosum
and pass into the inferior sagittal sinus; the superficial
middle cerebral veins that cross the sylvian fissure to enter
the sphenoparietal sinus on the inferior margin of the
sphenoid ridge; and the inferior cerebral veins that drain the
lower portions of the lateral surface of the temporal lobe
and the undersur-faces of the occipital and temporal lobes
and empty into the transverse and tentorial sinuses. Of the 3
to 12 (average, 6.8) superficial superior cerebral veins per
hemisphere, the number anterior and posterior to the central
or rolandic vein are close to the same (55). The veins
draining the corresponding part of the medial and lateral
surfaces of the superior margin of the cerebral hemisphere
usually join before entering the superior sagittal sinus. The
vein of Labbe, which extends from the sylvian fissure to the
transverse sinus, is the largest inferior cerebral vein. There
are usually no veins between the medial aspect of the
occipital pole and the transverse and straight sinuses, but
there are frequently several bridging veins (range, 2 to 7)
between the lateral surface of the occipital pole and the
transverse sinus (55).
There are also numerous bridging veins crossing the
interval between the superior surface of the cerebellum and
the sinuses in the tentorium. They are more numerous
medially than laterally (21).
Figure 3.27. A-F. Superior view. A. The superior part of the cerebral hemisphere has
been removed to expose the lateral ventricles. The frontal horn (Front. Horn) extends
into the frontal lobe (Front. Lobe). The body of the lateral ventricle (Body Lat. Vent.) is
deep to the frontal and parietal lobes (Par. Lobe). The atrium extends posteriorly toward
the occipital lobe (Occip. Lobe). The thalamostriate vein (Thal. Str. V.) courses along the
junction of the caudate nucleus (Caudate Nucl.) and the thalamus toward the foramen of
Monro (For. Monro). The anterior caudate veins (Ant. Caud. V.) course on the caudate
nucleus in the lateral wall of the frontal horn. The superior choroidal veins (Sup. Chor.
V.) course on the choroid plexus (Chor. Plex.) and join the thalamostriate vein near the
foramen of Monro. Medial atrial veins (Med. Atr. V.) course along the medial wall of the
atrium. The superior sagittal sinus (Sup. Sag. Sinus) courses in the edge of the falx. B.
Enlarged view. The septum pellucidum (Sept. Pell.) separates the lateral ventricles. The
anterior caudate and thalamostriate veins pass toward the foramen of Monro. The small
anterior superficial thalamic vein (Ant. Superf. Thal. V.) crosses the thalamus near the
anterior thalamic tubercle (Ant. Thal. Tuber.). The choroidal fissure (Chor. Fiss.) is
located between the fornix and thalamus. The bulb of the corpus callosum (Bulb Corp.
Call.) is in the medial wall of the atrium. The cingulate gyrus (Cing. Gyr.) wraps around
the corpus callosum (Corp. Call). C. Enlarged view of the frontal horns. The anterior
septal veins (Ant. Sept. V.) pass medially on the posterior surface of the genu of the
corpus callosum (Genu Corp. Call.) and turn posteriorly on the septum pellucidum. The
anterior caudate veins cross the head of the caudate nucleus. The posterior septal veins
(Post. Sept. V.) cross the medial wall of the body of the lateral ventricle. On the left side,
the anterior septal, thalamostriate, and superior choroidal veins course toward the
foramen of Monro. On the right side, the thalamostriate vein is absent and most of the
lateral wall of the body is drained by a large thalamocaudate vein
Figure 3.27. G-I. Superior view (continued). G. Another specimen. The thala-mostriate
veins receive the superior choroidal, anterior septal, anterior thalamic, and anterior
superficial thalamic veins and pass through the choroidal fissure, just behind the foramen
of Monro. The striae medullaris thalamic (Str. Med. Thal.) pass along the superomedial
margins of the thalami. H. Another specimen. The tela choroidea (Tela) extends across
the roof of the third ventricle above the internal cerebral veins. A large superior
superficial thalamic vein on the left side receives several small choroidal veins (Chor. V.)
and joins the anterior part of the internal cerebral vein. The anterior caudate, anterior
septal, anterior thalamic, and superior choroidal veins converge on the anterior end of the
internal cerebral vein. I. Another specimen. The right internal cerebral vein receives
duplicate thalamostrlate veins, called the anterior (Ant. Thal. Str. V.) and posterior (Post.
Thal Str. V.) thalamostriate veins. The right lateral atrial vein (Lat. Atr. V.) joins the
posterior thalamostriate vein. On the left side, a single large thalamostriate vein passes
through the foramen of Monro to join the internal cerebral vein. The inferior sagittal sinus
(Inf. Sag. Sinus) courses in the lower margin of the falx. (From Ono M, Rhoton AL Jr,
Peace D, Rodriguez R: Microsurgical anatomy of the deep venous system of the brain.
Neurosurgery 15:621-657, 1984.)

(Thal. Caud. V.), which receives the posterior caudate vein (Post. Caud. V.) and passes
posteriorly in the striothalamic sulcus (Str. Thal. Sulc.). D. The body of the fornix has
been removed at the junction of its attachment to the crura posteriorly and the columns
anteriorly. The removal of the tela choroidea in the roof of the third ventricle (3 Vent.)
exposes the internal cerebral veins (Int. Сет. V.) above the massa intermedia (Massa
Inter.). The choroid plexus on the right side has been removed along its attachment to the
tenia choroidea (Tenia Chor.). The anterior caudate, anterior septal, anterior superficial
thalamic, and superior choroidal veins converge on the left thalamostriate vein at the
foramen of Monro. The medial atrial veins unite to form a common trunk. The posterior
longitudinal hippocampal veins (Post. Long. Hippo. V.) course on the dentate gyri
(Dentate Gur.) and join the internal cerebral veins. The right posterior longitudinal
hippocampal vein unites with the thalamocaudate vein before entering the internal
cerebral vein. E. Another specimen. The fornix has been removed. The anterior caudate
veins pass along the lateral wall of the frontal horn and join the thalamostriate vein on the
left side and a thalamocaudate vein on the right side. The superior choroidal, superior
superficial thalamic (Sup. Superf. Thal. V.), and anterior septal veins join the internal
cerebral veins near the foramen of Monro. On the right side, the lateral wall of the body
is drained by a large thalamocaudate vein. A large anterior caudate vein passes along the
superolateral angle of the right lateral ventricle to join the thalamocaudate vein. F.
Enlarged view. The tributaries converging on the anterior end of the internal cerebral
vein at the foramen of Monro include the anterior septal, anterior caudate, thalamostriate,
superior choroidal, anterior thalamic (Ant Thal. V.), and anterior superficial thalamic
veins.
Figure 3.28. A and B. Cisternal veins. A. Anterolateral view. The insert shows the
direction of view. The frontal (Front, Lobe) and temporal (Temp. Lobe) lobes have been
retracted away from the floor of the anterior (Ant. Fossa) and middle cranial (Mid. Fossa)
fossae. The veins converging on the anterior end of the basal vein (Basal V.) below the
anterior perforated substance (Ant. Perf. Subst.) are the deep middle cerebral veins (Deep
Mid. Cer. V.) from the sylvian fissure (Sylvian Fiss.); the olfactory vein (Olf. V.), which
drains posteriorly along the olfactory tract (Olf. Tr.) near the gyrus rectus (Gyr. Rectus);
the frontoorbital veins (Front. Orb. V.), which drain the orbital gyri (Orb. Gyr.); the
inferior striate veins (Inf. Str. V.), which exit the anterior perforated substance; and the
anterior cerebral veins (Ant. Cer. V.), which are joined above the optic chiasm by the
anterior communicating vein (Ant. Comm. V.). The peduncular vein (Ped. V.} passes
around the cerebral peduncle (Ped.) above the oculomotor nerve (III) and joins the
median anterior pontomesencephalic vein (Med. Ant. Pon. Mes. V.) in the midline and the
basal vein laterally. The infundibulum (Infund.) passes inferiorly behind the anterior
clinoid process (Ant. Clinoid), optic nerve (Optic N.), and internal carotid artery (Int. Car.
A.). The lateral anterior pontomesencephalic vein (Lat. Ant. Pon. Mes. V.) joins the vein
of the pontomesencephalic sulcus (V. of Pon. Mes. Sulc.) below and the basal vein above.
The inferior thalamic veins (Inf. Thal. V.) arise behind and the premamillary veins
(Preman. V.) arise in front of the mamillary bodies. The inferior ventricular vein (Inf.
Vent. V.) exits the temporal horn above the parahippocampal gyrus (Parahippo. Gyr.) and
enters the basal vein. An uncal vein (Uncal V.) passes medially from the uncus. The
trochlear nerve (IV) courses near the tentorial edge (Tent. Edge). B. Lateral view, right
side. The temporal lobe has been elevated, as shown in the insert. The tentorium (Tent.)
extends along the side of the brain stem. The basal vein passes around the brain stem and
joins the vein of Galen (V. of Galen). The tributaries of the basal veins lateral to the brain
stem include the lateral mesen-cephalic vein (Lat. Mes. V.), which courses in the lateral
mesencephalic sulcus; the inferior ventricular vein, which drains the roof of the temporal
horn; the anterior hippocampal vein (Ant. Hippo. V.), which courses along the sulcus
between the uncus and the parahippocampal gyrus; the anterior longitudinal hippocampal
vein (Ant. Long. Hippo. V.), which courses along the dentate gyrus; and the medial
temporal veins (Med. Temp. V.) from the inferomedial surface of the temporal lobe. In the
pineal region, the basal vein receives the lateral atrial vein (Lat. Atr. V.) from the lateral
wall of the atrium. The internal cerebral veins (Int. Cer. V.) pass above the pineal body.
The superior vermian (Sup. Ve. V.) and superior hemispheric (Sup. He. V.) veins from the
cerebellum and the vein of the cerebellomesencephalic fissure (V. of Cer. Mes. Fiss.)
from the fissure between the midbrain and cerebellum ascend to join the vein of Galen.
Tectal veins (Tectal V.) drain the colliculi. A transverse pontine vein (Trans. Pon. V.)
crosses the pons.
Figure 3.28. С and D. Cisternal veins (continued). C. Posterior view. The insert shows the
direction of view. The occipital (Occip. Lobe) and parietal (Par. Lobe) lobes have been
retracted to expose the termination of the internal cerebral and basal veins in the vein of
Galen. The internal occipital (Int. Occip. V.) and posterior pericallosal (Post. Pericall. V.)
veins join the internal cerebral vein. The posterior longitudinal hippocampal vein (Post.
Long. Hippo. V.) passes along the dentate gyrus (Dentate Gyr.) and joins the medial atrial
vein (Med. Atr. V.). The lateral mesencephalic, posterior thalamic (Post. Thal. V.), and
inferior ventricular veins join the basal vein. Tectal veins pass from the superior (Sup/.
Coll.) and inferior colliculi (Inf. Coll.). The medial (Med. Gen. Body) and lateral (Lat.
Gen. Body) geniculate bodies are below the pulvinar. The inferior sagittal sinus (Inf. Sag.
Sinus) and the vein of Galen join the straight sinus (Str. Sinus). D. Right anterolateral
view with the anterior portion of the right cerebral hemisphere removed to expose the
upper brain stem and the third ventricle (3 Vent.) in the midline. The brain stem was
sectioned at the level of the cerebral peduncle. The anterior cerebral veins join the deep
middle cerebral vein to form the basal vein. The basal vein encircles the brain stem and
along its course receives the peduncular, inferior ventricular, anterior hippocampal,
anterior longitudinal hippocampal, posterior thalamic, lateral atrial, lateral anterior
pontomesencephalic, and lateral mesencephalic veins. The superior vermian vein receives
the superior hemispheric and tectal veins and the vein of the cerebellomesencephalic
fissure. The paraterminal (Paraterm. V.) and anterior pericallosal (Ant. Pericall. V.) veins
join the anterior cerebral vein. The internal cerebral vein courses in the velum
interpositum (Vel. Interpos.) in the roof of the third ventricle (3 Vent). The collateral
eminence (Coll. Eminence) sits above the collateral sulcus (Coll. Sulc.) in the floor of the
temporal horn. Septal veins (Sept. V.) cross the septum pellucidum (Sept. Pell.). The
choroid plexus (Chor. Plex.) passes through the foramen of Monro (For. Monro) to reach
the roof of the third ventricle. (From Ono M, Rhoton AL Jr, Peace D, Rodriguez R:
Microsurgical anatomy of the deep venous system of the brain. Neurosurgery 15:621-657,
1984.)
Figure 3.29. A-D. A. Lateral view of the left side. The temporal (Temp. Lobe) and frontal
(Front. Lobe) lobes have been elevated, as shown in the insert. The tentorium (Tent.) has
been opened above the cerebellum. The basal vein (Basal V.) arises below the anterior
perforated substance (Ant. Perf. Subst.), passes around the cerebral peduncle (Ped.), and
joins the vein of Galen (V. of Galen; dashed lines). The veins converging on the anterior
end of the basal vein are the olfactory veins (Olf. V.), which pass along the olfactory tract
(Olf. Tr.); the inferior striate veins (Inf. Str. V.), which descend through the anterior
perforated substance; the deep middle cerebral veins (Deep Mid. Cer. V.), which pass
medially from the sylvian fissure (Sylvian Fiss.); and the anterior cerebral veins (Ant.
Cer. V.), which pass across the optic chiasm. The tributaries of the basal veins lateral to
the brain stem include the peduncular vein (Ped. V.), which passes around the cerebral
peduncle; the lateral mesencephalic vein (Lat. Mes. V.), which courses in the lateral
mesencephalic sulcus; and the inferior ventricular vein (Inf. Vent. V.), which drains the
roof of the temporal horn. Tributaries of the inferior ventricular vein are the anterior
hippocampal vein (Ant. Hippo. V.), which courses along the sulcus lateral to the uncus;
the anterior longitudinal hippocampal vein (Ant. Long. Hippo. V.), which courses along
the dentate gyrus; and the medial temporal veins (Med. Temp. V.) from the inferomedial
surface of the temporal lobe. In the pineal region, the basal vein receives the lateral atrial
vein (Lat. Atr. V.) from the lateral wall of the atrium. The internal occipital vein (Int.
Occip. V.) from the medial surface of the occipital lobe joins the internal cerebral vein.
The superior vermian (Sup. Ve. V.) and superior hemispheric (Sup. He. V.) veins from the
cerebellum and the vein of the cerebellomesencephalic fissure (V. of Cer. Mes. Fiss.)
ascend to join the vein of Galen. The optic nerve (Optic N.) passes above the carotid
artery (Car. A.). The optic tract (Optic Tr.) terminates in the lateral geniculate body (Lat.
Gen. Body). The infundibulum (Infund.) passes inferiorly in front of the mamillary bodies
(Mam. Body). The uncus protrudes over the free edge (Tent. Edge) of the tentorium above
the oculomotor nerve (III). The parahip-pocampal gyrus (Parahippo. Gyr.) is medial to
the collateral (Coll. Sulc.) and rhinal (Rhinal Sulc.) sulci. The medial geniculate body
(Med. Gen. Body) is superolateral to the inferior (Inf. Coll.) and superior (Sup. Coll.)
colliculi. The pontomesencephalic sulcus (Pon. Mes. Sulc.) separates the pons and
midbrain. A transverse pontine vein (Trans. Pon. V.) crosses the pons. B. The tip of the
temporal lobe has been displaced posteriorly. Tributaries converging on the basal vein
below the anterior perforated substance include the deep middle cerebral, insular (Insular
V.), inferior striate, olfactory, and anterior cerebral veins. In its course around the
midbrain, the basal vein receives the peduncular, lateral mesencephalic, and inferior
ventricular veins. The uncal veins (Uncal. V.) drain the semilunar (Semilunar Gyr.) and
ambient (Ambient Gyr.) gyri. The premam-illary vein (Premam. V.) joins the peduncular
vein. The anterior communicating vein (Ant. Comm. V.) connects the paired anterior
cerebral veins above the optic chiasm. C. Enlarged view of the region of the inferior
ventricular vein. It exits the ventricle through the choroidal fissure, passes near the medial
and lateral geniculate bodies, and receives the uncal, anterior hippocampal, anterior
longitudinal hippocampal, and medial temporal veins. The anterior hippocapmal vein
arises in the anterior hippocampal sulcus (Ant. Hippo. Sulc.). The brachium of the
inferior colliculus (Brach. Inf. Coll.) is directed from the inferior colliculus toward the
medial geniculate body. D. Enlarged view. The veins converging on the region of the
great vein are the basal, internal cerebral (Int. Cer. V.), lateral atrial, superior vermian,
internal occipital, and tectal (Tectal V.) veins and the vein of the cerebellomesencephalic
fissure. The lemniscal trigone (Lemniscal Trig.) is posterior to the cerebral peduncle.
Figure 3.29. E-H. E. The posterior part of the basal and lateral atrial veins has been
removed (dashed lines) to expose the veins in the quadrigeminal cistern. The tectal veins
arise from the region of the quadrigeminal plate and pass posteriorly to join the basal vein
and the vein of the cerebellomesencephalic fissure. The veins on the superior surface of
the cerebellum converge above the apex of the vermis to form the superior vermian vein.
The internal occipital vein has been divided near its origin. The epithalamic veins
(Epithal. V.) arise in the region of the pineal body. The vein of Galen enters the straight
sinus at the apex of the tentorium (Apex. Tent.). F. The orientation is shown in the insert.
The temporal horn (Temp. Horn) has been opened between the superior (Sup. Temp.
Gyr.) and the middle temporal (Mid. Temp. Gyr.) gyri to expose the veins crossing the
roof and floor of the temporal horn. The inferior ventricular vein drains the anterior part
of the roof and receives the amygdalar vein (Amygd. V.) from the ventricular surface of
the amygdaloid nucleus (Amygd. Nucl.). The lateral atrial vein drains the posterior part of
the roof. The transverse hippocampal veins (Trans. Hippo. V.) pass medially across the
hippocampus in the floor of the temporal horn and through the junction of the fimbria of
the fornix and hippocampus to reach the basal vein. The inferior choroidal vein (Inf.
Chor. V.) courses on the choroid plexus. The medial atrial vein (Med. Atr. V.) drains the
medial wall of the atrium. G. Enlarged view. The tenia fimbria is a small ridge on the
edge of the fimbria along which the tela choroidea and choroid plexus are attached. The
choroid plexus has been detached and reflected upward. The inferior ventricular and
inferior choroidal veins pass through the choroidal fissure near the inferior choroid point
(Inf. Chor. Point), which is defined as the inferior end of the choroidal fissure. The
transverse hippocampal veins cross the floor of the temporal horn. Я. The neural
structures forming the roof of the temporal horn have been removed, the choroid plexus
has been reflected upward, and the choroidal fissure has been opened to expose the
surface of the subiculum and the dentate gyms (Dentate Gyr.) facing the ambient cistern.
A posterior superficial thalamic vein (Post. Superf. Thal. V.) joins the posterior
longitudinal hippocampal vein (Post. Long. Hippo. V.) on the dentate gyrus. The calcar
avis forms the lower half of the medial wall of the atrium. Both the collateral eminence
(Coll. Eminence) in the floor of the temporal horn and the collateral trigone (Coll. Trig.)
in the floor of the atrium overlie the collateral sulcus on the inferior surface of the
temporal lobe. The pes hippocampus (Pes. Hippo.) is the bulbous, digitated anterior part
of the hippocampus. (From Ono M, Rhoton AL Jr, Peace D, Rodriguez R: Microsurg-ical
anatomy of the deep venous system of the brain. Neurosurgery 15:621-657, 1984.)
Figure 3.30. A. Posterior view. Insert shows the orientation. The occipital lobe (Occip.
Lobe) has been retracted, and the tentorium (Tent.) has been opened to expose the
termination of the internal cerebral (Int. Cer. V.) and basal (Basal V.) veins in the vein of
Galen (V. of Galen.). The internal occipital (Int. Occip. V.), posterior pericallosal (Post.
Pericall. V.), and posterior longitudinal hippocampal (Post. Long. Hippo. V.) veins drain
into the internal cerebral vein. The lateral mesencephalic (Lat. Mes. V.), posterior
thalamic (Post. Thal. V.), and inferior ventricular (Inf. Vent. V.) veins join the basal vein.
The lingual gyrus (Lingual Gyr.) is below the calcarine sulcus (Calc. Sulc.). The anterior
part of the parahip-pocampal gyrus (Parahippo. Gyr.) is lateral to the uncus. The medial
geniculate body (Med. Gen. Body) is below the pulvinar. B. Another specimen. The
occiptal lobe has been removed to expose the atrium and the glomus of the choroid
plexus (Chor. Plex.). The basal vein courses below the pulvinar. A posterior septal vein
(Post. Sep. V.) crosses the roof and medial wall of the body of the lateral ventricle (Body
Lat. Vent.). A thalamocaudate vein (Thal. Caud. V.) joins the internal cerebral veins
above the pineal body. The lower layer of tela choroidea (Tela) in the roof of the third
ventricle is attached to the habenular trigones (Hab. Trig.). The superior choroidal vein
(Sup. Chor. V.) drains into the internal cerebral vein, and the inferior choroidal vein (Inf.
Chor. V.) drains into the basal vein. The oculomotor nerve (Ш) passes along the medial
margin of the cerebral peduncle (Ped.). The lateral atrial vein (Lat. Atr. V.) joins the basal
vein above the superior colliculus (Sup. Coll.). The lateral mesencephalic vein ascends
anterior to the brachium of the inferior colliculus (Brach. Inf. Coll.). The caudate nucleus
(Caudate Nucl.) is lateral to the thalamus. C. Right posterolateral view of another
specimen. The superior vermian vein (Sup. Ve. V.) receives the vein of the
cerebellomesencephalic fissure (V. of Cer. Mes. Fiss.) and the superior hemispheric veins
(Sup. H. V.). The tectal veins (Tectal V.) drain the region of the superior and inferior
colliculi (Inf. Coll.). D. Another specimen. The internal cerebral vein has been elevated to
show the tectal veins joining the superior vermian vein and the vein of the
cerebellomesencephalic fissure. The trochlear nerve (IV) arises below the inferior
colliculus. E. Midsagittal section of the pineal region. The internal cerebral vein courses
in the velum interpositum (Velum Interpos.) above the massa intermedia (Massa Inter.).
The velum interpositum is located between the layers of tela choroidea in the roof of the
third ventricle (3 Vent.). The internal cerebral vein receives the medial atrial vein (Med.
Atr. V.) from the lateral ventricle (Lat. Vent.) and the epithalamic veins (Inf. Epith. V.)
from the region of the pineal body. The tectal veins join the superior vermian vein and the
vein of the cerebellomesencephalic fissure. The vein of Galen and the inferior sagittal
sinus (Inf. Sag. Sinus) drain into the straight sinus. The fourth ventricle (4 Vent.) is
behind the pons. F. Inferior view. The cerebellum has been removed by dividing the
superior (Sup. Cer. Ped.), middle (Mid. Cer. Ped.), and inferior cerebellar peduncles just
posterior to the floor of the fourth ventricle. The colliculi are above the superior
medullary velum (Sup. Med. Vel.). The right basal vein enters a sinus in the tentorium
(Tent. Sinus), rather than joining the vein of Galen. The posterior mesencephalic (Post.
Mes. V.), internal occipital, posterior pericallosal, and posterior longitudinal hippocampal
veins drain into the internal cerebral veins. The epithalamic veins arise in the region of
the pineal gland. The vein of the cerebellomesencephalic fissure drains into the superior
vermian vein. (From Ono M, Rhoton AL Jr, Peace D, Rodriguez R: Microsurgical
anatomy of the deep venous system of the brain. Neurosurgery 15:621-657, 1984.)
Sellar Region
The purpose of this section is to review the anatomy of
the cranial base important to the various operative
approaches to the region of the sella turcica and third
ventricle. It deals with the sella turcica, sphenoid bone,
sphenoid sinus, cavernous sinus, and pituitary gland.
Sphenoid Bone
The sphenoid bone is located in the center of the cranial
base (28, 40-42). Some part of it is exposed in transcranial
operations through the anterior, middle, and posterior
cranial fossae and in subcranial approaches through the
nose and orbit (Figs. 3.31 and 3.32). The intimate contact
of the body of the sphenoid bone with the nasal cavity
below and the pituitary gland above has led to the
transsphenoidal route being the operative approach of
choice for selected tumors involving the third ventricle.
The neural relationships of the sphenoid bone
are among the most complex of any bone: the olfactory
tracts, gyrus rectus, and posterior part of the frontal lobe
rest against the smooth upper surface of the lesser wing; the
pons and mesen-cephalon lie posterior to the clival portion;
the optic chiasm lies posterior to the chiasmatic sul-cus;
and the second through sixth cranial nerves are intimately
related to the sphenoid bone. All exit the skull through the
optic canal, superior orbital fissure, foramen rotundum, or
foramen ovale, all foramina located in the sphenoid bone.
The sphenoid bone has many important arterial and venous
relationships: the carotid arteries groove each side of the
sphenoid bone and may bulge into the sphenoid sinus; the
basilar artery rests against its posterior surface; the circle of
Willis is located above its central portion; and the middle
cerebral artery courses parallel to the sphenoid ridge of the
lesser wing. The cavernous sinuses rest against the
sphenoid bone, and in-tercavernous venous connections
line the walls of the sella turcica and dorsum sellae.

Figure 3.31. Osseous relationships of the sphenoid bone. The sphenoid bone is outlined
in each view. A. Anterior view. B. Superior view. C. Lateral view. D. Inferior view.
(From Rhoton AL Jr, Hardy DG, Chambers SM: Microsurgical anatomy and dissection
of the sphenoid bone, cavernous sinus and sellar region. SurgNeurol 12:63-104, 1979.)
 Figure 3.32. A to D. Sphenoid bone. Anterior views. A. Conchal type sphenoid bone. B.
Bone with presellar type sphenoid sinus. C. Bone with sellar type sphenoid sinus and
well-defined sphenoid ostia. D. Bone with sellar type sphenoid sinus with poorly defined
sphenoid ostia and obliquely oriented sphenoidal septae.

In the anterior view of the skull the sphenoid bone
forms part of the posterior wall and roof of the orbit. In
the lateral view the greater wing of the sphenoid bone
projects above the zygoma, and the pterygoid plates
project below in the lateral view.
In the anterior view the sphenoid bone resembles a bat
with wings outstretched (Figs. 3.31 and 3.32). It has a
central portion called the body; the lesser wings, which
spread outward from the superolateral part of the body;
the two greater wings, which spread upward from the
lower part of the body; and the superior orbital fissure,
which is situated between the greater and lesser wings.
The vomer, the pterygoid processes, and the medial and
lateral pterygoid plates are directed downward from the
body. The body of the sphenoid bone is more or less
cubical and contains the sphenoid sinus. The superior
orbital fissure, through which the oculomotor, troch-lear,
and abducens nerves and the ophthalmic division of the
trigeminal nerve pass, is formed
on its inferior and lateral margins by the greater wing and
on its superior margin by the lesser wing. The inferior
surface of the lesser wing forms the posterior part of the
roof of each orbit and the exposed surface of the greater
wing forms the posterior wall of the orbit. The optic canals
are situated above the superomedial margin of the superior
orbital fissure. The sphenoid ostia open into the sinus.
In the superior view the pituitary fossa occupies the
central part of the body and is bounded anteriorly by the
tuberculum sellae and posteriorly by the dorsum sellae. The
chiasmatic groove, a shallow depression between the optic
foramina, is bounded posteriorly by the tuberculum sellae
and anteriorly by the planum sphenoidale. The frontal lobes
and the olfactory tracts rest against the smooth upper
surface of the lesser wing and the planum sphenoidale. The
posterior margin of the lesser wing forms a free edge called
the sphenoid ridge, which projects into the lateral cerebral
fissure to separate the
 Figure 3.32 E-H. Sphenoid bone (continued). E. Posterior view. F. Lateral view. G.
Superior view. H. Inferior view. (From Rhoton AL Jr, Hardy DG, Chambers SM:
Microsurgical anatomy and dissection of the sphenoid bone, cavernous sinus and sellar
region. Surg Neural 12:63-104, 1979.)

frontal and temporal lobes. The anterior clinoid processes
are located at the medial end of the lesser wings, the middle
clinoid processes are lateral to the tuberculum sellae, and
the posterior clinoid processes are situated at the
superolateral margin of the dorsum sellae. The dorsum
sellae is continuous with the clivus. The upper part of the
clivus is formed by the sphenoid bone and the lower part by
the occipital bone. The carotid sulcus is lateral to the body
of the sphenoid bone. The superior aspect of each greater
wing is concave upward and is filled by the tip of each
temporal lobe. The foramen rotundum, through which the
maxillary division of the trigeminal nerve passes, is located
at the junction of the body and greater wing. The foramen
ovale transmits the mandibular division of the trigeminal
nerve and the foramen spinosum transmits the middle
meningeal artery. When viewed from in-feriorly, the
vomer, a separate bone, frequently remains attached to the
anterior half of the body
of the sphenoid, and its most anterior portion separates the
sphenoid ostia.
The pterion and the "keyhole" are two important
anatomical landmarks in the region of the greater wing in
the lateral view (Fig. 3.31). The pterion is located over the
upper part of the greater wing. The "keyhole" is located just
behind the junction of the temporal line and the zygo-matic
process of the frontal bone several centimeters anterior to
the pterion. A burr hole placed over the pterion will be
located at the lateral end of the sphenoid ridge. Bone in the
region of the pterion is often removed to improve the
operative exposure along the sylvian fissure. A burr hole
placed at the keyhole will expose the orbit at its lower
margin and dura over the frontal lobe at its upper margin.
Sphenoid Sinus
The sphenoid sinus is subject to considerable variation
in size and shape and to variation in
the degree of pneumatization (Figs. 3.32 to 3.34) (3, 7,
12). It is present as minute cavities at birth, but its main
development takes place after puberty. In early life, it
extends backward into the presellar area and subsequently
expands into the area below and behind the sella turcica,
reaching its full size during adolescence. As the sinus
enlarges, it may partially encircle the optic canals. When
the sinus is exceptionally large, it extends into the roots of
the pterygoid processes or greater wing of the sphenoid
bone and may even extend into the basilar part of the
occipital bone. As age advances, the sinus frequently
undergoes further enlargement associated with absorption
of its bony walls. Occasionally there are gaps in its bone
with the mucous membrane lying directly against the dura
mater.
There are three types of sphenoid sinus in the adult:
conchal, presellar, and sellar types, depending on the
extent to which the sphenoid bone is pneumatized. In the
conchal type the area below the sella is a solid block of
bone without an air cavity. In the presellar type of
sphenoid sinus, the air cavity does not penetrate beyond a
vertical plane parallel to the anterior sellar wall. The sellar
type of sphenoid sinus is the most common, and here the
air cavity extends into the body of the sphenoid below the
sella and as far posteriorly as the clivus. In our previous
study in adult cadavers, this sinus was of a presellar type
in 24% and of the sellar type in 75% (36). The conchal
type is infrequent in the adult.
The septae within the sphenoid sinus vary greatly in
size, shape, thickness, location, completeness, and
relation to the sellar floor (Fig. 3.35). The cavities within
the sinus are seldom symmetrical from side to side and
are often subdivided by irregular minor septae. The septae
are often located off the midline as they cross the floor of
the sella. In our previous study a single major septum
separated the sinus into two large cavities in only 68% of
specimens, and even in these cases the septae were often
located off the midline or were deflected to one side (36).
The most common type of sphenoid sinus has multiple
small cavities in the large paired sinuses. The smaller
cavities are separated by septae oriented in all directions.
Computerized tomograms of the sella provide the
definition of the relationship of the septae to the floor of
the sella needed for transsphenoidal surgery. Major septae
may be found as far as 8 mm off the midline (36).
The carotid artery frequently produces a ser-pigenous
prominence into the sinus wall below the floor and along
the anterior margin of the sella (Figs. 3.33 and 3.34) (7,
36). Usually, the
optic canals protrude into the superolateral portion of the
sinus, and the second division of the trigeminal nerve
protrudes into the inf erolateral part. A diverticulum of the
sinus, called the op-ticocarotid recess, often projects
laterally between the optic canal and the carotid promi-
nence.
Removing the mucosa and bone from the lateral wall of
the sinus exposes the dura mater covering the medial
surface of the cavernous sinus and optic canals. Opening
this dura exposes the carotid arteries and optic and tri-
geminal nerves within the sinus. The sixth cranial nerve is
located between the lateral side of the carotid artery and the
medial side of the first trigeminal division. The second and
third trigeminal divisions are seen in the lower margin of
the opening through the lateral wall of the sphenoid sinus.
In half of the cases the optic and trigeminal nerves and the
carotid arteries have areas where bone 0.5 mm or less in
thickness separates them from the mucosa of the sphenoid
sinus, and in a few cases the bone separating these
structures from the sinus is absent (8, 36). The absence of
such bony protection within the walls of the sinus may
explain some of the cases of cranial nerve deficits and
carotid artery injury after transsphenoidal operations (18).
The bone is often thinner over the carotid arteries than over
the anterior margin of the pituitary gland.
Diaphragma Sellae
The diaphragma sellae forms the roof of the sella turcica.
It covers the pituitary gland, except for a small central
opening in its center, which transmits the pituitary stalk
(Fig. 3.36). The diaphragma is more rectangular than
circular, tends to be convex or concave rather than flat, and
is thinner around the infundibulum and somewhat thicker at
the periphery; the opening in its center is large when
compared to the size of the pituitary stalk. It frequently is a
thin, tenuous structure that would not be an adequate
barrier for protecting the suprasellar structures during trans-
sphenoidal operation. An outpouching of the arachnoid
protrudes through the central opening in the diaphragma
into the sella turcica in about half of the patients. This
outpouching represents a potential source of postoperative
cerebrospinal fluid leakage (18).
Pituitary Gland
When exposed from above by opening the diaphragma,
the superior surface of the posterior lobe of the pituitary
gland is lighter in color than the anterior lobe, and the
anterior lobe wraps
Figure 3.33. Stepwise dissection of the lateral wall of the right half of a sellar type
sphenoid sinus and adjacent structures (see text under "Incisural and Cister-nal Veins").
A. The sphenoid sinus and sellar area are divided in the midsagittal plane. The optic nerve
(Optic N.) is seen proximal to the optic canal. The optico-carotid recess separates the
carotid prominence and optic canal. The septum in the posterior part of the sinus is
incomplete. B. The sinus mucosa and thin bone of the lateral sinus wall are removed to
expose dura mater covering the carotid artery (Carotid A.), the second trigeminal division
(V2) just distal to the trigeminal ganglion, and the optic nerve. C. The dura is opened to
expose the carotid artery, the optic nerve in the optic canal, the second trigeminal division
below the carotid artery, and the abducens nerve (VI) between the first trigeminal
division (V1) and the carotid artery. D. Lateral view of the specimen showing area of the
cavernous sinus. The oculomotor (HI) and trochlear (IV) nerves are seen above. The
intra-cavernous portion of the carotid artery is seen medial to the trigeminal root (V) and
the ophthalmic, maxillary, and mandibular divisions (V3) of the trigeminal nerve. The
petrous portion of the carotid artery is seen in cross section below the trigeminal nerve.
The opening into the sphenoid sinus is located between the first and second trigeminal
divisions. E. Trigeminal nerve is reflected forward to expose the carotid artery, the
trigeminal impression, the artery of the inferior cavernous sinus (Art. Inf. Cav. Sinus),
and the abducens nerve, which splits into three bundles as it passes around the carotid
artery. (From Fujii K, Chambers SM, Rhoton AL Jr: Neurovascular relationships of the
sphenoid sinus: A microsurgical study. J Neurosurg 50:31-39, 1978.)
 Figure 3.34. A. Anterior views of a sellar type sphenoid sinus. The anterior wall of the
sella is removed to expose the pituitary gland. The specimen was split at the midline. The
air cavity is wider below than above, as is typical in a well-pneumatized specimen. The
optic canals are above. Carotid prominences are lateral to the sella. The trigeminal
prominence is below the carotid prominence. B. Anterior views of a sellar type sphenoid
sinus. The specimen is opened slightly to provide a better view of the lateral wall and the
carotid and trigeminal prominences. C. Anterior view of a sellar type sphenoid sinus.
Mucosa, dura, and bone of the lateral wall of the sinus are removed to expose
parasphenoidal segments of the carotid artery. Sympathetic nerves (Symp. N.) are anterior
to the left carotid artery. The orbital contents appear laterally. D. Anterior views of a
sellar type sphenoid sinus. Specimen is spread slightly to show the abducens nerve (VI)
and the ophthalmic (V1), maxillary (V2), and mandibular (V3) divisions of the trigeminal
nerve (V). (From Fujii K, Chambers SM, Rhoton AL Jr: Neurovascular relationships of
the sphenoid sinus: A microsurgical study. J Neurosurg 50:31-39, 1978.)
around the lower part of the pituitary stalk to form the a tendency for the pars tuberalis to be retained with the
pars tuberalis (Fig. 3.37). The posterior lobe is more posterior lobe. Intermediate lobe cysts are frequently
densely adherent to the sellar wall than the anterior lobe. encountered during separation of the anterior and posterior
The gland's width is equal to or greater than either its lobes.
depth or its length in most patients. Its inferior surface
usually conforms to the shape of the sellar floor, but its Pituitary Gland and Carotid Artery
lateral and superior margins vary in shape because these The distance separating the medial margin of the carotid
walls are composed of soft tissue rather than bone. If there artery and the lateral surface of the pituitary gland usually
is a large opening in the diaphragma, the glands tends to varies from 1 to 3 mm; however, in some cases the artery
be concave superiorly in the area around the stalk. The su- will protrude through the medial wall of the cavernous
perior surface may become triangular as a result of being sinus to indent the gland (Fig. 3.37) (3, 14, 36). Heavy
compressed laterally and posteriorly by the carotid arteries arterial bleeding during transsphenoidal hy-pophysectomy
(Fig. 3.36). As the anterior lobe is separated from the has been reported to be caused by carotid artery injury, but
posterior lobe, there is may also be caused by a tear in an arterial branch of the
carotid artery

Figure 3.35. Septa in the sphenoid sinus. The broken line
on the central diagram shows the plane of the section of
each specimen from which the drawings were taken, and
the large arrow shows the direction of view of the
specimens. The planum is above, the dorsum and clivus are
below, and the sella is in an intermediate position on each
diagram. The heavy dark lines on the drawings show the
location of the septae in the sphenoid sinus. A wide variety
of septae separate the sinus into cavities that vary in size
and shape, seldom being symmetrical from side to side.
(From Renn WH, Rhoton AL Jr: Microsurgical anatomy of
the sellar region. J Neurosurg 43:288-298, 1975.)
(e.g., the inferior hypophyseal artery) or by avulsion of a
small capsular branch from the carotid artery (18).
If the carotid arteries indent the lateral surfaces of the
gland, the gland does lose its rounded shape and conforms
to the wall of the artery, often developing protrusions above
or below the artery. Intrasellar tumors are subjected to the
same forces, which prevent them from being spherical, and
the increased pressure within the tumor increases the
degree to which the tumor insinuates into surrounding
crevices and tissue planes. Separation of these extensions
from the main mass of gland or tumor may explain cases in
which the tumor and elevated pituitary hormone levels
recur although the hormone levels fell to zero immediately
after adenoma removal.
Intercavernous Venous Connections
Venous sinuses may be found in the margins of the
diaphragma and around the gland (36). The intercavernous
connections (Fig. 3.38) within the sella are named on the
basis of their relationship to the pituitary gland; the anterior
intercavernous sinuses pass anterior to the hypophysis, and
the posterior intercavernous sinuses pass behind the gland.
Actually, these intercavernous connections can occur at any
site along the anterior, inferior, or posterior surface of the
gland. The anterior sinus is usually larger than the posterior
sinus, but either or both may be absent. If the anterior and
posterior connections coexist, the whole structure
constitutes the "circular sinus." Entering an anterior
intercavernous connection that extends downward in front
of the gland during transsphenoidal operation may produce
brisk bleeding. However, this usually stops with temporary
compression of the channel or with light monopolar
diathermy, which serves to glue the walls of the channel
together.
A large intercavernous venous connection called the
basilar sinus often passes posterior to the dorsum sellae and
upper clivus. The basilar sinus connects the posterior aspect
of both cavernous sinuses and is usually the largest and
most constant intercavernous connection across the
midline. The superior and inferior petrosal sinuses joint the
basilar sinus. The abducens nerve often enters the posterior
part of the cavernous sinus by passing through the basilar
sinus.
Cavernous Sinus
The cavernous sinus surrounds the horizontal portion of
the carotid artery and a segment of the abducens nerve
(Figs. 3.33, 3.36, and 3.39). The oculomotor, trochlear, and
ophthalamic divisions of the trigeminal nerve are found in
the roof and lateral wall of the sinus (11, 14, 29, 36). The
lateral wall of the cavernous sinus extends from the
superior orbital fissure in front to the apex of the petrous
portion of the temporal bone behind. The oculomotor nerve
enters the roof of the sinus lateral to the dorsum sellae. The
trochlear nerve enters the roof of the sinus posterolateral to
the third nerve, and both nerves enter the dura mater
immediately below and medial to the free edge of the
tentorium. The ophthalamic division of the trigeminal nerve
enters the low part of the lateral wall of the sinus and runs
obliquely upward to exit through the superior orbital fis-
sure. The abducens nerve enters the posterior wall of the
sinus by passing through the dura lining the upper clivus
and courses forward between the intracavernous carotid
artery medially and the ophthalmic division laterally. It fre-
quently splits into multiple rootlets in its course lateral to
the carotid artery.
 Figure 3.36. A. Superior view of the cavernous sinus, anterior and posterior lobe of the
pituitary, intracavernous portion of the carotid artery, and meningo-hypophyseal trunk
with its three branches: the inferior hypophyseal, tentorial, and dorsal meningeal arteries.
The ophthalmic artery arises from the anterior surface of the carotid artery above the
clinoid and enters the optic canal under the optic nerve. The dorsum was removed to
expose the posterior lobe of the pituitary. The sixth cranial nerve (CN VI) receives a
branch from the dorsal meningeal artery and courses laterally around the carotid artery.
The dural ostium of the third cranial nerve (CN III) (left) is in the roof of the cavernous
sinus, and the right third cranial nerve enters its dural ostium. The carotid artery is
exposed in the medial part of the foramen lacerum (left). B. Superior view of the sellar
region showing optic nerves, carotid arteries, and the third cranial nerve (CN Ш). Carotid
arteries bulge into the pituitary fossa. C. Superior view of the sellar region and both
cavernous sinuses. The carotid artery indents the lateral margin of the pituitary gland, and
a tongue of pituitary extends over the top of the artery. The sixth cranial nerve (CN VI)
passes through the duramater and around the lateral margin of the carotid artery. The
third cranial nerve enters the roof of the cavernous sinus lateral to the dorsum sellae. The
third through sixth cranial nerves are seen in the lateral wall of the cavernous sinus. D.
Superior view of the sellar region. The optical chiasm is reflected forward. A congenitally
absent diaphragma exposes the superior surface of the gland. The third cranial nerve is
posterior to the carotid arteries. The right ophthalmic artery arises below the optic nerve.
(A and С are from Harris FS, Rhoton AL Jr: Anatomy of the cavernous sinus: A
microsurgical study. J Neurosurg 45:169-180, 1976. В and С are from Renn WH, Rhoton
AL Jr: Microsurgical anatomy of the sellar region. J Neurosurg 43:288-298, 1975.)

The branches of the intracavernous portion of the
carotid artery are the meningohypophyseal trunk, the
artery of the inferior cavernous sinus, and McConnell's
capsular arteries (Figs. 3.32, 3.36, and 3.39). The
ophthalmic artery may also take origin from the carotid
artery within the sinus in few cases (36). The most
proximal branch of the intracavernous carotid artery, the
meningohypophyseal trunk, usually arises below the level
of the dorsum sellae near the apex of the curve between the
petrous and intracavernous segments of the artery. The
three branches of the meningohypophyseal artery are the
tentorial artery (of Bernasconi-Cassinari), which courses
toward the tentorium; the inferior hypophyseal artery,
which courses medially to sup-

Figure 3.37. A. Pituitary gland: superolateral view. The
posterior lobe is a lighter color and has a different
consistency than the anterior lobe. The pars tuberalis
partially encircles the stalk. The gland is concave around
the stalk. B. Pituitary gland: inferior view. Note the
relationship of the anterior and posterior lobes. C. Pituitary
gland: anterior and posterior lobe separated. The pars
tuberalis partially encircles the stalk. (From Rhoton AL Jr,
Hardy DG, Chambers SM: Microsurgical anatomy and
dissection of the sphenoid bone, cavernous sinus and sellar
region. Surg Neurol 12:63-104, 1979.)
ply the posterior part of the capsule of the pituitary gland;
and the dorsal meningeal artery, which perforates the dura
of the posterior wall of the sinus to supply the region of the
clivus and the sixth nerve.
Figure 3.38. Six sagittal sections of the sellar region
showing variations in the intercavernous venous con-
nections within the dura. The variations shown include
combinations of anterior, posterior, and inferior
intercavernous connections and the frequent presence of a
basilar sinus posterior to the dorsum. Either the anterior
(lower center) or posterior (lower left) intercavernous
connection or both (top center) may be absent. The anterior
intercavernous sinus may extend along the whole anterior
margin of the gland (lower left). The basilar sinus may be
absent (lower right). (From Renn WH, Rhoton AL Jr:
Microsurgical anatomy of the sellar region. J. Neurosurg
43:288-298, 1975.)
The artery of the inferior cavernous sinus originates from
the lateral side of the horizontal segment of the carotid
artery distal to the origin of the meningohypophyseal trunk
(14). It passes above the abducens nerve and downward
medially to the first trigeminal division to supply the dura
of the lateral wall of the sinus. In a few cases it arises from
the meningohypophyseal trunk.
McConnell's capsular arteries, if present, arise from the
medial side of the carotid artery and pass to the capsule of
the gland, distal to the point of origin of the artery of the
inferior cavernous sinus (14).
Parkinson's Triangle and the Intracavernous Portion of
the Carotid Artery
Parkinson described a triangle within the lateral wall of
the cavernous sinus through which the intracavernous
portion of the carotid artery and its branches might be
exposed for the surgical treatment of carotid-cavernous
fistulas
 (29). The boundaries of the triangle are the lower border of
the fourth nerve superiorly, the upper margin of the fifth
nerve inferiorly, and the slope along the dorsum sellae and
clivus posteriorly (Fig. 3.39).
Parkinson opened into the cavernous sinus by incising
the dura within Parkinson's triangle starting approximately
6 mm below the dural entrance of the third nerve and
extending anteriorly for 2 cm parallel to the slope of the
third and fourth nerves and retractng the leaves of the dura.
The intracavernous course of the extra-ocular nerves can be
located through this opening. Retracting the ophthalmic
division of the trigeminal nerve inferolaterally exposes the
ab-ducens nerve between the trigeminal nerve and the
carotid artery. We found in previous studies that it may be
difficult to expose all branches of the intracavernous
portion of the carotid artery through this opening (14).

Discussion
The surgical approaches to the third ventricle may
require transcortical or transcallosal incisions; division or
displacement of the fornix; opening of the lamina
terminalis, septum pellu-cidum, and floor of the third
ventricle; and dissection and separation of the tumor from
the quadrigeminal plate, the optic nerves, chiasm, and
tracts, the pituitary gland and its stalk, the cerebral
peduncles, and all of the walls of the third ventricle.
Injury of some structures exposed in approaching the
third ventricle, such as the olfactory and oculomotor
nerves, the optic pathways, and the quadrigeminal plate,
causes deficits that are well defined and that correspond to
the area injured. The sacrifice of other neural structures has
produced variable results: in some cases there was no
deficit, and in others the deficit was transient or permanent
or resulted in the loss of life. Struc-

The trigeminal root is reflected laterally to show a second

Figure 3.39. Superolateral view of the pituitary gland, branch of the sixth cranial nerve as it passes lateral to the
right cavernous sinus, and intracavernous structures carotid artery. C. The trigeminal root is reflected forward,
including the carotid artery and the third (CN III), fourth exposing the carotid artery in the foramen lacerum. A
(CN IV), and sixth (CN VI) cranial nerves. A. The lateral sympathetic nerve bundle is on the surface of the carotid
dural wall of the cavernous sinus is removed. The tortuous artery in the foramen lacerum. Three rootlets of the sixth
carotid artery bulges superiorly, pushing the interclinoid cranial nerve are seen passing around the carotid artery.
ligament and cavernous sinus roof upward and indenting The outline of the carotid artery is marked with a broken
the lateral margin of the pituitary gland. The inferior line in the areas where it is out of view in the petrous bone
hypophy-seal artery passes to the pituitary gland. The third and in the cavernous sinus. (From Harris FS, Rhoton AL Jr:
and fourth cranial nerves enter the roof of the cavernous Anatomy of the cavernous sinus: A microsurgical study. J
sinus by passing through the interclinoid ligament. The Neurosurg 45:169-180, 1976.)
sixth cranial nerve on the left side enters the dura posterior
to the dorsum and passes laterally around the left carotid
artery. The sixth cranial nerve is above the superior
margin of the trigeminal sensory (CN Vs) and motor (CN
VM) roots, and only the first division (CN V1) is exposed
distal to the ganglion. B. Further dural removal exposes
the trigeminal root and its second (CN V2) and third (CN
V3) divisions. The foramen lacerum is exposed lateral to
the gasserian ganglion.
tures sacrificed with variable results include the anterior
and posterior parts of the corpus cal-losum and one or both
of the fornices. Callosal incisions have resulted in disorders
of the inter-hemispheric transfer of information, visuospa-
tial transfer, the learning of bimanual motor tasks, and
memory and also in deficits including alexia, apraxia, and
astereognosis (20, 34, 46, 52, 56). Division of the fornix on
both sides may cause a memory loss (16, 19, 49). The
cerebral retraction needed for the anterior and posterior
interhemispheric approaches and the cortical incisions for
the transventricular surgical approaches have caused
convulsions, hemiplegia, mutism, impairment of
consciousness, and visual field loss (16, 23, 33).
Manipulation of the walls of the third ventricle may cause
the following disorders: hypothalamic dysfunction as man-
ifested by disturbances of temperature control, respiration,
consciousness, and hypophyseal secretion; visual loss due
to damage of the optic chiasm and tracts; and memory loss
due to injury to the columns of the fornix in the walls of the
third ventricle (23, 24). Dissection in the area of the
quadrigeminal plate may cause disorders of eye movement,
edematous closure of the aqueduct of Sylvius, blindness
from edema in the colliculi or geniculate bodies, and
extraocular palsies due to edema of the nuclei of the nerves
or the central pathways in the brain stem (6). Splitting the
superior part of the cerebellar ver-mis may cause cerebellar
edema and brain stem injury (27).
Sacrifice of branches of the superficial and deep venous
systems has produced inconstant deficits. Before sacrificing
these veins, one should try to work around them, displace
them out of the operative route, or place them under
moderate or even severe stretch (accepting the fact that
they may be torn) if it will yield some possibility of their
being saved. Another option is to divide only a few of their
small branches, which may allow the displacement of the
main trunk out of the operative field. Dandy noted that not
infrequently one internal cerebral vein had been sacrificed
without effect, and on a few occasions both small veins and
even the great vein of Galen had been ligated with recovery
without any apparent disturbance of function (4-6). On the
other hand, it seems that injury to this complicated venous
network may cause diencephalic edema, mental symptoms,
coma, hyperpyrexia, tachycardia, tachypnea, miosis,
rigidity of limbs, and exaggeration of deep tendon reflexes
(2, 17, 47, 48). Occlusion of the thalamostriate and other
veins at the foramen of Monro may cause
drowsiness, hemiplegia, mutism, and hemor-rhagic
infarction of the basal ganglia (16). Obliteration of veins
coursing between the cerebrum and the superior sagittal
sinus anterior or posterior to the rolandic vein or occlusion
of the anterior part of the sagittal sinus, although usually
not causing a deficit, may be accompanied by hemiplegia
(46). Sacrificing the internal occipital vein or the bridging
veins from the occipital pole to the superior sagittal or
transverse sinuses may cause hemianopsia (47, 54).
Cerebellar swelling after transection of the bridging vein
between the cerebellum and tentorium has been reported
(27).
Numerous arteries including the internal carotid and
basilar arteries and the circle of Willis and its branches are
frequently exposed during the removal of tumors of the
third ventricle, but only infrequently are any of these
sacrificed. Symon reported that perforating branches of the
posterior communicating artery might be sacrificed in the
subtemporal approach to cranio-pharyngioma with a
resulting infarct in the basal ganglia, but without obvious
deficit (50). Infarction in the distribution of the
thalamoperforating branches of the posterior cerebral artery
may cause coma and death after the removal of a suprasellar
tumor (55). The choroidal arteries are frequently exposed in
the approaches through the roof of the third ventricle, but at
that point they have given off most of their neural branches.
Arterial lesions at the anterior part of the circle of Willis are
more likely to result in disturbances in memory and
personality, and those at the posterior part of the circle are
more likely to result in disorders of the level of con-
sciousness and are frequently combined with disorders of
extraocular motion (32, 45, 49). Injuries to the superior
cerebellar artery in approaches to the posterior part of the
third ventricle may cause a cerebellar deficit.
Lesions in the anterior incisural space and in the anterior
part of the third ventricle may be approached by the
unilateral subfrontal, bifron-tal, frontal-interhemispheric,
frontotemporal, subtemporal, transsphenoidal, anterior
trans-ventricular, and anterior transcallosal routes. Tumors
located anterior to Liliequist's membrane between the optic
chiasm and the dia-phragma sella are commonly operated
on by the transsphenoidal or subfrontal approach. The
transsphenoidal approach is preferred if the tumor extends
upward out of an enlarged sella turcica and is located
above a pneumatized sphenoid sinus. The subfrontal
intracranial approach is reserved for those tumors in the
chias-
matic cistern that are not accessible by the trans-
sphenoidal route because they are located entirely above
the diaphragma sellae, extend upward out of a normal or
small sella, or are located above a nonpneumatized
(conchal) type of sphenoid sinus. The subfrontal approach
permits exposure of the tumor within the anterior incisural
space by four routes: (a) the subchiasmatic approach
between the optic nerves and below the optic chiasm; (b)
the opticocarotid route directed between the optic nerve
and carotid artery; (c) the lamina terminalis approach
directed above the optic chiasm through a thined lamina
terminalis; and (d) the transfrontal-transsphenoidal ap-
proach obtained by entering the sphenoid sinus and sella
through the transfrontal craniotomy (43). The
subchiasmatic approach is used if the subchiasmatic
opening is enlarged by the tumor. The opticocarotid route
is selected if parasellar extension of the tumor widens the
space between the carotid artery and the optic nerve and
the tumor cannot be reached by the subchiasmatic
approach. The lamina terminalis approach is selected if the
tumor has pushed the chiasm into a prefixed position and
extends into the third ventricle to stretch the lamina
terminalis so that the tumor is visible through it. The
transfrontal-transsphenoidal approach is selected if the tu-
mor grows upward out of the sella, the sphenoid sinus is
pneumatized and the tumor does not stretch the lamina
terminalis or widen the opticocarotid space, and a prefixed
chiasm blocks the subchiasmatic exposure. A bifrontal
craniotomy may be used if the tumor extends forward in
both anterior cranial fossae and cannot be removed by a
unilateral subfrontal exposure. The frontotemporal
(pterional) approach is used for a tumor arising from the
sphenoid ridge or anterior clinoid process, one arising
above the diaphragma and extending along the sphenoid
ridge or into the middle cranial fossa, or a lesion ac-
cessible through the spaces between the optic nerve and
carotid artery or between the carotid artery and the
oculomotor nerve. The frontotemporal approach may be
combined with a temporal lobectomy to expose lesions
extending into the middle incisural space.
The anterior transcallosal approach is suitable for
lesions located in the anterosuperior part of the third
ventricle or extending out of the superior part of the third
ventricle into one or both lateral ventricles near the
foramen of Monro. The transcallosal approach is easier to
perform than the transventricular approach if the
ventricles are of a normal size or are minimally enlarged.
The anterior transventricular approach is suita-
ble for approaching tumors in the anterosuperior part of the
third ventricle, especially if the tumor has a major extension
into the anterior part of the lateral ventricle on the side of
the approach. It is more difficult to expose the anterior part
of the lateral ventricle on the side opposite the craniotomy
through the transventricular than through the transcallosal
approach. The trans-ventricular approach enters the lateral
ventricle in a favorable location for exposure of the superior
half of the anterior part of the third ventricle by opening the
choroidal fissure or for biopsy or removal of the tumor
through an enlarged foramen of Monro, and the
transcallosal approach enters the lateral ventricle in a
satisfactory position for exposing the superior part of the
third ventricle by separating the halves of the body of the
fornix in the midline.
The ventricular veins provide valuable landmarks in
directing one to the foramen of Monro and the choroidal
fissure during operations directed through the lateral
ventricles. This is especially true if hydrocephalus, a
common result of third ventricular tumors, is present
because the borders between the neural structures in the
ventricular walls become less distinct as the ventricles
dilate. The thalamostriate vein is helpful in delimiting the
junction of the caudate nucleus and the thalamus because it
usually courses along the sulcus separating these structures.
The fact that the ventricular veins converge on the
choroidal fissure assists in identifying this fissure, which is
situated on the periphery of the thalamus. Opening through
the fissure in the body of the ventricle will expose the
velum inter-positum and the roof of the third ventricle,
opening through it in the atrium will expose the quad-
rigeminal cistern and the pineal region, and opening
through it in the temporal horn will expose the crural and
ambient cisterns.
In the transcortical operative approach through the
middle frontal gyrus or the transcallosal approach through
the anterior part of the corpus callosum, the veins in the
frontal horn are seen to drain posteriorly toward the
foramen of Monro because the choroidal fissure does not
extend into this area (26). The anterior caudate, anterior
septal, superior choroidal, and thalamostriate veins usually
join the internal cerebral veins at or near the foramen of
Monro. However, these veins may pass through the
choroidal fissure behind the foramen of Monro to enter the
velum interpositum and course adjacent to the internal
cerebral vein for a considerable distance before joining the
internal cerebral vein. The junction of the thalamostriate
vein with the in-
 ternal cerebral vein as seen on the lateral angio-gram
usually forms an acute angle at the posterior margin of the
foramen of Monro; however, the thalamostriate vein may
pass through the choroidal fissure and join the internal
cerebral vein posterior to the foramen of Monro. The in-
ternal cerebral vein is not seen upon opening into the
frontal horn because it courses in the roof of the third
ventricle below the body of the fornix. The anterior part of
the internal cerebral vein can only be exposed by opening
through or displacing the structures forming the roof of the
third ventricle.
One method of increasing the exposure of the roof of the
third ventricle is to section a column of the fornix
anterosuperior to the foramen on one side, but this will
permit the exposure of no more than a short anterior
segment of the internal cerebral vein. To prevent the
complications associated with sectioning the fornix, Hirsch
et al. sectioned the thalamostriate vein at the posterior
margin of the foramen of Monro, rather than damaging the
fornix to enlarge the opening in the roof of the third
ventricle (16). They stressed that interruption of this vein
was harmless; however, some of their patients developed
drowsiness, hemiplegia, and mutism, and occlusion of the
veins at the foramen of Monro has caused hemorrhagic
infarction of the basal ganglia. Other routes to the anterior
part of the third ventricle are by the interforniceal approach,
in which the body of the fornix is split in the midline and
the tela choroidea below the fornix is opened to expose the
internal cerebral veins, or the sub-choroidal approach, in
which the choroidal fissure is opened between the fornix
and thalamus, thus allowing the fornix to be pushed to the
opposite side to expose the structures in the roof of the third
ventricle (1, 53). The subchoroidal and interforniceal
approaches have the advantage of giving access to the
central portion of the third ventricle by displacing, rather
than dividing, the fibers in the fornix. They also provide a
more favorable angle for visualization of the third ventricle
than the transforaminal approach. These interforniceal and
subchoroidal approaches are uniquely suited to lesions in
the superior half of the third ventricle below the roof and
behind the foramen of Monro. In both approaches, the tela
choroidea below the fornix must be opened to expose the
internal cerebral vein and the third ventricle. In the
subchoroidal approach, the right half of the fornix and the
choroid plexus are displaced to the left side and the third
ventricle is entered through the resulting longitudinal
opening. A wider opening of the
third ventricle may be provided by displacing the
thalamostriate vein and extending the opening into the
foramen of Monro. However, occlusion of this vein at the
foramen of Monro has caused hemorrhagic infarction of the
basal ganglia (16). The maximal limits of the opening are
determined by the limits of displacement of these vessels
and their branches. The close relationship of the genu of the
internal capsule to the foramen of Monro should be kept in
mind when operating in this area. The genu of the internal
capsule nearly touches the lateral wall of the ventricle in
the area lateral to the foramen of Monro near the anterior
pole of the thalamus.
Approaches to the middle incisural space include the
posterior frontotemporal, subtemporal, temporal-
transventricular, and lateral suboccip-ital routes. The
subtemporal approach with elevation of the temporal lobe is
commonly used to expose lesions in the cisterns around the
inci-sura. Hemorrhage, venous infarction, and edema after
retraction of the temporal lobe during this approach are
minimized by placing the lower margin of the craniotomy
and the dural exposure at the cranial base so as to reduce
the need for retraction and by avoiding occlusion of the
bridging veins, especially the vein of Labbe. The ten-torium
is frequently divided to increase the exposure or to
decompress the brain stem when mass lesions are impacted
in the incisura. Resection of part of the parahippocampal
gyrus facilitates exposure of the upper part of the middle
incisural space. A transventricular approach using a cortical
incision in the nondominant inferior temporal gyrus may be
used if the lesion involves the temporal horn, choroidal
fissure, hippocampal formation, or upper part of the middle
incisural space (15). A cortical incision in the
occipitotemporal gyrus on the inferior surface of the
temporal lobe has been used to minimize visual and speech
deficits in exposing the temporal horn of the dominant
hemisphere (15). After entering the temporal horn, the
surgeon opens the choroidal fissure to expose the middle
incisural space. The trochlear nerve is the cranial nerve
most frequently injured in the middle incisural space. It can
be injured when the free edge is divided and is so thin and
friable that it may rupture from gentle retraction on the
leaves formed by dividing the tentorium.
Lesions in the posterior part of the third ventricle and
the posterior incisural space may be approached from
above the tentorium along the medial surface of the
occipital lobe using an occipital transtentorial approach,
through the posterior part of the lateral ventricle using a
poste-
rior transventricular approach, and through the corpus
callosum using a posterior interhemi-spheric transcallosal
approach, or from below the tentorium through the
supracerebellar space using an infratentorial
supracerebellar approach. The infratentorial
supracerebellar and occipital transtentorial approaches,
which are most commonly selected for pineal tumors, may
be combined with incision of the tentorium approximately
1 cm lateral to the straight sinus.
The infratentorial supracerebellar approach is preferred
for most lesions in the pineal region because the deep
venous system that caps the dorsal aspect of pineal tumors
does not obstruct access to the tumor. The approach is best
suited to tumors in the midline that grow into the lower
half of the posterior incisural space, displacing the
quadrigeminal plate and the anterior lobe of the
cerebellum. The occipital transtentorial approach is
preferred for lesions centered at or above the tentorial edge
if there is not a major extension to the opposite side or into
the posterior fossa, and for those lesions located above the
vein of Galen. The posterior transcallosal approach, in
which the splenium is divided, would be used only if the
lesion seems to arise in the splenium above the vein of
Galen and extends into the posterior incisural space (6).
The posterior transventricular approach provides adequate
exposure of the atrium and posterior portion of the body of
the lateral ventricle and would be the preferred approach
to a tumor involving the posterior incisural space if the
tumor extends into the pulvinar or involves the atrium or
the glomus of the choroid plexus. The preferable approach
to the ventricle is through the superior parietal lobule,
although Van Wagenen (51) approached the pineal region
through the atrium of the lateral ventricle using a cortical
incision in the superior temporal gyrus.
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4
Surgery of the Third Ventricle: Regional Embryology

IvanS.Ciric,M.D.

The success of a neurosurgical procedure depends
among other factors on the operative approach chosen and
the surgical technique used. The development of modern
neurosurgical techniques (including microsurgery, laser
vaporization techniques, and more recently, stereotactic-
endoscopic procedures) has made easier and safer the
complete removal of tumors in sites previously deemed
inaccessible or associated with a high incidence of
morbidity and mortality. As for the surgical approaches
chosen, they have been modified over the years in
accordance with the neurosurgeon's ever increasing
knowledge of anatomy and physiology of the area under
consideration. Understanding of the embryological planes
of development should also enter into consideration in
choosing the surgical approach to an intracranial tumor,
especially in the region of the third ventricle.
cerebral vesicle (32). Posterior to Rathke's pouch and sac,
the cerebral vesicle evaginates to form the pituitary stalk
and posterior lobe. Rathke's sac eventually gives rise to the
anterior pituitary, which remains separated from the
surrounding cerebral vesicle, the stalk, and the posterior
lobe by a layer of mesoderm that eventually differentiates
into the structures of the diaphragma sellae and the pituitary
gland capsule (9). It is not surprising, therefore, that a
variety of lesions of different embryological layers can
occur in and around the third ventricle. The peculiarities of
the embryological development of various lesions will
reflect in how they relate not only to the

Third Ventricle and the Pituitary Region

The third ventricle develops from the dience-phalic
vesicle at the rostral end of the neural tube during the third
week of gestation. Soon thereafter, the third ventricle
becomes surrounded by the rapidly developing cerebral
vesicles except along its roof, which begins to invag-inate,
trapping the surrounding mesoderm (Fig. 4.1). Pia mater
that eventually invests the floor of the third ventricle
forms from the layer of mesoderm adjacent to the ventral
surface of the diencephalic vesicle (3). Rathke's pouch
and sac form from an invagination of the distal end of the
stomodeum into the overlying mesoderm and

Figure 4.1. Development of the third ventricle (see text).

third ventricle, but also to the arachnoid membrane. A text
on surgery of lesions in and around the third ventricle
should include a discussion of the regional embryology of
both, lesions abutting against the outer boundaries of the
third ventricle as well as those occupying its interior. This
chapter includes discussion of the developmental anatomy
of pituitary adenomas, craniopharyn-giomas, and
neuroepithelial cysts of the third ventricle and of pineal
region tumors. In addition, in each instance an attempt is
made to explain the neuroanatomy of the lesion with the
developmental anatomy of the area under consideration and
to correlate these with the choice of surgical approach to be
used.
Pituitary Adenomas
Pituitary adenomas develop as intraparenchy-mal lesions
of the anterior lobe (Fig. 4.2) (7). Initially, they consist of a
microscopic conglomerate of tumor cells arranged in sheets
of uniform, polygonal cells with indistinct cell boundaries.
These microscopic adenomas can be found in
approximately 20% of routine, postmortem examinations of
the pituitary (13). Immunoper-oxidase staining will show
that these microad-enomas frequently consist of a variety of
hyper-secreting cells with one cell type predominant (27).
The initial impetus for the development of a microadenoma
is not known. It is conceivable that prolonged use of
estrogen-containing contraceptives will stimulate prolactin
secretion in a previously hormonally inactive
microadenoma (37). Approximately 10% of functioning
prolac-tin-secreting microadenomas will show substantive
growth over a period of 5 years (45). As they
Figure 4.2. Intraparenchymal stage of pituitary tumor
development.
grow, microadenomas compress the surrounding normal
anterior pituitary tissue into a relatively tough
pseudocapsular layer that blends imperceptibly with the
periphery of the usually softer and, in the central part, more
necrotic, and at times hemorrhagic adenoma (7). To assure
a complete removal of a microadenoma, one should also
resect this pseudocapsule along a cleavage plane between it
and the surrounding normal, yellow-orange anterior
pituitary tissue. A surgical cure is therefore possible in this
first, intra-parenchymal stage of pituitary (micro)adenoma
development.
Depending on the direction of its growth, a pituitary
microadenoma will eventually reach the pituitary gland
capsule along its superior, lateral, or inferior surface (Fig.
4.3). The pituitary gland capsule will become distended and
fragmented. Thus, it is common to find, after opening the
dura mater, a pituitary macroadenoma still enveloped by an
attenuated and partially fragmented pituitary gland capsule.
It is only after this thin layer is incised that a spontaneous
extrusion of tumor tissue occurs. During this second or
sellar stage of their development, pituitary adenomas can
still be removed completely and selectively along the
pseudocapsule cleavage plane between the tumor and the
surrounding, normal anterior pituitary. In about 10% of
cases, the tumor will be locally invasive into the sur-
rounding dural structures (11).
As pituitary adenomas continue to grow, they do so in
the direction of least resistance, namely, toward the
diaphragma sellae, which is covered by the arachnoid
membrane. As they extend
Figure 4.3. Sellar stage of pituitary tumor development.
through the diaphragma sellae, pituitary adenomas
displace, rather than penetrate, the arachnoid membrane in
a superior direction (11). Thus, they preserve their original
extraarach-noid location in relationship to all of the impor-
tant intraarachnoid neurovascular structures. Indeed, even
pituitary adenomas that invaginate the floor of the third
ventricle and reach as high as the foramen of Monro are in
fact separated from these structures by a layer of
arachnoid membrane (Fig. 4.4). It is primarily for this rea-
son that an extraarachnoid, transsphenoidal approach to
pituitary adenomas is preferable in the majority of patients
(Fig. 4.5) (20). A transcranial approach, on the other hand,
requires transgression of the subarachnoid space with all
of its important neurovascular structures (Fig. 4.5). When
the adenoma has reached the suprasellar space it is
classified as a pituitary macroade-noma with suprasellar
extension. Utilizing the transsphenoidal approach, a gross
total removal of a macroadenoma, as evident from the
absence of any demonstrable tumor tissue on the post-
Figure 4.5. The transsphenoidal approach (large arrow) to
operative computerized tomographic (CT) scan, can be pituitary tumors is confined to the extraarach-noidal space.
achieved in about 40% of cases. On the other hand, a The transcranial approach (small arrows) requires
complete removal of a macroadenoma, as evident from the transgression of a double layer of arachnoid and of the
endocrine cures achieved, will be possible in only one- intervening subarachnoid space.
quarter of such cases (11). A gross total removal of a mac-
roadenoma will depend on a number of factors such as the roadenoma with a straight suprasellar extension of less than
direction of its growth, the height of the suprasellar 2 cm is still amenable to a gross total tumor removal. In
extension, the width of the diaphragma sellae, the contrast, an anterior, posterior, or lateral tumor growth and
adenoma consistency, and the presence or absence of any pituitary adenomas with suprasellar extension of more than
dural invasion. Utilizing the transsphenoidal approach, a 2 cm can rarely be removed in a gross total fashion. A
mac- constricted diaphragma sellae usually constitutes a
contraindication for a transsphenoidal approach. Soft,
pulpy, and especially hem-orrhagic and cystic lesions are
easier to remove in a gross total fashion as compared to
hard, septate lesions. Finally, dural invasion precludes a
gross total tumor removal.

Craniopharyngiomas
During the development of Rathke's sac and its
subsequent anterior-superior rotation, columnar epithelium
from the hypophyseal duct will be brought into contact
with the infundibular area (Fig. 4.6) (43). When this occurs
before the development of the pia mater from the
mesoderm that separates Rathke's sac from the dience-
phalic vesicle, these cell nests will be embedded into the
neuroepithelium of the diencephalic floor. As the pia mater
develops about the fifth week of gestation, these cell nests
will be incorporated into the subpial space (Fig. 4.7) (10)
where they may undergo squamous metaplasia (17).
Intraventricular Craniopharyngiomas develop from an
endophytic growth of the squamous epithelium directed
toward the third ventricular cavity (10). Proliferation of the
squamous

Figure 4.4. Suprasellar stage of pituitary tumor de-

velopment. Note displacement rather than penetration of
the arachnoid membrane by the tumor.
 tuitary, they will be excluded from the subpial space by the
formation of the pia mater (Fig. 4.9). Depending on their
initial position in relationship to the stalk, these extrapial
cell nests may give rise to either a completely
intraarachnoid (Fig. 4.10) or a partially intra- and partially
ex-traarachnoid craniopharyngioma (10). When the lesion
is completely extrapial, a gross total sur-

Figure 4.6. Anterior-superior rotation of the anterior

pituitary with implanted epithelial cell nests from the
hypophyseal duct.

Figure 4.8. Partial intraparenchymal, subpial cra-

niopharyngioma.

Figure 4.7. Epithelial cell nests from a hypophyseal duct

implanted into the neuroepithelium and covered by the
developing pia mater.

epithelium, however, usually proceeds in an ex-ophytic

fashion toward the subarachnoid space. In that case, the
lesion will be partially intrapar-enchymal, subpial, and
adherent to the neural structures of the hypothalamic floor
(Fig. 4.8) (10, 18). The partially intraparenchymal cranio-
pharyngiomas cannot be removed completely. These
patients have a normal sella turcica, con-traindicating the
transsphenoidal approach.
When the cell nests from the hypophyseal duct remain
adherent to Rathke's sac or are suspended in the Figure 4.9. Epithelial cell nests from the hypophyseal duct
mesenchyma of the infundibular area, separated from the suspended in the mesenchyma surrounding the
developing anterior pi- neuroepithelium.
Figure 4.10. Extrapial, subarachnoid craniopharyn-
gioma.
gical removal should be possible utilizing micro-surgical
and laser vaporization techniques. In patients with
extrapial intraarachnoid cranio-pharyngiomas, the sella
turcica is also normal, precluding the transsphenoidal
approach. A partially intraarachnoid and partially
extraarachnoid craniopharyngioma, a rather frequent oc-
currence, is usually associated with a large sella, making a
transsphenoidal approach possible. Because of their
partial intraarachnoid location, a removal of these lesions
will inevitably result in a breach of the arachnoid
membrane and a per-ioperative cerebrospinal fluid fistula
requiring repair.
When the hypophyseal duct cell nests remain attached
to the upper surface of the developing anterior pituitary or
are brought into contact with the lowermost part of the
stalk, a craniopharyngioma arising in this location will
grow within the sella and thus behave as a pituitary
adenoma in that it will continue to grow outside the
arachnoid membrane (Fig. 4.11) (10). These tumors are
eminently resectable utilizing the transsphenoidal
approach (21). Because of their high cholesterol content,
intrasellar craniophar-yngiomas are easily distinguishable
from pituitary adenomas on a magnetic resonance
imaging (MRI) study.
It is obvious, therefore, that craniopharyn-
Figure 4.11. Extraarachnoidal craniopharyngioma.
giomas have a different relationship to the arachnoid
membrane from pituitary adenomas, which remain outside
the arachnoid membrane regardless of their size.
Craniopharyngiomas can be completely within the
arachnoid membrane, partially intra- and partially
extraarachnoid, or completely extraarachnoid.
Neuroepithelial (Colloid) Cyst of the Third Ventricle
By the fourth to fifth week of gestation, the rostral end
of the neural tube has enlarged into the diencephalic and
the two hemispheric vesicles (3). The initial slitlike
communication between the diencephalic and the cerebral
vesicles is the early choroidal fissure. It enlarges anteriorly
to form the foramen of Monro. While the lateral
diencephalic wall and the opposing walls of the
hemispheric vesicles undergo rapid proliferation to form
the thalamus and hypothalamus, the basal ganglia and the
lobes of the cerebral hemispheres, the roof of the
diencephalon, and the immediately adjacent dorsal wall of
the hemispheric vesicles fail to proliferate. Instead, they
undergo a U-shaped infolding resulting in the duplication
of the overlying mesoderm, which thus gives rise to the
velum interpositum. Further infolding of the fibrovascular
stroma of the
early velum interpositum along the medial wall of the
lateral ventricles gives rise to the choroid plexus (Fig. 4.1)
(12). A similar process of invag-ination of the fibrovascular
stroma from the velum interpositum into the diencephalic
vesicle leads to the formation of the choroid plexus in the
roof of the third ventricle. The infolded fibrovascular
stroma of the choroid plexus remains covered, however, by
a thin layer of neuroepi-thelium that merges imperceptibly
with the surrounding ependyma at the base of the choroid
plexus. Thus, the mesenchymal stroma of the choroid
plexus is in a strict anatomical sense extraventricular. The
corpus callosum develops as a connection between the two
cerebral vesicles. The fornix develops as a bundle of fibers
between the temporal lobe and the hypothala-mus. The
segment of the medial wall of the cerebral vesicles between
the corpus callosum and the fornix fails to proliferate and
persists as the septum pellucidum (12).
Neuroepithelial (colloid) cysts develop when the
neuroepithelium of the diencephalic roof begins to
invaginate into the third ventricle with a subsequent partial
sequestration of a cystlike structure. In the majority of
cases, the cyst remains firmly attached to the choroid
plexus (Fig. 4.12). According to this concept of their origin,
the so-called colloid cysts of the third ventricle are best
described as neuroepithelial cysts (4, 12, 38).
The surgical approaches to lesions in the anterior and
middle sections of the third ventricle should follow the
planes of embryological development of the diencephalic
area (5, 33). This is best executed either along the midline
through
Figure 4.12. Development of neuroepithelial (colloid)
cyst.
the corpus callosum (14, 29, 39) or from a lateral direction
through the lateral ventricle (28). The third ventricle can
then be reached through a distended foramen of Monro (14,
28); through the septum pellucidum and the velum
interpositum, reaching into the third ventricle between the
two internal cerebral veins (2, 8, 31); or through the
choroid fissure itself (44). Although sectioning of the
fornix anterior to the foramen of Monro, division of the
thalamus striate vein (23), and removal of the anterior
tubercle of the thalamus have been advocated to enlarge
the foramen of Monro, these maneuvers are usually not
necessary and should probably be avoided altogether.
Pineal Region Tumors
Pineal gland contains a variety of cells of different
origin. The predominant cell type is the pineocytoma, a
modified neuroepithelial cell that relates closely to
interlobular vessels and contains melanin (22). Other
component cell types include glial cells, rarely true
ganglion cells, neu-roblast-like cells, fibroblasts,
lymphocytes, and related cells, connective tissue, and
vessels (22). The development of the pineal gland
continues through the first decade of life when connective
tissue septi containing blood vessels penetrate the
parenchyma of the pineal gland and separate it into
anastomosing cords and, indeed, into the first half of the
second decade, when laminated calcified bodies, so-called
calcospherites, develop in the pineal in their adult form.
The classification of pineal neoplasms has undergone an
evolutionary change since del Rio-Hortega described in
1932 two main cell types in the human pineal gland (16).
According to Russell and Rubinstein (35), pineal region
tumors can be classified into four main categories. The
most common type are tumors of germ cell origin. The
germ cells derive from the yolk sac endoderm and can
migrate through the embryo. Thus, they can give rise to
tumors in diverse anatomical locations, although usually in
such midline structures as the brain, mediastinum,
retroperi-toneum, and gonads. The most common germ cell
tumor is germinoma (dysgerminoma, atypical teratoma).
Less common are teratomas, embryonal carcinomas,
endodermal sinus tumors, and choriocarcinomas (listed in
order of increasing malignancy).
Tumors of the pineal parenchymal cells and
pineocytomas constitute approximately 20 to 25% (15, 30).
Pineal cells have the capability to differentiate into tumors
with divergent histolog-ical makeups. Thus, these tumors
may assume
the appearance of ganglionic tumors, astrocyto-mas, or
retinoblastomas (34). Indeed, all three components have
been found in human pineal neoplasms (40). This is in
keeping with the phy-logenetic relationship of the pineal
cell with both the neurons and the photoreceptor cells of
fish and amphibians (22). Glial tumors and tumors of other
cell types, especially meningiomas and benign cysts, are of
particular interest to neurosur-geons and should always be
included in a differential diagnosis.
From this brief embryological discussion, it is obvious
that surgical approaches to pineal tumors depend not only
on their location, but also on their histological type. A
detailed discussion of the various surgical approaches to
the pineal region is beyond the scope of this chapter. Al-
though some controversy exists as to whether "pineal
tumors" should be operated upon or only radiated (1, 25),
it seems more appropriate to consider this issue in light of
the histological nature of the lesion. Thus, a correct
pretreatment diagnosis arrived at by CT scanning (menin-
giomas), MRI (cholesterol, fat-containing lesions such as
dermoid tumors, teratomas), or stereo-tactic biopsy (2)
(germinomas, gliomas) is a prerequisite for choosing the
optimal treatment. Although hormonal markers may give a
hint as to the histological nature of the lesion, they still fall
short of providing an accurate histological diagnosis.
In conclusion, it could probably be said that treatment
of pineal region tumors should be tailored not only to the
location of the lesion and its relationship to the
surrounding neurovascular structures, but also to the
presumed histological nature of the lesion. Thus, it seems
reasonable to suggest that such benign lesions as some ter-
atomas, dermoid cysts, meningiomas, and cystic
formations can be cured with surgical excision (41). In
contrast, malignant gliomas are best treated with
stereotactic biopsy and radiation therapy. Whether tumors
of germ cell origin should be treated with radiation
therapy and shunting (19, 24, 25, 42), with adjuvant
chemotherapy (25) in some instances (germinomas,
choriocarcinomas), or with surgical excision (6, 26, 36)
followed by radiation therapy and chemotherapy has not
been settled. The trend has been toward a more aggressive
approach that favors partial resection followed by
radiation therapy (25).
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callosal, interforniceal approaches for lesions af
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ventricle. J Neurosurg 39:230-235, 1974.
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5
Physiological Consequences of Complete or Partial
Commissural Section
Joseph E. Bogen, M.D.
Complete section of the corpus callosum, which has
come to be used increasingly as a treatment for medically
intractable epilepsy (88), is regularly followed by a wide
variety of neurological and neuropsychological deficits.
The deficits that are most apparent immediately after
operation make up the acute disconnection syndrome
(110). Those deficits that persist make up the stabilized
syndrome of hemisphere disconnection (12, 14, 15, 100).
Partial section of the corpus callosum to facilitate the
operative approach to deep midline lesions may produce a
fraction of the full syndrome, depending upon the part of
the corpus callosum that has been cut as well as the
amount and nature of any associated extracallosal damage.
In general, most of the disconnection deficits, both acute
and chronic, are not present as long as the splenium is
spared (4, 52). But certain partial sections do entail a few
inevitable deficits, as well as some common
complications, whose recognition is important for the
surgeon utilizing the transcallosal approaches. In this
chapter I present first the syndromes, acute and chronic,
consequent to a complete cerebral commissurot-omy
(including the corpus callosum and the underlying dorsal
hippocampal commissure, the ventral hippocampal
commissure between the fornices, the massa intermedia,
and the anterior commissure). This is followed by
comments on those particular aspects of the full-blown
syndrome that are apt to appear with different partial
sections. One should keep in mind that cal-losal lesions,
surgical as well as naturally occur-
ring, are often accompanied by damage to or pressure upon
neighboring structures, resulting in several distinct types of
signs: (a) signs of hemisphere disconnection, (b)
neighborhood signs, and (c) nonlocalizing signs such as
men-ingismus or signs of increased intracranial pressure. In
this chapter, attention is given mainly to signs of the first
type. A recent history of studies of the corpus callosum
explains how the disconnection signs have come to be
understood and emphasized (12). Other extensive reviews
are available (8, 16, 27, 28, 37, 42, 70, 80, 81, 106).
Historically Salient Signs
Before callosal syndromes are considered in detail, it is
useful to have an overall view of those signs of hemispheric
disconnection that have been emphasized historically and
whose reality has been confirmed by more recent investiga-
tions.
After hemisphere disconnection in the human, unilateral
tactile anomia, left hemialexia, and unilateral apraxia are
typical. That is, a righthander with complete cerebral
commissurotomy cannot name aloud objects correctly
manipulated (hence, recognized) with the left hand, cannot
read aloud written material presented solely to the left half-
field of vision, and cannot execute with the left hand
actions verbally named or described by the examiner,
although these actions are readily imitated when
demonstrated. The apraxia usually recedes within a few
months, whereas the hemialexia and unilateral anomia can
persist for years.
 The relationship of apraxia to the corpus cal-losum was
pointed out by Liepmann and Mass (71). They considered
the corpus callosum instrumental in left hand responses to
verbal command: the verbal instruction was comprehended
only by the left hemisphere and the left hand followed
instructions delivered by a route involving callosal
interhemispheric transfer from left to right and then by what
we now call "contra-lateral control," that is, by right
hemisphere control of the left hand. Necessarily then,
callosal interruption would result in an inability to follow
verbal commands with the left hand although there would
be no loss of comprehension (as expected from a left
hemisphere lesion) and there would be no weakness or
incoordination of the left hand (as expected from a right
hemisphere lesion). We now recognize the notion that
spatial or pictorial instructions understood by the right
hemisphere may require callosally mediated in-
terhemispheric communication for correct right hand
execution. This right-to-left aspect of callosal function was
not part of Liepmann's original callosal concept although, in
retrospect, it seems a natural corollary. Liepmann himself
considered the left hemisphere to be the organizer of
complex (particularly learned) motor behavior. Whether
and in what way the left hemisphere is dominant for skilled
movements generally (and not just those linguistically
related) are currently matters of active controversy (56, 58,
63, 66, 115).
Acute Disconnection Syndrome (As Observed in Right-
Handers Operated from the Right Side)
During the first few days after complete cerebral
commissurotomy, the patients commonly respond
reasonably well, with their right limbs, to simple
commands. But they are easily confused by three- or even
two-part commands, each part of which is obviously
understood. The patients often lie quietly and may seem
mildly "akinetic," although cooperating when stimulated.
There is sometimes an "imperviousness" resembling that
often seen with naturally occurring genu lesions (2, 12).
The patients are often mute even when willing to write
short (usually one-word) answers. This mutism is of special
interest and is discussed in more detail under
"Postcallosotomy Mutism."
The left-sided apraxia to verbal command is usually
severe and can be mistaken for hemiple-gia. Similarly, a
disregard for the left half-field of vision can be mistaken
for a hemianopsia. Left side weakness in the first week or
so due to
retraction edema in the right hemisphere sometimes
confounds the picture. The neurological status is difficult to
evaluate not only because the seemingly flaccid and
unresponsive left extremities may exhibit coordinated
movements, but also because, as the patient improves, there
may be competitive movements between the left and right
hands. Moreover, some patients have focal motor seizures,
manifested by clonic contractions on alternating sides of the
body and without loss of consciousness, occasionally fol-
lowed by transient unresponsiveness of whichever limbs
were involved. The patients commonly have bilateral
Babinski signs as well as bilaterally absent superficial
abdominal reflexes.
Well-coordinated but repetitive reaching, groping, and
grasping with the left hand sometimes resembles a grasp
reflex; grasp reflexes may actually be present bilaterally for
a day or two. When forced grasping cannot be elicited (by
inserting two fingers into the patient's palm from the ulnar
side, with some distal stroking), it is nevertheless possible
in most cases to demonstrate a proximal traction response
(PTR) (i.e. the patient is unable to relax the hand grip when
the examiner pulls so as to exert traction on the elbow and
shoulder flexors). The left arm hypo-tonia, the left arm
PTR, the responses bilaterally to plantar stimulation, and
the mutism were regularly observed in our cases; two
representative graphic summaries are shown in Figures 5.1
and 5.2.
Figure 5.1 indicates the intensity and duration of mutism
and other features of the acute disconnection syndrome in
our first patient, W.J. (21-23). His commissural section was
done without entering the third ventricle; two exposures,
before and behind the rolandic veins, made it possible to
confirm under direct vision that his callosal section was
complete. The patient's condition worsened at the end of
the first week, associated with an alkalotic hyponatremia
present on Days 5 to 7 (the patient had had diabetes insipi-
dus ever since his previous head injury, and vas-opressin
was used throughout his hospital stay). When the
hyponatremia was corrected, the patient rapidly improved
with respect to alertness and left side coordination, with
subsidence of the hypotonia and PTR. But some degree of
mutism persisted for another month. This patient's mutism
as well as that of several others has been described in detail
elsewhere (11). As discussed below, the duration of mutism
seems to be related to the extent of extracallosal damage; in
this case there was distinct atrophy of the right frontal lobe
quite evident at the time of operation, as
 Figure 5.1. Features of the acute disconnection syndrome as observed postop-eratively in
Patient W.J., a man aged 48 at the time of operation on Feb. 2, 1962. The capital letter N
means "none" (i.e., normal). A solid block in black indicates a marked deficit, whereas
interrupted black bars mean that the deficit was present but mild, the observations having
been made by the author (J.E.B.). Where the solid block or interrupted bars are gray, the
observation was made by someone else, usually a resident.

Figure 5.2. Features of the acute disconnection syndrome as observed postop-eratively in

Patient N.G., a woman aged 30 at the time of operation on Sept. 5, 1963. The symbols
are the same as for Figure 5.1.

well as a left parietotemporal electroencephalogram
(EEG) focus and bitemporal EEG foci on sphenoid
recordings (92).
Figure 5.2 shows the daily postoperative observations
of key features of the acute disconnection syndrome in
Patient N.G. (13, 18, 23). Her anterior commissure and
massa intermedia were sectioned under direct vision after
opening into the third ventricle between the fornices.
Recent magnetic resonance imaging studies have con-
firmed that her callosotomy was complete and that there
was a paucity of extracommissural damage. That her
extracommissural damage was slight is probably important
with respect to the relatively brief duration of her mutism.
Her postoperative course was overall quite smooth (small
amounts of vasopressin were used on Days 3 to 6). Even
so, there was a marked left apraxia to verbal command for
many weeks. There was also, as in every one of our 12
right-handers
tested after complete commissurotomy, a persistent anomia
in the left hand.
The left hand anomia has been such a regularly
appearing, easily tested, and persistently present
phenomenon that a separate section, "Unilateral (Left)
Tactile Anomia," is devoted to its further description.
N.G.'s postoperative course was summarized at the end
of a month by the author:
Two hours after operation the patient did not react to
pain and an hour later there was bilateral flexion to
sternal rub. An hour later there was a good grip on the
right to request, the right toe sign was positive and the
entire left side was flaccid. In succeeding hours the left
side remained flaccid to passive motion and to verbal
request but the patient used both hands together to pull
the covers over her chest. Hyperreflexia and positive toe
sign on the right side subsided after several days; a tonic
grasp and proximal traction response on the right rapidly
decreased but could be intermittently elicited as late as a
week postoperatively. On the first postoperative day
there was occasional mumbling including "yes"and "no,"
on the second day there was intelligible speech and on
the third day the patient was well oriented for place and
person although not for time and did not recognize her
husband. Disorientation for time and date and
intermittent inability to recognize the doctors persisted
for nearly two weeks. Complete apraxia, tonic grasp and
PTR remained pronounced on the left side for two
weeks. By the end of the third week, the left grasping had
largely subsided; no verbal instructions were followed
with the left hand but poses and gestures were copied
excellently. The patient graduated from wheelchair to
walker after two weeks but continued to have difficulty
controlling the left leg. By the fourth week the patient
was walking very well although still apraxic with the left
hand.
A positive Babinski sign has been present not only
contralateral to the retracted hemisphere but also, for at
least a day or two, on the ipsilat-eral side. An ipsilateral (as
well as contralateral) toe sign was also seen in our one
patient operated from the left, Patient C.C. (9, 23). The best
explanation for this ipsilateral Babinski sign is probably
that the diaschistic shock effect on the unexposed
hemisphere after an extensive cal-losal section is sufficient
to depress for a few days the corticofugal inhibition of the
primitive extensor response (10, 107). In any event, the
Babinski signs rapidly subside bilaterally and are not
present over the long term (24). An ipsilateral Babinski
sign is usually not observed when the callosal section is
partial.
It is not possible to include here all of the daily progress
notes on this patient, who had a rather smooth, almost ideal
postoperative course after a complete section, but the
following provides some idea of the patient's status at the
end of 2l/2 weeks:
Progress Note of Sept. 23, 1963
The patient has progressed rapidly in the past week
and is now up walking; she eats by herself without
difficulty and discusses things at some length although
after a lengthy conversation she tends to become a little
bit confused and says, "you people must have taken out
my brains."
When the patient walks she tends to have a slight
shuffle but there is no asymmetry. However, if one asks
her to walk on her heels she does this readily with the
right foot but does not do it with the left foot. If one asks
her to walk standing up on her tiptoes she again does this
only with the right foot; she could not rise up on either
the heel or the toe of the left foot. The hand is
progressing and whereas some days ago there was a PTR
on the left the patient now has no difficulty letting go
with the left hand when asked to do so, even if
considerable stretch is applied to the flexor joints.
However, apraxia of the left hand continues in that the
patient has considerable difficulty carrying out any com-
mand with the left hand and often, while laughing,
reaches over with the right hand to make the left hand
behave in a more appropriate or precise fashion. When
the patient was asked to put her left hand on her head she
could not do this, but when she was asked to imitate the
examiner when he put his left hand on his head she did it
without any difficulty. She was then asked, "now put
your left hand on your head" and she did this right away.
She was then asked, "put your left hand on your left ear"
and the left hand went on top of the head. This could
easily be duplicated with any combination of move-
ments; that is, the patient would be shown how to do
something and do it excellently with the left hand and
then she would be asked to do something else and the
hand would do what she had previously just done. . . .
Without warning, I put my hand in front of my forehead
so that a finger was placed in each supra-orbital notch
with the palm of my hand up over my forehead and the
little finger sticking out to the side. No sooner had I done
this without saying anything, when the patient's left arm
went up in complete imitation, to the exact positioning of
the fingers. After her arm was lowered, the patient was
then asked, "just lift your arm up in the air." The left arm
went up with palm on the forehead, in an imitation of the
previous peculiar position.
Reflex testing showed no asymmetry; the knee jerks
were quite hyperactive bilaterally but the reflexes at the
ankle, biceps and triceps were normal. Plantar
stimulation produced some withdrawal on each side with
no suggestion of dorsiflexion. Testing with the pinwheel
disclosed that on the left the patient felt the pinwheel to
be somewhat less sharp than the corresponding parts of
the right side; this hypalgesia is similar to what she had
before surgery and is quite distinct from the "shock-like"
sensation which W. J. has on the left side of his body.
Vibratory sense is apparently quite normal on the right
side but the patient is not cooperative enough to give
reliable results over the left side.
As the severity of the acute disconnection syndrome
subsides in a week or so, a phenomenon variously called
"intermanual conflict" or "the alien hand" appears. Almost
all complete com-
missurotomy patients manifest some degree of
intermanual conflict during the early postoperative period.
For example, a few weeks after operation, Patient R.Y.
(23) was seen buttoning his shirt with one hand while the
other hand was following along just behind undoing the
buttons.
Intermanual conflict was observed after com-
missurotomy by Wilson et al. (110) and by Ake-laitis (1),
who called it "diagnostic dyspraxia." The phenomenon has
been described in many case reports of callosal infarcts or
tumors. Even our youngest patient (L.B.) with no
appreciable apraxia to verbal command in the long term,
manifested this "alienation" 3 weeks after operation.
While doing the block design test uniman-ually with his
right hand, his left hand came up from beneath the table
and was reaching for the blocks when he slapped it with
his right hand and said, "That will keep it quiet for a
while." Such behavior progressively subsides after cal-
losotomy, probably because of other integrative
mechanisms supplementing or replacing com-missural
function. More recently, examples of intermanual conflict
have been reported in detail by Rayport et al. (87) and
Ferguson (43).
In rare instances, the intermanual conflict may reappear
even years later. An example is the following from a
follow-up examination done on Feb. 26, 1973. (Patient
A.M. was operated on Jul. 7, 1964, at age 31).
The most interesting finding in the entire examination
is the frequent occurrence of well-coordinated
movements of the left arm which are at cross-purposes
with whatever else is going on. These sometimes seem
to occur spontaneously, but on other occasions are
clearly in conflict with the behavior of the right arm.
For example, when attempting a Jendrassic
reinforcement, the patient reached with his right hand to
hold his left, but the left hand actually pushed his right
hand away. While testing finger-to-nose test (with the
patient sitting), his left hand suddenly started slapping
his chest like Tar-zan.
The patient follows verbal instructions readily with
the right hand, but poorly if at all with the left hand,
although he can raise and lower the left arm with
considerable reliability, the defect being more obvious
the more distal the joints involved in the requested act.
After a variety of maneuvers (the left hand often
following a visual demonstration fairly well) it was
possible to test the grip of the left hand while keeping
the thumb extended—so it was apparent that there is a
negative Wartenberg thumb sign on the left as well as
on the right.
In most patients, the intermanual conflict progressively
subsides in a few months or even weeks. Patient N.G.
had only mild intermanual conflicts in the hospital and
none were noted after her return home. Her status 5
months post-operatively was as follows:
Progress Note of Feb. 2, 1964
N.G. is doing excellently. There is still some lack of
initiative and an occasional defect in memory, but
otherwise her husband and she were both delighted with
her progress when I visited them in their home today.
The surgical wound has healed well and has a good
cosmetic appearance except for a small depression in the
most anterior burr hole. She has no headaches.
The patient is eating well and has gained weight
although she has been doing calisthenics each morning to
the TV. She sleeps well except for an occasional nocturia
(she needs no help with personal care); she recently had
a urethral dilatation and she takes mandelamine 4 times a
day along with her Dilantin 100 mg and Mebaral 50 mg.
She has had no seizures (in particular no convulsive
movements) unless one wishes to suspect as seizures an
occasional inattention and some numbness of the left
side. This absence of seizures is in spite of the fact that
the patient has had two menstrual periods since surgery,
the most recent a few weeks ago. The numbness of the
left side of the body is apparently continuous at a low
level, but once or twice a day it is quite bothersome for 5
to 10 minutes at a time. It involves more the leg (thus
resembling her aura before surgery) and also the arm but
not the face.
In spite of the "numbness" the patient has no disability
with the left hand, which she uses quite naturally for
dressing, cooking, etc. Although she occasionally has
trouble fastening her bra behind her back she says that
she dresses with ease and demonstrated for me two-
handed tying of shoe laces, this being done in a manner
indistinguishable from normal. The patient also shuffled
a pack of cards and dealt them deftly. She dealt one-
handed with either hand (slightly better with the left) and
at my request she unbuttoned and rebuttoned the top of
her blouse with her right hand while simultaneously
dealing cards with the left hand.
The patient wrote well with the right hand but could
make no legible characters with the left hand on several
trials. However, copying of designs was somewhat better
with the left. Her deficit with the right hand appeared to
be a deficit of conceptualization whereas the deficit in
the left hand appeared to be one of muscular
coordination. It is of interest that neither the patient nor
her husband could recall any incident of intermanual
conflict since her arrival home.
On blindfold testing today, the patient followed my
verbal commands with the left quite well, her unilateral
apraxia seemingly overcome. However, the anomia was
still present in the left hand to full extent. I repeatedly
demonstrated this with various objects while her husband
sat watching in open mouthed silence (Fig. 5.2).
The patient's personality seems to me essentially
unchanged from before surgery; she laughs easily and
appropriately. Her husband says she talks less ("she used
to talk my ear off") but that she socializes well with her
neighbors. She is perhaps a little more interested in
sexual activity than before the operation. Her memory
occasionally fails in that she may sometimes accompany
her husband somewhere and on the next day ask him
what they did. The memory loss occasionally takes the
form of absent minded-
 ness; while helping her husband prepare lunches for the
family, "she sometimes puts 2 or 3 slices of lunch meat
in a sandwich instead of one."
During my visit the patient was quite interested and
alert and not only responded appropriately to questions,
but spoke spontaneously on a number of subjects and did
not appear to have any memory difficulties at this time.
Her husband makes each night a list of housework for
her to do the next day, and, "she does everything well;
but if I forget to make the list, she will just sit around the
next day and do nothing." He makes out a menu and she
cooks the meals. "I used to have trouble getting things to
come out at the same time," she said, "but the meals are
better now." (Her husband nodded agreement.)
N.G. remained seizure-free for 8 years and then had
status epilepticus a few months after her family physician
discontinued her anticon-vulsant medication (13). Her
seizures were readily controlled when her medication was
reinsti-tuted, and her EEG abnormalities cleared during the
next 18 months. When N.G. was examined in November
1984, she continued to be seizure-free, to maintain her
household efficiently, and to participate in laboratory
studies at Cal Tech. Her left-handed anomia was still
readily demonstrable 21 years postoperatively. This persist-
ence of unilateral tactile anomia was also true of all of our
other patients (17).
Chronic, Stabilized Syndrome of Hemisphere
Disconnection
Overall Effects
Within a few months after operation, the symptoms of
acute hemisphere disconnection become compensated to a
remarkable degree. In personality and social situations the
patient appears much as before. However, when input is
lateralized (i.e., presented to only one hemisphere) each
hemisphere can be shown to operate independently to a
large extent. Each hemisphere seems to have its own
learning processes and its own separate memories.
Split-brain patients soon accept the idea that they have
capacities of which they are not conscious, such as left-
hand retrieval of objects not nameable. They may quickly
rationalize such acts, sometimes in a transparently
erroneous way (46). But even many years after operation
the patients will occasionally be quite surprised when some
well-coordinated or obviously well-informed act has just
been carried out by the left hand. This is particularly
common under conditions of continuously lateralized input
(116, 118).
Visual Effects: Double Hemianopia
Visual material can be presented selectively to a single
hemisphere by having the patient fix his
gaze on a projection screen onto which pictures of objects
or symbols are backprojected to the right, left, or both
visual half-fields using exposure times of 0.1 second or
less. The patients can read and describe material of various
kinds in the right half-field essentially as before operation.
When stimuli are presented to the left half-field, however,
the patients usually report that they see "nothing" or at most
"a flash of light." The disconnection (if it includes the
splenium) can sometimes be demonstrated with simple con-
frontation testing. The patient is allowed to have both eyes
open but does not speak and is allowed to use only one
hand (sitting on the other hand, for example). Using the free
hand, the subject indicates the onset of a stimulus, such as
the wiggling of the examiner's fingers. With such testing
there may seem to be a homonymous hemianopia in the
half-field contralateral to the indicating hand. When the
patient is tested with the other hand, there seems to be a
homonymous hemianopia in the other half-field.
This situation must be distinguished from the much more
commonly occurring extinction or hemiinattention deficit
from a hemispheric lesion, in which the patient tends to
indicate only one stimulus when the stimuli are in fact
bilateral (109). An observable difference is that the double
hemianopia is a symmetrical phenomenon (the deficit
occurs on each side) whereas extinction or hemiinattention
is typically onesided, more commonly for the left side.
In most patients there eventually appears a condition in
which no field defect can be demonstrated by a casual
confrontation technique. This apparently depends mainly
upon the ability of each hemisphere to direct the head and
eyes. For example, if the patient is instructed to point with
the right hand and if the examiner then wiggles the fingers
in the patient's left visual half-field, the patient's head and
eyes quickly turn to the left and then the right hand points
to the correct target.
If turning of the head is prevented, a leftward glance will
suffice for the patient's need for a cue. Or the right hand
may point to the left visual half-field as soon as it is
apparent that there is no suitable stimulus in the right visual
half-field. This "cheating" by the left hemisphere can often
be detected by providing no stimulus at all. Furthermore, if
stimuli are presented simultaneously in both visual half-
fields, only the stimulus in the right half-field is described
by the patient, that is, by the left hemisphere. There is
usually no verbal response to the stimulus in the left visual
half-field until the left hemisphere realizes
that the patient's left hand is also in action, pointing to the
left half-field stimulus.
When a patient has been tested repeatedly, so that the
occurrence of bilateral stimuli can be anticipated, both
stimuli may be identified by a single hand; if using the
right hand, the patient will point first to the right and then
to the left half-field. In those patients who have been fre-
quently tested, the appearance of a stimulus in the left
visual half-field is occasionally recognized in spite of our
attempts to circumvent the various cross cueing strategies.
However, even in our patient who does the best (L.B.),
performance on confrontation testing of visual fields is still
distinguishable from normal.
Auditory Suppression
After cerebral commissurotomy, the patient readily
identifies single words (and other sounds) if they are
presented to one ear at a time. But if different words are
presented to the two ears simultaneously ("dichotic
listening") only the words presented to the right ear will be
reliably reported (40, 79, 95).
This large right ear advantage is usually considered the
result of two concurrent circumstances: (a) the ipsilateral
pathway (from the left ear to the left hemisphere) is
suppressed by the presence of the simultaneous but
differing inputs, as it is in intact individuals during
dichotic listening (65, 103). (b) The contralateral pathway
from the left ear to the right hemisphere conveys
information that ordinarily reaches the left (speaking)
hemisphere by the callosal pathway and that has now been
severed. Although left ear words are rarely reported, their
perception by the right hemisphere is occasionally
evidenced by appropriate actions of the left hand (50).
Contralateral ear suppression commonly appears after
hemispherectomy or the creation of another large
hemispheric lesion. Because there is usually suppression
of the right ear by left hemisphere lesions, suppression of
the left ear by a left hemisphere lesion has been called
"paradoxical ipsilateral extinction." Further observations
have led to the conclusion that, whether the lesion is in
the left or the right hemisphere, if it is close to the midline
the suppression of left ear stimuli is probably attributable
to interruption of interhemispheric pathways (32, 76, 96).
Unilateral Apraxia
The degree of left hand dyspraxia is subject to large
individual differences. Immediately after operation all of
our patients showed some left-sided apraxia to verbal
commands such as "Wig-
gle your left toes" or "Make a fist with your left hand." Left
limb dyspraxia can be attributed to the simultaneous
presence of two deficits: poor comprehension by the right
hemisphere (which has good control of the left hand) and
poor ipsilateral control by the left hemisphere (which un-
derstands the commands). Subsidence of the dyspraxia,
therefore, can result from two compensatory mechanisms:
increased right hemisphere comprehension of words or
increased left hemisphere control of the left hand. The
extent of ipsilateral motor control can be tested by flashing
to right or left visual half-field sketches of thumb and
fingers in different postures for the subject to mimic with
one or the other hand. Responses are poor with the hand on
the side opposite the visual input, simple postures such as a
closed fist or an open hand being attainable after further
recovery. As recovery proceeds, good ipsilateral control is
first attained for responses carried out by the more proximal
musculature. After several months, most of the patients can
form a variety of hand and finger postures with either hand
to verbal instructions, such as, "Make a circle with your
thumb and little finger" and the like. Even many years later,
however, some degree of apraxia can be demonstrated
(115).
Somesthetic Effects
The lack of interhemispheric transfer after hemisphere
disconnection can be demonstrated with respect to
somesthesis (including touch, pressure, and proprioception)
in a variety of ways.
Cross Retrieval of Small Test Objects
Unseen objects in the right hand are handled, named, and
described in normal fashion. In contrast, attempts to name
or describe the same objects held out of sight in the left
hand consistently fail. In spite of the patient's inability to
name an unseen object in his left hand, identification of the
object by the right hemisphere is evident from appropriate
manipulation of the item, showing how it is used, or by
retrieval of the same object with the left hand from among
a collection of other objects screened from sight. What
distinguishes the split-brain patient from normal is that
excellent same hand retrieval (with either hand) is not
accompanied by the ability to retrieve with one hand
objects felt with the other.
Cross Replication of Hand Postures
Specific postures impressed on one (unseen) hand by the
examiner cannot be mimicked in the
opposite hand. Also, if a hand posture in outline form is
flashed by tachistoscope to one visual half-field, it can be
copied easily by the hand on that side but usually not by the
other hand.
A convenient way to test for lack of interhem-ispheric
transfer of proprioceptive information is as follows: the
patient extends both hands beneath the opaque screen (or
vision is otherwise excluded) and the examiner impresses a
particular posture on one hand. For example, one can put
the tip of the thumb against the tip of the little finger and
have the other three fingers fully extended and separated.
The split-brain patient cannot mimic with the other hand a
posture being held by the first hand. This procedure should
be repeated with various postures and in both directions.
Cross Localization of Finger Tips
After complete cerebral commissurotomy there is a
partial loss of the ability to name exact points stimulated on
the left side of the body. This defect is least apparent, if at
all, on the face and it is most apparent on the distal parts,
especially the finger tips. This deficit is not dependent upon
language; it can be shown in a nonverbal (picture
identification) fashion, in which case the deficit is present
in both directions (right-to-left and vice versa).
An easy way to demonstrate the defect is to have the
subject's hands extended, palms up (with vision excluded).
One touches the tip of one of the four fingers with the point
of a pencil, asking the patient to then touch the same point
with the tip of the thumb of the same hand. Repeating this
maneuver many times produces a numerical score, about
100% in normals for either hand. In the absence of a
parietal lesion, identification of any of the four finger tips
by putting the thumb tip upon the particular finger can be
done at nearly 100% level by the split-brain patient. One
then changes the task so that the finger tip is to be
indicated, not by touching it with the thumb of the same
hand, but by touching the corresponding finger tip of the
other hand with the thumb of that (other) hand. Sometimes
the procedure should be demonstrated with the patient's
hand in full vision until the patient understands what is
required. This cross localization cannot be done by the
split-brain patient at much better than chance level (25%),
whereas most normal adults do better than 90%.
An incompetence to cross localize or cross match has
been found in young children (44) possibly because their
commissures are not yet fully functioning (113).
Verbal Comprehension by the Right Hemisphere
Auditory comprehension of words by the disconnected
right hemisphere is suggested by the subject's ability to
retrieve with the left hand various objects if they are named
aloud by the examiner. Visual comprehension of printed
words by the right hemisphere is often present; after a
printed word is flashed to the left visual half-field, the
subject is often able to retrieve with the left hand the
designated item from among an array of hidden objects.
Control by the left hemisphere is excluded in these tests be-
cause incorrect verbal descriptions given immediately after
a correct response by the left hand show that only the right
hemisphere knew the answer.
While the disconnected right hemisphere's receptive
vocabulary can increase considerably over the years, this
single word comprehension is rarely accompanied by
speech. The most extreme cases (to date) of right
hemisphere language ability in right-handed (and left hemi-
sphere-speaking) split-brain subjects are two with right
hemisphere speech, both with the anterior commissure
uncut (75, 93). Right hemisphere language in the split-brain
subject has other limitations, with syntactic ability being ru-
dimentary at best. After studying a few cases in great depth
for over 10 years, Zaidel concluded:
Whereas phonetic and syntactic analysis seem to
specialize heavily in the left hemisphere, there is a rich
lexical structure in the right hemisphere. The structure of
the right hemisphere lexicon appears to be unique in that
it has access to a severely limited short term verbal
memory, and it has neither phonetic encoding nor
grapheme-to-phoneme correspondence rules . . . [this]
represents the limited linguistic competence that can be
acquired by a nonlin-guistic, more general purpose (or
other purpose) cognitive apparatus (117).
Right Hemisphere Dominance
After commissurotomy, each hemisphere can be tested
separately, demonstrating in a positive way those things
that each hemisphere can do better than the other, rather
than inferring what a hemisphere does from loss of
function when it is injured. Representative reviews are
included in the References (16, 69, 83, 99, 118). The
rapidly growing literature on hemispheric specialization
was thoroughly summarized by Brad-shaw and Nettleton
(25) and by Trevarthen (105) and more recently was
discussed by Gordon (51).
Unilateral (Left) Agraphia
Right-handers can write legibly, albeit not fluently, with
the left hand. This ability is com-
monly lost with callosal lesions, especially those that cause
unilateral apraxia. An inability to write to dictation is
common with left hemisphere lesions, almost always
affecting both hands. The left hand may be dysgraphic if
affected by a right hemispheric lesion, such as a frontal
lesion causing forced grasping. That the left dysgraphia
after callosal sectioning is not simply attributable to an
incoordination or paresis can be established if one can
demonstrate some other ability in the left hand requiring as
much control as would be required for writing. The left
hand may spontaneously doodle or it may copy various
designs or diagrams. It is not so much the presence of a
deficit but rather the contrast between certain deficits and
certain retained abilities that is most informative.
Simple or even complex geometric figures can often be
copied by a left hand that cannot write or even copy
writing previously made with the patient's own right hand
(9, 19, 67, 115).
Unilateral (Left) Tactile Anomia
The most useful single sign of hemisphere disconnection
is unilateral tactile anomia: this is an inability to name or
to describe an object when it is felt by one hand whereas it
is readily named (or well described if the name is
unknown) when it is placed into the other hand or when it
is presented either to vision or to audition. This unilateral
tactile anomia was present in every one of our complete
commissurotomy patients, in the left hands of 12 right-
handers and in the right hand of our 1 left-handed patient.
Others have repeatedly confirmed this finding, and it has
also been observed when the patient has had a callosotomy
sparing the anterior commissure (46, 74).
Not only is unilateral anomia quite regular in its
appearance, but it is also quite persistent, whenever
appropriately tested, for as long as 20 years (17) (and
longer, as shown by my more recent testing). In additon to
its regularity and its persistence, the demonstration of this
sign requires a minimum of equipment and time, and the
interpretation of results is usually quite clear. Of the many
maneuvers developed in the laboratory to test split-brain
patients, this is the principal one to be adopted as part of a
routine neurological examination.
Although there are many signs of brain bisection (as
described), one of the most convincing ways to
demonstrate hemisphere disconnection is to ask the
patient to feel with one hand and then name various small,
common objects such as a button, coin, safety pin, paper
clip, pencil
stub, rubber band, or key. Vision must be excluded. A
blindfold is notoriously unreliable; it is better to hold the
patient's eyelids closed, put a pillowcase over the patient's
head, or use an opaque screen.
The patient with a hemisphere disconnection is generally
unable to name or describe an object in the left hand
although he readily names objects in the right hand.
Sometimes the patient will give a vague description of the
object although unable to name it, but there is a contrast
with the ability to name the object readily when it is placed
into the right hand.
To establish hemisphere disconnection, other causes of
unilateral anomia, particularly aster-eognosis (or a gross
sensory deficit) must be excluded. The most certain proof
that the object has been identified is for the subject to
retrieve it correctly from a collection of similar objects.
Such a collection is most conveniently placed in a paper
plate about 12 to 15 cm in diameter, around which the
subject can shuffle the objects with one hand while
exploring for the test object. Even without evidence of
correct retrieval, aster-eognosis can be reasonably excluded
by observing the rapid, facile, and appropriate manipulation
of an object despite an inability to name or verbally
describe it.
In testing for unilateral anomia, the examiner must be
aware of strategies for circumventing the defect. For
example, the patient may manipulate it to produce a
characteristic noise, or the patient may identify a pipe or
some other object by a characteristic smell and thus
circumvent the inability of the left hemisphere to identify,
by palpation alone, an object placed in the left hand.
Syndrome after Corpus Callosotomy
When the corpus callosum is sectioned in its entirety at
one sitting the acute disconnection syndrome appears in
almost all respects as it is seen after a complete cerebral
commissurotomy including the anterior commissure and
massa intermedia. This state after callosotomy includes
transient mutism; hence this symptom when it follows a
complete section is not reasonably ascribed to molestation
of third ventricular structures (Fig. 5.3). Moreover, mutism
does not necessarily follow a frontal commissurotomy that
does include molestation of the third ventricular structures
but spares the splenium. These two observations taken
together suggest that post-commissurotomy mutism
requires explanation on some other basis than in terms of
third ventricle retraction.
 Figure 5.3. Degree of mutism (marked, mild, or none) after operation on 15 patients with
medically intractable epilepsy. Thirteen patients underwent complete commissurotomy
and 2 patients (D.M. and N.F.) underwent frontal commis-surotomy (52). The symbols
are the same as for Figure 5.1.

Staying out of the third ventricle does avoid some
problems, including transient diabetes in-sipidus. And there
may be less likelihood of aseptic meningitis or other
complications leading to hydrocephalus, a point that was
often advanced by Wilson and colleagues (59, 110).
Experiments with monkeys have shown that if the
anterior commissure is left intact it can compensate for loss
of the splenium with respect to interhemispheric transfer of
certain kinds of visual information (57). But the anterior
commissure cannot compensate completely for splenial loss
in the human because hemialexia usually is present after
splenial section. Indeed, most of the stabilized syndrome
seen after a complete cerebral commissurotomy is also seen
(i.e., has not been compensated) after a callosotomy sparing
the anterior commissure (46, 74). This is perhaps not
surprising because the anterior commissure is only Vioo the
size of the corpus cal-losum. On the other hand, we can
appreciate how significant it might be when we consider
the wealth of information that is conveyed over one
optic nerve—the diameter of which is about the same as
that of the anterior commissure. This question is
complicated by the fact that the size of the anterior
commissure is quite variable; a diameter difference of 3 or
4 times has been reported (112). The discrepancy between
monkeys (transfer of learning by the anterior commissure)
and humans (inability of the anterior commissure to
compensate for callosotomy) may reflect differences
between recently acquired memories as opposed to long-
standing ones. Current evidence suggests that memory
deficits can be expected after commissurotomy that
includes the anterior commissure, even when the splenium
is spared (30, 78, 114).
Syndrome after Frontal Commissurotomy
By "frontal commissurotomy" we refer (52) to section of
the anterior two-thirds of the corpus callosum together with
anterior commissurotomy; section of the anterior
commissure was done under direct vision and the third
ventricle was entered between the two fornices so the
 Figure 5.4. Frontal commissurotomy: Sketched here are the structures sectioned during a
frontal commissurotomy. This includes most of the corpus callosum (sparing the
splenium), the ventral hippocampal commissure (between the forn-ices), and the anterior
commissure.

section also included the ventral hippocampal commissure
(Fig. 5.4). The same operation was used on a few
occasions by Wilson et al. (110).
When the splenium is spared, as it is in the case of
frontal commissurotomy, very little of either the acute or
the chronic disconnection syndrome is seen. In particular,
mutism did not occur in our four operations for intractable
seizures with bitemporal foci. Because these patients had
retraction within the third ventricle to allow section of the
anterior commissure under direct vision, the mutism in
cases with more extensive section (i.e., complete
commissurotomy) was not likely of third ventricular
origin. Moreover, all of these four had retraction of the
medial aspect of the right frontal lobe, comparable with
that in the complete cases; retraction on the supplementary
motor cortex does not therefore seem to be a sufficient
explanation for the mutism after callosotomy, an issue
discussed in more detail under "Postcallosotomy Mutism."
In the long term, Preilowski could show some deficits of
motor coordination in two of our pa-
tients with frontal commissurotomy (85). But exhaustive
testing for the usual disconnection deficits (as described
under "Chronic, Stabilized Syndrome of Hemisphere
Disconnection"), has shown that, with retention of the
splenium, such deficits should not be expected (17, 47, 52,
55). Memory deficits have been observed after complete
commissurotomy and also in lesser degree after frontal
commissurotomy sparing the splenium. This is probably in
part attributable to deficits in combining linguistic
representations with visual or spatial images. We need
further research using a wide variety of memory tests
before and after operation, particularly with prolonged
follow-up.
Syndrome after Callosotomy Sparing the Splenium
Section of the corpus callosum that spares the splenium
(as well as the anterior commissure) but is otherwise
complete can be readily accomplished via an exposure
anterior to the rolandic
 Figure 5.5. Anterior callosotomy. This sketch shows how anterior callosotomy differs
from frontal commissurotomy, which is illustrated in Figure 5.4. There are two principal
differences: the anterior commissure is spared, and third ventricle is not entered by
separating the fornices.

bridging veins (Fig. 5.5). This procedure, which avoids
entry into the third ventricle, has come to be the most
popular version of commissural section for epilepsy. After
this operation one does not observe most of the acute
disconnection syndrome. This smoother postoperative
course is not surprising because the acute disconnection
syndrome does not usually occur after frontal com-
missurotomy, which is essentially the same procedure plus
section of the anterior commissure and massa intermedia.
Absence of significant mutism with callosotomy sparing
the splenium has been reported by Rayport et al. (87) as
well as in personal communications to myself from M.
Rayport, M. Apuzzo, J. Vries, J. Wada, and G. Yasargil. On
the other hand, a recent abstract by Ross et al. (91) reported
transient (1 - to 10-day) mutism with this procedure. This
difference could depend upon the amount of retraction,
particularly if there has been retraction of the left
hemisphere below the falx as well as the usual right hemi-
sphere retraction. Or it might reflect differences in the
criteria of the observers. Perhaps most important are
differences in the patients; even a lesser callosal section
may be followed by mutism when it is associated with a
concurrent thalamic lesion.
Midcallosal Section
The most common variant of callosal section is an
incision through the trunk sparing not only the splenium
but also most of the genu as well. Such an incision affords
ready access to both foramina of Monro with practically no
obligatory physiological cost as presently assessable (3, 4,
52, 72, 84, 94, 111). With some possible exceptions
(occasional brief mutism, inconstant auditory effects, tactile
transfer deficits) any impairments after callosal trunk
section are typically of the neighborhood type; for example,
the language deficits allegedly secondary to callosal trunk
section have been reported in only one
case, one in which the callosum was approached in a
right-hander by retraction of the left hemisphere (36).
Mutism in Special Cases
Mutism can be expected, at least for a time, if partial
callosal section is done in a right-hander to remove or to
biopsy a right thalamic lesion; this conclusion is based on
three personal cases and two cases of others on which I
was consulted. Mutism for several weeks followed
callosal trunk incision for the removal of a colloid cyst in
a case in which right thalamic injury had occurred during
a previous emergency ventriculostomy (personal
communication from Dr. Paul LaPrade). But significant
mutism did not appear after callosal trunk section in five
other personal cases including a small left thalamic
arteriovenous malformation (AVM) (not resected) and
two small AVMs of the septum (with resection in both
cases). As mentioned under "Syndrome after Frontal
Commissurotomy," no mutism appeared after frontal
commissurotomy in four of our epilepsy patients and no
mutism was seen in two personal tumor patients (both still
being followed after 10 and 13 years) with quite extensive
mid-callosal section for a third ventricle craniophar-
yngioma and a third ventricle glioma (84).
Inconstant Auditory Effects
As pointed out under "Auditory Suppression," a
naturally occurring lesion near the callosal trunk can
result in suppression of one ear when tested dichotically.
Hence, one might except similar changes after section of
the callosal trunk. A few changes have sometimes been
detected (personal communications from E. Zaidel and
from E. Teng); this requires further investigation. In any
case, the auditory effects are unlikely to be of clinical
importance, although one can anticipate certain patients
(for example, a symphony conductor) in whom slight
auditory alterations might be quite important.
Effects on Tactile Interaction?
The somesthetic nontransfer described under
"Somesthetic Effects" has not been detected in most cases
of midcallosal section. But if the task is made more
difficult, so that normal individuals commonly make
mistakes, some deficits (as compared with normal
subjects) have been elicited (7, 64). Further studies along
this line will no doubt be forthcoming; they are clearly
needed and the growing popularity of this approach will
afford frequent opportunities for both pre- and
postoperative testing.
Posterior Callosal (Splenial) Section
Whereas more anterior section of the corpus callosum
entails minimal long term physiological cost, section of the
splenium (Fig. 5.6) commonly causes a left hemialexia (33,
62, 73, 104, 108). This inability to read in the left visual
half-field may be accompanied by so-called color anomia,
an inability to give the names of colors presented to the
patient's view although the colors can be matched and the
patient can give (speak or write) the color names of objects,
for example, "yellow" when asked the color of a banana
(49). When the hemialexia and associated deficits are most
severe they can be mistaken for a left homonymous
hemianopsia. Although use of a tachistoscope is more
precise, it is not necessary because the deficit has often
been demonstrated without such equipment. In a recent
review (101), hemialexia is considered of two types: an
inability to match written words with objects and an inabil-
ity to read aloud written words or letters. Both of these are
said to be mimicked by the condition of visual hemineglect.
The foregoing hemideficits may not prove totally
disabling for most persons, although they can be so in
individuals whose occupations involve seeing large groups
of symbols more or less simultaneously, such as a
symphonic score. Where the splenial disconnection can be
quite crippling for almost any literate person is when the
callosal lesion is combined with a left occipital lesion or
indeed any lesion causing a right hemianopsia. Such
individuals typically have al-exia without agraphia; that is,
they can write but are unable to read, even what they have
just written correctly to dictation. This remarkable
dissociation of reading from writing has been known for
nearly a century (6, 35). One explanation is as follows:
When the patient has a right homonymous hemianopsia
resulting from a left occipital lobe lesion, nothing can be
seen, much less read, in the right half-field. Hence, visual
information can reach the left hemisphere language zone
only from the left half-field via the right occipital cortex
and transfer via the splenium. If another (pr confluent)
splenial lesion has disconnected the right occipital cortex
from the left hemisphere, the left hemisphere retains
competence to write to dictation but no longer has access to
information arriving in the right occipital lobe from the left
visual half-field.
As its proponents have recognized, there are some
difficulties with this explanation of alexia without agraphia.
These patients can often name objects or pictures of objects
visualized in the left half-field, showing that information
can reach the language zone from the left half-field. More-
 Figure 5.6. Posterior callosotomy: In this operation, in addition to the splenium, part of
the dorsal hippocampal commissure has been divided as it is usually adherent to the
undersurface of the corpus callosum.
over, alexia without agraphia can occur without an
accompanying loss of the right visual half-field (54, 61).
And alexia without agraphia can occur in cases with the
splenium largely intact. Reading seems to be a multistage
process that can be disturbed in a variety of ways (54, 60,
68). One can readily see that if splenial section were
accompanied by left occipital damage the patient might be
unable to read altogether and not just be hemialexic. Hence,
retraction of the left occipital pole is to be avoided in
approaching the splenium, although there may be situations,
such as an AVM in the medial aspect of the left occipital
lobe, where it seems necessary. In one such personal case,
the patient was "cured" of her AVM and was still able to
read albeit with difficulty, but she lost entirely her ability,
said to have been phenomenal, to sight read music for the
piano. Approaching the splenium from the left may be
preferable in the rare case where a left-hander has been
shown to be a right hemisphere speaker, preferably by use
of the Wada carotid amobarbital technique.
Postcallosotomy Mutism
After complete section of the cerebral commissures,
there was in almost every case a postoperative period of
mutism, of varying duration, during which speech was
absent or extremely sparse, although comprehension and
writing were retained. The patient did not talk even when
quite cooperative and having some ability to write. This
emissive deficit lasted, in milder form at least, in 11 right-
handed patients for nearly 3 months, 3 days, 20 years, 4
weeks, 4 months, 2 days, 4 weeks, 2 weeks, 1 week, 4
weeks, and 4 weeks (see Fig. 5.3). In 1 left-hander (P.D.)
mutism lasted 8 months. In all cases, there was little if any
paraphasia; when ability to talk returned there was no
nominal amnesia; in some cases there was a definite lack of
bodily spontaneity and motor initiative for a time, but only
partially correlated in duration with the loss of speech. As
the mutism subsided, there was a stage of partial recovery
that usually included hoarseness or whispering, but without
para-
 phasia, anomia, or novel semantic or syntactic errors,
except for 1 righthander (C.C.) operated from the left.
After complete cerebral commissurotomy there was
almost always at least some degree of mutism. The
notable exception in our series (see Fig. 5.3) was Patient
M.K., whose convulsive disorder, beginning on the left
side, was associated with a right ventricular dilatation as
well as a left footdrop present since childhood. Compen-
sation as a result of this right cerebral atrophic change
may have contributed to the absence of postoperative
mutism. On the other hand, this was our only case in
which a very large bone plate (nearly a hemicraniotomy)
was left out and replaced later to minimize pressure
effects during postoperative swelling.
Clearing of the mutism occurred in all cases but one.
This patient (A.M.) continues, even years later, to speak
very little—and when he does speak, his speech is poorly
phonated and badly articulated. He had severe brain
damage before the operation and we believe that he was,
to an unusual degree, dependent upon a compensatory
function of his corpus callosum for artic-ulatory control.
In this case, the prolonged speechlessness was almost
certainly not attributable to callosal section alone. This
case further illustrates the previously emphasized point
that postcommissurotomy deficits depend in large part
upon the nature and amount of preexisting, extracallosal
damage (11, 52, 100).
Postcommissurotomy mutism was originally considered
a simple neighborhood sign, a partial akinetic mutism
from retraction affecting the anterior end of the third
ventricle (29, 90) during section of the anterior
commissure. However, a number of patients have now
been seen with similar retraction, but a spared splenium,
who did not become mute, including N.F. and D.M.
(shown in Fig. 5.3).
In contrast to the cases of complete commissurotomy, in
these (and two other patients, D.B. and B.K.) all of the
same structures (including the massa intermedia and the
anterior commissure) were severed except the splenium
and there was no immediate postoperative mutism (52).
Such cases afford evidence not only against a third
ventricle origin for the mutism, but also against a right
supplementary cortex origin. On the other hand, Ross et al.
(91) reported mutism after anterior callosal section but not
after posterior callosal section. How to reconcile this ap-
parent conflict is one task of this section, as well as for the
future.
After complete callosotomy in two stages, Ray-
port et al. (87) observed in three of eight cases a marked
decrease in spontaneous speech unaccompanied by
paraphasia or comprehension deficit or inability to sing.
The authors suggested that, in these most affected cases,
mixed hand dominance may have been an important
consideration. Of particular importance was the absence of
any language or speech problem after the first stage
(rostrum, genu, and most of the trunk). The mutism
appeared only after the second stage (splenium and
remainder of the trunk). This result does not totally
eliminate retraction on supplementary motor cortex as a
partial contributory cause, but edema probably did not play
a role because the second stage followed the first by 2
months, 36 months, and 19 days. Rayport and colleagues
have suggested that mutism could result from an
interhemispheric conflict (see also Ref. 11). But they
emphasize more the aspect of mixed dominance, which
might indicate a greater role than usual of the corpus
callosum in the production of speech, as was probably the
situation in Patient A.M. (Fig. 5.3) and possibly the patient
reported by Sussman et al. (102).
The role of the corpus callosum in speech may be much
greater in certain patients. We can probably be reassured
with respect to the risk of severe postoperative mutism by a
favorable response to carotid amobarbital testing. This test
can give ambiguous results, but it can, we believe, be used
to exclude a critical dependence upon the commissures.
That is, if the patient continues to speak intelligibly when
the hemisphere minor for speech is narcotized, then dis-
connection of this minor hemisphere will probably not
deprive the patient of an essential resource with respect to
speech production.
Although severe, long term mutism may occur only
when callosal section is done in certain patients who are
peculiarly dependent for speech on these pathways, there
remains to be explained the mutism lasting several weeks
in callosotomy patients without either widespread damage
or anomalous lateralization from other causes.
A diaschisis secondary to deafferentation of speech areas
accounts for the deficits in terms of left hemisphere
dysfunction even when the left hemisphere is unmolested.
This interpretation is consistent with the appearance of a
right Babinski sign (a sign of left hemisphere malfunction)
and it may help to explain why our patients (and those of
Rayport) whose spleniums were spared had no mutism.
This means that the diaschisis of the left hemisphere (from
a complete section) must affect the speech "centers" or
"circuits" more than it affects writing "centers"
 or "circuits." This implies, in turn, that the writing function
is more robust or resistant in some sense than that for
speech, in spite of having developed later in both
phylogenesis and ontogenesis.
A more speculative possibility is that speech usually
requires interhemispheric integration for control of the
larynx and other midline structures in the following sense:
One can suppose that left hemisphere speech ordinarily
includes a corollary discharge (97) to the other hemisphere.
When the commissures are completely severed a
downstream interhemispheric conflict occurs at the level of
the motor nuclei for the larynx, which results in dysphonia.
This explanation is consistent with most of the evidence. In
particular, it fits the case of one patient (M.K.) who had no
mutism at all—this was the patient with right hemisphere
atrophy from childhood. It also fits the report of Sussman et
al. (102) that their patient uttered several complex
sentences shortly after operation although he was otherwise
speechless for 16 months.
Those concerned with the normal physiology of speech
will be more interested in the temporary (several weeks to
months) mutism after splenial section (either as part of a
total calloso-tomy or as a second stage) than the long-
lasting mutism (many months to years) of those whose
anomalous laterality is associated with longstanding
cortical lesions. But for the surgeon using a transcallosal
approach to the third ventricle, neither of these is apt to be
as important as transient mutism (several days to weeks)
after section of callosal segments (such as the trunk) well
anterior to the splenium.
The mutism reported by Ross et al. (91) lasted 1 to 10
days; hence, it is more relevant to the problems of third
ventricle access than the severe, prolonged type of mutism.
We have already alluded to the notion that the lack of
speech could be considered a mutism of the type often
associated with akinesia of either cingulate or subfron-tal
origin. This suggests that we think of the
postcommissurotomy state as a sort of "forme fruste" of
akinetic mutism, in which the mutism is much more evident
than is the akinesia. The occurrence of mutism in
callosotomy cases without entry into the third ventricle
could be explained as the result of subf rontal retraction
during section of the rostrum. Arguing against this is the
paucity of postoperative mutism in four of our patients
(D.M., N.F., D.B., and B.K.) whose splenium was spared
but who underwent section of both the rostrum and the
anterior commissure under direct vision.
The cause for transient mutism may be differ-
ent from one case to the next, and in any given case there
may be more than one factor operative, (a) The
commissural fibers may have been acting in a
compensatory fashion because of previous brain injury, (b)
Speech may require some absolute number of relevant brain
connections. In a marginal case the callosotomy may be
sufficient to bring the number of connections below the
minimum required, (c) The callosotomy may produce a
diaschisis in the speaking hemisphere, from which it
recovers only slowly, (d) The cal-losum may carry a
corollary discharge for speech output whose sudden loss
results in downstream interhemispheric conflict, (e)
Temporary circul-tory alterations (particularly of the
internal cerebral veins) may transiently derange the more
sensitive functions of the basal ganglia. (f) Damage to one
or the other fornix may be contributory, (g) Trauma to the
anterior third ventricle during division of the anterior
commissure or during division of the rostrum from in front
may be relevant in some cases, (h) Supplementary motor
cortex dysfunction may be contributory in some cases, (i)
Decussating fibers (for example, from medial frontal cortex
to opposite basal ganglia) may be relevant so that their
interruption plus medial frontal cortex edema combines to
produce mutism when associated with a thala-mic or striatal
lesion.
Concluding Remarks
The multifactorial causation of postcalloso-tomy mutism
affords a measure of our ignorance, representing as it does
the difficulties in predicting the likelihood of this usually
transient but nonetheless distressing malfunction. On the
other hand, the very existence of this riddle affords an
opportunity for someone to unravel it. Likewise, the lack of
replicable signs or symptoms from section of the anterior
two-thirds of the corpus callosum represents a territory still
unknown and awaiting exploration.
That the transcallosal approach to the third ventricle is
largely without obligatory physiological cost is both a boon
to the operator and a challenge to the scientist.
Neurosurgeons have historically been both therapeutic and
investigative, and we can expect that continued exploi-
tation of the transcallosal approach will benefit our patients
both at the time of treatment and by augmenting our
understanding of what Bremer (26) once called, "the
highest and most elaborate activities of the brain."
Acknowledgment
I am grateful for library assistance from S. Zeind and
staff, including P. Logan, C. DeCicco, L. Walden,
and V. Caullay of the Huntington Memorial Hospital, and
for word processing by Sally Johnstone.
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6
Pathological Correlates of Amnesia and the Anatomical Basis
of Memory
Antonio R. Damasio, M.D., Ph.D., and Gary W. Van Hoesen, Ph.D.
The early understanding of the structural basis of human
memory derived from the anatomical study of two distinct
groups of patients. The first comprised patients with
Wernicke-Korsakoff's psychosis. The second was made up
of patients with temporal lobectomies performed to
alleviate seizures refractory to medical treatment. The
current views on the anatomy of memory draw from a
much larger base of data, including not only the study of
such classical cases, but also recently described partial and
global amnestic syndromes associated with focal lesions in
(a) the basal forebrain, (b) the lateral and polar temporal
cortices, and (c) the association cortices of separate
sensory modalities. Additionally, the study of senile
dementia of the Alzheimer type is contributing important
understanding in this area.
In this chapter we review these recent developments and
indicate why they enlarge our working concept of the
relation between brain structure and memory. We also
review the anatomy of the system most frequently involved
in memory disorders, the limbic system, and note some
fundamental aspects of the neuropsychological testing of
the amnesias.
Amnesia Associated with Medial Temporal and
Diencephalic Damage
Decades of histopathological study of alcoholic patients
with amnesia have revealed damage in diencephalic and
mesencephalic regions. The consistent lesions in the
hypothalamus, espe-
cially in mamillary bodies, and the dorsomedial nuclei of
the thalamus have been related to the memory impairment.
Considerable controversy has surrounded the issue of
whether the mamillary bodies or the thalamic lesions are
crucial in causing the amnesia (41). Our view is that, if the
damage is bilateral, both loci can be associated with
memory impairment. Quite commonly, this is not even an
issue as both loci are involved. The reasonable conclusion
is that these structures are part of a system of cortical and
sub-cortical neural units necessary for learning, recall, and
recognition (11, 86). Future and more detailed analysis of
this type of data may well result in the inclusion, as part of
this system, of additional structures in the high, para-
midline brain stem. Nonetheless, the currently available
correlations are quite unequivocal, so long as it is kept in
mind that extensive neurochemical changes accompany this
disorder and undoubtedly play a crucial role.
The work on temporal lobectomies has also led to
unequivocal correlations. Patients with extensive,
unilateral, temporal excisions develop a partial amnesia
that affects predominantly verbal or nonverbal material
depending on whether the lobectomy is placed in the
dominant or non-dominant hemisphere (45). The inclusion,
in the excision, of parahippocampal cortex, hippocampus,
and amygdala seems necessary for the appearance of
amnesia (93). On the other hand, patients with bilateral
damage of the medial temporal lobes encompassing the
hippocampal formation, the overlying parahippocampal
gyrus,
 and part of the amygdala developed a major an-terograde
learning defect (65).
The best-studied subject with such a lesion, Patient
H.M., was operated on in the 1950s and still gives no
evidence of learning, at a conscious level, any material that
he has come in contact with since then (15, 73). This
anterograde amnesia covers material learned in any sensory
modality. The exception is the learning of some visuomotor
skills, which he has clearly mastered without being aware
that learning has taken place (13). H.M. can neither recall
nor recognize anterograde material of contextual and
generic types. The terms generic or semantic used in
association with memory denotes knowledge about the
basic properties of a stimulus, such as class membership
and function. Contextual or episodic memory denotes
knowledge of a specific stimulus, its relationship to other
stimuli in a given situation, and its relationship to the per-
ceiver and may contain a temporal element. The concepts of
episodic and semantic memory were proposed by Tulving
(74). The largely equivalent terms contextual and generic
are our own. This anterograde defect covers both verbal and
nonverbal information. In contrast to this pervasive
anterograde defect, H.M. has only a small retrograde
memory impairment. The patient retains normal memory
for persons, objects, and experiences up to the age of 16
years, when he started having seizures. That means that his
contextual and generic memories are normal up to that age.
For the period beyond the age of 16 years, there is a
recently uncovered contextual memory impairment,
noticeable when the patient is compared with controls (14).
The defect is far less marked than the anterograde
impairment.
Both H.M. and the patients with alcoholic Kor-sakoff's
syndrome have normal perception, language, and motor
function and preserved intellectual skills that allow them,
both in real situations and in laboratory testing, to exhibit a
large range of intelligent behaviors (11, 15). Although
some cognitive strategies are impaired, the disorder of
recall, recognition, and learning dominates the clinical
picture. The only other impairment of significance in these
amnestic patients has to do with emotion and affect. Most
of these patients have some disturbance of affect, emotional
display, or motivation. But these disturbances are mild in
comparison to the memory disorder (11, 15).
Both H.M. and the patients with alcoholic Kor-sakoff's
syndrome preserve their knowledge of skills and are able to
acquire new visuomotor skills. Their "procedural" memory
and "proce-
dural learning" are spared, i.e., their knowledge of "how" to
act in some specific circumstances is preserved. This
contrasts with their "declarative" memory and "declarative"
learning, i.e., their knowledge of "that," which is impaired
(12). We might take this qualification a bit further by
saying that, in the retrograde compartment of their memory,
only the contextual component of declarative knowledge is
disturbed, whereas the generic component of declarative
knowledge is intact.
None of these patients has difficulty recognizing the
myriad separate items that compose their universe in their
essential, generic nature or the function of those
components, i.e., they can recognize any human face as a
face, any dog as a dog, any house or airplane as such, the
beauty of a landscape as beauty indeed. Their disturbance
pertains only to those memories in which a particular
person, animal, object, quality, or experience must be
placed in the context of the subject who was previously in
contact with them, i.e., assigned a specific relation to the
beholder and maybe even a temporal position. The
hallmark of these amnestic disorders is the contrast between
the vast store of intact generic knowledge and intellectual
skills and the gross impairment of contextual knowledge
(17).
Recent Developments
Amnesia after Medial and Lateral Temporal Lobe Damage
Recent developments in the understanding of the
anatomical basis of amnesia include the description of cases
in which the profile of amnesia and the anatomical lesions
correlated with it were considerably different. One of the
most significant is the description of a global amnestic
syndrome, similar to that seen in H.M., but with a far more
pervasive retrograde amnesia encompassing all previously
acquired contextual memory (18). In addition to the
predictable bilateral medial temporal lobe lesions, that
syndrome is associated with bilateral lesions in both lateral
aspects of the temporal lobe including its pole, bilateral
insular cortices, and bilateral lesions in the basal forebrain
region. The cause is herpes simplex encephalitis. Further
investigations are necessary to establish unequivocal
correlations between some features of the syndrome, espe-
cially the overwhelming retrograde amnesia, and the
different sets of paired lesions seen in such cases. But a
reasonable working hypothesis is that damage to the polar
and lateral temporal cortices and the insular cortex is the
best corre-
late of the retrograde amnesia. Those are the areas
conspicuously spared in amnestic patients who have a
largely preserved retrograde memory, such as H.M.
Amnesia after Basal Forebrain Damage
Another important development is the description of an
amnestic syndrome encompassing an-terograde and
retrograde memory, milder than that reported with
temporal lobe damage and related exclusively to
contextual material, caused by unilateral or bilateral
lesions of the basal forebrain area (18, 85). This is the area
that includes the substantia innominata (which contains a
large part of the nucleus basalis of Mey-nert), the diagonal
band nuclei, the nucleus ac-cumbens and septal nuclei, and
part of the for-nix. These lesions are caused by vascular
damage in the territories supplied by the anterior
communicating artery, anterior cerebral artery, and
recurrent artery of Heubner. The immediate cause is
rupture of aneurysms in one of these arteries. The exact
pathological mechanism for this damage is varied—
infarction due to ischemia in a vascular territory subject to
sudden loss of blood flow, infarction due to embolism
from the aneurysmal sac, or direct damage by hemorrhage
from ruptured aneurysm. Not uncommonly, there is
additional damage in one of the orbitofrontal regions
(especially in gyrus rec-tus) and occasionally in the medial
frontal lobe, especially in the subcallosal portion of the
cin-gulate gyrus. The amnesia is more or less pure
depending on how much additional damage of this type is
present. A component of the basal forebrain, the nucleus
basalis of Meynert, is the site of some changes in its
cholinergic neurons in Alzheimer's disease (91) and these
changes might be related, in part, to the amnesia seen in
Alzheimer's patients.
This area is of obvious special importance to
neurosurgeons engaged in the treatment of aneurysms or
in the management of third ventricle tumors. It is apparent
that damage in this region, whether or not it involves the
fornix, is likely to cause memory impairment. Because
that impairment may be only partial, the potential for
missing its presence or minimizing its importance is
considerable. Such impairments may cast a major shadow
on what might otherwise be an uneventful recovery from a
successful operation.
Amnesia in Alzheimer's Disease
No less important has been the description of specific
and preponderant pathological involvement of the
entorhinal cortex and subiculum in
Alzheimer's disease (31). The entorhinal cortex is located
along the anterior part of the parahip-pocampal gyrus. The
subiculum is a component of the hippocampal formation.
Both entorhinal and subicular cortices serve as staging
areas for input to and output from the hippocampal for-
mation. The net effect of such lesions is to disconnect the
hippocampus from the cerebral cortex and from a variety of
subcortical structures in the limbic system and
diencephalon. This isolation is incompatible with normal
function and must be no less devastating than surgical
resection or vascular or encephalitic damage. In practice,
after such lesions develop, the hippocampus will no longer
be able to operate on the basis of the multimodal cortical
inputs that normally reach it via the perforant pathway that
originates in the superficial layers of the entorhinal cortex
(32). As if that were not impairment enough, however, the
lesions of Alzheimer's disease also block the exit of outputs
at the level of the subiculum. These selective lesions are
likely to be a major cause, perhaps the principal cause, of
the contextual amnesia that hallmarks the early phase of
Alzheimer's disease.
Other Developments
Other important new findings in the field of human
amnesia include: (a) the realization that syndromes such as
that of visual agnosia can be understood as disorders of
visually triggered memory that impair the recognition,
recall, and learning of certain types of visual stimuli (16,
20, 21); (b) the description of defects in learning related to
unilateral lesions capable of compromising the processing
of information conveyed from one sector of the body alone
(i.e., a learning defect of material presented in one hand
only (61, 62)); (c) the description of cases of amnesia with
lesions of the medial thalamic nuclei caused by stroke or by
direct injury (25, 70); and (d) the clarification of a question
regarding the role of the temporal stem in the development
of amnesia caused by medial temporal lobe damage. The
hypothesis that the amnesia associated with medial
temporal lesions might be related to section of the temporal
stem rather than damage to the hippocampus proper has
been posited (30). Recent experimental work in the
monkey, specifically designed to test the temporal stem
hypothesis, failed to support the claim (94). Furthermore,
because the temporal stem carries some of the outputs from
the hippocampus, it would be only natural that its damage
might lead to amnesia. That certainly does not disqualify
the hippocampus from a role in memory.
Anatomical Underpinnings of Memory
Reflection on this vast body of classical and recent
anatomical and cognitive findings permits the elaboration
of a more comprehensive list of neural systems crucial to
memory processing. It also permits some hypotheses about
the way in which they integrate in a network. Finally, it is
possible to venture a relatively specific functional role for
some key components of the network. We start this section
by reviewing the anatomy of the limbic system.
Limbic System Anatomy
The preceding material provides abundant evidence that
many parts of the limbic system play a critical role in
normal human memory, as well as in other behaviors that
play a supportive role in this essential process. A review
and update on limbic system anatomy is thus of special
importance for neurosurgeons as they are often called to
operate in its multiple areas or in its immediate vicinity.
Cortical Structures of the Limbic System
The cortical areas that form the limbic lobe are included
in nearly all definitions of the limbic system. They include
such major cerebral entities as the cingulate gyrus dorsally
and the para-hippocampal gyrus ventrally. These are
demarcated clearly in the human brain by the cingulate and
collateral sulci, respectively. Bridging areas such as the
subcallosal gyrus and the posterior orbital, anterior insular,
temporal polar, retro-splenial, and retrocalcarine cortices
link the cingulate and parahippocampal gyri. Together,
these form a continuous ring around the corpus callosum,
thalamus, and upper brain stem. In general, they are
uninterrupted by major sulci.
The cortical areas that form the limbic lobe differ widely
in their cytoarchitecture and include Brodmann's areas 23,
24, 25, 27, 28, 29, 35, 36, and 38. These are not true
isocortical areas. Instead, they fall into the categories of
periallocortex and proisocortex (63). They are intermediate
in structural complexity (Filimonoff's mesocortex (23))
between the less elaborate allo-cortices and the more
elaborate isocortices. They are characterized by an incipient
or absent layer IV, an accentuated layer II, and heavy,
largely unsegregated, layers V and VI.
Subcortical Structures of the Limbic System
The subcortical structures of the limbic system are
numerous and vary widely among authors. For reasons that
will be discussed more fully, it
seems appropriate to include the amygdala, septum,
anterior thalamus, habenula, and interpe-duncular nucleus.
Basal forebrain areas such as the substantia innominata,
and, particularly, the nucleus basalis of Meynert are
relatively new additions to lists of subcortical limbic
system structures. The latter is a widely scattered collection
of large hyperchromatic neurons that extends from the
septum to the midbrain in a position anterior and lateral to
the hypothalamus and ventral to the basal ganglia.
Particularly large clusters of these neurons are found
beneath the anterior commissure and along its lateral
excursion into the temporal lobe. Many of them are
contained within the substantia innominata. They have
widespread projections to all of the cerebral cortex (22, 35,
37, 42) and provide the major source of acetylcholine to it
(44). Heavy input is directed toward the motor cortices.
Interconnecting Pathways of the Limbic System
The third and final constituent of the limbic system is a
number of interconnecting pathways of different structures
and magnitudes. Some of these link various parts of the
limbic lobe. Others link the limbic lobe with subcortical
limbic structures. Still others interconnect subcortical struc-
tures. A final group of pathways link the cortex of the
limbic lobe and subcortical limbic structures with the
hypothalamus and related structures such as the preoptic
area. Few of these are entirely pure pathways. Most are
dominated largely by one of these types of connections. A
list of the major pathways would include the cingulum, the
uncinate fasciculus, the fimbria-fornix, the stria medullaris,
the stria terminalis, the ventroamygdalofugal pathway, the
medial forebrain bundle, the mamillothalamic tract, the
mamillotegmental tract, and the habenulointer-peduncular
tract or fasciculus retroflexus of Meynert. Many additional
connections of limbic system structures travel in well-
known association and commissural pathways of the
cerebral hemisphere such as the internal, external, and
extreme capsules and the corpus callosum and anterior
commissure. (Fig. 6.1 provides a summary of limbic
system anatomy.)
Limbic System Efferent Projections
A full review of all limbic system connections is beyond
the scope of this chapter, so we will highlight only those
findings that in recent years have altered the classical
thinking on this topic. Historically, it has been the
convention to view limbic system anatomy in the context
of hypo-
Figure 6.1. These illustrations depict schematically some of the major neuroan-atomical
components of the limbic system on views of the medial surface of the cerebral
hemisphere. A. Limbic system landmarks and sulcal boundaries. B. The major cortical
entities of the limbic system, the so-called limbic lobe. C. The subcortical structures of
the limbic system. D. The approximate location of major limbic system pathways that
interconnect its various components with each other and with the hypothalamus.
thalamic function (40). There has been good reason for this
because major interconnecting lim-bic pathways like the
fimbria-fornix and stria terminalis terminate on the neurons
of various hypothalamic nuclei. The hypothalamus is an
important effector center for the control and regulation of
both the endocrine system and the autonomic nervous
system. Although the structural basis for
hypothalamoendocrine interactions, both humoral and
vascular, is more generally understood, it has only been in
recent years that the structural basis for hypothala-
moautonomic interactions has been elucidated. For
example, it is now clear that specific nuclei of the
hypothalamus project to sympathetic and parasympathetic
centers in both the brain stem and spinal cord (64). These
are centered largely in the paraventricular, dorsomedial, and
posterior nuclei. Moreover, there is now evidence that
certain subcortical components of the limbic system itself,
such as the central amygdaloid nucleus, project to brain
stem autonomic centers as well (28, 29, 57). Such
projections, as well as those mediated via the
hypothalamus, validate the classical emphasis on limbic-
hypothalamic interactions in the regulation of autonomic
and endocrine effectors.
There is now good evidence that subcortical limbic
system structures can affect brain areas known to regulate
somatic effectors as well. The findings entail direct
amygdaloid projections to motor-related areas of the
cerebral cortex (6, 38, 56) and to the striatum (36).
Additionally, the nucleus basalis of Meynert projects
powerfully to the motor and premotor cortices (42).
The cortical areas of the limbic system also have
extensive projections to key central components of the
motor system. For example, the anterior part of the
cingulate gyrus projects extensively to the premotor and
supplementary motor cortices, and this part of the cingulate
gyrus receives extensive input from the remainder of the
limbic lobe and several subcortical parts of the limbic
system (83). It is a focal point for limbic influence on the
motor cortices. Moreover, there is evidence demonstrating
that the cortices of the limbic lobe project also to
subcortical motor structures such as the caudate nucleus
and pu-tamen (7, 81, 88) and pons (87). In total, these
constitute a major afferent source for motor-related parts of
the cerebral hemisphere. Therefore, it now seems
appropriate to view the limbic system in the context of all
effectors, autonomic, endocrine, and somatic as well.
Limbic system structures also have extensive and
widespread projections to associative parts
of the cerebral cortex. These are mediated via limbic lobe
and amygdaloid projections to the frontal, parietal, and
temporal association cortices (5, 7, 43, 53, 56, 60, 84).
Such projections, although largely elucidated in recent
years, were a major element of Papez's deductions, when
he suggested, nearly a half century ago, that the radiations
of the cingulate gyrus project not only back into his circuit,
but to the cerebral cortex as well, where he believed the
"psychic coloring" of sensations took place (55).
Unfortunately, this important and major element of Papez's
thinking has received far less emphasis than those relating
to his so-called circuit.
Limbic System Afferent Connections
As discussed previously, it seems clear that there are
extensive limbic system efferents that affect endocrine,
autonomic, and somatic effectors as well as associative
areas of the cerebral hemisphere. The existence of such
outputs raises the question of afferent input to limbic struc-
tures and makes the understanding of this topic critically
important. New information regarding limbic system input
has been slow to accrue because progress in this area has
been linked solidly to the development of newer and more
sensitive neuroanatomical tracing methods. A renewed
interest in the organization of the connections of the
cerebral cortex in general has also been decisive (34, 52,
67, 77). In higher mammals, limbic system structures
receive a large part of their input directly from the cerebral
cortex and especially from cortical areas designated as
associative in function (76). Such connections are well
illustrated by direct cortical projections to the amygdala (1,
27, 75, 82, 92) described in nonhuman primates.
Neocortical projections converge on the lateral nucleus of
the amygdala. These arise largely from the temporal cortex,
but insular and frontal projections have been described as
well (24, 46, 75). In general, these projections are highly
organized in terms of topography. For example, the visual
association cortex of the lateral temporal lobe projects to
the dorsolateral part of the lateral nucleus, whereas the
auditory association cortex projects to its more ventrolateral
parts. Temporal polar cortical projections to the lateral
nucleus terminate in the medial parts of the nucleus, as do
insular and orbitofrontal projections. The basal amygdaloid
nuclei receive extensive input from the cortex of the limbic
lobe, including the cingulate, temporal polar, and perirhinal
cortices as well as the subiculum (82).
The hippocampal formation receives its major
cortical input from the entorhinal periallocortex. The sum
of this projection is known as the per-forant pathway and it
forms an overlooked, but major fiber system in the
temporal lobe (71, 79). Input to the entorhinal cortices is
derived from both subcortical and cortical structures. The
former include the amygdala and septal area, as well as
several midline thalamic nuclei (33). The latter, the
cortical projections, are extensive. Major projections
originate in the subicular cortex (60) and in the olfactory
cortex and cortical amygdaloid nuclei (39). Collectively,
these represent allocortical projections. Large periallocorti-
cal projections arise from the presubicular and
retrosplenial cortices (68, 69). Proisocortical projections
arise from the posterior parahippocam-pal, temporal polar,
perirhinal, and posterior orbital cortices (78-80). Lastly,
isocortical input arises from the cortex of the superior
temporal gyrus (4) and the banks of the occipitotemporal
sulcus (84). In total, these projections represent a large and
diverse source of cortical input to the hippocampal
formation. They bring modality-specific and multimodal
cortical information to the structures of the hippocampal
formation.
It is plausible to believe that these sources of cortical
input to the entorhinal cortex and hippocampal formation
provide these structures with a rich variety of input
relating to the sensory environment. For example,
posterior parahippo-campal and parietooccipital
projections would be expected to carry visual or
visuosomatic information because these areas receive
input from peristriate visual association cortices (69). Pro-
jections that arise from the superior temporal gyrus (66)
would be expected to convey auditory input because these
areas receive direct projections from cortical areas that
surround the primary auditory cortex. Projections that
relay through the insular cortex, amygdala, and perirhinal
cortices to the entorhinal cortex and hippocampal
formation would be expected to convey somatic and
perhaps gustatory information. Olfactory input arises
directly from the olfactory bulb as well as from the
prepiriform cortex that forms the anterior part of the
parahippocampal gyrus.
Such connections would be expected to provide
unimodal channels of influence from all sensory
modalities, as well as bimodal and multimodal channels.
Some areas of the cortex that send direct projections to
entorhinal cortex are themselves multimodal because they
receive cortico-cortical association projections from areas
related to more than one modality. Moreover, many other
areas of the limbic lobe receive direct input
themselves from multimodal and sensory-specific
association cortices, and in turn project to the entorhinal
cortices, creating the potential for nearly all combinations
and permutations of simple and complex sensory inputs.
Finally, the association cortices undoubtedly play a dual
functional role because they are related, on the one hand, to
the analysis and synthesis on sensory information (54) and,
on the other, to the preservation of memories. Thus, the
input to the entorhinal cortices is likely to be a composite,
relating to both past and current sensory and cognitive
experiences relative to all modalities.
It should be apparent from this discussion that
experimental studies have altered classical thinking to a
considerable extent. It is no longer tenable to view the
limbic system as a group of interconnected structures whose
input arises largely from its own components and whose
output affects only other components of the system. Indeed,
extensive intralimbic system connections do exist and form
the substance of many elements of classical neuroanatomy.
In line with the early deductions of Papez and MacLean,
limbic system structures do receive sensory input and,
although there were early difficulties in demonstrating this
with experimental methods, it is now recognized that these
inputs are extensive and highly complex. Some of them
arise directly from sensory association areas adjacent to the
primary sensory areas, whereas others arise from
multimodal association cortices that, themselves, receive
input from two or more sensory association cortices. In
some instances, certain limbic structures receive these
categories of sensory association input directly, whereas in
other instances they are relayed indirectly. There is still
insufficient neurophysio-logical and functional data to
characterize all of these fully. Nonetheless, given what is
available, it is plausible to believe that they convey a rather
sophisticated digest of the sensory environment that is
linked often to the state of the organism in terms of
relevance, motivation, and attention. In short, they arise
from areas spread along the chain of intrahemispheric
sensory stations where an external stimulus is analyzed
elementally and then put together again in appropriate
perceptual categories and context. In many instances these
are multidimensional. One might conceptualize this as a
unit in association cortex that responds only when criteria
such as form, color, and orientation are combined appropri-
ately and/or if linked with the appropriate drive.
We do not know precisely what limbic system structures
do with such information, but func-
tional and clinical studies point clearly to the fact that
different areas subserve substantially different functions.
For example, damage to the anterior cingulate cortex can
lead to a pronounced amotivational and akinetic state, with
withdrawal from social and interpersonal interactions and
impoverished motor activity. Posterior orbitofrontal
damage may alter social behavior but it seldom involves the
same social withdrawal. It is characterized instead by
disinhibi-tion and social and sexual inappropriateness.
Motor activities as well may tend toward disin-hibition.
Basal forebrain changes, for example, in the case of
ruptured anterior communicating aneurysms, that damage
the septum, nucleus basalis, and columns of the fornix, may
lead to a distinct memory impairment, but disinhibition and
personality disorders may be manifest as well. Temporal
polar and amygdaloid pathology are linked solidly with
emotional changes of several varieties as well as perceptual
and sexual
dysfunction. Finally, hippocampal and parahip-pocampal
lesions lead to few of the behavioral changes discussed
previously, but cause, instead, irreversible alterations in
memory, a global amnestic disorder markedly skewed in
the direction of new learning.
Thus, it is inappropriate to view the limbic system as
having a single function, although an involvement with
memory is clearly the most visible of its roles. Without a
doubt certain of its structural elements are more important
for some behaviors than others, but in general, multiple
behaviors than others, but in general, multiple behavioral
changes accompany nearly any focal limbic disorder.
Additionally, it seems clear that limbic system structures
act in consort with many other parts of the nonlimbic brain
and have a decisive interaction with those areas subserving
sensation, cognition, motor function, endocrine control and
autonomic regulation. In short, it forms key elements of a
multitude of

Figure 6.2. This is a photomicrograph of a Nissl-stained coronal section from the human
brain at the level of the optic chiasm. The neuronal cell groups that form the nucleus
basalis of Meynert and surrounding surface and subcortical structures are highlighted.
neural systems that involve many brain areas and which line nuclei such as the paraventricular nucleus. They
subserve many complex behaviors. occupy a position between the reticular anterior pole at the
thalamus and the dorsome-dial thalamic nucleus, directly
Anatomical Concerns Relating to Surgery in the Vicinity over the third ventricle. In fact, the nucleus reuniens is
of the Third Ventricle directly dorsal to the ependymal cell lining. Both it and the
paraventricular nucleus provide a major source of input to
Access to operable abnormalities in or around the third
the entorhinal cortex (26, 33) (see Fig. 6.3). Moreover, the
ventricle requires, in most instances, a surgical approach
nucleus reuniens projects also to the hippocampus (26).
that compromises the integrity of certain limbic system
Little is known about their input, but nonspecific brain stem
structures. Memory impairments are not an unusual
sources would be expected. In consort with
postoperative complication andrepresent a matter of
substantial concern during the immediate postsurgical
management period or even longer afterward. The fimbria-
fornix system, a major interconnecting limbic system
pathway, is frequently the neural structure of concern
because it wraps nearly around a major portion of the
diencephalon and the fornix has a long interstitial course
through it enroute to termination sites in the preoptic and
hypothalamic areas.
The validity of the concern for fornix damage, in
totality, might be challenged for several reasons. Foremost
is the fact that there is little agreement in the literature as
to whether fornix integrity is essential for normal memory.
Indeed, it carries significant input to the hippocampal
formation as well as significant output from nearly all
parts of this collection of structures (72). However,
significant other input and output pathways would remain
intact so that disruption of the fornix would not totally
disconnect the hippocampal formation. In fact, nearly all
of its connections with the association cortices would be
structurally patent. It seems more plausible to us to believe
that fornix damage in consort with damage to other neural
systems critical for normal memory are collectively the
culprit. Basal forebrain nuclei, thalamic nuclei, and a
major, often overlooked, subcortical limbic pathway could
play a role.
The first would constitute the nucleus basalis of Meynert
that lies largely in the substantia innominata (see Fig. 6.2).
It extends beneath the basal ganglia and pallidum from the
midline of the hemisphere to the temporal lobe. Its largest
component lies relatively close to the midline and only a
few millimeters from the third ventricle. As discussed
previously, it provides the major cholinergic input to the
cortex. Fornix damage could disrupt cholinergic input to
the hippocampal formation and, in combination with
nucleus basalis pathology, would deprive all cortex from
much of its normal cholinergic innvervation. Figure 6.3. This is a darkfield photomicrograph of the
A thalamic nucleus of major concern would be the anterior thalamus of the rhesus monkey showing the
nucleus reuniens and other associated mid- location of retrogradely labeled neurons in the anterior
thalamus and nucleus reuniens after a horseradish
peroxidase injection into the entorhinal cortex of the
parahippocampal gyrus. These nuclei provide a strong input
to various parts of the ventromedial temporal lobe
including the hippocampal formation. Note their close
proximity to the third ventricle.
fornix damage, the hippocampal formation would be
partially deafferented and deeffer-ented.
The inferior thalamic peduncle (49) is seldom classified
as a subcortical limbic system pathway, but should be
elevated to that status. It carries a major component of
amygdaloid output and notably a major connection with the
dorso-medial thalamic nucleus (1, 47, 48, 56) (see Fig. 6.4).
Its course does not have a large anterior-posterior extent,
but it travels only a few millimeters from the third ventricle
as it swoops in a dorsal direction beneath and medial to the
globus pallidus. In fact, it intermingles, in part, with the
ansa lenticularis, a topographic feature that has precluded
its identification as an entity.
In summary, recent experimental neuroana-
tomical observations suggest that significant dorsal, lateral,
and ventral surgical damage around the third ventricle
would disrupt major connections of other limbic structures
that form neural systems related to certain aspects of nor-
mal memory. This may not be heartening to the
neurosurgeon. However, selective strategies might be
exercised during the surgical procedure, when possible, to
lessen the destruction or edema that might compromise
these limbic structures.
Model Network for Memory
The picture that emerges currently from this combination
of clinical and basic science findings indicates that: (a) the
intactness of modal sensory association cortices is essential
for the establishment of individual traces of memory.

Figure 6.4. This darkfield photomicrograph shows major parts of the ventro-
amygdalofugal pathway and the inferior thalamic peduncle in a coronal plane from the
rhesus monkey. Tritium-labeled amino acids were injected into the amygdala and tissue
sections were processed for autoradiography. The ventroam-ygdalofugal pathway
connects the amygdala with the basal forebrain and hypo-thalamus, as well as with other
limbic system structures. The inferior thalamic peduncle branches posteriorly at the
approximate level of the anterior commissure. It enters the thalamus from an anterior and
ventral location and conveys amygdaloid output to the dorsomedial thalamic nucleus.
The process seems to require input from limbic structures
and possibly also from brain stem nuclei responsible for
specific neurochemical in-nervation. The latter include the
locus coeruleus, nucleus basalis, nucleus of the raphe, and
ventral tegmental area, which provide the cerebral cortex
with intrinsic norepinephrine, acetylcho-line, serotonin
and dopamine, respectively, (b) The modal traces of
memory are stored in the modal sensory association
cortices, (c) The establishment of multimodal contextual
memory is dependent upon a complex anatomical system
that includes medial temporal regions, basal forebrain
structures, diencephalic structures, and some
neurochemically specific brain stem nuclei, as well as
subcortical connections interrelating these components.
The combined function of these units is: (a) the
computation of interrelationships between the several
modal stimuli that constitute experiential episodes and are
linked by temporal and spatial bonds, among others; (b)
the storage of the records of that computation, in the form
of a multiple entry, cross indexed catalog, capable of
permitting recall and recognition from the standpoint of
any of its constituents.
The store of the abstract records of contextual
relationships is possibly dependent, at least in part, upon
lateral temporal lobe structures interacting with medial
temporal structures such as the amygdala especially. For
some types of contextual memory, frontal lobe structures
may be important as well.
Preoperative and Postoperative Assessment of
Memory
The effects of neurosurgical procedures on memory are
best determined by comparison between preoperative and
postoperative performance in neuropsychological tests
and general behavior.
When it is possible to complete both preoperative and
postoperative neuropsychological assessment, patients can
serve as their own controls. The results of such a complete
study are useful not only for the management of the pa-
tient—especially in terms of planning the rehabilitation
procedures—but also for the proper reporting of surgical
results and for potential clinical research projects. In fact,
such complete information is necessary if further
cognitive experimental procedures are contemplated for a
patient who will participate in future investigation
protocols. Here we outline the fundamental principles and
procedures for this assessment
and provide appropriate references for those who may want
to pursue details of testing.
Memory should be examined in two settings, at the
bedside and in the neuropsychological laboratory. At the
bedside, patients should be tested for: (a) orientation to
time, place, and personal information—inquiry should
include birthdate, address, and a statement as to why the
patient is in the hospital; (b) recognition of doctors' and
nurses' faces; (c) naming of doctors' and nurses' names; (d)
recognition and naming of family members; (e)
identification of the location of the patient's room within
the hospital and within the ward, using both actual
displacement and maps (either is applicable in immobilized
patients); and (/) recall of recent events. The patients should
produce an account of special medical procedures in which
they have participated, a list of recent visitors (including
the topics of conversation and times of the visits), and an
itemization of major news events acquired through TV or
newspaper.
Behavior in the clinical setting (presence of geographic
disorientation, reaction to meals and nursing care) will
often provide a good tell-tale sign of memory impairment.
More detailed and comprehensive assessment of memory
can be accomplished only with special laboratory studies.
Neuropsychological assessment aims at scrutinizing
memory in comparison to other behaviors such as problem
solving (e.g., tests of intelligence (90), visual perception
(8), constructional ability (51, 58), and language (10)).
Deficits of memory may occur either as isolated
impairments or as part of a more pervasive cognitive
impairment. This comparison is critical for determining the
effects of disease and of neurosurgical procedures and for
planning the rehabilitation of the patient.
Laboratory assessment of memory must comprehend
both anterograde and retrograde memory processes. Within
the anterograde compartment, corresponding to the epoch
after the onset of disease, three stages of memory should be
examined. The first is immediate memory, which is most
frequently tested with tasks of memory for digital
sequences. In amnestic patients this stage of memory
processing is almost invariably intact. The second stage is
short term memory for verbal and nonverbal material,
which can be assessed with a variety of learning tasks using
word lists (59), word pairs (50, 89), reproduction of
geometric designs (9), or recognition of new faces (i.e.,
previously unfamiliar). The final stage of anterograde
memory to be examined is the long term and recognition of
previously familiar
material. As an example, patients should be required to
recall a word list that they were asked to learn 30 minutes
before. This can be followed by a recognition task, in
which the original target words are mixed in with distractor
items. Patients with a specific disability of recall may
produce a normal performance on the recognition task. The
inability to perform a delayed memory task carries very
different implications if it is caused by an inability to retain
any information as opposed to an inability just to recall
information.
The other major area of laboratory study is the
assessment of retrograde memory. Every patient should be
evaluated for the recall and recognition of personal
biographical material (such as wedding date, details on
friends and relatives, educational background, graduation
dates, special trips and vacations, family pets, etc.).
Obviously there are no available standardized tests for this
type of process and great care should be given in
constructing the appropriate personal assessment of each
new subject. Information for these tests can easily be
provided by the family and the results of questioning can be
confirmed with relatives. Nonpersonal retrograde memory
can be assessed with a standardized test such as the Boston
remote memory test (3), which quizzes the patient on public
events and on recognition of the faces of celebrities
(political, entertainment, and sports personalities from the
1920s to the 1970s).
Acknowledgments
We thank Paul Eslinger, Ph.D., for his help with the
section dealing with neuropsychological assessment. Betty
Redeker prepared the manuscript. Photographs are by Paul
Reimann.
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Commentary A
Memory in Man: A Neurosurgeon's Perspective
Henry D. Garrefson, M.D., Ph.D.
Intact memory function is an essential component of the
human condition in coping with everyday life. Inability to
retain and utilize new information as a result of an
intracranial neu-rosurgical procedure is a complication
potentially more devastating to the patient's long term re-
habilitation and return to productive life than is the
occurrence of a severe hemiparesis. In humans the limbic
system together with its major association areas in the
neocortex and subcorti-cal nuclei form the primary
substrate for normal memory function. During the past
decade major advances in our understanding of this
anatomical substrate have been made through careful pre-,
intra-, and postoperative testing of patients undergoing a
variety of neurosurgical procedures involving the limbic
system and its association areas. The human brain's
division of specialized memory functions between
dominant and non-dominant hemispheres for speech has
made this study more complex. One consequence has been
the lack of an adequate animal model with which to study
many aspects of memory function as seen in humans.
The anatomy of the limbic system and its association
areas have already been discussed in some detail in
Chapter 6. The areas of particular concern to the
neurosurgeon are the vascular territory of the small
perforating branches of the distal A1 segment of the
anterior cerebral and the anterior communicating arteries
(i.e., the substantia innominata, the anterior septal com-
plex, and the descending columns of the fornix (1, 2); the
hippocampal complex of the mesial temporal lobe
together with its association areas in the lateral temporal
cortex; and finally the parietooccipital association areas of
the dominant hemisphere for language. The columns of
the fornix in the area of the foramen of Monro play a less
certain role in global memory function.
Substantia Innominata and Anterior Septal Complex
with Adjacent Descending Columns of the Fornix
Entrance to the anterior third ventricle through the
lamina terminalis for evacuation of
tumor is surprisingly well tolerated. As long as the
subsequent tumor removal does not extend beyond the walls
of the tumor, disturbance of consciousness and memory
does not occur. However, disruption of the very fine
perforating vessels arising from the distal portion of the A1
segments of the anterior cerebral artery and from the
anterior communicating artery (10, 11, 13) will routinely
produce a significant global anter-ograde memory
disturbance of the episodic or contextual variety. These
vessels can to the naked eye mimic fine arachnoidal strands.
It is essential that operation in this region be done under
magnification for their adequate protection. These fine
perforating branches must be looked for and preserved
during anterior communicating artery aneurysm clipping as
well as during tumor resection in this same vicinity. The
memory abnormality produced is due to bilateral ischemic
damage of the immediately adjacent descending columns of
the fornix and the mesial portions of the adjacent substantia
innominata and nucleus basalis as well. Identification and
preservation of the larger and anatomically quite variable
recurrent arteries of Huebner, arising anywhere from 1 cm
proximal up to 3 mm distal to the anterior communicating
artery, are not enough to prevent this memory defect. Lesser
and more transient degrees of memory impairment due to
ischemic insult from incomplete injury to or spasm of these
small perforating vessels may persist for as long as 10 to 12
weeks.
Hippocampal Complex and Lateral Temporal
Lobe Cortex
Attention was sharply focused on the functional role of
the mesial temporal lobe structures by the appearance of a
devastating memory deficit in a patient, H.M., who
underwent bilateral resection of the amygdala and
hippocampal structures for intractable epilepsy (14). An an-
terior subfrontal approach was used in this patient, sparing
the remainder of the temporal lobe structures. H.M. showed
an almost complete inability to retain and recall, after a
brief distraction, any new material presented to him, with
the exception of a very slight, subtle retention of
 some new motor skills after extended periods of practice.
He remains able to read and reread the same literature with
enjoyment without ever being aware that he has done so
previously and, similarly, rework the same puzzles without
showing any practice effect.
In humans, memory function is partially segregated
between the two cerebral hemispheres on the basis of
whether there is a significant language component or verbal
label for the material to be remembered.
Verbally keyed memory function resides primarily in the
dominant hemisphere for speech. The dominant hemisphere
for speech is not synonymous with the dominant
hemisphere for handedness (12). In a group of 262 patients
without evidence of left hemisphere damage, 96% of right-
handers and 70% of non-right handers (ambidextrous and
left-handed) were left hemisphere-dominant for speech.
They were shown to have speech disturbance after
amobarbital injection into the carotid circulation of the left
hemisphere and not after a similar injection on the opposite
right side. Only 15% of the ambidextrous and left-handed
group had speech function clearly lateralized to the right
hemisphere, with the remaining 15% showing evidence of
bilateral speech representation. Although none of these 262
patients showed evidence of gross structural lesions, they
were being investigated for the management of intractable
epilepsy. The translation of these results to the nonepileptic
population must therefore be done cautiously. It is of
particular interest and some concern that 4% of the right-
handed patients in this study showed definite lateralization
of speech function to the right hemisphere.
Nonverbal memory function resides primarily in the
nondominant temporal lobe for speech. Nonverbal memory
deals with material for which there is no ready language
label to assist memory function in both recognition and
recall of this material. Recognizing a previously seen face
out of a group of faces or an abstract pattern of lines out of
a group or series of such abstract patterns are examples of
nonverbal memory. Memory of spatial relationships seems
to be a nondominant mesial temporal lobe-mediated
function (15). Recall of deliberately memorized spatial
information, such as recall of a specific location and of a
learned path through a stylus maze, is impaired after
excision of the right but not the left hippo-campal region.
Automatic encoding of where we have seen something,
even though deliberate attention was not paid to its location
at the time, is a common experience that also seems to de-
pend on the right (nondominant) hippocampus.
The absence of an adequate animal model for the study
of the human type of temporal lobe memory function
suggests that clarification of many aspects of neocortical
participation in memory function will continue to be slow
in appearing. Although the bilateral lesions in H.M.
included the amygdala, uncus, and hippocampus, it has
been subsequently shown that bilateral lesions of the
amygdala and uncus alone do not produce memory deficit.
Similarly, bilateral sectioning of the temporal stem has not
produced memory impairment (19). Care must be taken not
to duplicate the clinical outcome seen with H.M. by
unilateral surgical resection of the amygdala and
hippocampal complex in a patient who has sustained
significant prior damage to the opposite mesial temporal
lobe structures through trauma or some other disease
process.
Ojemann and coworkers recently showed that the lateral
temporal cortex of the dominant temporal lobe plays a
significant role in verbal memory (3, 6-9). Specific loci for
interference with verbal memory produced by cortical
stimulation of the dominant lateral temporal cortex during
either the input or the recall phase of memory testing have
been found in the mid- and posterior-temporal areas of the
first and second temporal convolution, both anterior to and
posterior to the primary temporal speech area. Cortex ad-
jacent to the posterior temporoparietal speech areas seems
to be involved in the input storage of short term verbal
memory, whereas cortex adjacent to the anterior language
area of the frontal operculum is involved in retrieval of
short term verbal memory. Resection of thus identified
lateral temporal cortical areas anterior to the primary speech
cortex in the temporal lobe produced definite verbal
memory deficits even when the hippocampus was spared.
Conversely, tailoring the temporal lobe cortical resection so
as to spare these identified areas of verbal memory function
permitted anterior temporal lobe resection including the
amygdala (but sparing the hippocampus) without producing
any measurable verbal memory disturbance. Ojemann and
Creutzfeldt have recently documented an increase in the
neuronal firing rate in these dominant temporal lobe
association areas when naming is an input memory stimulus
but not during naming when it is not an input to memory.
Cortical stimulation studies in the nondominant hemisphere
have shown discrete localization of short term nonverbal
memory in the posterior first temporal gyrus, further
reinforcing the evidence for a significant lateral temporal
cortical role in short term memory. Short term memory for
line orientation and
face identification ("visuospatial material") is specifically
interfered with by stimulation of the posterior
nondominant right first temporal gyrus (3). Spatial
functions, including memory, seem to be as discretely
organized in the nondominant hemisphere as are verbal
functions, again including memory, in the dominant
hemisphere.
Wieser and Yasargil reported that selective unilateral
microsurgical resection of the amygdala and hippocampus
with sparing of the lateral temporal lobe structures in the
dominant temporal lobe did not produce significant
impairment of verbal memory tasks (18). The same type of
resection in the nondominant temporal lobe did, however,
produce slight impairment of maze learning. These results
were considered preliminary by the authors, with more
detailed testing of nonverbal and verbal memory functions
being planned.
Columns of the Fornix at the Level of the Foramen of
Monro
Reported results of bilateral sectioning of the columns
of the fornix at the level of the foramen of Monro are
conflicting (5). Sweet and coworkers in 1959 described a
patient who sustained a severe contextual or episodic
memory deficit after bilateral sectioning of the columns of
the fornix during the removal of a colloid cyst of the third
ventricle (16). Whitty and Lishman in 1966 quoted Cairns
as having indicated that bilateral forniceal sectioning
could be carried out without producing memory
disturbance (17). A similar observation was made by W.E.
le Gros Clark and coworkers in 1938 (4). A group of
patients with apparent bilateral lesions of the fornix in the
immediate vicinity of the foramen of Monro with no
apparent significant memory deficit have been
summarized in some detail by Horel (5). It seems probable
that additional abnormality must accompany bilateral
forniceal damage for a flagrant amnestic syndrome to
appear. An adequate study of the effect of unilateral
sectioning of the columns of the fornix on memory is not
available. Enlargement of the foramen of Monro by poste-
riorly directed dissection under magnification with
appropriate microsurgical instrumentation is benign when
increased exposure through the foramen of Monro is
absolutely necessary. Sectioning of one or both of the
columns of the fornix is rarely required and should be
avoided. The unilateral destruction of structures important
in memory function usually requires more careful
psychometric testing than simple casual bedside
observation of memory function to document the often
subtle effects of such procedures.
Parietooccipital Association Areas of the Dominant
Hemisphere
The assignment of a disturbance in memory function as a
primary etiological factor in explaining impairment of
reading or writing secondary to focal lesions in the
dominant parie-tooccipital lobe requires some thought.
These deficits have been termed a dyspraxic form of
memory impairment. Although the primary motor, tactile,
and visual skills seem to be intact, the patient is unable to
use these primary modalities for certain forms of visual
recognition or written expression. Subtle forms of these
deficits may be seen after a dominant hemisphere parietal
transcortical approach to the area of the trigone and the
dorsal surface of the thalamus. These deficits may be
noticed clinically only if these functions are important to
the patient and are routinely used in his daily activities.
More widespread utilization of pre- and postoperative test
batteries for the evaluation of parietooccipi-tal function
would help to advance our understanding of these functions
in a manner similar to the progress that is now being
achieved in understanding the function of the "silent" areas
of the temporal lobe.
References
1 . Damasio A: The anatomical basis of memory dis
orders. Semin Neurol 4:223-225, 1984.
2. Damasio A, Graff-Radford N, Eslinger P, Dimasio
H, Kassell N: Amnesia following ventromedial le
sions of the frontal lobe. Arch Neurol 42:263-
271, 1985.
3. Fried I, Mateer C, Ojemann G, Wohns R, Febio P:
Organization of visuospatial functions in human
cortex: Evidence from electrical stimulation.
Brain 105:349-371, 1982.
4. Gros Clark WE le, Beattie J, Riddock G, Dott NM:
The Hypothalamus. Edinburgh, Oliver and Boyd,
1938.
5. Horel JA: The neuroanatomy of amnesia: A cri
tique of the hippocampal memory hypothesis.
Brain 101:403-445, 1978.
6. Ojemann GA: Brain organization for language
from the perspective of electrical stimulation
mapping. In The Behavioral and Brain Sciences.
Cambridge, Cambridge University Press, 1983, pp
189-230.
7. Ojemann GA, Dodrill CB: Intraoperative tech
niques for reducing language and memory deficits
with left temporal lobectomy. Presented at Epi
lepsy International, Hamburg, November 1985.
8. Ojemann G: Organization of short-term verbal
memory in language areas of human cortex: Evi
dence from electrical stimulation. Brain Lang
5:331-340, 1978.
9. Ojemann GA, Dodrill CB: Verbal memory deficits
after temporal lobectomy for epilepsy: Mechanism
and intraoperative prediction. J Neurosurg
62:101-107, 1985.
10. Perlmutter D, Rhoton AL: Microsurgical anatomy
 of the anterior cerebral-anterior communicating-
recurrent artery complex. J Neurosurg 45:259-272,
1976.
1 1 . Perlmutter D, Rhoton AL: Microsurgical anatomy
of the distal anterior cerebral artery. J Neurosurg
49:204-228, 1978.
12. Rasmussen T, Milner B: The role of early left brain
injury in determining lateralization of cerebral
speech functions. Ann NY Acad Sci 299:355-
369, 1977.
13. Rhoton AL, Perlmutter D: Microsurgical anatomy
of anterior communicating artery aneurysms.
Neurol Res 2:217-251, 1980.
14. Scoville WB, Milner B: Loss of recent memory
after bilateral hippocampal lesions. J Neurol Neu
rosurg Psychiatry 20:11-21, 1957.
15. Smith ML, Milner B: The role of the right hippo-
campus in the recall of spatial location. Neuro-
psychologia 19:781-793, 1981.
16. Sweet WH, Talland GA, Ervin FR: Loss of recent
memory following section of fornix. Trans Am
Neurol Assoc 84:76-82, 1959.
17. Whitty CWM, Lishman WA: Amnesia in cerebral
disease. In Whitty CWM, Zangwill OL (eds): Am
nesia. Washington, DC, Butterworths 1966, pp
36-75.
18. Wieser HG, Yasargil MG: Selective amygdala hip-
pocampectomy as a surgical treatment of mesio-
basal limbic epilepsy. Surg Neurol 17:445-457,
1982.
19. Zola-Morgan S, Squire LR, Mishkin M: The neu-
roanatomy of amnesia: Amygdala-hippocampus
versus temporal stem. Science 218:1337-1339,
1982.
7
Anatomy and Physiology of Consciousness:
Syndromes of Altered Consciousness Related to
Third Ventricular Surgery
Gilbert A. Block, M.D., and Jerome B. Posner, M.D.
Both clinical and experimental evidence assign an
important role to structures surrounding the third ventricle
in the regulation of motor function and consciousness. The
hypothalamus and its surrounding structures are especially
important as a reticular system integrator. The general as-
pects of the anatomy, physiology, and pathology of
consciousness were extensively reviewed by Plum and
Posner (67). In this chapter, we discuss the
pathophysiology of abnormal states of consciousness,
primarily hypersomnia and akinetic mutism, that arise
when third ventricular lesions damage the hypothalamic
region. We also present an integrated model of
neuroanatomical and neurochemical properties as they
relate to the syndromes of the third ventricle.
Anatomy and Chemistry of the
Hypothalamic Region
The hypothalamus is the ventral portion of the
diencephalon. It surrounds the inferior third ventricle and
is separated from the thalamus by the hypothalamic
sulcus. Rostrocaudally it extends from the preoptic area to
the mamillary bodies, merging caudally with the
periventricular gray of the midbrain.
The hypothalamus has a highly complex cellular
organization with multiple efferent and afferent
projections. Traditionally it has been subdivided into
anterior, medial, and posterior portions, but it is more
easily described functionally
by longitudinal subdivisions (Table 7.1) (10). The major
hypothalamic nuclei, their presumed function, and their
afferent and efferent connections are listed in Table 7.2.
The complex anatomical organization and the vast number
of connections and fibers of passage through this region
hamper our ability to determine completely the function of
individual hypothalamic nuclei.
Fibers passing through the hypothalamus are of major
importance in the consideration of altered states of
consciousness. The majority of these ascending and
descending fibers travel in the medial forebrain bundle
(MFB), which links the limbic forebrain with the lower
reticular regions (Table 7.3). This multidirectional pathway
constitutes the major longitudinal fiber system of the
hypothalamus. The fibers that compose the MFB are not
limited to the preoptic and lateral regions of the
hypothalamus but convey information to midline thalamic
structures as well. Fibers originating from bed nuclei that
comprise the MFB terminate in most of the structures that
are believed to regulate consciousness (42, 60, 95).
The neuropharmacology of the hypothalamus includes
norepinephrine, dopamine, serotonin, and acetylcholine
pathways and is at least as complex as its anatomy.
Neurotransmitter systems have been carefully studied using
modern techniques that include immunocytochemical
methods, fluorescence, lesioning, and punch biopsy for
enzymatic assay (23, 34, 65, 66). The
213
norepinephrine (NE) distribution in the hypo-thalamus
parallels the distribution of dopamine-beta-hydroxylase.
The majority of the NE cells are found in Al and A2 cell
groups as well as the locus coeruleus. Transection of the
ventral nor-adrenergic bundle results in a significant reduc-
tion of the norepinephrine content of the preoptic area.
Most hypothalamic dopamine is probably syn-
thesized in situ in the soma of the arcuate, ven-tromedial,
and periventricular nuclei. The remainder arises from axons
of passage arising from the mesotelencephalic cell groups
(A8, A9, A10). Serotonin and tryptophan hydroxylase are
present in the highest concentrations in the su-
prachiasmatic nucleus. The majority of serotonin originates
from axons arising from the raphe nucleus (79).
Hypothalamic acetylcholine has been demonstrated by
acetylcholinesterase histochemistry and measurement of
choline ace-tyltransferase activity (26). The highest concen-
trations of choline acetyltransferase are found in the
paraventricular, arcuate, and dorsomedial nuclei. Surgical
deafferentation of the median eminence significantly
reduces the choline acetyltransferase levels in the arcuate
and dorsomedial nuclei, indicating the existence of extra-
hypothalamic cholinergic neurons with axon terminations
or axons in passage in these regions. Satoh et al. (80)
demonstrated that the only choline acetyltransferase-
positive hypothalamic neurons are found in the
magnocellular preoptic nucleus.
Taken together, the neurochemical data indicate that,
with the exception of the dopamine in the
tuberoinfundibular tract, the majority of the monoamine
and acetylcholine content of the hy-
pothalamus arises from axons in passage or ax-ons
terminating in the hypothalamus. These neurotransmitters
are carried by fibers comprising the MFB, thus
neurochemically linking the limbic-forebrain and limbic-
mesencephalic areas.
Functions of the Hypothalamus
Acute and chronic experimental preparations (53, 72,
92) have established the role of the hy-pothalamic region
in the regulation of the following functions:
neuroendocrine, thermoregu-lation, feeding, emotional
output, autonomic control, osmoregulation, and
consciousness. Definitive localization of these functions to
precise anatomical regions of the hypothalamus is made
difficult by the complex overlapping functions of different
hypothalamic regions. Despite these limitations, certain
gross functional generalizations are possible (for review,
see 70).
Neuroendocrine Functions
Neuroendocrine functions of the hypothalamus have
been extensively investigated. Lutein-
izing hormone-releasing hormone is predominantly
localized to the preoptic area and the arcuate nucleus,
whereas thyrotropin-releasing hormone is found in highest
concentration in the dorsomedial nucleus. Corticotropin-
releasing factor localizes to the paraventricular nucleus but
seems not to colocalize with either oxytocin or vasopressin.
Growth hormone-releasing hormone (GHRH) localizes to
the caudal portion of the arcuate nucleus, with the majority
of GHRH-positive axons projecting directly to the median
eminence.
Thermoregulation
Thermoregulatory functions are encoded in the preoptic-
anterior hypothalamic areas, which regulate heat loss,
whereas the posterior hypothalamus contains centers for
both heat loss and heat production (4, 17, 20, 21). The
preoptic anterior hypothalamus contains neural thermo-
detectors as well as a comparator-resistance network that
integrates thermal signals. Effector signals are sent to the
posterior hypothalamic region, which activates heat loss
systems. The
premamillary region contains neurons that function as a set
point generator. Stimulation of this region activates heat
loss mechanisms. Large posterior hypothalamic lesions
eliminate the integrating mechanisms, prevent heat loss and
heat production, and thus result in poikiloth-ermy.
Feeding
Feeding experiments have shown that stimulating the
ventromedial medial nucleus interrupts feeding behavior,
whereas bilateral lesions result in a transient hyperphagia
with eventual stabilization of caloric intake at a higher
level. In association with the increased intake of food is the
decrease in the level of activity. Lateral hypothalamic area
lesions result in aphagia and can also cause hypokinesia.
Stimulation of this area activates feeding behavior
mechanisms. The firing rates in the neurons of both of these
areas are modified by a wide variety of factors including
glucose, free fatty acids, olfactory and sensory inputs, and
various neurotransmitters. Acetylcholine, acting via
muscarinic receptors, causes excitation of lateral
hypothalamic neurons and either excitation or inhibition of
ventromedial neurons, depending on the units recorded.
Similarly, norepinephrine has an excitatory effect on lateral
hypothalamic neurons yet can have an excitatory or
inhibitory effect on ventromedial neurons. The precise role
of these neurotransmitters in the regulation of feeding
behavior remains to be further elucidated. Lesions in either
of these areas have been reported to decrease the level of
activity. Electrophysiolog-ically, the decrease in activity is
reversible (potentially) by stimulation of the lateral
hypothalamic region or the administration of cholinergic or
adrenergic agonists.
Emotional Output
Rage responses occur after lesions are made in the basal
hypothalamus, particularly the ventromedial nucleus (74).
As the cell bodies of the ventromedial nucleus also lie
among the fibers of the MFB, it is unclear whether the
production of rage behavior with ventromedial nucleus le-
sions is secondary to destruction of MFB fibers or intrinsic
nuclear damage.
Autonomic Control
Early research demonstrated that the hypothalamus has a
profound influence on multiple organ systems by virtue of
its role in integrating autonomic nervous system function.
Electrical stimulation of anterior and posterior hypothala-
mic regions produces changes in autonomic
function by virtue of action on descending telen-cephalic
pathways that course through the hypothalamus, as well as
on integrating centers in the hypothalamic periventricular
regions. Lateral hypothalamic stimulation results in in-
creased parasympathetic tone in both animals and humans,
with resulting bradycardia, hypotension, and miosis.
Posteromedial and ventral stimulation results in increased
sympathetic tone.
Osmoregulation
Water balance and osmolarity are controlled via
hypothalamic integration of signals from os-moreceptors
and the neurosecretory response with output of vasopressin
to various stimuli. The preoptic region contains
osmoreceptors responsive to intracellular dehydration.
Stimulation of this area in response to contracted blood
volume causes increased fluid intake. Stimulation of lateral
hypothalamic osmoreceptors, although resulting in
increased thirst and polydyp-sia, may cause this by an
effect on increasing arousal via stimulation of fibers in
passage in the MFB.
Consciousness
Sleep and wakefulness are both dynamic processes.
Wakefulness alternates cyclically with both slow wave
(SWS) and paradoxical sleep (rapid eye movement, REM).
SWS can be subdivided into four stages, each characterized
by a progressively slower electroencephalogram (EEC)
frequency and a greater depth of sleep. In humans,
approximately 1.5 hours after the onset of sleep, EEG
desynchronization occurs, associated with diffuse
sympathetic activation and electromyographic quiescence.
During this stage, REM and pontogeniculate-occipital
phasic spikes occur and the arousal threshold is greatest.
In humans, REM sleep occupies 20 to 25%, stage II
SWS occupies 50%, and stage IV SWS occupies 15% of
total sleep time. Although sleep phylogeny varies,
generalizations can be made in humans from animal
experiments because SWS and activated sleep (REM)
occur in all mammals.
Lesions and transections at various levels of the nervous
system affect sleep and consciousness in different ways.
The effects of surgical lesions are difficult to interpret
because of imprecision in making highly localized lesions
in animals and the lack of precise reporting of the specific
postmortem pathological findings in humans. Nevertheless,
certain classical experiments of investigators and of nature
provide important insights into specific ascending and de-
scending pathways required for the maintenance
of normal consciousness and normal sleep-wake cycles:
The classical intercollicular high mid-brain transection
(cerveau isole) produces hyper-somnia and SWS (6). In
chronic preparations, there is an eventual return to a
desynchronized EEG and increased activity awakening
even if the posterior diencephalon is damaged by the
lesion. Recovery of the awake EEG probably is due to
intact lateral hypothalamic regions or mesencephalic-
pontine limbic structures. Isolated lateral hypothalamic
lesions result in somnolence in cats, whereas in monkeys
they cause both hypokinesia and somnolence (72). Ranson
thus proposed that the posterolateral hypothal-amus is
necessary in maintaining the normal waking state and that
removal of downward-projecting systems results in
hypersomnia (73).
Nauta showed that lateral-caudal transection of the
hypothalamus but not mamillary or rostral lesions caused
somnolence (57). Transections at the preoptic-
suprachiasmatic level resulted not only in persistent
wakefulness but also in sham rage. He suggested that
media forebrain fibers, terminating in and traversing the
lateral hypothalamic area, were necessary for maintaining
cortical wakefulness. Bilateral posterior hypothalamic and
subthalamic lesions, destroying the ventromedial nucleus
of the thalamus, posterior hypothalamic nuclei, MFB, and
mamillothalamic tract, cause somnolence and an increased
arousal threshold (54). Fifty percent of the animals recover
from the somnolent state but remain hypokinetic.
Recovery from somnolence indicates that the continued
hypokinesis reflects a continued depression of pathways of
which the rostral reticular formation is only one part. Stud-
ies by Shoham and Teitelbaun (81) have demonstrated that
lateral hypothalamic lesions, which destroy the
ventromedial nucleus, MFB, and inferior thalamic
radiations, also cause somnolence and hypokinesia.
Cortical high voltage slow waves persist in all animals, but
subcortical recordings indicate the presence of organized
states of sleep and waking. These animals demonstrate
hypokinesia and decreased endogenous arousal similar to
humans in a persistent vegetative state. Even when
engaged in automatic motor acts, cortical electrical activity
remains slow. Thus, persistent hypokinesia represents
continued subcortical activity functionally disconnected
from the cortex.
A neurochemical basis of sleep was first proposed by
Jouvet (27). He noted that monoamines induced and
maintained certain sleep periods. Serotonin from the raphe
nucleus induced and maintained SWS by acting on the
preoptic-basal forebrain areas, whereas norepinephrine,
from
the locus coeruleus, was thought to play a similar role in
REM sleep. Serotonin was further believed to induce REM
sleep by acting on the locus coeruleus. Thus, serotoninergic
raphe neurons and noradrenergic cells of the dorsal pontine
tegmen-tum regulated sleep directly or indirectly by acting
on other neurotransmitter systems. Although there are
various data to support these contentions, there are also
contrary results in which marked decreases in serotonin
after parachloro-phenylalanine administration and MFB
lesions did not specifically disrupt sleep (48, 49).
A more complex mechanism of interactive reciprocal
control mechanisms has been proposed. It implies that
differing abnormalities may cause hyper- or hyposomnia.
Hernandez-Peon et al. (22) implicated the importance of a
cholinergic reticular system in the induction of sleep, and
Jouvet (27) believed that cholinergic-monoami-nergic
interactions help regulate sleep.
There are four major groups of cholinergic (choline
acetyltransferase-positive) cells in the central nervous
system (64, 73): (a) rostral column (basal forebrain), (b)
caudal column (mid-brain/pons), (c) local circuit neurons in
dopa-mine-rich forebrain areas, and (d) motor neurons. The
rostral portion (medial septal nucleus, preoptic area, rostral
substantia innominata) of the basal forebrain cholinergic
system primarily innervates the cingulate gyri and other
telence-phalic limbic structures (5). The cholinergic soma
in the brain stem are most prominent in the dorsolateral
pontine tegmentum. Rostrally these cells are seen in the
periaqueductal gray matter, which merges with the
cholinergic soma of the nucleus parabrachialis dorsalis.
Smaller populations of cholinergic cells are scattered in the
tegmental reticular formation. A6 noradrenergic cells of the
locus coeruleus are cholinoceptive as indicated by the
positive acetylcholinesterase histochemistry (33). Similarly
the raphe nucleus also seems to be cholinoceptive.
Retrograde degeneration of the cholinoceptive raphe
neurons is seen after MFB radiofrequency lesioning. The
existence of two antagonistic cholinergic systems has been
proposed by Jouvet (27). The first consists of a ventral
tegmental pathway that follows one course of the MFB
from the preoptic area and lateral hypothalamic area to the
midbrain. Injection of acetylcholine into this area results in
the induction and maintenance of sleep. Lesions of this area
are followed by insomnia. The cholinergic giant cells of the
pontine reticular formation are involved in the regulation of
REM sleep onset through interactions with both the
cholinoceptive locus coeruleus and raphe nucleus.
 The simplistic view that monoamines are the primary
sleep generators is not supported by neurochemical
evidence indicating more complex regulatory mechanisms.
Further, electro-physiological data do not support a
simplistic monoamine theory that is based on one-to-one
interactions between the raphe and locus areas. The firing
rates of locus coeruleus and raphe cell groups do not
temporally correlate with specific sleep states, although
these cell groups probably play a permissive role in SWS
and REM sleep. There is, however, an antagonistic
relationship between serotonin and norepinephrine in sleep-
wake regulation (49). Lesions of the raphe nucleus, which
receives dendritic connections from the locus coeruleus,
cause insomnia and increased norepinephrine turnover. An
increase in SWS and REM sleep is seen with locus
coeruleus or dorsal noradrenergic bundle lesions; these le-
sions result in a concomitant decrease in fore-brain
norepinephrine and increase in 5-hydrox-yindoleacetic acid.
The increased serotonin turnover is probably secondary to
loss of direct or indirect noradrenergic inhibiton of raphe
neurons.
The circadian rhythm of the sleep-wake cycle is
regulated by the suprachiasmatic nucleus (SCN). This
nucleus is unique in that it receives direct retinal
projections (45, 47). Lesions of this nucleus cause the loss
of cortisol, drinking, and motor circadian rhythms (46).
Swanson and Cowan have traced SCN afferents to the
ventro-medial and arcuate nuclei, and thus this region may
serve as a primary clock for neuroendocrine as well as
behavioral rhythms (44, 62, 93). Stimulation of this area
also alters the oscillatory activity of the lateral
hypothalamic neurons (63).
Bilateral lesions of the SCN completely eliminate the
circadian rhythm of the sleep-wake cycle but have no effect
on REM or total sleep time (24), whereas anterior
hypothalamic lesions have no effect on circadian rhythms
(25). This has been confirmed by Mouret et al. (52), who
showed that bilateral SCN lesions do not quantitatively
affect SWS or REM sleep. Although the majority of SCN
neurons are inhibited by ionto-phoresed serotonin and
stimulated by acetylcho-line, there is no definitive effect of
raphe lesions on sleep-wake cycle rhythms (61).
Clinical Disorders
Hypersomnia
Hypersomnia can be defined as a subacute or chronic
state of prolonged periods of normal sleep. Hypersomnic
patients can be roused but
lapse rapidly into sleep. Clinical cases of hyper-somnia
have been associated with a wide variety of third
ventricular lesions. With the majority of these lesions
(Table 7.4) there has been widespread infiltration or
destruction of the hypo-thalamus or marked thalamic
invasion. In certain instances (12, 37), more focal lesions of
ventromedial or lateral hypothalamic nuclei were noted,
lesions in regions that interrupt multiple fiber tracts
contributing to the MFB. The cases of hypersomnia with
encephalitis (12, 75) have shown predominant changes in
the caudal and posterior portions of the hypothalamus. It
seems, therefore, that the more posterolaterally the lesion
occurs, the more likely hypersomnia will result. This is in
accord with the experimental data.
Akinetic Mutism
Akinetic mutism, also termed the persistent vegetative
state, is a term originally coined by Cairns (7) to describe
the clinical syndrome of apparent wakefulness with the
absence of behavioral cortical function in patients with nor-
mal sleep cycles. The term is sometimes used to describe
patients who are in fact awake but vary in activity from
absolute akinesia and mutism to a hypokinetic state without
mutism. The syndrome has been reported with a wide
variety of lesions, including those in the midbrain/rostral
pons tegmentum, the posterior third ventricle (7, 55, 71, 76,
77), the bilateral cingulate gyri (2, 9, 11, 14, 59), and the
bilateral basal ganglia (36).
Experimental studies on akinetic mutism have yielded
conflicting results. Mutism with and without akinesia has
been produced in dogs and cats after periaqueductal gray
lesions (83, 84). These results were not confirmed in
subsequent experiments in which caudal periaqueductal le-
sions resulted in neither akinesia nor mutism (83).
Akinetic mute states reported with anterior cingulate gyri
lesions have also been cast into doubt in light of other
experimental and clinical data. Bilateral ablation of area 24
in monkeys does not result in akinetic mutism (1, 13, 19,
31, 82, 87, 88, 96). In fact, normal or increased
vocalization has been seen in monkeys after bilateral
cingulate lesions (13, 19, 31, 41, 85-88, 92). The majority
of human studies have failed to demonstrate an effect on
speech production, and bilateral anterior cingulate gyral
lesions have not produced akinetic mutism (38, 68, 69, 98).
The reported cases of akinetic mutism in humans after
bilateral cingulate lesions were cases in which the akinetic
mutism resulted from
anterior cerebral artery occlusion or aneurysmal
hemorrhage and rupture. This indicates that there was
more widespread damage and it thus seems unlikely that
akinetic mutism results from isolated cingulate lesions.
Akinetic mute states have also been reported with lateral
hypothalamic lesions, which may
also result in aphagia and adipsia (18, 43, 72). This area is a
region of convergence and interconnections between the
limbic-forebrain and the limbic-brain stem regions (48, 50,
51). This area contains the lateral and MFBs, which carry
the fiber tracts mentioned earlier as well as the
pallidohabenular efferents that traverse the lat-
eral hypothalamic area and the ventromedial nucleus
(VMN) (58). It has recently been suggested that akinetic
mutism is not the result of intrinsic hypothalamic nuclear
damage but of ascending A8/A9/A10 dopaminergic fibers
in the MFB. In these studies akinetic mutism was
experimentally produced by 6-hydroxydopamine injections
into the MFB, substantia nigra or ventral teg-mental area
and was reversible by apomorphine. However, (a) 6-
hydroxydopamine is a nonspecific agent affecting all
catecholaminergic neurons, (b) MFB injections affect
multiple ascending and descending projections (60, 95), (c)
reversal of this state may represent nothing more than apo-
morphine-induced stereotypic behavior, and (d)
apomorphine is a mixed dopaminergic agonist-antagonist as
well as a serotoninergic agonist in receptor assays. Indeed,
the administration of spiroperidol, a dopaminergic
antagonist, causes no akinesia or alteration of
electromyographic activity in rats (28). Although Ross and
Stewart have reported the successful use of bromocryp-tine
in akinetic mutism (77), we have been unable to replicate
this.
Akinetic mutism associated with bilateral basal ganglia
lesions is clinically similar in certain respects to akinetic
mutism seen in association with third ventricular lesions.
These patients demonstrate apparent cognitive impairment
with marked hypokinesia or akinesia. Unlike the index case
of Cairns (7), they are able to perform complex behavioral
tasks after stimulation, and on further careful testing they
differ from Cairns' case in that they show multiple deficits
of cognitive functions. Laplane et al. (36) have proposed
that the apparent "psychic akinesia" in these patients is
secondary to interruption of the pallidohabenular afferents.
However, their patients had normal visual-spatial activities
in spite of isolated pallidal lesions, which have been
previously reported to cause deficits in visual-spatial tasks
(91). The explanation for this discrepancy is unclear.
In summary, akinetic mutism has been reported with a
variety of lesions and its association with third ventricular
lesions probably results from improper execution of motor
planning (40). Thus, perceptual abilities and motor pro-
grams are intact. Pathologically, akinetic mutism probably
results from the interruption of multiple ascending and
descending activating fibers that traverse the lateral and far
lateral hypothalamic regions.
Clinical Correlations
Table 7.4 details all of the cases of akinetic mutism with
or without hypersomnia for which
there are sufficient clinical data and either x-ray or
pathological data. Lesions of the third ventricle and
surrounding structures in humans that cause abnormalities
of consciousness fall into three categories: akinetic mutism,
hypersomnia, and akinetic mutism with hypersomnia. The
table includes only those cases in which there was no
evidence of increased intracranial pressure. Further, where
patients were said to be apathetic, this was interpreted to
indicate a degree of hypokinesia. In a lesser number of
patients with third ventricular lesions, other related clinical
abnormalities of hypothalamic dysfunction were seen.
Hypersomnia or akinetic mutism with hypersomnia are
much more common than akinetic mutism alone. A review
of the available pathological data does not allow us to
determine the localization of discrete lesions causing
hypersomnia with or without akinetic mutism. The few
cases of pure akinetic mutism with bilateral pallidal lesions
were investigated only by computerized tomography, thus
not eliminating the possibility of microscopic pathological
changes elsewhere in surrounding third ventricular struc-
tures.
Akinetic mutism alone or in association with
hypersomnia is, in general, seen with less extensive lesions,
although there is a fair degree of overlap. Therefore, it
seems that akinetic mutism and hypersomnia represent a
continuum of clinical dysfunction associated with third
ventricular lesions.
Conclusions
The alterations of consciousness associated with lesions
of the third ventricle are hypersomnia and akinetic mutism.
These conditions constitute a clinical spectrum of
abnormalities of normal arousal and attending mechanisms.
These deficits result primarily when there has been
interruption of multiple ascending and descending fibers in
the medial (and perhaps lateral) forebrain bundle. The
resulting deficit is probably dependent upon the severity of
the insult as well as its localization, i.e., hypersomnia
without akinetic mutism is more apt to occur after large
posterolateral hypothalamic lesions, whereas more discrete
lateral lesions (or far lateral lesions) produce akinetic
mutism. The neu-rochemical mechanisms and specific
pathways involved in the pathogenesis of these abnormal-
ities are unclear and can only be inferred from the
experimental data. It seems that the basal "tone" is such
that, without excitatory arousal systems, we would be
asleep all the time. Experimental data indicate that
acetylcholine is both
inhibitory and excitatory with regard to arousal; the
cholinergic cells in the pontine giant cells probably
facilitate sleep, whereas descending ax-ons from the basal
forebrain cholinergic activating system that terminate in
the posterolateral hypothalamus are probably involved in
arousal. Similarly, serotoninergic input from the raphe
facilitates sleep and cortical synchronization, whereas
noradrenergic input from the locus coe-ruleus inhibits
sleep. The role of dopaminergic input is unclear, as is the
role of the suprachias-matic nucleus. The reported
insomnia that is said to occur with anterior lesions may be
secondary to interruption of raphe efferents to the
suprachiasmatic region; however, this is not at all clear.
There should, however, be a rational mechanism for
instituting pharmacological therapy for patients with
akinetic mutism or hypersomnia in association with third
ventricular lesions that are not surgically accessible or are
unresponsive to operation. We propose the use,
sequentially, of three different classes of pharmacological
agents that have a theoretical basis for causing arousal.
The first of these is methysergide, a serotoninergic
antagonist. The rationale for this is that interruption of
raphe outflow results in insomnia with a concomitant
increase in norep-inephrine turnover, and methysergide
therapy thus may result in arousal. Second, physostig-
mine, a cholinesterase inhibitor with little tox-icity, can be
tried to increase basal forebrain cholinergic drive. From
the clinical trials of this drug in Alzheimer's disease (94),
there seem to be no "sedating effects" of this drug. This
indicates that the sleep-facilitatory role of the pontine giant
cells may be minimal. Third, as noradrenergic input seems
to have an overall effect of decreasing sleep, it would then
be appropriate to use either a monoamine oxidase A
inhibitor or another nonspecific agent that increases central
noradrenergic drive. Whether more specific alpha or beta
adrenergic agonists would be of benefit is unclear as the
pharmacology has not been further defined.
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8
Deep Veins
Robert R. Smith, M.D., Robert A. Sanford, M.D., and Henry H. Schmidek, M.D.
It must be a tribute to humanity's inquisitive nature that
Galen and his followers were able to outline the system of
veins and arteries on the internal surface of the brain. In a
society in which human dissection was banned, it was al-
most 1500 years later, during the Renaissance, that
Vesalius, Michelangelo, and da Vinci were able to confirm
and elaborate upon these early observations. William
Harvey's work, published in 1628, provided physiological
significance. Kaplan (30) and Browder et al. (7) further
elucidated this system via stereoscopic examination and,
finally, the angiographic methods introduced by Moniz (35)
became a powerful diagnostic, as well as scientific, tool for
anatomical studies.
From the traditional viewpoint, the cerebral venous
system can be divided into three primary systems. (a) The
deep cerebral veins drain blood away from the midline
structures, the deep white matter, the basal ganglia, and the
diencephalon toward the superficial venous system and
venous sinuses. (b) The superficial veins coalesce on the
pial surface and convey blood from the outer zone of 1 to 2
cm of cortex into larger veins that communicate finally with
the dural venous sinuses. (c) The cranial dura mater is
composed of two layers that split and receive the
contribution from both the superficial and deep venous sys-
tems. As a result of development of the telen-cephalon in
humans and primates, the deep cerebral veins are covered
and obscured, although for the most part they also drain
major neuronal masses. The deep venous system is, by
common
agreement, that system which drains into the great cerebral
vein. This structure, the vein of Galen, is a short vessel,
about 2 cm in length, that originates under the splenium of
the corpus callosum from the union of the two internal cer-
ebral veins. These two veins and those that empty into it are
of prime concern to the third ventricular surgeon. The great
cerebral vein also receives blood from the basal veins as
well as branches from the pericallosal vein, the internal
occipital vein, the posterior mesencephalic vein, and the
precentral cerebellar and superior ver-mian veins. Thus,
venous obstruction in the third ventricle may also be
accompanied by venous stasis or venous infarction in the
posterior cranial fossa.
Anatomy of the Deep Venous System
The internal cerebral veins are formed at the level of the
interventricular foramen by the union of the anterior septal
and the thalamostri-ate veins (Fig. 8.1). The internal
cerebral veins pass posteriorly, parallel to each other
entering the tela choroidea of the third ventricle. From here,
they pass through the velum interpositum to the level of the
splenium of the corpus callosum. At this point or slightly
below it, they join with the basal veins of Rosenthal to form
the great vein of Galen. The vein of Galen passes first
inferiorly and then superiorly before entering the straight
sinus. The internal cerebral vein has few direct tributaries
of its own. However, one or two direct lateral veins may
pass from the thalamus, caudate, or choroid plexus of the
lat-
 Figure 8.1. Structural relationship of the deep veins to the ventricular system.

eral ventricles to enter the internal cerebral vein directly.
The thalamostriate vein or posterior terminal vein drains
the caudate nucleus, internal capsule, and deep white
matter of the posterior frontal and parietal lobes and is
formed by two main veins, the anterior and posterior
terminal veins. The posterior terminal vein, or caudate
vein as it may be called, originates at the level of the
atrium, passes in the groove between the caudate nucleus
and thalamus anteriorly, and receives transverse caudate
veins and medullary veins from the body of the caudate
nucleus and deep white matter of the posterior, frontal, and
parietal lobes, respectively, and the striate veins from the
lentiform nucleus. The thalamostriate vein passes through
the intraventricular foramen, creating the angiographic
landmark, the
 venous angle. At that point, the thalamostriate vein is
joined by the anterior terminal vein and the superior
choroidal vein. The thalamostriate vein is crossed at the
intraventricular foramen by the choroid plexus of the lateral
ventricle, which passes posteriorly in the interventricular
foramen to enter the third ventricle. The anterior septal vein
joins the thalamostriate somewhat more medially and
inferiorly, passing usually superior to the choroid plexus
(9).
The anterior cerebral veins, formed by the union of
several intramedullary veins, drain the deep white matter of
the frontal lobe. Uniting anterior to the head of the caudate
nucleus, these usually form one vein, the anterior septal
vein, which runs medially, curving along the septum
pellucidum to pass lateral to the columns of the fornix,
where it joins the ipsilateral thalamostriate vein forming the
internal cerebral vein.
The superior choroidal vein courses over the superior
aspect of the thalamus beneath the choroid plexus of the
lateral ventricle and terminates in the internal cerebral vein
or the thalamostriate vein, providing the major venous
drainage of the plexus.
In the roof of the lateral ventricle, there are several veins.
For the most part, these pass across the roof, draining into
the internal cerebral vein. Two of these have names: the
direct lateral vein and the veins of the posterior horn. The
veins of the thalamus drain into the internal cerebral vein,
also thalamostriate veins. These enter the internal cerebral
vein inferiorly. From the lateral position, the atrial veins
course along the floor of the atrium of the lateral ventricle
to enter the internal cerebral vein just before the two join.
The internal cerebral vein then receives the pineal vein, a
precentral cerebellar vein, and a posterior ventricular vein
before joining the basal vein of Rosenthal (38).
In the peripheral circulatory bed, 70 to 80% of the blood
volume at any one time is housed in the venous system.
Thus, if the same relationship exists within the intracranial
space, min-ute-to-minute changes in intracranial pressure
(ICP) might be almost entirely dependent upon cerebral
venous capacity. If the veins were only passive tubes, then
venous blood volume would change only as related to
events on the arterial side. As it turns out, although
regulation of arterial blood flow and volume varies
considerably, the venous volume remains more or less
constant under normal operating conditions. There is some
evidence that extremes of ICP, such as that associated with
plateau waves, may be due to venous compression. The
pressure in cerebral
veins is only slightly above that of normal cere-brospinal
fluid (CSF) pressure and yet 70% of the blood volume is
found in these structures. Thus, any small change in venous
caliber could produce major changes in volume. Little,
however, is known about the myogenic response in the
cerebral vein. Although a rich adrenergic network is found
along the surface of major cerebral veins, at most only a
few contractile fibers are present. Smooth muscle cells are
occasionally found in large collecting veins but, in smaller
cerebral veins, these are nonexistent. It is known, however,
that cerebral veins contract spasmodically due to a number
of causes, including stroking and manipulation. It may be
that contractile elements in the periendothelial cells cause
the reaction. Venules on the pial surface contract as much
as arteries when noradrenaline is placed upon their surfaces
or when the cervical sympathetic chain is stimulated. Auer
and colleagues showed that beta receptor blockade did not
alter adrenergic venoconstriction but alpha blockade did (2-
4). In normal cats, sympathetic stimulation significantly
decreases ICP through venoconstriction of superficial
vessels. Little is known about intraparenchymal vessels or
the deep venous system. Both substance P and vas-oactive
intestinal polypeptide cause dilation of pial veins and
arteries (19). By contrast, when serotonin is applied to the
outer wall of cerebral veins, these vessels are strongly
constricted (3). The endothelial cells of cerebral veins are
connected by tight junctions and thus there is a biochemical
and enzymatic barrier within the veins like that
demonstrated in arterial beds. Under pathological
conditions, such as trauma, hypertension, embolism,
inflammation, or perhaps neoplasia, the venous barrier may
be disturbed. The venous barrier is also influenced at
increased ICP levels, beginning at 20 and 30 mm Hg.
Venous extravasation occurs during acute ischemia and
other conditions in which the arterial barrier is also broken.
The clinical significance of venoregulatory function and the
blood-brain barrier within the deep cerebral system has yet
to be defined.
Angiographic Patterns
From the diagnostic point of view, the deep cerebral
veins are much more important than the superficial veins.
The angiographic pattern of the veins that drain into the
internal cerebral vein is especially useful in localizing
neoplasms involving the basal nuclei and midline corpus
callosum. These veins are normally midline, placed one
against the other at the roof of the
third ventricle in the tela choroidea. The configuration is
such that they outline the roof of the third ventricle in
lateral projection (46). At the foramen of Monro, the bend
upward slightly and reach their highest point, forming an
elliptical curve, the anterior slope of which is approxi-
mately equal in length and arc to the posterior slope. The
thalamostriate vein, situated in the inferior and lateral
aspect of the lateral ventricular wall, outlines the
approximate size of the lateral ventricle on the
anteroposterior projection. If the ventricles are enlarged,
this arc becomes much wider. If the ventricle is narrowed
due to medial displacement, the arc is flat and reduced.
The angle made by the junction of the thalomostriate vein
and the internal cerebral vein has been called the venous
angle. At this point, the septal vein, extending backward
from the frontal horn of the lateral ventricle on each side,
usually joins the internal cerebral vein. In most cases, this
is situated at the foramen of Monro; occasionally,
however, the junction is much more posterior. This
anatomical variant has been referred to as a false venous
angle. Several methods have been offered to determine
whether the position of the foramen of Monro is normal or
abnormal but, because of aberrations in head shape, the
internal cerebral vein may differ among individuals. The
arc of the internal cerebral vein is also higher in children
than in adults. When doubt exists, it should be remem-
bered that the foramen of Monro is situated directly above
the dorsum sellae. In the case of a false venous angle, the
junction is much more posterior. The internal cerebral vein
is humped when a mass displaces the foramen of Monro
posteriorly.
There are numerous anastomoses between the
superficial veins and the deep veins allowing blood to
flow from one system to the other. Medullary veins are
sometimes seen radiating toward the ventricular wall from
the cerebral hemisphere. Ordinarily, they are not visible
except under pathological conditions, such as arterio-
venous malformations or tumors. Occasionally, a posterior
callosal vein is seen at the junction of the vein of Galen;
this indicates the inferior margin of the splenium of the
corpus callosum.
Little can be said about venous filling. Ordinarily, the
deep cerebral veins fill later than the superficial ones.
However, in about 20% of normal individuals they fill
simultaneously. The deep arteriovenous circulation time is
about 4.25 seconds whereas the carotid-jugular time has a
mean about twice that long. A prolonged circulation time
is associated with low carbon dioxide
tension, and neoplasms may produce local slowing of the
circulation. Diffuse increased ICP may also slow total
circulation time. A regional decrease in the circulation time
may be caused by tumors that shunt blood or cerebral
infarction associated with the so-called luxury perfusion
syndrome, status epilepticus, and, of course, arteriovenous
fistulas (46).
The position of the internal cerebral vein is a reliable
indication of midline shift and hernia-tion. The vein of
Galen is less reliable because it is fixed as it joins the
straight sinus. The internal cerebral vein can be recognized
on the anteroposterior view of the angiogram by tracing the
thalamostriate vein to the anterior portion of the internal
cerebral vein and then following it upward. If the internal
cerebral vein is shifted and the anterior cerebral artery is
not, there is a fair indication that a tumor is situated deeply,
often in the posterior frontal region or in the thalamic area.
If the vein is displaced more than the anterior cerebral
artery, the mass is probably situated posteriorly. If the
artery is shifted more, the mass is more anterior.
The configuration of the deep veins may be helpful in
defining the position of tumors near the midline. Those
anterior to the venous angle cause humping of the internal
cerebral vein and posterior displacement of the venous
angle (Fig. 8.2). When there is elevation of the septal vein,
the major tumor mass usually occurs anterior to the
foramen of Monro (Fig. 8.3). The internal cerebral veins
divide the thalamus into an upper one-third and a lower
two-thirds. Mass lesions
Figure 8.2. "Humping" of the internal cerebral vein and
distortion of the thalamostriate vein due to a large left
frontal tumor associated with tuberous sclerosis.

Figure 8.3. Elevation of the internal cerebral vein and
septal vein due to a large pituitary adenoma.
within the thalamus elevate the thalamostriate vein, causing
opening of the venous angle. There may also be separation
and midline displacement of the internal cerebral veins.
Tumors of the pineal gland cause elevation of the posterior
portion of the internal cerebral vein, usually without
displacement of the basal vein of Rosenthal (46).
The midline veins are useful in delineating and preparing
surgical approaches to a third ventricular mass. Colloid
cysts of the anterior-superior portion of the third ventricle
usually cause flattening of the internal cerebral vein in its
posterior portion while the anterior one-third describes a
sharp curve concave downward. When the cyst projects
predominantly into one lateral ventricle, the internal
cerebral vein is flattened throughout its entire length on
both sides. Sometimes there is elevation of the septal vein
on the side toward which the cyst protrudes. On the
contralateral side, the septal vein may be lower.
Fortunately, with the current availability of multiple
imaging systems, diagnosis of corpus callosal masses does
not depend upon angio-graphic data exclusively. However,
the chief an-giographic feature of these neoplasms is eleva-
tion of the pericallosal artery with depression of the internal
cerebral vein. There may be closure of the venous angle
(Fig. 8.4). Likewise, there is rarely need today for attention
to the deep veins in pituitary neoplasms. However, large
pituitary lesions cause elevation of the internal cerebral vein
as well as the septal vein (Fig. 8.3). Upward displacement
of the basal vein confirms subten-
Figure 8.4. Closure of the venous angle due to a large
frontal lobe metastasis.
torial extension of these lesions. Angiography is still useful
to demonstrate hypertrophied choro-idal vessels, including
the choroidal vein, which develops hypervascularity in
neoplasms such as intraventricular tumors and papillomas,
rarely encountered in the third ventricle. Angiography and
venography may also be useful in differentiating intraaxial
from extraaxial neoplasms that invade the third ventricle.
Angiography is useful in evaluating cranial base brain stem
lesions. Posterior displacement of the basilar artery or the
anterior pontomesencephalic venous plexus is seen with
extraaxial masses that arise from the cranial base. Intrinsic
brain stem masses displace these vessels anteriorly.
Disorders of the Deep Venous System
Although the disorders that afflict the deep venous
system are not confined to pediatric age group, these
diseases have been recognized more often in infants,
neonates, and young children. In neonates and especially
among premature infants, intracranial hemorrhage, notably
the sub-arachnoid variety, has been one of the most com-
mon causes of death and morbidity. In this age group,
bleeding from the subependymal matrix at the level of the
foramen of Monro and in the head of the caudate nucleus is
the most common cause, occurring in perhaps as many as
50% of those with a birth weight of less than 1500 g (14,
15). Hemorrhage from the choroid plexus occurs in
premature infants, but much more commonly in full-term
infants (18). The predisposing factors leading to
hemorrhage in these regions have
been widely debated. At the foramen of Monro, the
thalamostriate vein and the choroidal veins join at an acute
angle forming the internal cerebral veins. It was reasoned
that hypoxemia, hy-percarbia, and the need for mechanical
ventilation predispose this angle to torsion, hyperemia, and
subsequent hemorrhage (17). Others have implicated the
use of respirators and their role in raising intracranial
venous pressure. At present, although the cause of the
condition is unknown, hypoxia, hypercarbia, and acidosis
in premature infants apparently set the stage for the
development of the disorder (13, 17).
The clinical presentation may fall into one of three
categories. A rapid deterioration in neurological function
associated with apnea, seizures, and coma is the most
devastating variety. The second is characterized by
intermittent signs and symptoms with changes of tone and
spontaneous movement. The third category is disclosed by
screening low birth weight infants with computerized
tomography (CT) or ultrasonography and apparently the
disorder is asymptomatic in these individuals (21). Most
physicians favor ultrasonic scanning of the premature
infant in the neonatal unit in preference to CT, but both
are useful diagnostic tools. Because the head circum-
ference often does not change with primary infant
intraventricular hemorrhage, clinical signs may be late-
appearing. The hemorrhages may be graded on the basis
of radiographic and ultrasonic findings. In Grade 1, the
hemorrhage is purely subependymal. In Grades 2 and 3,
intraventricular hemorrhage with and without ventricular
dilatation occurs. In Grade 4 hemorrhage, the mass of
hematoma dissects into the parenchymal substance of the
brain. Mortality is highest in those infants with the lowest
birth weight and the most severe hemorrhage (15).
Progressive hydrocephalus requiring treatment is
associated with the higher grades (15).
Figure 8.5. A. Obstruction of the foramen of Monro and
Angiomas and arteriovenous malformations affect the hydrocephalus due to an enhancing mass in the lateral and
deep venous system. Nodular high density masses with third ventricular wall. B. A large dilated internal cerebral
marked enhancement after intravenous contrast material vein draining a frontal parietal arteriovenous malformation.
are hallmarks of this diagnosis. Angiography normally Although the diagnosis was suspected on the basis of CT,
reveals a pyramid-shaped mass of vessels situated the operative approach to midline enhancing lesions should
not be undertaken without angiography.
peripherally, but feeding toward the deep veins. Occa-
sionally, massive dilatation of midline veins may block
the foramen of Monro or aqueduct of Sylvius, leading to cified in some cases of the Sturge-Webber syndrome (37),
ventricular enlargement (Fig. 8.5). In children, venous leading to the hypothesis that thrombosis in the deep
angiomas and hemato-mas have produced seizures and system may contribute to the diffuse cerebral signs
subarachnoid hemorrhage and obstructed midline CSF occasionally associated with this disorder.
pathways. Probst also noted that the deep medullary veins Although aneurysms of the vein of Galen are not
and internal cerebral veins were not opa- contained within the third ventricle, the arteries and veins
that make up this malformation affect the third ventricle
structurally. The greatly enlarged venous aneurysm draws
arterial feeders from the anterior superior border, receiving
both anterior cerebral arteries, the lenticulostri-ate arteries,
thalamic perforators, and both the
anterior and the posterior choroidal arteries. Occasionally,
the superior cerebellar arteries may be involved. In infants,
the greatest contributor seems to be the posterior choroidal
artery, which is situated inferiorly and laterally. In older
children, however, these vessels are located anteriorly and
superiorly. Greatly dilated veins resting upon the posterior
third ventricle and the cerebral aqueduct vein may obstruct
outflow tracts, producing hydrocephalus. In older children,
subarachnoid hemorrhage has been a complicating feature.
In neonates, congestive heart failure is a common mode of
presentation.
Angiographic studies confirm the CT diagnosis in all but
those in whom the aneurysm has clotted, which presents as
an avascular mass. In these cases, the deep venous system,
including the internal cerebral veins, vein of Galen, and
straight sinus, may not fill on the late phase of the
angiogram. It is presumed that these vessels are obstructed
by thrombus (49).
Age and presentation are important in making
therapeutic decisions about vein of Galen malformations.
Shunting may be all that is necessary in older children
presenting with hydrocephalus. The dilated arteries and
veins may also be approached directly interhemispherically,
although mortality and morbidity are extremely high (48).
After coagulating and dividing perforating branches from
the anterior cerebral arteries, the surgeon divides the corpus
callosum. In the parietal region, the two choroidal arteries
are usually seen entering the large dilated venous channel
anterolaterally. These major feeders should be clipped or
coagulated. Once nutrient arteries have been occluded, the
vein of Galen progressively shrinks although it usually re-
mains quite bulbous (48). Removal of the dilated venous
channel, as advocated by Smith and Do-nat, is usually not
feasible or warranted. Unfortunately, in many cases, other
congenital central nervous system lesions are present and a
successful outcome does not necessarily follow. Many of
these infants, even though the malformation has been
successfully obliterated, are mentally or physically
retarded.
Isolated thrombosis of veins in the deep cerebral venous
system is being more frequently recognized. Information
obtained in the operating room correlates poorly with
occlusion due to trauma or infection. In the latter instance,
there is widespread involvement of several members of the
deep venous system and anastomotic channels. This often
leads to so-called venous infarction. Spontaneous occlusion
of the deep cerebral veins is largely a disorder, again, of
infancy and childhood. In our cases, the disorder was
associated with diarrhea and vomiting (40). The usual
history is that of a poorly developed, undernourished child
appearing in acute distress. The infant is usually dehydrated
and febrile, and the anterior fontanelle bulges. Serum
electrolytes are often abnormal, and it is not unusual with
deep venous occlusion to find cranial nerve abnormalities.
Often, the thrombosis extends into the straight sinus, the
vein of Galen, and the internal cerebral veins.
Intraventricular hemorrhage in the lateral and third
ventricles and subarachnoid hemorrhage have been seen in
two of our cases. There is often severe cerebral edema.
Because the cerebellar system drains into the vein of Galen,
widespread deep venous thrombosis often leads to venous
infarction in the cerebellum. Isolated internal cerebral vein
thrombosis has been described, often without neurological
deficit. Embolic occlusion of the internal cerebral veins has
also been described in over 20 cases. Infarction in the
medial basal ganglia and thalamus with intraventricular
hemorrhage has been the usual morphological pattern (47).
Thrombosis of the internal cerebral vein is also associated
with birth injury.
Spontaneous occlusion of the deep cerebral vein is
extremely rare. Again, dehydration and vomiting are the
usual underlying causes, although Towbin (47) described
deep vein occlusion and bilateral sinus thrombosis with
occlusion of the confluence in a 74-year-old man with
multiple sites of thrombus. He presented with progressive
weakness, paralysis, and coma. In that case, congestive
heart failure was a predisposing factor along with debility
and dehydration. Unaccountably, the disorder affects fe-
males with almost twice the frequency as males, possibly
because of the use of oral contraceptives. Likewise,
occlusion of superficial cerebral veins and sinuses has been
associated with systemic cancer. For some unknown
reason, these disorders spare the deep system.
Surgical Venous Anatomy
The pathological process and its anatomical location
within the third ventricle largely dictate the operative
approach. Because of the essential nature of the central
venous structures, each operative method must successfully
deal with these veins.
Anterior third ventricular lesions may be approached
safely by various methods. The lamina terminalis approach,
although of historical significance (22, 28, 32, 43), gives
extremely limited
 exposure and therefore has been abandoned by most
surgeons. Recently, Suzuki redescribed this approach and
reported 17 cases without operative mortality (44).
The transcortical approach, as initially advocated by
Dandy in 1933, provides easy access to the lateral
ventricle via a small cortical incision (16). In the presence
of hydrocephalus, cortical collapse with removal of CSF
may complicate surgical efforts due to tearing of the
midline draining veins.
This approach, however, obviates sacrificing major
parasagittal draining veins. Only the small lateral veins of
the roof of the lateral ventricle need to be sacrificed, and
this is usually well tolerated. Access to the third ventricle
is limited, however, via the foramen of Monro. In
pathological conditions such as the colloid cyst that pen-
etrates the foramen and is located primarily within the
lateral ventricle, the transcortical approach has great
appeal.
To enter the third ventricle from the lateral ventricle,
the foramen usually must be enlarged either at the
expense of the columns of the fornix anteriorly (31) or at
the expense of the thalamo-striate vein posteriorly (26).
Should damage occur to the opposite fornix by surgical
manipulation or compression by tumor, severe short term
memory deficit may occur (24, 27, 29, 45). Some
surgeons, interestingly, report no memory deficit with
bilateral injuries to the columns of the fornix (6, 10, 46).
Bengochea performed bilateral section of the fornix for
control of epilepsy in 12 patients without memory loss Figure 8.6. Transcallosal approach to the third ventricle
(6). showing the thalamostriate vein and internal cerebral vein.
Posterior extension of the foramen by section of the In this case, the thalamostriate vein has been coagulated
thalamostriate vein was without significant sequelae in and divided to enlarge the foramen of Monro posteriorly.
Hirsch's series of 10 patients (26). In our own series, only
1 venous infarction has occurred among 5 patients in lows the pericallosal arteries to be separated and the corpus
whom the thalamostriate vein was sacrificed (Fig. 8.6). callosum sectioned in a bloodless fashion. At this point,
There is a rich anastomotic network between the deep most authors (20, 31, 39, 41) advocate entrance into the
medullary veins and the superficial medullary veins that lateral ventricle, with access into the third ventricle via the
connect to pial cortical veins (28). In most cases, the foramen of Monro. The same anatomy is now encountered
thalamostriate vein may be taken safely. It drains a as previously described. Section of the thalamostriate vein
portion of the lenticular nucleus and thalamus but is our preferred method of enlarging the foramen.
relatively little of the internal capsule (42). Posterior The advantage of the trans-corpus callosal approach is
enlargement of the foramen of Monro increases exposure, threefold: either foramen of Monro or both may be
but the angle of visibility within the third ventricle may inspected by veering left or right through the septum, small
severely restrict the surgeon's options. lateral ventricles do not hinder exposure, and the angle of
The venous anatomy is also important in approaching surgical exposures may be varied in an anterior or posterior
the third ventricle through the corpus callosum. The direction, thereby increasing the amount of third ventricle
angiogram should be carefully reviewed and the initial inspected. The choroid plexus overlies the thalamostriate
interhemispheric exposure planned to avoid sacrifice of vein in most cases and careful removal or retraction is
major parasagittal draining veins (1). The operating necessary to prevent troublesome bleeding.
microscope al- Instead of deviating from the midline and entering the
lateral ventricle, continued midline
dissection between the f ornices allows direct entry into the
third ventricle (1, 5, 8, 12, 34, 36). Although Walter Dandy
originally described the transcallosal approach in 1922
(16), Busch suggested the interforniceal approach in 1944
(9). This modification exposes the internal cerbral veins,
which must be carefully retracted and spared. Caron et al.
described two cases in which the internal cerebral veins
were obstructed without ill effects during the removal of
pinealomas (11). It is known that extensive venous hemor-
rhagic infarcts may occur in the infant with spontaneous
occlusion of the internal cerebral veins.
The extent of callosal section needed to expose the third
ventricle varies according to the position of the lesion.
Usually 2.5 to 3 cm of incision at the level of the genu is
well tolerated. Corpus callosal section may be used to
expose the posterior third ventricle, but the vein of Galen
must be avoided and the hippocampal commissure should
be preserved to prevent major memory loss (25, 52). Yoshii
et al. presented the case of a 42-year-old woman who
survived spontaneous occlusion of the vein of Galen,
inferior sagittal sinus, and straight sinus (51). George
occluded the vein of Galen safely in two patients harboring
vein of Galen malformations, although the extensive
collateral circulation in these patients may have been
protective (40).
The traditional surgical sanctity of the deep venous
system suggests that these veins may not be sacrificed with
impunity. There is some evidence to indicate that gradual
reduction of the lumen of any major vein may not cause the
same neurological dysfunction associated with abrupt
occlusion. Obstruction due to a large neoplasm seems better
tolerated than surgical occlusion. With reference to the deep
venous sinuses, intra-operative deaths have been reported
after straight sinus ligation. Merli and Carteri (33),
however, resected a large infratentorial menin-gioma that
involved a segment of the straight sinus, and there was no
postoperative complication. As far as the vein of Galen is
concerned, both primates and dogs apparently tolerate ab-
rupt occlusion (23). In a survey of program directors made
by us, however, 47% believed that infarction would follow
surgical occlusion of this deep vein in humans. There is
little information concerning the basal vein of Rosenthal
although hemianopsia has been reported after surgical
occlusion of the internal occipital vein.
Many surgeons question the safety of operative occlusion
of the internal cerebral vein. Thirty-five percent of the
surgeons surveyed believed
that cerebral infarction would follow surgical ligation of
the internal cerebral vein (40). It may be that sacrifice of
this vein is justified if a total resection is to be performed
for a life-threatening neoplasm. As far as the thalamostriate
vein is concerned, an anastomotic system exists between
the deep and superficial system. However, 15% of the
surgeons surveyed felt that venous infarction was to be the
expected sequela of thalamostriate vein occlusion (40).
Thus, these experienced neurosurgeons recognize a definite
risk for venous infarction. For the septal vein and other
communicating veins into the deep system, there is little
information and little evidence that obstruction would
produce any ill effects. Thus, it should a surgical maxim
that the deep veins, unless they must be sacrificed, should
be preserved. The taking of the terminal vein, the
thalamostriate vein, and even the internal cerebral vein can
be accomplished with low risk if the procedure is justified.
Surgical occlusion of the great vein of Galen and even the
straight sinus can be carried out, but apparently with
greater risk.
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9
Pathological Lesions of the Third Ventricle and
Adjacent Structures
Richard L. Davis, M.D.
The region of the third ventricle has a large variety of
tissues and structures and the pathological processes in the
area are extremely varied. The menu of possible lesions is
thus broad. In this chapter we attempt to group lesions by
site, but it must be appreciated that pathological processes
in adjacent areas can impinge on a nearby site.
Mass Lesions within the Third Ventricle
Neoplasms
Astrocytomas
Tumors of glial, most commonly astrocytic, lineage are
the most common neuroepithelial neoplasms in this area.
Their symptoms are amazingly variable, and most
peculiar symptom complexes have been described (18).
Although very difficult to diagnose in the past, the advent
of the computerized tomographic (CT) and magnetic
resonance imaging scanners has made the diagnosis of
mass lesions in this area more attainable in a timely
manner, so that some of our modern therapies can be
given to the unfortunate patients so afflicted.
Juvenile Pilocytic Astrocytoma. One of the most
common tumors to fill the third ventricle and involve
adjacent structures is the juvenile pilocytic astrocytoma,
the astrocytoma most commonly seen in the cerebellum
(42). This tumor most commonly arises from the floor of
the ventricle, although it also may arise from the optic
pathways and impinge on the ventricle (Fig.
9.1) (41). It is a slowly growing lesion and mainly
compresses adjacent structures with only a narrow zone of
invasion (Fig. 9.2). Only exceptionally have these tumors
been reported to undergo malignant transformation (1).
These tumors may also arise from the neurohypophysis,
and the term "infundibuloma" has been applied to these
neoplasms.
The tumors may be grossly cystic, although this feature
is less common here than in the cerebellar examples. They
are often spongy and vary in color from gray to pink.
Histologically, the tumors, like their cerebellar
counterparts, have a biphasic pattern with compact
pilocytic zones, most often around blood vessels, alternat-
ing with looser protoplasmic astrocytic areas, often with
microcysts. There may be considerable variation from area
to area with relation to the prominence of the two
component zones. In addition, in some of these tumors
there are areas that contain what appear to be
oligodendroglia, with cells with a central dark-staining
nucleus and a perinuclear halo. These zones rarely contain
mineral, as is so commonly observed in typical
oligodendrogliomas.
There may be very prominent vascular proliferation; this
may be so prominent that it leads the unwary to "upgrade"
the tumor because of the association of vascular
proliferation with increased growth potential. This
interpretation is unjustified in the case of this neoplasm.
In some examples multinucleate giant cells are seen,
often in association with large granular, apparently
membrane-bound masses, the nature

Figure 9.1. Gross photograph of a juvenile pilocytic
astrocytoma of the third ventricle. The patient had had
symptoms for some years and had undergone a negative
exploration of the posterior fossa. This was, of course,
before modern neurodiagnostic techniques.
Figure 9.2. Low power photomicrograph showing the
relatively sharp border of a juvenile pilocytic astrocytoma.
Although there is no "capsule," the tumor quite abruptly
stops, and normal though compressed tissue is present.
Hematoxylin and eosin; original magnification x 10.
of which is still uncertain. Mitotic figures are distinctly
uncommon, although they have been seen in some of the
posterior optic nerve tumors, some of which have shown
relatively aggressive biological behavior. There is often
involvement of local leptomeninges, although seeding by
this route is almost unknown.
Fibrillary Astrocytoma. Fibrillary astrocyto-mas may
arise from any structure related to the third ventricle. They
are primarily infiltrating tumors, although they may form a
mass lesion as part of their expression. They are most com-
monly solid tumors, although cysts may be present and may
be prominent. In this area they most commonly arise or at
least present as thalamic lesions. Histologically, these
tumors show infil-
tration of the preexisting background tissue by neoplastic
astrocytes that can be deceptively innocent-appearing. But
more commonly, there are varying degrees of anaplasia
apparent in the tumor at the time of its diagnosis. There is a
gradual merging of this tumor with the glioblastoma
multiforme and all degrees of malignancy exist in the
spectrum of this group of neoplasms. In the series of
infiltrating astrocytomas and glio-blastomas studied at
UCSF, there was a clear correlation between the degree of
anaplasia and the median survival (11, 26). As biological
malignancy increases there is a general increase in the
cellularity, the amount of nuclear atypia, the presence of
cytoplasmic variability, the nuclear/ cytoplasmic ratio, the
number of mitotic figures, the amount of endothelial
proliferation, and the presence of necrosis. There is also a
general tendency to an increase in the degree of anaplasia
with time, although there are significant exceptions to this
generalization (10, 11). Thus, although there is often a
progression of a tumor from a moderately anaplastic
astrocytoma to a glioblastoma multiforme over a period of
years, this does not always pertain, and a tumor may retain
its original morphology and growth potential for many
years. In fact, with some tumors, notably the juvenile
pilocytic astrocytomas, the tendency is to retain the
original morphology and the attendant slow growth
potential for the duration of the neoplasm.
Protoplasmic Astrocytoma. Protoplasmic astrocytomas
are relatively rare tumors wherever they occur. They
theoretically arise in gray matter where protoplasmic
astrocytes usually are found, are generally circumscribed at
least early in their development, and (although they are in-
vasive) are early a possibly surgically treatable tumor.
However, too often at the time of diagnosis they have
already become invasive and also have assumed the
morphology in some areas of fibrillary astrocytoma and the
increased growth potential of this lesion. In fact, the
common coexistence of the protoplasmic astrocytoma in a
nuclear area with infiltrating fibrillary astrocytoma in
adjacent white matter is so frequent that this progression is
considered to be expected.
Subependymal Giant Cell Astrocytoma. The
subependymal giant cell astrocytoma is the tumor
associated most commonly with tuberous sclerosis. It is
thus far an exclusively intraventricular tumor composed of
extremely large astrocytes most often with a minimal
background of glial fibers. The cells are very large, 2 to 4
times the size of gemistocytes, and have large vesicular
nuclei with prominent nucleoli. Mitotic
figures may be present, but are usually not prominent.
Very often the mass of cytoplasm and the nuclear character
suggest that the tumor is neu-ronal in origin, and recent
data support the often biphasic nature of this neoplasm.
These tumors, often confused with gemistocy-tic
astrocytomas, have a relatively slowly progressive course.
They most often do not recur, and progression to
glioblastoma multiforme is unknown or at least unreported.
Tuberous sclerosis may present with such a tumor and this
tumor is considered by most to be diagnostic of this
disease. These tumors most often occur in the lateral
ventricles and often slip out easily when encountered,
presenting as "sausages" that easily are removed. Third
ventricular examples of this tumor have been reported;
they are clearly rare, but must be included in the
differential diagnosis of third ventricular lesions, especially
in the neonate or infant. Patients with tuberous sclerosis
occasionally have additional infiltrating brain tumors, so
that a progressive course may be due to the additional
lesion.
Subependymal Glomerate Astrocytoma. Subependymal
glomerate astrocytomas, or sub-ependymomas, are rare
third ventricular tumors. They most commonly arise from
the floor of the ventricle and have been seen in the
company of other rest elements, namely squamous
epithelial rests. They most commonly grow slowly in other
sites, but there are few data relative to their growth rate in
this environment. In other areas they are amenable to total
surgical extirpation, although it must be doubted that this
would be successful in the third ventricle and its sur-
rounds.
From the foregoing it must be appreciated that there is
little experience with this tumor in this site, so that
prognostications based on actual data are not available.
Other Astrocytomas. There is little experience with the
other astrocytomas occurring in this area. Theoretically
any astrocytoma may occur here, but the remaining
tumors, the gemis-tocytic astrocytoma, the astroblastoma,
and the adult pilocytic astrocytoma are so rare that there is
no recorded experience with their biology in this site.
Glioblastoma Multiforme
Glioblastoma multiforme is the most common primary
tumor in the cerebrum of adults and, although it arises
most frequently in the white matter, it commonly early
involves adjacent gray matter and so may involve the
stuctures in and around the third ventricle. This tumor is
usually
rather fast-growing, and even in vigorously treated cases
the median survival is about 1 year. The structure adjacent
to the third ventricle most commonly involved is the
thalamus, with the tumor extending into the third ventricle
from this nuclear mass (Fig. 9.3). As elsewhere, the tumor
is multiform both grossly and microscopically, with areas
of necrosis, softening, and alternating adjacent areas of
increased firmness. These are poorly limited lesions, fading
off into the surround usually without a clear margin. In
cases where the margin is grossly apparent, histologi-cal
examination usually shows this to be false, with infiltration
of the adjacent areas by tumor not appreciated grossly.
Histologically, the tumors are usually quite classical,
with hypercellular areas with nuclear and cytoplasmic
pleomorphism, a background of glial processes, and
vascular endothelial proliferation. Necrosis with or without
the typical pseudopallisading of nuclei may also be present.
In the adjacent areas of infiltration there may be tumor
showing much less anaplasia, and areas of edema and
gliosis may also be present. Mitotic activity may be present,
but is not usually very prominent. In fact, extremes of
mitotic activity suggest that the tumor may be a metastasis
masquerading as a glioblastoma. Primary lung tumors are
particularly prone to this mimicry.
Quite clearly, glioblastoma multiforme arising in the area
of the third ventricle is an almost universally fatal situation.
In this site neither operation nor radiation nor any of the
adjuvant therapies are likely to be greatly successful, and
major physical incapacity and mental impairment are likely
as early consequences and as continuing symptoms. Spread
across the midline is a frequent and not unexpected
occurrence.
Figure 9.3. Gross photograph of glioblastoma multiforme
extending into the third ventricle from the thalamus. Note
that the fornix is also infiltrated.
Ependymoma
Although ependymomas are relatively rare tumors of the
third ventricle, they may arise in the floor, walls, or roof of
this structure. As elsewhere, they are usually relatively
slowly growing mass lesions, with relatively little invasion
of the adjacent tissues. They usually cause symptoms by
compressing the adjacent structures and by blocking the
ventricular system. As with other neoplasms in this area,
removal by surgical means is almost impossible and, even
with the best adjuvant therapy, effective control is not to be
expected.
Grossly, ependymomas are firm to soft, usually delimited
lesions, protruding into the ventricle and compressing
adjacent structures. They are gray to pink and rarely show
either necrosis or hemorrhage. Histologically, they are
usually rather typical ependymomas, with prominent
gliovascular structuring forming the typical per-ivascular
rosettes so commonly seen with this tumor. Less
commonly, ependymal rosettes may be seen, and there may
be prominent areas with a dense background of glial
processes.
Other Neuroepithelial Tumors
Although conceivably any neuroepithelial neoplasm may
arise in this area, all other such tumors are exceedingly
rare, except by involvement by extension. Thus,
neuroblastomas may extend to involve the third ventricular
area, but primary tumors of this type almost never arise
here. So, too, for the medulloepitheliomas, ependymoblas-
tomas, and even primitive neuroectodermal tumors.
Choroid plexus tumors can be found here, and even
gangliocytomas have been reported (5, 15), but they are
unusual.
Germinal Neoplasms
Germinal neoplasms, specifically the germi-noma, were
recognized as occasional tumors that often produced a triad
of clinical symptoms when located in the floor of the third
ventricle (9). This triad includes visual loss, loss of libido,
and diabetes insipidus. When this occurs in young adult
males germinoma is quite likely. Why germino-mas should
involve the floor of the third ventricle is unclear, but they
have as good a reason to arise there as in the pineal body.
More recently other germinal neoplasms have also been
seen in this site, and probably yet others will be described
as time goes on.
The gross and microscopic features are identical to those
of the same tumors as they arise in the pineal body and are
described under "Pineal Area Lesions."
Metastatic Tumors
Metastatic tumors are the most common tumors found in
the brains of adults. Although they may be seen in any site
in the central nervous system (CNS), one of the more
common sites in the third ventricular area is the floor of the
third ventricle and the hypophysis cerebri (Fig. 9.4) (38).
Carcinomas of the lung in men and of the breast in women
are the most frequently seen in these areas, but neoplasms
from other primary sites have also been seen. These tumors
are usually found at autopsy, typically as incidental
findings, but they may present clinically as pituitary tumors
or be found during therapeutic hypophysectomy.
Histologically, they are typical metastases, with necrosis,
nuclear and cytoplasmic atypia, mitotic activity, and often
adjacent vascular endothelial proliferation. However,
pituitary adenomas may show some atypia, and it is only
by being aware of the possibility that one may make the
proper diagnosis if the metastasis is more subtle in its
presentation.
Craniopharyngiomas and Related Cysts
The term "craniopharyngioma" has been used in a
variety of different ways by different authors. Some have
used it to designate any tumor of supposed Rathke pouch
origin, excepting pituitary adenomas, and others have used
it in a more restricted sense of the adamantinomatoid
craniopharyngioma (29). Thus, care must be used with this
term so that correct communication occurs.
The adamantinomatoid craniopharyngioma is one of the
more common childhood brain tumors. It usually presents
as a result of compression of the adjacent pituitary gland,
the hypophysis, or the optic pathways. It may arise within
the sella or be a suprasellar or even intraventricular mass
within the third ventricle (Fig. 9.5). It is usually a slowly
growing tumor, but may present abruptly, perhaps as a
result of hemorrhage within the tumor. Neuroradiographic
studies commonly show mineralization within the mass.
Pathologically, the tumor is grossly multicystic with
several varieties of cyst contents. Some cysts contain flaky,
grumous material, others show liquid or colloid-like
material, and yet others show the "motor oil" fluid so
characteristic of this disease. The tumor is most often
sharply delimited, with a thin, fibrous capsule and firm
gliotic tissue in the adjacent compressed brain.
Histologically, the tumor is most interesting. There is a
delicate fibrovascular stroma, most often with loose
connective tissue, and thin-walled vascular channels. On
this connective

Figure 9.4. A. Metastatic carcinoma from the breast
infiltrating and enlarging the pituitary stalk. B. Metastatic
carcinoma from the lung in a mamillary body. C.
Metastatic carcinoma from the lung in the pituitary stalk.
tissue is a basal layer of columnar epithelium with
transitions to an intermediate stellate layer, which then
shows maturation in one or both of
two directions. There may be maturation to stratified
squamous epithelium, with the production of cysts with
masses of keratin, often with mineralized masses of large
dead keratinized cells (Fig. 9.6), and there may be
maturation toward glandular epithelium, with cuboidal or
columnar epithelium lining the cysts with a liquid or col-
loidal cyst contents. Very often both types of cysts are seen.
The "motor oil" cysts develop in two different ways. They
may arise from cystic change within the stellate layer of
epithelium or from cystic change in the loose connective
tissue. Although rare, a few reports in the literature describe
the presence of partially or fully formed teeth in these
tumors. Considering the multiple
Figure 9.5. Gross photograph of an adamantinomatoid
craniopharyngioma in the third ventricle. The patient died
during pneumography; the needle tracts are visible in the
corpus callosum.
Figure 9.6. Photomicrograph of an adamantinomatoid
craniopharyngioma showing the basal "picket fence" layer
of epithelium resting on loose connective tissue and
showing transitions to a stellate layer of keratinized
epithelium. Hematoxylin and eosin; original magnification
x 40.
types of epithelium present in most tumors, this may not be
as surprising as it initially seems.
With recurrence, the relationship of the epithelial
components to the connective tissue and to the brain tissue
may be markedly altered, and masses of tumor tissue may
be present within the ventricles, displacing and apparently
invading brain at some distance from the primary site (Fig.
9.7). Because of the multicystic nature of this tumor it may
be possible to ameliorate symptoms by aspiration of the
cyst contents (16).
One of the curiosities of the reaction to compression by
this tumor is the frequent dense Rosenthal gliosis that is so
commonly seen in the compressed adjacent brain (Fig. 9.8).
It is so common a finding that an experienced neuropathol-
ogist can predict the presence of an adamantinomatoid
craniopharyngioma by this finding. It also can cause some
diagnostic concern because the juvenile pilocytic
astrocytomas so frequently contain these peculiar
degenerating astrocytic fibers.
An interesting variant of this tumor (in fact, it may be a
quite distinct lesion) is the "papillary" craniopharyngioma.
Because it also contains stratified squamous elements, it
can be confused with the adamantinomatoid type (14).
Colloid Cysts
Colloid cysts are the most common intraventricular
tumor in this site. They typically arise in the anterior-
superior zone of the ventricle, characteristically blocking
one or both foramina of Monro. The origin of the cysts has
been the subject of much controversy and remains unsettled
Figure 9.7. Gross photograph of the brain of a woman who
had had several surgical procedures attempting to alleviate
her relentlessly progressive craniopharyngioma. Tumor can
be seen within the third and lateral ventricles and within
the basal ganglia.
(3). Probably most frequently their symptoms are those of
intermittent obstruction of the foramina of Monro, with
acute hydrocephalus of the lateral ventricles. However, this
lesion may be the cause of relatively sudden death; this is
well documented in the literature and has been supported
by my personal experience of three such cases (27).
Grossly the tumors are sharply circumscribed, with a
thin wall and a gelatinous or semiliquid center. They may
be tiny, measuring only a millimeter or two with the
incidental lesions or masses several centimeters in diameter
(Fig. 9.9). Even lesions large enough to cause symptoms in
many may not do so in all.
Histologically, the lining of the cyst wall may
Figure 9.8. Photomicrograph of a recurrent cranio-
pharyngioma showing a mass of keratinized epithelium
with a densely gliotic area, with some Rosenthal fibers.
Hematoxylin and eosin; original magnification X40.
Figure 9.9. Gross photograph of a colloid cyst of the third
ventricle that had caused relatively sudden death by
obstruction of the foramina of Monro. The patient's
complaints had been of sudden severe headaches, often
relieved by minor analgesics. She died leaving the
emergency room of the hospital.
vary in its epithelial composition (22). Most of the cysts
have a single layer of flattened cuboidal or columnar cells
lying on a basement membrane on a thin layer of fibrous
connective tissue. Less commonly, the epithelium will be
more complex, the least common being a pseudostratified
layer of columnar epithelium (Fig. 9.10).
At the electron microscopic level there is even more
complexity, with the origins of these peculiar lesions not
being settled even at high magnification (20, 21, 25).
Other Cysts
Both epidermoid and dermoid cysts may arise in this
area (Fig. 9.11). These masses are often more solid than
cystic. Epidermoid cysts are composed of a thin layer of
maturing stratified squamous epithelium with much
keratinized desquamated epithelium within the cyst (6).
The dermoid tumors are more complex, and the contents
of the cyst may reflect that complexity. Although the
stratified squamous lining is prominent and may vary in
thickness and degree of keratiniza-tion markedly from
area to area, the appendage structures usually are more
eye-catching. Both sweat and sebaceous glands may be
quite prominent, hair may be grossly evident, and support-
ing dermal structures such as piloerector muscles, fat, and
even occasionally teeth may be present.

Inflammatory Lesions
Abscess
Inflammatory processes are rarely a cause of symptoms
in the area of the third ventricle. However, even if rare,
this must be considered when approaching a lesion in this
site. The abscesses
Figure 9.10. Photomicrograph of the wall of colloid cyst
showing the epithelial wall of pseudostratified columnar
ciliated epithelium. Hematoxylin and eosin; original
magnification x 40.
Figure 9.11. Gross photograph of an epidermoid cyst
compressing the anterior third ventricle.
are almost always of hematogenous origin, and a variety of
organisms may be involved. The lesions almost always
originate within the adjacent parenchymal structures,
although rarely there is an abscess that begins within the
ventricle itself. As would be expected the abscess begins
with a focus of acute inflammation and extends to involve
adjacent structures. In the brain there is a delay in the
formation of the fibrous wall around the inflammatory
process and thus a delay in the production of an effective
barrier to the extension of the inflammatory process. This is
because there are no fibroblasts within the substance of the
CNS except in and around the blood vessels and in the
meninges.
Unless a diagnosis is made very early in the course of
such a process, the outcome must be expected to be fatal
and, even if made early, the prognosis must be grim. If
pyogenic organisms have ready access to the ventricular
system and subsequently the subarachnoid space, the pos-
sibility of rapidly disseminated pyogenic meningitis is
apparent and a fatal outcome is not surprising.
The rare finding of an apparently healed
(evolved) intraventricular abscess also should engender no
surprise, for less virulent organisms do occasionally infect
humans. However, such cases must remain conjectural
without a history that strongly suggests the possibility and
circumstances that support the history.
Granulation Tissue
Although the possibility of granulation tissue causing a
mass lesion in or around the third ventricle must be very
small, this possibility must be part of the total differential
diagnosis of mass lesions in this area. The causes remain
obscure, although hemorrhage and trauma must be high on
the list of possible causes. Even very low grade infections
must also be considered as possible etiologies in such a
situation. However, this should not be a high possibility in
any differential diagnosis lacking a suggestive history.
Granulomas
Most of the granulomatous processes that afflict humans
do so in rather a more generalized manner than
involvement of the area of the third ventricle specifically.
However, the possibility remains that such a lesion might
cause symptoms localized to this area. Any of the
granuloma-causing diseases might in fact localize to this
area and, although rare, might cause symptoms of a mass in
the area of the third ventricle. The causes of such a lesion
are almost endless, but must include almost any organism
that might result in granulomatous inflammation, including
tuberculosis, any of the fungi, and the indolent bacteria that
are occasionally associated with a granulomatous
inflammatory process.
Infestations
Infestations are relatively rare in the urbanized society of
the United States. With increasing travel opportunities there
have been more cases of infestations within the U.S. These
numbers can be expected to increase as travel to less
developed areas becomes more common and the population
of the U.S. continues to add immigrants from these areas. It
is well known that there is a significant incidence of
cysticercosis in the Mexican-American population of the
southwest, and the diagnosis of CNS cysticercosis in
California and the other states of the para-Mexican tier is
well established. However, with the spread of these
immigrants to other areas the diagnostic possibility must
also be spread.
We have seen a remarkable variety of symptoms
associated with CNS cysticercosis, ranging
from the classical repeated pyogenic meningitic picture to
the child with a mineralized granuloma with seizures to the
adult with unilateral intermittent hydrocephalus. Anyone
with a history of travel to or residence in an area that is
endemic for pig tapeworm infestation must be considered
at risk, for if this disease is not considered it is not
diagnosed, even by the pathologist, because the tissue is so
unfamiliar that the diagnosis may be missed.
Should the cyst be found and removed at operation (2),
the organism will most often be dead, and the characteristic
features are the dense crenelated hyaline lamina that is the
residum of the wall of the organism. The internal structures
are less characteristic, although the scolex, if found, is
again diagnostic. This is one of those circumstances in
which knowledge of the possibility of the disease is almost
essential to its correct diagnosis because the pathological
picture is not well known to the majority of pathol-ogists in
the U.S.
Choroid Plexus Hemorrhage and "
Xanthogranulomas"
Hemorrhage into the Choroid plexus is a very common
phenomenon, as every neuropathologist knows, although
this is not well documented in the literature. Evidence of
this hemorrhage is seen in almost every autopsy on
individuals over the age of 30 years, in the form of
intrachoroidal loose fibrous connective tissue with chronic
inflammatory cells, macrophages filled with he-mosiderin
and often with focal cholesterol crystals and foreign body
giant cells (Fig. 9.12); these
Figure 9.12. Photomicrograph of a mass from a third
ventricular Choroid plexus removed after a sudden ictus.
Cholesterol clefts, foreign body giant cells, and chronic
inflammation are obvious, as is the recent hemorrhage.
Hematoxylin and eosin; original magnification X 40.
foci have often been given the name of "Xantho-
granulomas," although they are not true neoplasms. They
cause symptoms very rarely and most often are an
incidental finding at autopsy (36, 37). Occasionally they
may be presented by the neurosurgeon for frozen section
diagnosis when he has unwittingly gotten into the trigone
of the lateral ventricle when searching for a tumor. Even
less commonly one sees recent hemorrhage into the
Choroid plexus causing symptoms and rarely resulting in
death. In the latter circumstance, the hemorrhage has been
into the Choroid plexus of the third ventricle, and the
mechanism of disability and death has been obstruction of
the foramina of Monro (Fig. 9.5).
Histologically, in recent hemorrhage there is hematoma
in the parenchyma of the Choroid plexus, with a reaction
dependent On the age of the lesion. Very early there may
be polymorpho-nuclear leukocytes; later, macrophages
become prominent, often filled with hemosiderin; later
still there may be some transformation of the extravasated
blood into cholesterol break-down products with
macrophages and even foreign body giant cells, thus, the
name "xanthogranu-loma."
Although rare, Choroid plexus hemorrhage must be
considered when there is a sudden ictus in a younger
individual with evidence of hydrocephalus and a dense
mass in the anterior third ventricle on CT scan. This is a
potentially curable disease if recognized.
Mass Lesions in the Walls of the Third Ventricle
Neuroepithelial Tumors See the
previous discussion.
Inflammatory Reactions
Sarcoidosis
Sarcoidosis is a rare disease that commonly involves the
CNS. It most commonly involves the meninges, but
localized involvement of the hy-pothalamus, especially
the lower walls of the third ventricle, is well known. The
reason for this localization is completely cryptic. Grossly,
one sees ill-defined areas of firmness with gray
discoloration and, histologically, the crisp gran-ulomas
without necrosis replace the hypothala-mic nuclei, with
gliosis of the adjacent structures (Fig. 9.13). Schaumann
bodies and asteroid structures are almost never seen in the
CNS (Fig. 9.13, inset).
Sarcoidosis is a diagnosis of exclusion, and
Figure 9.13. Photomicrograph of Sarcoidosis in brain, with
crisp, well-defined granulomas without necrosis.
Hematoxylin and eosin; original magnification x 40. Inset.
Shaumann body in CNS sarcoidosis. Hematoxylin and
eosin; original magnification x 160.
that diagnosis must be repeatedly questioned. One must
continue to search for an organism so a treatable disease is
not missed.
Histiocytosis
Involvement of the hypothalamus with histiocytosis X is
well known to clinical neuroscien-tists, although it is not a
matter of common knowledge among generalists. Any of
the pathological processes that bear this name may involve
this area, but most frequently it is the less malignant forms
that do so. The mixed histiocytic response that is seen in
the tissue is nonspecific; the peculiar cells characteristic of
Gaucher's disease may be present. Most commonly, the
patient will not have an established diagnosis and will
present with diabetes insipidus or another hy-pothalamic
syndrome. Usually a needle biopsy shows nonspecific
pathological findings and then other features of the disease
are discovered in other areas of the body. Fortunately, most
often the disease responds to radiation therapy, although
more malignant courses sometimes ensue.
Lymphocytic (Granulomatous)
Hypophysitis
Although scattered examples had been described in the
earlier literature, it was only relatively recently that the
entity or entities of lymphocytic (granulomatous)
hypophysitis were delineated pathologically and to a lesser
extent clinically (4). These lesions, which present as a rapid
onset loss of vision, most often in a recently pregnant
woman or one in the late third trimester, pathologically
show a chronic granulomatous
hypophysitis with prominent plasmacytic infiltration, often
prominent lymphoid follicles, and various degrees of
fibrosis of the pituitary gland. The appearance is similar to
that of Hashimoto's struma of the thyroid, and the obvious
possibility of origin in autoimmune phenomena has been
proposed. Studies are now under way to test this
hypothesis.
Until the diagnosis can be made clinically, however,
biopsy may be necessary for diagnosis, especially without
the "typical" clinical presentation.
Cysts See previous and following discussions.
Pituitary Tumors and Rathke Pouch Lesions
Tumors of the adenohypophysis are among the more
common tumors to afflict humans, especially females. We
are far more adept now at diagnosing small tumors of this
structure and dealing with endocrine-active lesions before
they begin to cause symptoms because of pressure on
adjacent structures. The advent of CT scans, computerized
reconstructions, and radioimmu-noassay has allowed us to
detect more lesions at far earlier stages. Now
microadenomas are well known and are successfully dealt
with using the transsphenoidal approach with its minimal
morbidity and rapid recovery.
Our much larger experience with a larger number of
lesions has confirmed something that was well known to
experienced neuropathologists in earlier times, namely, that
the classical descriptions of pituitary adenomas by the
terms "chrom-ophobic," "eosinophilic," and "basophilic"
are almost without meaning and should be abandoned as far
as routine diagnostic terminology is concerned. Further,
mixed tumors are relatively common, and histologically
there is no accurate way to predict whether a given tumor is
producing or secreting a hormone without demonstrating
the existence of that hormone in the tumor cells and by
showing elevated levels of the hormone in the serum.
With all that said, there are a number of different patterns
in tumors of the anterior pituitary, the pars intermedia, and
less commonly the pars tuberalis. Any of the
adenohypophyseal portions may give rise to neoplasms and
some will occur is less expected sites.
Also, the normal pituitary gland is subdivided into
lobules of cells, usually of multiple cell types, surrounded
by delicate fibrovascular septae. In the normal gland the
lobules are quite regular in
size, which may be emphasized by a reticulin stain.
Further, most tumors have a thin fibrous capsule, and
grossly most have a soft consistency approaching that of
toothpaste, although others are much more fibrous and
tough.
Probably the most common histological appearance is of
sheets of relatively uniform tumor cells with a rich vascular
supply but without the lobular subdivision seen in the
normal gland (Fig. 9.6). Depending on the amount of
artifact in the material, this may appear as a very compact
cellular tumor or as a looser, even sinusoidal lesion.
Because the latter is also seen as a subtype, this can be
confusing. In some tumors there is sufficient artifact so that
there is the appearance of two types of tumor cells, one
with much more granular basophilic cytoplasm and the
other with more eosinophilic cytoplasm. The former often
stand out as small cords of cells in the background of the
other cells. In fact this appearance is most often the result
of delayed fixation and, at the immunohistochemical and
electron microscopic level, all of the tumor cells are
similar.
Next most common is the tumor with lobules of varying
size, most much larger than the lobules of the normal
gland. These can be very confusing because they closely
mimic the normal glandular endocrine pattern, but the large
size of the lobules and their irregularity betray their
neoplastic nature. Most often the cells are all of the same
type and in many instances they are larger than normal.
The sinusoidal patterns is next most common, the tumor
at low magnification appearing as sinuous bands of wavy
cords of cells, often separated by almost sinusoidal thin-
walled vascular channels.
One of the most confusing morphological pictures seen
in pituitary adenomas is a pattern of cells with processes
extending toward vessel walls, simulating the appearance
of ependy-moma. Adding to the confusion is the often-ac-
companying appearance of round nuclei surrounded by
clear cytoplasm mimicking the "halo" of
oligodendroglioma. The concurrence of these two cell types
is of course well known in glial neoplasms, and thus an
erroneous diagnosis of glial tumor can easily be made. This
appearance is so common that among the experienced there
is a rule to the effect that, when a tumor looks like an
ependymoma in some areas and an oligodendroglioma in
others, always think of pituitary adenoma.
To add to the confusion, contrary to earlier dogma,
mineralization in pituitary tumors does
occur and it occurs also in both glial and men-ingeal
tumors, so that the pattern of mineralization is of no
assistance in differential diagnosis.
Necrosis may be a prominent feature of some tumors. It
is expected in patients showing the syndrome of pituitary
apoplexy, but often confuses the diagnosis of tumors
under more routine clinical circumstances and may lead to
the erroneous diagnosis of malignancy, either primary or
metastatic (38). Metastasis to the pituitary area is not
unknown and may present as a mass lesion (38).
Hemorrhage, too, may add confusion and yet may be a
prominent feature of pituitary tumors. Fibrosis, either
focal or rather generalized, is seen with great frequency in
pituitary neoplasms and cannot be used as a reliable index
of previous operation or radiotherapy.
Thus, until a larger experience suggests reliable
parameters of malignancy, this diagnosis must be
reserved for extraordinary cases and must be given with
cautions about indications for aggressive therapy. I have
found it useful to describe the features that are of concern
and give a concerned although guarded prognostic indi-
cation, explaining our lack of good reliable morphological
markers for malignancy in this organ.
Other Lesions
Although extremely rare, other lesions can cause
symptoms because of obstruction of or pressure on the
third ventricle or the surrounding structures (30).
Pineal Area Lesions
Teratomatous Lesions Including Cysts
It is essential that this section begin with a discussion of
some of the semantic traps that lay in wait for the
innocent beginning a study of tumors of the pineal region.
Even well-experienced pathologists have fallen victim to
the clouds of words that fog this area of pathology.
Although it is not now possible to prove, it seems likely
that del Rio Hortega was the major cause of our modern
confusion. According to his translators, he used the term
"pinealoma" for the tumor that we today (mostly)
recognize as a germinoma occurring in this peculiar site
(32). It is also clear that Hortega was enough convinced of
the origin of this tumor from the cells of the pineal body
that he insisted that this organ contained the two cell types
that are present in the tumor. Thus, if you carefully read
modern histology texts, even to the last editions, you will
find discussion of the two cell types found in the pineal
body and references to Hortega to back
this up. Almost all also include a copy of his diagram of the
cellularity of the pineal body, including the description of
the two cell types.
That Hortega was aware of the reality that the pineal
gland contains only one morphological cell type at least at
the light microscopic level is indicated by the descriptions
of the pineal parenchymal tumors elsewhere described; he
clearly knew that these tumors, that he called "pineo-
cytomas" and "pineoblastomas," were derived from pineal
parenchymal cells or cells that resembled them very
closely. Yet, he at least legitimized the term "pinealoma"
down to this generation, where it still causes much
confusion.
In an attempt to end this confusion, I will divide the
tumors that arise in the pineal body into two major groups:
those that are germinal in type, resembling more the tumors
that arise in the testes or ovaries, and those of
neuroepithelial origin, resembling the cells of the pineal
body itself or cells resembling other neuroepithelial
structures (7, 8).
In approaching tumors in the pineal area one must be
aware of the possible problems and how to deal with them
in the best interests of the patient. After much thought I
have concluded that a histological diagnosis is a desirable
bit of information in dealing with pineal area tumors; I also
realize that a significant group oppose that position and
believe that, because germinomas compose almost 50% of
pineal tumors, this should be the diagnosis of exclusion and
that a therapeutic "trial" of radiation will "prove" the
diagnosis. Although there is little question that a
germinoma will "melt" with radiation, there is also little
question that a teratoma will not or at least that the other
teratomatous elements will not. Thus, although there may
be a miraculous decrease in the mass or even a reversion to
normal, this does not mean that the problem is gone. In
those patients in whom other teratomatous elements are
present, there will be an almost inexorable increase in mass
over time, with recurrence of the mass and the ultimate
demise of the patient. Additionally, with some of the ger-
minal tumors there is the possibility or probability of spread
to other CNS sites or even systemic metastases (12, 13).
Having considered these possibilities, I think that biopsy
of pineal area tumors is desirable. Although needle or
direct biopsy may not demonstrate the total histological
type of the lesion, it cannot do less well than no biospy at
all. Should the tumor prove to be totally germinoma on bi-
opsy, then radiation can possibly prove curative; if other
elements are present, then the poorer
prognosis associated with such lesions can be shared with
the patient earlier.
Further, being painfully aware of the anatomical
isolation of the pineal area, I cannot but urge caution in the
surgical approach to this structure. It seems to me that the
Creator did not intend frequent neurosurgical intervention
in this area. Although I like to think that total removal of
neoplasms is desirable, I also think that patient survival is
important, and trauma to the midbrain, an almost
unavoidable accompaniment of major resection in this area,
is not associated with a long, happy, enjoyable, and pro-
ductive life. Thus, I strongly support whose who espouse
biopsy proof of diagnosis, but I do not believe that "total"
surgical extirpation is necessarily wise.
Germinal Tumors
Although the cell of origin of germ cell tumors in the
pineal body is not certain, there is no question that tumors
of this type are the most frequent in this site (12, 23, 24, 31,
35, 40).
Of the germinal tumors arising in the pineal body, the
most common is the germinoma, a tumor histologically
identical to the seminoma of the testes or the
dysgerminoma of the ovary. This is the tumor given the
not-to-be-repeated name of "pinealoma" in the older and
unfortunate more recent literature. It has two cell types, a
large, germinal cell with a large, vesicular nucleus, most
often reniform or oval, and a prominent nucleolus. The
cytoplasm is usually ill-defined and finely granular. The
"other" cells of this tumor are the bystanding lymphocytes
that are very often a quite prominent part of this tumor (Fig.
9.14). There is occasionally in the pineal a
Figure 9.14. Photomicrograph of a pineal germinoma
showing the lymphocytic areas adjacent to the germinal
neoplasm. Hematoxylin and eosin; original magnification x
40.
granulomatous "response" to the tumor, although this is
probably less common than in other sites. There is often
mitotic activity among the large tumor cells, and there is
frequently a good deal of nuclear atypia.
Although the microscopic aspects of the germinoma
most often get the greatest attention, the gross aspects are
equally confusing because they may be so variable. This
tumor is usually soft, is often well-demarcated, and may be
solid or cystic. There is often invasion of the adjacent
structures and spread via cerebrospinal fluid (CSF)
pathways; even systemic metastases, presumably via
ventricular shunts, have been recorded (17). The nearby
fornices may be diffusely involved, and this was thought to
be the mode of spread to the third ventricle when that site
presented as the "primary" before we were aware that this
tumor might arise primarily in the third ventricle.
Compression of adjacent structures is the mode of
clinical presentation, with Parinaud's syndrome or less
commonly such symptoms as precocious puberty.
This tumor, once clinically apparent, tends to grow
relatively rapidly and seed via CSF pathways. The tumor is
sensitive to radiation, but it often spreads widely, and total
neuraxis radiation is probably advisable in almost all cases
if subarachnoid seeds are not to develop. Because this
tumor accounts for almost half of the pineal region tumors,
it has given many radiotherapists too much confidence in
treating tumors of this area, and the nonresponding tumors
have come back to haunt some of our colleagues because
of their lack of knowledge of the complete spectrum of
tumors that occur in this area.
This spectrum of tumors is indeed large, for all of the
germinal neoplasms may occur in the pineal region, singly
or in combination. Although they will be discussed
individually, at least from the histological standpoint, it
must be appreciated and will be repeatedly emphasized
that all combinations do occur.
Mature teratomas are, although less frequent, a common
component of the germinal neoplasms in this area. As
might be expected they consist of the same tissues seen in
these tumors elsewhere. Mature tissues of ectodermal,
mesoder-mal, and endodermal origin in various combina-
tions make up these tumors (Fig. 9.15). They commonly
also have less well-differentiated components, and
combinations of adult tissues with more primitive
malignant components are all too common. Thus varying
combinations of mature squamous epithelium, glandular
tissue of several
Figure 9.15. Low power photomicrograph of a pineal Figure 9.16. Photomicrograph showing focal area of
teratoma with a mixture of mesodermal, ectodermal, and embryonal carcinoma in a teratoma. Hematoxylin and
endodermal elements. Hematoxylin and eosin; original eosin; original magnification x 40.
magnification x 10.

types, mixtures of the several connective tissue

components, loose fibrous tissue, cartilage, bone, and
smooth and striated muscle may be seen (Fig. 9.8). And,
perhaps not surprising considering the site, neuroepithelial
components are quite common, with even retinal elements
being seen rather commonly. Additionally, there may be
added the glandular elements of the endo-derm, with
recognizable gastric, small intestinal, or colonic
epithelium, along with the appendages such as pancreas or
liver.
Unfortunately, all too often other more malignant and
embryonal components are also present. Piled-up zones of
primitive columnar cells, forming ill-defined acini, or
complex glandular structures with large, polymorphic
nuclei with coarse chromatin, many mitotic figures, and Figure 9.17. Photomicrograph of a focus of yolk sac
granular ill-defined cytoplasm is the histological picture of carcinoma in a pineal teratoma. Hematoxylin and eosin;
embryonal carcinoma (Fig. 9.16). In the variant of this original magnification x 100.
tumor called "Teilum" tumor, or yolk sac carcinoma, the
masses of epithelium protrude into a glandular center hemorrhagic component. This also is one of the few pineal
resembling the primitive stage of development of the yolk tumors that may metastasize system-ically, and some, as a
sac (Fig. 9.17). result, have doubted that it is really primary in the pineal
These are primitive, highly malignant tumors, and region, believing that it might have arisen in the gonads,
unfortunately they tend to spread in the CNS as they do but have gone undetected in that site.
elsewhere, so that CSF seeding is an expected This tumor may be seen in association with one or more
complication of these tumors. Further, they are not as of the previously described teratomatous tumors, as is the
sensitive to radiation therapy and higher radiation doses case with all of this group of neoplasms.
are necessary for basic control. There has been a great deal of interest in the association
Another of the variants of teratomatous tumors that of the pineal germinal tumors with some of the
occurs rarely in the pineal region is the choriocarcinoma. immunological markers associated with germinal tumors in
This tumor is histologically identical (as are the other other sites (13). Thus, the presence of antibody to
teratomatous tumors) to the genital tumors of the same carcinoembryonic antigen or chorionic gonadotropin may
name. Unfortunately, it also has similar growth be helpful not only in diagnosis but also in following the
characteristics, with rapid increase in size, and a frequent results of treatment and in determining relapse, but to date
the results are not definitive, and absolute determiners are
not yet available.
Neuroepithelial Tumors structure of the normal pineal body in an exaggerated way,
with cells and nuclei that closely resemble the parent
The most common neuroepithelial tumors of the pineal
structure. There are usually few mitotic figures, and
area are the tumors derived from pineal parenchymal
necrosis is distinctly rare. The tumor is usually grossly
elements, the pineocytoma and the pineoblastoma. Other
defined, although there may be gross evidence of local in-
pineal parenchyma-derived tumors also occur, but are much
filtration. The tumor is usually solid, but cystic examples
rarer.
have been reported. Hemorrhage and necrosis are not
The most common pineal parenchymal tumor is the
usually a gross feature; after therapy, such changes may be
pineoblastoma. This tumor, identical at the light
seen.
microscopic level to the medulloblastoma, also shares the
Histologically, this tumor grows as sheets and lobules of
ability of the cerebellar tumor to spread widely and early to
cells with prominent vesicular nuclei, often with prominent
other sites via CSF pathways (19, 33). Grossly, the tumor is
nucleoli, but without evidence of rapid growth, i.e., there
usually soft, somewhat demarcated, pink, and friable. Even
are rarely many mitotic figures. Necrosis is also distinctly
at an early stage, there may be evidence of infiltration of
uncommon. The cytoplasma is as prominent as is the
adjacent structures, with resultant poor delimitation at the
cytoplasm of the pineal cells normally, i.e., there is little to
periphery. Histologically, the tumor is highly cellular with
be seen at the light level except for delicate processes
small nuclei and little in the way of cytoplasm (Fig. 9.18).
forming the background and the mass of processes seen in
Like the medulloblastoma, the pineoblastoma often shows
the center of the rosettes (Fig. 9.19). The vessels may be
varying degrees of differentiation, more frequently toward
prominent, but endothelial proliferation is not prominent.
the neuroblastic/pineocytic elements than toward the glial
There are usually areas in which the exaggerated Homer
elements, as is true of the medulloblastoma. Thus, one sees
Wright rosettes previously noted are found with ease, but
the exaggerated Homer Wright rosette also seen in the
this may not be the dominant histological feature. In a few
pineocytoma, with a large circlet of dark-staining small
cases there are areas with a dense glial mass similar to that
nuclei surrounding a mass of tangled processes, much
found in the core of many normal pineal bodies, with a
larger than the usual Homer Wright rosette, with 10 to 15
dense meshwork of background glial processes, with few
or more nuclei in the circle.
cell nuclei, usually typically astrocytic, and without
This tumor, as suggested previously, also tends to seed
evidence of significant cellular proliferation. Rosenthal
the neuraxis widely early in its course, and it must be
fibers may be very prominent within these areas. However,
presumed that CSF spread has occurred at the time of
these masses are most often several times the mass of the
diagnosis. We have used therapy identical to that for
normal pineal body as a whole, and it seems clear that they
medulloblastoma, but thus far have too few patients to
are part of the neoplastic process. The whole potential of
assess the results meaningfully.
differentiation in these tumors is amazing and, although
The pineocytoma is the next most common tumor in the
probably
pineal area. This tumor mimics the

Figure 9.19. Photomicrograph of a pineocytoma with

Figure 9.18. Photomicrograph of a pineoblastoma with rosettes with intertwining processes being prominent
small cells resembling those of medulloblastoma. features. Hematoxylin and eosin; original magnification x
Hematoxylin and eosin; original magnification x 100. 40.
not all types have been appreciated, many have been well
described (19, 28, 39).
In very rare cases one may see transitions from
pineoblastoma through pineocytoma to indolent
astrocytoma all in the same tumor. Our experience is
insufficient to know the biology of the latter types of
tumor, and for the present we are assuming the worst and
treating these patients as if they had a pure pineoblastoma.
Because all of the basic neuroepithelial cellular elements
exist in this area, it is not surprising that tumors derived
from these elements arise in this area, although
uncommonly. Thus, the spectrum of astrocytic,
ependymal, and most rarely oligodendroglial neoplasms
may be seen in this area. We have even seen primary
lymphomas, at least presenting as pineal neoplasms.
Tumors of the meninges, connective tissue, and blood
vessels may also be expected sooner or later to give rise to
neoplasms of this gland or at least in this area.
Metastases
Although rarely clinically apparent, metastases to the
pineal body, like the other areas of the nervous system, are
more common than is generally appreciated. In over 25
years of routine histological examination of pineal tissue,
metastatic tumors have been found with more frequency
than had been expected with almost no evident symptoms
that could be ascertained from the clinical record. The
possibility of metastasis must be borne in mind, especially
when dealing with biopsy material. When presented with
tissue showing only singular differentiation, one must
consider the possibility of metastatic carcinoma or even
metastatic sarcoma.
Although not considered a significant problem,
neoplasms, especially glial, may spread from adjacent
sites in which they might be more common. Good sense
and judgment must prevail.
Other
As suggested, involvement of the pineal area by tumors
from adjacent tissues must be expected. Thus,
meningiomas, vascular malformations, and other mass-
increasing lesions from adjacent areas will sooner or later
involve this tissue (34).
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10
Tumor Markers in Third Ventricular Neoplasms
Henry H. Schmidek, M.D., Adam Borit, M.D., and Steven L Wald, M.D.
The ability to diagnose cancer by a laboratory assay of
blood, urine, or cerebrospinal fluid has been a desirable
objective for many years. Ideally such a marker would be
specific to a disease and positive only in the presence of
neoplasia. The myeloma proteins discovered in 1846 are
closest to this ideal. Interest in tumor markers was re-
kindled by the discovery of а-fetoprotein (AFP) in
1963 and of carcinoembryonic antigen in 1965.
Among primary central nervous system (CNS)
tumors a variety of biochemical markers have been
identified (Table 10.1). A disease-specific marker is
important because it would allow differentiation of
the benign from the malignant tumors, help define
the tumor's histological subtype, allow monitoring of
the efficacy of treatment by changes in marker levels,
and permit early detection of asymptomatic
recurrences. Tumor markers also have the advantage
over, for example, exfoliative cytology in being
quantifiable.
Once it is possible to identify and quantitatively
determine tumor marker signals that will reveal the
presence of tumor, the localization and treatment of
the neoplasms bearing markers can be explored for
diagnosis and potentially for treatment. For example,
the in vivo localization of tumor growth can be
accomplished using antibody manufactured to the
marker, labeled with radioisotope, injected, and then
localized using radioscintigraphy or
radioimmunoscintigraphy. This technique, which has
been applied to the
diagnosis of asymptomatic lymp node metastases, is
potentially useful in the diagnosis of germ cell tumors
using antibody to AFP or the beta subunit of human
chorionic gonadotropin (bHCG) or to malignant
neural tumors using the polyamines. An example of
this approach is the recent report of monoclonal
antibody imaging of normal-sized retroperitoneal
lymph nodes for the detection of metastatic colon
cancer in lymph nodes judged normal in size and
appearance on computerized tomographic (CT)
scanning and at operation (36). Therapy may involve
conjugation of a chemotherapeutic agent to a tumor-
specific antibody to direct chemotherapeutic agents or
isotopes to cancer cells in vivo.
All cell markers identify one or more specific cell
constituents by immunological, enzymatic assay, or
analytical chemical methods, although a specific
compound detectable by chemical methods may also
serve as an antigen detectable by immunological
methods. As a practical matter almost all markers are
detected by immunological methods and their major
application is in tumor diagnosis and in research.
Markers discussed in this chapter are those that
have established diagnostic implications in
neuroncology and are specifically relevant to lesions
within or adjacent to the third ventricle. Metastatic
tumors will not be discussed; they are rare in this
region and would necessitate a fragmentary
description of many markers.
The primary neoplasms of the pineal region

are germ cell tumors, pineal parenchymal tumors, or (a
small number of) mesenchymal tumors and cysts (9, 10, 48,
49).
Germ Cell Tumors
Human germ cell tumors account for between one-half
and two-thirds of tumors in the pineal region and they
comprise a group of interrelated neoplasms. The
totipotential cells of origin of teratomas may remain
undifferentiated, resulting in an embryonal carcinoma, or
embark upon lines of differentiation of extraembryonic ele-
ments, either vitelline (yolk sac tumor) or tropho-blastic
(choriocarcinoma). The entire group of these tumors
includes germinoma (atypical teratoma), embryonal
carcinoma, choriocarcinoma, endodermal sinus tumor,
teratocarcinoma, and mixed tumors consisting of
combinations of these elements. The germinoma is the most
com-
mon of these tumors arising in the CNS (23-25, 29, 31,
56).
All of these tumors resemble the germ cell tumors of the
gonads and other extragonadal sites biologically and
histopathologically, although they originate within the
pineal gland, the suprasellar area ("ectopic pinealoma"), or
the anterior and posterior third ventricle. Germ cell tumors
originate in diencephalic centers that are synaptically
entrained in the regulation of go-nadotropic activity.
Gonadotropins are implicated in determining the site of
origin of intra-cranial germ cell tumors and seem to
function as carcinogenic inducers. The neuroendocrine
events of puberty have an activating influence in the
expression of malignant behavior among these neoplasms.
The question of the multicen-tric origin of the anterior-
posterior third ventricle tumors seeding from an anterior or
posterior third ventricular germinoma remains unresolved.
When the tumor is present in the anterior third ventricle it
tends to fill the floor and invade the walls of the ventricle
and may extend into the infundibulum, pituitary gland, and
optic nerves. Rarely an intracranial germ cell tumor
originates outside the diencephalic region, such as in the
cerebellar vermis.
The last 10 years have seen a marked increase in our
knowledge of various tissue-specific antigens. These
substances are capable of provoking the synthesis of an
antibody by the b cells of the immune system. Compounds
vary in their ability to elicit the initial or subsequent
production of antibody, and species vary in their ability to
respond to the initial or subsequent antigenic challenge.
Very few small molecular weight chemicals are able to
elicit an antibody response by themselves, but larger
compounds (such as poly-peptides) are usually adequate
for this purpose. Polypeptides or proteins containing a
polysac-charide moiety are especially good antigens. An
antigenic site (epitope) of a chemical compound consists of
only a few monomers such as amino acids or
monosaccharides of macromolecules. The same antigenic
site may be present in more than one specific molecule,
which can lead to antigenic cross reactivity and
misidentification of molecules. Radioimmunoassay (RIA)
is the current technique most widely used to measure the
concentration of antigens in blood or cerebrospinal fluid.
The method combines the immunological method with that
of quantitative detection of radioactivity (55, 62).
In performing a RIA, the antigen sought is highly
purified and radiolabeled usually with iodine-125 or iodine
Bl. A known quantity of this labeled antigen is placed in a
test tube and used
as the standard. A quantity of the patient's serum or blood
that contains an unknown quantity of the (unlabeled)
antigen is placed in a test tube, a known quantity of
antiserum (antibody) to the sought antigen is then added to
the mixture of standard and unknown, and the
immunological reaction is allowed to take place. In this re-
action, the primary antibody contained in the antiserum
reacts with both the labeled and unlabeled antigens. With
manipulation of the quantities of the reactants used, it can
be arranged that some of the labeled antigen will remain
free, i.e., will not react with the primary antibody.
Thereafter, the antibody is bound and the free antigens are
separated. This separation is usually achieved by adding a
secondary antibody that is specific against the primary
antibody to the mixture. This secondary antibody is pro-
duced in a different species from that in which the primary
antibody is produced. The addition of the secondary
antibody to the reaction mixture precipitates only the
complex of primary antibody with the antigen. Thus, the
free antigen remains in the supernatant fluid and the two
types of antigen (bound and free) can be separated. Instead
of a secondary antibody, other means of effecting this
separation can be used, such as staphylococcal protease A,
which combines with the FC portion of the
immunoglobulin G (IgG). The labeled antigen, either in
the precipitate or in the supernatant fluid, can be measured
and the equation (total radiolabeled antigen — free labeled
antigen = bound labeled antigen) gives the quantities of
labeled antigen in free and bound forms. Standard curves
can be constructed by systematically varying the amount
of unlabeled antigen (unknown sample) to fixed amounts
of labeled antigen and primary antiserum (antibody). The
ratio of the labeled antigen that is bound by the primary
antibody in the presence of varying quantities of unlabeled
antigen and in the absence of unlabeled antigen gives the
quantity of unlabeled antigen in the unknown sample.
The two major specific markers of germ cell tumors are
AFP and b HCG. Although present in some germinomas,
placental alkaline phospha-tase is not a fully established
marker for this group of tumors (40). Both AFP and b
HCG are measured by RIA of serum and cerebrospinal
fluid.
AFP
AFP is a 70-kilodalton glycoprotein that is thought to be
the fetal equivalent of albumin, initially discovered in the
serum of fetal mice and in the serum of adult mice with
hepatocellular
cancer. AFP is produced by the yolk sac and the fetal liver
and is suppressed around the time of birth but reappears in
the serum in the presence of hepatoma or teratocarcinoma.
The tumor cells producing AFP are the malignant
counterparts of the cell populations producing AFP during
development (3, 50).
After fertilization and the morula stage of development,
differentiation proceeds to the formation of the inner and
outer germ cell layers. The inner germ cell layer forms the
endoderm, which further differentiates into the visceral and
parietal layers. The cells of the visceral endodermal layer
are characterized by a thin basement membrane and the
synthesis of AFP on Day 7 of mouse development. The
gene responsible for directing this synthesis is silent until
that time and is then activated, resulting in the production
of AFP until birth when it is then turned off, only to be
derepressed when certain cells undergo malignant
transformation later in life. The visceral endodermal tissues
give rise to the fetal yolk sac, the liver, the gastrointestinal
epithelium, and their corresponding tumors, the yolk sac
(endodermal sinus) tumor, the hepatoma, and
gastrointestinal adenocarcinomas (2, 27,41, 54).
Occasionally, other tumors express this compound. Of
the tumors originating within the CNS, only the yolk sac
tumor, embryonal carcinoma, and mixed germ cell tumors
produce it in appreciable quantities. AFP and other
compounds, such as alpha-1-antitrypsin, are particularly lo-
calized in the hyaline globules characteristic of the yolk sac
tumor; however, one must be aware of metastatic tumors
producing this compound, particularly the extracranial
germ cell tumors.
Human Chorionic Gonadotropin (HCG)
HCG is a hormone produced by cells of the placenta,
especially the syncytiotrophoblasts. This marker is used in
establishing the diagnosis of pregnancy and in making the
diagnosis of trophoblastic disease. HCG is a 30-kilodalton
glycoprotein composed of an alpha and a beta subunit. The
alpha subunit of HCG is identical to the alpha subunit of
the pituitary gonadotropins, follicle-stimulating hormone
and luteinizing hormone (LH) and of thyroid-stimulating
hormone. The beta subunit of each of these hormones is
unique and characteristic. Identification of HCG is
performed through RIA of the beta subunit in serum, urine,
or cerebrospinal fluid. Aside from its production during
pregnancy, choriocarcino-mas, adenocarcinomas of the
lung, hepatomas, and malignant melanomas may also
occasionally produce this marker. Some neoplasms produce
 the alpha, others the beta, and still others both HCG
subunits. In the CNS, choriocarcinomas, embryonal
carcinomas, certain mixed germ cell tumors, and certain
metastatic tumors manufacture b HCG and indicate the
existence of these neoplastic cells (17, 18, 51).
The clinical experience with the use of tumor markers in
the diagnosis and subsequent management of third
ventricular neoplasms is limited by the relatively infrequent
occurrence of these tumors; however, significant
experience exists with the use of these markers in the
management of patients with testicular tumors, 95% of
which arise from primordial germ cells identical to those
found in and around the third ventricle. As with the
intracranial tumors these neoplasms occur as germinomas,
malignant teratomas, or mixed cell tumors. AFP and b
HCG were surveyed in a series of patients with testicular
tumors. Even in cases of pure seminomas (germinomas) the
b HCG level is occasionally elevated, a finding explained
by pathological studies demonstrating that some
germinomas contain syncytiotropho-blastic cells. Probably
10 to 20% of "pure" testicular seminomas produce b HCG.
Sano found that three of five cases of intracranial
germinomas secreted b HCG (47).
In a study of 10 patients with intracranial germinomas in
whom plasma AFP and b HCG was measured, Pomarede et
al. found the AFP elevated in 1 patient, the b HCG elevated
in 3 patients, and the LH elevated in 1 patient, probably
because of cross reactivity with HCG (42).
Assay of the secretion of AFP and b HCG by
nonseminomatous testicular tumors has shown that
approximately 40% of these cases demonstrate elevations
of one of these markers, and that during the course of the
disease the two markers, if present together, do not
necessarily quantitatively parallel each other. One reason
for this observation is the difference in the half-lives of the
two markers. The half-life of AFP is 5 days and that of b
HCG is 30 hours. AFP may therefore remain elevated for
days to weeks after radical tumor removal whereas the b
HCG level will fall rapidly. In addition, the production of a
marker substance is only one of the biological activities of
these cancers, and tumor cells that have ceased to produce
these markers are not necessarily dead. The level of marker
may drop to normal before the clinical and radiographic
disappearance of the tumor (34).
The investigation of pineal region tumors and of ectopic
pinealomas includes measurement of both AFP and b HCG
levels in serum and cerebrospinal fluid. The frequency of
occurrence of pos-
itive values among this group of heterogeneous tumors is
not known. A germ cell tumor may be present and both of
these markers may be negative on repeated examinations.
When positive, the presence of AFP is specific for a
malignant neoplasm possessing endodermal sinus ele-
ments, although it has been reported in association with a
"pure" germinomatous tumor (42). b HCG may be positive
in some pineal region germinomas, although they are
particularly characteristic of one of the other germ cell
tumors. In Jooma's series of pineal tumors there is a case
of a germinoma with elevated blood and cerebrospinal
fluid b HCG levels that then fell in response to
radiotherapy and with CT resolution of the lesion (28).
Among six male patients with other germ cell tumors,
markers were sought in three cases and were present in
two of these patients. One patient had elevation of both
AFP and b HCG, and the other had elevation of only AFP.
In two of these six cases precocious puberty occurred in
conjunction with the germ cell tumors probably because
the b HCG produced by the malignant teratoma stimulates
the interstitial cells of the testis to secrete androgens. In
one of these cases the b HCG, testosterone, and AFP levels
in the blood were elevated and subsequently fell during
radiotherapy.
Non-Germ Cell Tumors: Pineal
Parenchymal Tumors
The non-germ cell tumors of the pineal region include
neoplasms that arise from the pineal parenchymal cell, the
pinealocyte (pineocytoma, pineoblastoma, and mixed
forms of these tumors), or from glial cells (astrocytoma,
ependymoma, and mixed forms of these tumors). Pineal
parenchymal cells contain the enzymes that mediate the
synthesis of norepinephrine, serotonin, and melatonin from
tryptophan. N-Acetyltrans-ferase and hydroxyindole-O-
methyltransferase (HIOMT) are involved in this process,
and N-acetyltransferase is the rate-limiting enzyme for
melatonin formation. The enzyme HIOMT is a specific
marker for the site of melatonin formation.
Some controversy exists concerning the specificity of
melatonin as a marker because this hormone is also
synthesized by the retina, in red blood cells, peripheral
nerves, gastrointestinal tract, the hypothalamus, Choroid
plexus, and by the malignant melanoma. Within this
limitation there is considerable interest in this subject be-
cause of methodological improvements that now allow the
accurate assay of melatonin in spite of its small molecular
weight and many structural
analogs. Melatonin quantification is performed by
bioassay, spectrofluorometric assay, RIA, or the gas
chromatography-mass spectrometric technique. Each
approach exploits a different biological, chemical, or
physical property of melatonin and each assay has a
characteristic sensitivity and specificity. Pending the
establishment of a definitive assay method, the best doc-
umentation of the accuracy of a given assay method is a
scatter plot with linear regression analysis of paired data
for the test method and a reference method based on an
alternative analytical principle. At present RIA methods
yield values in agreement with those based on bioassay or
on gas chromatography-mass spectrom-etry, although of
the different methods the latter technique is probably the
most accurate. Melatonin levels in plasma, serum, and
cerebrospinal fluid tend to be similar. Melatonin circulates
in the blood of humans, is excreted in the urine, and
demonstrates a diurnal rhythm, being maximal during
darkness (11, 66).
Alterations in the pattern of melatonin secretion in the
presence of a third ventricle tumor have been described in
only a few cases. Neuwelt and Lewy (38) reported the pre-
and postoperative 24-hour melatonin assays of a 17-year-
old boy with obstructive hydrocephalus and a partially
cystic, calcified pineal tumor. The tumor enhanced on the
infusion CT scan, and AFP and b HCG assays were
negative. Examination of the cerebrospinal fluid for
malignant cells was also negative. After removal of a low
grade pineal region astrocytoma, the plasma melatonin
level, assayed by gas chromatography-mass spectrom-etry,
became unmeasurable. There are also occasional reports of
altered (elevated) levels of melatonin in the serum of
patients with a pineoblastoma (4). Melatonin has been
identified in a few pineoblastomas, in the rare
medulloblastoma, and in tumors that may be primary CNS
melanomas. Kennaway et al. (30) described a patient with
a pathologically verified pineoblastoma in whom
melatonin could not be detected
in the serum on several examinations and another patient
with a pineal germinoma in whom the melatonin level was
elevated (59). HIOMT, the enzyme required for the last
step in melatonin synthesis, has been demonstrated in vitro
within the cells of a metastatic pineal parenchymal tumor,
indicating that melatonin and probably other hormones are
produced by some of these tumors.
Other Neuroectodermal Tumors
The neuroectodermal neoplasms around the third
ventricle resemble their counterparts throughout the CNS
and their markers are the same as for other neuroectodermal
tumors (Table 10.2). The neurofilament proteins and glial
fibrillary acidic protein (GFAP) are useful in diagnosis;
others, such as neuron-specific enolase (14-3-2 protein) and
the SI00 proteins, are less specific and contribute little
further diagnostic information (37, 52, 53, 64, 67).
Neurofilament Proteins
Three proteins with molecular weights of 200, 145, and
68 kilodaltons together form the orga-nelle known as the
neurofilament. In vitro the 68-kilodalton component
assembles into morphologically normal intermediate-sized
filaments by itself. Neurofilament is one of the five, ap-
proximately 10-nm-thick, intermediate-sized filaments
thought to be specific for neurons and certain
neuroendocrine cells. Within neurons it is the axons that
stain most consistently, indicating the distribution of most
of the neuronal intermediate filaments in these cells. That
the Bodian silver stain stains mostly neurofilaments has
now been proven using antibodies to the neurofilament
proteins on sodium dodecyl sul-fate-polyacrylamide gel
electrophoresis of rat whole spinal cord homogenate (15,
16).
The predominantly axonal localization of neu-
rofilaments is useful as a more specific method of detecting
axons. These proteins are rarely found in primitive
neuroectodermal tumors and,
when detected, are seen only in a small percentage of the
tumor cells. In tumors in which differentiation toward
neurons is well advanced, such as ganglioneuroblastoma,
ganglioneuroma, or ganglioglioma (including the
hypothalamic gan-glionic hamartoma), the positivity is
more extensive and corresponds to the degree of
histological differentiation. Luteinizing hormone-releasing
hormone (LHRH) antigen has been demonstrated in the
neuronal cells (perikarya and axons) of the rare
hypothalamic ganglionic hamartoma. The LHRH is
manufactured in neurons of various nuclei of especially the
infundibular and mamillary regions of the hypothalamus.
The axons of these neurons, just as in the case of the other
hypothalamic releasing factors, secrete their produce into
the portal venous system of the median eminence from
whence it reaches the cells of the anteior pituitary. The
presence of LHRH in these tumors correlates with the
known occurrence of precocious puberty in some of the
affected patients. Such a tumor nodule may serve as an
"accessory" hypothalamus. This tumor is histo-
pathologically similar to gangliogliomas at other sites and
thus contains the neurofilament (neurons) and GFAP (glial)
markers (42a). In addition, neurofilaments have also been
identified in pheochromocytomas and in the oat cell carci-
noma of the lung. Teratomas may contain neu-rofilament-
positive neurons or endocrine cells (15, 39,42a).
Neurofilament proteins are specific to the cells and
tumors of the neuronal series, as well as to certain cells and
tumors of the diffuse endocrine system, and the
pathological categorization of these can be important in the
study of tumor types. To date assay of these proteins in
tissue fluids has not proven of value in the diagnosis of
third ventricular neoplasms.
Glial Fibrillary Acidic Protein (GFAP)
GFAP is a single intracellular protein with a molecular
weight of approximately 50 kilodal-tons. It is the specific
constituent of the 10-nm-thick, intermediate-sized filaments
of the various types of astrocytes and ependymal cells. Its
specific function in these cells is unknown. GFAP is
detectable in the absence of gliofibrillo-genesis, perhaps in
a soluble form. Astrocyte-like cells are also present in the
pineal and pituitary and astrocytomas occur there. Some
schwannian cells may also contain this protein (5-8, 70).
The applicability of the peroxidase-antiperoxi-dase
(PAP) method to formalin-fixed and paraffin-embedded
tissues has led to its widespread
use to identify neural antigens such as the GFAP. This
technique uses a primary antibody against the specific
tissue antigen to be identified as well as a link (secondary)
antibody generated against the immunoglobulins of the
species in which the primary antibody was produced. The
link antibody is followed by the PAP complex, the anti-
peroxidase component of which is generated in the same
species in which the primary antibody was produced.
In addition, before using the primary antibody, normal
serum from the same species from which the link antibody
was obtained (to reduce nonspecific staining) and H2O2 (to
inactivate endogenous peroxidase) are used sequentially.
Tryp-sinization enhances the sensitivity of detection of
certain antigens. Because the PAP complex is colorless,
certain chromogens are used to visualize the complex. The
PAP method is more sensitive than immunofluorescence,
and routinely processed tissues can be used in this method;
thus it is more useful than immunofluorescence when a
frozen section is not available. After immunoperoxidase
staining has been completed, the tissue section can be
counterstained with hematoxylin, thereby demonstrating
the nuclear morphology (12, 13, 20, 26, 33, 60, 61). An
alternative method to PAP, the ABC method, is also
becoming common (22, 57, 69).
GFAP is present in astrocytes, ependymal cells, the
normal pineal parenchyma, all types of astrocytomas, and
ependymomas. In these situations vimentin, the
mesenchymal intermediate filament, is also present. There
is a very rough inverse relationship between the quantity of
GFAP present and the tumor's histological grade of
malignancy. In low grade astrocytomas around the third
ventricle many of the tumor cells contain appreciable
amounts of GFAP, whereas in glioblastomas many of the
cells may be GFAP-negative. In the region of the third
ventricle the pilocytic astrocytoma is the most common
form and cells in these tumors may contain Rosenthal
fibers (8, 70, 71).
Two patterns of GFAP positivity have been described in
astrocytomas. In the more common pattern, the perikarya
as well as the processes contain immunoreactive material;
in the other pattern, mostly the cell processes and only a
few perikarya stain for GFAP. In ependymomas, cells of
all of the structural components may contain GFAP:
ependymomatous tubules, gliovascular rosettes, and the
diffuse areas. Many of the neural tumors in the vicinity of
the third ventricle, aside from the astrocytoma and ependy-
moma, contain a few GFAP-positive cells. These
include the Choroid plexus papilloma, oligodendroglioma,
ganglioglioma, primitive neuroectodermal tumors
(medulloblastoma, medulloepi-thelioma, pineoblastoma,
neuroblastoma, reti-noblastoma), capillary
hemangioblastoma, and craniopharyngioma. In
oligodendrogliomas, astrocytes are frequently intermixed
with the tumor oligodendrocytes. One of the components
of a ganglioglioma is astrocytic. Among the primitive
neuroectodermal tumors, differentiation in an astrocytic
direction occasionally occurs. The GFAP-positive cells in
capillary hemangioblas-tomas and Craniopharyngiomas
are thought to be reactive cells included within the
tumors. Teratomas may contain GFAP-positive astrocytes
and ependymal cells.
Studies of GFAP in the cerebrospinal fluid of patients
representing a wide spectrum of neurological disease have
shown elevations in association with a variety of both
neoplastic and non-neoplastic states. No specific disorder
is consistently associated with elevated cerebrospinal fluid
levels, although the only tumors to show cerebrospinal
fluid levels of greater than 500 mg/ ml are glioblastomas
and anaplastic astrocytomas (21).
Various compounds such as carbonic anhy-drase or
galactocerebroside have been suggested as markers of the
oligodendroglial cell, but none has been proven clinically
useful (32, 43). Current methods allow myelin basic
protein (MBP) and other components of myelin to be
detected in the cell body of oligodendroglia-synthesizing
myelin sheath but not in the adult oligodendro-cyte or in
the oligodendroglioma. Few studies have detailed the
distribution of myelin basic protein in CNS tumors.
Studies in experimentally induced schwannomas, rat cell
gliomas, cultures derived from human
oligodendrogliomas, and an astrocytoma have shown
either no MBP or inconsistent results. Jones and Whitaker
found the cerebrospinal fluid of patients with a variety of
brain tumors to contain no MBP except in one case when
an intratumoral hemorrhage had occurred before lumbar
puncture (7, 27, 58, 68).
The Polyamines
The polyamines, putrescine, spermidine, and spermine,
are small cationic molecules with unfortunate names that
are related to nucleic acid metabolism and cellular
proliferation (Fig. 10.1). Increased polyamine biosynthesis
occurs coincident with periods of cell proliferation or the
release of polyamines from dead or dying tumor cells.
Extensive studies particularly by the Brain Tumor
Research Group at the University of Cal-
ifornia, San Francisco, and by others (14, 19, 35, 46) have
shown that, although the value of these indicators is limited
by the frequent occurrence of false-positive and false-
negative values, they have a distinct and specific usefulness
in highly proliferative tumors such as glioblastoma multi-
forme and medulloblastoma located in or adjacent to the
ventricular system. It is among these neoplasms that
consistent elevations of cerebrospinal fluid polyamine
levels can be demonstrated to parallel the progression or
regression of a tumor, frequently preceding other evidence
of tumor recurrence. Tumor tissue concentrations of
polyamines seem to be indicative of a tumor's malignancy.
Even though no data presently exist for third ventricular
germ cell tumors or pineal parenchymal tumors, some of
these would be expected to produce high levels of pol-
yamines that could then be used to monitor these tumors.
Using an amino acid analyzer Marton et al. carried out
serial polyamine determinations by the ion-exchange
chromatographic separation method (35). In 16 patients
with medulloblastoma, 75 cerebrospinal fluid polyamine
determinations were performed and gave no false-positive
values and only 1 false-negative value. The polyamine
values provided an excellent correlation with the patient's
condition as evaluated by the neurological examination, the
CT and iso-topic scans, cerebrospinal fluid cytology, and
myelography. In all cases the putrescine levels were
elevated above that of other disease states, although
elevated putrescine and sperimidine levels have been
reported in the presence of hydrocephalus and
encephaloceles. Polyamine determination is of potential
value in pineal region tumors because they fulfill the
criteria of proximity to the ventricular system, rapid
proliferation, and the potential of recurrence within the
spinal fluid pathways (1). Recently, radiolabeled putrescine
has been used as a probe in an experimental brain tumor
model. In a preliminary report by Volkow et al. (65) using
transplanted rat gliosarcoma, the in vivo uptake of
[14C]putrescine was 35 times greater in tumor than in
normal brain and 95% of the injected polyamine cleared
within 5 minutes. These findings demonstrate the potential
efficacy of putrescine as a positron emission tomography
tracer for brain tumors.
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 11
Radiology of Third Ventricular Lesions
Eddie Kwan. M.D., Samuel M. Wolpert, M.B., S.Ch., Steven P. Smith, M.D., and
Michael T. Modie, M.D.
The third ventricle is a narrow funnel-shaped midline
cerebrospinal fluid (CSF)-containing compartment lined
with ependymal cells in direct communication
anterosuperiorly with each lateral ventricle through the
foramen of Monro and posteriorly with the aqueduct of
Sylvius. It has a roof, a floor, and an anterior, posterior, and
two lateral walls. A multitude of disease processes involve
the third ventricle, leading to characteristic alterations of
the anatomy. Thus, a clear understanding of the normal
radiological anatomy is necessary to characterize properly a
pathological process and formulate a differential diagnosis.
Currently available techniques for examination of the
third ventricle include: high resolution computerized
tomography (CT), with or without intravenous contrast
administration, metriza-mide CT-ventriculography and
cisternography, and selective cerebral angiography. In most
cases there is no need for metrizamide administration; high
resolution CT together with sagittal reformatting are
adequate. In problem cases, metrizamide studies can
provide excellent detail of the third ventricle. Angiography
retains a major role in the diagnosis of suspected
aneurysms, vascular malformations, and certain tumors.
In neonates, the anterior fontanel serves as an acoustic
window for examination with real time ultrasound.
Ventricular size and position, the internal sonographic
architecture of lesions (i.e., cystic versus solid), and
parenchymal hemorrhage are well displayed.
Magnetic resonance imaging (MRI) has devel-
oped rapidly since the publication of diagnostic quality
images in 1980 (44). Although still undergoing intensive
development and investigation, MRI offers several unique
features: increased sensitivity and tissue discrimination
compared to x-ray CT (7), freedom from potential side
effects of ionizing radiation (6), direct mul-tiplanar (e.g.,
axial, sagittal, or coronal) imaging capability, and lack of
the beam-hardening artifact encountered with posterior
fossa CT.
Radiological Anatomy
Roof
The roof of the third ventricle, extending from the
foramen of Monro anteriorly to the supra-pineal recess
posteriorly, has a slightly upward convex contour. It is
defined anatomically by the fornix, the tela choroidea, the
paired internal cerebral veins and the great vein of Galen
(best seen on lateral views in the late venous phase of
selective internal carotid angiograms).
The body and crura of the fornix and the hip-pocampal
commissure (which interconnects the crura) are not well
seen on CT scans either in the axial plane or with sagittal
reformatting because of the lack of contrast between these
structures and the surrounding neural tissue. However, the
anterior limbs of the fornix (the columns), highlighted by
CSF in the lateral and third ventricles, are well seen on
axial scans at the level of the foramen of Monro. MRI
displays the fornix in its entirety on sagittal images. The
septum pelluci-dum, which is attached inferiorly to the
superior
surface of the body of the fornix, is tallest anteriorly and
shortest posteriorly. The septum pel-lucidum is best seen
in the coronal plane on CT scans. At the posterior end of
the septum pellu-cidum, the crura of the fornix and the
hippocam-pal commissure fuse with the splenium of the
corpus callosum.
The medial posterior choroidal artery (MPChA) arises
from the peduncular segment of the posterior cerebral
artery (PCA), extends posteriorly and medially, and enters
the lateral portion of the quadrigeminal cistern. It then
contributes to the blood supply of the quadrigeminal plate
and pineal gland. Crossing anterior and lateral to the
pineal gland, the MPChA penetrates through the layers of
the tela choroidea, supplies the Choroid plexus just
inferior to the roof of the third ventricle, and lies adjacent
to the internal cerebral veins. The roof of the third
ventricle is outlined during infancy and childhood by the
cistern of the velum interpositum, a triangular or
diamond-shaped space formed by infolding of arachnoid
over the third ventricular roof. This CSF-con-taining
space represents a superior and anterior extension of the
quadrigeminal cistern. The cistern of the velum
interpositum becomes obliterated by adulthood.
The body of the fornix defines the cistern of the velum
interpositum superiorly, and the epithelial roof and
Choroid plexus of the third ventricle and adjacent tela
choroidea define it infe-riorly.
The lateral margin of the third ventricular roof is
defined by the choroidal fissure, bounded by the lateral
margin of the body of the fornix and the superomedial
surface of the thalamus. The crus fornix and the pulvinar
are posterior. The
choroidal fissure is in direct communication with the
retropulvinar cistern and can occasionally be identified in
the axial plane during metrizamide CT-cisternography.
Anterior Wall
The anterior wall of the third ventricle extends from the
foramen of Monro above to the optic chiasm below. The
superior margin is bounded by the columns of the fornix
and the rostrum of the corpus callosum. Immediately below
the foramen of Monro, the anterior commissure indents the
anterior wall and continues inferiorly for about 10 mm as
the lamina terminalis. The anterior wall terminates at the
optic recess, just above the optic chiasm. These anatomical
landmarks are well seen on either metrizamide ven-
triculography or cisternography in the lateral projection. CT
of the anterior wall region can also be accomplished with
thin sections (2 mm or less) in the axial plane, followed by
sagittal reformatting (Fig. 11.1 A). MRI is capable of
imaging the anatomy of the anterior third ventricle in the
sagittal plane without the use of intrathecal contrast or the
need for computer reformatting.
The thalamostriate vein, septal vein, and superior
choroidal vein unite to join the internal cerebral vein; this
junction, the venous angle, is U-shaped and
angiographically marks the foramen of Monro (Fig. 11.IB
and C). In some cases, however, the junction lies behind
the foramen— a false venous angle. The Choroid plexus of
the lateral ventricle and the distal branches of the MPChA
also pass through the foramen of Monro. An inconstant
vessel, the precallosal artery, may arise from the anterior
communicating artery (ACoA) and cross cephalad in front
of the lamina

Figure 11.1. A. Normal third ventricle. Sagittal reformatted image of a metrizamide CT-
cisternogram outlining the optic (o) and infundibular (i) recesses of the third ventricle.
Note the diaphragma sellae (arrowheads) above the pituitary gland (white arrow). The
anterior wall of the third ventricle, mamillary bodies (m), and tegmentum of the midbrain
(t) are also well visualized.
 Figure 11.1. В and С. Normal third ventricle.
terminalis to supply the rostrum of the corpus callosum.
The ACoA also gives rise to multiple small perforating
arteries supplying the lamina terminalis. The precallosal
artery and the perforating branches from the ACoA are
rarely seen on routine selective internal carotid arteriog-
raphy. The A1 segments of the anterior cerebral arteries
(ACAs) cross over the optic chiasm on either side of the
optic recess. These arterial relationships can be best
appreciated on thin
section direct coronal CT through the optic chiasm.
Floor
The floor extends from the chiasm posteriorly to the
aqueduct of Sylvius. The external landmarks outlining the
floor from anterior to posterior include the optic chiasm,
infundibulum, tuber cinereum, mamillary bodies, posterior
perforated substance, and tegmentum of the mid-
brain. The infundibular recess of the third ventricle
indents the infundibulum of the pituitary gland (Fig.
11.1 A). The chiasm, optic tract, infundibulum, and
mamillary bodies are best seen on metrizamide CT-
cisternography, whereas the optic and infundibular
recesses are best imaged with metrizamide
ventriculography in the lateral view.
The posterior communicating artery (PCoA), the
P1 segment of the PCA, and the apex of the basilar
artery lie below the optic tract. Multiple small
perforating arteries arise from these vessels to supply
the structures along the floor of the third ventricle.
These perforating branches can be seen routinely on
magnification vertebral arteriography. The anterior
choroidal artery (AChA) provides a vascular supply
to the optic tract and the optic radiations. The
hypophysis is supplied by two vessels: the inferior
and superior hypophyseal arteries. The inferior
hypophyseal artery is a branch of the
meningohypophyseal trunk of the precavernous
internal carotid artery (IСA), whereas the superior
hypophyseal artery is a small branch of the
supraclinoid ICA. The terminal branch of the
superior hypophyseal artery also supplies the tuber
cinereum. The superior and inferior hypophyseal
arteries are not seen normally, even on lateral
magnified selective internal carotid arteriography,
and their visualization indicates a pathological
process in the parasellar region or the development of
collateral pathways in cases of vascular occlusive
disease. The only major venous structure that abuts
the third ventricular floor is the anterior
pontomesencephalic vein (APMV), coursing along
the floor of the ventricle, the anterior surface of the
tegmentum, and the belly of the pons, finally draining
superiorly and posteriorly into the posterior
mesencephalic vein. The venous phase of selective
vertebral arteriograms demonstrates the APMV.
Posterior Wall
The suprapineal recess, extending between the tela
choroidea and the superior surface of the pineal
gland, forms the posterosuperior boundary of the
third ventricle. Below the suprapineal recess, the
pineal gland extends posteriorly into the
quadrigeminal cistern. The pineal recess indents the
gland as a notch dividing the gland into an upper
compartment attached to the habenu-lar commissure
and a lower compartment attached to the posterior
commissure. The aqueduct of Sylvius defines the
posteroinferior limits of the third ventricle.
Metrizamide ventriculog-
raphy delineates the suprapineal and pineal recesses.
If calcified, the habenular commissure and the
pineal gland can be demonstrated on plain films or CT
scans. The habenular commissure calcification has a
characteristic С shape, whereas the pineal gland
calcification is usually irregular and speckled.
Occasionally, the pineal calcification is shell-like
because of the development of a small cyst within the
pineal gland. The major vessel supplying the posterior
third ventricle is the MPChA. On a lateral vertebral
arteriogram, the MPChA has a characteristic M
configuration and is located between the
thalamoperforating arteries anteriorly and the lateral
posterior choroidal artery posteriorly.
The deep venous system of the supratentorial
compartment is located both anterior and posterior to
the pineal gland. The most important venous
structures in this region are the paired internal
cerebral veins, which course posteriorly along the roof
of the third ventricle (Fig. 11.IB and C). These veins
deviate slightly from the midline as they approach the
pineal gland, joining to form the great vein of Galen
beneath the splenium of the corpus callosum.
Originating at the lateral angle of the body of the
lateral ventricle, the direct lateral vein drains medially
into the internal cerebral vein, just anterior to the
pineal gland. Another important landmark, the medial
atrial vein, traverses the choroidal fissure and drains
into the internal cerebral vein just posterior to the
pineal gland. Other major venous structures that
converge in the pineal region include the precentral
cerebellar vein (draining superiorly), the basal vein of
Rosenthal (draining posteromedially), and the internal
occipital vein (draining anteromedially into the great
vein of Galen). Both selective internal carotid and ver-
tebral arteriograms must be obtained to demonstrate
all of these venous structures.
Contrast-enhanced CT with sagittal reformatting
demonstrates the relationship of the pineal gland to
the major neighboring venous structures. Subtle
lesions in the periaqueductal region may require
metrizamide CT-ventriculography and CT-
cisternography.
Lateral Walls
The lateral walls of the third ventricle are lined by
ependyma and are bordered by the hypothalamus
inferiorly and the thalami laterally. Several
commissures bridge the third ventricle and form parts
of its boundary. The largest of these is the massa
intermedia, situated in the upper half of
 tion axial CT scanning, the columns of the fornix and the
massa intermedia are often seen.

Cross Sectional Imaging Techniques

In adults, contrast-enhanced CT is performed after the
intravenous administration of contrast material containing
42 g of iodine. In children, intravenous contrast is
administered at a dose of 2 ml of 30% contrast material per
pound of body weight.
For metrizamide CT-ventriculography, the volume and
concentration of metrizamide depends on the size of the
ventricular system. For normal-sized ventricles, a dose of 3
to 5 ml of metrizamide at a concentration of 170 mg of
iodine per ml is adequate. Massive hydrocephalus requires
the use of a larger volume of contrast in a higher
concentration. Contrast may be instilled via ventricular
puncture or directly into an indwelling ventricular shunt
catheter.
For metrizamide CT-cisternography, one performs
lumbar puncture with a 22 gauge needle and then 3 to 5 ml
of metrizamide at a concentration of 170 mg of iodine per
ml are injected. Because metrizamide possesses a higher
specific gravity than CSF, the contrast agent flows ce-
phalad into the basal cisterns as the patient assumes the
Trendelenberg position. CT scanning may commence
within minutes of contrast instillation. Because of the low
dose of contrast agent, metrizamide CT-cisternography
may be performed safely as an outpatient procedure.
Neonatal ultrasound scanning is performed with a
portable real time sector scanner through the anterior
fontanel, with the use of 5-MHz transducer. The transducer
may be swept anter-oposteriorly to obtain optimal coronal
sections and is angled laterally to produce parasagittal
images. Cranial ultrasound is technically feasible until
closure of the anterior fontanel, which generally occurs at 9
to 12 months of age.
Several excellent reviews of basic MRI physics are
available (6, 23, 64, 72). The proton (1H), by virtue of its
abundance and physical characteristics, is best suited for
imaging available paramagnetic species found in biological
tissues (93). Protons act like spinning tops and tend to line
up in the presence of a strong external magnetic

a high signal intensity. B. A T2-weighted spin-echo image

demonstrates reversal of the relative signal intensities of
CSF, white matter, and gray matter.
Figure 11.2. Normal axial MRI scans. A. A heavily Ti-
weighted inversion recovery image demonstrates excellent
discrimination of the lower intensity gray matter and the
higher intensity white matter. Lower intensity structures are
dark; higher intensity structures are white. CSF and cortical
bone signals are low to absent. Fat in the diploic space and
scalp produces

Figure 11.3. Normal sagittal and coronal MRI scans. A. A
midline sagittal image from a heavily T1-weighted spin-
echo sequence demonstrates excellent delineation of the
aqueduct of Sylvius. Note the detailed depiction of
normal structures: corpus callosum, fornix, optic chiasm,
mamillary bodies, quadrigeminal plate, brain stem, fat in
the marrow space of the clivus, and fourth ventricle. B. A
coronal T1-weighted image provides sharp contrast
between the high intensity optic chiasm and the adjacent
low intensity of CSF. Note the absence of signal in the
lumen of the cavernous and supraclinoid portions of the
ICAs (arrowheads), with high intensity from the
surrounding slowly flowing blood in the cavernous
sinuses (particularly on the reader's right). The pituitary
gland (white arrows) lies
field, producing within the tissue sample a macroscopic
vector called magnetization.
A preselected radiofrequency pulse imparts energy to
these spinning, aligned protons. The pulse produces two
important outcomes: first, the spins of the individual
protons become synchronized (i.e., become coherent) and,
second, the magnetization vector is tipped away from
alignment with the external magnetic field. When the
radiofreqeuncy pulse stops, the protons "relax" back toward
alignment with the applied external field. In this relaxation
phase, some of the absorbed energy is radiated from the
tissue as a radiofrequency signal. Protons emit the energy at
different radiofrequencies depending on preselected
position-encoding spatial gradient fields. By analysis of the
emitted radiofrequency spectrum, the intensity and location
of the emitted radiofrequency is established and an image is
constructed.
The intensity of the emitted radiofrequency energy
(signal intensity) depends upon four factors: mobile proton
density, longitudinal relaxation time (T1), transverse
relaxation time (T2), and, in the case of vascular structures,
flow rate. Most important in determining final image con-
trast are the intrinsic tissue characteristics, T1 and T2. T1
denotes the time required to achieve maximal net
magnetization and is a function of interactions between
individual protons and their surrounding molecular
environment, or lattice. T1 is therefore referred to as the
"spin-lattice relaxation time." T2 measures decay of the
radiofrequency signal from excited tissue and relates
closely to loss of coherence within the sample. Because this
dephasing of proton spins occurs as a result of interactions
with other spinning nuclei, it is referred to as the "spin-spin
relaxation time." Regrowth of the net magnetization vector
in the direction of the external magnetic field is not
equivalent to loss of coherence within the tissue sample
and, therefore, knowledge of T1 does not predict the T2
value of the same tissue.
Pulsing sequences such as inversion recovery and spin-
echo are available to accentuate differences in T1 or T2
selectively within the sample (Figs. 11.2 and 11.3). In a
"T1-weighted image," for example, regional differences in
T1 are highlighted and tissues with short T1 values
generate stronger signals than tissues with longer T1 val-
ues. Inversion recovery sequences have the
superior to the aerated sphenoid sinus and lamina dura of
the sellar floor. Sinus air and compact bone produce little
or no signal.
greatest sensitivity to differences in tissue T1 values. By
selection of pulse sequence parameters, heavily T1-
weighted spin-echo imaging is possible. In conventional
gray scale display, regions with strong signals appear white
and areas of weak or absent signals appear darker. Con-
versely, structures with a long T2 will generate strong
signals (and thereby appear white) on heavily T2-dependent
spin-echo sequences, whereas structures with a shorter T2
generate weak signals and appear darker.
Lesions along the Roof of the Third Ventricle
Congenital Lesions
Cavum of the Septum Pellucidum, Cavum Vergae, Cavum
of the Velum Interpositum
Congenital anomalies represent a major portion of
lesions along the roof of the third ventricle. Cavum of the
septum pellucidum (CSP), cavum vergae (CV), and cavum
of the velum interpositum (CVI) are the most common.
These anomalies are typically discovered incidentally on
CT scanning (see Fig. 11.5). The CSP and the CV lie in the
same plane above the third ventricle and commonly occur
together. Embryologically, involution of these two cavae
commences posteriorly and extends rostrally; therefore, a
CV never occurs in the absence of a CSP. On CT scanning,
the cavae have the attenuation of CSF. The CSP is located
anterior and the CV posterior to the vertical plane formed
by the columns of the fornix. On both axial and coronal
scans, the CV always lies superior to the internal cerebral
vein. This anatomical relationship differentiates the CV
from cystic lesions of the third ventricle, which always lie
inferior to the internal cerebral vein.
True cysts may arise from the septum pellucidum (22),
blocking the foramen of Monro and causing obstructive
hydrocephalus. Ventricular obstruction is a differential
feature distinguishing these true cysts from a simple CSP.
The first two cases of pathological cysts in the septum
pellucidum were reported by Dandy in 1931. Since then,
other cystic lesions in this region have been described,
including neuroepithelial (colloid) cysts, cysticerosis cysts,
ependymal cysts, cystic gliomas, superior extension of
cystic Craniopharyngiomas, epidermoids, and dermoid
cysts.
A CVI, as already described, is a normal structure in the
infant brain. However, it can be confused with other CSF-
containing lesions in the
pineal region. Dilatation of the suprapineal recess in
conjunction with either massive hydrocephalus or partial
agenesis of the corpus callosum can mimic a CVI.
Metrizamide CT-ventric-ulography defines the exact
anatomy.
True arachnoid cysts of the velum interpositum also
occur, distorting the quadrigeminal cistern and to a lesser
degree the ambient cistern. An arachnoid cyst in this region
can be differentiated from a CVI by metrizamide CT-cister-
nography: an arachnoid cyst will generally not fill with
contrast, whereas a CVI will. These lesions may even
extend superiorly and laterally along the choroidal fissure
into the trigone of the lateral ventricle.
Agenesis of the Corpus Callosum
Agenesis of the corpus callosum is the next most
common congenital anomaly that occurs in the roof of the
third ventricle. It can be associated with hydrocephalus,
interhemispheric cysts, posterior fossa extraaxial cysts,
lipomas and other midline craniofacial anomalies (41). Em-
bryologically, the degree of callosal defect depends on the
stage at which developmental arrest occurs. Complete
agenesis occurs before the 12th gestational week. Partial
agenesis occurs later during intrauterine life and is thought
to result from a vascular or inflammatory insult. Because
the corpus callosum develops in an anteroposter-ior
direction, partial agenesis often involves the body and the
splenium of the corpus callosum and leaves the rostrum
intact. However, isolated agenesis of the rostrum has been
reported.
The primary radiological method for the diagnosis of
agenesis of the corpus callosum is CT in the axial and
coronal planes (Fig. 11.4). The frontal horns and bodies of
the lateral ventricles are widely separated, and the foramina
of Monro are enlarged. Separation of the posterior part of
the bodies of the lateral ventricles occurs in cases with
isolated posterior callosal agenesis. Enlargement of the
occipital horns and suprapineal recess is easily
demonstrable. The anterior interhemispheric fissure abuts
the anterior wall of the third ventricle because of the
absence of the rostrum of the corpus callosum. The medial
wall of the lateral ventricle is concave because of
protrusion by the cingulate gyrus and Probst's bundle (the
latter represents ectopic longitudinal callosal fibers that
failed to cross the midline during embryogenesis). The
third ventricle is high-riding, situated between rather than
below the lateral ventricles. Hypoplasia of the falx is often
associated with agenesis of the corpus callosum.
 Figure 11.4. Agenesis of the corpus callosum. A. Contrast-enhanced CT scan. Part of the
anterior interhemispherie fissure is seen in the usual location of the rostrum of the corpus
callosum [arrows). The anterior horns are slightly separated. B. Coronal reformatted
image demonstrates the high-riding third ventricle (white arrows), which separates the
adjacent frontal horns (black arrowheads). The high density above the third ventricle
represents the internal cerebral veins.

Lipomas involving the genu of the corpus callosum
occur in approximately 50% of cases of agenesis of the
corpus callosum. Calcification along the periphery of the
lipoma is often associated with this anomaly.
Angiography is seldom necessary to diagnose agenesis
of the corpus callosum. If carried out in
problem cases the vertically oriented "wandering"
pericallosal artery and the high-riding, separated internal
cerebral veins are distinctive (97).
Diencephalic Cyst
If the septum pellucidum is also absent, the roof of the
third ventricle may balloon dorsally
and result in an interhemispheric or diencephalic cyst (41)
(best imaged on direct coronal CT scans). The CT
appearance of a diencephalic cyst associated with agenesis
of the corpus callosum may mimic an interhemispheric
arachnoid cyst.
Septooptic Dysplasia
Another rare congenital lesion deserving attention is
septooptic dysplasia, first described by deMorsier. Patients
with this condition often present clinically with
hypothalamic or pituitary dysfunction (predominantly
deficiency of growth hormone [GH], thyroid-stimulating
hormone, adrenocorticotropic hormone, and antidiuretic
hormone). CT findings are combined optic nerve and optic
chiasm hypoplasia, absence of the septum pellucidum,
squaring of the frontal horns with flattening of the roof of
the third ventricle, and inferior pointing of the
anteroinferior margin of the frontal horns (70). These
changes are best seen in the direct coronal projection. The
pituitary stalk may be enlarged when there is associated
diabetes insipidus. Enlargement of the optic recess (a
remnant of the primitive optic ventricle) can be
demonstrated on sagittal reformatting of thin section
metrizamide CT-cister-nography. Hypothalamic
dysfunction and typical CT findings need not be present in
all patients with this syndrome. Absence of the septum pel-
lucidum is found in approximately 75% of the reported
cases. Other midline anomalies including harelip, cleft
palate, and absence of the olfactory bulb and tract have
been reported in patients with septooptic dysplasia.
Neoplastic Lesions
Tumors along the roof of the third ventricle usually
manifest themselves by obstruction of the foramen of
Monro.
Colloid Cyst
Colloid cysts are unsually spherical or ovoid and range in
diameter from a few millimeters to 9 cm. Although
generally originating from the roof of the third ventricle,
colloid cysts arising from the septum pellucidum have been
reported, with associated widening of the septum (21).
These lesions are usually homogeneous and hy-perdense on
noncontrast CT (36) (Fig. 11.5). However, cysts isodense
with either the surrounding brain or CSF have also been
reported. Most colloid cysts demonstrate minimal en-
hancement on postcontrast scans. High attenuation on a
precontrast scan is presumably due to desquamated
secretory products from the cyst wall with high protein
content and hemosiderin.
If the suspected colloid cyst is isodense, metrizamide
ventriculography will establish the diagnosis.
Glioma
Glioma involves the roof of the third ventricle, usually as
an inferior extension of a primary tumor involving the
corpus callosum. The CT appearance is the same as that of
gliomas involving the lateral walls of the third ventricle
(discussion follows under "Lesions Affecting the Lateral
Walls of the Third Ventricle").
Subependymal Giant Cell Astrocytoma
Subependymal giant cell astrocytomas usually occur in
the walls of the lateral ventricles after malignant
degeneration of hamartomas associated with tuberous
sclerosis (5). The roof of the third ventricle is involved if
the tumor grows inferiorly. Radiological description of this
entity is presented under "Intraventricular Lesions."
Subependymoma
Subependymomas are rare in the septum pellucidum
(45), constituting 5% of all reported cases (84). They are
histologically benign, lobu-lated, and sharply demarcated
from surrounding tissue. Growth is by expansion toward
the ventricle, in contradistinction to gliomas, which enlarge
by infiltration of surrounding structures. Subependymomas
are associated with less edema than are gliomas.
Subependymomas are isodense or slightly hyperdense on
noncontrast scans. The enhancement pattern of this tumor
is rather homogeneous, but not intense. The larger tumors
(4 to 5 cm in diameter) frequently demonstrate cyst
formation, focal calcification, and hemorrhage due to
vessel degeneration.
Lymphoma
Primary central nervous system (CNS) lymphoma, an
uncommon tumor (less than 1.5% of primary brain tumors),
most often occurs in patients with primary
immunodeficiency or im-munosuppression secondary to
organ transplantation. Primary CNS lymphomas involve
the roof of the third ventricle by inferior extension of tumor
originating in the corpus callosum. In addition, commonly
encountered tumor foci occur, particularly in the basal
ganglia, as well as in the thalamus, periventricular white
matter, and cerebellar vermis (32). The lesions are often
mul-tifocal. On the noncontrast CT scan, the lesions are
usually isodense or slightly hyperdense. Edema and mass
effect are significantly less than with metastases of
comparable size. The
 Figure 11.5. Colloid cyst. A. A noncontrast axial CT scan demonstrates an intrinsically
dense colloid cyst splitting the leaves of the septum pellucidum adjacent to the columns
of the fornices. Note the incidental cavum of the septum pellucidum [arrows)
immediately anterior to the cyst. B. Sagittal reformatted image depicts the mass near the
foramen of Monro (anterior is to the reader's left).

enhancement pattern is homogeneous, well cir- are extremely rare, in contradistinction to their frequency in
cumscribed, and intense (similar to meningiomas). Low primary gliomas. Angiography often shows a relatively
density centers within the lesions avascular mass.
Epidermoid and Dermoid Cysts
Epidermoid and dermoid cysts rarely involve the roof of
the third ventricle. Epidermoid cysts outnumber dermoid
cysts among intracranial tumors and have a tendency to
occur away from the midline structures. The radiological
differential diagnostic features are described under
"Lesions Affecting the Anterior Wall of the Third
Ventricle."
Vascular Lesions
Aneurysm of the Vein of Galen
Aneurysm of the great vein of Galen is a rare midline
arteriovenous malformation. The clini-

Figure 11.6. Vein of Galen aneurysm (with associated dural AV malformation). A.

Postcontrast CT scan image demonstrates a large, densely enhancing mass in the
posterior third ventricle and straight sinus. Note multiple enhancing arterial feeding
vessels. B. Lateral view of the arterial phase of an intraarterial left ICA digital angiogram
demonstrates enlarged feeding arteries from the meningohy-pophyseal trunk [three
rowheads), cavernous branches of the ICA [single arrowhead), pericallosal artery [single
arrow), and dural branches of the posterior cerebral artery [double arrows). C. Lateral
view from the late arterial phase of a selective vertebral arteriogram demonstrates a huge
vein of Galen aneurysm, continuing inferiorly as a posterior fossa venous varix. The sella
and clivus have been outlined in this subtraction image. D. Anteroposterior view from the
late arterial phase of the vertebral arteriogram documents the midline location of the vein
of Galen aneurysm. Note the tortuous basilar artery [arrow).
cal presentation depends on the age of presentation
and on the volume of blood shunted through the
malformation (28). In newborns, cardiac failure and
cranial bruits are the most common presenting signs.
In older children with a lesser degree of
arteriovenous (AV) shunting, the clinical picture is
that of an enlarging head due to obstructive
hydrocephalus secondary to aqueductal compression
by the dilated venous varix. Cranial bruits, seizures,
and subarachnoid hemorrhage may also be present.
Radiologically, this entity can be divided into two
groups: (a) malformations supplied by a few large
arterial feeders with almost direct shunting between
the varix and the enlarged vein of Galen and (b)
angiomatous malformations originating in the
thalamus and basal ganglia, with a slow-flowing
shunt draining into the dilated galenic venous
system (59).
On a noncontrast CT scan, a fusiform midline
structure of homogeneously increased attenuation is
located along the superior and posterior aspects of
the third ventricle. The lesion connects with an
enlarged torcular by a dilated midline channel
representing the straight sinus. The arterial feeders
to the dilated venous varix prominently enhance in a
characteristic serpiginous pattern (Fig. 11.6A). Other
CT findings include hydrocephalus caused by
compression of the aqueduct by the venous varix or
defective CSF re-sorption secondary to intracranial
venous hypertension and patchy areas of low
attenuation distinct from the malformation, related to
ischemia resulting from steal of blood away from the
surrounding brain parenchyma by the malformation.
Even though contrast-enhanced CT demonstrates
both enlarged arterial feeders and draining veins,
bilateral selective internal carotid and vertebral
arteriography is needed for surgical planning. Vein
of Galen malformations are commonly supplied by
distal branches of the АСА, AChA, PCA, posterior
choroidal arteries, and thalamoperforating arteries
(Fig. 11.6B). Spontaneous thrombosis of aneurysms
of the great vein of Galen is unusual, potentially
mimicking a pineal region tumor on CT. Aneurysms
can diminish in size after thrombosis.
Inflammatory Lesions
Cysticercosis
The diagnosis of a cysticercotic cyst involving the
septum pellucidum (30) should be considered if (a)
there are other calcific lesions within the brain
parenchyma, (b) the basal cisterns are dis-
torted because of meningeal involvement, (c) in-
traventricular cysts are present (99), and (d) com-
municating hydrocephalus is present. Cisternal and
ventricular involvement can be confirmed with
metrizamide CT-cisternography or ventric-ulography.
Subacute cysticercosis, i.e., dying larvae, can
occasionally show ringlike or nodular enhancement
after intravenous contrast administration (49).
Postinflammatory Gliosis of the Foramen of Monro
Rarely, a web of gliosis in response to inflam-
matory disease can occur in the foramen of Monro,
leading to unilateral obstruction of the lateral
ventricle. Neither contrast-enhanced CT nor
metrizamide CT-ventriculography dependably outline
the gliosis in these cases, although the latter test will
confirm obstruction of the foramen.
Lesions Affecting the Anterior Wall of the Third
Ventricle
Neoplastic Lesions
Meningioma
Meningiomas arising from the planum sphen-
oidale, olfactory groove, medial aspect of the
sphenoid ridge, diaphragma sellae, and tubercu-lum
sellae can all extend superiorly to deform the anterior
wall of the third ventricle. Meningiomas of the
planum sphenoidale may cause hyperostosis or
blistering of the bone, pneumo-sinus dilatans (an
upward bowing of the cortex of the posterior ethmoid
or anterior sphenoid air cells) (47), or pneumatization
of the anterior cli-noid processes. These findings are
easily discernible on plain films or bone window CT
images. Meningiomas only rarely cause bony erosion.
On noncontrast CT, meningiomas commonly appear
hyperdense because of microscopic psammoma body
calcifications. Enhancement is homogeneous (Fig.
11.7) except when necrotic, cystic, hemorrhagic, or
lipomatous components exist within the tumor.
Because of their extraaxial origin, meningiomas
characteristically have a long, smooth, broad-based at-
tachment to the planum and the spheroid ridge and
superior extension is modest relative to other
suprasellar lesions of comparable size.
Angiography is indicated in patients with suspected
meningiomas to confirm the diagnosis and outline the
vascular anatomy before operation. The most
characteristic sign of a planum sphenoidale
meningioma is elevation of the per-
 Figure 11.7. Planum sphenoidale/tuberculum sellae meningioma. A. Postcon-trast
axial CT scan demonstrates a homogeneously enhancing midline mass in the
floor of the anterior fossa and the suprasellar region. B. Sagittal reformatted
image defines the broad-based attachment of the mass to the tuberculum sellae
and planum sphenoidale.

icallosal and frontopolar arteries above the floor of the
anterior cranial fossa. Downward displacement of the
supraclinoid ICA and subsequent closing of the
carotid siphon may occur. Significant displacement of
the АСА and its branches from the midline is not a
constant finding. Lesions arising from the planum
sphenoidale or the tuberculum region can lead to
encasement of the carotid artery; this finding denotes
nonresecta-bility. Posterior ethmoidal branches of the
ophthalmic artery may enlarge to supply a planum
sphenoidale meningioma. In addition, a direct
anastomosis between the middle meningeal and
ophthalmic arteries potentially provides additional
blood supply to the tumor. If a meningioma erodes
through the roof of the orbit, the ophthalmic artery
may become stretched and encased.
The intermediate phase of angiography dem-
onstrates a homogeneous tumor blush that persists
well into the late venous phase. Large planum
sphenoidale meningiomas elevate the septal vein and
displace the anterior portion of the internal cerebral
vein posteriorly.
Meningiomas arising from the tuberculum sel-
lae derive their principal blood supply from men-
ingeal branches of the cavernous IСA. Tubercu-lum
meningiomas can also elevate the A1 segment of the
АСА.
Epidermoid Tumors
Epidermoid tumors arise from ectodermal cell
inclusions within the neural roof at the time of
neural tube closure between the third and fifth week
of embryogenesis. These lesions comprise less than
1 % of all intracranial tumors. Due to their slow
growth rate and soft cheeselike consistency,
epidermoids expand initially within CSF cisterns
along pathways of least resistance. However, they
can later deform and rotate adjacent neural
structures. Epidermoid tumors near the anterior third
ventricle may extend anteriorly along the floor of the
anterior cranial fossa or inferiorly to involve the
parasellar region, middle fossa, cerebellopontine
angle cistern, interpe-duncular fossa, and prepontine
cistern. Epidermoids in the suprasellar region often
produce symptoms by compressing the visual
pathway and the cranial nerves located within the
cavernous sinus. Symptoms are typically long-
standing and less severe than with other intracranial
tumors of comparable size.
On noncontrast CT, epidermoids characteristically
have attenuation values approaching those of CSF
(25). This finding reflects the variable proportions of
low density cholesterol, high density keratin, and
desquamated epithelial debris. Capsular calcification
rarely occurs. Intrinsically dense epidermoids with
attenuation values of 80 to 120 Hounsfield units
(HU) on noncontrast CT have been reported in the
posterior fossa (12), but not as yet in the floor of the
anterior cranial fossa. As a rule, because of their
relative avascularity, epidermoids do not enhance
after intravenous contrast administration.
Metrizamide CT-cisternography is very useful for
the diagnosis of epidermoid tumors. The interstices
of epidermoids trap metrizamide, and the CT
appearance is analogous to the "cauliflower" sign
shown on pneumoencephalograms. Epidermoid
tumors, even though benign, can recur if not
completely excised. Spontaneous rupture of
epidermoids may occur, resulting in chronic
granulomatous arachnoiditis and communicating
hydrocephalus.
Lymphoma and Leukemia
Lymphomatous and leukemic deposits can occur
in the frontal lobe or the surrounding dura
mater with deformity of the anterior third ventricle.
The CT appearances of these deposits have already
been described and may closely mimic those of
meningiomas.
Demyelineating Disease
Abnormal enhancement of the white matter tracts
along the roof and anterior wall of the third ventricle
has been reported in Type 2 adrenoleu-kodystrophy
(ADL) (27) and in Alexander's disease (52).
Enhancement is due to disruption of the blood-brain
barrier secondary to an inflammatory response. In the
acute phase of Type 2 ADL, prominent enhancement
is noted in the rostrum and genu of the corpus
callosum. Other areas of white matter tract
involvement include the internal capsule, cerebral
peduncles, corona radiata, and forceps major. Type 2
ADL is also characterized by the absence of
symmetrical decreased attenuation in the peritrigonal
white matter and the absence of an advancing margin
of contrast enhancement proceeding anteriorly,
features characteristic of Type 1 ADL. The CT pattern
of Type 2 ADL has not been reported in other types of
leukodystrophic, neoplastic, or infectious processes.
Type 2 ADL should be considered when insidious
personality changes, mental deterioration, and
disturbances of gait and vision occur in a young boy.
Laboratory evidence of adrenal insufficiency need not
be present. Brain biopsy is necessary for definitive
diagnosis.
Alexander's disease is a rare leukodystrophy of
uncertain pathogenesis, also demonstrating abnormal
enhancement along the anterior aspect of the third
ventricle. All proven cases have been sporadic.
Clinical manifestations usually develop during the
first year of life, with progressive retardation and an
enlarging head circumference. During the acute phase
of Alexander's disease, symmetrical, well-demarcated
areas of low attenuation involve the deep cerebral
white matter and basal ganglia. After intravenous con-
trast infusion, prominent enhancement appears in the
anterior columns of the fornices, caudate nuclei,
subependymal white matter, optic radiations, and
forceps minor. Again, this constellation of CT
findings has not been reported in other
leukodystrophic, neoplastic, or infectious processes.
Characteristically, megalocephaly without
hydrocephalus is present in patients with Alexander's
disease. Because there is no known biochemical
marker in these patients, a brain biopsy is necessary to
establish the diagnosis.
Lesions Affecting the Floor of the Third Ventricle

Neoplastic Lesions

Optic Nerve and Hypothalamic Glioma

Optic nerve glioma occurs infrequently, accounting for
0.6 to 1.2% of primary intracranial tumors. CNS
neurofibromatosis is present in 14 to 36% of patients with
optic nerve glioma. Lesions confined to the optic nerve
occur more frequently in prepubertal children, whereas
chiasmal lesions are more common in adolescents. In large
series, approximately 30% of the tumors involve the
prechiasmatic portion of the optic pathway, with the
remainder involving the anterior third ventricle, the optic
chiasm, and the optic tract (Fig. 11.8). Lesions involving
the posterior optic pathway are considered unrest-able
because of invasion of the thalamus and medial temporal
lobe.
Histologically, two distinct types of glioma arise in the
optic pathway, benign and malignant. The benign type
occurs more commonly in childhood, tends to be localized
to the optic nerve (with or without chiasmal involvement),
and usually behaves indolently. However, malignant
degeneration of these tumors has been documented. The
malignant type is less common, tends to occur in middle-
aged patients, and may initially mimic optic neuritis
clinically (48). Malignant optic nerve glioma may be fatal
in a relatively short time. These tumors are often centered
in the optic chiasm or optic tract, with infiltration of the
hypothalamus and medial temporal lobe. Hypothalamic
dysfunction often occurs later in the course of the disease.
On CT, the normal optic nerve and optic chiasm are
isodense with brain parenchyma and do not enhance with
intravenous contrast administration. The normal chiasm has
a smooth contour with a U or boomerang shape on axial
sections and a dumbbell shape on coronal images. The optic
recess of the third ventricle is filled with CSF and has a
teardrop configuration above the chiasm on direct coronal
scans. The average chiasm normally measures 1.8 cm trans-
versely, 0.8 cm in the anteroposterior direction, and 0.4 cm
vertically (24).
The CT appearance of optic nerve glioma is variable
(83). Uniform or fusiform enlargement of the nerve, as well
as irregular thickening, are the most common presentations
(Fig. 11.9). Rarely, optic nerve glioma demonstrates calcifi-
cation before radiotherapy.

Figure 11.8. Optic chiasm glioma. A. Postcontrast axial CT

demonstrates an enhancing suprasellar mass with a cyst
[white arrow). The tumor extends posteriorly along the
optic tract (open arrow). B. A scan at a higher level
documents extension posteriorly along the optic tract
toward the lateral geniculate body (open arrow).

Figure 11.9. Optic nerve glioma. Top. Fusiform en-
largement of the right optic nerve extends back to
the optic chiasm (arrow). Bottom. On a scan
obtained 2 mm inferior to the upper image, note the
unilateral optic canal enlargement and the enlarged
optic nerve (arrow).
The radiological appearance of optic nerve glioma
is sometimes indistinguishable from that of optic
nerve meningioma. Both lesions often enlarge the
optic canal. The clinical history, sex, and age of the
patient are helpful in this regard.
Chiasmatic gliomas have a globular appearance
with a vertical dimension greater than 0.6 cm (24).
Intrathecal metrizamide may be necessary for the
diagnosis of small lesions. On non-contrast CT,
chiasmatic gliomas are isodense to slightly
hyperdense. The majority of tumors enhance. If
extension into the anterior third ventricle occurs,
obstructive hydrocephalus may develop.
Hemorrhage into chiasmatic gliomas and
intratumoral cystic degeneration are not uncommon.
The major consideration in the differential di-
agnosis of optic chiasm glioma is hypothalamic
glioma. Extraaxial tumor growth from the chiasm
indents the inferior third ventricle, resulting in
capping of the tumor by the CSF-con-taining
ventricle. Conversely, growth of lesions originating
in the hypothalamus characteristi-
cally leads to obliteration of the anterior and inferior
third ventricle. Early on, hypothalamic glioma causes
sideways displacement of the inferior third ventricle,
as the tumor arises just lateral to the midline (57). In
most cases it is impossible to differentiate an optic
chiasm glioma from a hypothalamic glioma (26).
After radiotherapy, extensive dystrophic cal-
cification due to mineralizing microangiopathy may
involve the entire optic pathway. This diagnosis is
easily established by CT.
Angiography plays a limited role in the radiological
evaluation of lesions of the optic chiasm and should
be performed only to exclude an aneurysm or a
meningioma. The internal carotid arteriogram often
demonstrates lateral displacement of the supraclinoid
ICA and upward bowing of the A1 segment of the
АСА. With invasion of the optic tract and medial
temporal lobe, displacement and encasement of the
cisternal segment of the AChA occurs, in keeping
with the anatomical proximity of this artery to the
optic tract. On vertebral angiography, a chiasmatic
glioma may cause displacement and stretching of the
thalamoperforating arteries. If the tumor is of
sufficient size, venous phase films demonstrate
elevation of the internal cerebral vein and evidence of
hydrocephalus. The high density on nonenhanced CT
and homogeneous blush on angiography characteristic
of meningiomas are absent from studies of chiasmatic
gliomas.
Pituitary Adenomas
CT scanning allows direct identification of the
pituitary gland, infundibulum, cavernous sinuses,
neighboring arteries, and bony sella tur-cica. CT
detects intrasellar microadenonas (3 to 4 mm in
diameter) and extension beyond the sella (95).
Adenomas of any histological types or degree of
secretory activity may invade the suprasellar cistern,
cavernous sinuses, or sphenoid bone. Prolactinomas
are the commonest pituitary adenomas associated with
suprasellar extension, followed by endocrine-inactive
adenomas and GH-secreting adenomas (94).
Normal pituitary tissue possesses no blood-brain
barrier and enhances in proportion to the blood-iodine
level. Macroadenomas, tumors larger than 10 mm in
diameter, usually enhance homogeneously and can
produce expansion or erosion of the sella turcica.
Central areas of low attenuation from cystic
degeneration or prior hemorrhage occur often in
macroadenomas (69, 95) (Fig. 11.10).
Lateral invasion into the cavernous sinus is difficult
to detect radiologically unless there is

Figure 11.10. Pituitary macroadenoma. A direct coronal CT
image demonstrates a pituitary macroadenoma with
suprasellar extension. Note the sloping of the sellar floor
(open arrows). A low density area (indicating either a cyst
or necrosis) is seen within the tumor [arrow).
asymmetrical bulging of the cavernous sinus because the
macroadenoma and cavernous sinuses enhance equally. On
direct coronal scans, tumor encroachment on the CSF space
in the chias-matic cistern indicates supersellar extension.
Metrizamide CT-cisternography permits exact delineation
of the optic chiasm in problem cases.
Angiography is indicated if there is difficulty in
distinguishing a macroadenoma from a men-ingioma or an
aneurysm. The angiographic features, in addition to major
vascular displacements, include a vascular tumor blush and
abnormal enlargement of the meningohypophyseal trunk
and the superior and inferior hypophyseal branches of the
ICA. With extensive lateral growth, the tumor may
parasitize supply from the middle meningeal artery.
Cavernous sinus venography may provide further
information regarding possible cavernous sinus invasion.
Calcification is infrequent in pituitary adenomas.
Curvilinear calcification within a sellar or parasellar mass
obligates the exclusion of an aneurysm or dolichoectasia of
arteries in the circle of Willis.
Sellar enlargement, sloping and unilateral thinning of the
floor, erosion of the dorsum and posterior clinoid
processes, and frank extension into the sphenoid sinus are
well demonstrated by CT. Anatomical information
regarding the sphenoid sinus septa is useful in planning
trans-
sphenoidal surgery. Facial bone and hand films
demonstrate bony overgrowth in acromegaly.
The first sign of a pituitary adenoma may be pituitary
apoplexy, with the acute onset of severe headache and
visual field abnormalities. A CT scan reveals a suprasellar
mass with high attenuation, indicating acute hemorrhage
within the adenoma (76, 95). Although uncommon, a
blood-fluid level may be seen within the mass. Mixed
density within the tumor is encountered more often, with
cystic nonenhancing regions probably representing residua
of previous infarction or hemorrhage. Correlation with
history and CSF studies is vital, as a pituitary abscess and
an uncomplicated pituitary adenoma may also exhibit ring
enhancement with central areas of low attenuation.
Craniopharyngioma
Craniopharyngioma accounts for 5 to 10% of all
childhood brain tumors and 50% of suprasellar tumors in
the pediatric age group (34, 95). A second smaller peak
occurs during the sixth and seventh decades. Cyst
formation and calcification are prominent. Approximately
85% of Craniopharyngiomas are totally or partially cystic
(73). Cystic regions are typically of lower attenuation on
noncontrast CT than are truly solid components of the
tumor, but may be isodense or even hyperdense. Braun et
al. attributed increased attenuation in the cystic component,
encountered in 4 of 63 surgically resected tumors, to a high
intracystic protein concentration (11). Contrast
enhancement is limited to the capsule and solid portions of
the tumor. Childhood Craniopharyngiomas typically exhibit
some degree of contrast enhancement, whereas adult
tumors are often poorly enhancing (34, 63).
Calcification may be rimlike and peripheral, central,
combined peripheral and central, or even present in
adjacent brain parenchyma. In children, CT demonstrates
calcification in almost all cases. Tumors in adults may
calcify but in a smaller percentage of cases.
Commonly observed bony changes include sellar
enlargement and erosion of the dorsum sellae.
CT scanning after contrast administration is virtually
diagnostic of craniopharyngioma in a child if at least two of
the cardinal features of calcification, cyst formation, and
contrast enhancement are present in a suprasellar mass
(Fig. 11.11). In adults, however, meningiomas, pituitary
adenomas, and aneurysms may demonstrate calcification
and enhancement and are indistinguishable from some
Craniopharyngiomas.
 Figure 11.11. Craniopharyngioma. A sagittal reformatted CT image after contrast
administration demonstrates a suprasellar tumor with rimlike calcification superiorly
[arrows). The suprasellar component enhances. Anterior is to the reader's left.
Craniopharyngiomas are generally large tumors at the
time of diagnosis, averaging 3.5 cm in diameter in a large
pathological series (73). Modern CT scanners, operating
in the direct coronal projection, accurately define
intrasellar and suprasellar portions of the tumor. CT
detects involvement of the optic chiasm and surrounding
vascular structures and encroachment on surrounding
neural tissue or bone. Postoperative scans are useful for
evaluation of the amount of residual tumor and for
possible reaccumulation of cyst fluid. In cases requiring
further refinement of anatomical detail, metrizamide CT-
cis-ternography is a useful adjunct (42).
Angiographic findings are limited to displacement of
surrounding vessels because Craniopharyngiomas are
avascular tumors (63, 69).
Meningioma
In addition to those arising from the tubercu-lum sellae
and medial sphenoid ridge, meningiomas may arise at
other sites in the vicinity of the inferior third ventricle:
diaphragma sellae, cavernous sinus, optic nerve sheath at
the level of the chiasm, or the tentorial incisura, with
growth into the posterior suprasellar and prepon-tine
cisterns (63, 95). The radiological characteristics of
meningiomas were discussed under "Lesions Affecting
the Anterior Third Ventricle." Like tuberculum sellae
meningiomas, diaphragma sellae tumors present as
enhancing masses filling the suprasellar cistern. The
characteristic vascular displacement is elevation of the
A1 segments of the anterior cerebral arteries.
Diaphragma sellae and tentorial incisural meningiomas
cause enlargement of the branches of the
meningohypophyseal artery.
Suprasellar Germinoma
Suprasellar germinoma ("ectopic pinealoma") may be
suspected clinically in patients presenting with diabetes
insipidus, visual disturbances, and anterior pituitary
dysfunction (91). The striking male preponderance in
pineal region germinomas is not duplicated with suprasellar
germinomas. Patients with this condition generally do not
have a concomitant lesion in the posterior third ventricle.
Noncontrast CT demonstrates an isodense to slightly
hyperdense mass filling the suprasellar cistern. Infiltration
of the surrounding brain results in blurred, ill-defined
margins. Calcification is absent. Moderate, uniform
enhancement is the usual pattern. Germinoma may infiltrate
along the infundibulum, walls of the third ventricle, and
subependymal regions of the frontal horns and produces
abnormal enhancement of these structures.
Metrizamide ventriculography reveals upward convexity
of the anterior third ventricular floor. The optic and
infundibular recesses may be effaced and displaced
posterosuperiorly.
Cerebral angiography demonstrates vascular
displacements characteristic of a suprasellar mass. The
mass is usually avascular and does not produce abnormal
prominence of the meningohypophyseal trunk, as would
often occur with meningiomas or pituitary adenomas.
Dermoid, Epidermoid, Teratoma
Epidermoids may closely mimic suprasellar arachnoid
cysts, and the CT attenuation may approximate CSF.
Metrizamide CT-cisternography confirms the diagnosis
when contrast agent outlines the tumor interstices.
Dermoid cysts and benign teratomas may occur in the
suprasellar region and mimic Craniopharyngiomas (95).
The radiological features of dermoids and teratomas are
discussed under "Lesions Affecting the Posterior Wall and
Pineal Region."
Metastases
Metastatic disease of the pituitary gland produces
radiological signs indistinguishable from those of invasive
adenomas (95). An enhancing tumor mass may destroy the
bony sella. Primary sites include carcinoma of the breast,
lungs, kidney, and colon. Metastases to the infundibulum
produce masses within the suprasellar cistern, and
hypothalamic involvement is possible.
Tuber Cinereum Hamartoma
Tuber cinereum (hypothalamic) hamartomas are
associated with infantile or early childhood isosexual
precocious puberty and seizures (40). These hamartomas
appear on CT as nonenhanc-ing masses, 1 to 2 cm in
diameter, located in the posterior suprasellar cistern (57).
Hamartomas may displace the basilar artery and brain stem
posteriorly and occasionally attain sufficient size to distort
the anterior third ventricle (57, 63). Calcification within
hamartomas is rare. Lack of enhancement is sufficiently
characteristic for some authors to recommend diagnosis on
purely clinical and neuroradiological grounds.
Angiography is helpful if the diagnosis remains in doubt
after CT scanning. Abnormal vessels and a tumor blush are
not encountered. The distal basilar artery and APMV are
displaced posteriorly, and the PCoAs may be displaced lat-
erally.
Bony changes are unusual, but local erosion of the
dorsum sellae may occur. Roentgenograms of the hands
document inappropriately advanced bone age. Metrizamide
CT-cisternography detects small masses otherwise not seen
on routine CT scans.
Other rare causes of suprasellar masses, often with
marked contrast enhancement, include choristomas
(granular cell myoblastoma) (86, 90) and, in children,
idiopathic granulomatous disease. The radiological features
of these rare disorders are not specific and the lesions
cannot be
distinguished from the more common suprasellar masses.
Inflammatory Lesions
Chiasmatic Optic Neuritis
In cases with isolated symmetrical enlargement of the
optic chiasm, chiasmal optic neuritis is indistinguishable
from glioma by CT criteria alone (31). Because the median
age of presentation of the two is similar, only a therapeutic
trial of corticosteroids differentiates neuritis from glioma.
Serial CT scans document resolution of chiasmal swelling
as patients with chiasmal optic neuritis improve clinically.
Histiocytosis X
Histiocytosis X produces characteristic bony erosive
lesions and often involves the hypothalamus, producing
diabetes insipidus (20). The disease affects children more
commonly, males outnumbering females.
Noncontrast CT reveals a soft tissue mass within the
suprasellar cistern, often with an associated low density
region within the hypothalamus. Miller et al. reported
enhancement of the hypothalamic and suprasellar lesions in
three of their five cases of histiocytosis (63). Deformity and
flattening of the floor of the third ventricle can occur.
Angiography generally reveals an avascular mass.
The diagnosis of histiocytosis X can be made in patients
with CNS symptoms (diabetes insipidus or
panhypopituitarism), a suprasellar mass, and bony lesions.
The skull, followed by the femur and pelvis, are the most
commonly affected bones. Geographic calvarial lytic
lesions are common, with beveled margins produced by
unequal involvement of outer and inner tables. Involvement
in the periapical regions of the mandible produces an
appearance of "floating teeth." Mas-toid destruction and
soft tissue changes within the middle ear commonly result,
usually sparing facial nerve function. Sellar destruction and
sphenoid erosions are uncommon and unrelated to the
development of diabetes insipidus.
Sarcoidosis
CNS sarcoidosis causes a variety of neuroradiological
manifestions and may be the first evidence of the systemic
disorder (14). Approximately 4 to 7% of all patients with
sarcoidosis develop CNS involvement (54).
A common pattern of CNS sarcoidosis is granulomatous
leptomeningitis, involving the basal meninges,
hypothalamic region, floor of the third
ventricle, infundibulum, and optic chiasm. Hydrocephalus
is a common complication, resulting from either
intraventricular or extraventricular arachnoiditis and
adhesions. Extensive contrast enhancement of the basal
leptomeninges occurs in these cases, similar to that seen
with other granulomatous meningitides (e.g., tuberculous
or fungal).
Parenchymal granulomas are often widespread and may
coalesce to form masses mimicking primary neoplasms.
The suprasellar region is the most common intracranial
site for mass lesions of sarcoidosis. Hemispheric,
subfrontal, intraventricular, and periaqueductal foci have
also been reported. The lesions are characteristically
hyperdense on noncontrast CT and demonstrate marked,
uniform enhancement. Calcifications may occur.
Sarcoid masses are typically avascular at an-giography.
Sarcoid angiitis is rarely demonstrated.
Bony destruction may present as well-defined calvarial
lytic lesions, characteristically without marginal sclerosis.
Optic foraminal enlargement (due to sarcoidosis involving
the optic nerve sheath) and enlargement of the sella
turcica have also been reported. Rarely, sarcoidosis
produces reactive sclerosis of the orbital plates, sphenoid
bone, and pterygoid plates.
CT is particularly helpful in the follow-up of patients
undergoing corticosteroid treatment.
Vascular Lesions
Giant Intracranial Aneurysms
Giant aneurysms have a diameter greater than 2.5 cm
and usually present clinically as space-occupying lesions.
Giant aneurysms of the carotid bifurcation and basilar
artery may extend superiorly to compress the optic
chiasm, deforming the anterior wall and floor of the third
ventricle (37). Rarely a giant basilar aneurysm obstructs
the posterior third ventricle. Giant aneurysms should be
constantly borne in mind in the radiological differential
diagnosis of calcified masses in the suprasellar region,
and full angio-graphic evaluation should be conducted if
any doubt remains.
Giant intracranial aneurysms can be divided into three
types, partially thrombosed, completely thrombosed, and
nonthrombosed. Each of these types has specific CT
findings (85).
A partially thrombosed giant aneurysm is the most
common type in clinical practice (Fig. 11.12). A
noncontrast CT scan usually demonstrates curvilinear
calcification in an interrupted
pattern. The lumen of the lesion has an inhom-ogeneous
attenuation reflecting the thrombosed part (high
attenuation) and the portion with free-flowing blood (low
attenuation). After intravenous contrast administration the
relative density of these two components reverses,
indicating homogeneous enhancement of the free-flowing
blood within the patent lumen. In addition, a ringlike
pattern of contrast enhancement, either continuous or
interrupted, may be detected at the periphery of these
lesions. This peripheral enhancement represents the rich
network of vasa vasorum along the wall of the giant aneu-
rysm. Angiography is necessary to confirm the diagnosis.
Often the parent vessels drape over the unopacified portion
of the aneurysm. Angiography alone underestimates the
size of partially thrombosed aneurysms.
Completely thrombosed giant aneurysms are sharply
delineated, slightly hyperdense, round lesions on both
noncontrast and postcontrast CT. Because the contents are
static and thrombosed, the density on noncontrast and
contrast-enhanced scans is the same. Because of their
extraaxial location, giant aneurysms can deform the
suprasellar cistern. Partial calcification and enhancement of
the aneurysm wall occur.
The walls of nonthrombosed aneurysms often have little
or no calcification. These lesions are slightly hyperdense on
noncontrast CT and enhance homogeneously. Areas of low
attenuation in the brain parenchyma, presumably represent-
ing ischemia or atrophy secondary to the mass effect of
these lesions, have been described adjacent to giant
aneurysms. However, these zones of low attenuation are
less extensive than those with intracranial neoplasms of
comparable size.
Other techniques to confirm the diagnosis of a
nonthrombosed giant aneurysm are dynamic CT, MRI, and
digital intravenous angiography. Dynamic CT scanning
provides rapid sequential measurement of attenuation
values. After a rapid intravenous injection of a bolus of 40
ml of iodinated contrast agent, repetitive scanning is
obtained through the suspected lesion. Aneurysms
characteristically demonstrate a rapid wash-in peak
occurring between 6 and 11 seconds postinjection, with
washout of the contrast agent by 20 seconds. A
recirculation peak appears at 32 to 48 seconds (75). The
main differential diagnosis is from a meningioma. Attenua-
tion values of meningiomas also rise rapidly to a peak, but
this is followed by a flat washout phase. This plateau
characteristically occurs at 30 to 40 seconds and is due to
retention of contrast material within the meningioma. There
is
 no recirculation peak. Thus, the major differences in the
time-density curves distinguishing tumor from giant
aneurysm are the persistence of contrast enhancement
shown by the plateau and the absence of a recirculation
peak. MRI characteristics of aneurysms are discussed under
"Appearance of Lesions on MRI."
Digital intravenous angiography (DIVA) uses an
antecubital fossa or preferably superior vena caval catheter
for the bolus injection of 40 ml of 76% iodinated contrast
material. DIVA produces simultaneous opacification of the
giant aneurysm and the arteries of the circle of Willis. Even
though dynamic CT and DIVA may confirm the diagnosis
of giant aneurysm, conventional in-traarterial angiography
remains essential for exact anatomical delineation before
operation. For this reason, we advise that the expeditious
work-up of an aneurysm bypass dynamic CT and DIVA
and commence with selective arteriography.
Craniopharyngiomas, planum sphenoidale and
diaphragma sellae meningiomas, and suprasellar
germinomas can all mimic nonthrombosed giant
aneurysms. Associated findings of hy-perostosis and
pneumosinus dilatans, if present, provide helpful clues to
the diagnosis of menin-gioma. The margins of germinomas
are rarely as well defined as those of aneurysms. In
addition, subarachnoid and subependymal tumor seeding
occurs with germinomas, representing a differential feature
of this entity.
Basilar Artery Ectasia
Atherosclerotic ectasia of the calcified basilar artery may
encroach upon the inferior third ventricle (Fig. 11.13). In
severe cases the third ventricle may become partially
obstructed and hydrocephalus ensues.
Chiasmal Apoplexy
Chiasmal hemorrhage may be secondary to rupture of
small venous angiomas or arteriove-nous malformations or
to hemorrhage into a chiasmatic glioma (58).
CT scanning reveals a high attenuation mass in the
suprasellar region. In Maitland's group of four patients
(58), enhancement accompanied hemorrhage into a
chiasmatic glioma. Carotid arteriography is often normal
but sometimes
represents opacified flowing blood within the patent
portion of the aneurysm. Note secondary hydrocephalus
due to obstruction of the third ventricle. C. Lateral film
from a selective ICA angiogram demonstrates opacification
of the patent portion of the aneurysm lumen, confirming the
diagnosis.

Figure 11.12. Giant supraclinoid carotid artery aneurysm.

A. Lateral skull film demonstrates curvilinear calcification
in the suprasellar region [arrow). B. Direct coronal
enhanced CT displays the calcified rim of the aneurysm
enclosing thrombus within its dome [arrows]. A high
attenuation area [large white arrow)
 diffusion of metrizamide across the cyst wall, in
contradistinction to the "cauliflower" appearance in
patients with epidermoid tumors.
In the appropriate clinical setting, the ventric-ular-
cisternal form of cysticercosis may mimic a suprasellar
arachnoid cyst (18).
Other Lesions
Deformity and enlargement of the optic chiasm and
distortion of the suprasellar cistern can oc-

Figure 11.13. Basilar artery ectasia. A calcified ec-tatic

basilar artery [black arrow) deforms the third ventricle
[white arrows) and the right cerebral peduncle.

demonstrates venous abnormalities in the suprasellar

region.
Congenital Lesions: Arachnoid Cysts
Suprasellar cysts may originate from the epen-dyma of
the third ventricle as well as from the basal arachnoid (1).
Multiplanar CT is especially valuable in outlining the
anatomical relationships. On axial CT, a large rounded or
oval CSF density structure fills the suprasellar cistern and
third ventricular region. Hydrocephalus involving both
lateral ventricles is usual in symptomatic patients. The
rounded cyst often lacks the posteroinferior tapering
characteristic of the enlarged third ventricle of aqueduct
stenosis. However, this appearance alone is not
sufficiently reliable for firm diagnosis. Cysts may also
cause flattening of the upper brain stem and colliculi.
Even with direct coronal CT scanning, delineation of the
compressed third ventricle is often impossible. Contrast
enhancement and calcification of the cyst wall are
characteristically absent.
Metrizamide CT-ventriculography is crucial for the
evaluation of hydrocephalus associated with a possible
arachnoid cyst (1, 96). With aqueduct stenosis,
metrizamide fills the enlarged third ventricle; with
suprasellar arachnoid cysts, contrast should outline the top Figure 11.14. Herniation of the third ventricle and optic
of the cyst. chiasm into the sella turcica. A. Normal metrizamide
Metrizamide CT-cisternography may be necessary in cisternogram of the suprasellar region. Note the normal
troublesome cases, particularly if the CT appearances optic chiasm [arrows). B. Metrizamide cisternogram
mimic those of an epidermoid tumor. The test will demonstrates a filling defect in the suprasellar region
[arrows). Compare with the normal (A). C. Sagittal
demonstrate either immediate entry of contrast agent into reformatted image from the metrizamide cisternogram seen
the cyst or slow in В illustrating downward herniation of the inferior
recesses of the third ventricle into a partially empty sella
[arrows). Reformatted images were crucial to the proper
characterization of the filling defect seen in the suprasellar
cistern on the axial image.
cur in adhesive perichiasmatic arachnoiditis (16, 83)
secondary to prior hemorrhage, iophendylate
cisternography, operation, or infection. The CT diagnosis is
possible given the appropriate clinical history.
Finally, downward herniation of the anterior recesses of
the third ventricle and the optic chiasm can occur in the
empty sella syndrome (16) due to deficiency of the
diaphragma sellae (either primarily or secondary to prior
transsphenoidal operation or ischemic necrosis of the
gland). In these patients, deformity of the optic chiasm in
conjunction with an area of low attenuation within the sella
presents a confusing picture on the contrast-enhanced CT
scan alone. If, however, the infundibulum can be seen
extending toward the floor of the sella turcica, the diagnosis
is facilitated. Metrizamide CT-cisternog-raphy allows a
definitive diagnosis (Fig. 11.14). The third ventricle can
also herniate into the sella turcica in patients with
obstructive hydrocephalus due to lesions at the level of the
aqueduct.
Lesions Affecting the Posterior Wall and Pineal Region
Neoplastic Lesions
The development of high resolution CT scanning in the
1970s combined with widespread utilization of the
operating microscope revolutionized the diagnosis and
treatment of pineal region mass lesions. Although the
histological features of pineal region masses cannot be
definitively predicted by noninvasive techniques, the
differential diagnosis is usually limited and a single tumor
type may often be identified as most probable.
Germ cell tumors of the pineal region can be divided into
germinomas and embryonal carcinoma and its derivatives,
choriocarcinoma, yolk sac tumor (endodermal sinus tumor),
and teratoma/teratocarcinoma. Such tumors may be rel-
atively "pure" histologically or comprised of several
different subtypes. The incidence of pineal tumors is shown
in Table 11.1.
Germinoma
Germinomas account for approximately half of all pineal
region tumors (29, 51, 82). This tumor may originate in the
pineal or parapineal region, secondarily engulfing or
displacing the intact pineal gland. The majority of cases
occur in adolescent boys.
Noncontrast CT demonstrates an isodense to slightly
hyperdense mass (35, 98, 100). Calcifi-
cation of the tumor itself is rare. Cyst formation is also
unusual. Smaller lesions are well defined, but the borders of
larger lesions may be indistinct due to infiltration of tumor
cells into adjacent neural tissue. In either case, edema of the
surrounding brain is unusual. After contrast administration,
diffuse uniform enhancement is typical (Fig. 11. 15A), but
not invariable. The normal pineal gland calcification
appears displaced (Fig. 11.15B) or engulfed by the
enhancing tumor mass. Abnormal enhancement in the basal
cisterns and walls of the lateral ventricle indicates seeding
via CSF pathways. Leptomeningeal spread occurs in
approximately 8 to 15% of cases. Although unusual, cases
of simultaneous masses in the pineal region and suprasellar
region ("ectopic pinealoma") have occurred.
CT is useful in the follow-up of these highly
radiosensitive tumors. The usual response to external beam
radiation is total resolution within 6 weeks. However,
tumors with cystic components on the initial study have
demonstrated relative resistance to radiotherapy.
Embryonal Cell Carcinoma
As with the commoner germinoma and teratoma,
embryonal cell carcinoma is most often encountered in
young adolescent boys (66, 100). Noncontrast CT
demonstrates a slightly hyperdense mass, often containing
calcium (35, 51). The endodermal sinus variant may
develop cysts. Diffuse enhancement after contrast is the
usual pattern. The lesions may infiltrate surrounding
structures or be well circumscribed. Edema of surrounding
brain is scant or absent. Seeding of tumor may occur via
CSF pathways, and massive intratumoral hemorrhage is
occasionally encountered. Am embryonal carcinoma is
highly vascular at angiography.

Figure 11.15. Germinoma (two cases). A. A sagittal
reformatted CT scan image demonstrates an inhomo-
geneously enhancing mass [arrow) deforming the pos-
terior third ventricle [top). This pattern is unusual. The
more typical pattern of homogeneous enhancement is seen
in the scan of another patient [bottom). B. Postcontrast
axial CT scan illustrates displacement of pineal
calcification [arrow) by the expanding tumor.
Benign Teratomas
The pineal region is the most common intracranial
location for benign teratomas. A preponderance of cases
occurs in young men (81).
CT scans reflect the gross pathological features of these
tumors. Low attenuation (-70 to —30 HU) regions
predominate, representing fatty portions of the tumors
(Fig. 11.16). Bone and dental elements are easily seen.
Soft tissue components may be isodense to normal brain
and demonstrate contrast enhancement. Although often
large and irregularly shaped, teratomas are non-invasive
and present well-defined borders (51,
81). Spontaneous rupture of cystic elements into the
subarachnoid space and ventricles has been documented by
CT. The CT appearances of dermoid cysts closely mimic
those of teratomas.
Angiographic manifestations of teratomas are scant,
usually limited to the vascular displacements surrounding
an avascular mass. A faint tumor blush is encountered
occasionally.
Glioma
Gliomas in the pineal region and posterior third ventricle
comprise 10 to 25% of masses in this region (51,100).
There is no sex predilection, and most patients are young.
The spectrum of glial tumors described in this region
includes astrocytoma, glioblastoma, ependymoma, and
ganglioglioma. Although the pineal gland contains
fibrillary astrocytes, most pineal region gliomas originate in
parapineal structures, such as the corpora quadrigemina or
the posterior thalamus (81).
CT characteristics of gliomas are outlined under
"Lesions Affecting the Lateral Walls of the Third
Ventricle." Prominent enhancement is encountered
occasionally in exophytic components.
Angiographic findings are variable, depending on the
grade of the tumor and its exact location. Encasement of
the basilar artery has been reported.
Pineal Cell Origin
Less than 20% of pineal region tumors represent true
pineal cell neoplasms (100). Benign pineocytomas and
malignant pineoblastomas may exist in either pure or
mixed forms (29, 51). In most series, mixed types and
pineoblastomas predominate. Unlike the situation with
germ cell tumors, the sex incidence is equal. Mean age at
presentation is 10 years.
Pineal cell tumors are isodense to slightly hy-perdense
before the administration of contrast agent. Abnormal
calcification within these tumors is characteristic.
Pineocytomas may be cystic. Enhancement is dense and
uniform. The tumors may appear either well defined or
infil-trative.
Pineoblastomas frequently disseminate via CSF
pathways (Fig. 11.17) and may also metastasize outside the
CNS. At angiography, pineal cell tumors are usually
moderately vascular, but avascular masses have been
described.
Lipoma
Although the corpus callosum is the most common site
for intracranial lipomas, the pineal region may harbor
lipomas originating in the quad-
Figure 11.16. Teratoma. A. A postcontrast axial CT scan demonstrates calcification
surrounding a fat-containing tumor (arrows) in the posterior third ventricle. B. Sagittal
reformatted CT image depicts the fat-containing tumor in the posterior third ventricle
[arrows). Note the marked enlargement of the anterior third ventricle. Anterior is to the
reader's left.

Figure 11.17. Pineoblastoma. A. Abnormal enhancement
in the ambient and sylvian cisterns {arrows) indicates
seeding of tumor along the CSF pathways. The tumor
(best seen on a higher scan) is a faint area of
enhancement in the quadrigeminal plate area. В. А
postmetrizamide CT scan of the lumbar spine demon-
strates a drop metastasis to a lumbar nerve root [arrow].
rigeminal plate, velum interpositum, or ambient cistern
(98, 100). Lipomas occur in children or adults.
These tumors exhibit a fat density on nonen-hanced CT
(-100 to -40 HU). However, small
lipomas may seem to have significantly higher attenuation
values because of the partial volume averaging of
surrounding brain with the fat density of the tumor.
Enhancement is characteristically absent. The CT
differential diagnosis should include dermoid cyst and
teratoma.
Figure 11.18. Arachnoid cyst. A. A quadrigeminal cistern
arachnoid cyst [arrow) compresses the posterior third
ventricle and aqueduct. The ventricles are shunted. B. A
metrizamide CT-ventriculogram demonstrates
noncommunication of the cyst with the ventricular system.
Meningioma
Pineal region meningiomas share the CT characteristics
of meningiomas elsewhere: isodense to slightly hyperdense
masses with uniform enhancement. Calcification is
variable, as is tumor blush at angiography. These tumors
may arise from the pineal gland itself, the velum interpos-
itum, or the falx-tentorium junction (80).
Metastases
Metastases may involve the pineal region and posterior
third ventricle (62). Tumor types include breast, lung,
melanoma, and adenocarci-noma (primary site unknown).
The CT appearance of pineal region metastases is variable;
multiplicity of lesions provides the only distinguishing
radiological feature. Individual metastases may be isodense
or slightly hyperdense, with variable degrees of edema and
enhancement.
Epidermoids
Epidermoid cysts occur rarely in the pineal region. The
radiological features were presented under "Lesions
Affecting the Anterior Wall of the Third Ventricle."
Congenital Lesions: Arachnoid Cysts
Arachnoid cysts and glial cysts of the pineal region share
similar CT characteristics. The cysts may be either
developmental or acquired secondary to postinflammatory
or posthemor-rhagic adhesions. The cysts may involve
either the cistern of the velum interpositum, the quad-
rigeminal plate cistern, or both (62).
Cyst outlines may be smooth, lobular, or irregular.
Metrizamide CT-cisternography confirms the diagnosis by
demonstrating noncommunication with the normal
subarachnoid space or a slow diffusion of metrizamide into
the cyst (Fig. 11.18).
Vascular Lesions
Aneurysm of the great vein of Galen was discussed
under "Lesions along the Roof of the Third Ventricle."
Lesions Affecting the Lateral Walls of the Third
Ventricle
The most common lesions involving this region are
primary brain tumor and hypertensive hemorrhage
originating from the basal ganglia and thalamus.
Neoplastic Lesions
Glioma
Primary brain tumors have variable appearances on CT.
On noncontrast CT, low grade as-
trocytomas commonly present as an area of ill-defined low
attenuation with a subtle mass effect. Although
glioblastomas can have increased, decreased, or mixed
attenuation on noncontrast CT, the mixed attenuation
pattern together with a high degree of white matter edema
is most common (65% of cases) (88). Hemorrhagic, ne-
crotic, or cystic components are frequent. Low grade
astrocytomas typically do not show contrast enhancement.
Glioblastomas have variable appearances on contrast-
enhanced CT, the most common being a thick, irregular,
ring-shaped rim of enhancement surrounding a low density
center (Fig. 11.19). Coronal CT scans show a typical
anatomical picture (Fig. 11.20). Cystic gliomas may have a
single, small, enhancing mural nodule. Although CT scans
cannot predict the histological features of primary brain
tumors, the degree of contrast enhancement roughly paral-
lels the histological grade.
On cerebral angiography, AV shunting and
neovascularity characterize a glioblastoma, whereas
nonspecific mass effect is the most common finding with a
low grade astrocytoma.
Unfortunately, other common diseases share many of the
same CT characteristics as gliomas. The ring-shaped
enhancement associated with primary brain tumor is
usually thicker and more irregular than that of an abscess.
The thalami and basal ganglia are uncommon sites for
metastases. Homogeneous enhancement, extensive
surrounding edema, and multiplicity of lesions characterize
brain metastases.
MRI is more sensitive than CT alone in the detection of
low grade astrocytomas (8). MRI findings are discussed
under "Appearance of Lesions on MRI." The major
limitations of both CT and MRI are an inability to
demarcate dependably the tumor margin from peritumoral
vasogenic edema or radiation necrosis and an inability to
predict the specific histological grading of a primary CNS
tumor.
Lymphoma
Primary CNS lymphomas, although uncommon (less
than 1.5% of all intracranial tumors), have a predilection
for the corpus callosum, basal ganglia, and thalamic
regions. The CT characteristics and anatomical distribution
of these lesions were discussed under "Lesions along the
Roof of the Third Ventricle."
Subependymoma
Subependymomas are located most often near the fourth
ventricle (84), but can occur along the walls of the third
ventricle. Radiological features
 Figure 11.19. Thalamic glioblastoma. A and В (В 8 mm above A). A garland pattern of
enhancement surrounds a central low attenuation area of necrosis, findings often seen
with a glioblastoma. С Lateral magnified view of a selective vertebral arteriogram
demonstrates neovascularity [arrows) and stretching of the posterior choroidal arteries.

of subependymomas were discussed under "Lesions along
the Roof of the Third Ventricle."
Germinoma
Germinomas most commonly occur in the pineal and
suprasellar regions. In a Japanese series,
however, 10% of all intracranial germinomas primarily
involved the thalamic and basal ganglia region (53).
Although these lesions may be radio-logically difficult to
differentiate from high grade gliomas, the clinical features
of a slower progression, predominance in the prepubertal
boy, and
 Figure 11.20. Thalamic glioma. Coronal reformatted CT image illustrates invag-ination
of the trigone of the lateral ventricle [small arrows) by a parapineal region glioma. Note
the contralateral displacement of the internal cerebral veins [large arrows).

favorable response to radiation therapy often distinguish

germinoma from glioblastoma. After radiation therapy,
germinomas appear as low density areas without mass
effect or enhancement. The radiological features of typical
pineal germinoma were presented under "Lesions Affecting
the Posterior Wall and Pineal Region."

Vascular Lesions
Hypertensive Hemorrhage
The basal ganglia and the thalami are by far the most
frequent sites of spontaneous intracranial bleeding (from
40% to approximately 75% of all cases in large series) (74).
Isolated thalamic hemorrhages are extremely rare; most
cases also involve the internal capsule, basal ganglia, or
adjacent deep white matter. Thalamic hemorrhage
frequently extends into the ventricles (39). By far the most
common cause of thalamic hemorrhage is rupture of a
Charcot's aneurysm of the lenticulostriate arteries in a
patient with long-standing hypertension. Unusual causes of
thalamic hemorrhages include AV malformations,
cavernous angiomas, trauma, aneurysms, and hemorrhage
into vascular metastases (e.g., choriocarcinoma, melanoma,
renal cell carcinoma, or thyroid carcinoma).
Resorption of hematomas progresses from the periphery Figure 11.21. Hypertensive hemorrhage. A mixed high and
to the center. On noncontrast CT, hematomas evolve from a low attenuation mass lesion involves the basal ganglia and
hyperdense through an isodense to a hypodense phase over thalamus. This appearance on non-contrast CT is
2 to 3 weeks (Fig. 11.21). Contrast-enhanced CT during characteristic of the subacute phase of a hypertensive basal
ganglia hemorrhage. Note the compression of the third and
this period may demonstrate peripheral, thick, ring-like lateral ventricles.
enhancement, potentially mimicking a primary intracranial
tumor. This enhancement may remain for 6 to 9 months. Resolved hematomas on
noncontrast CT present as well-defined areas of low
attenuation with ipsilateral enlargement of the adjacent
ventricles. Occasionally, isodense gliosis can develop in
place of resolving hematomas.
Cavernous Angioma
Hemorrhage from cavernous angiomas may be
indistinguishable from primary hypertensive hemorrhage
by CT. Unruptured cavernous angiomas are generally
hyperdense on noncontrast CT because of
microcalcification (77). Mass effect and perifocal edema
are characteristically absent. The enhancement pattern is
variable. Cavernous angiomas are more common in the
cerebral hemispheres than the thalamic region, and the
lesions can enlarge slowly on sequential scans.
Cavernous angiomas are often missed on routine
angiography, but the angiographic detection rate
increases with the use of slow injections (16 ml of 60%
contrast material injected over 4 seconds) and prolonged
filming (68). The high rate of false-negative angiography
in cases of cavernous angioma relates to slow flow of
blood from the vascular system into the angiomas and to
stagnation of blood within the interstices of the lesions.

Intraventricular Lesions
Neoplastic Lesions
A tumor arising from within the third ventricle is rare.
Lesions of the Choroid plexus derive from ependymal
layers (Choroid plexus papilloma or carcinoma) or from
mesenchymal stroma (men-ingioma, vascular
malformation, cavernous angioma, hemangioma) that
infold during early em-bryogenesis. Giant cell
astrocytomas and colloid cysts are the most common
intraventricular tumors (65).
Choroid Plexus Papillomas/Carcinomas
Choroid plexus papillomas occur in patients of all ages.
The fourth ventricle is the most frequent location in
adults, and the lateral ventricle is the favored site in
children, usually before 3 years of age (60). The
incidence of Choroid plexus papilloma is 0.5% of Figure 11.22. Choroid plexus papilloma. A and B. Axial
intracranial tumors at all ages and 4% of intracranial (A) and sagittal reformatted (B) images from a postcontrast
neoplasms in patients under 12 years of age. Between 4% CT scan demonstrate an enhancing mass containing small
and 10% of all Choroid plexus papillomas occur in the cysts filling the third ventricle. Note extension through the
foramina of Monro [arrow, B) and associated
third ventricle (79, 92). Choroid plexus carcinoma tends hydrocephalus. C. Coronal plane ultrasound image depicts
to occur in the very young (under 2 years of age). the densely echogenic mass within the third ventricle
CT is the method of choice for the diagnosis of Choroid [arrows) and enlargement of the lateral ventricles.
plexus papillomas. On noncontrast CT, these lesions are
isodense to slightly hyperdense. Enhancement is intense
nant tumors, margination between the tumor and the
and homogeneous. In benign Choroid plexus papillomas
ventricular wall is irregular, with extra-ventricular
(Fig. 11.22), the margin between the tumor and the
extension and infiltration into the surrounding brain (71).
ventricular wall is well demarcated, whereas in malig-
Calcification, cysts, and hemorrhage are rare, occurring in
4% of cases. Cystic and hemorrhagic components occur
more frequently in carcinomas than in benign tumors.
Malignant degeneration of benign papillomas in children
occurs in about 20% of cases (92). Seeding of tumor within
the CSF occurs in both benign and malignant Choroid
plexus tumors.
 Because of the 4- to 5-fold overproduction of CSF,
generalized hydrocephalus and enlargement of the basal
cisterns characteristically occur in the absence of
intraventricular obstructive lesions. Intermittent
hemorrhage from this highly vascularized tumor, with
convexity block of CSF resorption, further aggravates the
existing hydrocephalus. A third ventricular Choroid plexus
papilloma, if large enough, can produce hydrocephalus by
obstructing the foramina of Monro.
Angiography aids in surgical planning. The principal
blood supply is by an enlarged MPChA. The angiographic
diagnosis of Choroid plexus tumor depends on finding a
persistent blush in the presence of enlarged arterial feeders
because normal Choroid plexus often exhibits a vascular
tangle and a small capillary blush. With Choroid plexus
carcinoma, additional findings are neo-vascularity and AV
shunting. In the venous phase, elevation and distortion of
the internal cerebral vein indicates the presence of the mass
within the third ventricle.
The diagnostic specificity of the CT and angiographic
findings in patients with Choroid plexus lesions is limited
because the appearance of a Choroid plexus papilloma is
similar to that of intraventricular meningiomas,
ependymomas, and cavernous angiomas. Angiography is
most useful in the exclusion of an intraventricular AV
malformation.
Ependymoma
Ependymomas constitute 6% of all intracranial gliomas
and are predominantly tumors of childhood and
adolescence. Ependymomas may arise in any part of the
ventricular system, but the fourth ventricle is the most
common site (approximately 60%). Supratentorially,
ependymomas arise most often near the trigone of the
lateral ventricle and less commonly within the third
ventricle (15% in Barone's series (2)). Ependymomas are
usually slowly growing and symptoms are due to
obstructive hydrocephalus and local infiltration of the brain
parenchyma. As ependymal cell rests are found far from the
ventricular system, these tumors may also arise within the
cerebral white matter at a distance from the ependymal
surface.
Solid tumor components are characteristically isodense.
The enhancement pattern is variable. Intratumoral cysts
occur commonly. Approximately 50% of ependymomas are
calcified (89). After operation and radiation therapy,
calcification in the residual tumor is more prevalent. An
ependymoma, if totally intraventricular, mimics
a Choroid plexus papilloma on CT. The CT scan also
detects local tumor recurrence and seeding of ependymoma
within the ventricles and cisterns (33).
Giant Cell Astrocytoma Associated with Tuberous Sclerosis
Tuberous sclerosis is a neurocutaneous syndrome with
dominant inheritance characterized by the triad of mental
deficiency, adenoma se-baceum, and seizures. The
hamartomas involve multiple sites: skin, brain, kidney,
heart, bone, and retina, with the skin and brain being the
most common. The tubers may undergo malignant
transformation to giant cell astrocytomas (55). These tubers
involve the lateral ventricle, third ventricle, foramen of
Monro, and septum pellucidum, in decreasing order of
frequency (5).
In spite of their large size, giant cell astrocytomas are
sharply circumscribed both on contrast-enhanced CT scans
(3) and gross examination. However, giant glial cells have
been detected in adjacent white matter at autopsy.
Symptoms develop when the tumor obstructs the CSF
circulation through the foramen of Monro with resultant
hydrocephalus. When the tumor is large, the exact site of
origin of the lesions is difficult to ascertain by CT or at
operation (Fig. 11.23). Giant cell astrocytomas, occurring
in isolation, may be difficult to differentiate from calcified
ependymomas. Tuberous sclerosis may be difficult to
distinguish from periventricular calcification associated
with toxoplasmosis and cytomegalic virus without an
appropriate clinical history.
Although angiography is usually not necessary for the
diagnosis of giant cell astrocytomas, when carried out the
findings vary (46) and can include marked hypervascularity
with pooling of contrast agent within the tumor, avascular
tumor, arterial ectasia and occlusion of cerebral blood
vessels remote from the primary lesion, and aneurysmal
change in small cerebral arteries. The last two findings
reflect the intrinsic dyspla-sia of the cerebral arterial walls.
Highly vascular giant cell astrocytomas can be
distinguished from other vascular malignant tumors by the
lack of early venous drainage.
Astrocytomas and ganglioneuromas not associated with
tuberous sclerosis can arise within the third ventricle. Most
intraventricular astrocytomas in the third ventricle occur
during the first or second decade of life. Hydrocephalus,
hypothalamic dysfunction, and memory deficits are the
most common presenting symptoms in these patients (4).
Astrocytomas commonly originate at the anterior column
of the fornix and
 may be attached to the ependyma by a pedicle. On CT,
these tumors may or may not enhance. Cystic degeneration
occurs in some cases.
Intraventricular Carniopharyngioma
Craniopharyngiomas originating within the anterior third
ventricle are rare. The presenting symptoms and signs are
due to obstructive hydrocephalus and hypothalamic
dysfunction. Diabetes insipidus and visual symptoms are
less common with intraventricular Craniopharyngiomas
than with those arising from the infundibulum. Cases of
intraventricular craniopharyngioma have all occurred in
adults. The radiological manifestations of
craniopharyngioma were discussed under "Lesions
Affecting the Floor of the Third Ventricle." Although CT
experience is limited, intraventricular Craniopharyngiomas
usually lack calcification and enhance homogeneously (61).
Metrizamide CT-ventricu-lography reliably establishes the
intraventricular location of these lesions.
Intraventricular Meningioma
Although very rare, an intra-third ventricular
meningioma should be included in the differential
diagnosis of any intrinsically dense lesion occurring in the
region of the foramen of Monro. Clinical symptoms result
from obstruction to the flow of CSF.
The major alternative diagnosis to be considered is a
colloid cyst. On noncontrast CT, meningioma and colloid
cyst are intrinsically dense and well circumscribed. The
enhancement pattern of meningiomas is more intense than
that of colloid cysts. In addition, the presence of calcium
helps to differentiate meningiomas from colloid cysts.
On vertebral angiography, a homogeneous tumor blush
and hypertrophied distal MPChA have been reported in
meningiomas arising from the anterior third ventricle (56).
Other tumors arising from within the third ventricle
include germinomas, epidermoids, teratomas, and
dermoids. Their characteristic CT findings were discussed
under "Lesions Affecting the Anterior Wall of the Third
Ventricle" and "Lesions Affecting the Posterior Wall and
Pineal Region." Hematogenous metastasis to the Choroid
plexus should also be considered in the differential
diagnosis of an enhancing intraventricular tumor.
Another extremely rare lesion that mimics an
intraventricular meningioma is an AV malformation
originating from the Choroid plexus of the third ventricle.
As reported by Britt et al. (13),

Figure 11.23. Giant cell astrocytoma. A. A noncon-trast

CT scan of a patient with tuberous sclerosis demonstrates
a largely cystic tumor containing calcification centered at
the foramen of Monro. B. Contrast enhancement along
the anterior margin of the tumor [arrow) indicates
malignant degeneration.
this variety of AV malformation appears heterogeneous
both before and after contrast infusion. Increased density
on nonenhanced CT resulted from hemosiderin deposited in
the capsule by an old hemorrhage.
Xanthogranuloma
Intracranial Xanthogranulomas usually adhere to the
Choroid plexus in the trigone of the lateral ventricle and are
often discovered as incidental findings. Anterior third
ventricular tumors may cause obstructive hydrocephalus
because of their strategic location. Radiologically, they
appear in-homogeneous and intrinsically dense on noncon-
trast CT, in contradistinction to the homogeneously dense
colloid cyst. Xanthogranulomas have low attenuation
centers because of their lipid and cholesterol content.
Punctate calcification is often present. The periphery of
these lesions may enhance (38). If only a contrast-enhanced
scan is performed, ringlike enhancement of a xantho-
granuloma might easily be confused with that of an abscess.
Chronic chemical meningitis has been associated with
Xanthogranulomas.
Xanthogranulomas are avascular on angiog-raphy. Even
though these lesions appear sharply circumscribed on CT,
surgical removal is technically more challenging than is the
case with colloid cysts because the fibrous capsule of the
xanthogranuloma is often densely adherent to the Choroid
plexus, fornix, and wall of the third ventricle.
Vascular Lesions
Hemorrhage into the third ventricle is a common clinical
entity, but seldom occurs as an isolated event. Aneurysm
rupture, trauma, and hypertensive hemorrhage originating
in the basal ganglia region are often associated with
hemorrhage into the third ventricle. Hemorrhage
originating from an AV malformation in the basal
ganglia/thalamic region can also dissect into the third
ventricle. In a series of 68 intraventricular hemorrhages
analyzed by Graeb et al. (39), the source of hemorrhage
was not identified in 12 patients after neuroradiological
evaluation. The cause of intraventricular hemorrhages in
this group is presumably rupture of angiographically
cryptic AV malformations located along the ependyma.
These patients have a better prognosis than patients whose
intraventricular hemorrhage is associated with aneurysm,
hypertension, or trauma.
AV malformations and cavernous angiomas originating
from the Choroid plexus are other rare causes of
intraventricular hemorrhage.
Obstructive hydrocephalus can be a complication of
intraventricular hemorrhage, but more frequently
communicating hydrocephalus results from adhesive
arachnoiditis and convexity block from associated
subarachnoid hemorrhage.
Infectious Lesion: Cysticercosis
Intracranial cysticercosis may have menin-geal,
parenchymal, and ventricular forms. Intraventricular
cysticercotic cysts generally cannot be diagnosed directly
by CT because their attenuation is similar to that of CSF.
The diagnosis should be entertained in the presence of
cystic or calcified parenchymal lesions, asymmetrical
enlargement of the involved basal cistern, or obstructive or
communicating hydrocephalus in patients with appropriate
clinical histories. Intraventricular cysticercosis can be
confirmed with metrizamide ventriculography. Cysticer-
cotic cysts may be mobile. Entrance of metrizamide into an
intraventricular cysticercotic cyst and enhancement of
intraventricular cysts have been reported (99). The latter
occurs only during the subacute phase of this infection (i.e.,
shortly after the death of the larvae with the subsequent
inflammatory response in the surrounding tissue). Entrance
of metrizamide into a third ventricular cyst is not
pathognomonic of cysticercosis because it has also been
reported with intraventricular arachnoid cysts and
ependymal cysts. Intraventricular cysticercosis can be di-
agnosed with certainty only if there is accompanying
radiological evidence of the parenchymal and meningeal
forms of the disease.
Congenital Lesion: Arnold-Chiari Type II Malformation
In patients with Arnold-Chiari Type II malformation, the
third ventricle is usually mildly dilated. With associated
aqueductal stenosis, however, third ventricular dilatation is
more prominent. On CT, the massa intermedia is unusually
large in 75% of patients with the Arnold-Chiari Type II
malformation. The enlarged massa intermedia frequently
lies close to the foramen of Monro. The anterior columns of
the fornix may be splayed or the wall of the third ventricle
may be tethered, creating a biconcave appearance of the
third ventricle (67). Infrequently, the massa intermedia
totally obliterates the third ventricular cavity, resulting in
fusion of the thalami across the midline. The large massa
intermedia does not enhance, a finding sometimes helpful
in differentiating the massa from an intraventricular tumor.
Associated stigmata of the Ar-
 nold-Chiari Type II malformation apparent on CT are an
enlarged foramen magnum, a low-lying fourth ventricle, a
small posterior fossa, scalloping of the petrous pyramids,
hypoplasia of the tentorium and the falx, beaking of the
tectum, inferomedial pointing of the floor of the frontal
horns, and interdigitation of the gyri along the
interhemispheric fissure.

Appearance of Lesions on MRI

Neoplastic Lesions
In general, primary brain tumors demonstrate prolonged
T1 and T2 times compared to normal brain (9, 17, 78) (Fig.
11.24). Significant overlap in T1 values exists between
benign and malignant tumors, and cystic regions within
either type of tumor may cause marked T1 prolongation.
Randell et al. (78) reported a focal decrease in T1 within a
malignant tumor due to hemorrhage. T1-weighted MRI is
particularly helpful in depicting Craniopharyngiomas,
lipomas, teratomas, and other lipid-containing masses
because of the short T1 of fat (44, 50) (Fig. 11.25). In
keeping with their variable lipid content, epidermoid tu-
mors may also have short T1 values or a T1 value longer
than that of surrounding brain (23). Calcification within
tumors may produce focal areas of signal absence.
Analysis of T2-weighted images is often complicated by
surrounding edema, which also exhibits a long T2 time
relative to brain tissue. Definition of the tumor-edema
interface may sometimes be achieved by alteration of the
pulse interval between excitation and the arrival of the spin
echo. In some cases, particularly meningiomas, tumor T1
and T2 values may be close to those of brain, and the
associated mass effect and edema provide the bulk of
findings on MRI. Experience with paramagnetic contrast
agents is accumulating, and preliminary images indicate
that alteration of the blood-brain barrier can be accentuated
in a manner similar to contrast-enhanced CT (19).
T1- and T2-weighted images provide complementary
information. In general, lesions are more conspicuous on
T2-weighted images, but may be missed by heavily T2-
weighted sequences alone if the lesion is surrounded by or
adjacent to CSF spaces (Fig. 11.24B).
Direct comparisons of the utility of contrast-enhanced
CT and MRI in the detection and characterization of
tumors are under way. Anecdotal

paralleling the occipital horns (arrows) are probably due to

interstitial edema.

Figure 11.24. Germinoma. A. A heavily T1-weighted

sagittal spin-echo image demonstrates a small mass of
low signal intensity involving the pineal region (arrow).
Note the compression of the aqueduct. B. A T2-weighted
axial spin-echo image of the same case. Note the
obscuration of the tumor by the high signal of the
surrounding CSF. Linear areas of high signal intensity
 reports document the superior detection of low grade
astrocytomas, pineal region germinomas, and brain stem
metastases by MRI, but no overall increase in
supratentorial tumor detection efficiency over CT has been
found in larger series (7, 10, 15). Efforts to predict specific
histological features of MRI lesions by analysis of T1 and
T2 changes have met with little success, as prolongation of
T1 and T2 characterizes cerebral infarction, edema,
demyelination, inflammatory disease, and many
degenerative processes.
Hydrocephalus
MRI is valuable in the detection of early interstitial
edema secondary to obstruction of CSF outflow. On T2-
weighted images, a high signal intensity develops in the
periventricular regions because of transependymal flow of
the CSF. Ventricular enlargement is easily detected, but the
most helpful contribution of MRI is its excellent,
predictable display of the size and configuration of the
aqueduct of Sylvius.
Vascular Lesions
MRI of giant aneurysms has been described (17, 44).
Short T1 regions within the aneurysms indicate clotted
blood, whereas areas of absent signal indicate either rapidly
flowing blood or mural calcifications (Fig. 11.26).
Racemose AV malformations present a complex picture:
low signal intensities are produced by rapidly flowing
blood within feeding arteries and larger draining veins,
whereas slower blood flow within the matrix of the
malformation gives rise to high signal intensity (64).
Hemorrhage presents a variable MRI appearance: very
acute bleeding appears dark on T1-weighted images
because of the long T1 However, progressive shortening of
the T1 of hemorrhagic lesions results in increasing signal
intensity from subacute and chronic hematomas (87). The
shortened T1 of hemorrhage (intraparenchy-mal or
extraaxial) persists long after hematomas become isodense
or hypodense to normal brain on CT scans (9). Coronal
images may be more accurate in identifying subdural
hematoma than are axial images.
The signal intensity of hemorrhage is high on T2-
weighted images.
Subarachnoid hemorrhage may be difficult to distinguish
on either T1- or T2-weighted images,

age at the same level as the CT scan reveals high signal

intensity within the mass due to its fat content. Note that
the area of calcification (arrow) produces little or no signal.

Figure 11.25. Teratoma. A. A postcontrast CT scan image

demonstrates a suprasellar mass with calcification (arrow).
Intrinsic high attenuation within the mass was also seen on
noncontrast CT scans (not shown). B. A heavily T1-
weighted axial spin-echo im-
Figure 11.26. Aneurysm. A. A T1-weighted axial inversion recovery image demonstrates
absence of signal from rapidly flowing blood within the lumina of the ACoA and bilateral
middle cerebral artery aneurysms [arrows). B. Oblique view from a selective ICA
angiogram confirms the ACoA aneurysm (arrow). Other aneurysms at the middle
cerebral artery bifurcations were also confirmed.
but is usually well demonstrated with conventional CT
scanning.
Sellar and Parasellar Lesions
Several studies of pituitary and juxtasellar lesions have
appeared (9, 43, 44). Pituitary adenomas,
Craniopharyngiomas, and giant aneu-rysms may be
differentiated according to the presence of fat or flowing
blood. Cavernous sinus invasion and suprasellar extension
of adenomas are well shown. Direct coronal and sagittal
imaging is particularly helpful in the diagnosis of sellar and
parasellar lesions. Empty sellas, hypothalamic hamartomas,
suprasellar teratomas, and colloid cysts of the third
ventricle have been demonstrated by MRI.
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12
Anterior Transcallosal and
Transcortical Approaches
William Shucart, M.D.

Lesions in the anterior third ventricle are uncommon; therefore, most surgeons have
limited experience with lesions of this region. Enthusiasm for operation has often been
dampened because surgical access to the anterior third ventricle requires disruption of
normal brain tissue and because many of these tumors are not resectable. Over the past
several years, however, there has been increasing interest in the diagnosis and treatment
of lesions in this area stimulated by increasing sophistication in imaging techniques,
refinements in surgical instrumentation, the realization that many lesions are removable,
and the development of surgical avenues that do not cause neurological deficits.

History
Historically, three approaches have been used to reach the anterior third ventricle: the
transcortical-transventricular approach going through a frontal lobe, the transcallosal-
transventricular approach, and the subfrontal approach through the lamina terminalis
(13, 18). More recently, computerized tomography (CT)-assisted stereotaxic biopsies
have been used to establish a diagnosis in third ventricular lesions (1).
The subfrontal approach has been used primarily for masses arising in the suprasellar
area that invaginate into the third ventricle. Both transventricular approaches have been
used for tumors arising within the third ventricle (4, 7, 9). The stereotaxic method is
generally used for lesions thought to be nonresectable.
The most commonly used approach for solely intraventricular lesions is probably the
transcortical-transventricular approach initially described by Dandy (5). He also
described a transcallosal approach that he used for posterior third ventricular lesions.
The anterior transcallosal approach has often been suggested (6, 12), but until recently
it was not used widely because of concern about the clinical effect of sectioning a
portion of the corpus callosum.
There have been suggestions in the literature since the 1940s that
sectioning the more anterior portion of the corpus callosum is not associated with distinct
symptoms, whereas complete callosal section has been shown to produce a broad array of
definite and persistent behavioral abnormalities (8). Since the 1960s, the surgical
literature has contained an increasing number of reports emphasizing the efficacy of the
transcallosal approach and confirming the predictions that there would be no specific
deficits referable to division of the anterior portion of the body of the corpus callosum (3,
11, 15-17). At present, there are advocates for both the transcallosal and the transcortical
approaches. The differences between and the advantages of these two approaches are
discussed in this chapter.

Surgical Approaches
The distinction between masses arising within and expanding the third ventricle and
those impinging from outside is important for determining the best operative approach,
but can be difficult. There are no certain clinical criteria to ascertain the origin of the
mass. Interference with normal functioning of the hypothalamic-pituitary axis and visual
field defects are most often seen with lesions arising subfrontally below the third
ventricle, but tumors growing within the ventricle may cause similar problems. CT or
magnetic resonance imaging with coronal and sagittal reconstructions often define the
exact anatomy and origin of the lesion (Fig. 12.1). Angiography may also be helpful in
evaluating the origin of the lesion by showing the displacement of the major arteries in
that area, particularly the branches of the anterior cerebral arteries.
If the lesion in the vicinity of the anterior third ventricle is small, the approach is best
determined by the presence or absence of a visual field disturbance; if present, the
approach should be subfrontal; if not, the approach should be transventricular. In cases
with large lesions and an associated visual field defect, a large craniotomy should be
performed to allow access to the subfrontal area and the use of one of the transventricular
approaches if needed.
If the ventricles are enlarged, which they usually are if a tumor is present, access to a
foramen of Monro and ultimately the third ventricle is easily accomplished with either
the transcortical or the transcallosal technique. Access to both sides of the third ventricle
is obtainable with either exposure but because of the angle of vision the view of the
ipsilateral portion of large lesions can be limited using the transcortical route. The line of
vision to the depths of the anterior third ventricle is better with the transcallosal method
(Fig. 12.2).
If the ventricles are small the transcallosal approach is far superior. Use of the
transcortical approach to the ventricle in the absence of hydrocephalus requires
disruption of a large amount of cortex and white matter, and the maintenance of
retraction can be difficult. This route also significantly limits mobility if departure from
the initial plane of entry into the lateral ventricle is needed.
The advantages of the transcallosal approach to the third ventricle are that the anatomy
is constant, the distance to the third ventricle is shorter than transcortically, there is
greater flexibility to explore the entire anterior-posterior extent of the third ventricle with
no disruption of hemispheral tissue, no cortical incision and therefore no anticonvulsants
are required, there is excellent unobstructed vision to the depths of the anterior third
ventricle, and ventricular size is irrelevant. Advantages of the transcortical-
transventricular exposure are that there is less chance of compromising an essential
draining vein going to the sagittal sinus and less chance of injuring the pericallosal
arteries.
Figure 12.1. Л. Standard horizontal CT scan showing large intraventricular mass. B.
Sagittal reconstruction showing clearly that the tumor is totally within the third and
lateral ventricles. C. Coronal reconstruction showing that the tumor is within the third
ventricle and extending primarily into the left lateral ventricle.
Figure 12.2. A. Comparison of angle of approach of transcallosal and transcort-ical
techniques. B. Ease of access to entire normal size anterior ventricular system using the
transcallosal approach. C. Transcortical approach to a dilated ventricular system; this
angle of approach allows less mobility than the transcallosal approach.
 As stereotaxic techniques are now so sophisticated, accurate, and safe they should be
used to obtain tissue for the diagnosis of third ventricular lesions thought to be
nonresectable on the basis of preoperative studies. If the diagnosis shows a lesion that is
treatable definitive surgery is performed.

Operative Technique
Transcallosal-Transventricular Approach
The patient is placed in the surgical headholder with the head straight and elevated
about 20°. A coronal skin incision provides the most flexibility, best demonstrates the
surface landmarks for proper placement of the bone flap, and is the most cosmetically
acceptable. A right-sided exposure is used in almost all cases so the coronal incision
should extend most inferiorly on the right side to a point approximately 1 cm anterior to
the external auditory meatus and approximately 2 cm above the zygoma. A curvilinear
incision is made parallel to and about 2 cm behind the coronal suture across the midline
toward the front of the left ear. The incision should be carried to the left far enough to
allow reflection of the skin flap at least 6 cm anterior to the coronal suture. This usually
requires an incision extending to a point approximately 5 cm above the left zygoma. The
scalp flap is reflected anteriorly and secured in the usual fashion. The coronal suture and
the junction of the sagittal and coronal sutures should be identified on the skull surface
(Fig. 12.3).
A triangular free bone flap is adequate for most procedures as maximal exposure is
required at the midline and not over the surface of the cortex. This is different from a
transcortical exposure in which a rectangular bone flap is necessary to expose a greater
portion of the cortical surface. The bone flap only need extend 6 to 7 cm laterally
because the exposure does not require significant displacement of the hemisphere. The
bone flap is made using at least two burr holes. One burr hole should be made with its
medial margin at the midline just behind the junction of the right coronal suture and the
sagittal suture. The second burr hole should be made with its medial margin at the
midline approximately 7 cm anterior to the first burr hole.
If the lesion in the third ventricle is very large or occupies a posterior position in the
third ventricle, it is sometimes helpful to place the bone flap more posteriorly. The burr
holes are each moved posteriorly about 2 cm so that the most posteriorly placed burr
hole would be 2 cm behind the coronal suture. This placement allows a little more direct
inferior line of vision for the surgeon. The major concern in moving the flap in this
fashion is the possibility of compromising a draining vein behind the coronal suture.
Greater access to the posterior portion of the third ventricle can be gained by lowering
the position of the patient's head on the operating table and angling the operating
microscope in a more posterior direction (Fig. 12.4).
The dura mater is stripped from the undersurface of the bone and the connection
between these two burr holes should be made with a Gigli saw (we avoid using the
craniotome in the area of the sagittal sinus). The remainder of the bone work can be
done using a craniotome or by placing a third burr hole approximately 6 to 7 cm to the
right of the midline equidistant from the two other burr holes. Several surgeons have
suggested exposing the entire width of the sagittal sinus, but this serves no useful
purpose and only increases the possibility of injury to the sinus. There should be no
retraction of the sagittal sinus, and the bony margin at the edge of the sagittal sinus helps
prevent inadvertent pressure
Figure 12.3. Relationship of skin incision (A) and burr holes (B) to cranial sutures.

against it by retractors. It is important to have the medial aspects of the two midline burr
holes at least at the lateral margin of the sagittal sinus so that the exposure goes straight
inferiorly and one is not obliged to work under a ridge of bone. If the exposure is not at
the midline the rim of bone must be removed using rongeurs. Removing the inner table
of bone over the sinus with an angled Kerrison rongeur is helpful. The bone edges are
waxed, the holes for wires to secure the bone when it is replaced
Figure 12.4. Possible alterations of microscope angle to provide views of different
regions of the third ventricle.

are made, and the wires are passed through the holes. After this, the dura mater is tented
to the surrounding pericranium in the usual fashion (Fig. 12.5).
The dural opening follows the outline of the bone flap with its base being hinged at
the sagittal sinus. The dural opening should go to the right lateral edge of the sagittal
sinus. At this point, if the ventricles are not enlarged, the patient is given 25 g of
mannitol intravenously to shrink the brain and decrease the need for hemispheral
retraction. If there is hydrocephalus, no dehydrating agent is given because there will be
marked relaxation of the brain when the ventricular system is opened. As the dura mater
is being elevated care is taken not to avulse any of the corticodural veins that may be
present. Although it is preferable to avoid sacrificing any draining veins from the cortex
to the saggittal sinus it is usually necessary to divide one or two to allow retraction of
the hemisphere. The veins anterior to the coronal suture can generally be sacrificed with
impunity, but if there is a very large draining vein it should be preserved if possible.
One or two traction sutures are placed through the base of the dural flap just lateral to
the sagittal sinus and are suspended over the crani-otomy to facilitate retraction of the
dura. The presence of the medial bony margin prevents too much pressure on the
saggittal sinus by these sutures. If the flap has been properly placed, the superior portion
of the falx and the medial portion of the cerebral hemisphere will be exposed. Only 3 to
4 cm of longitudinal free space between the hemisphere and falx are required for
adequate retraction. Since the medial margin of the
Figure 12.5. A. Reflection of scalp flap to provide room anterior to the coronal
suture. В Gigli saw used between the two medial burr holes С: Craniotomy
showmg the relationship of the sagittal sinus to the medial bone margin and the
dural incision [dashed line). D. Removal of the inner table of bone over the
sagittal sinus allowing excellent visualization while leaving the bone edge to
prevent undue retraction of or pressure on the sagittal sinus. E. Craniotomy
completed showing exposure of medial convexity and falx.
Figure 12.6. A. Relationship of the foramen of Monro to a line between the coronal
suture and the external auditory meatus. B. Line of incision through the corpus callosum,
well anterior to the motor cortex.

bone flap is 6 to 7 cm in length there is opportunity to select an area for retraction that
will compromise the smallest amount of venous drainage.
Before retraction of the right cerebral hemisphere from the falx, it is imperative to be
oriented to the landmarks that lead toward the proper portion of the corpus callosum. The
best guide is an imaginary line drawn from the coronal suture at the midline to the
external auditory meatus. This path will lead toward the midportion of the corpus
callosum (or slightly anteriorly), and if continued would go through the foramen of
Monro. The coronal suture is in the operative field and the external auditory meatus is
easily palpated through the drapes so this poses no difficulty. If the retractor is placed too
anteriorly and the line of retraction is located too anteriorly, abundant adhesions between
the frontal lobes will be encountered. There should be very few adhesions between the
frontal lobe and the falx. Rarely, one is able to identify the precentral sulcus on the
medial aspect of the hemisphere, and this can be used as a guide to the posterior limit of
the callosal division (Fig. 12.6).
The right hemisphere is gently retracted using a 15-mm-wide malleable retractor. The
line of retraction is straight down toward the bottom of the falx without deviation to
either side. As the inferior margin of the falx is
reached it becomes slightly more difficult to identify the midline, but this is not usually a
significant problem. The corpus callosum is identified by its very white color and not by
its relationship to the pericallosal arteries. The position of the arteries varies depending
on the size of the ventricular system. When retracting the hemisphere, one may see the
callosomar-ginal artery as it courses above the cingulate gyrus and mistake it for a
pericallosal artery. As retraction is continued and the actual pericallosal artery is seen on
the other side of the cingulate gyrus, one may mistake the gyrus for the corpus callosum,
thinking that the callosomarginal artery represents a pericallosal artery. The cingulate
gyrus, however, looks like typical cortex with its gray color and pial vasculature. It is
helpful to use two retractors to reach the corpus callosum, the 15-mm retractor against
the right hemisphere and a 10-mm retractor against the left hemisphere. The retractors are
gently "walked" down between the hemispheres until the strikingly white corpus
callosum is identified (Fig. 12.7). Neither pericallosal artery may be apparent if the
ventricles are enlarged, but there is no need to search for them if there is adequate corpus
callosum exposed to gain entry to the ventricular system. If both pericallosal arteries are
seen, it is best to go between them to avoid the division of penetrating branches going to
either hemisphere. Once the corpus callosum has been identified the hemispheral
retractor is removed, a protective covering of cottonoid, rubber, or something similar is
placed over the medial surface of the hemisphere, and then the retractor is fixed in place
at the depth of the incision, retracting the hemisphere laterally to expose the corpus
callosum. A 20- to 25-mm retractor is used to spread the pressure of retraction more
widely and to provide a gauge as to the length of the callosal incision. The callosal
incision generally need not be more than 2 to 3 cm in length. Before any further
retraction is done the corpus callosum is divided (Fig. 12.8).
The division of the corpus callosum is confined to the anterior third of the body and
the ease of division is related to its thickness. If there is

Figure 12.7. White corpus callosum seen at the depth of field with the right pericallosal
artery, right cingulate gyrus, and right callosomarginal artery seen to the right side. The
left cingulate gyrus is seen but the left pericallosal artery is not apparent.
Figure 12.8. A. Retraction of the right hemisphere laterally to expose the corpus
callosum. B. Retractors against both hemispheres showing both pericallosal arteries and
the right callosomarginal artery. C. Corpus callosum being divided after two small
pericallosal artery anastomoses have been sacrificed.
hydrocephalus the corpus callosum is usually quite thin with entry into the ventricles
being very easily accomplished. If the ventricles are not enlarged the corpus callosum
may be a centimetre or so thick and require considerably more dissection to get through.
The corpus callosum is avascular and can be divided with a blunt small dissector such as
a Penfield #4 or it can be divided using the bipolar cautery and a small suction (#5
French). As soon as the corpus callosum is divided, cerebrospinal fluid escapes from the
ventricle and the cerebral hemisphere relaxes in proportion to the ventricular size (i.e.,
the larger the ventricles the greater the hemispheral relaxation). At this point the
hemispheral retractor is repositioned over the edge of the corpus callosum. If further
retraction is required, a 15- to 20-mm wide retractor can be placed against the left side of
the callosal incision. If the second retractor is used, care must be taken not to create
pressure against the sagittal sinus (Fig. 12.9).
Once the corpus callosum is divided, orientation is accomplished by identifying the
major landmarks within the right lateral ventricle: the Choroid plexus, the thalamostriate
vein, and the septal vein. The foramen of Monro is found by following the Choroid
plexus and the thalamostriate vein anteriorly. The left lateral ventricle may be entered but
the direction of the Choroid plexus as it approaches the foramen of Monro will make this
immediately apparent. A cavum septum pellucidum may be entered and is confusing
because no intraventricular structures are seen. This usually becomes quickly apparent
and generally the presence of a cavum septum pellucidum has been noted on the
preoperative CT scan.
If the lesion being treated is in the lateral ventricle, the exposure obtained is usually
adequate for definitive treatment. If the lesion is in the third ventricle, the operation can
occasionally be performed through a dilated foramen of Monro (Fig. 12.10). If greater
exposure is needed the interforniceal or subchoroidal approaches should be utilized (2,
10, 14) (Figs. 12.11 and 12.12). The utilization of either of these latter two approaches
obviates the need for division of one of the fornices or removal of the anterior portion of
the thalamus to widen the foramen of Monro (Fig. 12.13). Utilization of the transcallosal
approach allows visualization of the depths of the third ventricle with great ease. Using
this approach, exposure can be obtained down to the upper portion of the basilar artery, if
the tumor extends that far (Figs. 12.14 and 12.15).
If there is hydrocephalus or if there is a probability that one of the foramina of Monro
will be compromised, the septum pellucidum should be fenestrated. In the presence of
hydrocephalus the septum is stretched quite thin and a fenestration of about 1 cm2 is
easily made. It is advisable to make the fenestration through the thinnest part of the
septum and avoid dissection near its base. If there is a cavum septum pellucidum both
walls should be fenestrated.
During dissection of lesions in the lateral ventricle a cottonoid is placed over the
foramen of Monro to help keep debris from getting into the cerebrospinal fluid. When
working in the ventricular system, one uses Ringer's lactate as an irrigating solution.
When the lesion has been removed the ventricular system should be thoroughly irrigated
to remove any debris and before closure there should be immaculate hemostasis. At this
point the retractors are removed and the dura mater is reapprox-imated in a watertight
fashion. The bone flap is replaced and the wound is closed in the usual fashion.
Ventricular drainage is rarely, if ever, necessary. Prophylactic antibiotics have not been
used unless there are other indications for their use, such as an abscess, and prophylactic
anticonvulsants have not been used.
Figure 12.9. A. Retractor placed over the cut edge of the corpus callosum. B. Same
exposure as A looking from posterior to anterior. C. View of the right foramen of Monro
showing Choroid plexus and the thalamostriate vein approaching the posterior portion of
the foramen and the septal vein approaching anteriorly. D. Less magnified view of C.
Figure 12.10. Cystic craniopharyngioma seen through a dilated right foramen of Monro.
Choroid plexus is slightly displaced laterally to show the location of the choroidal
fissure.

Figure 12.11. A. Choroid plexus displaced medially to show the underlying choroidal
fissure. B. View from posterior demonstrating access to the third ventricle via the
subchoroidal fissure.
Figure 12.12. A. Incision into the septum pellucidum. B. Leaves of the septum
pellucidum being bluntly separated. C. View from posterior showing interforniceal
access to the third ventricle after the leaves of the septum pellucidum are separated.
Figure 12.13. Autopsy specimen showing separated leaves of the septum pellucidum and
fornices to show normal planes that can be developed either between the fornices or
between a fornix and the thalamus (subchoroidal).

Figure 12.14. Apex of the basilar artery (bifurcation) seen through a dilated foramen of
Monro after removal of a craniopharyngioma.
Figure 12.15. A. Horizontal and coronal reconstruction of a cystic craniopharyngioma
extending from the sella up into the third ventricle. B. Comparable scans after a
transcallosal approach and removal of the tumor. The density in the right lateral
ventricle is a shunt catheter.

Transcortical-Transventricular Approach
There are many similarities between the transcallosal and the transcortical
approaches. The position of the patient in the surgical headholder and the coronal skin
incision are the same. The approach is best performed from the right side (the
nondominant hemisphere) unless it is being used for a lesion that is primarily in the left
lateral ventricle or is a third ventricular lesion with significant extension into the left
lateral ventricle. The bone flap extends approximately the same distance in the anterior-
posterior direction but much more exposure is needed over the cortical surface so a
rectangular bone flap that extends approximately 8 cm lateral to the midline is required.
The two medial burr holes are placed as they are for the transcallosal approach, but the
exposure of the lateral edge of the sagittal sinus is not as important and it is adequate if
the medial edge of the bone flap is a centimeter or so lateral to the midline. If the lesion
is very posterior in the third ventricle, some have advocated placing the bone flap a little
more posteriorly so that the coronal suture is roughly at the midportion of the flap. It is
preferable to limit the amount of bone removal behind the coronal suture to about 2 cm
to allow an adequate margin between the operative area and the motor cortex. When the
bone flap is removed, the dura mater is opened parallel to the edges of the bone flap
using the most medial portion along the sagittal sinus as the base of the dural flap,
which is reflected medially. It is not necessary to expose the lateral edge of the sagittal
sinus nor to elevate the dura mater enough to jeopardize the large cortical veins draining
into the sagittal sinus. A cortical incision is made paralleling the course of, and in the
center of, the middle frontal gyrus for a length of 3 to 4 cm (Fig. 12.16). If this approach
is used with normal size ventricles the longer incision is preferable because of the much
greater mass of hemispheral tissue that must be retracted to enter the lateral ventricle.
Dehydrating agents are used in these cases (usually osmotic diuretics). If the ventricles
are significantly enlarged, a smaller incision can be used because the cortical mantle is
thinner and the enlarged cavity provides excellent exposure down to the third ventricle.
When the incision has been made through the cortex the remaining dissection of white
matter to enter the ventricle is done bluntly using malleable retractors or Penfield
dissectors (Fig. 12.17). The plane of dissection should generally be directed toward the
foramen of Monro on the ipsilateral side. The anterior-posterior guideline is an
imaginary line drawn from the coronal suture to the external auditory meatus. The
medial-lateral guideline, particularly if the
Figure 12.16. A. Craniotomy landmarks for the transcortical approach. B. Relationship
of the craniotomy to the middle frontal gyrus. C. Relationship of the middle frontal gyrus
incision to the coronal and sagittal sutures.
Figure 12.17. A. Retractors opening up a gyrus incision.
B. Path of retraction to the lateral ventricle.

ventricles are not enlarged, is much more critical. The foramina of Monro are, for
practical purposes, midline structures. The plane should be directed from the middle
frontal gyrus toward the medial canthus of the contralateral eye. Such a plane will
generally cross the foramen of Monro or very close to it (Fig. 12.18). Twenty to twenty-
five-millimeter-wide malleable retractors are then used to maintain the exposure after
the underlying brain is covered with protective material. The intraventricular anatomy is
identified as described previously. This operation, once the ventricles are entered, is
identical to the transcallosal approach and the closure is performed in much the same
way (Fig. 12.19).
Some have advocated making the cortical incision in the superior rather than the
middle frontal gyrus. This approach avoids the benefits of the other approaches while
retaining the problems. The major advantage of a cortical incision is the decreased
chance of compromising the draining veins to the sagittal sinus. The chance of
damaging these veins is much greater with the superior frontal gyrus rather than the
middle frontal gyrus approach. The slight improvement in angulation for the surgical
approach obtained by using the superior frontal gyrus is not as good as that obtained by
using the interhemispheric approach and adds the problems of the cortical incision and
hemispheral retraction.
With either technique, fungating or diffuse gliomas can obscure intraventricular
landmarks and immediate orientation can be difficult. Pre-operative imaging techniques
so clearly display the anatomy that this usually presents little problem in the operating
room. Tumors involving the corpus callosum distort the anatomy and normal white
color of that structure, but the tumor is usually very obvious or there is some normal
corpus callosum that can be identified.
Complications
Most of the complications seen with operation of intraventricular lesions have been
related to the location and nature of the primary lesion rather than to the approach.
Examples of these are diabetes insipidus and akinetic mutism. The latter occurs with
tumors in or dissection of the anterior third ventricle, but can be seen transiently with
excessive retraction against both cingulate gyri. Aseptic meningitis has occurred in
approximately 15% of patients who have undergone intraventricular operations. It is
seen more often in patients who had tumors such as malignant astrocytomas, which
spill blood and necrotic tissue into the cerebrospinal fluid. All patients are treated with
corticosteroids preoper-
Figure 12.18. A. Anterior-posterior orientation to the foramen of Monro using an
imaginary line from the coronal suture to the external auditory meatus. B. Medial-
lateral orientation of the frontal gyrus using a plane from the middle frontal gyrus to the
medial canthus of the contralateral eye. С and D. Schematic presentation of the
approach to the foramen of Monro using the transcortical route.

Figure 12.19. A. Retractors separating hemispheral white matter after entry into the
lateral ventricle. B. Lateral view showing the anterior-posterior plane of hemispheral
retractors.

atively and for about 1 week postoperatively. The signs of aseptic meningitis
(headache, low grade fever, stiff neck) usually become apparent when the
corticosteroids are decreased or stopped. Each case has shown cerebrospinal fluid
changes consisting of moderate pleocytosis with a decrease in the sugar content, but no
organisms have been seen or cultured in any case. The patients responded
symptomatically to the reinstitution of corticosteroid therapy and required continued
treatment for 5 to 30 days.
In about half of the patients undergoing third ventricular operations, a
ventriculoperitoneal shunt has been placed before definitive operation because of the
severity of symptoms from increased intracranial pressure. With the transcallosal
approach the subsequent decrease in ventricular size did not create any problem at the
time of operation. In those patients without a shunt placed preoperatively, neither pre-
nor postoperative ventricular drainage was used. It would theoretically be possible to
see acute hydrocephalus or an increase in intracranial pressure in nonshunted patients
postoperatively if debris from the surgical procedure were to obstruct the aqueduct; we
have not seen that complication. The ventriculostomy created by dividing the corpus
callosum is probably not permanent but may function temporarily to help alleviate
hydrocephalus in the unshunted patient. The cortical incision in the transcortical-
transventricular approach may function in the same manner. In essentially all patients
we fenestrate the septum pellucidum to avoid the problem of a trapped or isolated
ventricle secondary to unilateral foramen of Monro occlusion.
 The two major complications in our experience using the transcallosal approach have
been related to compromise of venous drainage. In one case the sagittal sinus was
occluded by a retractor and led to venous infarction of the anterior portions of both
hemispheres. This is a complication that can and should be avoided by careful attention
to retractor placement. The other complication was related to venous infarction of the
right frontal lobe secondary to division of a very large vein draining from the brain to the
sagittal sinus. Despite the fact that this large draining vein was anterior to the coronal
suture, it clearly was an essential vein. We have seen this only once in a large number of
cases. The suggestion has been made that preoperative arteriography demonstrating the
venous drainage pattern can help in the selection of the proper side for the approach. We
have not found this helpful.
No significant clinical deficit subsequent to division of the anterior third of the body of
the corpus callosum has been seen. The deficit most likely to occur would be some
impairment of interhemispheral transfer of information. In our series, as well as others,
there has been no demonstrable deficit in any sphere including memory, performance, or
affect subsequent to division of this limited portion of the corpus callosum. We have not
seen any acute disconnection syndromes related to division of the corpus callosum.
The neurological deficits due to the transcortical-transventricular approach have
included contralateral hemiplegia and major motor seizures.
We have not seen the gastrointestinal hemorrhage others have reported with operation
in the third ventricle.

Summary
At present all lesions in the third ventricle are approachable at least to the extent of
obtaining enough tissue to make a definitive diagnosis. In masses thought to be
malignant or nonremovable a CT-assisted stereotaxic biopsy should be done. Surgical
access to the anterior third ventricle can be obtained using one of several different
approaches; the route utilized should be determined by the location of the lesion,
ventricular size, and associated signs suggesting involvement or lack of involvement of
structures outside the third ventricle. For lesions solely within the anterior third ventricle
a transcallosal approach is used, for lesions that seem to arise subfrontally but have a
significant third ventricular component a combined subfrontal-transcallosal approach is
used, and for practical purposes we no longer use the transcortical approach to the third
ventricle.
References
1. Apuzzo MLJ, Sabshin JK: Computed tomographic guidance stereotaxis in the
management of intracranial mass lesions. Neurosurgery 12:277-258, 1983.
2. Busch E: A new approach for the removal of tumors of the third ventricle.
Acta Psychiatr Neurol 19:57-60, 1944.
3. Cassinari V, Bernasconi V: Tumori della parte anteriore del terzo ventricolo.
Acta Neurochir (Wien) 11:236-271, 1963.
4. Cristensen JD: Third ventricle tumors: Clinical findings and surgical results
in 28 consecutive cases. Excerpta Med Int Congr Series 36:E61-E62, 1961.
5. Dandy WE: Diagnosis, localization and removal of tumors of the third ven
tricle. Bull Johns Hopkins Hosp. 33:188-189, 1922.
6. Ehni G: Interhemispheric and percallosal (transcallosal) approach to the
cingulate gyri, intraventricular shunt tubes, and certain deeply placed brain
lesions. Neurosurgery 14:99-110, 1984.
7. French JD, Bucy PC: Tumors of the spetum pellucidum. J Neurosurg 5:433-
449, 1948.
8. Gordon HW, Bogen JE, Sperry RW: Absence of deconnexion syndrome in two
 patients with partial section of the neocommissures. Brain 94:327-336, 1971.
9. Greenwood J Jr: Radical surgery of tumors of the thalamus, hypothalamus, and
third ventricle area. Surg Neurol 1:29-33, 1973.
10. Lavyne MH, Patterson RH Jr: Subchoroidal transvelum interpositum ap
proach to mid-third ventricular tumors. Neurosurgery 12:86-94, 1983.
11. Long DM, Chou SN: Transcallosal removal of Craniopharyngiomas within the
third ventricle. J Neurosurg 39:563-567, 1973.
12. Milhorat TH, Baldwin M: A technique for surgical exposure of the cerebral
midline: Experimental transcallosal microdissection. J Neurosurg 24:687-
691, 1966.
13. Rhoton AL Jr, Yamamoto I, Peace DA: Microsurgery of the third ventricle:
Part 2. Neurosurgery 8:357-373, 1981.
14. Scarff ТВ, Reigel DH, Lyons ТА: Transcallosal approach to the 3rd ventricle
in children. Neurosurgery 2:154, 1978 (abstr).
15. Shucart WA, Stein BM: Transcallosal approach to the anterior ventricular
system. Neurosurgery 3:339-343, 1978.
16. Van Den Bergh R, Brucher JM: L'abord transventriculaire dans les cranio-
pharyngiomes du triosieme ventricule: Aspects neurochirurgicaux et neuro-
pathologiques. Neurochirurgie 16:51-65, 1970.
17. Winston KR, Cavazzuti U, Arkins T: Absence of neurological and behavioral
abnormalities after anterior transcallosal operations for third ventricular
lesions. Neurosurgery 4:386-393, 1979.
18. Yamamoto I, Rhoton AL Jr, Peace DA: Microsurgery of the third ventricle:
Part 1. Neurosurgery 8:334-356, 1981.
13
Considerations in Transforaminal Entry
George Ehni, M.D., and Bruce Ehni, M.D.

Surgical Technique
The first consideration in planning transforaminal entry to a lesion in the region of or
within the foramen of Monro must be whether such an entry should be made. Foraminal
entry with a needle, freehand or with stereotaxic guidance, or by open operation may be
appropriate for masses whose nature is accurately perceived, but catastrophically
inappropriate for a mass that seems to be third ventricular in origin by computerized
tomography (CT) (20) perhaps, but that will bleed uncontrollably if it proves to be a
high-lying anterior communicating or basilar tip aneurysm — one of the classical
disasters in neurological surgery. Such an outcome results from having insufficient
information. Before foraminal entry is begun, vertebral angiography must reinforce CT
in case of doubt to avoid making the diagnosis of aneurysm at the moment the knife or
needle penetrates the capsule of the presumed colloid cyst (3, 13, 43). Bull and Sutton
(6), who gave precise directions for the conduct of pneumoventriculography when CT
was unknown and angiography was little used and hazardous, said that aneurysms
"cannot possibly be confused" (with colloid cysts), but they have been in the past and
may be again. Magnetic resonance imaging (MRI) should be useful in the identification
of a mass in the foramen of Monro or anterior third ventricle as an exophytic component
of a thalamic glioma for which foraminal entry might be found wanting.
The next consideration must be the choice of approach to the foramen. Shall it be
stereotaxic or freehand needle biopsy without craniotomy (4, 21, 27, 40)? Should it be
unilateral craniotomy and a transcortical approach through one (usually the right) lateral
ventricle to the foramen of Monro (5, 7, 13, 19, 25, 32, 38, 39, 50-52, 54)? Or should it
be an interhemispheric percallosal approach through the midline of the roof of the third
ventricle (2, 5, 7, 13) or percallosal into either the right or the left or both lateral
ventricles (1, 2, 15, 22, 27, 47, 49)?
Stereotaxic equipment and methods seem more attractive to some than is supported by
the relatively sparse literature advocating this method of treatment of colloid cysts. It
seems illogical to put a needle into a cyst, permitting aspiration of some of its content,
when total removal in a
single stage is feasible. Advantages claimed for the aspiration method of treatment
include foreknowledge of the nature of the mass by biopsy (4), negligible morbidity and
mortality, reduced time in the hospital, and a presumed permanence of good effect (4,
21, 27, 40). But relatively few procedures of this sort have been reported and the period
of postoperative observation is limited to fewer than 10 years. Patients have died of
recurrent colloid cysts when the initial extirpations were incomplete (4, 11, 32, 38, 47,
49) and there is little reason to think that aspiration of the cyst content will interrupt
continued elaboration of the product of the cyst lining. A cyst wall remnant is said to be
responsible for a recurrence rate of 10% (11). Another reason to eschew cyst puncture
is that the cyst content cannot be known until after the cyst is punctured, possibly with
spillage into the ventricular system. Not all of these cysts contain benign colloid or
cellular debris; in some, cholesterin crystals, hemosiderin, and mucus are present (6, 11,
18, 24, 37, 42, 45, 46, 48) and ventriculitis of the type provoked by the fluid of
Craniopharyngiomas and dermoid cysts may be anticipated.
Shunting of hydrocephalus due to a colloid cyst as definitive treatment is hazardous,
although the shunt may function well for a long period. When shunting patency fails on
some future date with immediate ventricular decompression unavailable, sudden death
may occur. Shunting or ventriculostomy before a definitive operation to effect rescue in
a deteriorating situation (8) or to allow for decompression and reduction of ventricular
size and a lessened probability of cortical collapse after cortical incision to a ventricle
(5) are sometimes useful tactics. Perhaps an aspirated colloid cyst will not refill nor a
shunt fail with dramatic and catastrophic suddenness, but such treatments must be
considered temporizing, incomplete, and less than wholly satisfactory solutions of a
problem best solved by total extirpation of the mass by a safe method (38).
Most surgeons base their preferences for the transcortical or the interhemispheric
method on safety, considering the level of skill and experience to be applied; ease of
access depending on whether the ventricles are large or small; liability to or freedom
from postoperative epilepsy, paresis, and other unwanted residues of the operation; and
quality of the end result. Another aspect that should be considered in choosing between
transcortical and percallosal approaches is whether the operation provides the most
versatile and useful access considering the position and nature of the lesion. If it has
been determined that the mass is eccentric, perhaps bulging out of the foramen of
Monro or bulging the adjacent septum pellucidum over to one side, or is invading the
caudate nucleus (9, 11, 30, 54) (and if the lesion has been proven not be an aneurysm),
a unilateral approach through the nondominant frontal lobe, particularly if the ventricle
is dilated, will provide excellent exposure and an opportunity for total removal with
minimal deficit, except for the high probability of subsequent seizures (4, 19, 32, 34,
39) and some risk of contralateral paresis if the incision is carried too far toward the
rolandic fissure or retraction is crudely applied. There is also, of course, the risk of
cortical collapse (5, 39). This approach gives a unilateral view of the septum
pellucidum and the interventricular foramen but, if there is nothing to be gained by
looking at the lesion from the side to which it is minimally, if at all, protuberant, the
total avoidance of veins bridging to the sagittal sinus and the pericallosal arteries if
using the interhemispheric approach may be considered an advantage.
Colloid cysts and other lesions within the third ventricle, even if of good size on
radiographic study, may not be visible on inspection of the region of the foramen of
Monro. The foramen may be slitlike and normal-
 looking, although just within it lies a cyst 1 or 2 cm in diameter. Surgeons have used a
cystoscope for ventriculoscopy to confirm the existence of a colloid cyst and have seen
nothing abnormal. The surgeon who has entered a ventricle through a cortical incision
and seen nothing abnormal may think that he should have chosen the opposite
hemisphere to wound. If he makes a window in the septum pellucidum he is unlikely to
see as well the foramen of Monro on the opposite side because of the unfavorable angle
of his line of sight with the axis of the foramen (Fig. 13.1) (2, 15, 22, 32). Despite this
occasional problem of not seeing a cyst in the foramen, ventriculoscopic inspection has
been recommended to give an opportunity for biopsy (40). Another source of confusion
may arise when lateral ventriculomegaly is revealed by CT without the cause being
seen— even on repeat CT and MRI. If positive contrast ventriculography is then done
and a "lesion" is revealed at the foramen of Monro, the "lesion" may

Figure 13.1. Coronal section through the region of the foramen of Monro. The bony
opening is generous to allow retraction of the hemispheres should the ventricles be small.
The craniotomy extends across the midline (Fig. 13.2) to permit the dural flap based on
the sagittal sinus to be pulled into a direct line with the falx, which may also be retracted,
allowing an uncompromised vertical view as well as one angled into either ventricle (A
and B). A dural flap based temporalward may or may not be required. Depending on how
one makes the opening in the corpus callosum between the pericallosal arteries, either or
both ventricles may be entered and the septum pellucidum may be fenestrated as required
or the two leaves of the septum may be separated for a direct entry between the fornices
to the midline tela choroidea of the third ventricle. The sight line of the transcortical
approach is good into the lateral ventricle and foramen on one side (C), but unfavorable
(inviting excessive retraction) through a window in the septum pellucidum into the
opposite ventricle (D).
 turn out to be a void in the contrast shadow if the films were made with the patient in
the hanging head position (valuable for pneumoventriculography only) without good
mixture of the contrast agent with all of the ventricular fluid. The experienced surgeon
should be little handicapped by not seeing anything in the foramen of Monro because
he will have anticipated this and will be ready to use an effective tactic that will reveal
the lesion and permit its removal.
A great virtue of the percallosal method is that it provides lines of sight (Fig. 13.1)
directly down the midline and 10 to 15° to the right and to the left, so that either the
right or the left lateral ventricle may be entered (15, 22) or the leaves of the septum
pellucidum may be separated for a midline entry into the anterior third ventricle (2, 5, 7,
13, 14, 22). The ability to view a lesion from both sides and from above may be of
particular value in cases where difficulty is experienced in separating the cyst capsule
from the Choroid plexus, the internal cerebral veins, or the tela choroidea of the third
ventricle and securing its sometimes vascular pedicle.
Occasionally large lesions may be imperfectly understood, as when the third ventricle
is obliterated by a possibly cystic mass elevating the floor of one or both lateral
ventricles adjacent to the region of the foramen of Monro. Angiography and CT may
leave unanswered the question of whether the lesion is a craniopharyngioma with an
infradiencephalic component that should be examined first. In such situations, one must
consider transforaminal entry with a possible subfrontal approach and the craniotomy
must be fashioned to permit a subfrontal extradural avenue for examination of the
region of the chiasm and the pituitary stalk and, subsequently, an avenue down the
midline if the lesion seems wholly or principally intraventricular (Fig. 13.2) (15).
Another consideration is the prevention or avoidance of hemisphere collapse in cases
complicated by massive ventriculomegaly (5, 39). Generous ventricular size makes
transcortical surgery easier and safer than if the ventricles are small (5, 7, 13, 19, 25, 32,
33, 38, 39, 50-52, 54), but an inability to seal the transcortical incision reliably in a
watertight fashion may argue for interhemispheric access because the small opening in
the corpus callosum is self-sealing once the retractors are removed and the ventricles
are filled with fluid.
The options available for dealing with masses in the foramen of Monro and for entry
into the third ventricle are several: one can perform freehand penetration of the foramen
of Monro with a stiff cannula oriented with reference to external landmarks (21) or use
stereotaxic guidance of a cannula or needle using a ventriculoscope (40) or devices in
conjunction with CT or more conventional guidance systems using radiographic films
(4, 27); one may work to and through the foramen of Monro with magnification after
exposure of the foramen through a cortical incision (5, 13, 19, 25, 32, 38, 39, 50-52, 54)
or through the corpus callosum (1, 2, 15, 22,27,47,49), utilizing tactics for reducing the
bulk of the intraforaminal lesion to facilitate total removal (11, 32, 38, 50); one may
enter percallos-ally, using the interforniceal approach down the midline between the
internal cerebral veins just back of the foramen of Monro and through the tela choroidea
of the third ventricle (2, 5, 7, 13) or the approach through the lateral ventricle, lifting the
Choroid plexus from the thalamus (12, 14, 25, 31, 51) or enlarging the foramen of
Monro by removing some of the substance of the anterior nucleus of the thalamus,
preserving the closely applied internal cerebral vein (11, 15, 19). Similarly the surgeon
may cut one or both forniceal columns (13, 32, 39) or divide the thala-
Figure 13.2. A craniotomy appropriate for transcallosal exposure on the right side in a
patient with small ventricles or who may require exploration of the chiasm. The low
frontal burr hole is directly on the midline and above the frontal sinus. The two holes on
either side of the sagittal sinus are staggered and may be safely connected by rongeur. A
Gigli saw provides thinner and more bevelled cuts than a high speed router. If the chiasm
is to be explored the dura should not be opened at the first opportunity, but only along
the sphenoid ridge to the region of the clinoid and then along the midline in the direction
of the low frontal burr hole.
 mostriate vein to provide improved access under the Choroid plexus and to the roof of
the third ventricle (12, 14, 25, 31, 51). Certain of these described procedures, although
perhaps technically feasible or even easy, carry unnecessary risks to the complete
recovery of the patient. A colloid cyst is invariably benign and should be essentially
curable.
Certain formerly used approaches are of historical interest only or are little used and
largely obsolete. Entrance into the third ventricle via the lamina terminalis (25, 29)
gives very limited access because of the tight proximity of the proximal pericallosal
arteries, the deep position and shortness of structure of the lamina terminalis between
the chiasm below and the anterior commissured superiorly, and the extreme sensitivity
to pressure and manipulation of the walls of the hypothalamus, which may cause severe
hypothalamic deficits.
The Dandy methods currently used include transcortical openings to the right and left
ventricles (used once each when his book was written (13)) and the anterior percallosal
method, which he did not use for colloid cysts, but did use for cysts of the septum
pellucidum and the cavum vergae. The posterior interhemispheric operation with
extensive section of the corpus callosum, which he called the "pineal approach," was
used by him 3 times, once on the left and twice to the right of the sagittal sinus for
colloid cysts. In his Case 2, illustrated by Figure 10 of his book, he kept to the midline
and entered the third ventricle between the internal cerebral veins, similar to the method
described by Busch in 1944 (7) except that Busch first entered the nondominant lateral
ventricle by cortical incision and subsequently gained the midline by splitting the
septum pellucidum. The pineal approach of Dandy is no longer used because of the
resulting hemisphere disconnection and the almost equal access provided by harmless
smaller anterior callosal openings and the use of the microscope (2, 15, 17, 22, 27).
For freehand puncture and aspiration of a cyst in the foramen of Monro, one used a
flexible shunt tube with an intraluminal obturator introduced 4 cm from the midline in
the coronal region, penetrating the frontal lobe on a line (from the frontal view) directed
toward the opposite inner canthus and on lateral view toward the external auditory canal
(21). A duration of success as long as 4 years has been claimed. The technique is said to
be simple, reliable, and safe. We and many others have used this method of entering the
foramen of Monro to introduce a catheter into the third ventricle for the instillation of
air or another contrast agent to make visible the anterior and posterior commissures of
the third ventricle and the ventricular walls preliminary to stereotaxic operations on the
thalamus, but have never tried to penetrate a cyst for therapeutic purposes. For
ventriculography, one uses a flexible catheter with little or no potential for damaging
any of the structures surrounding or inferior to the foramen of Monro in case the aim
should be less than perfect, but for the tough walls of colloid cysts an instrument with
penetration capability would be necessary. The possibility of wounding the internal
cerebral vein, Choroid plexus, fornix, thalamus, and hypothalamus is neither trivial nor
remote. Aspiration of the cyst content followed by ventriculoa-trial or peritoneal
shunting with the same tube is an instance of using two less than completely
satisfactory treatments in hope that, if one does not work, the other will. As already
mentioned, spillage of cyst content into the ventricular system is worrisome. Neither
would cyst content be suitable for conveyance to the heart and the general circulation.
Also, cyst content might easily obstruct the ventricular end of the tube used for
shunting. The cyst probably has a higher than realized refill potential,
said by some to be in the neighborhood of 10% (11), which must relate to the duration of
follow-up. As long as the cyst wall remains and as long as shunts are fallible, the
possibility of sudden death has not been eliminated.
Stereotaxic aspiration of a cyst may reduce the risk of damage to an internal cerebral
vein and other surrounding structures (4). Although the procedure may be elegant in
terms of the technology used and accuracy, one wonders about the true value of this
procedure. Little is gained by examining the cyst content because a generally spherical
unilocular structure in the interventricular foramen and anterior third ventricle can, for
practical purposes, only be a colloid cyst; aneurysms, tumors arising from the septum
pellucidum, fornix, and thalamus, and other masses should already have been ruled out
by CT, angiography, or MRI. There is danger of spillage of irritating content into the
ventricle, imper-manence of the therapeutic result, risk of future sudden death from acute
hydrocephalus, or the possible need for another procedure that might better have been
extirpative and curative in the first place.
Inspection of the foramen of Monro through the nondominant lateral ventricle entered
through the corpus callosum or a cortical incision is highly satisfactory and permits
colloid cyst extirpation and permanent cure. This should be considered the standard
method of dealing with colloid cysts and similar lesions. With smaller lesions up to a
centimeter in diameter, the foramen of Monro may be slitlike, with no evidence of a mass
within it as first seen. With larger lesions, up to 3 cm and more, the mass will have
spread apart the walls of the third ventricle just behind the foramen of Monro and the
foramen will be dilated a bit, allowing the pathological surface to be seen. There are
reports of cysts as large as 9 cm in greatest dimension (37); cysts presenting above the
third ventricle between the fornices and the leaves of the septum pellucidum (9-11); cysts
ruptured into the internal capsule and the caudate nucleus (30) or into both lateral
ventricles (54); and cysts with other special features (41, 53). The approach used must
suit the special circumstances.
If the mass has extended upward between the fornices and separated the leaves of the
septum pellucidum, perhaps more to the side of the approach so the foramen is overlain
by the bulging septum and so unseen, a reliable method of finding the foramen must be
used. The best method is to follow forward the Choroid plexus of the lateral ventricle
(50). Right where it disappears from view (perhaps under a bulging overhang of the
septum pellucidum that will have to be lifted up) will be found the foramen. Entering the
foramen and closely applied to the thalamus is the thalamostriate vein (Fig. 13.3).
Bounding the foramen superiorly and anteriorly is the fornix. Once the foramen is
located, its patency may be tested by catheterization with a Silastic (Dow Corning,
Midland, Michigan) shunt tube, using either the manufactured end with multiple
apertures or a surplus length cut very obliquely to make a filamentous tip. This may be
gently teased into the foramen and past the obstructing mass with no injury to either the
Choroid plexus or the vein. One intends not to penetrate the wall of the cyst at this stage,
but merely to feel the resistance of catheter passage between the cyst wall and the
thalamus.
If the cyst is not visible, the closed tip of a forceps should be introduced into the
foramen and gently opened, acting as a temporary retractor on the walls of the foramen.
This will permit one to see most lesions in the anterior third ventricle. If the catheter
passes with no resistance into the slitlike foramen and direct visualization with the
spreading forceps shows no evidence of a mass, one should use a #8 French urethral
catheter as a soft probe through the foramen; the mass may lie posterior or inferior to the
foramen of Monro. In either of these special circumstances the foramen is not the proper
route for extirpation of the lesion. Consideration must be given to entry through the roof
of the third ventricle directly down the midline behind the foramen of Monro by the
methods of Dandy (13) (Case 2; Fig. 10) Busch (7), or Apuzzo et al. (2) or by separating
the Choroid plexus just behind the foramen from its attachment to the thalamus and
going through the tela choroidea of the third ventricle laterally
Figure 13.3. View into the anterior right lateral ventricle through a high frontal
transcortical incision or one in the anterior corpus callosum angled to the right with
some retraction of the right cingulate gyrus, the right pericallosal artery, and the right
cut edge of the corpus callosum just behind the genu. The foramen of Monro may not be
seen beneath the overhang of a septum pellucidum bulging from a colloid cyst that has
dissected between and separated the columns of the fornix to lie between the leaves of
the septum pellucidum. To find it, follow the Choroid plexus forward to where it meets
the thalamostriate vein to enter the foramen. Colloid material may also dissect laterally
into the thalamus and caudate nucleus.
Figure 13.4. Diagramatic representation of a coronal section of the brain just posterior to
the foramen of Monro (not shown). The fornical columns are closely applied to the
rostrum of the corpus callosum and beneath lies the transverse fissure. Below this is the
roof of the third ventricle bearing the internal cerebral veins. A. The avenue of Apuzzo
et al. directly down the midline. B. The avenue of Busch, which gains the midline
beneath the corpus callosum from the lateral ventricle. Dandy's midline incision through
the posterior corpus callosum is not shown. D. The avenue of Deladsheer et al. and
others (see text) lateral to the Choroid plexus and the internal cerebral veins.
beneath the internal cerebral vein (14, 25, 31) (Fig. 13.4). Although colloid cysts take
origin from the tela choroidea just behind the foramen of Monro and in the region of the
paraphysis (10, 16, 23, 28, 35, 37, 44, 46, 53), there are circumstances that might cause
a cyst to appear in an aberrant position in the ventricle. Neuroepithelial cysts of this sort
can develop behind the paraphysis and even in the fourth ventricle (8, 10). Or a cyst
only lightly attached to the tela choroidea may be displaced posteriorly by the pressure
gradient developing in the lateral ventricles as a consequence of obstruction at the
interventricular foramen. Another possibility exists in the patient who has undergone
needle aspiration of a cysts or a less than complete extirpation, with the refilled cyst
lying in an aberrant location.
When the cyst or tumor is reasonably well seen an effort should be made, working
through the foramen of Monro, to free its anterior, inferior, lateral, and posterior
surfaces with a slender blunt probe such as a curved, ball-ended dissector. One should
not stroke superiorly around the mass because at this stage interruption of a possibly
vascular attachment or pedicle to the tela choroidea above would be inconvenient.
Unless the mass is small and seems inclined to deliver itself, it is unwise to attempt
removal of the lesion intact because the pedicle will be the last part to come through the
foramen of Monro and, if inadvertently disrupted, bleeding may occur from the roof of
the third ventricle — unseen and unsuspected until the third ventricle is filled with
blood.
A mass too large to squeeze out of the foramen is penetrated with a #20 or #21 spinal
needle held near its tip in a hemostat or a slender needle holder. Aspiration may then be
made with a 5-ml syringe connected to the needle by a short length of flexible tubing.
As material is being obtained the capsule shrinks simultaneously with the appearance of
fluid in the transparent tubing.
If the material is too thick for aspiration through the needle, a larger needle or even a
small caliber suction tip may be used. If the cyst content is semisolid or caseous, a
cruciate incision into the capsule will allow, by the use of a small, delicate sucker tip
and small ring curettes, fragmentation of the material and fairly complete evacuation.
One should never make a pushing force on such a cyst for fear of displacing it
posteriorly into the third ventricle and losing sight of it. The end of the sucker tip should
always be in contact with the interior of the cyst so as to maintain a slight grip on it, or
one may use a microaligator to hold the wall or fasten a length of suture material to the
wall of the cyst with a small microclip. A knot tied in the end will prevent slippage
through the clip.
The objective at this stage is to evacuate the cystic content completely to permit
delivery of the capsule by making gentle pulls on it at various sites around the opening
already made through the foramen of Monro. The pedicle will be the last part to be seen
as it passes through the foramen of Monro, which is then hemostatically divided. The
foramen should then be gently irrigated with a small volume of saline delivered through
the Silastic catheter. All of the saline return should be bloodless, with no need for
hemostatic sponge to be placed in the neighborhood of the foramen of Monro. If
bleeding occurs within the foramen of Monro, clips and cautery should be used
cautiously because one desires to retain patency of the thalamostriate and internal
cerebral veins (4, 11, 50) despite counterclaims of their dispensability (12, 14, 25, 31,
51). One may introduce a #8 French urethral catheter into the foramen and then slide
down a very small piece of gelatin sponge between the catheter and the bleeding point,
with the catheter serving as a counterforce against the wounded vein. The catheter
should be led outside the wound for removal in 12 to 24 hours, by which time the
Gelfoam will be firmly adherent to the vein, with little possibility of it obstructing the
aqueduct or allowing rebleeding.
If the interventricular foramen is too small to permit the tumor to be well seen or if
the tumor lies too far posterior to the foramen for removal
through it, the tumor may be approached through the roof of the third ventricle. Most
large masses not removable through the foramen will have widened the ventricle and will
have spread the tela choroidea and, thereby, the distance between the two internal
cerebral veins and fornices. A midline incision through the roof behind the foramen then
can be made; this was well shown in Figure 10 (Case 2) of Dandy's monograph on
tumors of the third ventricle (13) after what he called his pineal or posterior transcallosal
approach. A similar approach was later described by Edward Busch, but he used the
transcortical approach to a lateral ventricle and then opened the leaves of the septum
pellucidum (7). Apuzzo et al. (2) recently described a modified and refined perfectly
midline avenue into the third ventricle. One virtue of midline opening is that it can be
extended posteriorly almost without limit, increasing and improving the exposure of just
about anything in the third ventricle that arises from or is attached to superior structures.
As mentioned previously, a midline opening is not helpful for infradiencephalic tumors
invaginating into the third ventricle. The procedure of Dandy (13) minimized injury to
the columns of the fornix, which are separated posteriorly, but at the expense of cutting
the corpus callosum too far back by modern standards. Dandy's procedure also
minimized the possibility of injury to internal cerebral veins. However, in the case he
described one of the veins had to be ligated, apparently without complication, because
the cyst capsule was tightly attached to it (13). The critical obligation in this approach is
to remain so perfectly midline as to be looking down upon the roof of the third ventricle,
with the two internal cerebral veins directly visualized on either side, making the incision
carefully between them (Fig. 13.4). There is no cross connection between them, but if
bleeding occurs it is safer to put a small pledget of Gelfoam under a thin or narrow
cottonoid than to use cautery. One must be aware of anatomical variation, e.g., a single
internal cerebral vein.
The midline interforniceal approach of Busch (7) and Apuzzo et al. (2) requires
separation of the closely applied fornices and is somewhat worrisome because of their
vulnerability to bilateral injury. Such injury is, however, as yet undescribed. The fornix,
similar in construction to the optic nerve, may have similar sensitivity to damage. One
may be beguiled into thinking that no damage is done because the consequence of
modest forniceal damage must be carefully sought to be found, despite its disability
effect. The functions of the fornix and other parts of the limbic system in memory,
motivation, emotion, and other hard to quantitate features of human nature suggests that
it is prudent to avoid forniceal manipulation if at all possible (26, 36, 49).
An excellent method of third ventricular entry is that of Deladsheer et al. (14), Hirsch
et al. (25), Viale and Turtas (51), Cossu et al. (12), and Lavyne and Patterson (31), who
separate the Choroid plexus from the thalamus and enter the third ventricle beneath it and
the internal cerebral vein. The fine illustrations of Deladsheer et al. (14) and Cossu et al.
(12) are worth studying before using this method. The method entails manipulation of the
Choroid plexus and the thalamostriate vein, and there is some risk of interruption of one
of them. This method is not necessarily superior to the midline methods, and all have the
same indications. It may be more feasible technically when the two internal cerebral
veins are not clearly separate structures or when the effect of the intraventricular
neoplasm has been to stretch and broaden the veil of tissue attaching the vein to the
thalamus, making it easier to gain entry to the ventricle under and lateral to the right-
sided vein rather than medial to it.
 Enlargement of the foramen of Monro by removal of tissue from its posteroinferior
aspect, the anterior nucleus of the thalamus, has been mentioned as an alternative to
forniceal cutting (15, 19, 22). Despite the fact that the anterior nucleus and its contained
tract of Vicq d'Azyr is an important part of the limbic system, some of its substance can
be removed unilaterally, but the utility of doing so is small unless the thalamostriate
vein is also interrupted. The subchoroidal method of entering the ventricle behind the
foramen is clearly superior and seems to offer less danger to recent memory. If the
foramen needs enlarging only slightly, as when an evacuated cyst capsule remains just
too large to come through the foramen easily, the thalamostriate vein may be separated
from its attachment to the thalamus where it enters the interventricular foramen. With
gentle suction and the use of a micro-Love-Gruenwald forceps or a semi-sharp ring
curette, some anterior thalamic substance can be removed from beneath it.
Although surgeons who have removed third ventricular lesions with great success in
prior years sectioned one or both columns of the fornix (13, 32, 39), the consequence of
recent memory impairment and learning disability should forbid the use of this tactic.
Perhaps the human brain works just as well with only one fornix, but not knowing
everything that a fornix contributes to human behavior and competence makes for un-
certainty. At least as important, the lesion being operated upon may, because of features
not known when one fornix is cut, have interfered with the function of the other, or the
surgeon may damage the opposite fornix as he seeks to gain still better exposure.
Reports of the division of both forniceal columns without resulting deficit are highly
suspect. Lack of evidence of deficit most likely stems from insufficiency of knowledge
of forniceal function and examination during the period when forniceal division was
thought acceptable.
Thus, many considerations attend third ventricular entry. There are possibilities of
postoperative seizures, paresis, cortical collapse, impairment of frontal lobe function
due to division of bridging veins, damage to the pericallosal and tributary arteries, and
damage to deeper vascular structures such as the Choroid plexus, the thalamostriate
vein, the internal cerebral vein, and the choroidal arteries. The perils attending exposure
of these structures are immediate and so may seem of greater importance to the surgeon
than a depreciated quality of long term outcome that goes on outside his observation
once the patient is dismissed and at home. Injury to the limbic system from improper
handling may lead to serious functional impairment for the rest of the patient's life. This
system, well described elsewhere (26, 36), lies phylogenetically between the oldest parts
of the brain having to do with control of visceral function, cardiac, vascular, and
respiratory regulation, and crude types of locomotion and the neocortex, which lies atop
it and conceals it from view. The limbic system is concerned with motivation, emotion,
moods relating to eating and smell, sexual behavior, and behavioral responses to the
external and internal environment that far outlast provocative stimuli and contribute
immensly to distinctiveness of personality, memory, and mental competence.
The parts of the limbic system at risk in this operation include the cingulum and
cingulate bundle, the body and columns of the fornix, the termination of the
mamilothalamic tract of Vicq d'Ayzr, and the anterior nucleus of the thalamus. Even
deliberate lesioning or the excision of lengths of both cingulate gyri and the cingulum
bundles 2.5 cm long does not seem to have an unfavorable effect on behavior. On the
contrary, it may have an ameliorating effect on chronic pain and obsessive-compul-
sive states (15). The effect of forniceal lesions is, if bilateral, severe impairment of recent
memory and of the making of new permanent memory engrams. This is said not to occur
if only one fornix column is interrupted, but one can never be certain that the other
column is not impaired (15). Undoubtedly, much is to be learned about limbic structures,
and it may be surmised that in the future tests will be developed that show handicaps not
at present suspected. The appropriate attitude of a surgeon toward such structures should
be to inflict as little manipulative damage as possible. Something as gratuitous and
avoidable as sectioning the fornix or deep lesioning of the anterior nucleus of the
thalamus may change the patient's postoperative personality, drive, attitudes, emotions,
and capabilities in ways too subtle to be measured at present, but these changes may
significantly reduce his potential as an effective or perhaps superior human being.

Limbic System with Special Attention to Structures Involved in the Third

Ventricular Approach
The purpose of this section is to identify in humans the potential for disability after
surgical lesions are made in structures related to the third ventricular approach for the
removal of lesions from the diencephalon. We touch upon the anatomy of memory,
which has been covered in greater detail in Chapter 6. We also cover in some detail
lesions of the fornix, septum, mamillary bodies and mamillothalamic tract, nuclei of the
thalamus, and corpus callosum.
One facet that concerns us preeminently is disability to the function of memory
resulting from diencephalic surgery. We will discuss briefly the anatomy of memory
specifically and from there move onto structures in the neighborhood of the third
ventricle in greater detail.
The anatomy of memory is of some significance in neurosurgery, particularly in
surgery of the medial skull base, the diencephalon, and the temporal lobes, but getting to
the heart of this subject is difficult. Clini-copathological correlations have never been
clear enough to allow perfect determination of the neuroanatomical substrates in the
anatomy of memory. Recently utilized techniques such as horseradish peroxidase and
neurotransmitter tracing have produced far more information, but little more evidence of
the mode of operation, and have failed to answer important clinical questions regarding
humans. The search for the functional organ of memory has only proven to indicate that a
single entity cannot be found (14, 22, 27, 28, 31).
All memories, whether visual, verbal, or tactile, are probably stored in the neocortex in
the form of coded engrams holding a restricted number of items of information.
Presumably the longer a piece of information is held in memory, the more it is repeated.
With repetition its engram becomes more restricted and coded and more compressed. By
way of illustrating the importance of transmission of these presumed engrams, the fornix,
as small and anatomically insignificant as it seems in the human brain, contains 5 times
the number of neurons of the optic tract (19).
Weiskrantz (37) has offered a conceptual scheme of the function of memory, not as yet
translatable into a neurophysiological process. An event occurs initiating a "short term
trace" that lasts about 20 seconds and rapidly decays. The subsequent conversion of a
short term trace to a "long term trace" has been termed consolidation. Recall of short
term traces is a separate process from consolidation, supported by the observation that
the duration of retrograde amnesia (as in head injury) may decrease. Clearly, if a patient
can, at a later date, recall an event that he
 could not previously remember, the long term trace remained but could not be recalled.
Similarly, such patients in the absence of an attention disorder reflect accurate short
term memory even during the period of posttraumatic confusion (2).
In all likelihood the short term trace and immediate memory processes occur in the
cortex. The process requires initial registration, usually some visual or verbal repetition,
and short term hold. It seems possibly served by perisylvian language cortex and visual
association cortex (32). It is unlikely that much, if any, commissural transmission —
i.e., interhemispheric communication for storage, comparison, and retrieval—takes
place. The function of immediate recall is not threatened by surgical approaches to the
third ventricle (11).
As an immediate memory makes the metamorphosis to remote memory, it is
presumed to go from relatively uncoded cortical information to a compact engram that
can be read out at will. In the intervening time, the subcortical structures of the limbic
system and major parts of the thalamus have repeatedly encoded it, triaged it, stored it,
retrieved it, deciphered it, and transmitted it. By the time that it is a truly remote
memory, the limbic system may be little required. Until it is remote, however, the
memory is "recent" and as such is dependent on the subcortical white tracts and nuclei
of the limbic system and thalamus. The mechanism of limbic system ciphering seems to
be encoding into compact engrams, which with repetition become simpler and more
easily recovered (2).
Clinical states in which there may be recent memory disturbances include anoxia,
bitemporal lobectomy (26), herpes encephalitis, bilateral hippocampal infarction (24),
and Korsakoff's syndrome. Alzheimer's disease displays its first pathological changes in
the hippocampi; therefore, learning disability is presumably one of its first
manifestations. Tumors of the midline involving the fornices have resulted in amnestic
states (16, 17), as have tumors of the parasellar and suprasellar region, presumably
because of compression of the mamillary bodies, anterior fornices, thalamus, and
diencephalic white tracts (9, 20). Finally, trauma can affect the limbic system and
thereby memory. The hippocampi and amygdala are both known to have extremely low
electrical and epileptogenic thresholds; presumably by their sensitivity and by virtue of
their location near the bone and tentorium of the middle fossa, these structures are
sensitive to head injury. We will later see that neither the amygdala nor the entorhinal
cortex is thought to be important in the registration of recent memory. However, the
hippocampus does seem to be, and trauma to it causes the disturbed memory, storage,
and retrieval so prominent in traumatic amnesia. One may even go so far as to draw a
parallel between the dream states, fugue states, hallucinations, confusion, fear, etc., ex-
perienced by temporal lobe epilepsy patients and the same conditions seen in some
trauma patients. If, like Horel, one disbelieves the hippocampal theory, one may credit
the dysfunction produced in the temporal cortex and stem by trauma.
We see, then, that the function of recent memory involves a wide variety of
subcortical and particularly limbic structures and that dysfunction of recent memory can
be elicited by a variety of processes.
The basic limbic circuit was first described by Papez in 1937, and at the time it was
thought to be primarily concerned with olfaction and emotions. This view prevailed for
the next 20 years without much additional neuroanatomical or functional information.
Perhaps the exception to this was Brodal, who in 1947 thought sufficient evidence had
accrued to indicate that the circuit had nothing to do with olfaction. In the classical
Papez circuit, the hippocampi (Ammon's horn, subiculum, fimbriae, and
dentate gyrus) are connected by way of the fornix to the mamillary bodies. The
mamillary bodies are then connected by the tract of Vicq d'Azyr to the anterior
hypothalamus and from there to the cingulate gyrus. Since the time of Papez there has
been considerable information generated by clinicopathological and animal studies
adding to our knowledge and understanding of the limbic system. In Korsakoff,s disease,
Victor et al. have attached great importance to pathological conditions in the magno-
cellular dorsomedial thalamus (36). Similarly, Horel emphasized the dor-somedial
thalamus and disbelieved the idea that the hippocampi are central to the function of
memory (18). Spiegel and Wycis place orientation in time ("chronotaraxis"), often the
first problem experienced in Korsakoff's disease, in the anterior and dorsomedial nuclei
of the thalamus (29, 30). The weight of modern information makes the thalamus seem to
be more important in effect than the hippocampi so far as discrete lesions are concerned
in the production of amnestic states. Diencephalic white fiber tracts such as the anterior
commissure (18), inferior thalamic peduncle (18), and thalamocingulate tracts (22) have
been added to the list of structures thought crucial to recent memory. The temporal stem
to the dorsomedial thalamus, basal ganglia, and orbitofrontal cortex has also been
implicated (18). The anterior corpus callosum and anterior commissure (18, 40), neither
regarded as "limbic," have been recorded to cause clinical amnesia, perhaps by the loss
of interhemispheric transmission.
Certain of these structures important in the registration of recent memory are easily
damaged in third ventricular approaches and will be more specifically addressed later in
the discussion.
Remote memory is a function generally spared in all but severe degenerative diseases.
Patients with Korsakoff's syndrome or Kluver-Bucy syndrome after bitemporal
lobectomy will have surprisingly intact remote memory despite profound new learning
disability. The reason, of course, seems to be that the limbic system is not actively used
in the retrieval and decoding of remote memory. As currently understood, it takes wide-
spread cortical atrophy to impair remote memory. One never finds intact recent memory
in the presence of impaired remote memory.
More than 30 years ago in 1955, MacKay said that it was unwise to try to localize
memory as a function of any single portion of the nervous system (34). A single lesion
will probably not produce a deficit; rather there must be two or more (22, 23, 27-31).
Clinical and experimental evidence shows that mnestic derangements are evident with
lesions of the temporal cortex, parahippocampal cortex, cingulate gyrus, mamillary
bodies, thalamic nuclei, midbrain reticular formation, hippocampal formations, fornices,
hippocampal commissures, corpus callosum, thalamocingulate tracts, anterior
commissure, and inferior thalamic peduncles. There is no agreement on a "memory site,"
probably because there is no single site. We see, however, that recent memory
disturbances dominate the deficits likely to be produced by approaches to the third
ventricle primarily because of the subcortical and limbic nature of the operation.
The main problems in dissecting the memory circuit are two: (a) The pathological
conditions in human clinicopathological studies are too widespread (tumors, Korsakoff's
disease, encephalitis, infarcts, trauma), (b) Animal studies are difficult to design well,
execute, and interpret in a meaningful way. A third and probably less well understood
problem in clinicopathological and animal studies is that a chronic process such as
alcoholism will allow ongoing functional reorganization to proceed at a pace parallel
with the destruction of brain, thereby lending the impres-
sion that an individual is actually unimpaired until virtually all tolerance is used up.
Regarding memory and the third ventricular approach, certain features bear repeating.
The loss of many of the nuclei and fiber tracts in the limbic system will affect memory.
The hippocampus, once at the fore of memory theory, has become less eminent as
attention has been directed toward the diencephalon. Much of the older literature in
which normal mental status reportedly followed limbic injury must be viewed more
skeptically. In times past, forniceal injury, for example, was expected to provoke
olfactory or emotional disability whereas subtle memory and learning disabilities could
have been easily passed over. It is from this older literature that we have gotten certain
of our neurosurgical maxims, such as that unilateral limbic injury is well tolerated.
Subtle memory deficits may nowadays be expected to follow "minor" unilateral limbic
injuries (6, 27, 28, 31).
Medial Temporal Structures
In an effort to understand the importance of the diencephalic structures involved in
third ventricular surgery, one must have an understanding of their afferents. We discuss
these briefly before addressing those structures in the vicinity of the third ventricle.
Hippocampus
The hippocampal formation (Ammon's horn, subiculum, fimbriae, dentate gyrus)
receives its afferents from the medial septal nuclei via the dorsal fornix. The medial
septal nuclei are thought to drive the theta waves of the hippocampus. The
septohippocampal system receives, either indirectly or directly, input from most of the
neocortex and amygdala and much of the hypothalamus and from adrenergic,
dopaminergic, and serotonergic cell groups in the brain stem (33). The efferents from
the hippocampal formation then pass to the contralateral hippocampus via the
hippocampal commissure and over the fornix through the mamillary bodies into the
septum and into the hypothalamus and habenular nuclei and interpeduncular nuclei.
Hippocampal projections can be found as well in substantia nigra, central gray, pontine
gray, and corpus striatum. Of particular importance in this discussion, small efferents
also pass directly to the indusium griseum, cingulate gyrus, and medial septum via the
dorsal fornix, and a small number of efferents pass directly to the anterior thalamus,
bypassing the mamillary bodies. Furthermore, a number of fibers pass off the fornix into
the dorsomedial nucleus of the thalamus (35). These latter structures may well be
involved in tumors and operations of the diencephalon. Acting through the cingulate
cortex, habenular nuclei, and hypothalamus, the septohippocampal system in fact may
influence activity in most of the systems of the brain (33). Its major efferent system,
however, is that to the mamillary body. Because of the involvement of the mamillary
bodies in Korsakoff's syndrome, this massive connection of the hippocampus was
thought to implicate the fornix in memory. That contention remains controversial to this
day.
Glees and Griffith in 1952 and Scoville and Milner (26) were the first to implicate
lesions of the hippocampus as operant in memory deficits. Scoville and Milner noted in
particular a grave loss of recent memory in those cases in which the medial temporal
lobe resection involved the hippocampal complex bilaterally. In their noted case, H.M.,
a full-scale I.Q. minus memory quotient score of 45 was obtained. The hippocampus
was specifically suspect because of the lack of memory disturbances in other cases of
deliberate removal of the uncus and the lack of memory
deficit after temporal lobectomy without hippocampal removal. Scoville and Milner were
particularly impressed by the importance of the anterior hippocampus in the retention of
new memory.
The idea of a "memory circuit" involving the hippocampi, mamillary bodies, and
fornix took root with further clinical evidence, for example, ischemia of the hippocampi
responsible for amnesia shown by angiography revealing vertebrobasilar and
posterocerebral arterial disease (8, 24). The learning disability present in monkeys with
Kluver-Bucy syndrome had already been well established. There have been innumerable
animal studies purporting to solidify the central role of the hippocampus in memory.
The septohippocampal formation may well be at least as important in spatial
orientation as in memory (17, 18). In fact, it must be admitted that the studies in humans
implicate a wide area of the medial temporal lobe and the studies in animals are
inconclusive as to the hippocampi. Horel (18), for example, implicates the temporal stem
and medial temporal neocortex. Reviewing his own and other experimental results in
hippocampal lesions, he thinks that the spatial disorientation produced is productive of all
of the deficits of purported memory tasks. In a similar vein, Squire and Moore doubt that
the hippocampus is a source of mnestic deficits and believe that the dorsomedial nucleus
of the thalamus is foremost (31).
Despite the known severe memory deficits following bilateral medial temporal lobe
injury, then, the evidence implicating the hippocampi specifically is suspect. Reviewing
experimental evidence in animals, Horel suggested that learning and memory deficits
have not been documented in animals with either hippocampal or mamillary body lesions
but that spatial disorientation is common to mamillary, forniceal, and hippocampal
lesions (18).
The Amygdala
Despite its inclusion as a limbic structure and its close ties with many of the same
structures as the hippocampus, the amygdala is not thought to play a part in memory. The
amygdala has close ties with the hypothalamus and basal ganglion. It claims among its
afferents the periamygdalar cortex and each of the sensory association areas such as
visual, auditory, olfactory, and tactile association areas. Its efferents pass via the striae
terminalis to the hypothalamus and diencephalon and in the latter is included the
dorsomedial nucleus of the thalamus. Subsequently, they pass indirectly to the
telencephalon. Some efferents pass via the ventral amygdalofugal path to the
hypothalamus, and other efferents pass through the uncinate fasciculus to the ventral
insular and caudal orbito-frontal cortex (14, 19).
The effects produced by amygdala lesions are unlike those produced by other medial
temporal lobe injury. The amygdala, a complex organ of multiple nuclei, is active in a
large variety of disparate functions such as vegetative, emotional, and orienting.
Autonomic activity is changed by lesions of the amygdala, and by electrical stimulation
one can produce bradycardia, tachycardia, changes in respiratory rate, and changes in the
galvanic skin response. Lesions of the amygdala interfere with the organism's alerting
and orienting activity. There is an exaggerated dis-tractability and inability to respond to
new experiences.
Furthermore, aggression is either facilitated or inhibited by lesions of the amygdala
depending on whether the lesion is in the dorsomedial or lateral regions of the amygdala.
In animal studies, normal interaction with other animals of the same species is far
reduced. Only amygdala
lesions produce a general sluggishness and reduced ability to respond to "subtle social
signals" (19).
The amygdala comes up in discussions of memory primarily because the reduction in
orienting activity, arousal, and attention span impede the learning of new tasks in
animals. Furthermore, the expression of formerly learned responses is altered and may
surface in memory tests. However, there is little evidence that the amygdala is actually
involved in the retrieval of stored memory engrams. One can easily see, then, that poor
performance in general is the result of amygdala lesions, and lesions of the amygdala are
so general in their effect that it is hard to specifically define the deficits. Nevertheless, it
seems clear from the available information that this medial temporal lobe structure is
probably not responsible for much of the deficit in lesions of the hippocampal
formation-forniceal-mamillary Papez circuit.
The Temporal Stem
Deep in the medial temporal lobe, inferior to the insular cortex and dorsolateral to the
temporal horn of the lateral ventricle, lies the temporal stem, an important outflow path
of the temporal neocortex and amygdala. The stem, then, carries white fibers to
subcortical structures at the brain base. In particular, one projection goes to the medial
magnicellular part (emphasized by Victor) of the dorsal medial nucleus of the thalamus.
Other projections go to the pulvinar and midbrain, basal ganglia, and orbitofrontal cortex
(18). Temporal neocortex has been shown to be important in memory function by human
and animal electrical stimulation and by study of deliberate and natural lesions. If a large
amount of temporal lobe neocortex is damaged, a profound learning disability results.
Projections
Here we discuss the hippocampal-forniceal-mamillary link, as well as other
temporodiencephalic connections of importance in lesions of and surgical approaches to
the third ventricle.
The hippocampal formation projects via the fimbria and fornix to the posterior column
of the fornix and the hippocampal commissure; forniceal fibers also arise from the
periamygdaloid cortex. The fornix carries fibers in both directions, fibers being received
from and projected to cingulate cortex, the septal region, the thalamus, etc., but the main
direction is from caudal to rostral.

Fornix
The fornix is the main efferent bundle from the hippocampal formation (gyrus
dentatus, hippocampus, parahippocampal gyrus, subiculum, etc.), as discussed
previously. The hippocampal formation projects across to the contralateral formation via
the hippocampal commissure, and forniceal fibers then course rostrally above the
anterior third ventricle. Along the dorsal part and body of the fornix, fibers go to the
cingulate cortex and some fibers pass off into the dorsomedial nucleus of the thalamus
(35). Some forniceal fibers also originate in the periamygdaloid cortex, cingulate gyrus,
the indusium griseum, septal area, and hypothalamus. Above the anterior commissure,
the fornix gives rise to two large bundles. The precommissural fornix carrying fibers
mainly from the hippocampus proper (19) goes primarily to the lateral septal areas
anterior to the anterior commissure. The second and larger bundle, the postcommissural
fornix, carries fibers mainly from the hippocampal formation (subiculum and its
divisions) and is bound for the hypothalamus, thalamus, mamil-
lary bodies, rostral midbrain, and subthalamic region (19, 33). The fornix projects,
thereby, not only to mamillary bodies, but also to the septal area, preoptic hypothalamus,
dorsal and periventricular hypothalamus, anterior nucleus of the thalamus, median and
paramedian thalamus, supramamillary region, and central gray of the midbrain.
The consequence of section of the fornix is the basis of considerable controversy. At
present, one simply cannot say that clinical cases are interpretable as indicating that a
forniceal lesion guarantees production of a memory disturbance; other structures besides
the fornix are variably damaged by operations and natural lesions.
Garcia-Bengochea et al., working with forniceal lesions in monkeys and subsequently
therapeutic forniceal section in seizure patients, mentioned no adverse effects of forniceal
section (13). They treated 14 patients, presumably severing the body of both fornices in
each, producing no disturbance of memory. Such deliberate therapeutic section of the
fornix in humans was antedated by Dott (10) and Cairns and Mosberg (4), who sectioned
the fornix to remove brain tumor.
Cairns and Mosberg (4) presented 11 cases with 9 survivors of third ventricular tumor
removal. All patients underwent at least partial forni-cotomy. The result of follow-up in
these patients included the impression that forniceal section produced no deficit. In fact,
they reported a relief of memory deficit in 1 case. This, however, was done at a time
when the fornix was thought to have a primarily emotional and olfactory function and,
although these were specifically addressed, memory function was not. Admittedly, there
were a few cases in which transient memory disturbance was addressed, but ascribed to
the hydrocephalus preoperatively. In a similar vein, Dott (10) presented the use of the
transcortical transforaminal approach to third ventricular tumors in which he sectioned
the bodies of the fornix and part of the septum in two cases. This was done without
deficit, although he may have been looking more for olfaction and emotional disturbance
than for amnestic derangements. More recently, in a classical and celebrated case,
Woolsey and Nelson described an alcoholic patient with involution of the mamillary
bodies who subsequently developed a diencephalic metastatic pulmonary ade-
nocarcinoma (39). This tumor infiltrated the body of the fornices and posterior columns
bilaterally without the production of Korsakoff's syndrome. Nevertheless, there are
objections to this case on several points. The patient, being alcoholic, may have long
before developed other means of establishing recent memory retrieval, as has been
implied by Milner (34). Furthermore, the tumor, although largely infiltrating the fornices,
did leave a considerable number of fibers intact. Finally, formal neuropsychological
evaluation was not undertaken, and testing in such a situation must be careful because the
defect may be subtle and largely compensated for.
Squire and Moore noted that, at the time of publication of their article, there were 47
cases in the literature in which forniceal section did no harm versus 3 in which memory
disturbance could be legitimately ascribed to forniceal injury (31). One must not forget
the potential for confusion in the literature, however. Lesions of the far anterior fornix
seem to have less potential for memory or other deficits than lesions posterior or near the
hippocampal commissure (16, 21). One cannot compare the results of forniceal injury at
one level to forniceal injury at another and draw meaningful conclusions (31). Despite
the controversy and the presumed lack of detailed neuropsychological testing in many
reported cases, one cannot deny that there are instances of forniceal lesions in patients
with intact memory. However, we do not have the ability to predict which patient will
fare poorly and which will not.
 A certain volume of literature supports the contention that section of the fornices
produces serious memory disturbance, similar to that reported in hippocampal ablation.
Sweet et al. presented a patient in whom transfrontal section of the anterior fornices was
produced to ease removal of a large colloid cyst (34). This patient had a disabling
Korsakoff's syndrome postoperatively, which was ascribed to the forniceal division. This
patient was described as having marked impatience, a significant and lasting memory
deficit, a patchy retrograde amnesia, mild cognitive impairment, and general apathy.
Milner, in comments following the presentation, stated that neuropsychometrics
described a memory deficit not quite as bad as that following bilateral medial temporal
lobe section. Section of the anterior fornices in Sweet's patient was productive of a
difference in memory quotient to I.Q. of 13, as compared to bilateral hippocampal lesions
productive of differences as great as 30 and more (26, 34). One must be cautious in
ascribing this patient's recent memory disturbance to forniceal section, however, in that
there may well have been damage to the walls of the third ventricle productive of the
amnesia. Heilman and Sypert, in a noted case, described a patient with a poorly
differentiated glial neoplasm in the quadrigeminal cistern (16). This was surgically
removed, but aside from this there was no anatomical confirmation. The patient, both
preoperatively and postoperatively, had a severe deficit in memory, with a difference
between verbal I.Q. and memory quotient of 47, a severity comparable to that with
bilateral medial temporal lobe injury. The authors noted that this severe memory deficit is
in contrast to better tolerated more anterior lesions of the fornix and postulated that the
difference is due to the fibers coming off the fornix into the dorsomedial nucleus of the
thalamus given such importance by Victor et al. This difference has also been noted by
Lavyne and Patterson (21). In support of the idea that forniceal fibers course into the
dorsomedial thalamus from the posterior fornix, Valenstein and Nauta described their
occurrence in monkeys (35). Hassler and Riechert (15) described a female seizure patient
initially given an asymptomatic right anterior column forniceal lesion at the level of the
anterior commissure. Later a left column lesion was produced and the patient was found
to have a severe memory deficit without other behavioral change. Death occurred 8 days
later, apparently due to an unrelated cause, and bilateral forniceal injury was confirmed
as being productive of the amnestic derangement. Nevertheless, there are points of
controversy. The patient had a right medial frontal lobe glioma as well and left
hypothalamic softening, possibly including diencephalic fiber tracts and the anterior
commissure. The other right-sided lesion was near the inferior thalamic peduncles and
perhaps the temporal stem to the dorsomedial nucleus, and the case is thereby open to
criticism. Apuzzo described a transcallosal interforniceal approach in 11 patients (1). Of
these 11 known to have had forniceal manipulation, 4 had transient memory disturbances
on careful postoperative assessment. Although the fornices cannot be implicated exclu-
sively, this can be considered valid evidence of the importance of the forniceal system in
memory.
In a careful study avoiding the potential for task relearning, Gaffan reported
recognition memory impaired in monkeys operated on through a transcallosal approach
with bilateral anterior column forniceal tran-section (12). Similarly, Carr (5) described
recognition impaired after a transcallosal approach and section of the fornices of
baboons.
It has already been observed that two lesions are important in memory disturbances,
whereas one may not be (7, 23, 27, 28, 31). The controversy surrounding forniceal
section, with each school having its evidence, could be considerably cleared were it
generally acknowledged that these pa-
tients are not necessarily comparable. For example, forniceal section through frontal lobe
cortex may not be as devastating as forniceal section near the origin in the hippocampal
formation with possibly other limbic injury. A better question may be, does section of the
fornix provide better exposure (11)? Forniceal disturbance should be avoided if at all
possible because we cannot predict whether it will cause memory disturbance.
Septum
The septum reaches it highest degree of development in humans. It consists,
classically, of two large groups of nuclei, medial and lateral. The important nuclei in
primates and humans are found in front of the anterior commissure at the base of the
brain. The septum pellucidum in humans is not entirely comparable to the septal complex
of lower animals (19). The lateral group of septal nuclei is essentially composed of fibers
of the fornix and the hippocampal formations and commissure. The medial septal nuclei
consist of the diagonal band of Broca, the medial septal nucleus, and the septofimbrial
nucleus. The medial septal nuclei receive their input primarily from the lateral preoptic
and lateral hypothalamic nuclei. The medial septal nuclei send efferents back to the
hypothalamus and also to the hippocampus and habenula. The lateral septal nuclei
receive the majority of their input from the hippocampus and subiculum in a highly
topographical fashion. Some fibers also reach the lateral septal nuclei from the amygdala,
striae terminalis, piriform cortex, and other less important areas. Leaving the lateral
group, the septal group of nuclei project to the hypothalamus, ventral tegmental area, and
habenula. Projections from the cingulate cortex have been noted. A projection from the
septal region to the dorsomedial nucleus of the thalamus has also been suggested. Fibers
arising in the dorsomedial nucleus of the thalamus terminate in the diagonal band of
Broca in the septum.
Lesions made in the septal area affecting the important medial and lateral nuclei evoke
increased rage reaction and hyperemotionality. In experimental animals these changes
dissipate over time (19). Animals with septal lesions may also exhibit reduced
aggressiveness. Lesions may also produce an impaired ability to acquire passive
avoidance task learning in animals, somewhat similar to hippocampal injury. The septal
area, then, plays a role in the ability to interact with the environment, and lesions in the
septal area reduce the individual's ability to pay attention to subtle stimulation.
A large incision through the septum in association with transection of a fornix of the
fornices is to be avoided because these lesions would occur at the septal base and
threaten the important nuclei primarily. However, high in the septum pellucidum proper
under the corpus callosum, fenestration should not produce deficit.
Mamillary Bodies and the Mamilothalamic Tract
The mamillary nuclei in the posterior hypothalamus, as is well known, receive the
majority of their afferents from the subicular region of the hippocampal formation via the
postcommissural fornix. The efferents leave by two large tracts, the mamillothalamic
tract to the anterior nucleus of the thalamus and the mamillotegmental tract to the
tegmentum of the brain stem. The mamillary bodies, nested as they are in the
hypothalamus, are admixed with fibers of the medial forebrain bundle and other
important brain stem pathways. Lesions of the bodies, then, may implicate not only the
mamillary bodies, but other important rostral systems. Mamillary body lesions and
lesions of the mamillothalamic tract
 result in impairment of the ability to perform spatial discrimination (18, 19). Animals
with mamillothalamic tract lesions are loath to begin new responses to external
stimulation. The impairment should not be ascribed to global loss of memory.
The mamillary bodies are involuted or hemorrhagic in Wernicke-Kor-sakoff
syndrome. Korsakoff's patients are characterized not only by the mnestic loss, but also
by profound disturbances in attention, perception, and motivation (23). There is
widespread abnormality with cortical damage as well as diffuse periventricular
degeneration, however, and one simply cannot ascribe all of the memory and behavioral
disturbances to the mamillary injury alone. Nevertheless, this has had historical prece-
dent, essentially starting with Gudden. For example, Kahn and Crosby ascribed mnestic
derangements in their tumor patients to mamillary body injury and compression (20).
However, there are valid objections to this assumption and similar assumptions
elsewhere. One must admit that tumors of the mamillary region such as
craniopharyngioma and pituitary adenoma could just as well compress medial thalamic
or anterior thalamic structures. For example, one of Kahn and Crosby's patients had poor
verbal memory, but excellent tactile memory (overcoming his verbal memory
disturbance with the use of braille); this pattern has been ascribed to thalamic lesions
(23).
Dr. F. R. Ervin, in closing the discussion after Sweet's 1957 article, noted that neither
the Indian elephant nor the porpoise, both thought to have excellent behavioral memory
and spatial orientation, have mamillary bodies (34).

The Thalami: Diencephalic Amnesia

The mamillothalamic tract, one of the two main outflow tracts of the mamillary nuclei,
projects to the anterior nuclear group of the thalamus. The anterior thalamic nuclei also
receive direct input from the septohippocampal complex. The anterior nuclear group then
projects to and receives from the cingulum. Many of these projections that end up in the
cingulum continue on via the cingulate bundle, terminating in the hippocampal formation
(pre- and parasubiculum and entorhinal cortex) (14). Furthermore, the cingulate cortex
projects back to several thalamic nuclei. Primarily this is projection back to the anterior
nuclear group, but also the dorsomedial and ventromedial nuclei and ventroanterior and
lateral dorsal nuclei.
Lesions have been placed in the anterior nuclei as a means of treating a variety of
neuropsychiatric conditions such as uncontrollable aggression, schizophrenia, and
hyperkinesia (29, 30, 38). The neuroanatomical supposition is that the septum and
hippocampus may well play a role in the output of the cingulate gyrus via the anterior
thalamic nuclei. As pointed out by Speigel and Wycis (29), these connections control
emotional reaction, at least in part. Wood and Rowland do not allude to untoward side
effects of bilateral anterior thalamic stereotactically produced lesions in hyperactive
children; these children are described as virtually untestable in any case (38). Anterior
thalamotomy for depression, anxiety, schizophrenia, and pain disorders by Spiegel and
Wycis produced reduction in assaultive, aggressive, agitative, and maladaptive behavior
with the neurological side effect of "chronotaraxis" (confusion in time). However, most
of their lesions were in the dorsomedial nucleus.
Although the foramen of Monro may be enlarged by section of the fornix and septum,
it may also be enlarged by removal of some of the anterior tubercle of the thalamus.
There has been no reported case study
after such a unilateral lesion. In any event, the benefit to exposure is minimal in
comparison with subchoroidal entry of the ventricle.
Of considerably more importance in a discussion of potential harm to the limbic
system and the integration of memory is the dorsomedial thalamus. The dorsomedial
thalamus may be the critical lesion in patients with Korsakoff's syndrome (22, 29-31, 36).
The dorsomedial nucleus of the thalamus interacts intimately with the frontal cortex.
Considerable animal and human evidence has accrued that the medial thalamic lesion
produces amnesia and learning deficit even if unilateral and, in fact, the dorsomedial
nucleus has become preeminent in modern concepts of memory disturbance. Speedie and
Heilman ascribe intention, the focus of attention, and the control of interference to the
dorsomedial nucleus of the thalamus (27, 28).
The dorsomedial nucleus is the first and most severely affected nucleus in Wernicke-
Korsakoff syndrome. This is supported by the extensive study of the syndrome by Victor
et al. (36).
The physiological basis for medial thalamic function in memory is not known. The
area, however, is richly interconnected with other thalamic nuclei, the temporal stem, the
temporal lobes, the amygdala, and the orbital cortex. Amnestic derangement will
certainly result from a bilateral lesion of the dorsomedial nuclei; however, a unilateral
lesion can produce nmestic derangements whether dominant or nondominant.
Markowitsch has offered an extensive review. Neither animal nor human studies can
provide an absolutely clear-cut memory-related role of the dorsomedial nucleus, but it
may well be an important relay station. It seems to take not only a dorsomedial thalamic
lesion, but also another lesion in a memory-related pathway in tandem to produce the
memory deficit. Although Victor et al. favor the magnicellular nuclei as operative in the
registration of memory, Markowitsch favors the parvicellular part.
McEntee et al. studied a man in whom a metastatic pulmonary adeno-carcinoma had
invaded and destroyed the medial and posterior thalamus bilaterally with sparing of the
mamillary bodies, mamillothalamic tracts, and anterior thalamic nuclei (22). In addition
to his Korsakoff's psychosis, the patient had emotional lability, inattention, denial, and
visual agnosia for faces. Unfortunately, the fornices were not mentioned. Nevertheless,
this case supports the contention that abnormality of the thalami without abnormality of
the mamillary bodies can produce amnesia.
Spiegel et al. performed dorsomedial thalamotomy upon 30 patients for emotional
disturbance or pain (29). Of these, 19 experienced "chronotar-axis" (disorientation in
time) and 4 experienced disorientation in place as well. Apparently there was little other
learning disability in these patients and the deficiency was transient.
Exactly how the dorsomedial nucleus is functional in the registration of memory is
unknown. Valenstein and Nauta found that the hippocampal formation communicated
with the dorsomedial nucleus via the fornix in monkeys (35). In three other species, the
connection did not occur; it seemed to occur only in primates. The dorsomedial nucleus
also receives fibers from the amygdala, suggesting a "dual activation" by both the
hippocampus and the amygdala, thereby implying a regulating activity by these
structures via the dorsomedial nucleus of the prefrontal cortex in primates (19). Speedie
and Heilman suggested that a dorsomedial nucleus lesion will disrupt two separate limbic
pathways; the basolateral orbitofrontal thalamic amygdalar system and the medial
septohippocampal system (27, 28). A dorsomedial thalamic lesion, then, might of itself
satisfy the double lesion requirement of a mnestic derangement. A dorsomedial nuclear
lesion can be potent. It does not have to be bilateral to
 be disabling. In addition to disrupting the two limbic circuits, a unilateral
dorsomedial thalamic lesion may also induce frontal lobe signs. A domi-nent
dorsomedial lesion will produce verbal memory disturbance, whereas a
nondominant lesion will produce visuospatial memory disturbance (6, 27, 28).
Nevertheless, these disturbances are probably less severe than the deficits
produced by temporal ablation and in patients with Korsakoff's syndrome (27).
Additionally, these patients have diminished spontaneity and lack of initiative.
Patients with thalamic lesions of the dominant side will evidence not only
verbal memory disturbance, but also speech disturbances with perseveration,
neologisms, and anomia. It follows, then, that one should exercise caution in
manipulation of the thalamus when utilizing the subchoroidal approach (7).
Corpus Callosum
Short anterior incision of the corpus callosum, 21/2 cm long, will produce no
measurable deficit if independent of any other lesion (1). Nevertheless, the
frontal two-thirds of the corpus callosum is implicated in memory retrieval and
read-out. Memory retrieval is dependent on interhemispheric interaction (40). If
the corpus is sectioned, each of the independently acting disconnected
hemispheres is capable of storing and retrieving new information, but
interhemispheric communication is necessary for other associative processes. A
memory disturbance may well result, particularly if there is a requirement for
association. Such a task would be the word-paired associate learning task in the
Wechsler memory scale in which visual imagery support from the right
hemisphere is usually needed. Similarly, a large callosal lesion in a right-handed
patient would produce a motor dyspraxia in all tasks with the left hand, assuming
organized motor engrams of the left hemisphere. The cases of callosal apraxia
reported have been due to large lesions of the corpus callosum, such as large
surgical sections for seizure disorders, infarction, or hemorrhage. Other peculiar
abnormalities such as unilateral tactile anomia, hemialexia, and apathy seem to
occur only in patients with complete, very large, or progressive cerebral
commissurotomy. Even if just the splenium is spared, however, these deficits
may be transient (3). In some of the commissurotomy patients, callosectomy was
so extensive as to include the hippocampal commissure, and memory
impairment may well be on that basis (40).
It is evident from the literature that rostral callosectomy no larger than 21/2 cm
by and of itself will produce no detectable disturbance on formal
neuropsychometric testing. One must bear in mind, however, the admonition not
to disturb two structures (the corpus callosum and one other), either of which
might be operant in emotional and memory registration.
Summary
The neocortex seems to operate as an aggregation of columnar populations of
neurons, each functioning as a unit. Interaction between populations is regulated
by subcortical regions and this interaction generates a basic behavioral state and
memory. The reticular formation, hypothalamus, thalamus, and basal ganglia,
limbic system and related nuclei, mamillary bodies, and anterior and posterior
cingulate gyri all seem to operate in this fashion (25). The organization is
extremely complex, and attempting to arrive at a unitary concept of the
neuroanatomical substrate of memory, for example, is impossible at present.
The species difference between animals and humans may well invalidate much
of what has been assumed. For one example, the fornix in the mouse and rabbit
terminates almost entirely in the mamillary body,
whereas in the guinea pig and cat it terminates almost entirely in the central gray
substance (35). There is much conjecture and many assumptions in both the animal and
human literature and many times the investigator has not taken into account other limbic
areas involved besides the one of his focus. The potential for an incomplete lesion to be
collateralized or for functional reorganization to occur apace slower processes is hardly
taken into account at all. Reviews of the effect of lesions of the fornix often do not
distinguish the apparently high importance of the site of the lesion along the long axis of
the fornix.
Classically, the hippocampal formation, fornix, mamillary bodies, and possibly the
anterior nucleus of the thalamus were implicated in memory. Newer thought including
animal studies has added a large number of structures for our consideration. The
dorsomedial thalamus, pulvinar, inferior thalamic peduncle, anterior commissure,
anterior corpus callosum, temporal stem, diencephalic white fiber tracts,
thalamocingulate tract, and parietopetal thalamic nuclei have all been added. Expert re-
viewers do not agree on a "memory site" because there is no single site of storage of
memory. All of the foregoing structures are organs of relay. Furthermore, the literature is
replete with evidence that it takes more than a single lesion to produce a deficit in
emotion, memory, orientation, or arousal. A transcallosal approach to the third ventricle
will have necessitated a callosectomy. To add to this lesion deliberately or accidentally
forniceal, basal septal, dorsomedial thalamic, anterior thalamic, mamillothalamic, or
hypothalamic lesion is to invite at least transient disturbance of spatial orientation, verbal
or visuospatial memory, emotion, or arousal or an inability to interact with the
environment.
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Limbic System with Special Attention to Structures Involved in the Third

Ventricular Approach
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Neuropsychology. Oxford, Oxford University Press, 1979.
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14
Transcallosal Interforniceal Approach
Michael L J. Apuzzo, M.D., and Steven L Giannotta, M.D.

Historical Perspective
In 1944, Edward Busch published the description of a new approach for the removal of third ventricular
tumors (6). Troubled by difficulties associated with efforts to remove colloid cysts and more particularly
solid tumors through the foramen of Monro, he noted the following incidental surgical observation: "In
removing a tumor of the septum pellucidum we had the opportunity of observing in detail the roof of the
third ventricle from above and were impressed by its thinness and by the 'well-marked median raphe.' We
thought that perhaps it might be possible to divide the roof of the third ventricle in the midline, thus gaining
direct and satisfactory access to the ventricle itself." After substantiating the anatomical validity of such a
deduction in several postmortem brains, he undertook, with some trepidation, the first procedure employing
the interforniceal maneuver in a 48-year-old man with a colloid cyst. After a right frontal transcortical
lateral ventricular exposure, "the septum pellucidum was split just above the roof of the third ventricle. . . .
The roof of the third ventricle now bulged upwards and it was only necessary to start the division of the
roof at the most prominent point by means of a blunt hook, after which the intraventricular pressure
gradually completed the division, the tumor bulging upwards with every pulsation. The tumor was
punctured but seemed solid; it was cautiously lifted up and seen to adhere to the Choroid plexus. A clip was
placed anteriorly to the tumor and the stalk was cut through. The whole third ventricle was in full view."
Busch had thus described division and definition of the midline forniceal raphe with subsequent
perforation of the diencephalic roof along a natural plane between the two forniceal bodies. In a total of six
operated patients in which this maneuver was used to gain third ventricular access, no untoward effects
were observed. Little further commentary is available on the technique or the results of such a procedure.
Based on the techniques of Dandy (8) and van Wagenen (23), during the 1960s a series of papers
provided a substrate for the application of a strictly midline interhemispheric approach to the third ventricle
that incorporated the technique for entry described by Busch. Prompted by the split brain animal studies of
Sperry, Baldwin et al. (4) described a technique for medial cerebral incision in primates, which was later
undertaken with greater refinement by Milhorat and Baldwin (20), with the addition of the technical aid of
the operating microscope. The authors
Figure 14.1. Angled anatomical schematic diagram demonstrating major incisions in midline neural
structures to the third ventricular chamber.
Figure 14.2. Dorsal fornix view with anatomical elements of structure, line of incision, and silhouette of
the underlying third ventricle.
stressed, "The approach affords a unique and extensive view of the third ventricular chamber. . . .
Clinically, the transcallosal microdissection technique is of potential value in the exposure and removal of a
number of midline tumors."
In this chapter, we describe the technique of midline interhemispheric exposure via the corpus callosum
and the forniceal component of the roof of the third ventricular chamber (Figs. 14.1 and 14.2). This
technique affords excellent visualization primarily of the anterior and mid-third ventricular regions and may
be safely used in the absence of lateral ventriculomegaly (1-3).

Operative Corridor: Anatomy and Physiological Risks

The major topographic elements of the midline corridor that require identification and consideration
include the coronal suture, the sagittal sinus, the parasagittal veins, the falx cerebri, the cingulate gyrus, the
pericallosal arteries, the corpus callosum, the fornix and its components, the tela choroidea, the medial
posterior choroidal arteries, and the internal cerebral veins. Consideration of the consequences of injury to
each neural or vascular component is essential as a stepwise progression evolves through the corridor of
exposure.
Parasagittal Veins
Initial cortical visualization and manipulation of the parasagittal venous elements during the early stages
of exposure and subsequent retraction may cause proximal or remote cortical injury. Other than direct
manipulation, the consequences of potential venous infarction is an important consideration. Absolute
preservation of the venous tributaries is an important goal within the surgical process. It has been our
experience that appropriate placement of an economically sized bone flap may be suitably planned in
relation to venous anatomy as defined by cerebral angiography rather than strictly by bony landmarks.
Review of 100 angiograms (3) with particular attention to the distribution and confirmation of the
parasagittal venous complex in the region of the coronal suture has disclosed that 42 of the studies showed
evidence of significant venous tributaries from the mid- and posterior frontal lobe draining within 2 cm
anterior or posterior to the coronal suture. The majority (70%) of these venous tributaries entered the
sagittal sinus within the sector 2 cm posterior to the coronal suture, whereas 30% were evident in the
anterior 2-cm region. Sacrifice of these major tributaries could cause either cortical deficit or seizures.
Planning of bone flap placement in the pericoronal area and the extent and mode of brain retraction or
deformation should take into account the parasagittal venous anatomy as an important guiding factor (Fig.
14.3).
Corpus Callosum
Major callosal incision and limited but strategically placed interruption of callosal pathways have been
shown to result in disorders of interhemispheric transfer of information such as visual spatial transfer,
tactile informational transfer, and bimanual motor learning (12, 13). The issue of limited incision through
the superior genu and trunk has been addressed on a number of occasions (9, 11, 14, 18, 25). Jeeves et al.
(18) reported three patients who underwent 30-mm incision in the mid- and anterior corpus callosum for the
excision of third ventricular neoplasms. All were found to have deficits in transfer of tactile data, but not of
information obtained visually. None of the patients was aware of this inability or inconvenienced by it.
Winston et al. (25) studied four children ranging in age from 18 months to 10 years, who underwent 2-cm
longi-
Figure 14.3. The bone flap is placed with consideration of the major parasagittal veins in the pericoronal
area. Care is taken to avoid sacrifice of venous tributaries contributing to mid- and posterior frontal
drainage.

tudinal incision in the anterior body of the corpus callosum. None of the children demonstrated any of the
signs of commissural disconnection. Tests of dexterity in intermanual and intramanual sensory transfer
indicated successful interhemispheric transfer in spite of the young age of the patients tested and the
location of their lesions. Gordon et al. (14) studied two patients with nearly complete section of the body,
genu, and anterior commissure. No evidence of interhemispheric disconnection was evident. Apuzzo et al.
(3) studied six patients with 2.5-cm incisions in the callosal trunk. All patients could readily name objects
and numbers placed out of sight in the nondominant hand. Crossed and uncrossed localization of light
touch was accurate from right to left hands. Interhemispheric transfer of tasks requiring tactile feedback in
motor sequencing was successful and complete. These results indicated no measurable deficits in
interhemispheric transfer of somesthetic information or complex perceptual motor learning tasks requiring
continual sensory motor integration. Therefore, the majority of data support the concept that limited
incision of the callosal trunk effects a minimal physiological alteration.
*
Fornix
Once lateral ventricular entry has been effected, third ventricular lesions may be approached by a number
of surgical maneuvers that involve an element of manipulation of the fornix (1). These maneuvers have
been undertaken with trepidation because of the considered risk of amnesia during the postoperative period.
Review of the literature related to the role of the fornix and memory processes provides contradictory
opinions. The severe amnesia that has been attributed to damage of the hippocampus and mamillary bodies
has logically led to the prediction that alteration of the forniceal structure would likewise produce amnesia.
Review of available literature provides no consistently substantive evi-
dence of amnesia that has resulted from isolated forniceal injury. Dott (10) and Cairns and Mosberg (7)
reported patients who had no memory deficits after section of the fornix. Bengochea et al. (5) sectioned the
fornix bilaterally for epilepsy and noted no alterations in mentation in 12 patients. Woolsey and Nelson
described neoplastic destruction of the fornix without memory loss (26).
Hassler and Riechert (15) reported a patient who underwent bilateral fornicectomy for epilepsy. A lesion
was placed stereotactically in the column at the level of the anterior commissure by electrical coagulation.
The initial lesion was placed on the right and produced no amnesia. A second lesion in the left column 11
months later produced a severe memory deficit, however, autopsy revealed bilateral forniceal lesions with a
tumor of the right medial frontal lobe and softening of the left hypothalamus. Sweet et al. (22) reported a
patient with a colloid cyst of the third ventricle that was removed after bilateral sectioning of the column of
the fornix, with subsequent manifestation of a severe amnestic syndrome. Memory for remote events was
preserved, however; there was persistence of severe loss of recent events, which did not resolve during 2
years of follow-up. Horel (17) suggested that injury to the magnocellular medialis dorsalis during cyst
removal could be considered the cause.
Heilman and Sypert (16) reported a patient with amnesia and a glioma in the region of the hippocampal
commissure. After subtotal excision of the lesion, the patient manifested a profound and persistent amnestic
deficit. No structural verification for lesion site was reported. Memory loss has been reported after major
extensive commissurotomy in which the hippocampal commissure was sectioned (27).
In review, there are clear instances of destruction of the fornix with absence of detectable amnesia and
also cases in which fornix damage has been implicated in amnesia. These reports may be subject to various
interpretations based on the presence of attendant neural destruction or the lack of verification of structural
alterations.
Incision of the forniceal raphe and retraction of the body has not resulted in persistent amnestic
syndromes in our hands, with mentation evaluated not only by standard bedside examination, but also by
psychometric assessment (2, 3). The objective of the exposure is to take advantage of a natural plane of
cleavage. This exposure often requires no retraction of the forniceal elements beyond that produced by the
mass lesion within the third ventricular chamber.

Structural Definition
Preoperative radiographic assessment is directed toward the development of an absolute definition of the
anatomical substrate peculiar to the given patient. The goal is to obtain clear perspectives of the individual's
anatomy along the operative corridor and of all aspects of distortion and redisposition of anatomical
elements by the lesion. In general, high resolution computerized tomography (CT) in axial, coronal, and
particularly midline sagittal planes will accomplish adequate definition. Magnetic resonance imaging
(MRI) in multiple planes will augment CT and at times provide important information related to lesion
definition. Cerebral angiography provides important information related to cortical venous anatomy and
occasionally augments imaging data related to the vascu-larity of the lesion (Fig. 14.4).
Strict definition of surgical strategy and economy of tissue manipulation can be enhanced by careful
consideration of the precise midpoint of bone flap placement, the angulation of retractor placement to the
midpole of the lesion, and the distance of the corridor to the corpus callosum, fornix, and lesion. The size
and extent of callosal and forniceal incisions
Figure 14.4. Cystic intraventricular craniopharyngioma. A. CT with stippled calcium. B. MRI
demonstrating a sagittal view of the lesion with the anatomical corridor for entry. C. Venogram with the
coronal suture landmark [arrow) as a guide for the bone flap plan. D. Postoperative (24 hours) CT. In this
case the foraman of Monro (4 mm) was not distended by the mass, and some maneuver was clearly
required for fornix manipulation.

may be estimated preoperatively in relation to the apparent type, size, and disposition of the lesion within
the ventricle. The relation of the fornix to the corpus callosum and the area of the septum pellucidum may
be determined. There is considerable variability regarding not only the relationship of all normal
anatomical elements, but also the structural substrate deformed by the pathological process; absolute
definition of the entire complex will permit maximal economy of manipulation and thus provide for
ultimate safety and satisfactory management of the pathological process.

Operative Technique
After the induction of general anesthesia with endotracheal intubation, the patient is positioned supine
and the head is elevated 15 to 20° from the horizontal and supported by a Mayfield pin fixation headrest
(Fig. 14.5). Consideration is given to the placement of a left frontal ventriculostomy. This is used especially
in individuals with ventriculomegaly as an adjuvent for intraoperative intracranial pressure control and
postoperative pressure monitoring. High potency glucocorticoid preparations are used in all, and
prophylactic antibiotics are employed in patients with ventriculostomies.
A paramedian right side 6- x 4- X 3-cm trapezoidal free bone flap is most commonly used for calvarial
entry. Optimal placement for access to the foramen of Monro dictates that the bone flap be bisected by the
Figure 14.5. Patient is positioned in supine with head fixed in 20° of flexion from the natural longitudinal
axis.

Figure 14.6. Visual access to the entire chamber is possible within variables of angles of entry at the
cortical level.

coronal suture. However, to reduce the possibility of cortical injury we plan the bone flap in relation to the
specific cortical venous anatomy of the individual patient. Moving the bone flap posteriorly, although
increasing the proximity to the paracentral hemispheric region, may produce a more optimal angle for
corridor access to the forniceal body with raphe incision extending from the foramen of Monro posteriorly.
This angle of access (Fig. 14.6) affords optimal visualization of all third ventricular
regions, but particularly the anterior third. Predominantly anterior placement of the bone flap in relation to
the coronal suture promotes better visualization of the posterior third of the chamber. Depending on the
thickness of the skull, the bone flap is developed on the midline or 1 cm to the left of the midline (Fig.
14.7). Generous and absolute midline exposure is required for ease of identification of the interhemispheric
fissure, but also for minimization of retraction as the entry corridor is

Figure 14.7. Some options for developing the bone flap to assure midline exposure over 5 to 6 cm. With
calvaria thicker than 1 cm, exposure is facilitated by incorporating 1- to 1.5-cm contralateral paramedian
bone removal (D).
developed. The midline approach to the third ventricle, particularly in cases with small lesions (1 cm) and
no hydrocephalus, requires access to an absolutely sagittal plane in the line of the falx. Therefore, if this can
be initiated at a superficial level, retraction in the medial to lateral plane may be minimized. All retraction
and deformation of parasagittal brain parenchyma may be localized completely to a 5-cm anterior to
posterior plane.
A number of scalp incisions (Fig. 14.8) are appropriate to gain adequate calvarial exposure and meet the
individual requirements of cosmesis. However, we generally use a two-limbed curvilinear scalp flap. Once
scalp incision is initiated, furosemide and/or mannitol is administered to reduce cerebral mass, thus
facilitating interhemispheric exposure and minimizing the required force of retractor application.
After the application of dural tenting sutures, the Budde self-retaining retractor system (Fig. 14.9) is
brought into the field and appropriately installed in relation to the headrest for fixation. This system is
versatile and flexible, offering the opportunity to introduce either retraction or instrumentation in any
direction within the field and simultaneously offering a stabilization device for the surgeons' wrists and
hands. The instrumentation offers an anchoring base for retraction sutures and, thus, the ring component of
the system may be established adjacent to the operative field before the bone flap is fashioned.
A trapezoidal dural incision (Fig. 14.10) is developed with the broad base of the form positioned at the
line of the sagittal sinus. Traction sutures are applied so that the dural flap is reflected over the sagittal sinus
with an element of compression of this structure. These sutures are secured to the left side of the retractor
ring. Absolute exposure of the midline plane at the level of the superior falx is realized.

Figure 14.8. Various scalp incisions offer flexibility and economy of exposure at the midline in the
pericoronal area and allow ventriculostomy placement on the left.
Figure 14.9. A. Ring retractor installed after scalp incision. Here it is pictured after the initial set-up with
the bone flap turned and the dura mater reflected to the midline and secured to the left superior ring. B.
Microscope in position with bilateral ribbon retraction in the midline and the operator's hands stabilized by
the ring.

A self-retaining retractor arm with a 19-mm blade is prepared to be applied from the right side of the
field, and initial blunt retraction is undertaken at the falx-cortex interface with the broad end of a Penfield
(No. 1) instrument. Indentification of the inferior falx is achieved using this technique, and Biocol is
applied to the exposed medial and lateral cortical surfaces. This component of the exposure having been
developed, the operating microscope with either a 275-mm or a 300-mm lens is brought into the field. The
choice of objectives is related to the potential use of the micromanipulator laser adaptor and the individual
depth of field. With the use of a combination of blunt and sharp microinstrumen-tation, a midline plane is
then developed between the cingulate gyri. The retractor blade and Biocol are advanced to the corpus
callosum. The
Figure 14.10. A. Dural incision takes advantage of the full extent of the bone flap with approximation of
the midline and the sagittal sinus. B. Initial development of the midline plane at the sagittal sinus with
identification of the falx. The cortex will be deformed no more than 5 cm in the longitudinal plane. C.
Initial development of the exposure to the cingulate gyrus. Lateral retraction should not exceed 2 cm.
cingulate gyrus may occasionally be confused with the corpus callosum. However, the cingulate
gyrus is the distinctive tan-gray of the cortical pial surface, whereas the callosum is strikingly
white. With identification of the corpus callosum, the pericallosal arteries are readily identified
(Fig. 14.11, A and B). At the callosum the exposure may be enhanced by the placement of cotton
balls that are saturated with Ringer's lactate solution and cylindrically shaped to maintain the
longitudinal exposure at the anterior and posterior poles of the midline slot. A 3.5- x 1-cm
callosal exposure is the endpoint of this stage of the procedure (Fig. 14.13). The falx is
maintained as the midline reference with the original position of the pericallosal arteries serving
as a secondary landmark.
Having established callosal exposure and identified the pericallosal arteries, the surgeon plans
the callosal incision. This entry is 2.0 to 2.5 cm long and depends on variables related to the angle
of entry and the size of the lesion. Five French (5 F) irrigating suctions and multiple
microinstrumentations are utilized to mobilize the pericallosal arteries (Fig. 14.11С). In the
majority of cases, the right pericallosal artery is displaced 2 to 3 mm to the right in the
pericallosal cistern and incision of the callosum is initiated immediately to the right of the left
pericallosal artery. Again the falx serves as a midline reference point during the initiation of the
incision. Occasionally, with substantial third venrticular masses or ventriculomegaly there may be
a domelike configuration of the corpus callosum; shift of the midline may occur with
asymmetrical ventriculomegaly; rarely the falx is shifted; all of these variables will be apparent
on the preoperative imaging and should be anticipated. Interhemispheric dissection may be
complicated by midline shift or, as in cases of cysticercosis, adhesive arachnoiditis. The thickness
of the corpus will vary according to the extent of hydrocephalus. As dissection with a 5 F suction
commences, the surgeon should evaluate the point of callosal incision as it relates to underlying
anatomy. Depending on the point of incision and its relation to the anterior to posterior and
medial to lateral planes, the following entry points are possible: (a) right lateral ventricle, (b) left
lateral ventricle, (c) septum pellucidum with or without cavum, and (d) forniceal body (Figs.
14.12 and 14.13).
Study of preoperative sagittal imaging with particular attention to fornix anatomy and
disposition in relation to the corpus callosum, as well as the area and configuration of the septum
pellucidum, will orient the surgeon in relation to possible landmarks during callosal transit. As
callosal transit is completed one identifies the ependymal surface of the lateral ventricles. This
layer is readily appreciated because of its gray-black hue, and ependymal vessels are readily
visualized under magnification (Fig. 14.14). At this time, the line of attachment of the septum is
often identified, indicating that precise midline entry to the ventricular system has been achieved
(Fig. 14.14). If the septum is not appreciated, either right or left lateral ventricular entry is most
likely. The self-retaining retractor blade is then advanced to the inferior callosal margin and the
Choroid plexus is identified. This is the most striking and reliable landmark in the mid- and
anterior lateral ventricular system. It may be followed to the foramen of Monro with appropriate
orientation being gained in relation to this important central landmark.
In most cases the abnormality may be appreciated through the foramen of Monro, which is
quite variable in area. Anatomical perspective will vary according to entry angle (Fig. 14.15).
With identification of the foramen, the septal vein, septum pellucidum, forniceal structure, thala-
mostriate vein, thalamic tubercle, and head of the caudate are readily appreciated. Bipolar
coagulating forceps are used to fenestrate the sep-
Figure 14.11. A. Initial exposure of the corpus callosum with a single retractor and cotton balls at the
anterior and posterior poles creating a 3.5- x 1.5-cm area of visualization. B. Photomicrograph of the
callosal exposure with the anterior cerebral arteries in the midline. C. Coronal view with the double
retractor option. D. The anterior cerebral arteries are displaced toward the lateral callosal cistern. The falx
gives a midline orientation for the incision.
Figure 14.12. А, В, С. А 5 F suction irrigation device and bipolar forceps are used to incise the corpus
callosum over a 2.5-cm length. Note in В the options for ventricular entry.
Figure 14.13. Steps in retractor advancement in the sagittal plane with care to assure the
appropriate entry angle to the septum and the foramen of Monro.

Figure 14.14. Photomicrograph showing initial callosal resection with ependyma of the
left and right lateral ventricles with transverse veins and midline attachment of the
septum pellucidum.

_
Figure 14.15. Possibilities for field of view at the periforaminal region depending on sagittal entry angles
[А, В, С). The angle of visualization will affect access to the raphe and the predominant perspective of the
third ventricular chamber; A, mid and posterior; B, middle third; C, mid and anterior. В is optimal for
overall exposure.
turn, creating a single ventricular cavity in the event that a lateral ventricular shunt is required (Fig. 14.16).
At times septal leafs or a cavum facilitates identification of the raphe or midline division between the two
forniceal bodies. The septum serves as a landmark for guidance to the

Figure 14.16. A. The septum pellucidum is coagulated to the dorsal surface of the fornix. B. Visualization
of the left foramen is gained by retraction. C. Photomicrograph with the septum being coagulated and soft
glial tumor evident at the foramina of Monro bilaterally adjacent to forceps.
midline union of the forniceal columns and bodies superior and posterior to the anterior commissure and
medial and superior to the foramen of Monro (Fig. 14.17).
With midline entry, identification of the septum, and moderate ventriculomegaly, bilateral visualization
of the foramen of Monro is readily achieved without a left-sided retractor (falx, cingulum, and corpus).
The surgeon must remain cognizant of entry angles related to each level of the corridor as the perspective
of the foramen of Monro and thus the fornix and finally the third ventricular chamber will vary according to
minor angular sagittal variables. Minimal changes in entry angles may confuse the site of ventricular
visualization and access.
Having gained midline exposure with appropriate landmark orientation, the raphe is identified at the site
of septum attachment on the dorsal fornix (Fig. 14.17); incision is commenced at the level of the foramen
of Monro with a fine tip bipolar forceps and Sheehy canal knife (Fig. 14.18). The incision is carried
posteriorly for 1.0 to 2.0 cm (Fig. 14.19). The size and shape of the fornix in the midline are quite variable
and are influenced by individual variations and deformation by the pathological mass. What to expect
during operative transit is indicated by preoperative imaging studies. With completion of the incision, the
mass is readily identified (Fig. 14.20). The normal structures in the diencephalic roof including the tela
choroidea, Choroid plexus, internal cerebral veins, and posterior choroidal arteries are often attenuated or
displaced laterally by the presence of the mass. Secondary retraction at the level of the fornix is often not
necessary; however, a 5-mm retractor blade may be utilized to maintain exposure either initially or once
mass decompression has been partially achieved (Figs. 14.21 and 14.22). Access to the lesion may be
possible through the midline raphe incision with views of anterior and posterior poles enhanced by minor
alterations in retractor and microscope placements. Secondary manipulations of the lesion are possible
through the foramina of Monro. Utilization of laser instrumentation and the introduction of miniature
angular mirrors are accomplished readily.

Figure 14.17. Photomicrograph with the crest of the coagulated septum marking the
raphe of the fornix adjacent to the foramen of Monro distended by craniopharyngioma.
Figure 14.18. A. The junction of the septum and the fornix provides the landmark for the forniceal raphe, which may
be established and developed with a canal knife. В, С. The mass lesion is identified and the raphe is developed over a 2-
cm extent posteriorly from the foramen of Monro using bipolar forceps and a canal knife. D. A cystic lesion is incised
and drained causing relaxation of the tense forniceal displacement and initiating the requirement for retraction on the
forniceal body to maintain exposure.
Figure 14.19. Photomicrograph demonstrating initial dissection of the raphe during operation for a third
ventricular ependymoma.

Figure 14.20. Photomicrograph demonstrates craniopharyngioma distending the raphe after the initial
incision. The foramen of Monro is to the right of the field.

In developing the interforniceal plane, one should not exceed 2 cm posterior to the foramen of Monro
(Fig. 14.2). The surgeon must be cognizant of the hippocampal commissure in the posterior component of
the forniceal structure. There is evidence in the literature suggesting that compromise of this area may lead
to permanent memory impairment and, therefore, we have been reluctant to extend our incision posteriorly
into this region. Likewise, we have not carried the incision beyond the region
Figure 14.21. Photomicrograph with a 5-mm retractor blade on the right fornix in a case of
craniopharyngioma.

Figure 14.22. Use of the Budde ring retractor with multiple options exercised. The midline and posterior
parasagittal retractors are 19 mm (cingulum, corpus callosum). The anterior parasagittal retractor is 5 mm
(forniceal body).

of the column-anterior commissure interface. The extent of the incision as described provides excellent
visualization of all regions of the ventricle and in particular in the presence of a mass lesion, which
enhances the overall exposure by its deformation of surrounding structures.
At times the internal cerebral veins will be visualized. These have been retracted with self-retaining
instruments without morbidity.
Mass management strategy follows conventional standards of micro-surgical technique (Fig. 14.23).
After initial exposure of the intraventricular lesion, needle aspiration may be undertaken or the mass may
be incised and aspirated with a 5 F or 3 F suction. This may cause collapse
Figure 14.23. Lesion exposure and excision. A. Wall biopsy. B. Dissection of anterior pole (i), lateral
recesses (2), and posterior pole (3). C. The internal cerebral veins may be identified laterally displaced by
the mass expansion.

of the forniceal bodies into the midline and necessitate further retraction; in this case a 5-mm retractor blade
may be introduced from the right of the field. If the lesion is not cystic, after wall biopsy central
decompression may be achieved with either a carbon dioxide laser or bipolar coagulation and
microinstrumentation.
Once internal decompression is achieved, anterior and lateral components of the mass may be dissected
from the third ventricular wall with gentle traction on the lesion, developing the tumor-brain interface with
a Sheehy canal knife. With lateral dissection the internal cerebral veins
may be identified and followed to the foramen of Monro anteriorly. The Choroid plexus is often intimately
adherent to the junction with the thalamostriate vein. Fragments of tumor are removed, improving expo-
sure. Visualization of the third venticular floor (if intact) or the sellar content is readily appreciated as the
anterior and inferior poles are mobilized. Finally, the posterior component of the mass is approached.
Depending on entry angles, this may require minor alterations of head position by reverse Trendelenburg
maneuver, appropriate posterior angulation of the microscope, or the use of miniature mirrors (Figs. 14.24

Figure 14.24. A. Lesions may be manipulated simultaneously through the foramen of Monro and the
interforniceal entry. В, С Visualization of the posterior chamber, if limited, may be gained with an angled
dental mirror.
Figure 14.25. Completion of mass excision with an instrument in the foramen and the retractor removed.
There is redundant fornix secondary to mass displacement.

and 14.25). With mass excision extending from the diencephalic roof to the dorsum sellae, it is not unusual
to visualize the clivus, basilar circulation, and prepontine cistern at the completion of lesion excision. En-
counters with major venous and arterial structures are premeditated and defined by preoperative
radiographic studies.

Complications
Although a number of complications may be attendant to dissection of lesions within the third ventricle
(alteration of consiousness, gastrointestinal hemorrhage, increased endocrinopathy, visual loss, and other
signs of diencephalic injury), the major considerations in establishing the transcallosal interforniceal
corridor are the development of hemiparesis and memory loss (2, 3, 10, 17-19, 21, 24, 27).
With care related to midline entry in relation to the cortical venous anatomy and minimization of midline
retraction, the incidence of permanent paresis will approach zero and that of transient paresis will be less
than 10%.
Transient recent memory loss is the single most commonly encountered postoperative problem. This has
been observed in 30% of our personal series, with complete resolution of this symptom generally observed
within a 21-day period. This disorder of mentation is recognized as an amnesia for recent events that is
most striking 24 to 72 hours postoperatively, with gradual resolution thereafter. Seventy-five percent of our
cases manifested resolution of this problem within a 7-day period. All patients had returned to preoperative
base line status or improved to normal mentation at 3 months postoperatively. The manifestation of this
complaint was thought to be more related to the texture of the offending lesion than to the size of the lesion,
with firm masses creating more need for local manipulation and the transmission of pressure to adjacent
periventricular structures.
Utilization
Advantages
The transcallosal interforniceal corridor affords exposure of lesions primarily within the anterior and
mid-third ventricle with minimal phys-

Figure 14.26. A. Multiple view CT of a partially cystic craniopharyngioma with a limited basilar and a
significant third ventricular component. B. Early postoperative CT with a small asymptomatic frontal fluid
collection. Adequate access and complete removal was accomplished by interforniceal exposure.
 iological cost; in addition, exposure of the posterior component of the chamber may be effected. Lesions
with basal components may be approached (Fig. 14.26). The technique allows for adequate exposure of the
third ventricular chamber in the event of minimal ventricular enlargement or minimal mass expansion
within the region. Additionally, it allows for simultaneous manipulation of and approach to the region
through the foramen of Monro and the transforniceal corridor for added technical advantage. If the foramen
of Monro is small or the lesion is not well visualized, the maneuver offers extensive exposure of the third
ventricular chamber, aiding the comfort of the surgeon.

Limitations
Inherent limitations of the approach are stressed by lesions that are less than 1.5 cm in size and are
located primarily posterior in the chamber and by lesions that are primarily basilar with lateral extension
and present a restricted or narrow apex deforming the mid- and anterior fornix. For the latter, a combined
basal (for lateral access) and transcallosal midline approach is often required, whereas for the former a
direct posterior corridor should be considered.

References
1. Apuzzo MLJ: Transcallosal Interforniceal exposure of lesions of the third
ventricle. In Schmidek HH (ed): Operative Neurological Techniques: Indi
cations and Methods. New York, Grune and Stratton, 1982.
2. Apuzzo MLJ: Inforniceal exposure of the third ventricular chamber. In Samii
M (ed): Surgery in and around the Brain Stem and Third Ventricle. Berlin,
Springer-Verlag, 1.987.
3. Apuzzo MJ, Chikovani OK, Gott PS, Teng EL, Zee CS, Giannotta SL, Weiss
MH: Transcallosal, interfornicial approaches for lesions affecting the third
ventricle: Surgical considerations and consequences. Neurosurgery 10:547-
554, 1982.
4. Baldwin M, Ommaya AD, Farrier R, MacDonald F: Mesial cerebral incision.
J Neurosurg 20:679-686, 1963.
5. Bengochea FG, De La Torre O, Esquivel O, Vieta R, Fernandez C: The section
of the fornix in the surgical treatment of certain epilipsies. Trans Am Neurol
Assoc 79:176-178, 1954.
6. Busch E: A new approach for the removal of tumors of the third ventricle.
Acta Psychiatr Scand 19:57-60, 1944.
7. Cairns H, Mosberg WH Jr: Colloid cyst of the third ventricle. Surg Gynecol
Obstet 92:545-570, 1951.
8. Dandy WE: Diagnosis, localization and removal of tumors of the third ven
tricle. Johns Hopkins Hosp Bull 33.188-189, 1922.
9. Dimond SJ, Scammell RE, Brouwers EYM, Weeks R: Functions of the centre
section (trunk) of the corpus callosum in man. Brain 100:543-562, 1977.
10. Dott NM: Surgical aspects of the hypothalamus. In Clark WEL, Beattie J,
Riddoch GG, Doh NM (eds): The Hypothalamus: Morphological, Functional,
Clinical and Surgical Aspect. Edinburgh, Oliver and Boyd, 1938, pp 131-
185.
11. Gazzaniga MS, Risse GL, Springer SP, Clark E, Wilson DH: Psychologic and
neurologic consequences of partial and complete cerebral commissurotomy.
Neurology (NY) 25:10-15, 1975.
12. Geschwind N: Disconnexion syndromes in animals and man: Part I. Brain
88:237-294, 1965.
13. Geschwind N: Disconnexion syndromes in animals and man: Part II. Brain
88:585-644, 1965.
14. Gordon HW, Bogen JE, Sperry RW: Absence of disconnexion syndrome in
two patients with partial section of the neocommissures. Brain 94:327-336,
1971.
15. Hassler R, Riechert T: Uber einen Fall von Doppelseitiger Fornicotomie bei
sogenannter Teporaler Epilepsie. Acta Neurochir (Wien) 5:330-340, 1957.
16. Heilman KM, Sypert GW: Korsakoff's syndrome resulting from bilateral
fornix lesions. Neurology (NY) 27:490-493, 1977.
17. Horel JA: The neuroanatomy of amnesia: A critique of the hippocampal
memory hypothesis. Brain 101:403-445, 1978.
18. Jeeves MA, Simpson DA, Geffen G: Functional consequences of the trans
callosal removal of intraventricular tumours. J Neurol Neurosurg Psychiatry
42:134-142, 1979.
19. Long DM, Chou SN: Transcallosal removal of Craniopharyngiomas within the
third ventricle. J Neurosurg 39:563-567, 1973.
20. Milhorat TH, Baldwin M: A technique for surgical exposure of the cerebral
midline: Experimental transcallosal microdissection. J Neurosurg 24:687-
691, 1966.
21. Shucart WA, Stein BM: Transcallosal approach to the anterior ventricular
system. Neurosurgery 3:339-343, 1978.
22. Sweet WH, Talland GA, Ervin FR: Loss of recent memory following section
of fornix. Trans Am Neurol Assoc 84:76-82, 1959.
23. van Wagenen WP: Surgery of the hypothalamic region. Res Publ Assoc Res
Nerv Merit Dis 20:841-853, 1939.
24. Williams M, Pennybacker J: Memory disturbances in third ventricle tumours.
J Neurol Neurosurg Psychiatry 17:115-123, 1954.
25. Winston KR, Cavazzuti V, Arkins T: Absence of neurological and behavioral
abnormalities after anterior transcallosal operation for third ventricular
lesions. Neurosurgery 4:386-393, 1979.
26. Woolsey RM, Nelson JS: Asymptomatic destruction of the fornix in man.
Arch Neurol 32:566-568, 1975.
27. Zaidel D, Sperry KW: Memory impairment after commissurotomy in man.
Brain 97:263-272, 1974.
 15
Subchoroidal Trans-Velum
Interpositum Approach
Michael H. Lavyne, M.D., and RusselH. Patterson, Jr., M.D.

Excision of brain tumors lying within the anterior to middle portion of the third ventricle has been difficult
because of the surgeon's inability to open the ventricle widely and safely. Although it is possible to remove
small tumors from the anterior portion of the ventricle without opening the foramen of Monro, tumors within
the midportion are relatively inaccessible unless the foramen is enlarged. Traditionally this has been done by
opening the foramen anteriorly, sacrificing the ipsilateral column of the fornix. But this may result in severe
short term memory loss, especially if either the tumor or the operation compromises the contralateral fornix.
The second option, which we have chosen to utilize, has been to enlarge the foramen posteriorly (4). Dandy (1)
described the removal of a mid-third ventricular tumor after opening the foramen posteriorly and ligating one
of the "lesser veins" of Galen. However, most neurosurgeons have hesitated to sacrifice the vein, perhaps
because McKissock (5) warned of the dangers of creating venous hypertension in the ipsilateral basal ganglia
and internal capsule. This is not an important risk because there is excellent collateral circulation between the
superficial cortical and medullary venous systems, as well as between the posterior medullary venous system
and the galenic system. Hirsch et al. (3) and Deland-sheer et al. (2) were the first to describe the microsurgical
subchoroidal approach to the third ventricle and emphasized that the ipsilateral thalamostriate vein could be
coagulated and divided from the internal cerebral vein without risking venous hypertension in the ipsilateral
basal ganglion. Viale and Turtas (6) modified this approach to the third ventricle by operating in the "figure
eight" created between the thalamus and the ipsilateral internal cerebral vein posteriorly and the thalamostriate
vein and foramen of Monro anteriorly. To gain access to the mid-third ventricle using this modification, one
must heavily retract the body of the fornix, which could cause severe disturbance of short term memory.
Therefore, we view Viale's modifications as a hindrance rather than an improvement upon the approach of
Hirsch and Delandsheer.
Exposure of the lateral ventricle is attained either through a cortical incision in the second frontal gyrus or
through the corpus callosum in the midline. The transcortical route has the advantage that the key landmarks in
the lateral ventricle that guide the surgeon into the third ventricle are in the direct line of sight and, therefore,
less intraventricular retraction is required than is necessary after the transcallosal approach. On the other hand,
the approach through the corpus callosum minimizes injury to the frontal lobe and may be less epileptogenic.
In patients with massive ventriculomegaly due to associated hydrocephalus, the exposure is comparable with
either approach.
 Indications
Tumors that are primarily extraaxial and indent the floor of the third ventricle should be removed via a
subfrontal rather than a transventricular approach. These tumors arise from the sellar or parasellar region and it
is sometimes difficult to determine the site of origin even at operation. Pituitary tumors are the most common
type in this group, although epidermoid and dermoid tumors, meningiomas, atypical teratomas, ectopic
pinealomas, and metastases, as well as nonneoplastic lesions, including arachnoid cysts and sarcoidosis, have
been described. Tumors that are entirely confined within the ventricle and have not broken through the floor
are best handled by the subchoroidal or interforniceal approaches. These tumors are frequently attached to the
wall of the ventricles by pedicles through which they receive their blood supply. Low grade astrocytomas are
relatively common in children and when they arise in the hypothalamus or the optic chiasm grow into the
ventricular lumen, causing obstructive hydrocephalus as well as hypothalamic dysfunction. It is frequently
difficult to differentiate these gliomas from lesions originating from within the thalamus that extend into the
third ventricle. Other less frequently encountered tumors include ependymomas, papillomas of the Choroid
plexus, and meningiomas of the tela choroidea. Entirely intraventricular Craniopharyngiomas, which originate
from Rathe's pouch, have also been encountered. Vascular anomalies, including cavernous hemangioma, and
nonneoplastic cysts secondary to parasitic or tuberculous granulomatous disease round out the list of
exceptionally rare causes of obstructive hydrocephalus due to intraventricular abnormalities. If the patient has
hydrocephalus, the surgical exposure will be much easier to attain. On the other hand, if the patient has a
functioning ventricular shunt with normal or small-sized lateral ventricles, the transcortical incision, dissection,
and retraction required to gain access to the mid-third ventricle make this approach less attractive than the
transcallosal or transcallosal interforniceal approaches to the third ventricle. A specific example of this relative
contraindication is seen in a patient who was shunted for "aqueductal stenosis" a decade before the
development of a large third ventricular glioma (Fig. 15.1). In the face of small lateral ventricles, a
transcortical subchoroidal approach to the glioma was performed for biopsy. A subop-timal view of this third
ventricular tumor was attained because the small noncompliant lateral ventricle prevented adequate retraction
of the Choroid plexus, fornix, and thalamus. In patients recently shunted the ventricular cavity is still relatively
distensible, perhaps because of periventricular cerebrospinal fluid (CSF) accumulation. This enables the
surgeon to retract the fornix and basal ganglia gently without fear of damaging them. In this situation we would
prefer a stereotaxic biopsy to establish the diagnosis and, if that were not possible, the transcallosal interforni-
ceal approach would be utilized to obtain tissue for pathological examination. If the ventricular shunt catheter
had been placed through the right frontal approach, we would have performed a small cortisectomy around the
ventricular catheter to gain access to the small lateral ventricle and the intraventricular landmarks needed to
guide the surgeon to the third ventricle for tumor biopsy.
 Figure 15.1. These two contrast-enhanced CT sections show small lateral ventricles in a patient who was
shunted 10 years before the scan. The right hemi-cranium is smaller than the left. The shunt catheter passes
through the thalamus into the right lateral ventricle, but caused no deficits. The contrast-enhancing tumor
filling the velum interpositum emanates from the right thalamus. There is no evidence of periventricular low
density due to transventricular uptake of water, which suggests to the surgeon that the shunt has been
functioning properly for a long time.

Preoperative Evaluation
Patients harboring third ventricular tumors usually present with signs and symptoms of hydrocephalus due
to tumorous obstruction of CSF pathways or of pituitary or hypothalamic dysfunction due to direct invasion.
Patients are usually referred to the neurosurgeon with a computerized tomographic (CT) scan that has defined
the location of the lesion. Thin coronal sections, with and without intravenous contrast enhancement, should be
studied to give the surgeon a clear knowledge of the location of the tumor with respect to the confines of the
third ventricle and of the tumor's vascular pattern, which may help to determine the presumed preoperative
diagnosis (Fig. 15.2). One must also study the peritumorous venous drainage with a high quality cerebral
angiogram, preferably with magnification (Fig. 15.3). A digital arterial angiogram will not give the surgeon
optimal information about third ventricular venous drainage and therefore is not an acceptable substitute for a
standard angiogram. If the Venogram shows that the tumor has spread both internal cerebral veins laterally, we
would remove it without dividing the thalomostriate vein from the internal cerebral vein. In this situation
division of the septal vein from the internal cerebral vein may be necessary to enlarge the operative field from
the foramen of Monro to the posterior portion of the third ventricle. Conversely, if the internal cerebral veins
are together and displaced dorsally by the lesion, either or both the
 Figure 15.2. A. This preoperative CT scan shows a well-circumscribed lesion filling the anterior and
middle portions of the third ventricle, which is surrounded by edema. B. The speckled blood or calcium density
within the lesion enhanced after intravenous contrast infusion. No hydrocephalus is noted. C. The sagittal
reconstruction of the contrast-enhanced CT scan shows that the lesion is entirely confined within the third
ventricle. This cavernous angioma was removed utilizing a subchoroidal exposure of the third ventricle. D.
These operative photographs taken during the removal of this lesion show the view of the right lateral
ventricle, including the right thalamostriate, septal, and internal cerebral veins, the fornix, and the thalamus,
partially obscured by the small cottonoid. E. After both septal and thalamostriate veins were coagulated and
divided, the lesion within the third ventricular cavity was identified, biopsied, and vaporized with a CO2 laser.
Diagnosis: cavernous angioma.
 Figure 15.3. A. The lateral Venogram shows the configuration of the veins draining the lateral ventricles
into the internal cerebral vein. The venous angle made by the thalamostriate and internal cerebral vein is
"open" (more obtuse than normal) because of the presence of a mid-third ventricular mass elevating the course
of the internal cerebral vein (ICV) and partially obstructing the CSF pathways. The presence of direct venous
communications between the ICV and the thalamus is not evident on this Venogram, but the posterior portion
of the ICV is partially encased in tumor. The absence of many anteriorly draining parasagittal veins would
make the transcallosal approach as attractive as the transcortical approach to the right lateral ventricle.
B. Large thalamic perforating arteries from the top of the basilar artery and dilated medial posterior
choroidal arteries suggest that this third ventricular mass is a primary thalamic tumor.
 septal and ipsilateral thalamostriate veins are divided from the internal cerebral vein along the subchoroidal
route to the third ventricle.

Technique
In patients who are obtunded due to tumorous hydrocephalus, we first place a ventricular shunt and later
return the patient to the operating room for tumor biopsy or excision when the patient's level of consciousness
improves. The placement of the scalp incision is critical when inserting a shunt. We prefer a frontal placement
because the scalp flap can be utilized for definitive craniotomy (Fig. 15.4). The horseshoe right frontal scalp
flap is hinged toward the coronal suture so that the shunt material will not lay beneath the incision. (If the
transcallosal route is elected, the scalp flap crosses the midline. The patient is placed in the

Figure 15.4. A. The burr hole is placed in the midpupillary line anterior to the right coronal suture. A
horseshoe scalp flap is fashioned so that it is hinged posteriorly. B. Another way of approximating the location
of the single burr hole, which is utilized for the placement of the ventricular shunt catheter or as the centrum
for the craniotomy, is to mark the skin 10 cm rostral from the nasion and 3 cm to the right of the midline. C.
This conceptualization shows the sequence in which the saw cuts are made with the air-powered cranial saw
after the single perforation has been drilled. The last cut is along the midline to assure that venous bleeding, if
it should occur, can be controlled easily. Bleeding points are not coagulated, but rather are tamponaded with
pledgets of thrombin-soaked gelatin sponge.
 lateral position with the vertex elevated slightly above the equatorial plane so that the medial surface of the
brain falls away from the falx, obviating the need for firm retraction.) The scalp flap is fashioned so that a
single burr hole placed in the center of the flap 10 cm above the nasion and 3 cm to the right of the midline can
be used for placement of the

Figure 15.5. A. The dural opening. Rather than hinging the dura mater toward the midline in a horseshoe
fashion, we prefer to open the dura in a cruciate way to visualize as much of the cortex as possible. B. A small
cortisectomy is made after coagulating the pial vessels with a bipolar cautery. С. А 16 gauge Cone ventricular
needle is passed perpendicular to the cortex. Depending upon the thickness of the cortical mantle, the tip of the
needle will enter the frontal horn of the right lateral ventricle just anterior to the foramen of Monro.
 shunt catheter as well as for the small free bone plate needed for the craniotomy. The last saw cut is along
the midline so that potentially troublesome parasagittal venous bleeding can be controlled promptly with a thin
strip of thrombin-soaked gelatin sponge (Fig. 15.4.) The dura mater is opened in a cruciate fashion along the
diagonal and is reflected along each saw cut (Fig. 15.5). The small superficial cortisectomy is made in the
middle frontal gyrus and a 16 gauge Cone ventricular needle is passed into the right lateral ventricle (Fig.
15.5). A core of brain surrounding the needle track is removed so that the two 20-mm Silastic-coated
Greenberg retractors can be placed within the ventricle (Figs. 15.6 to 15.8). The remainder of the operation is
done with the help of the microscope. We prefer the 300-mm lens and the 12.5x oculars. The first key
anatomical landmark to be encountered is the Choroid plexus. The Choroid plexus is attached along the
superior and medial aspect of the thalamus at the choroidal fissure. After elevating the Choroid plexus, this
ependymal lining becomes apparent. By following the Choroid plexus anteriorly to the foramen of Munro, the
surgeon will also identify the subependymal course of the caudate and the thalamostriate veins as they run
toward the foramen of Monro (Fig. 15.9). In patients with massive hydrocephalus, decompression of the
ipsilateral ventricular CSF causes the septum pellucidum to bow out toward the collapsed ventricle, partly
occluding the foramen of Monro (Fig. 15.10). The septum should be fenestrated, allowing CSF from the
contralateral ventricle to escape. Care should be taken to puncture the midportion of the septum at least a few
millimeters away from the column of the fornix. The foramen of Monro will become apparent as the septum
returns to the middle. The Choroid plexus is elevated with the tip of the retractor blade revealing the dorsal
aspect of the thalamus (Fig. 15.12A). Cutting the leptomeninges rather than stripping them from the superior
aspect of the thalamus allows one to elevate

Figure 15.6. The artist has sketched an overview of the operative set-up. Note that the patient's head has
been rotated and the vertex has been tilted a few degrees to the left of the midsagittal plane. The retractor
blades are advanced to the edge of the cortisectomy so that the surgeon can easily view into the lateral
ventricle. The cortisectomy should be lengthened so that 25 to 35 mm of intraventricular exposure is obtained.
 Figure 15.7. The artist's drawings (A and B) and the operative photograph (C) delineate the intraventricular
anatomy. The Choroid plexus, septal vein, thalamostriate vein, thalamus, and fornix, as well as the tumor
filling the foramen of Monro, are seen.
 Figure 15.8. These drawings show coronal views of the approach to the midportion of the third
ventricular cavity.

the choroid plexus and dislocate it toward the midline. If the Choroid plexus is excessively
abundant, the surgeon may elect to coagulate and remove it. The subependymal veins that drain the
anterolateral aspect of the ventricle, the septal and thalamostriate veins, shed their subependymal
coat and join directly into the internal cerebral vein within the leaves of arachnoid called the velum
interpositum. Anteromedial thalamic and posteromedial thalamic veins join the terminal segments of
the internal cerebral vein posterior to this dissection. Visualization of these and occasional
anomalous direct lateral veins allows one to divide both the septal and the thalamostriate veins, if it
is necessary, to gain wider exposure of the third ventricle without fear of internal cerebral vein
thrombosis (Fig. 15.11). After the thalamostriate or septal vein is divided from the internal cerebral
vein (Fig. 15.12), the retractors are advanced along the medial wall of the thalamus and the body of
the fornix, respectively, to gain access to the third ventricle. Only leptomeningeal adhesions coursing
through the velum interpositum and the thin inferior pial layer underlying the ependymal membrane
prevent access to the third ventricle. The medial posterior choroidal arteries travel through the velum
interpositum and supply the Choroid plexus of the third and lateral ventricles as well as the posterior
medial aspect of the thalamus. The Choroid plexus of the third ventricle lies in the roof of the cavity,
but in the presence of a tumor it is usually atrophic, presumably as a result of chronically increased
intracranial pressure. Once the tumor is encountered, biopsy is taken with a small cup forceps (Fig.
15.1 ЗА). The tumor
 Figure 15.9. These two photographs (B and C) and the accompanying drawing (A) show the ventricular
anatomy in a formalin-fixed brain. The right frontal cortex has been removed. The artist has enhanced the
conceptualization of the microsurgeon's operative view by superimposing the subjacent third ventricle. B.
Coagulation and then division of the thalamostriate vein from the internal cerebral vein as the former leaves its
subependymal course over the thalamus. C. The remaining filmy strips of arachnoid that course through the
velum interpositum. Division of these strands allows the surgeon free access to the midportion of the ventricle.
 Figure 15.10. Left. The artist's conceptualization of the intraventricular anatomy clearly shows the Choroid
plexus and subependymal course of the caudate and thalamostriate veins, but the view of the foramen of Monro
has been obstructed by a ballooned septum pellucidum under pressure due to CSF in the isolated left lateral
ventricle. The surgeon perforates the septum so that CSF under tension can drain into the operative field. Right.
Aspiration of this CSF will allow the septum to drift out of the way, enabling the surgeon to identify the
foramen of Monro and the confluence of the septal and thalamostriate veins. The retractors gently depress the
thalamus and elevate the body of the fornix from right to left. Forceful retraction is not necessary. The tip of
medial retractor is bent slightly so that the column of the fornix can be gently elevated as well as dislocated
medially. Taking down the filmy strips of arachnoid in the velum interpositum may be necessary before one
enters the third ventricular cavity. Sometimes the tumor spreads apart both internal cerebral veins, and taking
the septal vein from the ipsilateral internal cerebral vein will allow one to retract the thalamus laterally a few
millimeters, giving the surgeon an excellent view of the tumor cavity.
 Figure 15.11. The communications between the deep thalamic veins and the internal cerebral vein. The
presence of the middle and posterior venous communications enables the surgeon to coagulate the septal or
thalamostriate vein without concern about the development of regional venous hypertension.
 Figure 15.12. A tumor being removed. A and D. The thalamostriate vein is divided from the internal vein,
and the leptomeninges in the velum interpositum are taken down.
В and E. A flat dissector is passed between the thalamus and the internal cerebral vein, and the Silastic-
coated retractors are advanced so that the medial retractor slightly dislocates the fornix and the lateral retractor
depresses the thalamus. The tumor can then be attacked between the internal cerebral vein and the thalamus
with standard microsurgical instruments, the laser, or the cavatron ultrasonic emulsifier.
С and F. After the tumor is removed one should be able to see the contralateral foramen of Monro and both
columns of the fornices.
 Figure 15.13. The artist has shown the three usual tools for removing the tumor: A, microvascular biopsy
forceps (for the avascular tumor); B, carbon dioxide laser (for the scirrhous tumor); and C, Cavitron aspirator
(for the gelatinous tumor).
 vascularity and consistency is assessed during this maneuver. Firm avascular tumors are vaporized with the
carbon dioxide laser (Fig. 15.13B) and soft tumors are removed with suction (Fig. 15.13C) or the Cavitron
ultrasonic emulsifier. Hemostasis is usually not a problem, and it is managed with bipolar cautery or cottonoid
pledgets soaked in throm-bin. By gutting the centrum of the tumor, the surgeon identifies the plane between the
tumor and the walls of the surrounding thalamus and hypothalamus. When possible, as in the case of
intraventricular craniopharyngioma or low grade glioma, the lesion is completely removed.
Virtually all of these patients are left with obstruction of the CSF pathways and, for this reason, a flanged
ventricular catheter is left in the lateral ventricle when the craniotomy is closed. The tube is passed through the
single burr hole made in the center of the free bone flap and is attached to an Ommaya reservoir (Fig. 15.14).
We usually elect not to convert the Ommaya reservoir to a functioning shunt until the patient demonstrates
clinical evidence of persistent obstructive hydrocephalus.

Figure 15.14. A. The relationship of the center-filling Ommaya reservoir to the scalp flap. At a later date the
ventriculostomy can be converted to a shunt if communicating hydrocephalus ensues. B. The tip of a
ventricular catheter in the frontal bow of the right lateral ventricle. The tip of the catheter should not rest near
the coagulated deep cerebral veins.
 When aspirating CSF through the catheter, it is possible to injure the subjacent deep cerebral veins stripped
of their ependymal cover. To prevent this complication, it is important to leave just enough catheter to pierce
the most superior aspect of the lateral ventricle.

Complications
Complications associated with this procedure have been few. Although the transcortical approach to the
ventricle has been associated with postoperative seizures, the use of perioperative anticonvulsant medications
has essentially eliminated this problem. An additional problem could be related to heavy retraction on the
thalamus, caudate, or body of the fornix. However, this potential problem is essentially eliminated by
coagulation and division of the thalamostriate vein from the internal cerebral vein, which gives the surgeon an
excellent view in the third ventricle from the level of the foramen of Monro to its most posterior portion. This
expanse will allow one to operate safely on anterior, middle, and posterior third ventricular lesions without
injuring the columns of the fornix. Whether interruption of one or both columns of the fornix will result in
permanent short term memory loss is controversial. We think that there has been enough unfavorable
experience with unilateral anterior fornicotomy to urge avoidance of this maneuver, especially when the
contralateral fornix could be compromised by the third ventricular tumor.
References
1. Dandy WE: Benign Tumors in the Third Ventricle of the Brain: Diagnosis
and Treatment. Springfield, IL, Charles С Thomas, 1933.
2. Delandsheer JM, Guyot JF, Jomin M, Sherpereel B, Laine E: Acces au
triosieme ventricle par voie inter-thalamo-trigonale. Neurochirurgie 24:419-
421, 1978.
3. Hirsch JF, Zouaoui A, Renien D, Pierre-Kahn A: A new surgical approach to
the third ventricle with interruption of the striothalamic vein. Acta Neurochir
(Wien) 47:135-147, 1979.
4. Lavyne MH, Patterson RH, Jr: Subchoroidal trans-velum interpositum ap
proach to mid-third ventricular tumors. Neurosurgery 12:86-93, 1983.
5. McKissock W: The surgical treatment of the colloid of the third ventricle: A
report based upon twenty-one personal cases. Brain 74:1-9, 1951.
6. Viale GL, Turtas S: The subchoroidal approach to the third ventricle. Surg
Neurol 14:71-76, 1980.
16
Subfrontal Transsphenoidal and Trans-
Lamina Terminalis Approaches
RusselH. Patterson, Jr., M.D.

Many surgeons favor a pterional approach along the sphenoid ridge to tumors involving the anterior third
ventricle, such as Craniopharyngiomas. The advantages of this approach are several. It is the shortest distance
from the scalp to the sella, it provides a glimpse of the tumor both behind and in front of the carotid artery, and it
avoids opening the frontal sinuses. However, the pterional approach has substantial disadvantages; the opposite
optic nerve and carotid artery are poorly visualized, tumor removal is difficult because one must operate with the
carotid arteries and optic nerves obstructing access, and the various arteries and nerves are positioned at a
peculiar angle that is difficult to conceptualize without a substantial amount of experience. For these reasons, I
prefer a straight frontal approach.
A frontal approach has some drawbacks but, fortunately, these are minor or can be readily overcome. The
surgeon may have to open the frontal and sphenoid sinuses, anosmia results in 30 to 50% of patients, and short
optic nerves may block access to the tumor. On the other hand, exposure of the tumor is better than by any other
approach with the consequence that the chances of damaging the optic nerves and major arteries are minimized.

Surgical Technique
The patient is positioned supine with two #20 spinal needles in the lumbar subarachnoid space for the
withdrawal of spinal fluid. We have had constructed for the operating table a thick mattress with a notch that
provides sufficient clearance for the lumbar needles (Fig. 16.1 A). At the appropriate time, spinal fluid is allowed
to flow by gravity through plastic tubes into a sterile 50-ml syringe with the plunger removed and taped
underneath the table. By means of a three-way stop cock on the syringe, spinal fluid in excess of 50 ml can be
removed from this reservoir for injection back into the patient at the end of the operation. A frame that holds a
Mayo tray clamps to the operating table. This is placed
Figure 16.1. A. Patient supine with table tilted head up about 20° and the lumbar spinal needle in place. The neck
is extended so that the floor of the frontal fossa is tipped back about 45° from the vertical, which will reduce the
need for frontal lobe retraction. B. The head is not rotated, which makes orientation around the sella easier (I,
surgeon; 2, assistant; 3, nurse; 4, anesthesiologist; 5, microscope base).
Figure 16.2. A. The neck is extended so that the roof of the orbits is tipped back about 45° from the vertical. B.
Position of Mayfield pin head holder.

approximately 20 cm caudal to the patient's brow, and an extra outrigger provides an additional surface on which
to place instruments. An ordinary back table as used in general surgery provides the reserve of instruments for
the nurse, who stands on a platform near the first assistant. The nurse is close enough that she can provide an
extra set of hands for irrigation or manipulation of the electrocautery, if necessary (Fig. 16.1B).
The operating table is tipped with the head elevated and the feet down. The neck is extended so that the roof
of the orbits, were they visible, would be tipped back approximately 45° from the vertical (Fig. 16.2A). This
means that the frontal lobe will tend to fall back by gravity from the roof of the orbit, which minimizes the
amount of retraction necessary to expose the region of the optic chiasm. The position probably will require the
surgeon to use straight eyepieces on the operating microscope, which is most conveniently done by having the
surgeon seated using a Mayo stand as an armrest (Fig. 16.1 A).
It is also possible to place the head in a neutral position with the roof of the orbit and the undersurface of the
frontal lobe positioned vertically, which is convenient for the surgeon because he can use angled eyepieces and
operate with his line of vision straight down. However, in this position the frontal lobe tends to fall over the optic
chiasm with the consequence that retraction pressure on the frontal lobe must be greater. Consequently, we
prefer the approach with the head thrown back and neck extended.
The head is held with the Mayfield pin head holder. This is not ideal for a coronal incision because invariably
the pin position compromises the incision to a degree. We usually put the double pins in the left posterior frontal
region and the single pin behind the right ear. It is then possible to drape for a coronal incision on the right side
that extends from near the zygoma to a point sufficiently past the midline to allow a bifrontal incision if desired
(Fig. 16.2B).
After the patient is positioned, the hair is shaved for about 4 cm behind the hairline. If the tumor is small and
the surgeon elects a unilateral
Figure 16.3. A and B. The coronal scalp incision is placed in the hair line, which varies from patient to patient.
The bone plate reaches the midline and is flush with the orbital roof. C. For complex tumors, such as
Craniopharyngiomas, a bifrontal bone plate is used. It can be carried to the zygoma insertion on either side,
although usually 4 cm on either side of the midline is adequate.

approach, the scalp incision is made from near the zygoma in front of the ear in the hairline across to the left side
of the midline. The incision, particularly if it is as low as the zygoma, must be kept within 1 cm of the helix of
the ear to avoid dividing the frontalis branch of the facial nerve. After making the incision, a soft tissue flap
consisting of scalp and temporal muscle is turned down toward the brow. Because the bone opening must be
made flush with the brow, it is important that the flap
Figure 16.4. В. Scalp and temporal muscle turned down toward the brow. В, С, and D. The dura mater is opened
transversely, dividing the sagittal sinus and falx in the case of a bifrontal exposure.

be turned down far enough to expose the supraorbital ridge and the insertion of the zygoma into the frontal bone
at the keyhole. Small tumors can be handled readily through a right frontal exposure alone, but larger tumors are
better exposed through a bifrontal craniotomy.
Whether the exposure is unilateral or bilateral, we prefer to make the first hole a trephine opening centered on
the midline just at the brow. The trephine makes for an easier passage through the frontal sinus than using a high
speed burr (Fig. 16.3). Most often the frontal sinus will be entered in the process, but sometimes it is possible to
preserve the mucosa by pushing it downward with an instrument before the trephine button
Figure 16.5. A. The retractor is put in obliquely along the roof of the orbit toward the optic chiasm. B. A more
direct exposure can be gained by sliding the retractor medially to the falx and retracting the gyrus rectus. The
danger is that the increased retraction pressure may damage the frontal lobe. С The tumor is exposed. The skull
opening must be flush with the floor of the frontal fossa to minimize retraction. Usually the frontal sinus is
opened widely.

is removed. An air drill may be used to place the other holes in the skull. One of them should be at the keyhole
on the right at the zygomatic process of the frontal bone, and others may be necessary in older patients in whom
the dura mater is likely to be adherent to the intertable of the skull. In case of a bifrontal exposure, one burr hole
is placed over the sagittal sinus approximately 4 cm posterior to the trephine opening and
Figure 16.6. A to C. Sometimes the brain is full and the chiasm is difficult to expose. In a unilateral approach,
splitting the sylvian fissure enough to expose A1 and M1 will allow more retraction. D. In a bifrontal exposure,
the olfactory tracts are dissected and preserved so that olfaction will not be lost. The frontal lobes are then
separated and retracted.

others are placed as needed in the skull to the left of the midline. The flap need not be large; 4 cm from the roof
of the orbit is enough (Fig. 16.4A).
It is possible to feel the roof of the orbit with an instrument from the medial trephine opening and also the
lateral opening in the skull at the keyhole. In this way, it is possible to use the craniotome to make an opening
flush with the roof of the orbit. The frontal sinus will be opened in most patients, but this is easy to repair at the
end of the procedure.
After the bone plate is removed, we request the anesthesiologist to open the spinal drainage system and begin
the removal of spinal fluid. Perhaps
Figure 16.7. Preservation of the olfactory tracts during bifrontal craniotomy. The sense of smell is retained.

30 to 60 ml of spinal fluid are removed at first, and during the course of the procedure additional fluid is
removed in quantities sufficient to keep spinal fluid from welling up around the optic chiasm. It is probably wise
not to remove all of the spinal fluid so that blood spilled at the operative site will be less likely to fill the
subarachnoid space. Brain relaxation is achieved by the position of the head, the withdrawal of spinal fluid, the
administration of 50 g of urea at the beginning of the procedure, and adjustment of ventilation to keep the pCO2
in the range of 28 to 30 mm
Hg.
The dura mater is opened starting at the keyhole and curving across toward the trephine opening (Fig. 16.4C).
The dural opening is started laterally to avoid any bridging veins draining from the cerebrum into the sagittal
sinus. In the case of a bifrontal exposure, the sagittal sinus and the falx are divided just above the glabella.
The microscope is then brought into the field and the surgeon sits using a draped Mayo stand as an arm
support and also as a convenient place to put commonly used instruments (Fig. 16.1 A). A self-retaining brain
retractor that attaches to the pin head holder has proved quite satisfactory (Fig. 16.5A). The older retractors that
attached to the skull opening take up so much room that they are not practical with the small opening that we
favor.
For the unilateral approach (Fig. 16.5B), retraction of the brain is begun laterally over the roof of the orbit, and
the olfactory tract is followed down to the region of the optic chiasm (Fig. 16.6C). The arachnoid around the
optic chiasm and optic nerves is divided, and we strive to expose both optic nerves as well as the optic chiasm
(Fig. 16.6D). If it is difficult to
Figure 16.8. If the optic nerves are long, it may be possible to extract the tumor from between the nerves. A
layer of arachnoid usually separates a craniopharyngioma from the arteries, which makes separation relatively
easy. However, the optic chiasm, hypothalamus, and pituitary stalk are often quite adherent to the tumor and
difficult to separate.

get adequate exposure of the chiasm, which will be the case if the optic nerves are long, it is often helpful to
divide the arachnoid in the sylvian fissure sufficiently to expose the middle cerebral artery (Fig. 16.6C). The
resulting separation of the frontal lobe and the temporal lobe allows better exposure of the chiasm. Gradually,
adequate exposure of the optic nerves and chiasm can be obtained. Usually it is wise to coagulate and divide the
olfactory nerve and try to have the retractor along or near the falx because of the advantages of a straighter
approach to the optic chiasm.
If the tumor is large, and often this can be anticipated from the preoperative roentgenographic studies, then a
bifrontal exposure is ad-
Figure 16.9. Comparison of tumor removal with long or short optic nerves.

vantageous. In this case a bone plate can be fashioned on the left side that is similar to the one on the right.
However, it is often unnecessary to go as far as the keyhole on the left side, and the sawcut can be stopped
perhaps 4 cm to the left of the midline. However, the sawcut still must be made flush with the roof of the left
orbit to minimize retraction of the frontal lobe (Fig. 16.4B). After removal of the bone plate on the left, the dura
mater is opened on the left side and the sagittal sinus and falx are divided at the glabella. It may be possible then
to retract the frontal lobe and dissect the olfactory tracts from the undersurface of the frontal lobe, preserving
them. This may be difficult, and often both olfactory tracts will be stretched in the process, leading to permanent
anosmia. Brain retraction then is not only posteriorly, but the frontal lobes are separated. Callosal branches of the
anterior cerebral artery are identified and followed to the region of the anterior communicating artery. This will
allow exposure of the entire optic chiasm, even if the optic nerves are long, and it gives excellent exposure of the
lamina terminalis (Fig. 16.6D). In a bifrontal craniotomy, ability to preserve the olfactory tracts is improved (Fig.
16.7).
In cases in which the optic nerves are long, the craniopharyngioma usually will be identified between the
nerves above the sella (Fig. 16.8A). The tumor is covered by a layer of arachnoid, and it is often possible to
extract the tumor by a steady pull on the capsule and dissection of arachnoid off the sides. The cystic tumors
provide the most difficulty because the cyst wall is quite delicate. It is easy to leave fragments of the cyst wall
inadvertently behind, and because the cyst wall is composed of neoplastic tissue the pieces will continue to grow.
Often the pituitary stalk, which can be identified by the vertical striations of the portal system, can be identified
and preserved (Fig. 16.6D).
In many patients, the optic nerves will be quite short and only a millimeter may exist between the chiasm and
the tuberculum (Fig. 16.9B). This space is not sufficient for resection of the tumor (Fig. 16.9 A).
Figure 16.10. A. If the optic nerves are short and the tumor is large and hard to break into small pieces, the
tuberculum sellae should be removed to protect the optic apparatus from injury. B. A flap of dura mater is peeled
back from the tuberculum and the sphenoid sinus is entered with a chisel. Often the sinus mucosa can be
preserved. С to E. The tuberculum and anterior wall of the sella are removed with bone instruments or a high
speed burr.

At this point, one can make a hole with a blunt instrument in the lamina terminalis and examine the tumor from
above. The lamina is sometimes difficult to distinguish from the optic tracts and chiasm, but it has a faint reddish
blush that identifies it. This is the place to make the hole. If the tumor is quite friable, it is sometimes possible to
remove a good deal of tumor from between the optic tracts. However, it may be that the tumor under the chiasm
is difficult to reach or that parts of the tumor will be so firm that manipulations to remove the tumor risk damage
to the optic tract. If this is the case, we recommend that the tuberculum sellae be removed. This is easy to
accomplish by cutting a flap of dura mater over the tuberculum and hinging it either down toward the chiasm or
up
 Figure 16.11. Removal of the tuberculum sellae (cadaver).

Figure 16.12. Craniopharyngioma with short optic nerves.

toward the crista galli. A chisel then can be used to make a hole through the planum sphenoidale into the
sphenoid sinus. The sphenoid sinus mucosa is quite thick and often can be preserved. Fine bone instruments are
then used to remove the bone in front of the sella between the optic nerves (Fig. 16.10). Another option is to
open the sphenoid sinus and remove the bone at the tuberculum with a high speed drill (Fig. 16.11). In either
case, the whole process takes no more than 15 minutes. The dura mater enclosing the circular sinus then is
coagulated and divided. A craniopharyngioma with short optic nerves is shown in Figure 16.12.
Figure 16.13. A. The dura mater is divided and pushed out of the way. В and C. Tumor is removed by pushing it
down and away from the chiasm into the sphenoid sinus from which it can be extracted without brushing the
optic apparatus.

With the tumor exposed through the lamina terminalis and the tuberculum removed, it is possible to push
chunks of tumor downward into the sphenoid sinus where they can be removed without fear of damaging the
optic apparatus (Fig. 16.13B).

Problems and Complications

The main difficulty with the procedure occurs with large tumors that are adherent to the underside of the
chiasm or to the hypothalamus. As a rule, steady traction and gentle dissection will free the tumor from both of
these structures, but it is to these structures that the tumor is most adherent. Restraint must be exercised in
separating adherent tumor from the optic chiasm. If the chiasm is stretched or vision is already impaired, small
amounts of manipulation can cause severe visual loss. Occasionally, prudence will dictate leaving tumor behind
in preference to causing blindness. Sometimes the tumor adheres to the carotid, posterior communicating, or
basilar arteries, but this is exceptional. For the most part
Figure 16.14. Appearance after the lamina terminalis is opened, the tuberculum sellae is removed, and the
craniopharyngioma is excised.

the tumor is insulated from the arteries by a layer of arachnoid, and separation is easy.
After tumor removal is completed, the hole in the sphenoid sinus is repaired by pushing the sphenoid sinus
mucosa down and stuffing the cavity of the sinus with fat (Fig. 16.14). Fat obtained from a patient undergoing an
operation in another room has been quite satisfactory (Fig. 16.15B). The fat is stuffed into the sinus cavity and
held in place by a few sutures placed across the top of the fat between remaining fragments of dura mater.
Previously withdrawn spinal fluid, if it is not blood-stained, is returned through the lumbar needles. This
maneuver flushes out air and refills the brain. We try to close the dura watertight, if possible, and then use more
fat to seal the open frontal sinuses. A flap of pericranium is cut from the underside of the scalp flap and sutured
to the dura near the cut edge of the opening in the skull (Fig. 16.15C). If the dura mater is shredded, we do not
patch it but place a sheet of gelatin sponge under the bone plate. The bone plate is repositioned and held with
sutures passed through drill holes. The trephine button is replaced and wedged into position with some gelatin
foam. Bone dust, silicone rubber glue, or acrylic cranioplasty material is used to fill the burr holes. The scalp is
closed in two layers without drainage.
The complications of the surgical procedure are few if retraction on the frontal lobe has been gentle. Anosmia
occurs in about 30% of the patients for whom a unilateral approach has been used and at least 50% of the
patients for whom a bifrontal approach has been used, even if the olfactory tracts are saved. Hypopituitarism is
common, but often this is present before operation. Diabetes insipidus is a likely consequence, but this can be
well managed with pitressin and desmopressin acetate and tends to self-correct. The worst endocrine
complication is diabetes insipidus occurring in a patient with adypsia. Because the patient has inadequate thirst
mechanisms, the fluids lost due to diabetes insipidus are not adequately replaced by oral fluids. This leads to
dehydration with high serum osmolalities and hypernatremia. We have seen this primarily in patients who have
had prior radiation therapy. It has been rare in patients undergoing operation for the first time or in patients
whose prior therapy has been only operation.
Figure 16.15. A and B. The sphenoid sinus is closed by packing it with fat and tacking back the dural flap with a
few sutures. С Fat is placed in the frontal sinus and, after the dura is closed, a flap of pericranium is placed over
the fat and tacked to the dura mater. D. The bone plate is replaced and the holes and saw cut are filled with
something like bone dust or silicone rubber.
17
Bifrontal Anterior
Interhemispheric Approach
Jiro Suzuki, M.D.

The first attempt to remove a tumor from the anterior part of the third ventricle was
that of Lewis (9) in 1910, operating on a craniopharyngioma. After the total excision of
a craniopharyngioma by Gordy et al. (4) in 1949, total removal of such lesions soon
became commonplace throughout the world, although the operative mortality rate was
high at 25 to 57% (4, 5, 10, 11). Subsequent to the advent of steroid replacement
therapy in 1952 (7) and, more recently, microsurgery, the operative mortality has
decreased, but several problems have remained. Moreover, because many tumors of the
anterior part of the third ventricle are imbedded in or surround the hypothalamopituitary
system, complete excision is not always the best therapy. In light of findings concerning
the nature of the tumor, its location, the patient's age, etc., it is desirable to attempt to
assure maximal prolongation of the patient's useful survival time and to take measures
that will minimize the possibility of recurrence (1,2). For these purposes, therapy—
including radiotherapy and chemotherapy—must be considered.
When, however, operation is to be performed, operative findings often influence the
decision of whether complete excision of the tumor is desirable. Shillito's caution (12)
to the neurosurgeon should be kept in mind: "Mature judgment is needed to determine
how far to go and when to stop." It is therefore essential to obtain an operative field of
maximal size and to use an approach that minimizes damage to brain tissue. We have
consequently devised a bifrontal interhemispheric trans-lamina terminalis approach
(Fig. 17.1) for mass lesions, such as Craniopharyngiomas, that are known to raise the
floor of the third ventricle and develop near the suprasellar region or to develop within
the third ventricle itself. Using this approach, we have obtained favorable operative
results (15).
Thus far, at least six approaches to the anterior third ventricle have been attempted.
They include (a) a subfrontal approach, (b) an interhemispheric trans-lamina terminalis
approach, (c) a pterional approach, (d) a subtemporal approach, (e) a transcallosal
approach, and (/) a transsphenoidal approach. For complete excision of a tumor,
however, it is best to use an approach that minimizes damage to the brain tissue and
Figure 17.1. Interhemispheric trans-lamina terminalis approach (bifrontal craniotomy).

cranial nerves and allows sufficient treatment of arterial hemorrhage during the surgical
operation.
Using the bifrontal interhemispheric trans-lamina terminalis approach, both the
anterior circle of Willis and the optic chiasm can be visualized and tumors within the
third ventricle itself can be excised by first making a small incision in the lamina
terminalis—which has often been widened and thinned by the tumor growth. Moreover,
favorable surgical results can normally be obtained using this approach because the
amount of damage to the brain and vessels is kept to a minimum. Needless to say,
optimal results will be achieved using this approach when operation is undertaken with
careful consideration of the anatomy, physiology, and pathology of the pituitary and
hypothalamic regions (Figs. 17.2 and 17.3).
Problems that arise during operations in this region are often due to the fact that, even
if the tumor is benign, such as craniopharyngioma, it may invade the brain substance
around the tumor itself. Moreover, a dense gliosis will normally surround the tumor.
With regard to the question of the tissue surrounding a craniopharyngioma, Sweet (16)
and Hoffman et al. (6) have argued that complete excision is possible due to the presence
of a layer of gliosis, which provides a margin of safety between the tumor and the
functioning neruons. In contrast, Ghatak et al. (3) and Shillito (13) have held that it is
hard to perform complete excision of the tumor without damaging neural tissue when
fingers of tumor invade the surroundings.
Figure 17.2. A sagittal section through the hypothalamus. A. Preoptic area. B. Lateral
hypothalamic area. C. Paraventricular nucleus. D. Anterior hypothalamic nucleus. E.
Supraoptic nucleus. F. Dorsomedial nucleus. G. Ventromedial nucleus. H. Arcuate
nucleus. I. Posterior hypothalamic nucleus. J. Mamillary nucleus.

In an autopsy study of six cases of craniopharyngioma, Kuboda et al. (8) found that
the thickness of the reactive gliosis was 0 to 2 mm and the distance from the tumor to
the hypothalamic nuclei was 0 to 3 mm (averaging 2 mm). Moreover, the vascular
distribution around the tumor generally was abundantly concentrated within the gliosis,
rather than within the tumor itself. Consequently, they concluded that dissection in cases
of strong adhesion or in cases likely to hemorrhage is, in effect, inviting severe sequelae
or a fatal outcome, an opinion with which we concur.
In pediatric cases, even if damage to small arteries is incurred during excision,
collateral circulation will develop and the plasticity of the brain is high. In contrast, in
adult cases, there is little neovascularization and plasticity is low. It is thought that
recovery from various sequelae is likely in pediatric cases, even after complete excision,
whereas it is likely that among adults there will be some whose sequelae are severe and
permanent. We therefore believe that the dissection and excision of tumors should be
dealt with in completely different ways for pediatric and adult cases.
Figure 17.3. Drawings of coronal sections through portions of the human hy-
pothalamus.
Figure 17.4. Preoperative CT scans. A. Plain CT scan demonstrates the cystic tumor
containing a solid mass within the third ventricle. B. Enhanced CT scan, showing a
cystic tumor with a strongly enhanced mass after the injection of contrast medium.

Figure 17.5. T1 image of MRI scan. The CSF and the cystic contents appear white
(increased MRI signal). The solid part of the tumor is shown as regions of decreased
image intensity. A. Coronal scan. B. Sagittal scan.

Details of our trans-lamina terminalis approach are described within the context of
reporting a typical case of a tumor of the third ventricle. The patient was a 24-year-old
man. He had experienced fatigue and a tendency toward somnolence for about 2 years
and reported having occasionally fallen asleep in the midst of important business
meetings. He was admitted to the hospital with the complaint of headache. Both
computerized tomographic (CT) (Fig. 17.4) and magnetic resonance imaging (MRI)
(Fig. 17.5) scans showed a solid mass with a cyst extending from the suprasellar region
to within the third ventricle. Angiograms did not reveal any notable abnormalities, such
as elevation of the A1 segment. Operation was performed under a preoperative
diagnosis of craniopharyngioma developing mainly within the third ventricle.

Surgical Technique
This section gives details of the surgical removal of the tumor in the anterior part of
the third ventricle by means of a bifrontal craniotomy and an interhemispheric trans-
lamina terminalis approach.
The patient is placed in the supine position, and the head is slightly extended with the
nose pointing straight up (Fig. 17.6). The skin incision is made a few millimeters behind
the frontal hairline and is extended inferiorly on both sides, without severing the
temporal branch of the facial nerve (Fig. 17.7). The skin flap is then folded anteriorly
over the periosteum and dissection is continued as far as the upper edge of the
 Figure 17.6. Position of head.

Figure 17.7. Bifrontal scalp incision behind the hair line.

orbits. Two burr holes are drilled directly over the midline—one at the middle of the
orbital ridge and the other 5 cm superiorly. Two further burr holes are then made
bilaterally at the junction of the orbital ridge, the zygomatic process of the frontal bone,
and the linea temporalis (Fig. 17.8). Because increased adhesion of the bone to dura
mater is sometimes found in elderly patients, two additional burr holes can be made on
both sides of the upper midline burr hole, taking suitable precautions against dural
adhesion. The craniotomy is begun once the dura mater has been sufficiently separated
from the inner table of the skull. Because the frontal sinus is opened in approximately
80% of our cases (Fig. 17.9), the following procedure is also required. First, a
nonstimulating antiseptic is
 Figure 17.8. Sites of burr holes.

Figure 17.9. The frontal sinus is opened after bifrontal craniotomy.

applied to all exposed regions, including the bone flap, and treatment of the frontal sinus
is begun. While the mucous membrane within the sinus is cauterized, it is stripped from
the bone and pressed toward the channels communicating with the nasal passage. Next,
the internal bone lamina of the sinus is rongeured away, and the dead space in the sinus
is reduced. Particularly the internal lamina of the lateral portions of the sinus must be
thoroughly scraped. Because of inflammation of the mucous membrane, it may become
thickened so that excess tissue will need to be excised. For the elimination of any dead
space, bone chips or bone dust obtained during craniotomy can be packed into small
recesses and bone wax can be applied to provide a level surface without any dead space
(Fig. 17.10). Antiseptics are then applied to this surface and hands are washed. The
development of a postoperative epidural hematoma is prevented by suturing the dura
mater to the pericranial tissues at six sites anteriorly and four sites posteriorly. Opening
of the dura mater is done as far anteriorly as possible along the edge of the orbita in a
configuration that resembles a double-U or the number 3 (Fig. 17.11).
Figure 17.10. Closure of the opened frontal sinus. The cavity is filled with bone dust. A
small amount of bone wax is smeared over the sinus opening.

Figure 17.11. Opening of the dura mater and division of the anterior part of the superior
sagittal sinus and falx. A ventricular drainage tube is inserted into the frontal horn of the
lateral ventricle.

The further anteriorly that the superior sagittal sinus is divided the better, because this
sinus becomes narrower anteriorly and damage to the bridging cortical veins just beneath
the dura mater can then be avoided. This precaution allows one to preserve the bridging
cortical veins as far as possible. In incision of the dura mater, it is important when
approaching the midline region to inspect the subdural space carefully to identify the
presence of bridging veins there. If this precuation is not taken, control of various points
of hemorrhage from severed bridging veins may become difficult. When such
hemorrhage is not easily controlled, the head can be elevated to decrease the venous
pressure. Care should be taken, however, not to elevate the head excessively because the
danger of air embolism is increased correspondingly.
Bringing a halt to hemorrhage from the superior sagittal sinus is safely and easily done
by means of cauterization. Only infrequently is the sinus
 Figure 17.12. Dissection of the right olfactory bulb.

Figure 17.13. Dissection of the left olfactory bulb.

so wide that it requires closure by suturing. Moreover, because there is a danger of the
suture slipping off during or after the operation, thereby producing a massive subdural
hemorrhage, cauterization is recommended. Furthermore, if the falx is also shortened by
means of cauterization, the obstruction of the operative field is reduced. By rongeuring
the ridge of the bone 3 cm from the midline at the right-sided craniotomy, a small
incision in the dura mater beneath can be made and a ventricular catheter 3 m in
diameter can be placed within the lateral ventricle after the frontal horn has been
punctured with a Dandy cannula. The catheter is then immobilized in the subcutaneous
tissue and led on top of the scalp and immobilized there. Cerebrospinal fluid (CSF) can
then be drained
 Figure 17.14. Dissection of the right olfactory tract.

Figure 17.15. Dissection of the left olfactory tract.

through the tube, thereby reducing the total brain volume and producing a small gap
between the dura mater and the brain itself. The surgical wound is kept moist with wet
gauze and not allowed to dry out, and the entire brain surface is protected with thin
cotton pledgets.
The operation then proceeds toward the olfactory bulbs. The region of the bulb is
easily approached by elevating the head a few degrees and viewing along the orbital
surface of the brain. The arachnoid membrane and small arterioles and venules adhere to
the olfactory bulbs, making it impossible to visualize the bulb directly. By cauterizing
those small vessels, one can see the bulb itself. This process is carried out by alternating
between the two sides until both bulbs are visible (Figs. 17.12 and 17.13).
 Figure 17.16. Completion of dissection of both olfactory tracts.

Figure 17.17. Blunt dissection of the interhemispheric fissure between the frontal
lobes.
The head, which had been previously elevated, is now lowered and the dissection of
the olfactory tracts, alternating between the left and the right, is greatly facilitated (Figs.
17.14 and 17.15). If a unilateral olfactory tract is completely dissected before the start of
dissection of the other, there is the danger of avulsion of the contralateral olfactory tract.
We therefore believe that it is important to dissect bluntly the olfactory tracts in
parallel—proceeding by alternating between the left and the right sides. In the dissection
of these tracts, pressure should not be applied inferiorly, but rather in a superior
direction. Even when adhering by only a single fine fiber, inadvertent traction during the
operation can lead to
Figure 17.18. The interhemispheric dissection should proceed in an "overhanging"
manner.

Figure 17.19. Exposure of the A2 segment interhemispherically.

the complete freeing of the olfactory tract and loss of olfaction, so that no region of
adherence should be overlooked.
By further dissection the trigonal area of the olfactory tract will be reached and from
there it is safe to proceed within the substance of the frontal lobe. Sufficient dissection of
the surrounding arachnoid membrane should then be undertaken without applying
pressure to the olfactory tract. By proceeding in this manner, alternating dissection of the
left and right olfactory tracts, it is unlikely that either tract will be damaged or that they
will be a hindrance during operation.
The olfactory tract should not be allowed to become dry during the operation, and care
should be taken to prevent the adherence of moistened cotton pledgets. Moreover,
uneven pressure on the pledgets as they are placed can lead to severance of the olfactory
tract and the nerves can
 Figure 17.20. Complete dissection of both A2 segments.

Figure 17.21. Exposure of the AComA and branches of the A2 segments.

be damaged due to heat conduction as a result of the coagulation of vessels in

this region. At the completion of dissection of the olfactory tracts, a small
portion of both optic nerves should be visible beneath the arachnoid (Fig.
17.16).
Next, the position of the head is further lowered, and the left and right frontal
lobes are bluntly dissected (Fig. 17.17). A key point at this time is that the
interhemispheric dissection should be done by proceeding forward in an
"overhanging" position (Fig. 17.18). In other words, the dissection is done such
that the distal A2 segment of the anterior cerebral artery (АСА) will appear (Fig.
17.19). After both A2 segments beneath the
Figure 17.22. Complete dissection of the small perforating arteries from A1 and A2
segments or from the AComA.

Figure 17.23. If necessary for a wider operative field, the AComA and chiasm can be
divided.

genu of the corpus callosum have been exposed, dissection proceeds toward the anterior
communicating artery (AComA)—thus allowing complete dissection of the frontal lobes
with a minimum of damage to brain tissue (Fig. 17.20). Branches of the A2 segment can
then be appreciated, but they must not be sacrificed (Fig. 17.21). Sometimes it is unclear
which vessel is the A2 segment on the left and right and, in such a case, it is important to
keep note of which and how many vessels on the left and on the right have been found.
Hemostasis of venous hemorrhage can usually be achieved simply by means of
applying a cotton pledget to the bleeding vessel. Often the A2 segment on both sides will
adhere at several locations. The A2 segments should be completely separated to left and
right and the course of the
Figure 17.24. The groove left in the chiasmatic region by compression can be seen after
complete dissection of both A1 segments and the AComA from the chiasm and optic
nerves. The tumor is visible through the lamina terminalis.

Figure 17.25. Dissection of the left internal carotid artery.

perforating arteries leaving from the A1 and A2 segments or from the AComA will
become evident (Fig. 17.22). Aspiration of the contents of any cysts will greatly
facilitate the dissection of those arteries from the anterior wall of the third ventricle and
separation of the perforating arteries to the left and right will allow visualization of the
tumor beneath the lamina terminalis. In cases where a larger operative field is required
and where the AComA is large enough that two vascular clips can be
Figure 17.26. Dissection of the right internal carotid artery. Bulging of the lamina
terminalis has disappeared because the cystic contents have already been aspirated.

Figure 17.27. The hypophysial stalk can be identified posterior from the chiasm.

applied, the AComA is divided and both the A1 and A2 groups of perforating arteries are
separated to the left and right, respectively. This procedure will provide a wide operative
field. However, the clips on the AComA might detach during operation, leading to
various difficulties, so this procedure should not be used unless a wider operative field is
required.
When the color of the optic chiasm has been altered because of compression from
below or tumor cell infiltration—and thus the postoperative recovery of chiasma
functions is thought to be unlikely—
 sectioning of the midline of the chiasm will provide the widest possible operative field
(Fig. 17.23). In such cases, needless to say, bitemporal hemianopsia will remain
postoperatively.
When using the bifrontal interhemispheric trans-lamina terminalis approach, the worst
possible circumstance is damage to arterial vessels during the operation. Regardless of
how hemostasis is ultimately achieved, severe brain damage is likely to have been
incurred. For this reason, the surrounding blood vessels must be identified and dissected
from the chiasm and optic nerves until they hang completely free from one another. In
Figure 17.24, a groove can be seen alongside the chiasm and bilateral optic nerves; these
blood vessel grooves in the chiasmatic region can be seen after complete dissection of
both A1 segments and the AComA. A tumor within the third ventricle can be seen to
bulge the lamina terminalis forward. Dissection proceeds along both A1 segments as far
as both internal carotid arteries (ICAs) (Figs. 17.25 and 17.26). Because the cyst has
been aspirated, swelling of the lamina terminalis has disappeared (Fig. 17.26). In this
particular case, there was no tumor within the sella and the pituitary stalk can be seen
clearly posterior from the chiasm (Fig. 17.27).
After the blood vessels in this region have been displaced posteriorly, a small incision
in the lamina terminalis, just anterior of the AComA, is made (Fig. 17.28).
In most cases of craniopharyngioma, the tumor elevates the floor of the third ventricle,
reducing the ventricular space and allowing the flattened walls of the third ventricle to
lie against one another. Consequently, the incision in the lamina terminalis will sever
both the superior and the inferior wall. A large tumor located in the anteroinferior
portion of the third ventricle will then be visible. This component of tumor will have
been the enhanced portion on CT scans, and the cystic contents will already have been
evacuated. Further dissection should proceed painstakingly. The number of thin cotton
pledgets should be counted as they are inserted one by one between the internal wall of
the third ventricle and the tumor. This procedure causes the tumor to rise gradually
toward the lamina terminalis as a result of displacement by the cotton pieces (Fig.
17.29). At this time, simply because the tumor is visible it should not be decided to
begin excision immediately. If piecemeal tumor excision were then to begin using
forceps, the interface with normal brain tissue would not be discernible, damage to brain
would be likely, and portions of the tumor would undoubtedly be left behind. Only after
the tumor has been dissected and carefully delimited and it has been determined that
damage to brain tissue will not be incurred should excision of the tumor itself be
performed. Because of removal of tumor tissue, the ventricular space may be further
increased so that the insertion of pledgets will let the tumor rise further into the visual
field. By repeating this procedure, the tumor is made still smaller and, in the end,
complete excision is achieved (Fig. 17.30).
During the entire excision procedure, arterial bleeding must be avoided. If venous
bleeding occurs, hemostasis can always be achieved by compression with a pledget if
sufficient patience is shown. Once the tumor has been completely excised, the cerebral
aqueduct can be seen at the deepest region of the third ventricle (Fig. 17.31); inferiorly,
the basilar artery and posterior cerebral arteries, superior cerebellar arteries, and
oculomotor nerves can also sometimes be exposed. Olfactory tracts that have previously
been sufficiently dissected will be preserved using these surgical procedures (Fig.
17.32).
Figure 17.28. A small incision in the lamina terminalis is made strictly in the midline.

Figure 17.29. Removal of the tumor via the lamina terminalis. Thin cotton pledgets are
inserted between the internal walls of the third ventricle and the tumor.

In achieving complete hemostasis, one should rinse the operative field repeatedly with
normal saline. Hemorrhage during the operation will flow into the recesses near portions
of the ICA, the A1 and A2 segments, the AComA, and the M1 segment and will collect
there. In such cases, the formation of a hematoma around these vessels is likely to cause
vaso-spasm postoperatively between the 4th and the 14th days. There are cases in which
the tumor itself has been successfully removed but the
Figure 17.30. The tumor is removed piecemeal and, in the end, complete excision is
achieved.

Figure 17.31. After the removal of the tumor, the cerebral aqueduct is well visualized
through the defect in the lamina terminalis.

patient has been lost because of vasospasm, and therefore the importance of complete
hemostasis must be kept in mind.
Nonetheless, regardless of how much care is taken during operation, some blood will
work its way down posteriorly toward the deep portions of the bilateral sylvian fissures
or into the space produced by tumor excision or anteriorly toward the chiasm. To prevent
that blood from remaining, the many cotton pledgets that have been inserted during
tumor excision must now be removed—taking care that none remain
Figure 17.32. The basilar artery and both superior cerebellar arteries can be seen. The
olfactory tracts are completely preserved.

Figure 17.33. Watertight closure of the dura mater.

behind. Once all pledgets have been removed, the dural opening is closed with
interrupted silk sutures, and aron alpha adhesive is smeared over them so that the suture
line is watertight (Fig. 17.33).
Two twist drill holes are then made in the skull flap that has been removed and stay
sutures, attached to the dura mater, are brought through the drill holes. The epidural
space is made as small as possible to protect against the postoperative development of
hematoma there and to allow the skull flap to be fastened in place (Fig. 17.34). The
frontal burr holes are filled with a cranioplasty material (methyl methacrylate) for
cosmetic purposes. The tube for continuous ventricular drainage (CVD) is brought out
through a counter incision and is maintained for postoperative control of intracranial
pressure. After muscle, galea, and
Figure 17.34. The dura mater is hitched up to the middle of the bone flap with silk
passed through twist drill holes.

Figure 17.35. Scalp closure. The CVD tube is immobilized on the skin.

skin are sutured, the CVD tube is wound two full turns on the scalp and carefully sutured
at several sites—thus completing the operation (Fig. 17.35).
An incision in the flattened anterior wall of the third ventricle has been made and
considerable trauma of the third ventricle has been incurred; therefore, steroids should be
administered before operation and body weight, water, and electrolyte balance should be
checked at hourly intervals. Moreover, detailed care must be provided to prevent
gastrointestinal bleeding and various infections. Of course, intracranial pressure is con-
Figure 17.36. Principal operative approaches to a tumor of the third ventricle in each
portion of the ventricle.

trolled by means of CVD, but a 2-week limit is recommended because of the danger of
infection, after which the CVD tube should be removed and a shunt operation should be
performed if intracranial pressure remains high.
CT scanning 1 week postoperatively confirmed complete removal of the tumor (Fig.
17.36). The postoperative status of this patient is satisfactory and he is now reappointed
as a computer technologist.

Indications
This approach is suitable for tumors of the anterior part of the third ventricle,
especially for tumors that develop anteriorly from the line joining the anterior ridge of the
foramen of Monro and the cerebral aqueduct. For tumors developing from the pineal
region, complete excision by opening only the lamina terminalis is not possible (Fig.
17.37).
Among tumors that grow mainly within the third ventricle, there are optic gliomas,
pituitary adenomas, Craniopharyngiomas, meningiomas, cavernous angiomas, and
arteriovenous malformations. In the case of suprasellar mass lesions that displace the
third ventricle inferoposter-iorly, however, this approach produces a wide operative field
and consequently good operative results without incurring any damage to the brain tissue
itself. For example, this approach is indicated in cases of giant suprasellar meningioma,
giant AComA aneurysm, and giant olfactory groove meningioma—for any of which
opening of the lamina terminalis is not required. Moreover, we use a bifrontal
interhemispheric approach in all cases of AComA aneurysm. The degrees of invasion and
of adhesion to the tissue surrounding the third ventricle can be anticipated by means of
MRI-CT scans, and total excision is never attempted when such adherence or invasion is
severe. It is also important that rigorous endocrine testing has been done preoperatively,
so that replacement of hormone can be begun before operation. Particularly
glucocorticoid replacement should be begun on the day before the operation.
The following are brief descriptions of three cases in which this approach was used for
the excision of a mass lesion.
Case 1
The patient was a 60-year-old man with a giant pituitary adenoma growing within the
third ventricle (Fig. 17.38A). The chief complaint was bitemporal hemianopsia.
Complete excision was done using this approach. Postoperatively transient diabetes
insipidus and hypernatremia appeared, but he was discharged in excellent condition after
2 months. Postoperative CT scan showed no residual tumor (Fig. 17.38B).
Figure 17.37. Postoperative CT scan shows total removal of the tumor. A. Axial scan.
B. Coronal scan.

Figure 17.38. Case 1. CT scans with contrast medium enhancement. A. Preoperative CT

scan showing a giant tumor of the third ventricle. B. Postoperative CT scan showing that
the tumor has been totally removed.
Figure 17.39. Case 2. CT scans with contrast medium enhancement. A. Preoperative CT
scan showing a tumor in the anterior region of the third ventricle. B. Postoperative CT
scan showing that the tumor shadow has disappeared.

Case 2
The patient was a 40-year-old man with a cavernous angioma in the seat ot the left
wall of the third ventricle (Fig. 17.39Л). He suffered from polydipsia, polyuria, and right-
sided homonymous hemianopsia. With the bifrontal trans-lamina terminalis approach, the
lamina terminalis was opened, revealing a conglomerate vascular tumor directly below.
The tumor was surrounded by a mudlike substance thought to be an old hematoma. These
findings suggested the occurrence of several previous hemorrhages within the lesion. The
tumor was totally excised and the patient was discharged in excellent condition (Fig.
17.39B).
Case 3
The patient was a 26-year-old man with an arteriovenous malformation extending
along the anterior wall of the third ventricle, along the medial walls of the frontal horns
of the lateral ventricles, and along the entire length of the corpus callosum (Fig. 17.40A).
With the same approach, the third ventricle was entered via the lamina terminalis to
reveal an irregular, bumpy internal surface of the third ventricle caused by the abnormal
vessels. The draining vein poured into the galenic vein, which courses on the superior
surface of the third ventricle. A silver clip was placed to the draining vein and total
excision of the arteriovenous malformation nidus of the lateral and third ventricles was
performed. Next the head was extended extremely and the abnormal vessels leaving both
A3 segments of the АСА along the corpus callosum were cauterized one by one (Fig.
17.40B). By making use of this head position when performing bifrontal craniotomy, it is
possible to observe from both sides of the falx as far as the posterior portion of the corpus
callosum.
Figure 17.40. Case 3. A. The angiogram before operation showing an arteriovenous
malformation at the third ventricle and corpus callosum. B. The angiogram after
operation showing disappearance of the arteriovenous malformation.

Summary
Advantages
The advantages of the bifrontal interhemispheric trans-lamina terminalis approach can
be summarized as follows.
1. The operative field is extremely wide, allowing visualization of all of
the important nerves and blood vessels at the base of the brain, including
the anterior half of the circle of Willis, both A2, M1 and M2 segments and
the perforating branches leaving from those segments, the olfactory
nerves, the optic nerves, etc. With the conventional unilateral subfrontal
approach these important structures are behind in a dead angle, and it
is more difficult to remove a tumor from the contralateral half of the
third ventricle.
2. No damage is done to the brain tissue, except the lamina terminalis
itself which, depending upon the nature of the tumor, is often widened
and thinned and shows reduced functional capacities.
3. When necessary, the AComA can be divided and, under some cir
cumstances, the optic chiasm can also be cut, providing a still larger
operative field.
 4. This approach is suitable not only for tumors within the third ventricle, but also for
many other lesions located on the midline of the anterior fossa.
Disadvantages
The disadvantages of this approach can be summarized as follows.
1. Treatment of the frontal sinus must be done with extreme caution
to prevent infection.
2. Additional care is needed when the superior sagittal sinus has been
divided.
3. Care must be taken to preserve the olfactory nerves (14).
These three points are not thought to be insurmountable demerits of the trans-lamina
terminalis approach and complications using this approach are in fact rare.
Pitfalls
Pitfalls that we have experienced during operations using this approach include the
following.
1. In elderly patients, there is sometimes severe adhesion of the bone
to the dura mater and damage to the dura mater may be incurred during
craniotomy.
2. The use of a large amount of bone wax to reduce the dead space of
the frontal sinus may result in an aseptic epidural abscess.
3. When the superior sagittal sinus has been cut and ligated with
sutures, the ligation of the severed end may become loosened during
operation or after closure of the dura mater and a large hemorrhage from
the venous sinus may occur.
4. When two clips have been placed on both severed ends of the
AComA, either clip may slip off during operation and control of the
subsequent hemorrhage from the AComA may be difficult.
5. A perforating branch may become separated from its trunk artery,
causing severe hemorrhage.
Complications
Finally, with regard to postoperative complications, the following points should be
mentioned.
1. Diabetes insipidus should be considered a virtual inevitability. It is
consequently essential to measure the urine output at 1-hour intervals
during and after operation and to check the water and electrolyte balance,
serum osmolality, etc. Before the appropriate period has been lost, des
mopressin acetate should be administered, thereby maintaining an ap
propriate water and electrolyte balance.
In pediatric cases, the diabetes insipidus is always transitory, whereas symptoms in
adults may be prolonged.
2. Gastrointestinal bleeding is rare when the trans-lamina terminalis
approach is used, but administration of cimetidine to protect against that
possibility is recommended.
3. Adrenal shock is also infrequently encountered, but steroids are
normally given starting preoperatively and continuing for 2 or 3 weeks
postoperatively. Care must be taken in the gradual reduction of the steroid
dose.
4. Intracranial pressure increases due to acute hydrocephalus. The
CVD instituted during operation should be continued postoperatively to
control intracranial pressure. In those cases where the pressure remains
high for 2 weeks postoperatively, control can then be obtained by means
of a shunt operation.
 5. Infection is a relatively frequent occurrence after operation of the
third ventricular region. Because steroids are also used postoperatively,
the administration of antibiotics is recommended as a preventive
measure.
6. CSF leakage may occur. There is often slow healing of the wound
after complete excision of a tumor in this region and CSF leakage from
the site of the scalp closure can easily occur. Because such leakage can
lead to infection, it is essential to make the dura closure completely
watertight.
These complications can normally be overcome in children, but may prove more
difficult in some adult patients.
References
1. Cabezudo JM, Vaquero J, Areito E, Martinez R, Sola RG, Bravo G: Cranio
pharyngioma: A critical approach to treatment. J Neurosurg 55:371-375,
1981.
2. Danoff BF, Cowchoch FS, Kramer S: Childhood craniopharyngioma: Survival,
local control, endocrine and neurologic function following radiotherapy. Int
J Radiat Oncol Biol Phys 9:171-175, 1983.
3. Ghatak MR, Hirano A, Zimmerman HM: Ultrastructure of craniopharyn
gioma. Cancer 27:1465-1475, 1971.
4. Gordy PD, Peet MM, Kahn BA: Surgery of craniopharyngioma. J Neurosurg
6:503-517, 1949.
5. Grant FC: Surgical experience with tumors of pituitary gland. JAMA
136:668-672, 1948.
6. Hoffman HJ< Hendrick EB, Humphreys RP, Buncic JR, Armstrong DL, Jenkin
RDT: Management of craniopharyngioma in children. J Neurosurg 47:218-
227, 1977.
7. Ingraham FD, Matson DD, McLaurin RL: Cortisone and ACTH as an adjunct
to the surgery of Craniopharyngiomas. N Engl J Med 246:568-571, 1952.
8. Kubota T, Yamamoto S, Kohno H, Ito H, Hayashi M: Operative procedures of
craniopharyngioma estimated by autopsy findings. Neurol Med Chir 20:341-
354, 1980 (in Japanese).
9. Lewis DD: A contribution to the subject of tumors of the hypophysis. JAMA
55:1002-1008, 1910.
10. Love JG, Marshall TM: Craniopharyngioma (pituitary adamantinoma). Surg
Gynecol Obstet 90:591-601, 1950.
11. Northfield DWC: Rathke-pouch tumors. Brain 80:293-312, 1957.
12. Shillito J: Paediatric Neurological Surgery. New York, Raven Press, 1978.
13. Shillito J: Craniopharyngiomas: The subfrontal approach, or none at all. Clin
Neurosurg 27:188-205, 1980.
14. Suzuki J, Yoshimoto T, Mizoi K: Preservation of the olfactory tract in bifrontal
craniotomy for anterior communicating artery aneurysms, and the functional
prognosis. J Neurosurg 54:342-345, 1981.
15. Suzuki J, Katakura R, Mori T: Interhemispheric approach through the lamina
terminalis to tumors of the anterior part of the third ventricle. Surg Neurol
22:157-163, 1984.
16. Sweet WH: Radical surgical treatment of craniopharyngioma. Clin Neurosurg
23:52-79, 1976.
18
Pterional Approach
George T. Tindall, M.D., and Suzie C. Tindall, M.D.

For more than 20 years the pterional (frontotemporal) approach has been used for the
surgical exposure and treatment of aneurysms located on the anterior portion of the circle
of Willis. Only in recent years has this approach become popular for exposing other
lesions situated in the suprasellar and parasellar regions. In 1972 Krayenbuhl et al. (4)
reported a series of 250 patients with cerebral aneurysms operated upon utilizing
microsurgical techniques. The good results achieved—83% of the entire series and 94%
of patients who were Grades 1, 2, or 3 preoperatively— showed the importance of
microsurgical techniques in the modern management of intracranial aneurysms. In their
publication, which emphasized a number of important principles of aneurysm
management, the authors described their relatively small osteoplastic frontotemporal cra-
niotomy with the bone flap centered on the pterion. Although this bony opening seems
relatively small compared to some of the bone flaps used in earlier years to expose
aneurysms and other lesions in the vicinity of the chiasm, when used with the operating
microscope and appropriate partial removal of the sphenoid bone it serves the purpose of
providing excellent exposure of the chiasmal region. As Krayenbuhl et al. (4) com-
mented, aneurysm exposure was achieved at the expense of the subarachnoid space and
the bony floor of the anterior fossa rather than by undue retraction of the brain. Also, in
this publication the authors described the use of a self-retaining retractor that ensured a
constant but minimal amount of retraction, a distinct advantage over the inconsistent and
sometimes dangerous use of hand-held brain retractors.
In 1975, Yasargil and Fox (8) reported their impressive results in 505 patients
operated upon for aneurysm. They described the pterional approach in considerably more
detail. Although it is difficult to assign any specific individual credit for developing the
pterional approach, it is certainly appropriate to give special mention to Yasargil for
providing the details and popularizing this particular approach.
The pterional approach described by Krayenbuhl and Yasargil resembles very closely
the anterior craniotomy approach described by Dandy for aneurysms on the anterior
portion of the circle of Willis. In his
excellent publications on the surgery of intracranial aneurysms (2, 3) he described a
craniotomy that with minor modifications could be considered an early version of a
pterional approach. In the procedure described by Dandy, the head was turned to the
opposite side and a concealed, curved anterior frontal skin incision within the hairline
was made. The extent of the bone flap removal was such that the sylvian fissure,
anterior temporal lobe, and lateral inferior frontal lobe were exposed. Dandy's approach
to the aneurysm was made by upward retraction of the inferior portion of the frontal
lobe, essentially the same procedure used in the modern pterional approach. His bone
flap was much larger than the one currently used and no attempt was made to drill the
sphenoid flush so as to provide deep exposure with minimal retraction. The major
difference between Dandy and modern neurosurgeons is, of course, the current use of
microtechniques, which were not available to Dandy and other neurosurgeons of his era.
In 1981, Rhoton et al. described a number of operative approaches to the third
ventricle, among them a frontotemporal approach that is similar to the pterional
approach for aneurysms except that it is extended further posteriorly into the temporal
region (6). These authors recommended this latter approach only if a tumor involving
the third ventricle was centered lateral to the sella or extended into the middle cranial
fossa. Symon advocated the use of a midtemporal approach, which is essentially a
pterional approach with temporal extension, for the operative removal of
Craniopharyngiomas (7). Based on 100 cases, he thought that this approach, which
provides access to lesions behind the optic nerves, makes it possible to achieve effective
tumor removal.
The pterional approach is used most frequently today for aneurysm surgery. It does,
however, have a place in the surgical treatment of lesions in the suprasellar and inferior
third ventricular regions. In general, the remaining comments in this chapter apply to
nonaneurysmal lesions accessible by the pterional approach.

Indications for the Pterional Approach

The pterional approach has limited application for lesions in or about the third
ventricle. From an anatomical standpoint, suprasellar and parasellar lesions that are
located within the cross hatched area in Figures 18.1 and 18.2 can be adequately reached
and surgically managed through a pterional approach. As shown in the coronal view
(Fig. 18.1), suprasellar lesions that extend laterally into the anterior and middle cranial
fossae are particularly suitable for the pterional approach. There is no limit to the lateral
tumor extension that can be managed by the pterional approach if the lateral extension is
ipsilateral to the surgical flap. The area depicted in the sagittal view (Fig. 18.2) extends
from the planum sphenoidale anteriorly to the basilar artery caudally and vertically from
within the sella to a point approximately 1.5 to 2.0 cm directly above the diaphragma
sellae.
From the standpoint of pathology, a variety of lesions can be expected in this
anatomical area and all are suitable for attempted excision by this approach. In many
instances an exact pathological diagnosis will not be apparent until frozen section
examination of biopsy material at the time of operation. A list of possible lesions
encountered in this area is shown in Table 18.1. In clinical practice, the most common
neoplastic lesions are Craniopharyngiomas and pituitary adenomas and the most
common vascular lesion is an aneurysm. However, the anatomical location of the lesion
in question is the primary concern in the choice of the pterional
Figure 18.1. Coronal view showing the region of parasellar access via the left pterional
approach.

Figure 18.2. Sagittal view showing the region of ideal access: from the planum
sphenoidale anteriorly to the basilar artery posteriorly; from the sella to 2.0 cm superior
to the diaphragm.
approach. Many of the lesions mentioned in the table are better handled by alternative
exposures if they extend outside the designated anatomical area.

Contraindications
Contraindications to the operative procedure are both general and specific. General
contraindications are those that mitigate against any major operative procedure and
include poor health, an unstable medical condition, or a septic process anywhere in or on
the body. Advanced age (i.e., >65 years) in itself is not a contraindication as long as the
patient's general health and medical condition are both good.
The only specific contraindication to the pterional approach would be in patients in
whom the lesion is primarily out of the region cross hatched in Figures 18.1 and 18.2.
This would include lesions that appear on computerized tomographic (CT) scan or other
diagnostic studies to be predominantly within the third ventricle (although a lesion
mainly in the third ventricle but with definite exophytic extension into the aforemen-
tioned cross hatched area can at least be biopsied and thus positively identified using the
pterional approach). Other circumstances that may be encountered, particularly invasion
of the cavernous sinus, do not, in our opinion, contraindicate the pterional approach.
Although a gross total excision of the lesion may not be possible in this latter situation,
nonetheless, a positive tissue diagnosis and a partial resection of a tumor can be
accomplished via a pterional approach.

Preoperative Evaluation
Patients presenting with lesions in or immediately below the inferior third ventricle in
an anatomical location suitable for the pterional approach will usually present with signs
or symptoms referable to increased intracranial pressure or ophthalmological or
neuroendocrine disorders (Table 18.2). It is important that the preoperative assessment
of each patient be individualized depending on age, duration of symptoms, major
complaints, etc., rather than applying a rigid protocol to each patient with a suspected
lesion in the suprasellar region.
Symptoms of increased intracranial pressure include nausea, vomiting, headache,
apathy, and lethargy and are usually progressive. These symptoms usually follow the
development of hydrocephalus due to obstruction of cerebrospinal fluid (CSF) flow
through the third ventricle. However, increased intracranial pressure may also simply
reflect the volume of the tumor or the amount of peritumoral edema. Headache may
occur in isolation and may be due to dural involvement at the skull base or irritation of
the fifth cranial nerve within the cavernous sinus.
 Ophthalmological involvement is common with lesions in the suprasellar region.
Visual acuity may be compromised in one or both eyes by either intrinsic (e.g., optic
glioma) or extrinsic lesions. An afferent pupillary defect (Marcus-Gunn pupil) may
accompany the diminished acuity. The type of visual field defect may give some hint of
lesion localization within the suprasellar area. A defect confined to one eye suggests
anterolateral localization compromising a single optic nerve; a junctional sco-toma
suggests anteromedial localization with compromise of the optic nerve at the anterior
chiasm; bitemporal superior quandrantanopsia or hemianopsia implicates chiasmal
compression from below; and a congruous homonymous hemianopsia suggests more
posterior involvement of the optic tract. Cavernous sinus invasion may be associated
with involvement of the third through sixth cranial nerves.
The large number of hypothalamic syndromes that can result from pathological
involvement of this structure include disorders of consciousness and sleep, cognition,
emotional behavior and affect, autonomic balance, caloric balance, and water-osmolar
balance. As a detailed discussion of these syndromes is beyond the scope of this chapter
the reader is referred to more definitive references, such as the publication of Plum and
Van Uitert (5).
Endocrinological involvement usually consists of varying degrees of hypopituitarism
due in most instances to involvement of the region of the median eminence or pituitary
stalk rather than to actual damage to the pituitary gland itself. This is understandable in
view of the fact that the portal venous system that traverses the stalk is the major
vascular supply of the adenohypophysis. Thus, interruption of the stalk results in
extensive necrosis of the anterior pituitary. Also, varying degrees of diabetes insipidus
(DI) can result from stalk impairment. Interestingly, in a patient with DI the subsequent
development of hypopituitarism is associated with significant amelioration of the DI.
The improvement is attributable to the low rate of glomerular filtration resulting from
growth hormone and adrenal steroid deficiencies and increased tubular resorp-
tion of water due to adrenal insufficiency. The clinical findings associated with
hypopituitarism are due to deficiencies in pituitary-target organ endocrine function and
are outlined in Table 18.2.

Endocrinological Testing
Endocrinological evaluation is important in patients with parasellar and suprasellar
lesions for the following reasons: (a) to determine whether there is deficient pituitary
function; (b) to monitor the effects of therapy (e.g., either a loss or a return of function
as a result of operation); and (c) to aid in following the status of a lesion in terms of
progressive growth or recurrence. It is important to assess the status of the pituitary-
adrenal and pituitary-thyroid axes before performing invasive diagnostic studies and
surgical procedures. Any deficiency in these axes should be replaced and, in the case of
the pituitary-adrenal axis, not only replaced but supplemented significantly before,
during, and immediately after invasive diagnostic and surgical procedures. The stress of
a major procedure in a patient with an undetected deficiency of endogenous adrenal
steroids can provoke an Addisonian crisis during the postoperative period which can, in
turn, be fatal unless recognized and treated quickly and appropriately.
Minimal endocrine testing for patients with lesions in the suprasellar region includes
an evaluation of the pituitary-target organ axes; tests recommended for this purpose are
listed in Table 18.3. From these data, pituitary endocrine function can be evaluated.
Additionally, in a patient in whom there is DI or a suspicion of DI, a water deprivation
test to evaluate antidiuretic hormone or vasopressin reserve should be performed. Also,
serum prolactin levels in patients with suprasellar lesions should be determined for two
important reasons. First, the suprasellar lesion in question and for which operation is
planned may be a pituitary tumor that secretes prolactin, a so-called prolactinoma. In
these cases levels of serum prolactin are usually in excess of 150 ng/ml and may even
exceed 1000 ng/ml. The second and a more likely cause for the elevated prolactin is
related to the "stalk phenomenon." The "stalk phenomenon" is that situation which
results when prolactin inhibitory factor (PIF), which is conveyed in the portal system, is
prevented from reaching the normal adenohypophysis. Structural lesions that compress
the pituitary stalk interfere with the delivery of PIF, a substance thought to be dopamine,
thus allowing the normal adenohypophysis to secrete an ex-
cess of prolactin. In these instances, prolactin levels are usually in the range of 70 to 100
ng/ml and should not exceed 150 ng/ml. Structural lesions (other than a prolactinoma)
that elevate serum prolactin by this mechanism are referred to as pseudoprolactinomas.

Tumor Markers and CSF Cytology

The presence of alpha-fetoprotein (AFP) or the beta subunit of human chorionic
gonadotropin (HCG) in the lumbar CSF may help to predict the pathological diagnosis
of a suprasellar mass. Elevated levels of CSF HCG are frequently seen in patients with
suprasellar germinomas, and elevated CSF levels of AFP have been reported in patients
with malignant teratomas that have yolk sac elements within them. If a germinoma is
suspected CSF cytological examination may give positive identification.

Neuroradiological Studies
Neuroradiological studies have changed significantly over the past several years and,
in general, have become more accurate from a diagnostic standpoint and safer and less
painful for the patient. CT scanning has made a major impact on neurological diagnosis
and has replaced procedures such as pneumoencephalography and polytomography. The
latest diagnostic breakthrough, magnetic resonance imaging, is almost certain to play a
major role in the treatment of these suprasellar lesions, but sufficient experience has not
yet accumulated to define its role.
Currently, recommended neurodiagnostic studies for patients with suprasellar lesions
include anteroposterior and lateral skull films and high resolution CT scans in both axial
and coronal views. A contrast-enhanced scan should be part of the routine CT
examination. Although not a routine procedure, conventional cerebral angiography or
high quality arterial digital angiography should be performed in patients with suprasellar
lesions if there is any doubt as to the pathological nature of the lesion from a review of
the skull x-ray films and CT scan and to determine the degree of vascularity of the
lesion. Vascular lesions and the extent of vascularity of certain tumors can only be
accurately defined by conventional angiography or high quality arterial digital
angiography. In our opinion, digital intravenous angiography does not provide adequate
quality imaging of these lesions.
In some patients, special studies such as metrizamide cisternography (MC) and
cavernous sinus venography (CSV) may be helpful in further defining the boundaries or
invasiveness of a lesion. In our opinion, MC may be indicated in patients with a
relatively small suprasellar tumor associated with a normal-sized sella turcica. In some
instances, we have found that the metrizamide study provides a more accurate depiction
of the boundaries of the lesion and its relationship to surrounding normal structures than
can be obtained from a routine CT scan. MC involves a lumbar puncture using a #22
gauge needle. After satisfactory placement of the needle tip in the subarachnoid space, 5
ml of metrizamide (190 mg/ml) is injected slowly. The contrast medium is allowed to
enter the basilar cisterns by gravity by placing the patient in a 60° Trendelenberg
position for 2 minutes. CT scans are then obtained using serial sections 5 mm thick in
both sagittal and coronal planes.
CSV, which is a rarely used procedure, is accomplished by transfemoral venous
catheterization of the inferior petrosal sinus and may help to determine whether the
cavernous sinus is invaded by tumor. It is relatively uncomfortable for the patient and
the amount of valuable diagnostic information provided by the test often leaves much
to be desired.
Technical Aspects of the Pterional Approach to Inferior Third Ventricular and
Parasellar Lesions
Before planning the procedure the surgeon should have adequately evaluated several
important factors about the patient. These include (a) the exact anatomical position of
the lesion in question; (b) the degree of extension, if any, into the frontal fossa, the
middle fossa, or the retroclival area and on which side; (c) the relationship of the lesion
to the major surrounding anatomical structures such as the optic nerves and chiasm, the
internal carotid artery and its major branches, the basilar artery, and the cavernous sinus;
and (d) the status of the intracranial pressure (ICP); i.e., whether normal or elevated. If
elevated, it is important that the cause of the elevation—hydrocephalus, mass effect, or
peritumoral edema—be identified so that an appropriate treatment program can be
considered or instituted before a definitive pterional approach to the lesion.
Preoperative Considerations
Once the exact anatomical position of the lesion has been ascertained and it has been
determined that the pterional approach is the appropriate surgical procedure for the
lesion in question, the surgeon must decide from which side the approach will be made.
If the lesion has significant lateral extension into the frontal or middle fossa, it should be
approached from the side of maximal lateral extension. If this is not a determining
factor, the lesion should be approached from the side of maximal visual loss. If neither
of these rules apply, we prefer to operate from the side of the nondominant hemisphere,
generally the right side.
If the patient has significant hydrocephalus and there is doubt that the parasellar lesion
can be resected completely, we advise performing a ventriculoperitoneal shunting
procedure at least several days before the definitive craniotomy. If the foramen of
Monro is compromised by the lesion, biventricular shunting is carried out. Careful
planning is necessary for placement of the shunt catheters and tubing so that the
incisions and the course of the tubing will not interfere with the pterional approach. If a
right pterional approach is planned, we position the left ventricular catheter
transfrontally and the right ventricular catheter transparietally, situating Rickham
reservoirs within the holes used for passage of the catheters and joining the distal
drainage tubing of both systems through a "T" connector above a suitable valve situated
beneath the mastoid fascia behind the right ear. This leaves the right frontal area free of
tubing at the time of definitive craniotomy (Fig. 18.3).
If there is significant peritumoral edema or tumor mass effect the patient is pretreated
with relatively high doses of steroids (6 to 10 mg of dexamethasone QID or the
equivalent) for several days before the definitive surgical procedure. We do not use
prophylactic anticonvulsants preoperatively unless a cortical resection is planned or the
lesion in question has invaded cortical structures.
In view of current cost containment awareness, routine type and cross match of the
blood of patients undergoing craniotomy by the pterional route are not performed unless
the lesion has the potential for rapid blood loss (e.g., meningioma, arteriovenous
malformation, aneurysm, etc.).
The patient undergoes a thorough shampoo with Betadine or a comparable antiseptic
soap on the night before the procedure, and the surgical area on the scalp is shaved
immediately before transport of the patient to the operating room. Usually, only that area
of the patient's scalp around the planned scalp incision is shaved.
Perioperative antibiotic coverage is not used as a routine unless: (a) the
Figure 18.3. Representation of biventricular shunt placement designed to facilitate right
frontal craniotomy.

patient has been previously shunted or has other previously implanted foreign bodies
(heart valves, vascular grafts, etc.); (b) it is anticipated that the operative procedure will
last longer than 5 hours; (c) the patient has a large frontal sinus that will be entered
during the procedure; or (d) the patient requires cardiac prophylaxis because of previous
rheumatic fever.

Patient Positioning
In most instances the patient can be placed in the supine position with a soft roll under
the ipsilateral shoulder. However, if the patient has a short, relatively nonflexible neck
or if significant neck turning might compromise jugular venous return, the lateral
decubitus position is used.
If the lesion is large, there is significant peritumoral edema, or there is some other
reason to believe that brain retraction will be difficult, a lumbar subarachnoid catheter or
18 gauge lumbar puncture needle may be inserted before positioning the patient. A
drainage bag with stopcock for on/off control by the anesthesiologist is connected to the
needle or indwelling catheter. During the dural opening and particularly during
elevation of the frontal lobe, the catheter can be opened to allow CSF to
 Figure 18.4. Fixation points of headrest before final positioning.

drain slowly. This procedure considerably facilitates exposure to the region of the
chiasm.
Placement of the head in a three-point skull fixation clamp is necessary to prevent any
unwanted head movement throughout the procedure. The device is applied with the
single pin in or near the midline on the forehead and the remaining two pins straddling
the occiput (Fig. 18.4). The head is then positioned appropriately for the approach.
Usually, the sagittal plane of the head is parallel to the floor with the pterion uppermost.
However, if the approach is to be directed more anteriorly into the frontal fossa or
retrochiasmatic region the forehead may be depressed slightly. If there is to be
significant dissection in the region of the tentorial hiatus and in subtemporal regions,
the vertex may be depressed slightly; if an approach to the basilar artery or supraclival
region is contemplated, the forehead may be elevated slightly.
Operative Procedure
Once the patient has been suitably positioned the scalp incision is planned before the
application of drapes. The usual incision is begun 1 cm anterior to the tragus of the ear
just at the zygomatic arch and is extended up just behind the hairline to the midsagittal
plane 3 cm anterior to the coronal suture. As depicted in Figure 18.5, the scalp incision
may be varied so as to permit more frontal exposure by bringing it across the center of
the head in a curvilinear fashion (this is cosmetically preferable to curving it down over
the forehead in front of the hairline) or to permit more temporal exposure by gently
curving it farther back above the ear and then proceeding in a frontal direction. Once the
planned incision is marked, the head is scrubbed with Betadine soap and reprepared
with Betadine solution and sterile towels and draping are applied circumfer-entially.
The use of a plastic shield such as Vi-drape isolates the exposed skin from the surgical
field. In most instances we inject lidocaine with 1:100,000 epinephrine subcutaneously
before making the scalp incision to aid in scalp hemostasis. Raney clips are used along
the scalp edges.
It is important to limit the amount of dissection in the subgaleal space between the
galea and the temporalis fascia anteriorly so as to avoid injuring the frontalis branch of
the facial nerve. With the electrocautery,
Figure 18.5. Variability of scalp incision to permit greater frontal or temporal
exposure.

the temporalis fascia and muscle are incised immediately beneath the scalp incision and
all layers are turned forward as a unit (Fig. 18.6). The temporalis muscle is dissected off
the skull far forward to the orbitofrontal angle and the superior orbital ridge and low
over the temporal fossa. The muscle can be retracted to achieve maximal exposure with
the use of rubber-banded sutures or fishhooks. A self-retaining retractor is used to
spread the superior aspect of the incision.
While turning the scalp and bone flaps, we administer 30 to 50 g of mannitol (20%
solution) i.v. If there is a possibility that increased ICP might be a significant problem,
40 mg of furosemide is also given. The arterial pCO2 is kept in the range of 25 to 30
torr during the procedure and the patient is paralyzed and mechanically ventilated.
The exact position of the bone flap will again depend upon the need for maximal
exposure in certain areas. The standard flap, as depicted in Figure 18.7) is usually
fashioned with four burr holes, one at the orbitofrontal angle, one over the middle of the
coronal suture, one in the midtemporal region, and one low in the temporal fossa. The
size of the flap is dictated somewhat by the surgeon's estimate of the amount of
retraction necessary for appropriate exposure of the lesion. It is better to err on the side
of the larger flap than to have to revise the flap during the procedure. For more
exposure in the subfrontal or perichiasmatic region the flap can be expanded anteriorly
by placing an additional hole over the supraorbital ridge. The presence of a large frontal
sinus with more than the usual amount of lateral extension that would obviously require
entry to achieve a pterional bone flap with an anterior extension is not a
contraindication to the use of this approach. In these cases, we would proceed to enter
the sinus, exenterate as much mucosa as feasible, and pack off the remainder of the
sinus with either muscle or adipose tissue held in place with dural tack-up sutures. For
more temporal exposure the single midtemporal hole can be replaced by two holes
placed more pos-
Figure 18.6. A. Incision with respect to bony landmarks. B. Course of the frontalis
branch of the facial nerve; dissection of the subgaleal space anteriorly should be limited.
C. The temporalis fascia and muscle are reflected as a unit.

teriorly. The options for bone flap placement are indicated in Figure 18.7. We prefer to
connect the orbitofrontal and subtemporal holes by ron-guering a channel between them
before completing the flap with the pneumatic craniotome. This permits better control of
the sometimes vascular sphenoid ridge and avoids inadvertent dural tears from the use
Figure 18.7. Burr hole placement in reference to bony landmarks with options for
increasing frontal or temporal exposure.

of the craniotome in the irregular terrain of the sphenoid ridge. Once the flap is
elevated, the dura mater is tacked up to small holes previously drilled obliquely in the
bone edges. Attention is then directed to the sphenoid ridge.
The lateral aspect of the sphenoid ridge is drilled away flush with the frontal fossa
(Fig. 18.8). This maneuver is combined with a small subtemporal craniectomy. The
importance of this aspect of the procedure cannot be overemphasized. If accomplished
correctly it provides for much better visualization of the deep structures and less
necessity for brain retraction later in the procedure.
The usual dural opening is shown in Figure 18.9. The initial opening
Figure 18.8. A combination of temporal craniectomy (A) and excision of the sphenoid
wing (B) develops a basal pterional exposure (C).

is curvilinear, 1.5 to 2 cm back from the sphenoid ridge, and the small dural flap is
tacked back over the ridge. Several cruciate incisions are made in the dura mater
overlying the frontal and temporal lobes. These dural flaps can be left in place for a
modest amount of brain protection during the remainder of the procedure. At this point
we place moist gauze sponges and cottonoids strategically over the exposed flap to
prevent excessive drying of the tissues and thrombin-soaked gelatin sponge with
cottonoids along the bone flap circumference to prevent oozing into the wound during
the remainder of the procedure.
 Figure 18.9. Dural opening.

A self-retaining retractor system of the surgeon's choice is set up (Fig. 18.10). Two
retractors, a frontal and a temporal, are generally used. The frontal is usually the wider
of the two retractors. Strips of moist cottonoid can be used between the brain and the
retractors. The frontal blade is carefully placed beneath the frontal lobe and gently
advanced, exposing first the ipsilateral olfactory nerve and then the optic nerve at the
anterior clinoid process (Fig. 18.11). The temporal blade is used for gentle retraction of
the anterior-superior temporal lobe. As this retractor is advanced, one needs to
visualize, coagulate, and incise any bridging veins from the surface of the temporal
lobe. A bridging vein torn later in the procedure because this step was not
accomplished adequately at the outset can be a source of frustration for the surgeon.
We prefer to use magnifying loupes of 2 or 2.5X for all parts of the procedure
described to this point. Once the retractors are set, the operating microscope is brought
into the field and used throughout the rest of the operation until closure is begun.
The microsurgical anatomy encountered during the pterional approach is depicted in
Figure 18.12. It is convenient to think of this anatomy in terms of three triangles—
frontal, middle, and posterior. The frontal triangle is that area bounded by the two
anterior limbs of the optic chiasm and the tuberculum sellae. The middle triangle is
bordered by the poster-olateral aspect of the ipsilateral optic nerve, the anterolateral
aspect of
Figure 18.10. Self-retaining retractor blades are applied along frontal and temporal
vectors.

the ipsilateral internal carotid artery, and the A1 segment of the anterior cerebral artery.
The posterior triangle is defined by the posterolateral aspect of the ipsilateral internal
carotid artery, the tentorial edge, and the retracted temporal lobe.
Working over the frontal retractor the surgeon first exposes the ipsilateral optic nerve
and the infrachiasmatic cistern by gentle dissection of the surrounding arachnoid. Entry
into the interchiasmatic region, or the frontal triangle, frequently results in a substantial
egress of spinal fluid, which facilitates brain relaxation. Moving the frontal retractor
posteriorly and after more arachnoidal dissection in the middle triangle the internal
carotid artery comes into view lateral and posterior to the optic nerve. With the addition
of temporal retraction, the tentorial edge, third cranial nerve, posterior communicating
artery, and interpeduncular cistern can be explored in the posterior triangle. With
slightly more retraction with the frontal retractor the anterior choroidal artery and the A1
segment of the anterior cerebral artery can be exposed. Working between and around
these structures it is possible to visualize adequately the anteromedial portion of the
contralateral optic nerve, the diaphragma sellae, the infundibulum, the contralateral
internal carotid artery, the ipsilateral posterior clinoid process, the superior portion of the
clivus, and the basilar artery.
The anatomical appearance may be altered significantly depending upon the
pathological condition in the area. In Figure 18.13 a cyst of a suprasellar
craniopharyngioma presenting itself in the interchiasmatic region spreading the optic
nerves apart is shown. Figure 18.14 shows the more solid part of this tumor as it
insinuates itself between and around the structures of the middle and posterior triangles.
Mass effects of such
Figure 18.11. A. The frontal blade is advanced to identify first the ipsilateral olfactory
nerve. B. Next, the anterior clinoid process and optic nerve are appreciated. C. The
temporal blade is advanced to enhance the lateral carotid exposure.

lesions may significantly distort and dislocate normal anatomical structures.

If the pathological character of the lesion is not immediately apparent upon initial
inspection, the surgeon should consider needle aspiration using a 20 gauge spinal
needle on a small syringe. If this maneuver is productive of arterial blood, the diagnosis
of an aneurysm not visualized on the preoperative studies can be made and a potential
catastrophe can be averted as the plan of management is altered.
Figure 18.12. A. The frontal triangle bounded by the two anterior limbs of the optic
chiasm and tuberculum sellae. B. The middle triangle bounded by the posterolateral
aspect of the ipsilateral optic nerve, the anterolateral aspect of the ipsilateral internal
carotid artery, and the A1 segment of the anterior cerebral artery. C. The posterior
triangle bounded by the posterolateral aspect of the ipsilateral internal carotid artery, the
tentorial edge, and the retracted temporal lobe.
Figure 18.13. Suprasellar craniopharyngioma with distortion of the interchiasmatic
region.

Figure 18.14. Distortion and displacement of the right optic nerve and carotid artery by
a tumor mass developing a tumor presence in the middle and posterior triangles.

The techniques used for resection will depend to some extent on the pathological
nature of the lesion as determined by gross inspection and frozen section biopsy. With a
cystic craniopharyngioma care should be taken to aspirate as much of the cystic
contents as possible to prevent contamination of the spinal fluid with this material,
which could lead to a postoperative chemical meningitis. Likewise, in dealing with a
germi-noma, which has the propensity to seed through the subarachnoid space, the area
around the tumor site should be protected by cottonoids and, as
much as possible, the tumor should be removed intact to prevent contamination of the
spinal fluid. Sharp dissection of the arachnoidal and anatomical planes using bipolar
coagulation, microscissors, and knives is preferable to a technique of pulling or tearing
with dissectors, although the latter instruments can be used to advantage to define the
planes initially. We believe that the limitations of exposure in this area make use of the
Cavitron ultrasonic surgical aspirator difficult. However, the carbon dioxide laser is
extremely helpful when dealing with tough, non-suckable tumor tissue such as may be
encountered in meningioma or solid craniopharyngioma. From the pterional approach
there will be certain areas that are blind to the surgeon such as the inferior surface of the
ipsilateral optic nerve and the hypothalamic recesses in the floor of the third ventricle. A
small 3-mm micromirror may help in visualizing such areas. The majority of the visible
tumor should be resected initially with the expectation that the component extending up
into the floor of the third ventricle may then collapse into the surgical field. Attempts to
pull at tumor outside of the field of direct vision can have serious consequences.
Tolerance of the normal anatomical structures encountered in the pterional approach
to surgical dissection can only be learned by experience. An optic nerve or chiasm
already stretched and distorted by adjacent tumor is extremely sensitive to any type of
manipulation. The same can be said for the third cranial nerve. In general, the large
vascular structures encountered in this approach will tolerate more manipulation than
the adjacent neural structures.
With completion of definitive removal of the lesion, hemostasis should be
meticulously obtained using bipolar coagulation and gentle irrigation with saline. The
anesthesiologist is asked to perform a sustained Valsalva maneuver on the patient to
evaluate hemostasis before closure. The self-retaining retractors are then removed under
direct vision.
Closure of the dura mater is accomplished with 4-0 absorbable Vicryl (polygalactin;
Ethicon, Inc., Somerville, New Jersey) suture and the aid of a pericranial graft if
necessary. The bone flap is firmly resecured using 26 gauge wire or 2-0 silk. The
authors use acrylic cranioplasty to fill all bony defects except the area of subtemporal
decompression. Careful attention is paid to reconstituting the normal contour of the
orbitofrontal angle and the burr hole sites in the superior aspect of the flap. Placing
acrylic in the region of the removed subtemporal and inferior sphenoid ridge may result
in an unacceptable bulge in this area, but using acrylic for the remaining bony defects
results in an excellent cosmetic result and the patient appreciates not being able to feel
the burr hole sites postoperatively. Closure of the temporalis muscle and fascia is with
2-0 absorbable Vicryl interrupted sutures. The galea is closed with interrupted 3-0
absorbable Vicryl sutures with buried knots. The skin is closed with a running,
continuous 3-0 or 4-0 nylon suture, which is removed 7 to 10 days postoperatively. A
small dressing is secured with paper-based tape.

Pitfalls during the Intraoperative Period

A number of pitfalls or technical mishaps can occur during the pterional approach.
We do not include every possible problem that can arise, but we do describe the more
common ones.
In developing the skin, fascial, and muscle incision, one must keep in mind the course
of the motor branch of the facial nerve that supplies the frontalis muscle. The nerve is
difficult to visualize during the course of the operation and can be damaged by undue
traction or dissection in the
subgaleal plane or divided during the skin and muscle incisions. Generally, one can
avoid injury to this branch by opening the temporalis muscle and fascia immediately
below the scalp incision and avoiding extensive dissection in the plane between the
galea and temporalis fascia anteriorly. The superficial temporal artery is taking on more
importance in the field of neurosurgery and we make an effort to preserve the largest
branch of this artery whenever possible.
A pitfall that one should strive to avoid is inappropriate placement of the bone flap;
with careful planning this can be avoided. The bone flap should be tailored to the
individual needs of the case, a point already emphasized. It is necessary to drill away
the lateral sphenoid ridge flush or this bony protuberance will partially block the
exposure of deeper structures.
Adequate relaxation of the brain is necessary for safe and effective brain retraction
and exposure of the inferior third ventricular and suprasellar areas. Occasionally, a
"tight" brain is encountered before or at the time of dural incision. When this occurs, the
operator should check to see that the usual measures for decreasing ICP are in use—i.e.,
hyper-ventilation to a PCO2 of 25 to 30 torr, mannitol, furosemide, steroids, and lumbar
drainage. If, despite these measures, the brain continues to bulge, the operating table
may be tilted to 10 to 15° of reverse Trendelenberg postiion, thus elevating the head
slightly. A readjustment of the head position may also help to improve venous drainage
and brain relaxation. If these measures fail, the frontal horn of the ipsilateral lateral
ventricle may be tapped to drain enough ventricular fluid to relax the brain sufficiently
for dural opening.
Placement of self-retaining brain retractors can give problems. A common problem is
for the retractor blade that is placed over the anterior temporal region to tear one of the
bridging veins and thus cause troublesome bleeding. This can be avoided by cauterizing
and dividing these veins as the retractor is carefully and slowly inserted. Another
problem encountered particularly by the inexperienced operator is to place the frontal
lobe retractor in too far and expose not the ipsilateral, but the contralateral olfactory
bulb, thus causing confusion as the latter structure is followed posteriorly. Some
difficulty may be experienced in exposing the retrochiasmatic area adequately so that a
lesion in this area can be excised. Exposure in this case may be facilitated greatly by
opening the arachnoid of the sylvian fissure before placing retractors. Excessive
retractor pressure and frequent alteration in retractor position are to be avoided as they
may lead to intracerebral swelling or hemorrhage.

Complications
The complications that potentially can follow the pterional approach are those that
can be seen after any neurosurgical intracranial procedure. Infection, hemorrhage, and
edema are the most common problems one is likely to encounter and each can be
detected by close postoperative observation and the use of the appropriate diagnostic
procedure, i.e., CT scanning. Complications peculiar or special to operation in the
parasellar region include visual loss, diabetes insipidus, varying degrees of hypopi-
tuitarism, and rarely coma due to hypothalamic damage. Visual loss is usually a result
of undue manipulation of the optic nerves or chiasm and is probably related to
impairment in blood supply, particularly from damage to the arterial supply that reaches
the chiasm inferiorly. Both diabetes insipidus and hypopituitarism can result from
injury to the pituitary stalk. Both endocrine deficiency states can be confirmed by
appropriate laboratory determination. The syndrome of inappropriate antidiuretic
hormone secretion can also follow operation in this area.

References
1. Daughaday WH: The adenohypophysis. In Williams RH (ed): Textbook of
Endocrinology, ed 5. Philadelphia, WB Saunders, 1974, pp 31-79.
2. Dandy WE: Intracranial Arterial Aneurysms. New York, Havner Publishing
Co, 1969, pp 103-132. (Fascimile of the 1944 edition reprinted by arrange
ment with Corness University Press.)
3. Dandy WE: Surgery of the Brain (A monograph from Lewis' Practice of
Surgery, Volume XII). Hagerstown, MD, WF Prior Co, Inc, 1945, p 405.
4. Krayenbuhl HA, Yasargil MG, Flamm ES, Tew JM: Microsurgical treatment
of intracranial saccular aneurysms. J Neurosurg 37:678-686, 1972.
5. Plum F, Van Uitert R: Nonendocrine Diseases and Disorders of the Hypo
thalamus. In Reichlin S, Balderssarini RJ, Martin JB (eds): The Hypothala
mus. New York, Raven Press, 1978, pp 415-473.
6. Rhoton AL, Yamamoto I, Peace DA: Microsurgery of the third ventricle: Part
2. Neurosurgery 8:357-373, 1981.
7. Symon L: Microsurgery of the hypothalamus with special reference to cran
iopharyngioma. Neurosurg Rev 6:43-49, 1983.
8. Yasargil MG, Fox JL: The microsurgical approach to intracranial aneurysms.
SurgNeurol 3:7-14, 1975.
19
Combined Approaches
M. Gazi Yasargil, Prof. Dr. med., Peter J. Teddy, D.
Phil., F.R.C.S., and Peter Roth

It has been known for many years that Craniopharyngiomas extending upward from
the infundibulum of the third ventricle to the foramen of Monro (whether unilateral or
bilateral, solid or cystic) cannot be completely removed using solely a frontobasal
(pterional) approach and par-achiasmal dissection, even after opening the lamina
terminalis. Although the basal and laterobasal portions of the tumor can be exposed by
this route, the most superior and superoposterior portions, within the posterior half of
the third ventricle, cannot be adequately dissected (Figs. 19.1 and 19.2).
A subtemporal approach to Craniopharyngiomas has not been used in Zurich. It
seems unlikely that complete removal of the tumors with large superior extension can be
achieved in this manner for the same reason as for the pterional approach. Transcortical,
transventricular operations are rejected for fear of producing porencephalic cysts or
postoperative epilepsy and because, although the contralateral aspect of the third
ventricle can usually be well demonstrated, it is difficult to control the ipsilateral
dissection. The transcallosal approach has been used for arteriovenous malformations of
the anterior third of the corpus callosum, colloid cysts of the third ventricle, and third
ventricular gliomas. The pterional approach has been developed to facilitate the repair
of aneurysms involving the circle of Willis. A combined paramedian-pterional approach
was utilized quite successfully in three cases of multiple aneurysms (middle cerebral
and/or basilar bifurcation with pericallosal aneurysm). The idea arose that
Craniopharyngiomas could also be removed completely and safely by using this
combined transcallosal and pterional operation. The transcallosal approach can be used
to dissect the superior, superoposterior, and superolateral aspects of the mass, especially
from the posterior half of the third ventricle and the origin of the aqueduct (Fig. 19.3).
Removal of the parachiasmatic and suprachiasmatic segments of the tumor within the
interpeduncular and ambient cisterns can be achieved from the frontobasal pterional
opening. This would allow dissection of
Figure 19.1. Schematic representation of the multidimensional growing tendency of
craniopharyngioma and its relation to the brain stem and the basal cisterns. A. Lateral.
B. Anteroposterior view.

Figure 19.2. Direction of growth of parachiasmal tumors: A. Into the basal cisterns. B.
Upward into the infundibulum without occlusion of foramina of Monro. С With
occlusion of both foramina of Monro. D. Paramedian expansion and displacement of the
third ventricle.

the mass from around the internal carotid artery and its branches. The bilateral A1
segments and the anterior communicating artery, the basilar bifurcation with both P1/P2
segments, both superior cerebellar arteries, and the mamillary bodies. This frontobasal
pterional approach is also effective for tumor dissection in the region of the optic
nerves, chiasm, optic tracts, and third nerves. A particularly useful technique in
removing
Figure 19.3. A combined approach (subfrontal-parachiasmal and transcallosal-
transforamlnal) is required for proper dissection in a case of superoposterior
expansion of the tumor into the third ventricle.

the preinfundibular retrochiasmatic portion of these tumors is opening the

lamina terminalis, delivering the tumor from beneath the chiasm to the
chiasmatic and lamina terminalis cisterns, with subsequent removal from
between the optic nerves (see Fig. 19.8).
This combined approach was successfully used in 22 procedures for very
large Craniopharyngiomas and in 2 cases of optic glioma arising from the optic
tract with medial extension into the third ventricle causing obstruction of the
foramen of Monro. We have also seen hypothalamic gliomas in three cases
growing superiorly toward the foramen of Monro and extending into the sub-
and prechiasmatic areas; these were removed using the combined approach. It is
not always possible to predict the true extent of third ventricular tumors on
preoperative computerized tomographic (CT) scans or angiograms. Often this
must be established by a comprehensive exploration.

Technique
Of critical importance to this operation is the proper positioning of the
patient. Particular care must be taken with regard to flexion of the neck (Fig.
19.4A) to bring the head into the correct degree of elevation. It is necessary to
make one's approach through the corpus callosum and
Figure 19.4. A. Position of the patient for a combined approach to a third ventricular
tumor. The arrows indicate the extent of the maneuverability available to the surgeon. B.
One skin flap for two separate craniotomies (frontal-paramedian and pterional). The
arrows indicate the surgical entrance for tumor dissection and removal.
foramina of Monro with the patient fully recumbent. This course would take a horizontal
line to its lowermost limit. The patient must therefore be supine with the head somewhat
flexed so that the surgeon is looking perpendicularly through the corpus callosum to the
foramina and along this projected line to the infundibulum (Fig. 19.4B). The slight
anterior tilting of the head is contrary to the normally adopted method of extending the
neck to reduce frontal lobe retraction, as in the anterolateral approach where the head is
also turned slightly to the left. As the head cannot easily be turned from right to left
during the operation, a compromise must be accepted. However, as we need to reach
midline structures there is little reason to require lateral tilt of the head. Furthermore,
almost without exception there is obstruction of the foramina of Monro in these patients
and nearly all have hydrocephalus. This helps the surgeon a good deal; after only a small
opening is made in the corpus callosum, cerebrospinal fluid (CSF) is released and the
frontal lobe falls back, thereby facilitating inspection of the parachiasmatic area with
minimal retraction. One practical point is that the table position may need to be quite
high and the arrangement of surgical drapes and instrument trays may not allow easy
alteration. The surgeon may need a platform for the frontolateral part of the operation,
but may sit for the transcallosal approach and dissection.
The skin incision can be bifrontal or unilateral but must cross the midline (see Fig.
19.4B). The important factor is to recognize the position of the coronal suture, which is
usually perpendicular to the foramen of Monro. Occasionally, gross chronic
hydrocephalus may produce distortion of the calvarium so that the coronal suture is
displaced (usually) backward. The general rule is, therefore, that the foramen of Monro
is on the perpendicular from the coronal suture line or up to 1 cm anterior to it (see Fig.
19.4B).
There is no need to turn a large bone flap, as under the same scalp flap two small
craniotomies can be made. In cases of pronounced hydrocephalus the transcallosal
approach is made first to facilitate release of CSF and minimize frontal lobe retraction
during the second stage. In cases of only moderate hydrocephalus (especially
Craniopharyngiomas) the frontolateral approach is made first. The sylvian fissure and
then the carotid and lamina terminalis cisterns are opened such that the parachiasmatic
extension of the tumor can be inspected and its relation to the optic nerve and tracts, the
internal carotid artery, the third nerve, etc., can be studied. In cases of severe
hydrocephalus and a tight brain, it may be necessary first to tap the lateral ventricle with
a brain needle before starting any form of dissection or retraction. For the parasagittal
craniotomy, three burr holes are fashioned—two in the midline (one 2 cm in front of the
coronal suture and the other 1 cm behind) and the third 2 cm lateral to the midline so that
a triangular free flap may be created and removed. The pterional craniotomy is carried
out in the standard fashion previously described (1). After dissection of the temporal
skin and muscle flaps four burr holes are made, the first behind the base of the
zygomatic process of the frontal bone, the second over the glabella, the third 3 cm
posterior to the first along the linea temporalis, and the fourth over the anterior part of
the squama temporalis. A small quadrilateral free flap that is quite adequate for the
frontobasal approach can thus be created.

Midline Approach
There are several points of surgical technique that are important when gaining access
to midline structures using the transcallosal approach.
Figure 19.5. The corpus callosum is longitudinally divided at the level of the coronal
suture. The dashed line indicates the site of the incision between the two pericallosal
arteries.

The craniotomy, although small (elongated anterosuperiorly), could be smaller yet if one
could positively identify the location of the bridging veins to the sagittal sinus. Direct
inspection determines the direction of the dissection, anteriorly or posteriorly, to these
venous structures that are to be preserved. If a large leash of veins is encountered,
dissection of their arachnoid sheath from the dura mater will permit mobilization.
Wrapping these venous structures in small muscle fragments limits venous oozing.
Occasionally, moderately sized veins must by necessity be sacrificed; excessive time
must not be lost attempting to preserve these structures.
Exploring the medial surface of the frontal lobe is generally straight-forward,
especially when the subarachnoid cisterns are dilated. Small veins crossing the
subarachnoid space are coagulated and divided as the frontal lobe is dissected free from
the falx. Separating the falx and cingulate gyrus is also usually straightforward.
Occasionally the falx is a fibrous network with numerous large defects. In this instance
the variable depth of the falx suggests fusion of the cingulate gyri in the midline. Care
must be taken not to confuse the opposed cingulate gyri for the corpus callosum. Under
these circumstances the callosomarginal arteries within their respective sulci may be
mistaken for the pericallosal vessels.
The callosomarginal and pericallosal arteries occasionally provide small branches to
the falx, but inadvertent avulsion is of no consequence. However, avulsion of the parent
vessels will lead to troublesome hemorrhage. Upon reaching the body of the corpus
callosum it is important to realize that there may be one to three A2 arteries (see Ref. 1).
The arterial pattern in this region must be carefully studied on the preoperative
angiograms and correlated with the surgical anatomy. One must always
Figure 19.6. A. The right foramen of Monro is obstructed by the expanding tumor. Sp,
septum pellucidum bulging to the right as the left foramen of Monro is blocked. Pl,
Choroid plexus. B. The septum is opened. Both foramina of Monro are visualized
obstructed by the tumor. C. Schematic representation of the transcallosal-transseptal
approach to both foramina of Monro.
inspect the lateral sulcus, beneath the cingulate gyrus, for accessory A2 vessels.
Normally, our dissection proceeds by approaching the corpus callosum between the two
pericallosal arteries; however, in some cases, anatomical variations will force us to
remain lateral to the right pericallosal artery. To avoid potential mechanical vasospasm
during dissection, cottonoids soaked with papaverine or phenytoin should be applied
locally (Fig. 19.5).
Using fine bipolar forceps, one makes a 10- to 15-mm opening into the corpus
callosum. This allows free flow of CSF and decompression of the right ventricle. Unless
there are natural openings in the septum pellucidum, the CSF of the left ventricle will
remain unvented and the septum pellucidum will bulge to the right, obscuring the view
of the surgeon. A 10-mm fenestrating incision in the septum pellucidum would
decompress the left ventricle, giving the surgeon good access to both foramina of Monro
(Fig. 19.6).

Dissection of the Tumor at the Foramina of Monro and in the Third Ventricle
The foraminal region should first be inspected to ascertain the course of the veins
running toward the internal cerebral veins. In particular, one should identify the septal,
frontal subependymal, thalamostriate, and smaller posteriorly to anteriorly directed
veins, all of which run to the posterior inferior corner of the foramen of Monro and are
usually covered by Choroid plexus. The foramen is usually grossly enlarged and it has
not been found necessary to mobilize the Choroid plexus and tela choroidea (Fig.
19.7A).

Figure 19.7. A. Dissection of the tumor. B. Third ventricle visualized through the
enlarged foramen of Monro after tumor removal.
 Dissection of the tumor then proceeds bilaterally within the foramina from the
posterior inferior corners and then further into the ventricles bilaterally. The tumor is
punctured and a central decompression is carried out. This permits a deeper inspection
and the massa intermedia may be seen (superiorly and posteriorly compressed and
displaced), together with the origin of the aqueduct. At this stage it is most important to
establish, if possible, a good plane between normal and tumoral tissue to prevent damage
to the periaqueductal structures and the delicate lateral walls of the dilated third ventricle
(Fig. 19.7B).
The infundibulum and subchiasmatic region may now be inspected and the tumor
dissected from these areas. This is generally quite safe in the midline; however, laterally
care must be exercised to avoid damage to the optic tracts. Deeper dissection reveals the
infundibulum, which may be membranous or actually breached by the tumor. Careful
exploration is necessary here as one quickly approaches the basilar bifurcation and
mamillary bodies; separation of the tumor from these structures is not difficult as there
are few arachnoidal adhesions present (see Fig. 11 A).
Within the interpeduncular cistern there is rarely serious bleeding from damage to
small arteries during dissection. However, rupture of some of the venous branches may
produce small hemorrhages that may be difficult to control by simple coagulation. In
such instances, small pieces of muscle held in place for a few minutes with a moist
sponge will usually be more effective in this sensitive area than excessive use of bipolar
coagulation.
The anterosuperior aspect of the third ventricle may now be inspected cautiously as
this is where lie the A1 segments, anterior communicating arteries, hypothalamic
vessels, and optic chiasm. If a large segment of tumor is still present and the anatomy is
unclear, the midline approach is discontinued and the dissection is carried further from
the frontobasal direction.
In general, there is a relatively well-defined cleavage plane between the wall of the
third ventricle and the tumor itself (at least in cases of craniopharyngioma). However,
careful inspection and early orientation are mandatory to avoid damage to the ventricular
wall. This may occasionally be complicated by the fact that the tumor may not lie
entirely within the ventricle—a fact not easily established on CT scan. The mass may
displace the ventricle to the right or to the left, indent it from below symmetrically or
asymmetrically, or lie within the third ventricle (see Fig. 19.2).

Pterional Approach
This standard approach has been described in detail elsewhere (1) and only an outline
is given here. After removal of the bone flap, the tension of the intracranial compartment
can be assessed and if necessary, through a small dural rent, CSF may be released by
puncturing the ventricle with a brain needle. One or two small dural rents are also cut
along the frontal or temporal portions of the planned dural incision to provide further
CSF release.
Pterional craniotomy is designed to take advantage of the natural planes and spaces
and to expose the base of the brain without significant brain retraction. One natural plane
is provided by the sphenoid ridge as it separates the frontal and temporal lobes. Another
is provided by the roof of the orbit projecting superiorly and indenting the basal surface
of the frontal lobe. These planes project from the surface of the brain to the parasellar
area and form the base of this pyramidal space, the apex of which is formed by the
junction of the frontal and temporal lobes. The
Figure 19.8. A. Right-sided pterional approach showing an anteriorly fixed chiasm. The
lamina terminalis is bulging and the tumor adheres to the anterior communicating and
hypothalamic arteries. B. The lamina terminalis is opened and the superoanterior portion
of the tumor has been dissected.

base of this pyramid may be enlarged by removal of bone from the sphenoid ridge and
by flattening of the orbital roof. The apex of the pyramid may be enlarged by opening
the basal sylvian fissure, thus forming a further pyramid-shaped working space with the
apex directed toward the limen insulae. The width of this pyramid is the shortest
distance from the calvarium to the sella.
The base of the pyramid is enlarged by using a high speed electric drill to smooth the
convolutions of the posterior lateral orbital roof adjacent to the frontal sphenoid suture.
The posterior ridge of the greater wing of the sphenoid is also flattened until a small
ridge representing the most lateral aspect of the lesser wing is reached. Any bleeding
from the bone is readily controlled by coagulation and the application of bone wax. If
the frontal sinus extends far laterally, it may be inadvertently entered, in which case the
mucosa is stripped from the bone and the sinus is plugged with a small piece of muscle
and sealed with an acrylic adhesive before being covered with bone wax at the end of
the procedure. The dura is opened in a semicircular fashion around the sylvian fissure,
arching toward the sphenoid ridge, and is retracted. The direction and sequence of
arachnoid dissection and Cisternal opening depend to some degree on the location of the
lesion. Both the sylvian cistern between the basal frontal and temporal lobes and the
lamina terminalis cistern are opened.
The apex of the pyramid is enlarged using sharp dissection with a round arachnoid
knife, and the sylvian cistern is entered at the level of the opercular frontal gyrus. The
arachnoid of the sylvian cistern should be opened on the frontal side of the superficial
middle cerebral veins.
Occasionally two or three frontoorbital venous tributaries crossing the sylvian fissue
must be sacrificed to complete the dissection of the most medial aspect of the fissure.
The sylvian cistern is then followed laterally around the orbital frontal gyrus, at which
stage the frontal lobe will be retracted away from the temporal lobe. The right carotid,
the lamina terminalis, and the interpeduncular cisterns are opened to release more CSF
and to expose the base of the tumor. Although the approach to midline tumors is
generally more frontomedially directed than for aneurysm surgery, the concept of
"enlarging the base of the pyramid" by flattening the posterolateral orbital roof remains
useful in minimizing retraction of the frontal lobe and in gaining maximal access to the
parachiasmatic region (Fig. 19.8).

Summary
The combined approach provides a systematic method for attacking and excising these
large Craniopharyngiomas. The initial step is lateral chiasmatic and subfrontal
evaluation via the pterional dural opening. The anatomical relationships of the tumor to
the optic nerve and tract, the internal carotid artery and its branches, the chiasm, and the
anterior cerebral vessels are determined by direct inspection. Tumor removal via the
subfrontal pterional approach is not undertaken until after the trans-

Figure 19.9. A to C. CT scan of an 11-year-old boy with craniopharyngioma occupying

the third ventricle. D. Coronal CT showing extension of the tumor into the third
ventricle and up to the foramina of Monro. Note bilateral hydrocephalus.
Figure 19.10. A. Anteriorly fixed chiasm visualized through the right pterional
approach. B. Tumor visualized through the foramen of Monro using the transcallosal
approach.

Figure 19.11. A. Basilar artery and its branches are now visualized through the opened
infundibulum of the third ventricle after tumor removal. B. The anterosuperior portion of
the tumor is removed through an opening of the lamina terminalis.
Figure 19.12. A to C. Postoperative axial CT scan showing radical removal of the tumor.
D. Coronal CT scan showing normal size ventricles and patent foramina of Monro.

callosal intraventricular approach to the tumor is completed. Frequently the basilar

cisterns are blocked by the presence of these large tumors, compounding the
hydrocephalus produced by obstruction of the foramen of Monro. Opening of the
superficial cisterns, frontal and temporal, associated with the sylvian fissure provides
escape for CSF otherwise blocked at the basal cisterns.
The next step is to proceed with the paramedian dural exposure and transcallosal
approach to the third ventricle. Upon opening into the lateral ventricles after the
placement of a septal window to control hydrocephalus, one can proceed with a direct
attack on the superior and superoposterior portions of the tumor, which is the major
advantage of the combined approach. After the superior and superoposterior aspects of
the tumor have been dissected and removed, the anatomical relationships of the foramen
of Monro, origin of the aqueduct, and lateral and
basal aspects of the third ventricle are established, and hemostasis is completed, one
reinspects the subfrontal area.
During this step, one removes residual tumor from the retrochiasmatic area,
interpeduncular cisterns, and optic tracts and nerves. Once one is satisfied with tumor
removal and hemostasis is complete one may then proceed with the fourth and final step,
the return to the transcallosal transventricular tumor bed to assure that no residual tumor
is present and that hemostasis is absolute (Figs. 19.9A to C, and 19.10-19.12).
Following these four steps of the combined transcallosal-pterional approach provides
the most detailed evaluation of the subfrontal and intraventricular anatomy and
simultaneously assures control of hydrocephalus. Tumors of this origin require precise
anatomical evaluation, meticulous dissection, and absolute hemostasis, all provided by
this combined approach.

Reference
1. Yasargil MG: Microneurosurgery, vol I, Microsurgical Anatomy of the Basal
Cisterns and Vessels of the Brain, Diagnostic Studies, General Operative
Techniques and Pathological Considerations of the Intracranial Aneurysms.
Stuttgart, Georg Thieme Verlag, 1984, p 371.
20
Transnasal Transsphenoidal Approach
Martin H. Weiss, M.D.

Tumors of the floor of the cranial vault, particularly those arising from and extending
along the midline, frequently impact upon the third ventricle as they extend superiorly
into the intracranial compartment. These masses (whether they be neoplastic,
inflammatory, or cystic) may derive from intradural or extradural sources as well as
extracranial processes that extend in a superior direction. Efficient extraction of these
lesions can frequently be accomplished most effectively by attacking them from the site
of origin inferior to the third ventricle utilizing a transnasal procedure, which can be
tailored to involve either intradural or extradural masses.

Historical Perspective
Schloffer, a rhinologist from Innsbruck, Austria, first recommended utilization of the
transnasal approach to intracranial neoplasms and reported the successful removal of a
pituitary tumor utilizing this approach in 1907 (5). Subsequent modifications by a
number of international as well as American neurosurgeons enabled Cushing to report a
15-year experience of some 231 transnasal operations upon pituitary tumors with a
mortality rate of 5.6%. This was significantly less than the early mortality figures for
transcranial approaches to the area of the sella; the primary sources of morbidity lay with
the difficulty in irradi-cating cerebrospinal fluid (CSF) fistulas developing during the
course of the procedure and the occurrence of meningitis as a consequence of persistent
CSF fistulas. As our results in the use of transcranial approaches to the sella and the
parasellar area dramatically improved, interest in the transnasal approach to skull base
lesions waned, particularly in the United States, even though our European colleagues
effectively persisted in these pursuits. Advances in microsurgical techniques rekindled
the North American interest in transnasal surgery led by the pioneering efforts of Jules
Hardy in his promulgation of the technique of transsphenoidal hypophysectomy (3); our
early successes with hypophysectomy of the normal gland in the treatment of
disseminated breast and prostate cancer as well as diabetic retinopathy encouraged
extension of
 this technique to pituitary tumors as well as parasellar lesions with significant degrees
of intracranial extension. The mortality rate in experienced hands with such approaches
consistently is significantly less than 1 % with postoperative radiographic confirmation
of radical resection of extensive lesions (2, 4). These considerations have led to
permanent inclusion of this technique in the neurosurgical armamentarium with
continued expansion of the indications for utilization of transnasal approaches to the
base of the skull (1-3).

General Guidelines
At present, lesions that optimally lend themselves to transnasal resection are midline
lesions of the skull base extending from the inferior aspect of the clivus (foramen
magnum) to the level of the planum sphen-oidale whether they be extracranial,
extradural, or intradural (Fig. 20.1). Varying degrees of lateral extension from the
midline may lend themselves to inclusion in these operative approaches depending upon
the experience of the surgeon and the broad base upon which such extension has arisen.
It has become commonplace to utilize combined procedures to approach extensive
lesions of the skull base that broadly involve the midline yet have considerable and
inaccessible lateral extension. In general, our strategy has been to utilize a transnasal
approach to these lesions initially to remove as much as possible of the tumor mass via
what we think is a significantly more benign procedure; residual lateral tumor can then
be approached via a transcranial intradural procedure in which tumor dissection will
have been minimized by the previous transnasal procedure. Utilizing these criteria we
have successfully approached lesions arising within the sphenoid sinus such as sphenoid
sinus muco-celes, lesions of the clivus such as chordomas, lesions of the sella such as
pituitary tumors and various intrasellar cysts, and lesions arising within the suprasellar
cistern such as Craniopharyngiomas and dysger-minomas.
There are relatively few contraindications to the implementation of this technique other
than those already mentioned with specific respect to extensive lateral extension. The
presence of a nonpneumatized sphenoid sinus complicates the surgical procedure and
may require more extensive utilization of radiographic conformation of position
intraoperatively, but the availability of appropriately sized high speed drills allows one to
obviate this problem with relative ease. The position of the intracaver-nous carotid
artery, in a similar fashion, adds a complicating dimension with respect to access to
structures or lesions lying superior to the carotid arteries. Indeed, major ectatic carotid
arteries may mitigate against a successful approach to a sellar or a suprasellar lesion
although this is an extremely rare finding. The presence of acute sinusitis is an obvious
temporary limiting factor that may delay but not prohibit the utilization of a transnasal
approach. In general, if the bulk of the lesion lies within the midline with a modest or
moderate degree of lateral extension, one would elect to approach these lesions
transnasally. However, if the vast majority of the lesion lies lateral to the midline with a
small degree of midline extension and invasion, one would utilize a standard transcranial
approach because it would be more likely to allow for radical tumor resection. A
previous rhinoplasty or submucosal resection for nasal septal deviation will also add to
the complexity of the intranasal dissection because of postoperative changes in the
relationship between the nasal mucosa and its adjacent structures, but appropriate
dissection planes can invariably be established even under such circumstances.
Figure 20.1. Suprasellar extension arising from a broad-based mass may be easily
approached via a transnasal transsphenoidal route. The lateral or anterior extension of a
mass that has a small or narrow basal attachment would limit access to the contents of
the tumor and is a relative contraindication to approaching via the transnasal route.

Approaches to intradural lesions offer the greatest technical challenge. Frequently,

such lesions extensively embrace the major vascular structures that cannot be readily
appreciated during the course of transnasal surgery. It has been my experience that
invasion of the cavernous sinus is best approached transnasally when such invasion has
occurred from a midline lesion. The exposure of the entire sella via the transnasal route
enables access to the extension of the tumor into the cavernous sinus well beyond that
which can be generated via a transcranial approach. On the other hand, in those cases in
which a tumor incorporates the carotid or basilar arteries within the substrate of the
tumor mass, one may not visualize the relationship of the tumor and such vessels via a
transnasal approach; one would therefore incline one's operative strategy toward a
transcranial approach under such circumstances.

Radiographic Considerations
Preoperative assessment of these lesions requires meticulous radiographic definition
of the extent of the lesion so that one can apply the selection criteria. In addition,
however, one must recognize the frequent involvement of the hypothalamic-
hypophysial axis by lesions so positioned, which impacts upon the risk factors. Any
lesion proximal to the pituitary or hypothalamus requires adequate endocrine evaluation
preoperatively to minimize the potential for an intraoperative or postoperative
catastrophe because of inadequate pituitary reserve. The two most
 important hormone axes that must be considered are those relating to cortisol and thyroid
release from their respective organs. Because many of these procedures call for the
concomitant utilization of exogenous glucocorticoids, the risk of intraoperative
hypocortisolemia is generally not a major factor. However, preexistent hypothyroidism
may become acutely manifest during the early postoperative period, making preoperative
recognition of this potential an essential consideration. Adequate reestablishment of a
euthyroid state requires approximately a week of treatment before surgical procedures
can be electively pursued. It has been our policy to evaluate a complete thyroid profile as
well as a baseline cortisol level preoperatively in anticipation of intraoperative manipula-
tion of the hypothalamic-hypophysial axis. The existence of normal hormonal activity
preoperatively obviously does not guarantee normalcy postoperatively, but a reasonable
understanding of preoperative pituitary function can help to mitigate against particular
perioperative complications.
Radiographic evaluation of parasellar lesions has been radically affected by the advent
of high resolution computerized tomographic (CT) scanning. Utilization of varying
window widths enables definition of bony landmarks (whether or not these are
pathologically involved) and of the extent of soft tissue extension and related vascular
distortion. CT scanning with a high resolution scanner utilizing contrast enhancement
along with coronal and sagittal reconstructions has enabled us to visualize the
peritumoral vasculature to the extent that preoperative angiography is rarely required. In
those cases in which questions of the existence of an aneurysm or vascular invasion by
tumor are of concern, intravenous digital subtraction angiography has frequently proved
to be an excellent alternative to selective angiography. Cystic lesions that involve the su-
prasellar cistern may defy adequate delineation by any of the aforementioned means.
Positive contrast CT cisternography has been a helpful resource in outlining such lesions.
Recently, magnetic resonance imaging (MRI) has allowed us to delineate the extent of
such lesions. MRI may, in the reasonably near future, replace CT scanning as the primary
or definitive imaging modality for such skull base lesions. The availability of these
advanced imaging forms has essentially eliminated the need for conventional
polytomographic studies in which visualization is limited to the definition of bony
structures, obviously of limited use.

Surgical Procedures
Considerations of operative technique begin with the induction of general anesthesia.
When a patient is defined as having compromised neurological function, most commonly
visual compromise due to tumoral compression, or when preexistent hypopituitarism is
defined, it is essential to administer adequate glucocorticoids before induction to
minimize the potential for an undesirable preoperative hemodynamic crisis or
intraoperative progression of neurological compromise. Patients with tumors of sufficient
extent to compress neural structures are given sizable doses of high potency
glucocorticoids (40 mg of methylpredniso-lone or 10 mg of dexamethasone) before
anesthesia induction. The placement of the endotracheal tube with respect to the mouth
itself is a significant consideration (Fig. 20.2A). The tube is best located slightly to the
left of the patient's midline so as not to put untoward traction on the lips and therefore
mitigate against satisfactory elevation intraoperatively. It is certainly reasonable to
include an esophageal stethoscope along with the endotracheal tube to monitor
pulmonary ventilation intraoperatively; it is essential to assess the status of the
endotracheal balloon to evaluate
Figure 20.2. A. The endotracheal tube should be placed to the left of the midline so as to
allow access easily from the patient's right side but not so far as to cause undue traction
on the lips and therefore impede elevation of the lip during the course of the procedure.
B. The patient is positioned in a supine position with the face parallel to the floor and
the head elevated approximately 15° above the heart. C. In the final position, the
surgeon (1) stands just to the right of the patient with the Mayo stand (2), the nurse (3),
the microscope base (4), and the assistant (5) around the head of the patient. The
anesthesiologist (6) stands to the left of the patient. The patient's right posterolateral
thigh is approximately positioned to allow access should a fascia lata graft be required.

the potential existence of any leaks that might allow intraoperative aspiration of blood,
mucus, or irrigating fluid accumulating in the posterior oropharynx during the course of
the procedure.
The vast majority of our operations are done under balanced anesthesia utilizing
nitrous oxide and narcotic, which allows us to awaken patients
Figure 20.3. Slight flexion of the head allows easiest visualization of the struc-
tures that lie caudal to the sella turcica whereas extension allows better visual-
ization of those structures lying anterior to the sella turcica (particularly the
planum sphenoidale and tuberculum sellae). For most situations, a neutral posi-
tion (head parallel to the floor) is optimal for access to the sella and suprasellar
structures.

rapidly postoperatively to assess their visual and neurological status.

Occasionally, inhalation anesthesia is required, particularly to control blood
pressure when there is a tendency to hypertension. In normotensive patients, we
prefer to keep the blood pressure at approximately a systolic of 100 mm Hg (a
mean of 70 to 80 mm Hg) to reduce venous ooze from the operative site.
Once anesthesia has been satisfactorily induced, we generally prefer to
position the patient supine with the face parallel to the ceiling with the head
elevated approximately 15° above the heart (Fig. 20.2, В and C). Flexion or
extension of the head from the position just mentioned can help in approaching
lesions either anterior or posterior to the sella turcica (Fig. 20.3). With the head
parallel to the ceiling, those intra- and suprasellar tumors most commonly
encountered may be most readily approached. However, if there is significant
extension inferiorly along the clivus, visualization is enhanced by some flexion
from this neutral position, whereas subfrontal extension of the tumor to a level
of the tuberculum or planum may be best approached with extension of the head
from this neutral position. One must also allow for exposure of the right superior
posterolateral thigh or the anterior wall of the abdomen to gain access for a
fascial or subcutaneous fat graft should that be necessary during the course of
the procedure.
Considerations of intracranial pressure control during this procedure generally
relate to assurance that venous drainage will be adequate to
Figure 20.4. A gingival incision leaving approximately 3 mm of a gingival cuff for
closure is made extending from the canine fossa to the contralateral canine fossa and is
carried down to the level of the subperiosteal plane of the maxilla. The dissection is
carried superiorly in a subperiosteal fashion to expose the upper aspect of the rostrum
of the maxilla, including the nasal spine and the lateral recesses. If there should be a
particularly prominent nasal spine or markedly heightened maxillary rostrum a
resection of these will enable better dissection along the floor and along the mesial
surface, avoiding any undue visual obstruction. Once the floor of the nose is readily
identified, the mucosa of the nose is dissected off the floor along its mesial aspect, with
the dissection then carried mesially up along the vomer and over the vomer to dissect
the mucosa from the quadrangular cartilage. The dissection is carried superiorly along
one side to free the mucosa from the quadrangular cartilage so that it can be visualized
posteriorly to recognize the attachment of the quadrangular cartilage to both the vomer
inferiorly and the perpendicular plate of the ethmoid posteriorly.

avoid venous congestion of the operative site. This is generally assured by positioning
the head above the heart to encourage venous drainage. Intracranial hypertension is
generally not a major problem in these cases except with lesions that grow sufficiently
superior to obstruct the fora-
Figure 20.5. Once the quadrangular cartilage is adequately visualized, it can be
mobilized from its attachment to both the perpendicular plate of the ethmoid and the
vomer so as to allow mobilization of the quadrangular cartilage to the side with the
overlying attached nasal mucosa. This allows visualization of the perpendicular plate of
the ethmoid and the superior aspect of the vomer for further dissection. Once the
quadrangular cartilage has been mobilized from the vomer and the perpendicular plate
of the ethmoid, a dissection is carried posteriorly along the perpendicular plate of the
ethmoid and the posterior-superior aspect of the vomer to the rostrum of the sphenoid
sinus. Identification of the sphenoid sinus ostia will indicate the superior aspect of the
rostrum of the sphenoid sinus so as to limit the extent of the section and also allow
access to the sphenoid sinus.

mina of Monro, generating secondary hydrocephalus. Under such circumstances,

reduction of intracranial pressure before the induction of anesthesia is generally
desirable. We have utilized direct ventricular cannu-lation (either unilateral or bilateral
depending upon interventricular communication) with removal of ventricular fluid
before induction to control such intracranial hypertension. Utilization of dehydrating
agents intraoperatively is rarely necessary or desirable, obviating the need for placement
of a Foley catheter with its potential attendant morbidity.
This operative procedure is performed through a "semisterile" field. As a
consequence, it is imperative to irrigate the operative field vigorously during the course
of operation to reduce the potential for contamination. A number of authors have
advocated the utilization of preoperative antibiotics to reduce the risk of postoperative
infection due to the semi-sterile nature of the operative field. We abandoned the use of
such agents some 12 years ago with no apparent untoward effect. Our infection rate
remains under 1% in our operative series. We do, however, irrigate vigorously with
bacitracin-impregnated lactated Ringer's solution (50,000 units/500 ml). We think that
this is the single most critical factor in reducing the potential for operative
contamination from the paranasal sinuses.
Figure 20.6. One can gain access to the entire extent of the clivus by directing the
dissection inferiorly along the vomer and the roof of the hard palate with dissection of
the mucosa of the nasopharynx from the clivus to gain access to lesions as low as the
foramen magnum. In this same manner a lesion lying over the tuberculum sellae and
even the planum sphenoidale can be approached by carrying the dissection anterior to
the sella turcica after the rostrum of the sphenoid has been resected.

Once the patient is adequately positioned after the satisfactory induction of

endotracheal anesthesia, a povidone-iodine preparation of the nasopharynx and
sublabial gingival area of the maxilla is carried out to reduce potential contamination
from these sources. The nasal mucosa and gingival mucosa are infiltrated with 0.5%
lidocaine containing epinephrine 1/200,000 and the nose is packed with cottonoids
impregnated with 5% cocaine to shrink the nasal turbinates. A gingival incision
extending from canine fossa to canine fossa is then made and carried down to expose
the rostrum of the maxilla (Fig. 20.4). The dissection should be carried in a
subperiosteal fashion to minimize the amount of blood loss and superiorly to identify
the entrance to the nose. A great variability has been encountered in the size of the
nasal spine, which may or may not require resection superiorly to allow adequate
visualization of the posterior aspect of the nasal pharynx. In addition, the superior
aspect of the rostrum of the maxilla is variable in height from the floor of the nose and
may require some resection inferiorly and laterally to increase the size of the nasal
cavity and allow smooth and direct dissection of the nasal mucosa from the floor and
mesial structures. Once this preliminary portion of dissection is completed, one must
remember to remove the nasal cottonoids before proceeding with the intranasal dis-
section. The mucosa is first dissected from the floor of the nasal canal along its mesial
aspect and then dissection is carried mesially and superiorly up along the vomer to the
junction with the quadrangular cartilage. There are multiple adhesive bands extending
from the basal mucosa to this junction, which must be meticulously dissected to avoid a
tear in the nasal mucosa. The dissection is then carried superiorly up along the inferior
aspect of the quadrangular cartilage, coming anteriorly to expose the columella at its
inferior portion (Fig. 20.5). The nasal cartilage can then be dissected free from the
superior aspect of the vomer along with the anterior aspect of the perpendicular plate of
the ethmoid so that the cartilage can be observed as it is mobilized away from the
midline with
Figure 20.7. In В one can appreciate resection of the rostrum of the sphenoid sinus
utilizing the sphenoid ostia to gain access to the sphenoid sinus with the punch. If the
sphenoid sinus is nonpneumatized or only partially pneumatized, one can use a high
speed drill to drill through the bone to gain access to the sella turcica. Under such
circumstances, radiographic or fluoroscopic control of the depth of the drilling
dissection is probably desirable because it may be difficult, under these unusual
circumstances, to appreciate the extent of drilling that has occurred.

the nasal mucosa to which it remains attached on one side. This allows visualization of
the vomer and the perpendicular plate of the ethmoid so that the dissection can then be
carried posteriorly to identify the rostrum of the sphenoid sinus. The perpendicular plate
of the ethmoid is an invaluable landmark in that it has never failed in guiding this
surgeon to the rostrum of the sphenoid sinus. The dissection at this point will be
dependent upon the area of particular involvement that one is addressing. In the unusual
situation in which a chordoma of the clivus extending as far down as the foramen
magnum is under surgical attack, one would want to dissect the mucosa of the
nasopharynx from the inferior posterior wall of the clivus to gain access to this
retrosphenoid structure. One would follow along the floor of the nose, utilizing the
landmarks of the hard and soft palate to establish the plane between the mucosa and the
clivus to gain access to this structure (Fig. 20.6). Ordinarily, one would utilize the
rostrum of the sphenoid as a landmark to gain access to the sphenoid sinus once both of
the sphenoid sinus ostia had been identified. In the usual course of events, where a
suprasellar cistern tumor with an enlarged sella turcica is compressing the third ventricle,
the sphenoid sinus ostia mark the anterior extent of the exposure with respect to the
sphenoid sinus that will enable adequate access to the suprasellar cistern (Fig. 20.7). The
rostrum of the sphenoid sinus can be readily removed, gaining access to its interior via
the ostia. Should one be dealing with a sphenoid sinus mucocele, radical exenteration of
the mucocele along with any remaining mucosa of the sphenoid sinus will allow one to
complete
Figure 20.8. Once the rostrum of the sphenoid sinus has been resected to allow
visualization of the full extent of the sphenoid, the sphenoid sinus mucosa should be
exenterated, which will help control any bleeding from this mucosa as well as avoiding
the potential for a postoperative sphenoid sinus mucocele. One must also note that there
is almost always a bony septum within the sphenoid sinus that also must be removed to
allow access to the entire extent of the floor of the sella turcica. Frequently, this septum
is somewhat eccentric and may not appear to be present to the untrained eye. Dissection
along one side of the septum only will give compromised exposure of the floor of the
sella with resultant compromise to the extent of resection of the intra- or suprasellar
contents.

the procedure at this point. Should the abnormality lie superior to the sphenoid sinus,
one should exenterate the sphenoid sinus mucosa to prevent the genesis of a
postoperative mucocele along with any undue bleeding from residual sphenoid sinus
mucosa (Fig. 20.8). If one is dealing with a chordoma of the clivus, it is imperative to
recognize that these are frequently if not always surrounded by a layer of cortical bone,
which must be drilled off before ready access to the intraclival chordoma can be
secured. One can recognize the chordoma capsule after resection of
Figure 20.9. Clivus chordomas are generally found overlying a layer of cortical bone
which must be drilled off to gain exposure to the capsule. These structures (remnants of
the primitive notochord) reside within the confines of the clivus in their original phase.
Once the capsule of the chordoma has been opened, one may readily remove the
moderately vascular and gelatinous internal contents of the chordoma. Utilizing this
technique, one can then progressively infold the capsule of the tumor so as to separate it
from its surrounding structures to gain access to the extracapsular space to enable a
radical resection. One must always remember that bone destruction is the hallmark of the
chordoma; it may either penetrate or intimately attach to the dura, preventing potential
complete resection utilizing these techniques.

the clival cortical bone; radical resection is then most readily accomplished by removal
of the central portion of the gelatinous chordoma and then folding in of the capsule (Fig.
20.9). These tumors are in general extradural tumors, which allow one to gauge the
extent of resection by identification of the dural margins. Limiting oneself to the
extradural compartment allows resection of the tumor while avoiding the potential for
surgical damage to the basilar artery or disruption of the arachnoid, necessitating a
grafting procedure to avoid a postoperative CSF fistula.
Figure 20.10. Once the floor of the sella has been removed so as to identify at each
lateral boundary the cavernous sinus and the circular sinus superiorly (an opening of
approximately 1.5 cm square), the dura is opened in a cruciate fashion so as to elevate
four dural flaps that will give maximal surface area of exposure in the form of a square.

In the unusual event that the dura mater is invaded, one may settle for an intracapsular
removal of tumor, allowing the capsule to occlude the opening in the dura mater, or one
may incise the dural margins surrounding the capsule longitudinally in an effort to
extract the intradural portion of the capsule. When possible under these circumstances,
preservation of the arachnoid will mitigate against the potential for a CSF fistula even
though the dura mater has been breached.
For those lesions arising within the sella turcica and extending superiorly it is
necessary to resect the floor of the sella before gaining access to the primary lesion. If
the floor has been markedly thinned by tumor expansion, one may simply chip off a
significant segment of the floor using a long small bone curette; a thick or normal sellar
floor can be easily opened using a high speed diamond drill while preserving the
integrity of the overlying dura. When working within and beyond the sella turcica, it is
easiest to utilize a cruciate incision when opening the dura so that, after elevating the
dural flaps, one is left with a square opening as opposed to a diamond-shaped opening.
A square shape maximizes the area of the dural opening (Fig. 20.10). Identification of
the arachnoid, once again, is of critical importance in an effort to avoid a CSF fistula
(Fig. 20.11). The arachnoid is actually a reasonably tough membrane which is, even in
the face of major suprasellar extension, generally intact so as to allow resection of the
tumor without disturbance of the overlying arachnoid.
Lesions arising primarily within the suprasellar cistern, such as a craniopharyngioma
arising from the pituitary stalk and growing superi-
Figure 20.11. Once the dural flaps have been elevated, access to the tumor both within
the confines of the sella and in the suprasellar cistern can be readily obtained utilizing
various curettes and scoops. The critical relationship between the tumor, diaphragma
sellae, and suprasellar arachnoid must be recognized because it is imperative to preserve
the integrity of the arachnoid to minimize or virtually eliminate the potential for a
postoperative CSF fistula.
Figure 20.12. A pure suprasellar tumor may be approached by carrying the bony
resection anteriorly over the tuberculum sellae with exposure of the dura mater lying
anterior to the circular sinus. A transverse incision is then made in the dura rostrum and
caudal to the circular sinus with coagulation of the circular sinus to allow transection of
the circular sinus and exposure of the suprasellar cistern without disturbing the pituitary.

orly, present a particularly interesting problem. In these cases, the sella turcica is
usually of normal size and one strives to preserve a normal pituitary gland while
resecting the suprasellar lesion. Under such circumstances, one optimally must resect
not only the floor of the sella turcica but also extend the bony resection superiorly to
remove the tuberculum sellae, which can be visualized through the sphenoid sinus
opening (Fig. 20.12). This will generally require crossing the circular sinus at the
anterior lip of the sella turcica, which generally can be readily accomplished. The sinus
is an intradural structure contained between the leaves of the dura so that a pure
extradural resection of bone should not compromise sinus integrity. Once the bone of
the tuberculum sellae has
Figure 20.13. If a CSF fistula is recognized at operation, one closes this fistulous
component with a fascia lata graft. The fascia is placed against the diaphragma sellae
within the intrasellar compartment. This is then held in position with a section of
quadrangular cartilage if that is readily available or, more recently, a small piece of
Marlex mesh. Fat taken from the subcutaneous tissue at the time of the fascial resection
is utilized to fill the sphenoid and hold the graft material in position.

been removed one would open the dura anterior to the circular sinus as well as inferior to
the circular sinus (along the floor of the sella) to isolate the circular sinus. One would
then coagulate and transect this sinus to gain direct visualization of the suprasellar
cistern, preserving the pituitary in its position. Under these circumstances, it is
frequently if not always necessary to open the arachnoid intentionally to drain out CSF
so that one may adequately visualize the suprasellar compartment.
Once the capsule of the craniopharyngioma is recognized, a needle may be inserted to
drain any cystic fluid. The contents can then be resected piecemeal with progressive
infolding of the capsule of the craniopharyngioma or other cystic lesions to effect a
radical removal of tumor. This
Figure 20.14. Once the retractor has been removed, the nasal mucosa is approximated
and tamponaded by placing a posterior and anterior nasal pack of Vaseline gauze. The
posterior pack is placed up against the rostrum of the sphenoid to hold the fat graft in
position when this is required. The gingival mucosa, which heals rapidly and readily, is
approximated with three inverted knot sutures.

same technique obviously allows for resection of those suprasellar tumors that extend
anteriorly over the tuberculum sellae and defy extraction via a resection solely of the
sellar floor.
Once the mass has been resected, attention must be paid to the need for obliteration of
the CSF fistula if one has been created (Fig. 20.13). Under such circumstances, we prefer
to use a fascial graft constructed from a small segment of fascia lata. The graft is placed
on the intradural side of the opening and then is held in position by a section of cartilage
wedged into the bony opening to hold the dura mater against the graft. The sphenoid
opening or the opening behind this graft is then filled with fat taken from the site of the
graft to buttress the graft into position. After removal of the self-retraining retractor, the
nasal mucosa is approximated and tamponaded by utilization of bilateral posterior and
anterior nasal packs (Fig. 20.14). The posterior nasal pack is placed up against the
sphenoid opening to prevent migration of the fat that may have been placed in the
sphenoid. If a graft is not necessary, strips of Surgicel (absorbable hemostat; Johnson &
Johnson, New Brunswick, New
Jersey) are placed down along the tumor bed, and the sphenoid sinus is not filled with a
fat graft. Approximation of the gingival mucosa before insertion of the nasal packs is
accomplished with three plain catgut sutures that create relative approximation of the
mucosal margins without an attempt at hemostasis, which is accomplished by the
insertion of the nasal packs.

Pitfalls
As with any operative procedure, anatomical variations or intraoperative
misadventures may occur. With the exception of the aforementioned variability in the
size of the nasal spine and height of the vomer and rostrum of the maxilla, most
anatomical variations can be anticipated on the basis of the preoperative
roentgenograms. There are a number of points during the course of the dissection that
may allow an individual to go astray. The first of these most commonly occurs during
the dissection of the nasal mucosa from the vomer, particularly in its transition to the
quadrangular cartilage. Because of dense adhesions at this level, it is easy to tear through
the nasal mucosa, resulting in entrance into the nasal cavity. A small tear, particularly
one that is unilateral, can be well tolerated and not prevent one from continuing with a
meticulous dissection to accomplish one's objectives. However, bilateral tears,
particularly with resection of the quadrangular cartilage when that becomes necessary,
can leave the individual with a large nasal perforation that can be quite symptomatic
with respect to respiratory noises and chronic nasal drainage. Beyond the mucosal
dissection, one must be concerned about the relationship of the parasellar vascular
structures to any sellar and suprasellar lesion. Invasion of the cavernous sinus is a
commonplace event under such circumstances, and one may frequently enter the
cavernous sinus to resect such invasive tumor without any undue or excessive morbidity.
Deviations in the course of the carotid arteries, however, can be of grave consequence;
one must exert extreme caution when opening the dura mater to make sure that an ectatic
carotid artery does not underlie the sellar dura mater. I have seen both carotid arteries
touching within the midline, emerging from the cavernous sinus as they traverse that
structure.
A graft that is not adequately secured to obliterate a fistulous opening in the
subarachnoid space will not inhibit the genesis of a postoperative CSF leak. A good rule
of thumb is to perform a Valsalva maneuver after insertion of the graft to assess the
integrity of the graft. There should be no CSF transgressing the graft. Finally,
inadequate insertion of nasal packs does not allow for adequate tamponade of the nasal
mucosa to inhibit postoperative bleeding from this site. Such bleeding can occur in a
retrograde fashion, resulting in the genesis of a suprasellar postoperative clot, or may
emerge through the pack or gingival opening, causing persistent bleeding through the
gingiva. Under the latter circumstances, reinforcement of the nasal pack will usually
result in sufficient tamponade. When retrograde hemorrhage occurs, however, it is
necessary to reexplore the operative site, extract any accumulated clot, and repack the
nasal mucosa.
If, during the course of the operative procedure, there is excessive bleeding from
within the cavernous sinus, this can be readily controlled by the application of a Surgicel
pack against the bleeding site. The pack is held in position for a good 10 to 15 minutes
to tamponade the bleeding site. Inadvertent entrance into the carotid artery at this level
presents a much more serious problem. This would call for the insertion of a permanent
pack to tamponade the bleeding site sufficiently while at the
same time avoiding excess compression of the artery, which could result in carotid
stenosis or occlusion. Such a pack can be temporarily fashioned from Surgicel while a
fascial or muscle graft is obtained from the preoperatively prepared leg. This graft would
be inserted directly against the bleeding site and then be held in position by a fat graft
that would come out through and fill the sphenoid sinus.

Complications
The above pitfalls and potential complications, although distinctly unusual, are
relatively specific to this technical approach. There are, however, additional potential
complications that relate to the neural structures involved with tumor progression. These
potential complications are, of course, inherent in any surgical procedure that undertakes
decompression of neural structures from such masses. If one should extend beyond the
confines of the arachnoid in extracting one of these masses via the transnasal route, there
is an obvious potential for entanglement of optic nerves, suprasellar carotid artery,
hypothalamus, and pituitary stalk. Interestingly, a number of sizable series in addition to
ours have demonstrated that the likelihood of such complicating factors seems
significantly less with the transnasal route rather than the transcranial route. The
incidence of visual recovery, for instance, seems to be at least as good if not better with
transnasal resection of suprasellar tumors as compared to the transcranial approach.
When it is necessary to breach the arachnoid utilizing the transnasal approach, extreme
caution must be exercised in assessing the extent of available tumor for resection
utilizing this technique. Any undue stress on adjacent structures and on tumor capsule is
to be avoided during the course of resection. If one remains confined to the
extraarachnoidal compartment, the potential for such complications is virtually
nonexistent.
It has become evident over the past 2 decades that compressive lesions of the third
ventricle arising from the suprasellar cistern or structures inferior to this may be resected
effectively and safely via a transnasal approach. The duration of operation is generally
significantly less than for transcranial operation in experienced hands, and the reported
mortality and morbidity is such as to make this procedure the optimal choice for
resection of such lesions.

References
1. Ezrin C, Horvath E, Kaufman B, Kovacs K, Weiss MH: Pituitary Surgery.
Boca Raton, FL, CRC Press, 1980, p 180.
2. Guiot G: Transsphenoidal approach in surgical treatment of pituitary ade
nomas: General principles and indications in non-functioning adenomas.
Excerpta Med Int Cong Ser 303:158, 1973.
3. Hardy J: L'exeresa des adenomas hypophysaimes par voie trans-sphenolpale.
Union Med Can 91:933, 1962.
4. Henderson WR: The pituitary adenomata: A followup study of the surgical
results in 338 cases (Dr. Harvey Cushing's series). Br J Surg 26:811, 1939.
5. Schloffer H: Erfulgreiche Operation Eiwes Hypophysewtunions auf Nasal-
lam. Weg WienKlin Wochamschr 20:621, 1907.
21
Anterior and Mid-Third
Ventricular Lesions: A
Surgical Overview
Michael L J. Apuzzo, M.D., Chi-Shing Zee, M.D., and
Robert E. Breeze, M.D.

Surgery of the anterior and mid-third ventricular region remains a challenging issue. In
spite of improvements in radiological imaging, diagnosis is often in doubt; however,
structural definition is realized to the extent that preoperative planning of surgical
strategies may be performed in greater detail than ever before. The advent of imaging-
directed ster-eotaxis (12, 73) now allows for histological assay, safe endoscopic visu-
alization, and occasionally excision of lesions in the region and must be considered a
vital element in the composite of strategical alternatives.
The development of microsurgical techniques and their utilization with a number of
operative corridors (144) and intraoperative maneuvers provide a variety of approaches
that may be undertaken according to the structural and histological presentation of an
individual lesion (145, 157, 168).
This chapter reviews structural presentations of the diverse pathological spectrum
affecting the anterior and mid-third ventricle, as well as the advantages and risks of
available operative corridors, in an effort to develop guidelines for strategies in the
management of these lesions.

Pathology: Patterns of Structural Presentation

In spite of a diverse spectrum of histological processes (48), the structural presentation
of masses affecting the anterior and mid-third ventricular region may be divided into
three major groups with secondary divisions (Figs. 21.1 and 21.2). Development of this
classification is pertinent to the selection of the appropriate surgical corridor for excision
and alternative management.
Extraaxial Intraventricular
These lesions are histologically benign masses with minimal areas of origin and
adherence to elements of the ventricular walls. Microscopic surgical planes are, in
general, well defined. This category consists of lesions of developmental, neoplastic,
vascular, and infectious etiologies and includes colloid cysts, Craniopharyngiomas,
epidermoids, dermoids,
teratomas, papillomas, cysticercosis cysts, ependymal cysts, granulomas, and
arteriovenous malformations (5, 24, 27, 38, 54, 63, 64, 65, 80, 83, 109, 114, 136, 137,
138, 149, 150, 152, 153, 156, 175, 178).

Intraaxial with Ventricular Component

These lesions originate within the neural or supportive elements adjacent to the
ventricle with concomitant mass producing ventricular compression or an exophytic
component growing primarily into the ventricular cavity. Within this group are lesions
that have extended to the region by local metastasis or by remote metastasis. Examples of
the group
include the spectrum of glial tumors that may affect the thalamus, hypothalamus, or
optic structures, medulloblastomas, and germinomas (19,57, 155).

Basal
These lesions have origin from structures within the skull or brain bases and extend
superiorly to involve the third ventricular cavity. These
are most commonly histologically benign and potentially excisable lesions with various
extents of origin and involvement of the basal structures. Such lesions are, in general,
developmental, neoplastic, vascular, or infectious in origin and include pituitary
adenomas, Craniopharyngiomas, chordomas, epidermoids, meningiomas, germinomas,
arachnoid cysts, cysticercosis cysts, and aneurysms (3, 16, 17, 57, 62, 90, 125, 126, 176).
It is important to consider that these processes may be secondarily subdivided into
lesions that (a) elevate the third ventricular floor or (b) disrupt the third ventricular floor
during their evolution. Those lesions that disrupt the third ventricular floor are clearly
visualized through the foramen of Monro.
Radiology: Role of Computerized Tomography and Magnetic Resonance Imaging
Computerized tomography (CT) is the primary diagnostic imaging procedure in the
evaluation of patients with anterior and mid-third ventricular lesions. With the
availability of CT, the role of skull roentgenography, skull angiography, and
radionuclide brain scanning has diminished markedly while pneumoencephalography
has been virtually eliminated. CT has certain advantages compared to these other
imaging modalities, including safety, economy of time, and information provided. These
features have made CT an integral part of the evaluation of patients with anterior and
mid-third ventricular lesions. Not infrequently, instillation of metrizamide into the
ventricular system is required to evaluate such lesions, and magnetic resonance imaging
(MRI) will undoubtedly be a helpful modality in the evaluation of patients with lesions
in this location. MRI has the advantage of increased soft tissue contrast and rapidly
provides multiplanar imaging. As experience accumulates, MRI may well replace CT.
Mass lesions in the anterior and middle portions of the third ventricle are not
common; they can be divided into three major groups:
Extraaxial intraventricular
These lesions are important because of their potential resectability. Histologically,
they are benign masses with minimal areas of adherence to the ventricular wall. Certain
intraventricular lesions can only be identified radiographically on metrizamide
ventriculograms or metrizamide CT ventriculograms. To confirm that one is dealing
with an intraventricular lesion, one must show that the lesion can be delineated by
metrizamide on all sides except for a small area of attachment.
Metrizamide studies will also demonstrate whether the lesion has smooth margins, a
characteristic feature in many of the intraventricular lesions. MRI is also potentially
useful in the evaluation of these lesions, and the availability of coronal and sagittal
images is an asset. By selecting optimal imaging sequences, demonstration of the
intraventricular location of these lesions surrounded by cerebrospinal fluid may be
possible.
Colloid cysts are the most common anterior third ventricular lesions in many series.
They are located in the roof of the third ventricle, arising from the most anterior
extremity of the tela choroidea. The findings of CT are highly characteristic in most
cases, a well-circumscribed, high attenuation mass being seen on the noncontrast scan
(18). A slight increase in attenuation is generally seen after intravenous contrast in-
fusion. Occasionally, the cysts may be isodense or only slightly hyperdense (128).
Widening of the septum pellucidum may be associated with colloid cysts (59). Large
colloid cysts commonly bulge into the foramen of Monro and can result in intermittent
hydrocephalus.
 Ependymomas are relatively rare tumors that are seldom found within the third
ventricle. On CT, ependymomas exhibit patchy contrast enhancement with cystic areas.
Ependymomas have a relatively high incidence of internal calcification (172, 189).
Distinguishing ependymomas from deeply located gliomas may be difficult. Both
tumors may have a lobulated appearance with contrast enhancement.
Intraventricular Craniopharyngiomas are extremely rare lesions. On CT, they may
present as enhancing lesions with and without calcification, not different from
suprasellar Craniopharyngiomas. Cystic areas within the lesion may also be seen.
Cysticercosis cysts can be freely mobile or adherent to the ventricular wall.
Intraventricular cysticercosis cysts generally require the instillation of metrizamide into
the ventricular system for their demonstration because their density tends to be similar
to ventricular fluid and they tend to be thin-walled (8, 190).
Choroid plexus papillomas of the third ventricle are very rare. They are usually
attached to the roof of the third ventricle, as are colloid cysts. However, in contrast to
the smooth margin of colloid cysts, a finely lobulated, irregular margin may be
appreciated with Choroid plexus neoplasms. In addition, calcification may be seen.
Meningiomas of the anterior third ventricle are rare. CT usually shows a high density
lesion before contrast administration, with homogeneous enhancement after contrast
infusion. Calcification is frequent; this is a feature not seen with colloid cysts (101).
Intraaxial Lesions with a Ventricular Component
These lesions include the spectrum of glial tumors that may affect the optic chiasm,
hypothalamus, and thalamus as well as germinomas and medulloblastomas. On CT,
gliomas may show variable density, whereas germinomas and medulloblastomas
generally have a slight increase in density before contrast infusion; with contrast they
are usually enhancing mass lesions (122). An intraventricular component of these
lesions is also seen as an enhancing mass. Differentiation of these lesions from
ependymomas may be difficult. Frequently, metrizamide ventriculograms or
metrizamide CT ventriculograms are necessary to determine the extent of
intraventricular involvement.
MRI can play a significant role in defining the lesion and demonstrating its
intraventricular involvement in axial, coronal, and sagittal planes. A major advantage of
MRI is that the optic chiasm and pituitary stalk can be readily identified on sagittal and
coronal images. The relationship between the lesion and the optic chiasm can be
delineated readily due to the difference in signal intensity between the lesion and the
optic chiasm, which can be achieved by selecting appropriate imaging sequences. Crit-
ical information regarding whether the chiasm is prefixed or superiorly displaced are
readily available on coronal and sagittal images. CT can demonstrate the location of a
normal optic chiasm. However, in the presence of an abnormal mass lesion, separation
of the optic chiasm from a mass lesion in the suprasellar cistern may not be possible
because of a lack of significant density difference. A further advantage of MRI is that
both internal carotid arteries can be identified in the parasellar region due to the lack of
signal from rapidly flowing blood. On the coronal images, the chiasmal carotid window
can be readily defined. Encasement or displacement of the carotid arteries by tumor
mass can be readily identified.
Basal

These lesions originate from structures at the base of skull or brain

and extend superiorly to involve the third ventricle. Lesions originating from the skull
base may produce bony changes on skull films and CT scans. Lesions originating from a
parasellar location may extend occasionally into the third ventricle causing foramen of
Monro obstruction. Those lesions with a significant intraventricular component may
obliterate the anterior third ventricle on metrizamide ventriculography. Intraventricular
lesions with only a small area of attachment to the ventricular wall may be shown to have
metrizamide surrounding the lesion on metrizamide ventriculography in contrast to
suprasellar lesions that extend to the third ventricle and obliterate that structure. In these
cases, no metrizamide will be visualized within the anterior third ventricle because it has
been compressed. MRI can provide information regarding changes involving the bone
marrow in the clivus. The relationship between the lesion and the brain stem or
suprasellar cistern can be well shown on sagittal images. Again, involvement or
displacement of the carotid arteries and optic chiasm by the lesion can be clearly demon-
strated. A disadvantage of MRI is its poor sensitivity in the detection of calcification in
lesions such as Craniopharyngiomas, chordomas, or os-teochondromas.
Osteochondromas and chordomas are examples of lesions arising from the skull base.
Their origin can be traced easily to the osseous structures of the skull base (16, 90).
Pituitary adenomas typically cause enlargement of the sella turcica with the bulk of
the lesion seen within the sella. There may be varying degrees of suprasellar extension.
With sufficient suprasellar extension, involvement of the anterior third ventricle can also
be seen. CT will demonstrate an enhancing mass lesion with or without cystic changes.
Calcification in adenomas is uncommon (147).
Involvement of the anterior third ventricle is common in Craniopharyngiomas. On
CT, they often present as enhancing lesions that are frequently calcified and not
infrequently contain cystic areas (56).
Suprasellar arachnoid cysts or cysticercosis cysts extending into the third ventricle
may be quite difficult to differentiate from cysticercosis cysts or ependymal cysts within
the third ventricle on CT. Metrizamide ventriculography or metrizamide CT
ventriculography is generally required to define these lesions.
Suprasellar meningiomas can be identified as high attenuation lesions with
homogeneous, intense contrast enhancement on CT scans. Suprasellar epidermoidomas
are low density lesions that occasionally have fatty values and that may show
calcification and contrast enhancement.
An aneurysm at the tip of the basilar artery may occasionally mimic a lesion in the
third ventricle and even cause obstruction at the foramina of Monro. Caution should be
exercised to avoid confusing an aneurysm of the basilar artery with a colloid cyst.
Careful CT analysis should permit diagnosis of an aneurysm, which should be
contiguous with the basilar artery. Of course, angiography provides definitive
information in such cases.

General Technical Principles of Transcranial Approaches to the Third Ventricle

The overlying objectives in surgery of this region relate to obtaining maximal
exposure and intraoperative flexibility for lesion access and manipulation (6, 144).
These objectives are to be obtained with minimal manipulation, injury, or sacrifice of
normal neural and vascular structures. Consideration of a number of principles is
essential for a satisfactory outcome.
Corridor Selection
Multiple alternatives are available for access to the third ventricular chamber.
However, for an individual lesion usually one corridor offers optimal exposure and
maximal intraoperative flexibility. Selection of the corridor is dependent upon adequate
structural definition on imaging studies as well as possibly angiographic or
ventriculographic assessments. Proper selection of the operative corridor will minimize
the "bottom line" neural manipulation, injury, or sacrifice.
Craniotomy Flap Position
The craniotomy flap position should approximate the skull base or midline to
minimize brain retraction and maximize exposure corridors. Ventricular or spinal
drainage as well as osmotic agents should be used to reduce the mass of retracted tissues
and the need for excessive retractor pressure. Only self-retaining retractor systems
should be used.
Incision of Neural Structures
Because the third ventricular chamber can be reached only with neural transit, neural
incision is frequently required. The incision required in the lamina terminalis, corpus
callosum, or forniceal raphe should be minimized within limits of safe or adequate
exposure.
Venous Preservation
The number of veins sacrificed during transit and at the site of the lesion should be
minimized. This principle applies to both parasagittal veins and veins of the galenic and
Paraventricular systems. Techniques of alternate routes of access as well as
displacement should be used before sacrifice. Cortical injury and deep venous
thrombosis are potential causes of major neurological deficit (20, 37, 79, 127, 164, 167).
Arterial Preservation
All arterial structures in the region of a mass displacement should be preserved.
Vessels should be displaced from the tumor capsule. Numerous important arteries are
encountered when removing tumors of the third ventricle. The posterior circle of Willis
and basilar apex appear below the floor. Perforating branches of the anterior circle are
intimately associated with the anterior wall. The posterior cerebral, pericallosal,
superior cerebellar, and choroidal arteries are adjacent to the posterior wall. Both
anterior and posterior cerebral arteries supply the roof. The internal carotid, anterior
choroidal, anterior communicating, and posterior communicating arteries supply
perforating branches to the walls. Disorders of memory, personality, and consciousness
are the cost of otherwise technically adequate procedures involving minimal vascular
injury or sacrifice.
Lesion Management
Every effort should be made to minimize trauma and the transmission of pressure to
normal structures in the region of the abnormality. This may be achieved not only by
obtaining adequate and comfortable expo-sure, but also by utilizing careful principles of
lesion excision. Mass presence should be minimized initially by internal
decompression. Initially, aspiration should be undertaken. Next the capsule should be
opened, a biopsy obtained, and intracapsular removal completed at high power
magnification by microsurgical technique with or without microsurgical adjuvents.
Only after this is completed should an effort be made to separate the capsule from the
neural and vascular structures. With decompression, a combination of brain pulsation,
microirrigation, and microdissection most often will produce satisfactory dissection
planes.
Operative Approaches
After the recognition and radiological definition of the pathological process in this
region, the goals of the surgical undertaking should include (a) definition of histology,
(b) maximal excision of the lesion, (c) relief of the alteration in cerebrospinal fluid
dynamics, and (d) relief of local signs and symptoms attendant to the regional mass.
A number of operative techniques (Table 21.1) are available and of safe and proven
value. Each must be performed appropriately from the technical standpoint and applied
properly to the structural and histological substrate if optimization of result is to be
realized.
Major operative categories include: (a) craniotomy by basal, superior, or combined
approaches; (b) imaging guidance stereotaxy; and (c) cerebrospinal fluid diversion.

Craniotomy
Basal
Masses with basal components and origin are appropriately exposed by a number of
alternative routes (Figs. 21.3 and 21.4). All are essentially extraaxial corridors.
Transsphenoidal
This approach offers excellent and rapid access of the sella turcica (184). In the event
that this structure is enlarged by the mass, even greater suprasellar access is available in
vectors that are in the line of sellar distension. Visual system and third ventricular region
masses are readily decompressed, particularly if lesions are cystic or soft.

Figure 21.3. Sagittal (A) and coronal (B) representations of corridors of access to the
anterior and mid-third ventricular region, as well as basal components of lesions
affecting the chamber.
 Lesion excision and surgical expectations are limited in the event that angular frontal
or temporal masses exist or when masses are solid in texture. In addition, excision of
dense Capsular components that may be adherent to vascular and neural structures is
rarely complete and is undertaken with risk (4, 41, 70, 100). Therefore, tumor excision is
generally limited to the removal of tissue within the tumor capsule, permitting the
capsule to retract from neural and vascular elements. A number of potential
complications must be considered with a transsphenoidal exposure (72, 144, 184): (a)
stretch injury of the infraorbital nerve, secondary to sublabial manipulation and
speculum insertion; (b) olfactory injury with misdirection of superior dissection; (c)
optic nerve injury with optic foramen fracture secondary to forceful retractor opening;
(d) multiple cranial nerve (optic, oculomotor, trochlear, trigeminal, abducent) and
carotid artery injury with cavernous sinus trauma; (e) carotid, trigeminal, or optic nerve
injury with forced retractor opening and forceful manipulation in the sphenoid sinus; (f)
optic nerve, chiasmal, circle of Willis, and hypothalamic injury with excessive
manipulation during tumor excision, and (g) cerebrospinal fluid fistula with arachnoid
disruption.

Transcranial (Fig. 21.5)

Subfrontal. Basal midline tumors with suprasellar extension may be readily
approached by the subfrontal route either unilaterally or bilaterally (134, 135). This
approach may be undertaken along midline or oblique frontal corridors. With the
midline corridor, angulation for visualization of the optic nerves and carotid arteries is
perhaps best in terms of general anatomical comprehension (Fig. 21.6). The surgeon can
work between the optic nerves and easily identify the pituitary stalk and carotid arteries.
The arachnoid of the anterior chiasmatic cistern is opened. Retraction and manipulation
of the optic nerves and chiasm is minimized. After internal decompression of the mass
by initial techniques of needle aspiration and microsurgical reduction of the interior of
the mass, microdissection of the capsule is undertaken.
In general, posterolateral exposure along the ipsilateral carotid artery and the visual
system is limited. This may be optimized by lateral extension of the basal component of
the bone flap to the pterion. With the utilization of a midline corridor, the
transsphenoidal (133) entry via the planum sphenoidale may be used if the chiasm seems
to be prefixed, and the lamina terminalis (often distended by the mass) may be incised to
offer tumor access or visualization. These maneuvers offer a secondary route for tumor
manipulation and delivery (91, 169, 170). The lamina terminalis entry is of value with
masses located above the sella turcica, but below the foramen of Monro, particularly if
the chiasm seems to be prefixed and subchiasmatic access is not available. In attaining
this exposure, care should be taken to preserve perforating branches from the anterior
cerebral and anterior communicating arteries. Midline incision of the lamina is optimal.
Lack of superior displacement of the A1 (horizontal) portion of the anterior cerebral
artery with a suprasellar mass often will be anatomically attended by a "prefixed"
chiasm (2). Such an angiographic observation usually indicates a primary anteroinferior
vector of chiasmal displacement as the evolving mass affects the normal anatomy of the
region.
The transsphenoidal approach is indicated if the chiasm is prefixed, the sinus is
aerated, opticocarotid access is limited, and the lamina terminalis is not distended by
tumor.
Pterional. The pterional approach offers the shortest transit from
scalp to sella turcica, as well as good anterolateral visualization of the ipsilateral carotid-
neurovisual pathway (Fig. 21.7). With opening of the medial sylvian fissure and use of
the opticocarotid and lateral carotid corridors, visualization of the retrosellar space is
realized (177). Such exposures are effective for suprasellar tumors where the chiasm is
prefixed. The opticocarotid corridor is utilized if asymmetrical superolateral extension
of the mass distends the interval between the optic nerve and the carotid artery,
particularly if the chiasm appears prefixed. Care must be taken to preserve perforating
branches from the internal carotid artery to the visual system.
When using this exposure, one must realize that the opposite carotid
artery and optic nerve are not fully visualized initially. Tumor removal is often difficult
because of the obstructing disposition of major neural and vascular structures, with
various nerves and arteries positioned at peculiar angles that are difficult to
conceptualize without considerable experience.
Subtemporal. The subtemporal corridor offers optimal exposure for lesions in the
posterior, parasellar, dorsum sella, and posterior perforated space regions (Fig. 21.8). If
sufficient mass is present, exposure of such a lesion may be gained via the pterional
opticocarotid approach. However, direct access for posterior suprasellar lesions is
optimized subtemporally. The major consideration with this approach is the posterior
communicating artery with its perforating branches to the region. In addition, medial
angulation of the tentorium may limit exposure. This approach requires extensive
temporal retraction and provides poor visualization of structures in the prepontine
cistern. The surgeon may visualize the ipsilateral posterior cerebral and superior
cerebellar arteries, but the contralateral structures are not fully visualized. In addition,
the ipsilateral third and fourth nerves are in the line of the approach.
All of the basal approaches, although providing access to basal components of an
offending mass, provide limited superior access or visualization.
Superior
These approaches offer exposure of the third ventricular via superior entry through
the trunk of the corpus callosum or the frontal cortex. These corridors are used for
exposure and excision of intraventricular lesions or intraventricular components of basal
lesions that are not accessible from a basilar approach (2, 16).

Transcortical
Originally described by Walter Dandy, this approach classically is undertaken
through the right middle frontal gyrus and is optimally used
in the presence of ventriculomegaly, which enhances exposure without the need for
excessive brain excision, retraction, or manipulation. It offers excellent visualization of
the ipsilateral foramen of Monro with a satisfactory visual alignment for lesions of the
middle and midanterior sections of the third ventricular chamber. It provides the optimal
angulation for use of the subchoroidal exposure, but a less satisfactory visual alignment
for the interforniceal maneuver or visualization of the contralateral
foramen. In addition to the sacrifice of neural tissue required, it is considered to have a
higher incidence of seizure complications than the transcallosal exposure. Guidance
during the pial-ependymal transit may be enhanced by using real time ultrasonography.
Transcallosal
The transcallosal corridor, gained by interhemispheric exposure of the body of the
corpus callosum in the pericoronal region followed by a 2- to 3-cm incision, offers the
major advantages of constant anatomy, shorter transit to the diencephalic roof, and
flexibility of exploration within the entire third ventricular cavity through the optimal
access provided by interforniceal exposure simultaneously with visualization of both
foramina of Monro. There is no disruption of hemispheric tissue and, importantly,
ventricular size is irrelevant (10, 110, 111, 162, 163, 166).
Section of the callosal trunk has been extensively evaluated and does not carry a
physiological cost currently considered to be measurable or recognizable (10, 21, 82).
However, the interhemispheric exposure carries the risk of contralateral hemiparesis (10,
162). The incidence of such a complication may be reduced by the utilization of
preoperative angiography as an adjunct to operative planning and refinement of operative
technique (10). Mutism, a rare complication, may be related to bilateral cingulate
retraction.
Both superior approaches offer exposure of the foramen of Monro and diencephalic
roof with optimal maneuvers for third ventricular entry including (a) transforaminal, (b)
transforaminal with ipsilateral forniceal column section, (c) subchoroidal, and (d)
interforniceal visualization (Fig. 21.9).
The goal of surgery is total excision with minimal trauma to adjacent neural tissues.
The amount of exposure required to accomplish this end will vary with the nature of the
pathological process and the skill and
experience of the operator. Requirements for exposure are variable, but knowledge and
familarity with each method of exposure of the third ventricular chamber is imperative
to expand the spectrum of options and thus the safety of the operative endeavor.
Each of these methods and options carries certain advantages and disadvantages (53).
Transforaminal Visualization. Transforaminal exposure may be op-
timized by the presence of a large lesion that distends the foramen, although this is not a
dependable feature of third ventricular lesions (Fig. 21.10). In such a case, if the
angulation of exposure is satisfactory, excision may be accomplished with minimal
midline manipulation. This is dependant in all cases on the texture of the individual
lesion and its resistance to methods of excision initiated by the operator. Often, espe-
cially in the presence of a firm lesion, inadequate access to the posterior and
anterosuperior component necessitates further exposure maneuvers.
Transforaminal Exposure with Unilateral Section of the Ipsilateral Column of the
Fornix. This method of enlargement of the area of exposure has been advocated in the
past. However, it is not recommended as other maneuvers afford greater exposure
without the sacrifice of neural elements.
Subchoroidal Visualization. This technique, which takes advantage of the natural
plane at the region of the lamina affixa, allows mobilization of both forniceal bodies
from ipsilateral to medial (Fig. 21.11). This approach provides access to the central
portion of the ventricle by lateral displacement of the fornix via the velum interpositum
(43, 49, 75, 98, 99, 179). It is suited for lesions in the superior half of the third ventricle
adjacent to the roof and posterior to the foramen. This exposure is expanded to include
directly the foramen of Monro by sacrifice of the thalamostriate vein at the foramen—a
maneuver that has not been recognized to initiate complicating events. This tolerance
confirms the capacity of collateral connections to shunt blood from the deep medullary to
the superficial subependymal venous systems. These collaterals are apparent in certain
pathological processes. In patients with a direct lateral tributary to the internal cerebral
vein, both the septal and thalamostriate veins may be safely sacrificed. The direct lateral
vein is similar to the thalamostriate vein; both receive transverse caudate tributaries,
although the direct lateral vein enters the internal cerebral vein 1 to 2 cm posterior to the
thalamostriate vein. With the presence of a mass and inadequate foramen exposure, this
maneuver will often provide satisfactory exposure without active retraction of the fornix.
Lines of visualization for this maneuver are optimized by the transcortical approach. In
our experience the transcallosal approach may be used as an initial stage before this
maneuver, but it is somewhat less satisfactory. A drawback of this technique is that, if a
lesion is small or moderately sized, retraction of the thalamus may be required to gain
adequate working visualization with the transcortical corridor.
Interforniceal Visualization. This maneuver (10, 11) takes advantage of a natural plane
of division between the columns and bodies of the fornices that opens into the
diencephalic roof (Fig. 21.11). This division is occasionally apparent with biventricular
exposure in the presence of a mass and is clearly evident in the presence of a cavum
septum pellucidum or septal leafs. It is readily defined by the passage of a
microinstrument at the line of the septal insertion in the presence of a mass. When
combined with the transcallosal approach, this maneuver affords complete exposure of
the third ventricular chamber and midline basal structures. In the presence of a
significant mass, active retraction is not required; the internal cerebral veins are
displaced by the mass or may be retracted for inferior or posterior visualization as
required. This maneuver is undertaken only if transforaminal exposure is inadequate or if
manipulation seems excessive. This exposure combined with bilateral foraminal
exposure as afforded by the transcallosal technique provides the most extensive exposure
of the third ventricular chamber.
 Although a number of problems related to the hypothalamic region and its elegant
functional components are possible (34, 106, 110, 111, 130), the major complication
experienced with micromanipulation of the midline diencephalic structures is transient
memory loss. This problem is observed with each of the previously discussed techniques
and is generally transient. It is considered to be related to direct and transmitted trauma
to the deep midline and paramedian structures.
Combined
A single corridor occasionally provides inadequate exposure for satisfactory and safe
excision of basal masses with simultaneous third ventricular involvement. In such cases
consideration must be given to an approach that combines features of both basal and
superior exposures.
Yasargil et al. (187) described simultaneous pericoronal and pterional bone flaps to
effect transcallosal and pterional exposures. Ehni and Ehni (53) described a large
frontotemporoparietal bone flap for multiple corridor exposure. We have developed a
miter bone flap (Fig. 21.12) that affords exposure of the cerebral midline in the
pericoronal region for transcallosal exposure and the entire frontal floor medial to the
pterion for subfrontal and lateral optic access. This flap may be developed after a
bicoronal incision and requires incision of the temporalis muscle in a quadrant cresent at
its posterior base. This flap has proved to be economical in terms of effort versus extent
of exposure and has proven to be ideal for basal masses with large mid- and anterior
sellar attachments. It is not recommended for masses with temporal components, which
will require more extensive temporal exposure. Transcortical exposure of the foramen is
easily accomplished. Subfrontal exploration is undertaken during the initial stage of the
procedure; superior corridors are established if required as a secondary step after the
extraaxial operation.

Imaging Guidance Stereotaxy

The wedding of computerized tomographic scanning or magnetic resonance scanning
and stereotactic techniques has added a new dimension to the management of
intracranial masses and most particularly lesions in the third ventricular region (7-9, 12,
13, 23, 85, 87, 88, 105, 129). Low risk biopsy may be achieved, providing guidance for
operative or nonoperative decision making (1, 44, 81, 108, 142). In addition, by using
ventriculoscopic (78, 180) techniques with imaging guidance stereotaxy, cystic lesions
may be aspirated (under direct vision) or excised with microinstrumentation. We have
used such methods satisfactorily with craniopharyngioma cysts, colloid cysts, and
cysticercosis cysts, totally excising cysticercosis cysts. Intracavitary brachytherapy of
neoplastic cystic lesions seems to provide either an alternative to craniotomy or a
postoperative adjuvant of substantive importance (68, 124).

Cerebrospinal Fluid Diversion

Biventricular shunting offers a method of management for lateral ventriculomegaly
and its attendant symptoms secondary to bilateral foramen of Monro obstruction. At
times third ventricular masses permit communication between the lateral ventricles via
the formina-anterior third ventricular complex. This may be indicated on imaging studies
or be established by ventriculostomy followed by metrizamide ventriculography.
Internalized ventriculoperitoneal or jugular shunting is occasionally required after direct
management of third ventricular masses. At craniotomy, third ventriculostomy (78) is
accomplished with trans-lamina terminalis exposures with lesion excision or perforation
of the region of the tuber cinereum (Fig. 21.13). Silastic (Dow Corning, Midland, Michi-
gan) conduits may be established from the prepontine cistern through the ventricle and
midline corridor to a subgaleally placed Rickham reservoir. Internal measures of fluid
diversion can be judged competent only by close observation of the patient with
intracranial pressure monitoring over a 48- to 72-hour period, followed by frequent
clinical and radiographic assessment.
Fenestration of the septum pellucidum is advisable with all direct third ventricular
exploration to preclude the need for bilateral shunting procedures.
Memory
In the microsurgical era, operation of the third ventricle with associated manipulation
of midline basal cerebral structures is often attended by postoperative manifestations of
an amnestic syndrome (34, 10-12). Fortunately this complication is usually transient
(days to several weeks
duration). This striking complication is observed in what is, in most cases, an otherwise
functionally intact patient, generating considerable concern and providing a major
obstruction to optimal patient performance. The fornix, the major interconnecting limbic
pathway and a major component of the diencephalic roof, is by "tradition" considered to
be the primary focus of neural injury in such cases. However, the substance of this belief
may be challenged. There is no agreement in the literature whether fornix integrity is
required for normal memory. Although this structure represents a major limbic pathway,
significant comparable fiber bundles would remain intact after isolated forniceal injury.
Importantly, nearly all hippocampal connections with the associated cortices would be
structurally patent. More logically, current data seem to indicate
that diffuse multifocal midline injuries to a number of areas concerned with the memory
process are collectively required for the amnestic syndrome (45, 61). These areas
probably include the basal forebrain nuclei, the thalamic nuclei, and the inferior thalamic
peduncle.
The basal nucleus of Meynert lies predominantly in the substantia innominata. This
structure extends inferiorly to the basal ganglia and pallidum from the midline to the
temporal lobe. Its major component lies adjacent to the midline millimeters from the
third ventricle (Fig. 21.14). This region provides major cholinergie input to the cortical
region. Fornix injury may alter cholinergie input to the hippocampal formation, which,
when combined with pathological basal nuclei, could impact upon all cortical
cholinergie innervation.
Important thalamic nuclei include the nucleus reuniens and other associated midline
nuclei such as the Paraventricular nuclei. These groups are situated between the anterior
pole of the thalamus and the dorsal medial thalamic nucleus directly over the third
ventricle. These nuclei provide major input to the entorhinal cortex. The nucleus
reuniens projects to the hippocampus, with logically afferent brain stem influence. With
associated forniceal injury, the hippocampal formation would be partially restricted from
afferent and efferent perspectives.
The inferior thalamic peduncle carries a major component of amygdaloid output and
provides a major connection with the dorsal medial thalamic nucleus. Both are
considered to be important anatomic elements of memory. This structure is limited in
anteroposterior extent, but is immediately adjacent to the third ventricle as it passes
inferior and medial to the globus pallidus.

Craniopharyngioma
Surgical Pathology
Although comprising between 1 and 4% of all primary intracranial neoplasms, this
histological entity represents one of the more common surgical problems in the third
ventricular region. Great variability in size is evident, with components of the lesions
often involving the sellar, suprasellar, and third ventricular compartments with
combinations of cystic and solid components (2, 92). As Craniopharyngiomas are classi-
cally considered to arise from rests of buccal epitheleum that accompany migration of
Rathke's pouch from the premature stomadeum upward to join the infundibulum and
form the pituitary gland and its stalk, the spectrum of compartmental and structural
variability is broad (48). Lesions may be totally intrasellar, intrasellar and extrasellar,
suprasellar only, or intraventricular only. The most common structural manifestation is a
suprasellar mass with displacement and/or disruption of the floor of the third ventricular
chamber. These lesions may be totally extraarachnoidal, but may also be intrapial with
finger-like projections invading neural tissue. The presence of this intrapial component
may be attended by intense glial reaction in adjacent brain. This reaction acts as an
impediment to establishing dissection planes in some cases and, particularly with cystic
lesions with fine membranes, may further complicate efforts at excision. This response is
variable in intensity and extent and, in certain cases, may provide a "buffer area" that
allows dissection exclusive of functioning neural tissue (159, 173, 174).
A major technical issue relates to involvement of the components of the circle of
Willis with elements of the neoplasm. Such intimate adherence often provides the major
limitation in excision (31, 32, 35, 36, 40, 52, 60, 67, 77, 84, 86, 94, 115, 116, 119, 123,
141, 151, 158, 171).
 Operative Techniques (Suprasellar)
For the purposes of this discussion the operative considerations for a
suprasellar craniopharyngioma without a temporal or major frontal component
are described. This may be considered, with some modification, a "traditional"
basal frontal exposure.
If hydrocephalus is present a left frontal ventriculostomy is established.
Bilateral ventriculostomies may be required in the event that complete
obstruction of the right foramen is present. Components of a right basal
frontotemporal exposure or a complete frontopterionotemporal craniotomy may
be performed. We have preferred a right frontal craniotomy that incorporates the
entire frontal floor from the midline to the sphenoid wing. This craniotomy is
accomplished by incising the temporalis muscle parallel to the frontal floor to
the region of the pterion and then extending the incision at right angles to the
base along the line of the coronal suture. A free bone flap is turned with the
crescent of temporal muscle at the posteroinferior base. This exposure offers
options of pterional and lateral wing excision and opening of the sylvian fissure
for added basilar and lateral exposure. The approach to the lesion is extraaxial
via a number of optional angular corridors. The medial subfrontal approach
offers optimal visualization of both optic nerves, but poor angulation for appre-
ciation of the lateral component of the optic nerve, carotid artery, and optic tract
anatomy. The laterofrontal corridor afforded by the posterior (lateral) exposure
affords such exposure and adds another intraoperative option. During initial
exposure the orbital surface of the frontal lobe is protected by Bicol (Trimedyne,
Santa Ana, СA) as identification of the optic nerve and tumor surface is made
under low power magnification. Self-retaining retractor systems are essential.
After exposure of the parasellar region, a number of options are available,
including the subchiasmal, opticocarotid, lateral carotid, transsphenoidal, and
translaminar exposures.
Selection of each of these options is related to anatomic presentation.
Therefore, an effort should be made to accomplish complete appreciation of all
elements of anatomic presentation and distortion of normal anatomic
relationships. The maximal exposure of tumor surface is the goal of this stage of
the procedure.
After initial tumor exposure the arachnoid layer is identified and incised, with
care being taken to preserve the margin of the tumor-arachnoid envelope.
Internal decompression by aspiration is the next stage of the excision, as even
minimal aspiration may enhance dissection planes at the tumor margins. Further
internal decompression is afforded by methods of aspiration, bipolar
cauterization, and sharp excision or laser vaporization (51). Care should be taken
in the presence of calcium to avoid transfer of excessive heat generated by laser
energy. It is preferable to crush calcium with microinstrumentation and remove
it piecemeal. Use of a 5 French suction-irrigation system with sharp dissection
within the tumor capsule-arachnoid envelope facilitates dissection. The major
feeding arteries are most often derived from the anterior circulation components
of the circle of Willis (anterior cerebral, anterior communicating, carotid, and
posterior communicating arteries). These small branches may be coagulated,
with care being taken to preserve feeding branches to the inferior chiasm and
tracts.
Capsular components are removed in sections, with care taken to avoid "blind"
or excessive traction.
Anatomic maintenance of the pituitary stalk is a major objective in any
microsurgical dissection in the sellar region and is a requirement for normal
pituitary function. With high-power magnification the stalk is
readily recognized by a distinctive striate pattern (portal system) that is directed
vertically from the inferior hypothalamic surface to the diaphragma region. This
structure is most often identified in the posterior or posterolateral tumor margins. At
completion of the excision, angular dental mirrors or endoscopes aid in regional
visualization.
Although considerable variability of opinion exists regarding the resectability of such
lesions, available data imply that initial direct exploration is the most appropriate
management, especially in lesions with solid components (36, 76, 77, 173, 174, 159).
Such action is required to assess properly the operability of these lesions. Major
objectives in the procedure include decompression of the visual system and reduction of
local mass effect at the foramen of Monro. With attainment of these goals the procedure
should probably be terminated if microdissection planes are obscure.
Radiation therapy (76, 95, 96, 146) should be initiated during the postoperative period
if operative knowledge or postoperative imaging indicate the presence of tumor or
residual calcium. Early recurrence (months) is most commonly cystic and should be
managed by imaging stereotactic methods with conduit/reservoir placement for drainage
and consideration of colloid-based radionuclide installation (14, 15, 93, 103, 104).
Reoperation is not precluded by previous operations and radiation treatment.
However, surgical expectations are less optimistic and risks increased in relation to the
initial procedure when dissection planes were optimal (77, 173). In the event that
reoperation is required, it is worthwhile to consider an alternate corridor. Guidelines for
exploration of the variations in structural presentations are detailed later in this chapter.

Colloid (Neuroepithelial) Cyst

Developmental and Surgical Pathology
Colloid cysts of the third ventricle are relatively rare lesions accounting for 0.5 to
1.0% of primary intracranial, neurally derived tumors. Many terms have been applied to
these lesions, including neuroepithelial cysts, neuroepithelial tumors, paraphyseal cysts,
ependymal cysts, epithelial cysts, Choroid plexus cysts, and cysts of the foramen of
Monro (47, 66, 89, 131, 132, 183, 192).
Although the first documented case a of colloid cyst of the third ventricle was
reported by Wallmann in 1858 (181), it was not until 1933 that Dandy (46) described the
radiological definition and surgical management of these lesions (185).
There has been considerable debate and controversy over the origin of the cyst. In
1910, Sjovall suggested that the cyst was a remnant of the paraphysis. The paraphysis is
a constant feature of human embryos in the 17- to 100-mm stage and lies at the rostral
end of the diencephalic roof. This widely accepted concept carried with it the belief that
such cysts occurred only at the anterior part of the third ventricle. In 1955, Kappers
suggested that, although occasional examples are paraphyseal in origin, most arise from
diencephalic ependymal pouches (160). The Choroid plexus has been proposed as an
alternate site of origin of such cysts. The term neuroepithelial cyst was proposed by
Shuangshoti and Netsky in 1966 (161). They proposed that these lesions may occur any-
where along the course of the central nervous system from the Choroid plexus or
ependyma, both being derived from a common neuroepithelium.
Most commonly, colloid cysts arise in the anterior superior part of the third ventricle
immediately posterior to the foramen of Monro (4, 28, 33,
59). They generally project inferiorly into the third ventricle and vary in extent
superiorly and rostrally. Attachments of various dimensions are present with the tela
choroidea of the third ventricular roof. Occasionally, the forniceal column superior to
the anterior commissure will be separated by the mass (41). This separation may involve
the leaves of the septum pellucidum. Generally, the cyst is well circumscribed, smooth,
and spherical with dimensions varying from 0.3 to 9 cm. The wall of the cyst is
composed of a layer of epithelial cells, either low columnar or cuboidal, and surrounded
by a connective tissue capsule (74). The cyst is filled with homogeneous viscous
material containing cellular debris. This material is variable in viscosity. Various
numbers of desquamated epithelial cells, leukocytes, red cells, gitter cells, and
cholesterol pigment have been described in the colloid material.
It is important to recognize that these lesions may occur posterior to the foramen of
Monro and that they may be attended by various degrees of aqueductal stenosis.
Symptomatology
Numerous perspectives relating to symptomatology are available in the literature.
Symptom complexes include the following.
Acute and Intermittent Increases in Intracranial Pressure
This causes the "classical" history of paroxysmal headache with changes in head
position. These episodes may be attended by vertigo, vomiting, alterations in conscience
level, alterations in mentation, seizure activity, vital sign aberrances, or cerebrospinal
fluid rhinorrhea. The predisposition to acute demise has been repeatedly stressed (30,
39, 55, 58, 102, 113, 117, 186, 188).
Chronically Increased Intracranial Pressure
In this complex chronic dementia alone or in combination with gait disturbances and
urinary incontinence are encountered (107).

Local Pressure Effects

These effects related to the mass include sensorimotor, extrapyramidal, and
autonomic disturbances and memory disorders (97).
Identification of the presence of these lesions by the "classical presentation" is
unusual. Long-standing, intermittent, nonspecific headache without attendant postural
exacerbations is the most frequently encountered complaint (39, 118).

Radiology
As has been noted, imaging studies provide the primary indicator toward suspicion of
this lesion, with masses generally presenting in the anterior third ventricle with attendant
lateral ventriculomegaly (154, 191). The spheroid masses are usually slightly
hyperdense, but may be isodense (50, 140). The lesion generally shows some elements
of uniform enhancement with contrast medium, but no ring enhancement has been
described (29). Attendant structural alterations include enlargement of the septum
pellucidum and collapse of the posterior third ventricle. Fullness of the posterior third
ventricle may be present if aqueductal stenosis is present.
Occasionally, such a lesion may be disclosed as a truly "incidental" finding with no
evidence of lateral ventriculomegaly. Focal enhancement may indicate the presence of a
xanthogranulomatous component.
Management
In spite of their benign histological character these lesions are life-threatening
(39). Although the absolute risk of demise has not been accurately determined,
there is no doubt that, because of their location and repeated documentations of
rapid and fatal neurological deterioration, definitive management to reduce the
cyst mass or maintain normal cerebrospinal fluid dynamics is most appropriate.
An element of controversy exists regarding the best method for treatment.
Arguments exist for the following management options: (a) biventricular
shunting, (b) stereotactic aspiration, and (c) direct excision.
Because of the potential incidence of aqueductal stenosis (30 to 40%), some
method of cerebrospinal fluid diversion may be required if option b or с is
exercised initially.
Stereotactic aspiration with imaging-guided techniques may be accomplished
at small risk and offers an apparently plausible management option (7, 12, 13, 22,
148). In our experience lesions less than 1 cm in diameter may be difficult to
puncture and aspirate; however, published experience indicates that cyst
aspiration is possible in 80% of lesions greater than 1 cm in diameter if a cannula
larger than 1.5 mm may be introduced. Use of this technique should be attended
by a meticulous and vigilant monitoring of ventricular size or intraventricular
pressure with a consideration of ventriculography postaspiration to assess
patency of the aqueduct of Sylvius. This technique requires expertise in the
utilization of such instrumentation and requires further evaluation and experience
before it can be uniformly endorsed for all cases. It is optimally undertaken with
endoscopic control.
In the event that craniotomy is undertaken, both the transcortical and
transcallosal corridors afford exposure of the foramen of Monro. Occasionally,
the forniceal raphe may be opened by the mass presence. With appreciation of
the mass at the foramen, aspiration should be undertaken with a #20 needle or #3
F suction after incision of the capsule. Miniature curettes may be introduced
within the cyst cavity to assist with reduction of the content volume. At all times,
care is taken to avoid traction or manipulation of the cyst attachment at the tela
choroidea adjacent to the foramen, which may cause venous or arterial injury.
After evacuation of the cyst contents, the wall may be coagulated and gently
delivered in fragments through the foramen. If the foramen is small or adequate
access for manipulation is not available, added exposure may be gained via
subchoroidal or interforniceal corridors.
After cyst excision, ventricular exploration may be afforded by fiber-optic
endoscopy or direct visualization if additional corridors have been established.
The development of a third ventriculostomy in the region of the tuber cinereum
may be considered at that time with or without a Silastic conduit being led
through the main operative corridor to a Rickham reservoir.
Subchoroidal or interforniceal corridors may be developed if the cyst is not
apparent at the foramen to identify the abnormality and provide a route for
manipulation and excision. In our experience "complete" third ventricular
exploration is optimally accomplished via the transcallosal-interforniceal
approach.
After cyst excision, monitoring of intracranial pressure is required for 48 to 72
hours.
Biventricular shunting as a definitive treatment may be considered. However,
70% of the patients will be unnecessarily shunt-dependent when the capabilities
of other operative methodologies are considered.
Selection of a Surgical Procedure
The selection of an appropriate surgical procedure may be governed by the presenting
structural substrate as defined on imaging studies. Many factors bear on such a selection
including those related to the individual patient, surgeon, and institution; however, our
approach to the utilization of management alternatives based on the presenting structural
substrate is detailed in Table 21.2.
Extraaxial Intraventricular Mass (6)
Masses contained within the third ventricular chamber are approached primarily via a
transcallosal corridor, which offers maximal options for midline exploration irrespective
of ventricular size (Table 21.2). If foraminal exposure is inadequate, interforniceal or
subchoroidal exposure is easily initiated.
Stereotactic excision, evacuation, and/or biopsy of cystic lesions is a primary
consideration.
Cerebrospinal fluid diversion as the isolated management of such a lesion, although
occasionally indicated because of patient factors such as age or medical fragility, is not
our primary choice. Selected cases are shown in Figures 21.15 to 21.21.
Intraaxial Ventricular Mass (6)
Such lesions with intraaxial components and ventricular involvement are often either
radiosensitive or managable by indirect means after stereotactic histological assay (Table
21.2). Management is based on information derived from stereotactic biopsy and
includes cerebrospinal fluid diversion with radiochemotherapy for malignant lesions and
transcallosal third ventricular exploration when a defined and separate intraventricular
component is present with histologically benign lesions. Cerebrospinal fluid diversion
without tissue assay is not considered a prudent alternative. Selected cases are shown in
Figures 21.22 to 21.27.
Basal Masses
Basal masses may be considered in three groups (Table 21.2): intrasel-lar-suprasellar,
suprasellar, and superior extension (third ventricular).
Intrasellar-Suprasellar Masses Intrasellar lesions (Table 21.2) with enlargement of the sella
and mid-
line suprasellar extension are optimally managed by the transsphenoidal corridor,
particularly if the lesion is cystic. In such cases with pneumatized sphenoid bones,
anterior sellar entry allows permanent fenestration of the cystic cavity. In the event that
frontal or temporal extensions are present, a craniotomy allowing access to the
appropriate fossa should be undertaken. If the sellar contour and volume are normal a
subfrontal approach is generally the most effective corridor.
Stereotactic drainage of cystic lesions with the establishment of permanent reservoirs
should be given consideration in the treatment of cystic lesions primarily in elderly or
medically fragile patients.
Suprasellar Masses
Suprasellar masses (Table 21.2) with midline subfrontal superior extension are
managed by a subfrontal exposure that allows options initiated on the basis of chiasmal
position. If radiographic assessments do not define the strict chiasmal and perichiasmal
anatomy, basilar exposure from the frontal midline to the pterion affords the optimal
exposure for the exercise of multiple options at the sellar region, including the initiation
of subchiasmatic, transsphenoidal, translaminal, opticocarotid, and lateral carotid
exposures.
Midline retrosellar masses are approached optimally through a pter-
ional corridor with opticocarotid and lateral carotid exposures. Consideration may be
given to subtemporal exposures particularly if a temporal component of tumor mass is
present.
Major subfrontal and temporal masses require exposure of their appropriate fossae.
Predominantly cystic masses in the suprasellar region are effectively managed by
stereotactic techniques in experienced hands; however, dependent on histology, an effort
at wall excision by an appropriate exposure should be considered.

Superior Extension Masses

When superior extension (Table 21.2) is apparent above the foramen of Monro and
the midline base is greater than 2.5 cm, an exposure that allows combined basal and
superior approaches is most appropriate.
If the basal component is less than 2.5 cm (midline), a transcallosal interforniceal
exposure will afford access that will allow complete excision of the lesion. In cases of
this type, the hypothalamic floor is not only elevated, but is in fact parted by the lesion
so that visualization of the tumor at the foramen of Monro is possible. Stereotactic
endoscopy has been recommended as an initial step before undertaking craniotomy for
midline exposure and lesion excision. If visualization of the lesion at the foramen is
realized, initial transcallosal exposure is appropriate; otherwise, initial subfrontal
exposure is indicated. Selected cases are shown in Figures 21.28 to 21.31.
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Commentary В
Technique and Strategies of Direct Surgical Management
of Craniopharyngioma
Alexander N. Konovalov, M.D.
At the Moscow N. N. Burdenko Institute of
Neurosurgery the problem of surgical treatment of
craniopharyngioma has always been given special attention.
About 1200 patients with these tumors have been observed
and treated. My personal experience in dealing with that
neurosurgical problem includes more than 300 cases in
which microsurgical removal of Craniopharyngiomas was
performed.
In 1974, we started microsurgical radical removal of
these tumors. Since that time our surgical technique has
evolved and our results have improved. However, this
problem is far from resolution and needs further serious
investigation.
Anatomical Variants of
Craniopharyngiomas
From the surgical point of view it is of great importance
to clarify the extension and exact localization of the tumor,
especially its relation to the third ventricle before operation.
In our practice we use the following classification of
Craniopharyngiomas according to the point of initial
growth and the relation to the third ventricle and to the
sella: endosuprasellar-extraven-tricular, and intraventricular
tumors (Fig. B.1).
Endosuprasellar Craniopharyngiomas
Small, purely intrasellar tumors are rare and can be
removed with the transsphenoidal approach. An
endosuprasellar craniopharyngioma starts to grow in the
sella and displaces upward the diaphragm, chiasm, optic
nerves, and third
ventricular floor. The pituitary stalk is usually seriously
damaged and included into the tumor capsule. In some
cases the diaphragm can be destroyed by the tumor as it
grows in various directions to reach a giant size.
Suprasellar-Extraventricular
Craniopharyngiomas
The point of initial growth of these tumors is on the level
of the pituitary stalk. The tumor destroys the stalk partially
or completely, spreads in various directions (retro-, para-,
an-tesellar), and displaces the third ventricular floor.
Intraventricular Craniopharyngiomas
If the tumor starts to grow at the level of the
infundibulum it destroys the floor of the ventricle and
penetrates into its cavity. There are two possible variants:
(a) the main part of the tumor occupies the third ventricle
(intraventricular type of craniopharyngioma) and (b) the
tumor spreads into the third ventricle as well as into the
extraventricular space.
All of these variants of Craniopharyngiomas are
summarized in Figure B. 1. This classification is just an
approximation. In practice it is not always easy to classify
the tumor according to these groupings, even at operation.
There may be mixed forms as the tumor can grow from
several points along the hypophyseal axis. In addition, we
have identified a group of giant Craniopharyngiomas that
spread far beyond the chiasma-sellar region.
 The precise diagnosis of the type of craniopharyngioma
and its relation to the third ventricle, optic pathways, sella,
and other structures is of great importance. Computerized
tomography (CT) and magnetic resonance imaging are the
best methods, but even they cannot in all cases determine
whether the floor of the third ventricle is penetrated or just
displaced by the tumor. Sometimes a preoperative
ventriculoscopy may help in defining the intraventricular
propagation of the craniopharyngioma.
Surgical Technique
Third Ventricular Craniopharyngiomas
In comparison with Craniopharyngiomas of other
groups third ventricular Craniopharyngiomas present the
greatest difficulty for radical removal. That is why many
surgical approaches have been suggested for their
management (trans-lamina terminalis, transcortical,
transcallosal, and others).
My surgical technique differs for variants of these
tumors and has changed significantly during the last 10
years. At first, trans-lamina terminalis access was
regarded as preferable. It was used in about two-thirds of
my 150 patients with intraventricular
Craniopharyngiomas. More recently, my attitude toward
this method of crani-
opharyngioma treatment has changed. I now prefer to
remove third ventricular tumors through the transcallosal
route alone or in combination with the subfrontal approach.
If there is exact information about the intra-and
extraventricular extent of the lesion, a wide right-sided
trepanation is used; its posterior edge reaches the coronal
suture and crosses the midline (Fig. B.2). It permits
transcallosal removal of the intraventricular part of the
tumor as the first stage and after that, if a basal portion of
the tumor is still inaccessible through the transcallosal
route, the subfrontal approach is used to extirpate the
extraventricular part of craniopharyngioma through the
lamina terminalis incision, under the chiasm, or through the
opticocarotid triangle.
Transcallosal Approach
The corpus callosum is divided between the anterior
cerebral arteries by a 2-cm incision. Then the tumor may be
removed through one and if necessary both foramina of
Monro (in both cases in incision is made in the septum
pellucidum). If the foramen of Monro is small it may be
enlarged by the anterior incision or the tumor may be
approached by splitting the fornix strictly in the midline.
By this method the upper part of the tumor can be widely
exposed. This permits
its radical removal (Figs. B.3 to B.6). I now use all of these
methods and the choice of the operative corridor depends
on the actual anatomical situation.
In comparison with the trans-lamina terminalis exposure,
the transcallosal approach has some important advantages:
the tumor is widely exposed, all parts of the third ventricle
are accessible, and all stages of tumor removal are under
visual control. With the transcallosal approach
important arterial branches supplying the diencephalon
can be preserved more effectively than with the basal
approach.
The first stage of tumor resection is opening of the
capsule and evacuation of the cystic fluid. The solid part
of the tumor can be removed with the help of an
ultrasound aspirator, although the size of this instrument
limits its usefulness in a narrow operative channel. The
basal suprasellar part of the tumor is usually hard and
contains
large calcifications. The removal of these calcified masses
is difficult and necessitates breaking the tumor into
fragments. This can be done by means of bipolar
coagulation. In some cases with large and very hard
calcified components we have successfully used a special
small ultra-sound knife. When the solid part is removed
the tumor capsule must be separated from the ventricular
walls and then removed in pieces.
After tumor ablation, there usually is an opening in the
ventricular floor through which one can see the pedunculi
and the basilar artery with its branches (Fig. B.6). The
basal part of large tumors inaccessible by the transcallosal
route must be extirpated by a subfrontal exposure during
the same operation.
Trans-Lamina Terminalis Approach
In all cases when the tumor was situated intra-
ventricularly a similar picture was revealed during
operation. The optic chiasm was very stretched by the
tumor and adjacent to the tuberculum sellae. The lamina
terminalis was expanded and thinned and the tumor was
usually
visible through it. After tumor puncture through the lamina
terminalis and evacuation of cystic fluid, dislocation of the
chiasm and optic nerves diminished our observation of the
sellar regions and the remnants of the pituitary stalk. The
incision in the lamina terminalis (on the average 1 to 1.5
cm long) is made strictly in the midline. At first, the solid,
calcified part of the tumor is removed; then the capsule is
gently separated from the ventricular cavity and resected
(Figs. B.7 and B.8). Using this approach, it is usually
impossible to visualize all details of the third ventricle,
which makes radical tumor removal difficult and
dangerous. Therefore, we prefer the transcallosal route and
use the lamina terminalis exposure rarely. The
extraventricular part of the tumor may be approached and
excised through the opticocarotid triangle.
Endosuprasellar Craniopharyngiomas
Tumors of this group can vary markedly in size and
suprasellar extension. The pituitary gland as well as the
pituitary stalk may be partially or completely destroyed. In
some cases the tumor
can penetrate into the third ventricle. In an overwhelming
majority of cases endosuprasellar Craniopharyngiomas can
be radically removed with the subfrontal approach (usually
right-sided).
After tumor exposure the capsule is widely opened
between the optic nerves, and the tumor contents—cystic
liquid, cholesterol masses, and calcification—are removed
as completely as possible; with capsule collapse, the vessels
passing over it can be more easily detached; they include
the posterior communicating artery, anterior choroidal
arteries, and small branches of the internal carotid arteries
to the diencephalic region.
Under the microscope, it is possible to distinguish
between vessels that merely pass across the capsule and
those that contribute to its blood supply. The latter are
coagulated and divided. Adhesion of the anterior cerebral
arteries to the tumor capsule occurs in cases of pronounced
antesellar and suprasellar growth.
As it is very important to preserve the vascular
connections of the infundibular part of the third ventricle
and pituitary gland, I try at the beginning to divide the
tumor from the remnants of the sella diaphragm, which
constitute the external layer of the tumor capsule. In some
cases it is possible to identify a place between these two
layers and preserve the posterior part of diaphragm with its
vascular net. If these attempts are unsuccessful the
suprasellar part of the capsule is thoroughly separated from
the chiasm, the third ventricular floor, and remnants of the
pituitary stalk and is excised just above the sellar entrance.
The next stage of the operation is removal of the
intrasellar part of the tumor with the help of a blunt
dissector. The tumor capsule is separated from the dura
mater of the sella. Manipulation must be very careful to
preserve the remnants of the pituitary gland, a fine strip of
light pink tissue lining the floor and posterior wall of the
sella turcica.
Complete removal of the endosuprasellar cra-
niopharyngioma usually results in a wide expo-
sure of the interpeduncular cistern, the brain stem, and the
upper part of the basilar artery with its branches (Figs. B.9
and B.10).
Suprasellar-Extraventricular
Craniopharyngiomas
This type of craniopharyngioma occurs more often in
adults than in children. The tumors are frequently situated
asymmetrically, displacing the hypophyseal stalk and the
third ventricle to one side. In the majority of cases
unilateral subfrontal access permits radical tumor removal,
but if most of the tumor growth is in the middle or
posterior fossa other approaches (such as subtemporal or
transtentorial) may be used.
Depending on the location of the tumor, its dissection
has been carried out between the optic nerves and also
through the opticocarotid triangle. The tumor capsule is
frequently thin and contains fluid, cholesterol masses,
yellow tumor tissue of a lobular structure, and collections
of calcium. Sometimes the tumor appears as dense
homogeneous tissue that includes the large vessels and
optic and oculomotor nerves. After evac-
uation of the cystic fluid and the solid part of the tumor that
can be removed more easily with the help of an ultrasound
aspirator, the capsule must be meticulously separated from
the optic pathways, the third ventricle floor, the sella dia-
phragm, and the carotid arteries and their branches and then
removed.
Giant Craniopharyngiomas
In this group we include tumors, usually cystic, that
spread far beyond the chiasmal-sellar region. These tumors
may occupy the anterior, middle, and even posterior fossae
or the ventricular system. Quite often the walls of the large
cystic cavities are so thin that they could hardly be
completely separated from the cerebral tissue and
particularly the arachnoid membrane. Besides the cysts
there are also solid portions of the tumor in which the
inmportant vessels and cranial nerves may be included.
About half of our cases of giant craniopharyngioma were in
children.
Depending on the predominant location of the tumor,
various approaches can be used (frontal,
temporal, transventricular, and others). Separation of the evacuation diminishes cyst size, facilitating extirpation.
important arteries and their branches, the cranial nerves,
and the diencephalic structures is the most critical part of Clinical Considerations
the operation (Fig. B.1 1). At the Burdenko Institute, Craniopharyngiomas are
Special attention should be given to careful hemostasis approximately as common in adults as in children. There is
because of the large operative field. The removal of large some difference in the presentations of different types of
cysts may result in brain collapse and rupture of the cortical craniopharyngioma in children and adults.
veins. In some cases, the cyst should be punctured repeat- Endosuprasellar, third ventricular, and giant
edly to evacuate fluid or an Ommaja system should be used craniopharynyn-giomas are more frequent in children.
before radical extirpation. Fluid Suprasel-lar-extraventricular (pituitary stalk) craniopha-
ryngiomas occur more often in adults (about one-half of
all cases).
We operate as radically as possible upon children with
Craniopharyngiomas to prevent a tumor recurrence. With
adults, especially aged patients, we are more conservative.
Reoperations are more difficult and dangerous because of
adhesions. Nevertheless, the radical removal of
Craniopharyngiomas in subsequent operations is possible.
Concerning palliative surgery on the ventricular system,
our policy is first to try to remove the tumor radically by
the direct approach. This is easier to do when the ventricles
are large than when they collapse after diversionary shunt
operations.
Commentary С
Diencephalic Structures at Risk in Third Ventricular
Surgery
Robert B. Page, M.D.
The median and paired third ventricle lies between the
two hemispheres of the brain and is filled with fluid.
Operating within it to remove a tumor or a parasitic cyst
should be relatively safe as long as its boundaries are not
violated. The problem presented to the surgeon when
faced with a tumor in the third ventricle is rather like the
problem presented to Willie Sutton when faced with a
payroll in a bank vault. It is to determine by what route
the vault (ventricle) can be entered and by what
techniques the payroll (tumor) can be removed so that as
little disturbance as possible will be created and the bank
(patient) will continue to function as before. To answer
that question for each individual job, we would do well to
emulate Mr. Sutton and "case the joint."
Anatomy of the Third Ventricle
The front wall of the third ventricle is formed by the
optic chiasm, the lamina terminalis, and the anterior
commissure. The optic chiasm and the anterior
commissure are fiber tracts through which information is
passed between neural structures of the two hemispheres.
The lamina terminalis, although not serving that function
in adulthood, is the embryological site of development of
the commissural plate, which differentiates into the
anterior, callosal, and hippocampal commissures (3). The
Supraoptic nuclei and the columns of the fornix lie in the
anterior wall of the hypothalamus, just dorsal to the optic
chiasm and just lateral to the lamina terminalis.
The organum vasculosum of the lamina terminalis (OVLT),
a structure implicated in body fluid homeostasis and
reproduction, lies beneath the anterior commissure in the
midline in the lamina terminalis. More dorsally, at the level
of the foramen of Monro lies the subforniceal organ (SFO),
which is also implicated in the maintenance of fluid
homeostasis (2).
The ceiling and floor of the third ventricle are also
attenuated. Its ceiling is vascular and is made up of the
Choroid plexus of the third ventricle, which is attached to
the thalamus along the tinea thalamica, and of the paired
internal cerebral veins. It is termed the velum interpositum.
Overlying that ceiling, as a roof over the attic, are the
hippocampal commissure and the crus of the fornices. The
floor of the third ventricle is formed by the mamillary
bodies (the ultimate destination of many fibers in the
fornix, which lies in its roof) and the tuber cinereum, the
site of attachment of the hypophyseal median eminence to
the hypothalamus.
The posterior surface of the third ventricle is formed by
the midbrain, the posterior commissure, the habenula, and
the pineal gland. The aqueduct of Sylvius serves as a
conduit carrying cerebrospinal fluid out of the third
ventricle and lies just beneath the posterior commissure.
The posterior wall of the third ventricle is attenuated only
at the posterior and habenular commissure and the
suprapineal recess. The lateral walls of the third ventricle
are stout and are made up of the nuclear masses of the
hypothalamus.
Approaches to the Third Ventricle
As a consequence of this architecture, the surgeon
is forced to enter the third ventricle by one of three
routes. The first is through the lamina terminalis (the
anterior wall). The second is through the forniceal
raphe, hippocampal commissure, and velum
interpositum or just lateral to the fornices through the
tinea thalamica (the roof). The third is through the
posterior commissure or the suprapineal recess (the
second story of the back wall). Entering from below is
barred by the attachment of the pituitary gland of the
brain. Entering from the side is barred by the nuclear
masses of the hypothalamus. Entering from the
posterior ventral aspect is barred by the connection of
the midbrain with the hypothalamus. The surgeon will
thus enter and leave the third ventricle by the same
routes as many fiber tracts that enter and leave the
hypothalamus, and the surgeon must perforce be
cognizant of them. While working in the third
ventricle, the surgeon will work next to nuclear
masses and fiber tracts of the hypothalamus and must
respect them lest alarms go off that cannot be safely
silenced.
Hypothalamus: General Anatomical Features
If the brain is sectioned in the midsagittal plane, the
medial wall of the third ventricle can be visualized. A
horizontal groove, the hypothalamic sulcus,
demarcates the thalamus above from the
hypothalamus below. The anterior margin of the
hypothalamus does not strictly correspond to the
anterior wall of the third ventricle (the lamina
terminalis). Instead it is defined by a line drawn from
the rostral margin of the optic chiasm to the anterior
commissure (5). In midsagittal section the
hypothalamus is frequently divided into three zones.
From anterior to posterior they are the Supraoptic, the
tuberal, and the mamillary regions. In coronal section
the hypothalamus is divided into a periventricular
(median), a medial, and a lateral zone. Finally, a
horizontal line drawn parallel to the anterior-posterior
commissural line and midway between the floor and
the hypothalamic sulcus separates the hypothalamus
into a dorsal and a ventral zone. This schoolbook
parcellation of the hypothalamus into a three-
dimensional grid (5) has several important
consequences for surgeons. First, ascending and
descending input from the brain stem and from the
medial forebrain areas, respectively, for the most part
enters the medial forebrain bundle—a tract coursing
through the lateral zone of the hypothalamus and far
from
the sites of surgical appraoch. Second, neurose-
cretory groups involved with regulating the indi-
vidual's ability both to survive and to reproduce lie in
the periventricular zone and are at risk during
surgical exploration of the third ventricle. Third,
chemosensory sites with the ability to sense sodium
concentration and glucose concentration lie in the
periventricular zone of the hy-pothalamus.
Specific Nuclei
The periventricular zone contains all of the
neurosecretory cell nuclei except the Supraoptic
nuclei (SON). These nuclear groups include the
Paraventricular nuclei (PVN) and the arcuate nuclei
(AN). The suprachiasmatic nucleus also lies in the
periventricular zone and its cells synthesize a
neurosecretory peptide—vasopressin. However, these
cells synapse with other neurons and do not make
neurohemal contact. In these suprachiasmatic cells,
vasopressin serves as a neurotransmitter or a
neuromodular and not as a neurosecretion. The
Supraoptic nuclei are em-bryologically derived from
the periventricular zone but migrate from it during
the course of brain maturation to take up a new
position over the optic tract (5). Similarly,
gonadotropin-re-leasing hormone (GnRH)-containing
cells are thought to migrate from the periventricular
zone into the preoptic area of the adult.
The PVN and AN are of particular importance; if
recent findings in laboratory animals are applicable
to humans, these nuclear groups are the primary sites
in which peptides and amines regulating the pituitary
gland's response to changes in the internal milieu and
the external environment are synthesized.
Corticotropin-releasing factor (CRF), arginine
vasopressin (AVP), oxyto-cin (ОТ), thyrotropin-
releasing hormone (TRH), enkephalin, and
somatostatin (SRIF) are also synthesized in cells
residing in the PVN. Axons of many of these neurons
terminate in the median eminence near the
fenestrated vessels of its primary capillary plexus.
Axons containing CRF, AVP, ОТ, TRH, or SRIF
leave the PVN laterally and course toward the medial
forebrain bundle. Upon entering the lateral zone they
turn to course downward toward the ventral surface
of the brain and then pass as a discrete fiber bundle
medially through the lateral retrochiasmatic area to
gain the midline and to enter the median eminence
from anteriorly. They terminate in its medial third
(7).
The Paraventricular nucleus may well serve as a
site for the integration of the autonomic neural and
the endocrine systems (10). For example, with
hypotension, neural traffic is increased over
the glossopharyngeal nerves and there is increased
input into the nucleus and tractus soli-tarius.
Connections between the nucleus solitar-ius and the
dorsal motor nucleus of the vagus and the lateral
reticular nucleus have been demonstrated. Ascending
noradrenergic systems originating in these nuclei
project to the parvo-cellular division of the PVN.
Some noradrenergic neurons terminate on AVP-
containing neurons in the PVN. Some of these
neurons, along with neurons containing CRF, project
to the median eminence. AVP and CRF released into
median eminence capillaries and carried by portal
routes to the pars distalis synergistically stimulate the
release of adrenocorpticotropic hormone (ACTH)
from corticotrophs and of beta-endorphin from
melanotrophs. ACTH can then enter the systemic
circulation to stimulate the release of corticosteroids
from the adrenal gland. The lateral reticular nucleus
also projects to the SON (1). Stimulation of the SON
results in release of AVP from axons terminating in
the neural lobe. AVP can enter the systemic
circulation to (a) conserve water loss to the kidney
and to (b) elevate blood pressure by stimulating
vasoconstriction and by sensitizing the gain and the
feedback response of the carotid bodies and hence
altering the neural traffic over the glossopharyngeal
nerves. AVP released in the neural lobe can also
cross (by short portal and capillary routes) into the
neighboring pars distalis to release beta-endorphin
from melanotrophs or ACTH from corticotrophs (6).
Some AVP-synthesizing cells in the PVN project not
to the median eminence but to the medulla where
they synapse with ascending noradrenergic cells
projecting back to the PVN. Some oxytocin-
containing cells in the PVN project to the
intermediolateral cell column of the spinal cord and
presumably alter sympathetic outflow. CRF
projections from cell bodies lying in the
Paraventricular nucleus can also alter sympathetic
tone. The details of this system are far from clear but
it seems evident that the PVN is a "site for the
integration of neuroendocrine and autonomic
mechanisms" (10). Less well localized are sites for
the integration of temperature control in the walls of
both the anterior and posterior aspects of the third
ventricle and sites for sensing the concentrations of
sodium and glucose in the circulating blood. It is
evident that cell systems subserving these functions
vital for homeostasis lie close to the walls of the third
ventricle and that the integrity of the ventricular
surface should be respected by surgeons entering the
third ventricle. The arcuate nucleus lies near the floor
of the
third ventricle. Many of its cell bodies contain
dopamine (11). Others are the site of the synthesis of
proopiomelanocortin (POMC) and of its derivatives
(ACTH, the melanotropins, beta-lipotro-pin, and beta-
and gamma-endorphin) (4). With the exception of
growth hormone-releasing hormone (8), hypothalamic
releasing and inhibiting hormones do not seem to be
synthesized in the arcuate nuclei. Dopamine,
synthesized in cell bodies in the arcuate nucleus and
released predominantly in the lateral thirds of the
median eminence, inhibits prolactin (PRO) secretion
by pituitary lactotrophs. The role of the processed
products of POMC in the median eminence is
unknown at present but endorphins may modify
gonadotropin, PRO, AVP, and ОТ secretion. The
significance of projections of ACTH-containing fibers
from the arcuate nuclei to the Paraventricular nuclei
where they contact cells containing CRF (4) remains
unknown.
The Supraoptic nuclei lie in the medial zone of the
Supraoptic region. They contain magno-cellular
neurons that synthesize either AVP or ОТ with their
associated neurophysins. In addition, some cells form
part of a third opioid system and contain dynorphins.
Dynorphins may coexist in the same neurons with the
classical neurosecretory peptides (12). Axons of the
Supraoptic nucleus project posteriorly to form the su-
praopticohypophyseal tract, which enters the median
eminence of the pituitary in the midline. The
supraopticohypophyseal tract passes through the
internal zone of the median eminence. Its axons
terminate on fenestrated capillaries in the neural lobe.
The preoptic area contains GnRH-containing cell
bodies that project directly to the median eminence
and terminate in its lateral thirds. These fiber
pathways join the fibers coursing medially from the
lateral retrochiasmatic area to form a funnel where
neuropeptide-containing pathways enter the median
eminence from the front (7). These fiber tracts pass
through the arcuate nuclei anteriorly as they descend
into the median eminence.
Frontal Approach
When approaching the third ventricle from the front
through the lamina terminalis, the surgeon will use a
subfrontal approach and gain access to the lamina
terminalis and the optic chiasm. In doing so, the
surgeon will expose the region of the anterior
perforated space and the preoptic area. The structures
at risk then include descending pathways from the
medial frontal lobe, which will enter the medial
forebrain bundle in
the lateral wall of the hypothalamus. Such structures pass close to
the surface of the brain in the region of the olfactory tubercle and
anterior perforated space and include projections from the septal
region destined for the mesencephalic tegmentum (5). Damage in
this region through excess retraction or damage to perforating
vessels originating from the anterior cerebral artery may result in
significant alterations of consciousness. Damage to higher cortical
function can be expected if the nucleus basalis of Meynert (the
origin of the major cholinergie projection to the cortex) is injured.
Changes in gonadotropic function are possible as GnRH-
containing cells lie in the preoptic area. The lamina terminalsi
itself is avascular and contains no neural tracts. The approach into
the third ventricle is safe as long as it is kept strictly in the
midline. The organum vasculosum of the lamina terminalis and
the subforniceal organ lie along the course of the approach. Both
of these structures have been implicated in salt and water
homeostasis (9). In addition, the SON lie just above the optic
chiasm and just lateral to the midline. Hence, disturbances in
water balance and conservation may be secondary to damage to
the SON or to the OVLT and SFO. In addition, memory deficits
may occur if the pillars of the fornices or if the SON are damaged
during the approach. Memory dysfunction has been reported both
with forniceal damage and with the loss or destruction of AVP-
secreting neurons. Such a deficit may recover as diabetes insipidus
improves.
Superior Approach
In the approach to the third ventricle from above, the fornices
are at risk as they lie within the operative field. However, no other
major input into the hypothalamus is present in this region.
Posterior Approach
The posterior approach through the suprapineal recess or
through a stretched and thinned posterior commissure also spares
the ascending and descending tracts leaving the hypothalamus
posteriorly. These tracts include the mamillary peduncle and the
dorsal longitudinal, fasciculus and lie well beneath the tectum of
the midbrain and out of the field of the surgeon.
Ventricular Floor
The floor of the third ventricle is at risk when the surgeon is
working within the third ventricle or beneath it as in the
transsphenoidal approach carried above the diaphragma sellae.
Damage to
the floor of the third ventricle will include the arcuate nuclei and
the neurosecretory tracts passing through it as well as the median
eminence itself as these systems are tightly packed within a small
space. Panhypopituitarism is to be expected.
The surgeon attempts to enter the third ventricle through
windows placed anteriorly, superiorly, and posteriorly. These
windows contain either no fiber tracts or fiber tracts such as the
hippocampal or posterior commissure, which can be divided
without apparent neurological deficit. Through these windows
the surgeon gains access to the third ventricle, but once within
the third ventricle one must take care not to violate its walls.
References
1. Day ТА, Renaud LP: Electrophysiological evidence
that noradrenergic afferents selectively facilitate
the activity of Supraoptic vasopressin neurons.
Brain Res 303:233-240, 1984.
2. Joseph SA, Knigge KM: The endocrine hypothal
amus: Recent anatomical studies. Res Publ Assoc
Res Nerv Merit Dis 56:15-47, 1978.
3. Loeser JD, Alvord EC Jr: Agenesis of the corpus
callosum. Brain 91:553-570, 1968.
4. Mezey E, Kiss JZ, Mueller GP, Eskay R, O'Dona-
hue TL, Palkovits M: Distribution of the pro-opi-
omelanocortin derived peptides, adrenocortico-
trope hormone, a-melanocyte-stimulating hor
mone and B-endorphin (ACTH, a-MSH, 0-End) in
the rat hypothalamus. Brain Res 328:341-347,
1985.
5. Nauta WJH, Haymaker W: Hypothalamic nuclei
and fiber connections. In Haymaker W, Anderson
E, Nauta WJH (eds): Hypothalamus. Springfield,
IL, Charles С Thomas, 1969, pp 136-209.
6. Page RB: Directional pituitary blood flow: A mi-
crocinephotographic study. Endocrinology 112:
157-165, 1983.
7. Palkovits M: Neuropeptides in the median emi
nence: Their sources and destinations. Peptides
3:299-303, 1982.
8. Sawchenko PE, Swanson LW, Rivier J, Vale WW:
The distribution of growth-hormone-releasing
factor (GRF) immunoreactivity in the central
nervous system of the rat: An immunohistochem
ical study using antisera directed against rat hy
pothalamic GRF. J Comp Neurol 237:100-115,
1985.
9. Simpson JB: The circumventricular organs and
the central actions of angiotensin. Neuroen-
docrinology 32:248-256, 1981.
10. Swanson LW, Sawchenko PE: Paraventricular
nucleus: A site for the integration of neuroendo
crine and autonomic mechanisms. Neuroendocri-
nology 31:410-417, 1980.
11. Szentagothai J, Flerko B, Mess B, Halasz B: Hy
pothalamic Control of the Anterior Pituitary. Bu
dapest, Akedemiai, 1968.
12. Whitnall MH, Gainer H, Cox BM, Molineaux CJ:
Dynorphin-A-(l-8) is contained within vasopres
sin neurosecretory vesicles in rat pituitary. Sci
ence 222; 1137-1139, 1983.
22
Posterior Transcortical
Approach
Kenichiro Sugita, M.D., and Kazuhiro Hongo, M.D.

Indications, Applications, and Contraindications

The posterior transcortical approach through the superior parietal lobe to the third
ventricle is not indicated for a lesion entirely within the third ventricle. It is indicated for
such lesions as posterior thalamic and posterior parathalamic tumors, which are related
to the posterior Paraventricular portion, and arteriovenous malformations around the
posterior half of the ventricle (around the trigone), which are located in the lateral wall
of the third ventricle. The approach can be made through a cortical incision in the
parietal lobe, even in the dominant hemisphere. The posterior transcortical approach is
contraindicated for lesions of the anterior portions of the thalamus and ventricle, for
which the anterior transcortical approach through the frontal lobe is used. A lesion
located solely in the third ventricle is best approached interhemispherically. The more
lateral to the midline is a lesion, the more useful is the transcortical approach (1-10, 13,
14).
In our own practice we have not used an approach through the middle temporal gyrus
to lesions of the posterior ventricular portion and the posterior thalamus because a
temporal approach to such lesions is likely to produce postoperative neurological
deficits such as hemianopsia and hemiparesis, although the distance involved in this
approach is shorter than that through the medial parietal incision. The temporal
approach is indicated only for lesions located lateral to the temporal horn and in the
temporal lobe. An approach through the lateral parietal cortical incision is inadvisable
because the areas involved are related to more important neurological functions, such as
speech and vision, than are involved in the medial approach.

Preoperative Evaluation and Radiographic Assessment

Exact radiological study is indispensable for the posterior transcortical approach.
Three-dimensional reconstruction of the preoperative computerized tomographic (CT)
scan is very helpful because it is often difficult to obtain topographical orientation
during the procedures for deep-seated lesions through a small cortical incision under an
operating microscope.
In addition to sagittal reconstruction of the CT scan, the new imaging by magnetic
resonance would also be very helpful where available. Angiog-raphy provides us with
much important information: How vascular is the lesion? Where do the main feeding
arteries come from? For a highly vascular tumor we should plan to attack during the
initial stage the side where the feeders are mainly located. How much have the important
veins been shifted?
When the preoperative CT scan shows a diffusely infiltrating lesion without a clear
border or with an extensive invasion into the bilateral hemispheres, radical operation
using this approach should not be attempted. There are also objections to direct surgical
attack on malignant tumors located in the periventricular region because of the
possibility of ventricular seeding during the transventricular approach.
When a lesion is small and seated deep from the ventricular floor, a two-stage
operation of stereotaxic exploration and direct attack is recommended. At the time of the
stereotaxic exploration a metal marker such as a piece of a hemoclip should be left in the
lesion in addition to taking a tumor specimen for histological study. The metal marker is
useful for the second operation.

Considerations of Position and Intracranial Pressure Control

The patient's position is prone with the head elevated higher than the heart level, to
achieve which the upper portion of the operating table is elevated about 35°. The
patient's head is positioned slightly chin-up so that the operating microscope can be used
perpendicularly in a sagittal plane. During the initial procedure from the skin incision to
exposure of the trigone the patient's head is kept perpendicular to the floor because in
this way the correct direction from the cortical incision to the ventricle is easily obtained.
After the ventricle is entered, the patient's head is rotated to the side of the lesion so that
we can use the microscope perpendicularly in a coronal plane during the procedure
around the lesion; the angle of rotation is usually about 20°.
The usual methods for controlling intracranial pressure, such as elevation of the
patient's head, hyperventilation, and the administration of mannitol, are indispensable
during the initial stage. Lumbar drainage of cerebrospinal fluid (CSF) is usually not done
because the ventricle is opened during approach and lumbar drainage might promote
tentorial herniation if the mass is large with perifocal edema. In some cases with
advanced noncommunicating hydrocephalus ventricular drainage is instituted in the
contralateral anterior horn before the craniotomy; the tap is helpful for the initial
approach until the ventricle is exposed and CSF is suctioned from the whole ventricular
system.

Pictorial Illustration of the Technique

Position of the Patient's Body and Head This is as
previously described (Fig. 22.1A).
Sugita Multipurpose Head Frame
This assembly (12) is an essential tool in this approach; it holds four tapered spatulas
that facilitate the approach through a small cortical incision with minimal damage to
normal brain tissue (Fig. 22.1B).
Skin Incision with Craniotomy
A U-shaped skin incision is made in the medial parietal area, 6x6 cm in size. The top
of the skin flap is made along the midline. The craniotomy
is 5 х 5 cm in size so as to correspond to the skin flap close to the sagittal sinus,
which is not exposed. The center of the craniotomy is about 4 to 5 cm posterior
to the central sulcus and 3 cm lateral to the midline (Fig. 22.1С).
Dural Opening, Ventricular Tap, and Cortical Incision
The dura mater is opened with an X-shaped incision. A ventricular tap needle
is inserted at the cortical surface slightly posterior to the center of the
craniotomy. The target of the tap is the trigone. The CSF is not drained from the
tap except in a case where the brain bulges with advanced hydrocephalus
because a direct approach to a collapsed ventricle is difficult. A cortical incision
less than 3 cm long is made coronally on the superior parietal cortex; the
approach to the trigone is made by coronal sectioning of the brain. Coronal
sectioning of the cortex and brain helps to minimize damage to the connecting
fibers of the corpus callosum. In a patient with advanced hydrocephalus the
incision should be made slightly posterior to the center of the craniotomy
because the brain sinks to the frontal side after the egress of CSF.
Brain Retraction with Four Tapered Spatulas
The operating microscope is used throughout the procedure after a successful
ventricular tap. The route from the cortical incision to the trigone is made by
sectioning the brain along the track of the ventricular tap. The approach is helped
by the application of four tapered spatulas that are held with four self-retaining
retractors. These retractors are set on the Sugita multipurpose head frame; in this
way spatulas can be applied from any point around the operating field. There are
two particularly important points regarding brain retraction. The first concerns
the application of tapered spatulas. Three kinds of tapered spatula are available,
differing in the width of the tip: 2, 4, and 6 mm. The application of tapered
spatulas enables us to obtain an ample operating field with less brain retraction,
and retraction with tapered spatulas results in less brain damage than retraction
with the usual spatulas. Another important point is that the brain is not retracted
with all four spatulas at a time but only with a pair; the other pair is kept loose.
The pair in use is changed whenever the side of the operative procedure is
changed. Retraction with a pair of spatulas facilitates visualization of a wider
operating field than retraction with four spatulas, even through a 3-cm cortical
incision. The self-retaining retractor must be light; our newly designed one made
of titanium weighs 180 g and is tapered. As it is so light it is possible to feel the
resistance of the brain and know how much the brain is retracted. Cotton patties
must be placed under the spatulas; they must be soft and thin with little tendency
to adhere to tissue (Fig. 22.2A).
Techniques of Dissection of Tumors
Usually it is difficult to discriminate thalamic and parathalamic tumors from
the normal structure of the ventricular floor even with high magnification of the
operating microscope because a thick normal ependymal layer covers the floor.
Only the topographical information obtained by preoperative CT scanning helps
us to decide which area of the ventricular floor should be sacrificed to advance
into lesions in the thalamus.
With a small and deep-seated lesion a direct approach to the lesion with
minimal damage to the normal structure is more difficult than with a large
lesion. Here intraoperative radiological study is helpful. Although the best
investigation is intraoperative CT scanning, intraoperative plain skull films are
also very helpful after a small hemoclip has been posi-
tioned in the bottom of the operating field. In addition to the two-stage operation
mentioned previously, open operation combined with the stereotaxic method is
recommended for dealing with small and deep-seated lesions.
We isolate the tumor from the surrounding critical tissues with a small cotton patty
held with bipolar coagulating forceps when the consistency
of the tumor is different from that of the surrounding tissues. The patties used
for the purpose are conventional cotton pieces sized 1 X 2 or 1 x 3 cm. The
patty should be changed frequently, usually every minute, because its surface
becomes too smooth with adhesion and absorption of the surrounding brain and
tumor tissues. Ideal dissection along the tumor border can be performed with
the rough surface of a new patty. We can feel the different consistencies
between the tumor and normal tissues through the small ball-shaped patty,
something like the old-fashioned method of finger enucleation. When a tumor
has no clear border, radical removal must not be attempted; only partial
removal is performed inside the safety zone that is determined from the
preoperative CT scan (Fig. 22.2B).
When the normal brain is completely isolated from the tumor the normal
areas should be protected with different kinds of cotton patty from the
bemsheets used for dissection: the bemsheets are hard whereas the patties are
soft. Using two different kinds of patty helps us to discriminate completely
finished areas from ongoing ones. When we check the area completely isolated
from the tumor a little later, its surface will often have developed a pathological
appearance due to clots and microbleeding.
Topographical Anatomy around the Third Ventricle
The topographical anatomy along the approach from the parietal cortex
through the trigone to the thalamus must be thoroughly understood. When we are
operating in the depth of the brain via a small transcortical route, the anatomical
orientation is sometimes lost, especially when we operate under a microscope. In
this approach the most important landmark is the shape of the trigone and the
three directions of the anterior, inferior, and posterior horns. If the ventricle is
missing the approach cannot be successful. We must master the topographical
atlas for stereotaxic surgery so that the size and location of the important
structures around the ventricle can be known in millimeters. The actual location
of a critical structure, however, will be different from normal because of the
tumor. During operation we must therefore keep in mind not only the normal
anatomy but also the pathological location of critical structures in each case, as
obtained from the preoperative CT scan.
The three topographical sections of Figures 22.2C and 22.3 are reconstructed
from the atlas of Schaltenbrand and Bailey (11); Section A is the topography
along the anterior route from the posterior parietal cortex to the thalamus,
Section В is along the central route, and Section С is along the posterior route.
The distance from the cortex to the ventricle is about 5 cm. The width of the
thalamus is 15 to 25 mm. The dorsomedial portion of the thalamus about 10
mm lateral and 15 mm ventral from the dorsomedial corner of the thalamus
(i.e., the pulvinar thalami and nucleus dorsomedialis) can be directly attacked:
this portion is, in our experience, relatively silent.

Pitfalls during the Intraoperative Period

The craniotomy must be made in the correct area to make a correct cortical
incision in the medial parietal lobe. When advanced hydrocephalus is present
the cortical incision should be made slightly to the occipital side in the window
of the small craniotomy because the slackened brain sinks to the frontal side
after the egress of CSF. Although the incision is less than 3 cm long the
arachnoid membrane around it should not be damaged because the arachnoid
protects against excessive elongation of
the incision by retraction. At the end of operation, however, the length will often have
increased to about 4 cm.
Unless the patient's head is perpendicular the approach to the trigone is occasionally
difficult. The orientation from the cortex to the trigone can be easily realized when the
head is perpendicular. A ventricular tap before transcortical incision is recommended:
tracing the tap facilitates entering the ventricle. After the ventricle is opened the patient's
head is rotated to the affected side.
The use of four tapered saptulas connected to self-retaining retractors and the Sugita
frame is one of the most essential techniques in this approach. Although four spatulas are
set up around the cortical incision, the brain around the route of approach should be
retracted with only two spatulas at a time. Retraction of only one side of the brain helps
to maintain a normal blood circulation in the other side. A larger operating field than the
cortical incision is obtained in this manner by changing the direction of retraction.
Retraction with four spatulas simultaneously does not enlarge the operating field much
and damages the brain tissue more than does the use of only two spatulas. Another
important point is that the observation angle of the microscope must be frequently
changed: tilting and sloping of the microscope reduces the need for brain retraction.
The communicating channels of the exposed ventricle located in the bottom of the
operating field must be obstructed during the procedure with large pieces of cotton patty
to prevent spread of blood to the entire ventricular system, especially when dealing with
a hemorrhagic tumor.
We occasionally become confused about the anatomical orientation during the
procedure around a deep-seated lesion through an operating microscope that provides us
a limited visual field, especially when we approach through a small cortical incision. To
keep our sense of direction, the most important landmark is the ventricle. When the third
ventricle has been exposed, the foramen of Monro and occasionally the entrance of the
aqueduct give us further information about the anatomical relationships. The more the
ventricle is exposed the more easily can we obtain anatomical orientation.
During removal of thalamic and parathalamic tumors that are located close to critical
structures such as the internal capsule and the optic radiation we must keep in mind the
three-dimensional topographic mapping reconstructed from the preoperative CT scan.
We should pay attention to the fact that the anatomical relationships are often far
different from normal in the case of large thalamic tumor; for example, we encountered a
case where the internal capsule was shifted more than 3 cm laterally from its normal
position.
The most difficult decision concerns how radically tumors in this area can be
removed. We have not encountered postoperative additional neurological deficits that
were permanent when only the tumor mass was removed, even in an area where the
thalamus and internal capsule would have been located in the normal brain. A relatively
safe zone to attack is the posterior dorsomedial area of the thalamus; this is the
anterolateral floor of the trigone. We should refrain from advancing in a deeply anter-
olateral direction from the trigone, especially when the tumor border is unclear.

Complications Associated with the Technique

It is said that an approach through the parietal lobe of the dominant hemisphere is
likely to cause the Gerstmann syndrome as a postoperative complication. However, we
have never experienced this in 43 cases operated through the parietal transcortical
approach, 20 of which were
on the left side. To minimize such postoperative complications the cortical incision
should be made as small as possible and retraction of the brain should be as little as
possible, with the aid of the four tapered spatulas connected to self-retaining retractors.
If the cortical incision is made in the far lateral area of the parietal lobe, there is a higher
possibility of such postoperative complications as homonymous hemianopsia or sensory
aphasia. The complication one must be most careful to avoid is injury of the normal
internal capsule and a large area of the normal thalamus. To avoid additional
neurological deficits the normal tissues should never be removed in the deep
anterolateral area around a tumor located in the thalamus. In this area one must leave a
small portion of the tumor when the tumor border is not clear.

Case Reports
Case 1
This 60-year-old man had had right hemiparesis for 3 months. The CT scan showed a
mass in the ventroposterior area of the left thalamus (Fig. 22.4). First, radiation therapy
was tried without effect. A stereotaxic exploration was performed 1 month before the
main operation, and a small piece of a silver clip was left in the lesion after the removal
of two pieces of tumor tissue, which were histologically determined to be benign
astrocytoma.
With the patient in the prone position a direct approach to the tumor was performed
through a left medial parietal corticotomy. After the trigone had been exposed an
incision was made in the portion anterolateral to the trigone, which was a roof of the
nucleus dorsomedialis. The tumor was found intramedullarly at a depth of 6 mm from
the bottom of the ventricle (Fig. 22.5). The small piece of clip that had been left was
very useful in getting the correct orientation to the tumor. The tumor had a hard capsule
and its center was cystic, containing cheeselike necrotic tissue. After removal of the
mass with the capsule, a thin
 arachnoid membrane and many small arteries were visible in the bottom of the dead
space; this was the third ventricle. After operation the right hemiparesis was slightly
worse for 2 weeks and then returned to the preoperative state. No postoperative
additional deficits were observed. The patient was able to walk.
Case 2
This 46-year-old man had only a brief (2-week) history of severe headache. A
transcortical approach was made through a 3-cm cortical incision in the right medial
parietal lobe. At a depth of about 6 cm the trigone of the right lateral ventricle was
encountered. After coagulating and resecting the choroidal plexus the ependymal layer
of the ventricular floor and the thalamic mass was entered. Decompression was readily
accomplished because many clots were found inside the tumor and its border was clear.
Blood loss was less than 100 ml. The histology diagnosis was Grade III astrocytoma.
The postoperative course was uneventful except for a transient left hemiparesis.
Irradiation was done (Fig. 22.6).

Case3
This 57-year-old man had complained of nausea, vomiting, headache, and anorexia for
more than 10 months. Slight right hemiparesis appeared a few weeks before operation. A
transcortical approach was made through the left medial parietal lobe. The trigone of the
left lateral ventricle was entered at a depth of 3 cm. Immediately a tumorous bulging was
found in the anterolateral wall of the trigone. The tumor was covered with a thin
ependymal layer, which was carefully peeled; the posterior border of the tumor was
delineated. The tumor was rather vascular; we had a difficult time coagulating the
bleeders. The medial wall of the trigone was free of tumor; communication to the
contralateral ventricle was made through the medial wall and CSF was drained. The
brain became slack. We began to remove the tumor by suction dissection. Most of it was
removable by suction; its color and consistency were different from those of the normal
brain. The two-suction method, with a large suction in the dominant hand and a small
one in the other, was useful at times. As we proceeded with suction dissection we found
that the anterior border was rather well demarcated. The lateral ventral extent of the
tumor was not followed too far because we knew from the preoperative CT
scan (Fig. 22.7) that the tumor had extended down to the midbrain. At the end of the
procedure, the space created in the depth measured 3 x 3.5 x 3.5 cm. Subtotal removal
with substantial decompression was believed to have been accomplished. The
histological finding was Grade II or III astrocytoma. Postoperatively right hemiplegia
appeared for several days and then mild hemiparesis continued. The patient was
transferred to another hospital for irradiation.

References
1. Castaigne P, Ron dot P, Ribadeau-Dumas JL, et al: Ataxie optique localisee
au cote gauche dans les deux hemichamps visuels homonymes gauches. Rev
Neurol (Paris) 131:23-28, 1975.
2. Castaigne P, Pertuiset B, Rondot P, et al: Ataxie optiquedans les deux hemi
champs visuels homonymes gauches apres exerese chirurgicale d'un ane-
vrysme arteriel de la paroi du ventricule lateral. Rev Neurol (Paris) 124:262-
268, 1971.
3. Cramer F: The intraventricular meningiomas: A note on the neurologic
determinants governing the surgical approach. Arch Neurol 3:98, 1960.
4. Dandy WE: Diagnosis, localization and removal of tumors of the third ven
tricle. Johns Hopkins Hosp Bull 33-188, 1922.
5. Gardner WJ, Turner CA: Primary fibroblastic tumours of the Choroid plexus
of the lateral ventricles. Surg Arch 66:804-809, 1938.
6. Hirsch JF, Zouaoui A, Renier D, et al: A new surgical approach to the third
ventricle with interruption of the striothalamic vein. Ada Neurochir (Wien)
47:135-147, 1979.
7. Kempe LG: Operative Neurosurgery. Berlin, Springer, 1968, vol 1, pp 196-
202.
8. Lapras C, Deruty R, Bret PH: Tumors of the lateral ventricles. Adv Tech
niques Neurosurg 11:103-167, 1984.
 9. Maurizio F, Mario S, Giulio M, et al: Meningiomas of the lateral ventricles. J
Neurosurg 54:64-75, 1981.
10. Okudera H, Kobayashi S, Sugita K: A simple three-dimensional display model
based on recorded CT scan films for surgical reference. Acta Neurochir
(Wien) 71:47-53, 1984.
11. Schaltenbrand G, Bailey P: Einfuhrung in die stereotaktischen Operationen,
mit einem Atlas des menschlichen Gehirns. Stuttgart, Thieme, 1959, vol 3.
12. Sugita K, Hirota T, Mizuno T: A newly designed multipurpose microneuro-
surgical head frame. J Neurosurg 48:656-657, 1978.
13. Tonnis W: Behsndlungsergebnis bei Geschwulsten des Seitenventrikels. Lan-
genbecks Arch Klin Chir 284:446-450, 1956.
14. Torre E, Alexander E Jr, Davis CH Jr, et al: Tumors of the lateral ventricles
of the brain: Report of eight cases, with suggestions for clinical management.
J Neurosurg 20:461-470, 1963.
23
Infratentorial Supracerebellar Approach
Bennett M. Stein, M.D.

The material in this chapter is based on over 90 operations for tumors of the pineal
region. Not accepting the premise that tumors of the pineal region are generally
malignant and therefore should be treated by a more conservative approach (1, 2, 6) (a
shunt operation to relieve hydrocephalus followed by indiscriminate radiation), I have
approached the problem in a more radical fashion that requires definition of the tumor
before the institution of therapy (24-27).
With an increased awareness of the pathology of these tumors from autopsy series and
histological confirmation at operation, it has become apparent that there are a wide
variety of tumor types existing in the pineal region (5, 10, 12, 19, 22, 30). These tumors
take origin from various structures, not only the pineal body but the tela choroidea,
thalamus, and midbrain. The tumors run a gamut from benign encapsulated tumors to
malignant invasive tumors that are prone to seed. The categorization that we have
adopted is based on the scheme of Rubinstein (21), which places the tumors into three
broad categories: (a) Germ cell tumors including the benign dermoids and epidermoids
ranging through the intermediate tumors of the mature teratoma type (Fig. 23.1) to the
extremely malignant, invasive, and prone to seed germinoma, embryonal carcinoma, and
choriocarcinoma, (b) Pineal cell tumors including the pineoblastoma and the
pineocytoma—the latter benign or malignant, (c) Supporting cell tumors including the
astrocytoma (Grade 1 to Grade 4), meningioma, ependymoma, oligodendroglioma, and
other rare tumors arising from cells in association with the pineal body but not actually
part of it.
The exact identification of these tumors allows a more enlightened form of therapy.
Some of the principles in the treatment of these tumors are old and well established, such
as the treatment of hydrocephalus by a shunt. Others are new and innovative, such as the
operative microsurgical resection of benign encapsulated tumors and the identification of
malignant tumors followed by radiation, chemotherapy, or combinations thereof. The
armamentarium of the neurooncologist has been broadened through the use of multiple
chemotherapeutic agents. The
cornerstone of our method of treatment rests on the development of a safe and effective
operative procedure. Accordingly, we have found that the only certain way to identify
and thereby effectively treat tumors of the pineal region is to obtain abundant tissue for
histological examination including light microscopy, histochemical studies, and electron
micros-copy. The use of computerized tomographic (CT) scanning with and without
contrast administration, angiography, biological markers (including the beta subunit of
human chorionic gonadotropin alpha-fetoprotein) (13,14) and more recently the
magnetic resonance imaging (MRI) scanner has not allowed us to identify the
histological nature of these tumors with a high degree of accuracy (Figs. 23.2 to 23.4).

Historical Perspective
The operative experience with pineal tumors is intriguing to review. Dandy (4) was
the first neurosurgeon to tackle tumors of the pineal region aggressively. At that time
operation on these deep-seated tumors was frowned upon by his colleagues (3). Dandy
was a student of the pineal body, studying the functions of the gland as well as
developing operative approaches to reach this region in the experimental animal and
humans. Unfortunately, microsurgical technique was not available to him at that time
and anesthesia for these difficult neurosurgical cases was in its infancy. With these two
strikes against him it was not unexpected that his operative mortality and morbidity
were high. Perhaps as a result of this and other fruitless attempts to remove or otherwise
surgically treat tumors of this region, the direct operative approach to pineal tumors fell
into a state of disrepute. However, other neurosurgeons developed and promoted various
operative techniques to explore the region. Whereas Dandy (4) utilized a parafalx,
parietal approach with resection of a portion of the posterior corpus callosum and
approach to these tumors through the deep venous system, Van Wagenen (29) used a
transventricular approach through the dilated trigone of the lateral ventricle (a rather
convoluted and involved approach dependent entirely upon the presence of
hydrocephalus). Poppen (15) fostered an approach above the tentorium either medial or
inferior to the occipital lobe, thereby approaching the tumor low and adjacent to the
deep venous system. None of the results from these various operative procedures,
however, were what one could call spectacularly successful. Krause (11) in the 1920s
with a primitive neurosurgical technique utilized the posterior fossa approach to the pin-
eal region and was able to explore the region successfully in three cases, removing some
of the tumors. We have exclusively used the operation as developed by Krause (18, 27).

Advantages and Contraindications

The Infratentorial Supracerebellar approach is essentially a posterior fossa approach to
the pineal region and in our estimation has certain advantages, (a) The approach is
central to tumors that are basically midline, (b) The exposure is excellent when carried
out with the patient in the sitting position and provides space comparable to that
obtained with supratentorial approaches, (c) The tumors are approached ventral to the
deep venous system, (d) There is no morbidity related to the parietal or occipital lobes as
is experienced with supratentorial exposures.
It is for these reasons that I prefer this approach and have used it in virtually all of the
cases of pineal region tumor and of some vascular malformations. This approach,
however, should not be used when the tumor extends dorsally, in which case it may
envelop or grow above the deep venous system. Neither should the approach be used
when the
tumor is large and extends laterally into the region of the trigone of the lateral ventricle
(Fig. 23.3). Occasionally, additional lateral exposure may be gained by cutting the
tentorium from the posterior fossa exposure. Fortunately, most of the tumors are of
modest size and do not extend to a major degree in the aforementioned directions.

Operative Exposure and Technique

As with any innovative operative approach to the central nervous system, utmost
attention to detail is absolutely essential in achieving the desired result. This statement
holds for the simplest operation such as a shunt to complicated ones such as the approach
to a basilar aneurysm or acoustic tumor. Obviously, the same principle applies when one
is reaching the central area of the brain with a limited degree of exposure (27). The
operation microscope is absolutely essential to these operations. It would be impossible
to perform them with headlight and loupes and this should not be attempted. Also the use
of long instruments is preferred because the distances are of significant magnitude. Some
of the conventional microsurgical instruments are not applicable to operation in this
region. Similarly, innovative instruments such as the laser and the Cavitron are used with
difficulty in this region because of the small exposure and the angulation required during
the operative approach. Nevertheless, these two instruments have added to the
armamentarium of the surgeon approaching tumors of this region.
Perhaps the most important aspect of the operative procedure is the positioning of the
patient so that the trajectory utilized is comfortable and effective in exposing the pineal
region. This aspect of the operation as well as other fine points are stressed in the
following discussion. Utilizing illustrations and operative photographs, a step-by-step
approach to this region is presented.
Patient Preparation
The patients are prepared for operation by the performance of CT scanning with and
without contrast administration. Especially helpful are coronal and sagittal reconstructed
views. More recently we have been using the MRI scanner to identify the location of the
tumor. Rarely, we perform arteriography. Some of the tumors are quite vascular but that
fact will be apparent at the time of operation and knowing it beforehand does not
reassure the surgeon or the patient or make the operation significantly easier. The
vascularity of these tumors derives from branches of the posterior medial and lateral
choroidal arteries. These can be sacrificed with impunity. Certainly, one does not want to
wander into a vascular malformation such as a vein of Galen annomaly or a true
arteriovenous malformation in this region. However, the presence of this type of lesion is
usually suspected through the use of the CT scanning and in these instances
arteriography is mandatory. Twenty-four to 48 hours before the operation, the patient is
given high dose steroids, which are continued. If the patient has untreated hydrocephalus,
this must be relieved at the time of the operation by ventricular drainage or the
performance of extrancranial shunting (ventriculoperitoneal shunt) at some time before
the definitive operative procedure. Interestingly, many of the operations that we have
carried out are referrals and in many of these patients shunts have been performed
previously; unfortunately in some of the cases radiation has also been given.
Nevertheless, it is absolutely critical to the operative procedure that the ventricular
system be thoroughly decompressed before the operation or during the operative
procedure. If more relaxation is required, we do not hesitate to use
mannitol. Often when the cisterna magna is exposed, the release of
cerebrospinal fluid (CSF)— even if a block exists at the level of the incisura or
the aqueduct — will relieve tension within the posterior fossa. The choice of
anesthesia is left to the anesthesiologist. Ours prefer the use of inhalation
anesthesia, which will generally raise intracranial pressure. This elevation,
however, can be defeated with hyperventilation and the appropriate use of
ventricular decompression and dehydrating agents. Spinal drainage is not
utilized in these cases. All of the operations are done with the patient in the
sitting position with the usual preparation for this position, such as Doppler
monitoring and elevation of the legs. Depending upon the preference of the
anesthesiologist, a central venous catheter may be utilized. Because of the
difficulty experienced in placing a central venous catheter either the evening
before or at the time of the operation, we have tended to abandon this
procedure. However, Doppler monitoring is essential to detect small amounts of
air entering the venous system. When this phenomenon is detected early, it is
possible to take measures to prevent further ingress of air to the venous system.
Positioning
The patient is positioned in a "sitting-slouch" position (Fig. 23.5A). The
patient's body is placed well down on the operating table, the shoulders are
supported with a firm pillow or sandbag, and the body is placed in a С
configuration. A small pillow is required under the lumbar lordosis to support
the back. The head is then grasped by the three-point vise type of head holder
and positioned with a moderate degree of flexion so that two fingers can be
placed between the patient's chin and the sternum. Care must be taken not to
overflex the head.
In discussing the positioning, an anecdotal tragic experience should be
recounted. We treated a patient with a large tumor of the pineal region that
turned out to be an infiltrating astrocytoma. One month before operation on the
pineal tumor, the patient was involved in an automobile accident; he was not
rendered unconscious but suffered from headaches afterward. The pineal tumor
was picked up on a routine CT scan done for headaches. There had been no
complaints referable to the neck. When positioning him in the characteristic
sitting-slouch position, the anesthesiologist noted that there was some difficulty
in controlling hypotension. The operation went well, and a modest portion of the
tumor was resected. In the recovery room, it was noted that the patient was
quadriplegic, but alert. Cervical spine films and a myelogram that evening
showed no abnormalities. One week later, flexion-extension views were taken of
the cervical spine. No abnormalities were noted as the quadriplegia persisted. At
that point, on a hunch that there might have been another disease process within
the cervical spinal cord, a CT scan with and without contrast infusion was
carried out. To our surprise, fractures dating back to the auto accident were
noted in the laminae and pedicles of C-5 and C-6. At the time of the CT scan
these were nondisplaced but obviously, with the degree of distortion of the
cervical and thoracic spine during the positioning of the patient, these fractures
permitted a guillotine effect on the cervical cord, resulting in quadriplegia.
Therefore, if there is any hint of abnormality in the cervical spine either acute or
long-standing, of necessity the position should be modified or the operative
procedure should be abandoned. Alternatively, we have not been comfortable
with the prone position nor have we tried the three-quarter prone position.
A self-retaining retractor of the Greenberg type is positioned with the holder
affixed to the operating table and the retractor post arranged in a U-shaped
fashion, open inferiorly around the operative procedure (Fig.
23.5В). These bars will be the recipients of the two retractor arms (position to be
detailed later), a remote irrigating system, and the tray for small cottonoids and
Telfa pads.
The operation microscope is arranged so that the inclined eyepiece is rotated
upward, allowing the surgeon to look down rather than straight ahead or upward.
A 275-mm objective is utilized. With this objective, it is possible to place long
instruments comfortably into the wound and to use the Cavitron aspirator with
the long curved tip. A television camera and the binocular observer arm are
located in the usual position on the microscope and the whole affair is covered by
a transparent drape.
Exposure
A forearm rest is arranged at the head of the table. This can be attached to the
seat upon which the surgeon sits or directly to the top of the table after the
hinged head piece has been removed. A long midline incision is performed. This
should extend down to approximately C-4 and up to the
region of the lambdoid suture, well above the torcular region (Fig. 23.6A). The extra
length of the incision is necessary to gain separation of the muscles and fascia from the
suboccipital region. If the patient's ventricular system requires decompression, a separate
incision is made to the right side in the region of the lambdoid suture to drain the trigone
of the lateral ventricle. The amount of CSF removed can be regulated during the
operation to obtain maximal relaxation of the posterior fossa contents, while not
overdraining the system. The midline incision is brought directly down through the
nuchal ligament to the bone of the suboccipital region. It is not necessary to denude the
first or second cervical spines of
their muscle attachments although the incision must go down to the posterior aspect of
these two structures. The craniectomy not involving the foramen magnum does not
require the removal of the oblique or recti muscles from C-l, C-2. A wide exposure of
the suboccipital bone, however, is necessary (Fig. 23.6B). A self-retaining retractor of
low profile is utilized to hold back the muscles and fascia (Fig. 23.6C). It is apparent
from Figure 23.9, which is a sagittal view, that the center of the route to the pineal gland
is just below the tentorium or in this case the torcular region. The remainder of the
craniectomy is only to provide access for the various instruments and the beam of the
operation microscope. Using the air drill, numerous burr holes are placed because the
bone is the thickest over the torcular and the sinus regions. A number of passes with the
drill in this area are necessary to at least thin out the bone so that rongeuring is done in
an effortless fashion. The craniectomy should extend just above the transverse sinuses
and include all of the torcular region so that the view is not obscured by overhanging
bone and the tentorium can be elevated ever so slightly by a self-retaining retractor.
Laterally, the craniectomy is carried out almost to the mastoid groove and inferiorly 1
cm short of the foramen magnum region. This provides a wide oblong-shaped
craniectomy (Fig. 23.6B). Again, the most essential portion of the craniectomy is that
uncovering the sinsuses and the torcular region.
At this point the surgeon may determine the pressure within the posterior fossa by
palpating the dura mater. If the dura is tense and nonpulsatile, then the ventricle must be
further decompressed or dehydrating agents must be instituted. It is folly to open the
dura of the posterior fossa with a tense cerebellum. There is little choice of the fashion in
which the dura is opened (Fig. 23.7). It is opened to expose maximally the superior
surface of the cerebellum. This requires a V-shaped incision with the limbs relatively
close to the midline so that the
"cathedral effect" of the tentorium does not obscure the central or midline view
and so that the dura in the central area may be retracted upward to the greatest
extent (Fig. 23.7B). Secondary incisions are then carried out laterally toward the
lateral sinuses so that, at the completion of the incision, there are three flaps, a
central one and two lateral ones, which reflect upward and expose the superior
surface of the cerebellum (Figs. 23.7С, 23.8). These flaps may be held upward by
stay sutures attached to rubber bands placed around the Greenberg retractor.
Inferiorly, the dura mater is left as a sling to support the cerebellar hemispheres
during retraction. As noted previously, if additional space is required, this may be
obtained by making a small opening in the arachnoid of the cisterna magna and
releasing CSF from this cistern. The Greenberg retractor is then arranged with
the various posts and bars as shown in Figure 23.7 A. This provides two self-
retaining retractors, a cottonoid tray, and a fixed
irrigating system, which is composed of a 16 gauge needle attached to intravenous
tubing and then to a syringe. The tip of the needle may be bent and then positioned with
the retractor so that the irrigation goes directly into the area of the pineal tumor when
this portion of the operation is attained. Before placement of the retractor blades, the
veins bridging between the cerebellum and the overlying dura mater must all be
coagulated and divided (Figs. 23.9 and 23.10). By gravity, with the patient in the sitting
position, the cerebellum will drop under most circumstances and immediately provide 1
to 1.5 cm of space between its surface and the tentorium (Fig. 23.8). At this point,
protective Telfa is placed over the cerebellum and a self-retaining retractor is placed into
the region of the incisura hard against the torcular and straight sinus, lifting these
structures upward. Another retractor usually 0.5-in. wide is
looped low to come over the cerebellum in the region of the vermis. This is bent in an S-
shaped fashion and depresses the cerebellum (Fig. 23.10A and B). The tip of this
retractor should be placed directly at the anterior aspect of the cerebellum. At this point
with the naked eye or with loupes it is possible to see the pineal region and in almost all
cases the arachnoid will be thickened and opalescent. The operation microscope is now
brought into the field and is used during the remaining portion of work on the tumor. The
thickened arachnoid in the region of the pineal tumor and the incisura is then opened
with a small arachnoid knife, long bayonet scissors, and the assistance of a long bipolar
cautery under
irrigation. The precentral cerebellar vein will be noted coming directly from the region
of the anterior vermis toward the great vein of Galen, which is just visible through the
thickened arachnoid (Figs. 23.11 and 23.12). The precentral vein may be coagulated
with impunity to release the anterior vermis, permitting further exposure of the pineal
region. A few small branches of the choroidal and superior cerebellar arteries may
be noted in the thickened arachnoid overlying the tumor, and these can be
indiscriminantly coagulated and divided. Care must be taken not to injure the large veins
laterally (the veins of Rosenthal running along the medial aspect of the temporal lobe).
At the time of this initial exposure the trajectory of the operation microscope is generally
in line with the vein of Galen and slightly dorsal to the main bulk of the pineal tumor.
Care must be taken not to continue to pursue this direction, for this will bring the surgeon
into conflict with this important deep venous structure (16). As soon as the vein of Galen
is identified, the trajectory of the microscope is angled downward 10 to 20°. At the same
time the inferior retractor is made to retract the cerebellum further, exposing a broad area
of the posterior aspect of the tumor (Fig. 23.13). It may be necessary to cut the
thickened arachnoid well out laterally just above the margin of the cerebellum to release
the cerebellum from this tethering. In Figure 23.11A the sequence of these incisions is
shown. First, the incision along the anterior border of the cerebellum (I and 2), then
division of the precentral cerebellar vein (3), and then cuts extending upward to the
region of the vein of Galen and the confluence of venous structures (4 and 5).
Tumor Management
The posterior face of most tumors will now be exposed adequately to permit progress
to further stages of the operation, including tumor removal. Small branches of the
choroidal arteries especially in vascular tumors will course over this posterior surface of
the tumor and can be coagulated with impunity (Fig. 23.11B). The tumor is then opened
with a fine long-handled knife and bayonet scissors. Coagulation is used where
necessary depending upon the vascularity of the tumor capsule (Fig. 23.14). Portions of
the tumor are then removed by tumor forceps for frozen tissue diagnosis. The accuracy
on these frozen tissues is about 50%, perhaps no more than the law of chance. This is
explained by the difficulty in diagnosing pineal region tumors on frozen tissue even by
an experienced pathologist and is one reason that we prefer open biopsy with abundant
tissue for permanent sections. The interior of the tumor then may be decompressed as
necessary (Figs. 23.14B and 23.15). In those tumors that are benign and encapsulated, it
is possible to dissect laterally, superiorly, and inferiorly around the capsule of the tumors
after gutting the interior. Many tumors are attached superiorly in the region of the velum
interpositum and sometimes laterally to the medial aspect of the pulvinar or the walls of
the third ventricle. Attachments inferiorly to the region of the quadrigeminal portion of
the midbrain vary according to the nature of the tumor but are generally modest in those
encapsulated benign tumors because of the small choroidal arteries bridging this gap. In
tumors that are exophytic or that fungate out of the midbrain, the area
of attachment will be broad and ill-defined and should not be violated (Fig. 23.16).
Various instruments may be used to core out the interior of the tumor. Some of the
tumors are extremely soft and, although varying in vascularity, may be suctioned by a 7
F suction tip. Other firmer tumors such as meningiomas, some astrocytomas, and
teratomas are variegated and much of them are firm, even calcified; this tissue requires
instrumentation such as the laser or Cavitron aspirator. With the long curved tip of the
Cavitron, it is now possible with some difficulty to place it into the operative area to
remove these central cores of firm, sometimes calcified
 tissue (Fig. 23.14B). Some of the teratomas have even contained structures resembling
malformed teeth, and these have been the most difficult to remove. Unfortunately, the
heavily calcified areas are often the most vascular. A long bipolar cautery is of
assistance in these maneuvers and the use of long tumor forceps, curettes, and scissors
can be combined to core out the interior of the tumors.
Once a large central portion of the tumor is removed, it will become apparent
whether the tumor is infiltrating or encapsulated. With infiltra-tive tumors, it is wise
not to attempt radical resections; these are tumors that best respond to radiation,
chemotherapy, or combinations thereof. Pursuing malignant infiltrating tumors into
surrounding structures will often lead to severe neurological deficits that may be
permanent.
The most difficult portion of encapsulated tumors to remove is that portion that
hollows out the midbrain or extends laterally into the trigone of the lateral ventricles.
Because of the sitting position the portion intimate to the midbrain is most difficult to
remove because it must be elevated and then microdissection techniques must be
carried out between it and the critical midbrain structures. This can be accomplished,
however, and it may be possible for a skilled assistant to hold the tumor up with forceps
while the surgeon works in this interface, coagulating and dividing the vessels. The
prepositioned irrigator is of immense help in this maneuver. As the tumor is gradually
delivered or the large decompression is made through the center of the tumor, openings
into the posterior third ventricle frequently occur. This gives the surgeon an excellent
perception of the relationship of his operative exposure and the third ventricle as related
to the tumor. Tumors with minimal attachment will often roll out at this point and large
pieces may be removed as a whole (Figs. 23.15 and 23.17). Again, particular attention
is paid to the attachment, especially to the velum interpositum, because a hole in the
internal cerebral veins or the vein of Galen will lead to profuse bleeding that is difficult
to control. Other than packing, it is difficult to place hemostatic agents on these
structures and have them stay in place. Similarly, an attempt to cauterize these
distended veins may lead to larger openings. With experience, it is possible to
determine which tumors are resectable and which should be left short of total resection
and also the tumors in which only a biopsy should be done. Surprisingly, we have
encountered our only severe difficulties — three mortalities — in patients with
malignant tumors that were highly vascular and difficult to manage at operation. Only
small portions of the tumors in these patients were removed and yet hemostasis was
inadequate, leading to massive postoperative hemorrhage and death. One of these cases
was a glioblastoma in which hemorrhage occurred 1 week after the operation,
presumably as a vessel was eroded. The other two hemorrhages occurred immediately
after operation on malignant pineocytomas where bleeding was difficult to control at
the time of operation. We have used all of the standard hemostatic agents and prefer
none over others. When total removal is possible, the tumor is usually not highly
vascular and hemostasis after such radical resections is usually quite easy.
CSF Diversion and Closure
In some cases where a block to the aqueduct remains after the central portion of the
tumor is cored out, it is possible to leave a small ventricular catheter through the tumor
into the third ventricle, subsequently leading it down and attaching it to the dura mater
while placing the distal end into the cisterna magna. This permits an internal shunting
of CSF much like a Torkildsen procedure and may be used in lieu of an extracranial
shunt. Once hemostasis is secured, we have not left metallic markers in the area,
foregoing this because of the possible use of MRI scanning. All protective mechanisms
are removed from the cerebellum and the dura is closed in a sling like fashion to
resupport the cerebellum and replace it to its normal position. All of the patients had
craniectomies and there has been no replacement of the bone. The muscles and fascia are
closed in appropriate layers, and we have used wound drainage for 12 hours. The patient
is kept in a sitting position, extubated, and taken to the recovery room where ventricular
drainage is continued as necessary. A high dose of dexamethasone is also continued.
Malignant Tumor Management
In the comprehensive treatment of these patients when malignant tumors are
encountered, our protocol mandates the performance of three CSF evaluations during the
postoperative period and myelography studying the lumbar and thoracic regions looking
for evidence of seeding. Wherever possible we have been removing CSF via either the
shunt system or the cisterna magna to evaluate it from a cytological viewpoint (8).
We have developed a protocol for the treatment of these patients which is founded on
a detailed identification of the tumor. This information plus the evaluation of CSF and
myelography has led us to the following treatment regimen:
Surgery
In those benign and encapsulated tumors that are totally removed no further treatment
is necessary (27). This group comprises approximately 30% of the tumors encountered
and consists of the low grade cystic or solid astrocytoma, dermoid, epidermoid, and
meningioma (20) and the
mature encapsulated three-germ layer teratoma. Some of the pineocytomas have fallen
into this cateogry, as has the rare ependymoma.
Radiation
Those tumors that have the features of a germinoma, including the small patches of
lymphocyte-like cells in the interstices and the larger nucleated cells, have a tendency to
spread in the region of the third ventricle or by seeding throughout the CSF spaces. Our
primary treatment has been radiation therapy. When seeding is not evident, radiation is
directed at the tumor and the region of the third ventricle. When seeding is apparent
from a myelogram or evaluation of the CSF, radiation is given to the entire neuraxis,
5500 rads to the tumor, 3500 rads to the entire brain, and 3500 rads to the spine (17, 28).

Chemotherapy
In tumors of the primitive embryonal or choriocarcinoma type, chemotherapy has
been the first line of defense. This consists of the Einhorn triple chemotherapy treatment
(7). In tumors that have received radiation treatment and recur, chemotherapy may
follow (9, 13, 23).

Results
Using this operative approach, we have had 3 mortalities out of 90 operative
experiences. These 3 mortalities occurred in patients with malignant tumors in which
hemostasis was a problem. Morbidity was generally temporary and consisted of
somnolence and disturbance of extraocular movements such as Parinaud's syndrome
(Fig. 23.18).

References
1. Camins MB, Schlestnger EB: Treatment of tumors of the posterior part of the third
ventricle and the pineal region: A long term followup. Ada Neurochir (Men)
40:131-143, 1978.
 2. Cummins FM, Taveras JM, Schlesinger EB: Treatment of gliomas of the third
ventricle and pinealomas: With special reference to the value of radiotherapy.
Neurology (Minneap) 10:1031-1036, 1960.
3. Cushing H: Intracranial tumors: Notes upon a series of two thousand verified
cases with surgical mortality pertaining thereto. Springfield, IL, Charles С
Thomas, 1933.
4. Dandy WE: Operative experience in cases of pineal tumor. Arch Surg (Chi
cago) 33:19-46, 1936.
5. DeGirolami U, Schmidek H: Clinicopathological study of 53 tumors of the
pineal region. J Neurosurg 39:455-462, 1973.
6. Donat JF, Okazaki H, Gomez MR, Reagan RJ, Baker HL Jr, Laws ER Jr:
Pineal tumors: A 53-year experience. Arch Neurol 35:736-740, 1978.
7. Einhorn LH, Donohue J: Cis-diamine dichloroplatinum, vinblastine, and
bleomycin combination chemotherapy in disseminated testicular cancer.
Ann Intern Мей 87:293-298, 1977.
8. Gindhart TD, Tsukahara YC: Cytologic diagnosis of pineal germinoma in
cerebrospinal fluid and sputum. Acta Cytol 23:341-346, 1979.
9. Ginsberg S, Kirshner J, Reich S, et al: Systemic chemotherapy for a primary
germ cell tumor of the brain: A pharmaco-kinetic study. Cancer Treat Rep
65:477-483, 1981.
10. Herrick MK, Rubinstein LJ: The cytological differentiating potential of pineal
parenchymal neoplasms (the pinealomas): A clinicopathological study of 28
tumors. Brain 102:321-332, 1979.
11. Krause F: Operative frielegung der vierhugen, nebst beobachtungen uber
hirndruck und dekompression. Zentbl Chir 53:2812-2819, 1926.
12. Neuwelt EA, Ginsberg M, Frenkel et al: Malignant pineal region tumors: A
clinico-pathological study. J Neurosurg 57:597-607, 1979.
13. Neuwelt EA, Frenkel EP, Smith RG: Suprasellar germinomas (ectopic pineal
omas): Aspects of immunological characterization and successful chemo
therapeutic responses in recurrent disease. Neurosurgery 7:352-358, 1980.
14. Ono N, Takeda F, Uki J, et al: A suprasellar embryonal carcinoma producing
alphafetoprotein and human chorionic gonadotropin; treated with combined
chemotherapy followed by radiotherapy. Surg Neurol 18:435-443, 1983.
15. Poppen JL: The right occipital approach to a pinealoma. J Neurosurg 25:706-
710, 1966.
16. guest DO, Kleriga E: Microsurgical anatomy of the pineal region. Neurosur
gery 6:385-390, 1979.
17. Rao YTR, Medini E, Haselow RE, et al: Pineal and ectopic pineal tumors: The
role of radiation therapy. Cancer 48:708-713, 1981.
18. Reid WS, Clark K: Comparison of the Infratentorial and transtentorial ap
proaches to the pineal region. Neurosurgery 3:1-8, 1978.
19. Ringertz N, Nordenstam H, Flyger G: Tumors of the pineal region. J Neuro-
pathol Exp Neurol 13:540-561, 1954.
20. Rozario R, Adelman L, Prager RJ, Stein BM: Meningiomas of the pineal region
and third ventricle. Neurosurgery 5:489-495, 1979.
21. Rubinstein LF: Cytogenesis and differentiation of pineal neoplasms. Hum
Pathol 12:441-448, 1981.
22. Schmidek HH: Pineal Tumours. New York, Masson, 1977.
23. Seigal T, Pfeffer R, Catane R, et al: Successful chemotherapy of recurrent
intracranial germinoma with spinal metastases. Neurology (Cleve) 33:631-
633, 1983.
24. Stein BM: The Infratentorial Supracerebellar approach to pineal lesions. J
Neurosurg 35:197-202, 1971.
25. Stein BM: Supracerebellar-infratentorial approach to pineal tumors. Surg
Neurol 11:331-337, 1979.
26. Stein BM: Surgical treatment of pineal tumors. Clin Neurosurg 26:490-510,
1979, ch 19.
27. Stein BM: Supracerebellar approach for pineal region neoplasms. In Schmi
dek H, Sweet W (eds): Operative Neurosurgical Techniques. New York,
Grune & Stratton, 1982, vol 1, pp 599-607.
28. Sung D, Harisiadis L, Chang CH: Midline pineal tumors and suprasellar
germinomas: Highly curable by irradiation. Radiology 128: 745-751, 1978.
29. Van Wagenen WP: A surgical approach for the removal of certain pineal
tumors: Report of a case. Surg Gynecol Obstet 53:216-220, 1931.
30. Whittle IR, Allsop JL, Besser M: Tuberculoma mimicking a pinealoma. J
Neurosurg 59:875-878, 1983.
24

Occipital Transtentorial
Approach
W.Kemp Clark, M.D.

Historical Perspective
Historically, tumors in the region of the pineal gland were treated by cerebrospinal
fluid diversion and radiation therapy (5). The chief reasons for this surgical nihilism
were the high operative mortality and morbidity associated with direct surgical
approaches to tumors in this area (2, 3, 9, 13, 15).
The older approaches to this region usually involved either an occipital lobectomy
with its concomitant permanent homonymous hemianopsia or division of some part of
the corpus callosum (4, 8, 14). Usually the splenium was divided. This results in a
partial cerebral disconnection syndrome with the patient having difficulty transferring
visual information from one hemisphere to the other.
These older approaches to this region often resulted in division of one or both internal
cerebral veins or even the vein of Galen itself (2). The literature is confusing as to the
exact results of this action. The collateral venous drainage from the deep galenic system
is through septal and choroidal veins. This may be adequate to carry the venous
circulation but, on the other hand, it may not. However, mutism, a flat affect, even coma
and death have been reported (12). Seizures and hemiplegia have also resulted from
these older approaches (13).
Other approaches to this region have involved the Supracerebellar infratentorial
approach (7, 11). To reach the pineal region, one must coagulate the veins draining the
cerebellar hemisphere. This may result in cerebellar venous infarction (7). The
advantages of the occipital transtentorial approach over the Supracerebellar
infratentorial approach have been described by surgeons using both approaches (10).

Advantages and Indications

The principle advantages of this approach over the supracellular are a greater ability
to mobilize the tumor and to visualize more of the third ventricle and better orientation
of the surgeon. An anatomical fact makes this approach feasible. There are no veins that
cross from the occipital lobe into the superior sagittal sinus. Therefore, no risk of
infarction
occurs by this approach unless the surgeon makes the mistake of ligating the inferior
cerebral vein. As this vein drains the occipital lobe into a transverse sinus, its interruption
produces edema in the occipital lobe. The vein lies quite lateral and should be outside the
usual operative exposure.
The occipital transtentorial approach was initially described by Jamie-son (5). He
operated without the use of the operating microscope. The addition of this instrument has
made the procedure both more effective and safer. The improved illumination and
magnification make it possible to gain access to the pineal region with substantial ease
(6).
Today, the indications for operation of pineal region tumors can best be outlined as
follows. In many conditions operation is the only curative procedure available. This is
true for aneurysms of the vein of Galen and for teratomas of the pineal gland itself.
During operation, one may obtain tissue for pathological diagnosis. This in itself is a
worthwhile goal, as it makes possible a better approach to therapy and prognosis.
Because chemotherapy is a distinct possibility in cases of germinoma of the pineal gland,
a tissue diagnosis of tumor type is a worthwhile reason to operate on these patients. The
mere act of operating on the patient regardless of the type of tumor results in reducing the
size of the tumor, reducing the burden to the patient. This will improve the chances of
radiation controlling the tumor. Finally, operative procedures in this region should result
in opening of the third ventricle into the subarachnoid space. This avoids the need for
shunt devices. Control of intracranial pressure without a shunt is a worthwhile goal and
can only be achieved by direct surgical approach to the tumor.
Turning specifically to the advantages of the occipital transtentorial approach, these
are many. This approach allows a great deal of exposure without sacrifice of any neural
tissue. It is remarkably free of complications or surgical difficulties. Access is gained to
the entire third ventricle, the superior cerebellar vermis, the upper fourth ventricle, and
the posterior corpus callosum. Excellent visualization of the normal anatomy and the
abnormality is obtained. All types of pathology existing in this location can be handled.

Positioning of Patient
The occipital transtentorial approach traditionally was done with the patient in the
sitting position with the attendant risks of air embolus (5). More importantly, in my
personal series, all visual field cuts postoperatively occurred in patients operated on in
the sitting position. Since changing to the semiprone position, we have eliminated this
complication.
If the patient is to be operated on in the sitting position, an indwelling catheter in the
right heart must be placed for aspiration of air. A Doppler probe should be placed on the
precordium. The most likely time of air embolus is when the bone flap is being turned or
when the dura mater is being opened. In the sitting position, care should be taken to be
sure that the patient is placed far enough forward that the operating microscope can be
brought into position without producing hyperextension of the surgeon's neck.
An alternative is the semiprone position (Fig. 24.1). This is the position preferred for
operations on aneurysms of the vein of Galen. Small children do not tolerate the sitting
position very well and it is easier to place them prone with the surgeon at the patient's
head. The disadvantages is that the anatomy is reversed and the surgeon must be
reminded of that fact.
Of the three possible positions the best is undoubtedly the park bench
(semilateral) (Fig. 24.2). It allows easy access to the area and does not produce inversion
of the anatomy. It has the additional advantage that the occipital lobe tends to fall away
spontaneously and thus retraction of it is avoided.

Patient Preparation
In preparation for the procedure, certain adjuncts have proven helpful. Corticosteroids,
usually dexamethasone in doses of 4 to 6 mg every 6 hours for 48 hours preoperatively,
is helpful. A ventriculostomy or a preoperative ventriculoperitoneal shunt for control of
intracranial pressure before direct approach to the tumor is also beneficial.

Instrumentation
The single most important instrument for the performance of this procedure is the
operating microscope. Our preference is for the Zeiss operating microscope with the
Contraves stand. A binocular observer tube, 35-mm camera, and TV camera are adjuncts
to the use of the microscope. It is our practice to bring in the microscope at the time of
opening of the tentorium or just after it has been opened. The microscope can be removed
from the operative field after the work in the pineal region has been completed and the
dural closure has begun.
Microsurgical instruments are of the usual types, the preference being for bayonetted
forceps, both sharp and blunt. Bipolar cautery is essential. The bipolar cautery forceps
must be long enough to reach into the depths of the wound. Usually a 7.5- or 8-in.
forceps will serve. Bayonetted scissors, usually curved slightly upward, are used to open
the arachnoid and do the dissection around the veins. An arachnoidal knife is sometimes
very useful in doing this part of the dissection.
Operative Technique
The details of the opening of the operative incision are critical (1, 6). For a right-
handed surgeon, a right occipital craniotomy is usually easier. For the left-handed
surgeon, it is usually the opposite side. In either case, the crux of the exposure lies in
ensuring that the bony opening is placed to be both across the midline to the opposite
side and at the level of the transverse sinus. What follows is a description for a right-
handed surgeon and is therefore a right occipital craniotomy.
The skin incision is made to the left side of the midline, beginning at
the level of the external occipital protuberance (Fig. 24.3). It is carried up approximately
7 to 8 cm and then turned across the midline laterally. This is important to make the
craniotomy on the down side of the skull, which ensures the use of gravity to help retract
the occipital lobe. The incision is again turned downward to end along the mastoid
groove. The scalp is then reflected downward. It is easiest to turn the scalp in one layer
including the periosteum. Hemostasis from the scalp is obtained in the usual manner. It is
our preference to use Rainey clips for this purpose. However, hemostats or Michelle clips
may be used.
After reflection of the scalp, the bony opening is made (Fig. 24.4). Burr holes are
placed on the right side along the midline just lateral to the superior sagittal sinus.
Usually two holes are sufficient as the length of the craniotomy flap is usually about 7
cm. Six burr holes are usually required, four on the right side and two on the left side of
the superior
sagittal sinus. Burr holes are then connected with the use of the Gigli saw or a
craniotome. The bone is removed by rongeurs across the superior sagittal sinus. The
bone flap is then removed as a free flap and kept sterile on the scrub nurse's table.
Next, removal of the occipital bone over the transverse sinus is carried out by rongeur.
It is not necessary to carry this completely into the posterior fossa, but the transverse
sinus must be visualized throughout its extent in the operative field. Bleeding from
either of the dural sinuses is easily controlled by using thrombin-soaked gelatin sponge
and gentle pressure.
The dura mater is opened as an L-shaped or T-shaped incision. In the first cases in our
personal series, the dura was opened in a conventional
horseshoe fashion, basing the horseshoe on the superior sagittal sinus. We have
abandoned this procedure because the roll of dura along the interhemispheric fissure
interfered with access to the lesion. If an L-shaped incision is used, it should begin
superiorly as close to the superior longitudinal sinus as possible. The incision is carried
inferiorly along the sinus to the level of the torcular. It is then turned laterally, close to
the transverse sinus. We leave a cuff of dura of sufficient size to enable a watertight dural
closure. Alternatively, we use an incision opening the dura along the sagittal sinus, then
along the transverse sinus, and finally obliquely up toward the superior lateral burr hole.
This incision has been used in most of our recent cases (Fig. 24.5A). It allows easier
access for retraction of the occipital lobe. In any event, the dura is then reflected upward
and outward, exposing the occipital lobe. Then, a self-retaining retractor may be gently
applied to the occipital lobe, retracting it laterally and superiorly. The crux here is to
avoid placing the retractor directly on the calcarine cortex, keeping it more to the
occipital pole than deep into the interhemispheric fissure (Fig. 24.5B). If the park bench
position is used, it is usually not necessary to retract the occipital lobe as it will fall away
spontaneously (Fig. 24.6).
Next, the tentorium is opened (Fig. 24.7A). This is done by making an incision parallel
to the straight sinus, approximately 1 to 1.5 cm from it. It is easiest to open the tentorium
going anteriorly. The surgeon is cutting
away from himself. The beginning incision is made at the junction of the straight sinus
and the torcular and is carried anteriorly toward the incisura. The tentorium is vascular
and the surgeon should be prepared to control the bleeding by bipolar coagulation or,
occasionally, by the use of clips. Retention sutures are placed to hold the tentorium
open, enabling visualization of the superior cerebellar vermis and the arachnoid over
the veins of the galenic system. Much of the difficulty encountered during earlier
operative procedures in this region was due to the tearing of this arachnoid, resulting in
damage to the underlying veins. Once, it was thought that the preoperative use of
radiation produced the thickening of the arachnoid. This is probably not the case as the
arachnoid in this area is always thick. It is necessary to free these veins from their
arachnoidal sheath to gain
access to the tumor (Fig. 24.7B). Using microsurgical technique, one opens sharply the
dense arachnoid over the deep veins. The first vein visualized is usually the vein of
Galen; next is usually the right basilar vein of Rosenthal, which enters the field laterally,
coming in to join with the internal cerebral vein. The internal cerebral vein and the
precentral vein of the cerebellum are usually the next veins visualized. The arachnoid is
dissected from the vein of Galen, the internal cerebral vein, and the basal vein of
Rosenthal. In most circumstances, it is necessary to
dissect the arachnoid off the right internal cerebral vein and the right basal vein of
Rosenthal only (Fig. 24.7B). However, it is possible to dissect the left with facility
should it be necessary to mobilize the veins to gain access to the lesion. Once the
arachnoid has been dissected free from the veins, the surgeon can deal with any lesion
of the superior vermis, quadrigeminal plate, posterior third ventricle, splenium, or
pineal gland (Fig. 24.8).

Lesion Management
In a typical pineal region tumor, the tumor mass lies deep to these venous structures
(Fig. 24.9). A more difficult situation arises when the tumor rises from the free edge of
the tentorium or the junction of the falx and the tentorium (Fig. 24.10). In this
circumstance, the veins will be carried anteriorly, producing the problem of identifying
them through the tumor. The surgeon must reduce the volume of the tumor using the
ultrasonic aspirator. Working cautiously along the lateral inferior margin of the tumor,
the surgeon can begin to identify the arachnoid and the veins. It is usually easier to deal
with meningiomas arising in this location by approaching their removal from lateral to
medial and from inferior to superior. However, no hard and fast rule can be made as
each case must be approached individually, and the most promising plane of dissection
should be pursued by the surgeon.
Intrinsic tumors, such as gliomas of the quadrigeminal plate or gliomas of the
splenium of the corpus callosum, will again take the deep venous structures posteriorly
toward the surgeon, and they may be displaced upward or downward depending on the
site of origin of the tumor. It is usually simple to identify an intrinsic tumor of either the
brain stem or the splenium by the lack of encapsulation of the mass. However, if a
primary pineal tumor is very large this may be rather difficult. Occasionally, the
identification of the capsule may prove difficult. The glioma in this region should be
cautiously excised and the third ventricle should be entered through its posterior aspect
in the pineal recess. This should be a large opening so that cerebrospinal fluid (CSF)
flow will be facilitated.
If the lesion dealt with is a vein of Galen aneurysm, the major feeders to the
malformation should have been identified by preoperative angiog-raphy. Their location
can then be confirmed by direct inspection by rotating the mass of the aneurysm until
they can be seen. These can be dividied between aneurysm clips. Thus, a thorough
centimeter by centimeter inspection of the wall of the vein of Galen is carried out.
Arterial feeders entering into it are either coagulated or clipped and divided. As this
dissection proceeds, the operator will note that the vein of Galen becomes progressively
bluer and less turgid, making it easier to complete the dissection. When the surgeon
feels that all arterial connections have been divided, a 25 gauge needle is introduced into
the vein of Galen and a blood sample is drawn. Simultaneously blood is drawn from a
peripheral vein. Determination of blood gases on the two samples is done and the values
should be the same. This indicates that the blood from the vein of Galen is venous and
that all arterial anastomoses have been interrupted.
If one is dealing with the typical pineal region tumor, the tumor should be entered by
sharp dissection and a biopsy obtained (Fig. 24.11). A frozen section will help with the
decision of how to proceed. If, as occasionally happens, the tumor proves to be a glioma
arising either from the quadrigeminal p?ate or from the corpus callosum, cytoreduction
of the tumor should be done cautiously and the CSF pathway should be opened.
 If the tumor proves to be of embryonal origin such as a teratoma or dermoid,
piecemeal or en bloc resection should be done. The surgeon should make every attempt
to remove the tumor completely.
If the tumor is a germinoma of the pineal region, thorough cytoreduction of the tumor
with removal of as much as possible should be carried out (Fig. 24.12). In any case, the
end stage is when one can visualize the interior of the third ventricle, seeing all the way
to the foramen of Monro. This ensures that there is no block of the CSF pathway.
 Pineal region tumors may extend inferiorly down under the vermis of the cerebellum
(Fig. 24.13A). If this is the case, that structure should be divided so that the lower pole
of the tumor may be identified, mobilized, and removed. Similarly, the tumor may
extend superiorly into the splenium of the corpus callosum (Fig. 24.13B). Usually it is
possible by reducing the tumor volume internally and delivering the capsule of the
tumor downward into the operative field to avoid having to divide the splenium. The
surgeon should be aware that opening the superior vermis of the cerebellum produces
little in the way of neurological deficit but too vigorous a division of the splenium will
produce a cerebral disconnection syndrome.
Through this approach, it is possible to operate on tumors of the
superior cerebellar vermis. Upon opening the tentorium, the surgeon will see the
culmen of the cerebellum (Fig. 24.1ЗА). Either the tumor presents on the surface
or it may be found subcortically by ultrasound or by needle. It is then approached
through a transcortical incision. The great advantage of approaching tumors in
the cerebellar vermis by this approach is the avoidance of manipulation of the
cerebellum. The tumor may be removed in toto or in part depending on its
histological characteristics without producing neurological deficit by retraction
or dissection within the cerebellum. Likewise, tumors lying in the superior part
of the fourth ventricle may be approached through the superior cerebellar vermis
by this approach, again with the advantage of approaching the tumor through the
shortest possible route.

Intraoperative Decisions
Clearly, the advantage of this procedure is the possibility of total excision of
the lesion. This is the nub of the whole operative procedure. There are a number
of points that enter into the decision to excise totally or simply to perform an
internal decompression. Similarly, there is a problem relating to when to stop the
internal decompression of a tumor. The factors that enter into the decision to
attempt total resection include the nature of the lesion, the location of the major
deep venous structures,
 the ease of the procedure up to the decision-making point, the age of the patient, and the
availability of adjunctive therapy.
Obviously the type of abnormality with which the surgeon is dealing is a critical
determinant of the possibility of total excision. It is rarely possible to excise a germ cell
tumor totally unless it is a teratoma. An occasional germinoma can be excised. For other
tumors that occur in this region, such as meningiomas, arachnoidal cysts, lipomas, and
gliomas, total resection becomes increasingly difficult. One is usually unable to remove
a meningioma if it is invading the dural sinuses. Total resection is also limited by the
location of the great veins, which typically are displaced anteriorly to meningioma when
one is working through tumor toward these vascular structures. Because most
meningiomas in this area are truly benign in terms of their growth characteristics, it is
usually not necessary to risk the patient's life and function in attempting a total removal.
Tumors that are intrinsic to the brain stem such as lipomas and gliomas cannot be
surgically resected except at the price of a ghastly neurological deficit. Here internal
decompression is the trick. How well the procedure has gone to the point of decision-
making for a total excision is also critical. If it has been a struggle with a number of
problems, such as blood loss or anesthetic difficulty, it is usually the better part of valor
to abandon the procedure. One can return another day for a second attempt. If things
have gone well and there are no problems with the patient in general, it is safe to
consider total resection if all other criteria are met.
The age of the patient is also a consideration. The surgeon should be more aggressive
in the younger age group. The availability of adjunctive therapy must be considered
because some of the germ cell tumors have been successfully managed with
chemotherapy and radiation.
The critical dimension for total excision is the ability of the surgeon to define a clean
plane between the tumor and the surrounding normal structures. As long as this plane
can be easily identified, it is possible to proceed toward total resection. This is a matter
of experience and judgment.
The question of when the tumor has been adequately reduced is again a matter of
surgical judgment. One must open the posterior third ventricle adequately to allow for
the normal flow of CSF. It is critical that the ventricular system be unblocked before
resection is abandoned; otherwise, the patient will require some type of shunt. One of the
purposes of the operation is to avoid the need for a shunt, with its concomitant problems
of intermittent obstruction or infection (Fig. 24.12).
Once the ventricular system has been decompressed, one must consider the amount of
tumor burden that remains to be treated by radiation, chemotherapy, or both. The best
estimate of this is how much normal tissue can be identified around the edges of the
mass. The direction in which the remaining tumor is going is also critical. For instance,
in a quadrigeminal plate glioma the remaining tumor is in the brain stem. It becomes
critical to stop excising the tumor before entering the brain stem proper. A very difficult
problem lies in the surgical treatment of lipomas in this region and here cytoreduction
should stop as soon as the ventricular system is decompressed. The margins between
lipomatous tumor and brain are extremely difficult to define, and the surgeon may injure
critical areas of the brain.

Closure
After removal of the tumor and local hemostatis, the retractor, if any, should be
removed from the wound, the wound thoroughly irrigated, and
the dura replaced and sutured (Fig. 24.14A). Although, it is not necessary to close the
tentorium watertight, a few sutures to prevent the occipital lobe from herniating
downward are worthwhile. Closure of the dura mater can be done either with interrupted
or running suture. The dura mater should be closed as watertight as possible (Fig.
24.14B). The bone flap is replaced and wired in position, and the small, narrow
craniectomy along the transverse sinus is repaired using stainless steel mesh as an onlay
cranioplasty (Fig. 24.14C). The scalp flap is then replaced and closed either in one layer
with mattress sutures or in the two-layer closure of the galea and the skin.
 Drainage using a suction-type drain such as the Jackson Pratt may be used. It should
be placed in the epidural space as an optional measure.

Summary and Complications

In summary, the occipital transtentorial approach to the pineal region, posterior third
ventricle, superior cerebellar vermis, quadrigeminal plate, and deep galenic venous
system has proven to be one of the most successful surgical procedures introduced
during the past 2 decades. The older approaches had unacceptable morbidity and
mortality. This has proven not to be the case with this approach. The complications of
this approach are the usual ones of any surgical intervention in the head. Infection,
osteomyelitis, and intracranial hemorrhage of various types are possible. In my
experience none have occurred. This may be a function of the relatively small size of
my series of these tumors. Specific complications using this approach include the
production of a homonymous hemianopsia. This is the direct result of improper
placement of the retractor with two vigorous a retraction of the occipital lobe. This may
be avoided by the use of hypertonic solutions during operation and the preexistent use
of ventricular drainage to reduce ventricular size. Finally, the use of the park bench
position produces falling away of the occipital lobe without retraction.
Other complications involve injury to the splenium of the corpus callosum. If this is
inadvertently or deliberately divided, the patient will be left with a cerebral
disconnection syndrome. This will produce difficulty in reading, as visual information
cannot be transferred from one hemisphere to the other.
Damage to the venous structures are the final specific problems related to this
approach. The easiest one to avoid is damage to the inferior cerebral vein, which drains
the occipital lobe. This should lie too far laterally to be of any concern to the operating
surgeon. It rarely is in the operative field but can be visualized occasionally lying just
lateral to the bony opening. Damage to the internal cerebral veins may result in mutism.
Damage to the vein of Galen may produce a similar effect. The secrete in avoiding
damage to the deep venous system is to open the arachnoid sharply under direct vision
with magnification.
In the case of intrinsic tumors approached through this exposure, it is possible to enter
into the quadrigeminal plate of the upper brain stem with disastrous results. However,
the surgeon should recognize that the goal in such a case is to open the third ventricle,
not to effect a great deal of tumor resection.
This approach to this anatomically deep region in the center of the brain has proven to
be effective, safe, and relatively simple to perform technically. It is a significant
advance in our surgical capacity to deal with tumors of the human nervous system.

References
1. Clark K: The occipital transtentorial approach to the pineal region, in Schmi-
dek HH, Sweet WH (eds): Operative Neurosurgery and Techniques. New
York, Grune and Stratton, 1983, pp 595-598.
2. Dandy WE: An operation for the removal of pineal tumors. Surg Gunecol
Obstet 33:113-119, 1921.
3. Glasauer FE: An operative approach to pineal tumors. Acta Neurochir (Wien)
22:177-180, 1970.
4. Horrax G: Treatment of tumors of the pineal body. Arch Neurol Psychiatry
64:227-242, 1950.
5. Jamieson KG: Excision of pineal tumors. J Neurosurg 35:550-553, 1971.
6. Lazar ML, Clark WK: Direct surgical management of masses in the region of
the vein of Galen. Surg Neurol 2:17-21, 1974.
 7. Page LK: The infratentorial Supracerebellar exposure of tumors in the pineal
area. Neurosurgery 1:36-40, 1977.
8. Poppen JL: The right occipital approach to a pinealoma. JNeurosurg 25:706-
710, 1966.
9. Poppen JL, Marino R Jr: Pinealomas and tumors of the posterior portion of
the third ventricle. J Neurosurg 28:357-364, 1968.
10. Reid WS, Clark WK: Comparison of the infratentorial and transtentorial
aproaches to the pineal region. Neurosurgery 3:1-8, 1978.
11. Stein BM. The infratentorial Supracerebellar approach to pineal lesions. J
Neurosurg 35:197-202, 1971.
12. Stern WE, Batzdorf U, Rich JR: Challenges of surgical excision of tumors in
the pineal region. Bull LA Neurol Soc 36:106-118, 1971.
13. Suzuki J, Iwabuchi T: Surgical removal of pineal tumors (pinealomas and
teratomas). J Neurosurg 23:565-571, 1965.
14. Van Wagenen WP: A surgical approach for removal of certain pineal tumors:
Report of a case. Surg Gynecol Obstet 53:216-220, 1931.
L5. Ward A, Spurling RG: The conservative treatment of third venticle tumors. J
Neurosurg 5:124-130, 1948.
25
Posterior
Intrahemispheric
Retrocallosal and
Transcallosal
Approaches
J. Gordon McComb, M.D., and Michael L J. Apuzzo,
M.D.

Historical Perspective
The posterior interhemispheric transcallosal approach to the pineal region was
originally described by Walter Dandy in 1915 using a canine model (5, 22, 35). Based
on his experience with 12 animals he suggested the feasibility of such an approach in
humans, and in 1921 he published his initial experience using this method with 3 cases
of pineal region masses (7). With the head in a lateral position with the right side up, an
extensive right midline parietooccipital bone flap was developed, the dura was reflected
over the sagittal sinus, and bridging veins were sacrificed. After midline exposure, the
posterior 3 to 4 cm of the corpus callosum was incised, providing visualization of the
vein of Galen, its tributaries, and the posterior third ventricle and quadrigeminal
regions.

In the first instance a silent cerebellar tumor had secondarily involved the region of
the pineal body and the corpora quadrigemina; after exposure of the tumor no attempt
was made to remove it, because of its infiltrating character. This case, however,
showed that a good exposure of this region is possible. On two subsequent occasions
tumors of the pineal body have been completely removed. In one case an
encapsulated tubercle of the pineal body... it measured 5 cm by 4 cm. The results of
this case demonstrated not only the feasibility of the removal of tumors of the pineal
body, but also the absence (in this case at least) of any injurious mental or physical
effects due to the operation.

In this chapter we describe modifications of this essential concept (7, 28) that, when
coupled with contemporary microsurgical instrumentation, allows safe exposure of the
pineal gland, posterior third ventricle, quadrigeminal cistern, and quadrigeminal
complex (Fig. 25.1) via a posterior interhemispheric corridor, which allows regional
entry and exposure via maneuvers of (a) tentorial incision, (b) falcine incision, (c)
splenial retraction, (d) incision of the posterior body of the corpus callosum, and (e)
splenial incision.
Operative Corridor: Anatomy and Physiological Risks
The major topographic elements of the posterior midline corridor that require
identification and consideration include the inion, the lamdoidal and sagittal sutures, the
sagittal sinus, the parasagittal cortical veins, the falx cerebri, the tentorium, the incisura,
the straight sinus, the vein of Galen and its tributaries, and the posterior trunk and
splenium of the corpus callosum (20, 21, 23, 31).
Consideration of the consequences of injury to each neural or vascular component is
essential as a stepwise progression evolves through the corridor of exposure.
Dural Venous Sinuses
During bone flap development and dural reflection, attention must be directed toward
maintaining the integrity of the sagittal sinus, which is exposed over its posterior third,
the lateral sinus, and the torcular Hero-phili (14, 17). Particularly, if the sitting position
is used aspiration of air must be avoided. With the retrocallosal approach, it may be
necessary to gain more exposure by incising the falx cerebri, which necessitates
dividing the inferior sagittal sinus or the tentorium parallel to the straight sinus (Fig.
25.2).
Parasagittal Veins
Although primary consideration must be given (9) to parasagittal venous tributaries
during anterior callosal approaches (1, 34), this is not an important issue in posterior
callosal approaches that involve the posterior third of the nondominant cerebral
hemisphere. The posterior one-third of the sagittal sinus receives few significant
tributaries, and the posterior, medial superior nondominant hemisphere is generally
without a detectable functional component (Fig. 25.3).
Deep Cerebral Veins (Galenic System)
The venous structures comprising the galenic system provide an apparent potential
threat to satisfactory outcome in surgical endeavors in this region (16, 21, 30, 32). Most
reports addressing the surgical approaches to the pineal region caution that these vessels
should not be compromised as either hydrocephalus or venous infarction could result.
The concept that hydrocephalus resulted from occlusion of the vein of Galen
originated with the work of Dandy in 1919 (6). However, subsequent studies by Bedford
(1934) (2), Schlesinger (1940) (28), and Hammock et al. (1971) (13) failed to confirm
this observation. The issue of venous infarction remains clouded. Clinical experience
with thrombosis of the vein of Galen has not added relevant information as the
circulatory and pathological changes that follow occlusion thrombosis are not selective
to the vein of Galen, but involve many of the veins comprising the deep venous system
and are often associated with other pathological processes such as inflammation or mass
lesions. Schlesinger (29) reported in 1939 that no valves are present in the deep or the
superficial venous systems of the brain and that there is free bidirectional commu-
nication between the two drainage pathways. Some of the vascular changes observed
after ligation of the vein of Galen in earlier studies potentially relate to operative
techniques rather than actual ligation of the structure. Any objections to technique seem
to have been avoided by Hammock et al. (13), who selectively occluded the vein of
Galen with clips, effecting minimal trauma to adjacent tissues. Pre- and postoperative
angiograms confirmed pre- and postocclusion vascular anatomy in the rhesus monkey.
The only circulatory change noted on the postclipping
angiogram was dilation of the adjacent venous pathways; there was no evidence of
thrombosis. Examination of the brains at various intervals after vein of Galen occlusion
showed no evidence of vascular infarction or encephalomalacia, but only dilation of the
diencephalic and choroidal vessels. Clinically these animals showed no untoward effects.
No study has detailed selective occlusion of the internal cerebral veins, basal veins of
Rosenthal, or precentral cerebellar veins, which in combination or total might deprive
access to collateral drainage pathways. Based upon available information, it seems that
isolated partial occlusion of the deep venous system should have no untoward
consequences. However, more detailed laboratory and clinical information is required
before an absolute statement may be made in this regard.
By necessity, the authors have occluded one or two of these tributaries without
evidence of clinical consequences. Dandy noted a similar clinical observation in 1936
(8). Caron et al. (4) described two cases in which both internal cerebral veins were
sacrificed without harmful effects.
Spectrum of Approach
The interhemispheric retrocallosal or transcallosal approaches allow a number of
corridors and exposures depending on individual patient anatomy and size and location
of the lesion (Fig. 25.4). Possible exposures of the quadrigeminal and posterior and
mid-ventricular regions are gained by a number of intraoperative maneuvers in
subsequent corridors: (a)
exposure of the posterior incisural margin, (b) incision of the tentorium with exposure of
the quadrigeminal cistern and posterior third ventricle, (c) incision of the falx (inferior
sagittal sinus) with enhanced contralateral visualization, (d) retraction of the splenium of
the corpus callosum with posterior third ventricular and superior quadrigeminal
exposure, (e) section of the posterior trunk of the corpus callosum with increased
exposure of the posterior and middle third ventricle, and (f) section of the splenium (if
unavoidable) to increase third ventricular exposure.
The individual anatomy and lesion (Fig. 25.5) will dictate the particular need for
exposure (25); however, a number of possibilities are evident dependent on the location
of the mass (Fig. 25.6): (a) Masses in the superior quadrigeminal cistern encroaching on
the posterior third ventricle may be approached with a retrocallosal and transincisural
corridor with or without sectioning of the tentorium and/or falx by either an 8-cm bone
flap extending from the torcular or a 6-cm bone flap 2 cm superior to the torcular, (b)
Lesions predominantly in the quadrigeminal cistern with minimal third ventricular
involvement may be managed by a 6-cm midline bone flap 2 cm superior to the inion.
Tentorial incision is generally required. (c) Lesions involving the posterior and mid-third
ventricular chamber with or without superior quadrigeminal involvement generally
require exposure that allows maximal flexibility of the corridor. In this case a 10-cm
midline bone flap extends from 2 cm superior to the torcular anteriorly. This allows
access to the posterior trunk of the corpus callosum as well as the posterior incisural
margin.
Structural Definitions
High resolution computerized tomography (CT) with and without contrast
administration and additional reconstructions in the coronal and sagittal planes usually
provide excellent detail of the region of the posterior third ventricle (Fig. 25.7).
Magnetic resonance imaging (MRI) with multiplanar views augments CT data and
provides further definition of vascular anatomy (Figs. 25.8 and 25.9). At present, only
the water content with various relaxation times can be measured on MRI, but it is antici-
pated that in future various doping compounds will become available to delineate further
the nature of the lesion. Small lesions in the posterior third ventricle can even be further
delineated by the addition of metri-
zamide (Fig. 25.10) to the ventricular cerebrospinal fluid (CSF) by way of a
ventriculostomy, which have often been placed previously to control raised intracranial
pressure (ICP). Unless there is question as to the vascularity of the lesion, there is little
need for angiography when the retrocallosal approach to the posterior third ventricle is
planned. For the more anterior transcallosal approach, it is suggested that angiography be
done if for nothing more than to delineate the location of the parasagittal draining veins
(1). This will allow better placement of the bone flap to minimize the number of these
veins that must be occluded and divided to gain access to the midline.

Operative Techniques
General Measures
The majority of patients with tumors in the region of the posterior third ventricle have
hydrocephalus. For control of the associated raised ICP,
many patients have received a ventriculostomy before coming to the operating room; if
not, one can be placed after the induction of general anesthesia. Antibiotics are given to
cover the perioperative period (at the beginning of the operation and for 24 to 48 hours
thereafter). As three-fourths of ventriculostomy infections are from Staphylococcus
species (approximately one-half of the total infections are Staphylococcus epi-dermidis
and one-fourth are Staphylococcus aureus), the antibiotics need to cover this group of
organisms. We are presently using vancomycin as 30 to 40% of the S. epidermidis
cultured at our institution are resistent to methicillin. Glucocorticoids have generally
been started 1 or more days before operation.
If a ventriculostomy is placed before operation, the ventricles are deliberately kept
moderately dilated by only draining CSF if the ICP exceeds 15 to 20 torr. This allows
decompression of the ventricles by further drainage of CSF intraoperatively when the
medial aspect of the right hemisphere is gently retracted from the falx cerebri, allowing
the corpus callosum or retrocallosal region to be adequately exposed. Rather than
inserting a CSF-diverting shunt preoperatively, the authors prefer an attempt to
reestablish CSF circulation by tumor removal, thereby obviating the need for shunting.
During the postoperative period, the presence of a ventriculostomy will allow
monitoring of ICP as well as determining whether CSF circulation has been adequately
reestablished. If the exposure is not adequate with CSF drainage, osmotic and
nonosmotic dehydrating agents may be used.
Intraoperative evoked response monitoring is a helpful and recommended adjunct
(12).

Position
Although a number of options in positioning are possible to obtain access to the
posterior hemispheric midline (15, 18, 19, 24, 26), the authors prefer placing the patient
in a right lateral decubitis (Figs. 25.11 to 25.13) or three-quarters prone position, with
the head fixed in a dependent oblique posture (Figs. 25.14 and 25.15). This head
position is developed by placing the superior sagittal sinus parallel to the floor and then
elevating the vertex 30° to 40° from the horizontal. This allows the dependent
hemisphere (usually the right) to fall away from the midline while the falx cerebri
supports the superior (left) hemisphere. Removal of CSF from the dilated lateral
ventricles, as most frequently is done, provides excellent exposure with minimal
retraction of the hemisphere. Compared to the sitting position (Figs. 25.16 and 25.17),
the surgeon enjoys a closer working distance and experiences less fatigue as his hands
and arms are at waist or chest level and not extended. The use of the hands are parallel
rather than one over the other as necessitated by sitting position. Another advantage is
that the position of the microscope to the patient can be varied over a greater distance,
gaining further visibility even though the corridor of access is narrow. Raising and
lowering the patient will add another degree of flexibility for the operative exposure and
reduces the manipulation necessary to reach the lesion. Of most importance is the fact
that the risk of air embolism is considerably reduced. Because of the clinical and
technical superiority of the dependent oblique head position we reserve the semi-sitting
position for excessively obese individuals in whom utilization of the dependent oblique
position would be unduly difficult or potentially threatening to pulmonary status during
a lengthy procedure (Figs. 25.18 and 25.19).
Retrocallosal Approach
Before draping, so as to observe readily the pertinent anatomical landmarks, one marks
the midline, the torcular, and the transverse sinus on the scalp. Either a linear, 2-limbed
mitre or an S-shaped incision may be used. Exposure should include the sagittal and
lambdoidal sutures to act as bone flap landmarks. The scalp is then injected with 0.25%
lidocaine, 1:400,000 epinephrine solution to reduce bleeding. Either three or four burr
holes are placed to develop the paramedian bone flap. The two medial burr holes are
placed directly on the midline 6 to 8 cm apart with the posterior burr hole at or just above
the torcular. If two lateral burr holes are placed, the most posterior one is at or just above
the transverse sinus. The lateral one or two burr holes need be no more than 4 to 6 cm off
the midline. Absolute midline exposure is imperative. In individuals with a thick
calvarium it is desirable to extend the bone flap over the midline. The dura mater is
separated from the overlying calvarium and a free bone flap is cut. The dura mater is
opened in a trapezoidal shape with the lateral extent of the opening at the point where the
hemisphere needs maximal retraction. The intact portion of the dura mater supports the
hemisphere. The infrequent bridging veins are coagulated and divided as necessary,
allowing the posterior parietal and occipital lobes to be easily retracted. Occluding and
dividing a bridging vein within the operative field should not significantly compromise
venous drainage in this portion of the hemisphere. Stay sutures are placed in the dura
mater just lateral to the superior sagittal sinus and retraction is obtained by securing the
ties to the Budde retractor ring. If a ventriculostomy is in place, it is
opened and the pressure is reduced to atmospheric while gentle pressure is applied to the
medial surface of the parietooccipital lobes to aid in expelling CSF from the ventricles.
The Budde self-retaining retractor system and the operating microscope are brought into
position. A 19-mm retractor blade is used and exposure of the incisural margin is rapid
as the falx is complete. Compression of the medial hemisphere is minimal and a 2-cm
slot is easily realized (Fig. 25.20). With the retrocallosal approach, it is not necessary to
separate the cingulate gyri or the pericallosal arteries. If the lesion is posteriorly directed,
it can be seen distending the dense arachnoid in the notch between the falx cerebri and
the
tentorium. If necessary, either the falx cerebri, the tentorium, or both may be divided to
gain additional exposure. The dura mater of the falx cerebri (Fig. 25.21) is cauterized
with a combination of straight or angu-lated bipolar forceps and is sharply incised,
usually with a #11 blade, after the inferior sagittal sinus has been occluded. Stay sutures
can be placed in the cut edges of the falx for further exposure or to apply traction to stop
bleeding from the inferior sagittal sinus if it continues. The tentorium (Fig. 25.22) is
divided in a similar fashion but lateral to the straight sinus. Stay sutures can also be
placed in the cut edges of the tentorium to gain excellent exposure to the posterior fossa.
A second 5/8-or 1/4-in. blade may be applied medially on the falx and a third V4-in.
retractor may be placed on the splenium to enhance exposure.
 It is generally not necessary to expose the splenium of the corpus callosum although
one needs to be cognizant of its location (Fig. 25.23). Occasionally retraction or partial
excision of a distended and thinned commissure may be necessary. The arachnoid is
divided as needed. The internal cerebral veins, basilar veins of Rosenthal, and precentral
cerebellar veins may or may not be encountered and are frequently displaced by the
tumor mass. Usually one can work around them but sometimes it is necesary to
coagulate and divide one or two of these vessels.
Tumor removal can be accomplished with a variety of techniques including aspiration,
bipolar coagulation, ultrasonic aspiration, and laser vaporization, depending upon the
consistency of the mass (Fig. 25.24).
Depending upon the location of the lesion and the degree of resection, the third ventricle
may or may not have been entered. Feeding arterial vessels are usually inferior and
lateral to the mass. If possible, these should be identified early in the dissection. One
frequently has some idea as to whether CSF circulation has been reestablished. The
ventriculostomy is closed and opened when the patient has returned to the intensive care
unit. No attempt is made to reinflate the ventricles by injecting fluid via the
ventriculostomy. The self-retaining retractor is removed. The dura mater is closed using a
running 4-0 Vicryl suture. Dural tenting sutures are placed if desired. Gelfoam is placed
over the exposed dura mater. The bone flap is replaced and fixed with #28 gauge wire.
The scalp is closed as a single layer using either interrupted 3-0 or 4-0 Vicryl sutures in
the younger patient or staple sutures in the adult. The skin edges are approximated with
Steri-strips if scalp bleeding is not a problem or a running subcuticular suture if it is.
Transcallosal Approach
If the lesion is totally confined to the posterior portion of the third ventricle without
extension beneath and posterior to the corpus callosum or there is significant middle
third ventricular extension it may be necessary to use a transcallosal approach to
augment exposure of the lesion. If possible, it is best to maintain the integrity of the
splenium of the corpus callosum. For this reason, the exposure needs to be such that a 2-
to 2.5-cm incision can be made in the body of the corpus callosum 2 to 3 cm anterior to
the tip of the splenium, thus leaving it intact (Fig. 25.25). As the approach is more
anterior, the calvarial opening needs to be moved accordingly. This necessitates that the
patient undergo angiography to determine the location of the major draining cerebral
veins so one can
position the bony opening to avoid dividing many of the major draining veins in the
posterior parietal region. The depth of the falx cerebri varies considerably, as does the
extent of the adhesions between the two hemispheres that must be divided before the
corpus callosum is reached. It is necessary to identify both pericallosal arteries to make
certain that the dissection to the corpus callosum is between them and not on their medial
aspect. The corpus callosum is easily identified as a glistening white structure that is
totally different from the cortex. After estimating the distance from the tip of the
splenium of the corpus callosum, one makes the posterior extent of the incision at least 2
to 3 cm anteriorly with a microsucter. A narrow (19-mm)-bladed self-retaining retractor
can be placed through the incision in the body of the corpus callosum. The dilatation of
the third ventricle either by tumor mass or hydrocephalus thins the corpus callosum and
posterior fornix, simplifying the dissection. The connective tissue of the tela choroidea is
next encountered. Lesions in this region tend to displace the internal cerebral veins
laterally, although on some occasions they can be found separated from the midline by
only a millimeter or two of connective tissue. Usually it is possible to coagulate and
divide the intervening connective tissue and displace the cerebral veins laterally but, if
necessary, one may be occluded and divided.
With large masses or significant hydrocephalus the dissection required to enter the
third ventricle can be surprisingly little; however, with small lesions and little
hydrocephalus, the depth of the operative corridor before reaching the third ventricle is
considerable. Sagittal MRI or CT will guide depth measurements. Entry into the third
ventricle is readily appreciated by noting the smooth ependymal surface and the
presence of CSF. Tumor removal can be accomplished with a variety of techniques.
After tumor excision the aqueduct of Sylvius can be observed. Closure is the same as
for the retrocallosal approach.

Utilization
The posterior interhemispheric retrocallosal and transcallosal approaches offer rapid,
direct, and safe exposure of the quadrigeminal and pineal regions and posterior two-
thirds of the third ventricle with minimal physiological consequence. By concurrent
utilization of the dependent oblique head position, the procedural exposure and ease of
intraoperative manipulation may be facilitated. The corridor may be used for access to
any mass or vascular lesion within these regions, irrespective to its size.
Considering the histological spectrum of tumors, diagnostic capability of imaging
devices, availability of biological markers, current imaging-guided stereotactic methods,
and therapeutic modalities, it seems that direct operation should be reserved for (a)
benign potentially excisable lesions and (b) malignant and mixed germinal tumors
where multimodal-ity therapy offers the best opportunity for palliation. Such lesions
may be considered largely radioresistant.
Advantages
Using the dependent oblique head position, gravity and CSF drainage are frequently
all that is required to obtain excellent exposure of the pineal region of the corpus
callosum. The lateral decubitus or 3/4 prone body position are well tolerated by the
patient and reduce the risk of air emboli. The retrocallosal approach is the preferred
corridor as it is not necessary to sacrifice any important intracranial structures. By
opening the falx cerebri, one has access to the opposite side and, by opening the
tentorium, the superior portions of the quadrigeminal region are exposed.
The dependent oblique position provides the surgeon with a comfortable working
position as the distance allows the hands to be placed by the side of the waist or at chest
level and the arms are not extended. In addition, the operating microscope can be used
over a wide arc, which is further increased by raising or lowering the operating room
table. The assistant surgeon and scrub nurse are conveniently located, which aids a
smooth flow of the operative procedure. The technique offers visualization of all
elements of the midline and posterior third ventricle and the pineal and quadrigeminal
regions with minimal physiological risks and minimizes the utilization of active
retraction. The corridor provides the shortest and most direct access to the pineal region
(26, 27, 31, 33).
Disadvantages
This corridor is advocated only for those lesions that are primarily in the pineal or
posterior third ventricular locations. It is not an appropriate approach for lesions of the
anterior third ventricle or those of the posterior fossa. In general, the galenic system and
its tributaries are encountered before the pathological structure. Optimal positioning is
difficult in large patients.

References
1. Apuzzo MLJ, Chikovani OK, Gott PS, Teng BL, Zee CS, Giannotta SL, Weiss
MH: Transcallosal, interfornicial approaches for lesions affecting the third
ventricle: Surgical considerations and consequences. Neurosurgery 10:547-
554, 1982.
2. Bedford THB: The nervous system of the velum interpositum of the rhesus
monkey and the effect of experimental occlusion of the great vein of Galen.
Brain 57:255-265, 1934.
3. Bogen JE: Physiological consequences of complete or partial commissural
section. In Apuzzo MLJ (ed): Surgery of the Third Ventricle. Baltimore,
Williams & Wilkins, 1987.
4. Caron JP, Nick J, Contamin F, Singer B, Comoy J, Keravel Y: Tolerance de
la ligature et de la thrombose aseptique des veines cerebraler profondes chez
l'homme. Ann Med Interne (Paris) 12:899-906, 1977.
5. Dandy WE: Extirpation of the pineal body. J Exp Med 22:237-247, 1915.
6. Dandy WE: Experimental hydrocephalus. Ann Surg 70:129-142,1919.
7. Dandy WE: An operation for the removal of pineal tumors. Surg Gynecol
Obstet 33:113-119, 1921.
8. Dandy WE: Operative experience in cases of pineal tumor. Arch Surg 33:19-
46, 1936.
9. Dandy WE: Benign Tumors in the Third Ventricle of the Brain: Diagnosis
and Treatment. Springfield, Thomas, 1933, p 171.
10. Foerster O: Das operative Vorgehen bei Tumor der Vierhugelgegend. Men
Klin Wochenschr 41:986-990, 1928.
11. Geschwind N: Disconnexion syndromes in animals and man. Brain 88:237-
294,585-644, 1965.
12. Greenberg RP, Ducker DP: Evoked potentials in the clinical neurosciences. J
Neurosurg 56:1-18, 1982.
13. Hammock MK, Milhorat TH, Earle K, DiChiro G: Vein of Galen ligation in the
primate: Angiographic, gross, and light microscopic evaluation. J Neurosurg
34:77-83, 1971.
14. Huang YP, Okudera T, Ohta T, Robbins A: Anatomic variations of the dural
venous sinuses. In Kapp JP, Schmidek HH (eds): The Cerebral Venous
System and its Disorders. New York, Grune and Stratton, 1984, pp 109-
167.
15. Jamieson KG: Excision of pineal tumors. J Neurosurg 35:550-553, 1971.
16. Kaplan HA: Results of obliteration of specific cerebral veins and dural venous
sinuses: Animal and human studies. In Kapp JP, Schmidek HH (eds): The
Cerebral Venous System and its Disorders. New York, Grune and Stratton,
1984, pp 275-282.
17. Kapp JP, Schmidek HH: Surgery of the cerebral venous system. In Kapp JP,
Schmidek HH (eds): The Cerebral Venous System and Its Disorders. New
York, Grune and Stratton, 1984, pp 597-623.
18. Kobayashi S, Sugita K, Tanaka Y, Kyoshima K: Infratentorial approach to
 the pineal region in the prone position: Concorde position. J Neurosurg 58:141-143,
1983.
19. McComb JG, Barky K: Lateral decubitus position for posterior fossa surgery
in children. Concepts Pediatr Neurosurg 5:207-213, 1985.
20. Ono M, Rhoton AL Jr, Barry M: Microsurgical anatomy of the region of the
tentorial incisura. J Neurosurg 60:365-399, 1984.
21. Ono M, Rhoton AL Jr, Peace D, Rodriguez RJ: Microsurgical anatomy of the
deep venous system of the brain. Neurosurgery 15:621-657, 1984.
22. Pendyl G: The surgery of pineal lesions—historical perspective. In Neuwelt
EA (ed): Diagnosis and Treatment of Pineal Region Tumors. Baltimore,
Williams & Wilkins, 1984, pp 139-154.
23. Pendyl G: Microsurgical anatomy of the pineal region. In Neuwelt EA (ed):
Diagnosis and Treatment of Pineal Region Tumors. Baltimore, Williams &
Wilkins, 1984, pp 155-207.
24. Poppen JL: The right occipital approach to a pinealoma. J Neurosurg 25:706-
710, 1966.
25. Raimondi AJ, Tomita T: Pineal tumors in childhood. Child Brain 9:239-266,
1982.
26. Reid WS, Clark WK: Comparison of the infratentorial and transtentorial
approaches to the pineal region. Neurosurgery 3:1-8,1978.
27. Rhoton A Jr, Yamamoto I, Peace DA: Microsurgery of the third ventricle: Part
2. Operative approaches. Neurosurgery 8:357-373, 1981.
28. Schlesinger B: The tolerance of the blocked galenic system against artificially
increased intravenous pressure. Brain 63:178-183, 1940.
29. Schlesinger B: The venous drainage of the brain, with special reference to
the galenic system. Brain 62:274-291, 1939.
30. Schmidek HH, Kapp JP: Traumatic and neoplastic involvement of the cere
bral venous system. In Kapp JP, Schmidek HH (eds): The Cerebral Venous
System and Its Disorders. New York, Grune and Stratton, 1984, pp 581-
595.
31. Seeger W (ed): Microsurgery of the Brain. New York, Springer-Verlag, 1980,
vol 1 and 2.
32. Smith RR, Sanford RA: Disorders and the deep cerebral veins. In Kapp JP,
Schmidek HH (eds): The Cerebral Venous System and Its Disorders. New
York, Grune and Stratton, 1984, pp 547-555.
33. Stein BM: The infratentorial Supracerebellar approach to pineal lesions. J
Neurosurg 35:197-202, 1971.
34. Sugita K, Kobayashi S, Yokoo A: Preservation of large bridging veins during
brain retraction. J Neurosurg 57:856-858, 1982.
35. Wilkins RH: History of surgery of the third ventricular region. In Apuzzo MLJ
(ed): Surgery of the Third Ventricle. Baltimore, Williams & Wilkins, 1987,
pp3-31.
Commentary D
Operative Management of Malformations of the Vein of Galen
J. Gordon McComb, M.D., and
Michael L J. Apuzzo, M.D.
It is necessary to differentiate between primary and
secondary vein of Galen aneurysms. In the secondary
form, the galenic system, including the inferior sagittal and
straight sinuses as well as the vein of Galen, is dilated in
response to an increased venous outflow from either an
adjacent or a remote angioma. The treatment for the sec-
ondary forms is the same as for angiomata in general. In
the primary vein of Galen malformation the arterial feeders
connect directly into the sack of the aneurysm, which is
thick and tough, making its rupture very unlikely. In some
cases there can be a small adjacent angioma in association
with what is predominantly a primary
vein of Galen aneurysm. Whereas hemorrhage is unusual in
the primary form, it is much more frequent when the
primary form is associated with an angioma (Figs. D.1 and
D.2). The comments that follow are directed to what is
predominantly the primary form of vein of Galen aneu-
rysm.
Clinical Features and Selection of Management
Modes
The management of vein of Galen aneurysms is best
considered in the context of the patients'
ages at the time of presentation. This consists of four
groupings: neonatal, infantile, childhood, and adult, as
characterized by Amacher and Shil-lito(2)(TableD.l).
The neonate presents at birth with massive high output
cardiac failure that responds little to maximal medical
therapy. The diagnosis is usually made by cardiac
angiography for a suspected heart anomaly and is
subsequently confirmed by computerized tomographic
(CT) scanning, although intracranial ultrasound can now
be considered an initial imaging technique. Surgical
intervention in an infant with intractable cardiac failure has
been nearly universally fatal; this demise is usually on a
cardiovascular basis because of poor myocardical
perfusion. More recently, embolization techniques are
proving to be of value. Using a transfemoral route
Berenstein and associates (7) have been able to diminish
the flow through the fistula significantly by one or more
embolization procedures (Fig. D.3). This technique is not
without risk as it is possible for the embolized material to
pass through the malformation and lodge in the lungs. A
more direct
approach has recently been described by Mickle (5). Coiled
copper wires are introduced into the aneurysmal sac
through the dura mater over the torcular after a burr hole
has been made at this location. This technique seems to
have greater success with fewer risks. By reducing the
shunting through the fistula one can bring the cardiac
failure under control. Rarely does the embolization
procedure result in complete obliteration of the feeding
vessels. It is uncertain whether the benefits of subsequent
direct operative intervention to remove the remaining
feeders are worth
 the risk. Such a decision is also dependent upon the
presence or absence of an associated adjacent angioma,
making the possibility of hemorrhage a consideration as
well. In spite of appropriate and successful medical and
surgical treatment of this malformation, the prognosis
might still be very poor. Norman and Becker (6) noted
extensive parenchymal changes in neonates with this lesion
dying shortly after birth without attempted surgical
intervention. This indicates that, in some neonates,
widespread irreversible parenchymal damage has occurred
by the time of delivery. The ability to predict those
neonates who will not respond to any form of therapy
remains to be established.
Hydrocephalus is usually the presenting factor in the
infantile group. These infants frequently had mild neonatal
cardiac failure that responded to therapy or resolved
spontaneously. In these patients it has been the authors'
approach to shunt the hydrocephalus if progressive but not
to attempt to treat the vein of Galen aneurysm surgically
unless there is evidence of hemorrhage, increasing
compression of surrounding neural structures, or additive
parenchymal damage from the "steal phenomenon" as
judged by progressive neurological deterioration and
changes on CT or MR imaging. Some of these patients
would be suitable for embolization but not those in whom
there is evidence of hemorrhage or increasing mass effect.
The childhood group may present with progressive
hydrocephalus or subarachnoid hemorrhage; the diagnosis
is then made by CT scanning and is further defined by
angiography. As with the infantile group, the approach
would be to intervene surgically in the presence of hemor-
rhage or mass effect. The hydrocephalus, if progressive,
would require shunting.
Patients in the adult group often present with
subarachnoid hemorrhage or symptoms and signs of a
pineal region mass. In these situations direct surgical
intervention is warranted. If hydrocephalus is present,
shunting should be undertaken before occlusion of the
malformation, as subependymal veins are often more
distended after occlusion of the malformation and pose a
risk with subependymal passage of instrumentation (8).
Operative Approach
The surgical approach has been described by Amacher
(1), Yasargil et al. (8), and Hoffman et al. (3). It is
advocated that a vein of Galen malformation be
technically considered like any other pineal lesion and
approached via a posterior interhemispheric route, as
described in Chapter 25.
Vascular Anatomy and Positioning
The most common arterial supply to these mal-
formations is from the anterior cerebral arteries, the
posterior cerebral and superior cerebellar arteries, and the
posterior thalamic perforators arising from the peduncular
segment of the posterior cerebral artery. This supply is
frequently bilateral (Fig. D.4). Therefore, the operative po-
sition and corridor must be determined with these facts
taken into consideration. A Supracerebellar subtentorial
attack is not appropriate as this approach will not allow
access to the more anterior arterial feeders. Although the
patient could be placed in either a sitting or a prone
position, either a lateral decubitus (pediatric) or 3/4 prone
dependent oblique position (adult) is favored (4).
Hypotensive anesthetic technique may be required during
dissection and collapse of the aneurysm dome.
Operative Technique
Basic elements of the approach have been defined in
detail in the previous chapter (4). A bone flap that extends
from the torcular 8 to 10 cm anteriorly (childhood and adult
cases) affords the optimal exposure required for isolation of
all vascular input (Fig. D.5). In these cases the exposed
cortex appears more vascular, and greater care than usual is
required as the interhemispheric
corridor is developed (cuneus region). The Budde ring
retractor system is indispensable as a retraction device and
hand stabilization platform. In the deep midline the
thickened arachnoidal membrane of the callosal, dorsal
ambient, and quadrigeminal cisterns is encountered and
opened. With the right side approach soft cottonoid
paddies are used to isolate the plane between the
malformation and the brain (Fig. D.6).
The ambient cistern is opened and the posterior cerebral
and superior cerebellar arteries are identified. Distal
segments of the anterior cerebral arteries are exposed over
the splenium and traced to the dome of the malformation.
In each case terminal feeding branches are divided at the
malformation, which may be manipulated without
significant risk of rupture because of the generally
thickened wall. Left lateral feeders may be identified by a
transfalcine exposure with elements of rotation and
collapse of the dome. A constant vigilance regarding
completeness of oc-
clusion requires observations of the color changes in the
vein of Galen. When its color changes from red to blue, all
feeders have been divided. If no change is observed after
occlusion of the distal pericallosal, posterior cerebral, and
superior cerebellar artery contributions, it is necessary to
explore the region of the large perforating posterior
thalamic vessels from the peduncular segment of the
posterior cerebral artery. This is accomplished by a
retrosplenial approach with depression of the malformation
with a cottonoid and retraction of the splenium with a 1/8-
or 1/4-in. self-retaining retractor blade. If no alternative is
comfortable, the splenium may be split to expose the
cistern of the velum interpositum. At the base of the cistern
the tela choroidea of the third ventricle is identified and
opened and the striae medullares, massa intermedia, poste-
rior commissure, and habenular trigone are visualized.
The posterior thalamic perforators may be identified
passing through the habenular trigone to the galenic
malformtion at its anterior base. If the superior exposure
fails to provide adequate visualization, the inferior surface
may be explored with deformation of the inferior and pos-
terior wall of the malformation. After these maneuvers the
malformation should be blue. Further checks include
Doppler auscultation and evaluation of the O2 and CO2
content of aspirated blood. If the sac is flaccid at the end of
the procedure it need not be excised, especially if doing so
might damage the hypothalamus or thalamus. Galenic
venous drainage need not be of concern when deciding
whether to remove the aneurysmal sac as venous drainage
by necessity has developed along other channels because of
the increased pressure.
The younger the patient, the more concern for
myocardial function and hemodynamics, both intra- and
postoperatively. Evidence of increasing heart failure must
be aggressively treated, including pharmacological support,
reduction of peripheral vascular resistance, and the with-
drawal of blood. Removal of the malformation in several
stages, especially in the younger patient, may be advisable.
Postoperative angiography is
indicated to assure that all fistulous connections have been
disrupted. The patient must be followed indefinitely for
signs of hydrocephalus and shunted if necessary.
References
1. Amacher AL: Vein of Galen aneurysms. In Wil-
kins RH, Rengachary SS (eds): Neurosurgery.
New York, McGraw-Hill, 1985, pp 1459-1465.
2. Amacher AL, Shillito J Jr: The syndromes and
surgical treatment of aneurysms of the great vein
of Galen. J Neurosurg 39:89-98, 1973.
3. Hoffman JH, Chaung S, Hendrick EB, Humphreys
RP: Aneurysms of the vein of Galen. J Neurosurg
57:316-322, 1982.
4. McComb JG, Apuzzo MLJ: Posterior Intrahemi
spheric retrocallosal and transcallosal ap
proaches. In Apuzzo MLJ (ed): Surgery oj the
Third Ventricle. Baltimore, Williams & Wilkins,
1987, pp 611-640.
5. Mickle JP: The transtorcular approach to vein of
Galen aneurysms—a preliminary report. Pre
sented at the 13th Annual Meeting of the Section
of Pediatric Neurological Surgeons of the Ameri
can Association of Neurological Surgeons, Salt
Lake City, Utah, December 11-13, 1984.
6. Norman MG, Becker LE: Cerebral damage in neo
nates resulting from arteriovenous malformation
of the vein of Galen. J Neurol Neurosurg Psy
chiatry 37:252-258, 1974.
7. Wisoff JH, Berenstein A, Epstein FJ: Vein of
Galen aneurysm: Combined treatment of emboli
zation and surgery. Presented at the 13th Annual
Meeting of the Section of Pediatric Neurological
Surgeons of the American Association of Neuro
logical Surgeons, Salt Lake City, Utah, December
11-13, 1984.
8. Yasargil MG, Antic J, Laciga R, Jaim KK, Boone
SC: Arteriovenous malformations of vein of
Galen: Microsurgical treatment. Surg Neurol
6:195-200, 1976.
26
Controversies,
Techniques, and
Strategies for Pineal
Tumor Surgery
Claude Lapras, M.D., and J. D. Patet, M.D.

Different approaches for operation in the pineal region have been proposed. After
various experiences we finally chose the occipital supra-and transtentorial approach as
the most convenient in cases of pineal tumors. We have now used it for 85 patients.

Controversies about the Approaches

Transcallosal Approach
The transcallosal approach as proposed by Dandy (1) was used in our first eight cases,
but problems were more frequent than advantages. We were unable to perform a total
removal in any case. The approach is performed along the falx at the level of the
parietooccipital junction. It is posteriorly free from veins to the superior sagittal sinus
but anteriorly the parietal bridging veins are often encountered and could be damaged by
excessive retraction; dividing these veins always initiates a mild hemiparesis or a
contralateral astereognosia. When the corpus callosum is reached, there are no
landmarks, the approach can be oblique, the pericallosal arteries are variable, and the
venous anatomy is not uniform. As the exposure is narrow, finding exactly where the
splenium is located is difficult. After dividing the corpus callosum, the internal cerebral
veins are dissected. Normally tumor removal is performed between the internal cerebral
veins or by retracting them laterally. Keeping veins displaced anteriorly is easy because
they are mobile, but posteriorly they join together to form the great vein of Galen and are
fixed on the midline; operation between or under them is dangerous and blind.
The transcallosal approach was proposed especially for superiorly developed tumors.
In these cases (Fig. 26.1 A), starting dissection by locating the internal cerebral veins is
difficult because the anatomy is modified. The veins are sometimes displaced laterally,
one vein may remain in the midline when the other is distorted laterally, or both may be
included in or hidden by the exophytic superior growth of the tumor.
The main arguments against using the transcallosal approach are
related to vascular pedicles and tumor extension. Vessels of pineal tumors are almost
exclusively situated posterior to the tumor. Arteries come from the medial branches of
the posterior choroidal arteries. With a superior approach they are seen only at the end of
the procedure. In contrast, they are initially and easily dissected by approaching
posteriorly. Small additional arteries run anteriorly and laterally from the distal branches
of the pericallosal arteries. They are never large enough to justify a superior approach.
Two or three short pineal veins tether the tumor under the vein of Galen. These short
tumoral veins are more safely divided after a posterior approach allowing one to dissect
below the vein of Galen then after a superior approach. Approaching through the corpus
callosum, anterior tumor extensions, exophytic as well as limited, are dissected first. At
this time and at this level it is impossible to know precisely whether the tumor invades
brain structures. The answer usually lies
posteriorly on the midline near the quadrigeminal plate or posteriorly and laterally near
the thalamopulvinar mass. Posterior approaches provide better conditions for the
judgment of tumor features.
Poppen (3) proposed performing the approach more posteriorly, through an occipital
bone flap, dividing only the splenium of the corpus callosum. But division of the
corpus callosum itself and even its visualization are not necessary. Operating along a
lower route across a sagittal opening of the tentorium is easier. This modified occipital
approach was described by Jamieson (2); we have used it since 1970.
Transcortical-Transventricular Approach
The transcortical-transventricular approach described by Van Wagenen (5) has the
main disadvantage of being too lateral. Operation is performed after entering the
posterior part of the lateral ventricle through a cortical incision located in the parietal
region. This approach is limited to the nondominant hemisphere. In the lateral ventricle,
the only landmark is the Choroid plexus and its hilum. The tumor, bulging behind the
thalamus beneath the posterior medial wall, is seen after Choroid plexus removal. The
route is direct and medial behind the hilum of the Choroid plexus and tangential to the
posterior thalamic mass. This approach is deep; the thalamic mass is restricting, and it
is difficult to work on the midline and more difficult beyond it. Removal is performed
through a narrow venous triangle made by the internal cerebral vein and the basilar vein
of Rosenthal. This approach was suitable to only two young patients and one recurrent
case. They presented with large pineal tumors developed almost completely laterally
toward a dilated lateral ventricle on the nondominant hemisphere.
Anterior Subchoroidal Approach
If the lateral ventricle is large, entering the frontal horn and posterior opening of the
foramen of Monro by section of the thalamostriate vein gives good access to the middle
and eventually the posterior part of the third ventricle. In the case of a pineal tumor, this
gives access only to the anterior tumor extension. This approach has the same
disadvantages as the transcallosal; the vessels are behind the tumor and the critical
region to check tumor infiltration is posteriorly and remote from the skull opening. We
have never used this approach for pineal operation.
Occipital Infratentorial Approach
Our experience with this approach (4) is limited. Its main advantage is that with
retraction of the upper cerebellum the surgical corridor is free of delicate nervous
structures. Theoretically, cerebellar retraction is easy. The sitting position is
advantageous. Sacrificing the bridging veins between cerebellum and tentorium is
without consequence but the addition of venous sacrifice to cerebellar retraction can
explain some persistent postoperative ataxia. In the case of a preoperative tonsillar
herniation, retraction could aggravate the situation. This danger was encountered in one
of our patients who manifested bradycardia after retractor application.
The main disadvantage of the infratentorial approach is the presence of the tentorium.
It is restricting, giving two lateral blind corners. The slope of the tentorium produces
restricted visualization on each side; therefore, it should be used for small tumors without
lateral extension. We found it difficult to perform hemostasis in front of a tumor
extending into the cavity of the third ventricle and to dissect the roof of the third
ventricle. Therefore, it seems better to use another approach for ante-
riorly developed tumors. Pineal tumors may also extend caudally into two
directions. Most commonly, the tumor extends posteriorly above the
quadrigeminal plate, filling the quadrigeminal cistern (Fig. 26.1B), displacing
the superior cerebellum, and finally being encased behind the brain stem and
cerebellum. With this approach it is difficult to remove the posterior extension
under direct view. The other posterior extension is into the dilated upper part of
the aqueduct of Sylvius (Fig. 26.1С) where a tumoral nodule can prolapse and
distend the brain stem. The bulging appearance of the quadrigeminal plate must
be carefully evaluated and differentiated from the tumor invasion. The
infratentorial approach is not optimal for this visualization or for removing the
nodule. However, the infratentorial approach seems appropriate for small pineal
lesions that are well cirumscribed, plainly situated in the midline, and associated
with small lateral ventricles. Retraction of the upper cerebellum is not modified
by ventricular size, whereas retraction of the occipital lobe needed for the
occipital supra- and transtentorial approach is more difficult when ventricles are
small spontaneously or after a lengthy delay between shunting and direct
operation.

The Occipital Supratentorial and Transtentorial Approach

Position
The approach is performed with the patient in the sitting position with the hips
completely flexed. The knees are semiflexed and the legs are elevated to the
level of the heart. The position is more fetal than sitting. A large belt is applied to
the abdomen to reduce peripheral venous volume and diminish blood pressure
variations associated with the sitting position. For the same purpose, elastic
stockings are used. The head is completely flexed anteriorly and turned slightly
downward toward the right side (Fig. 26.2). Head flexion and inclination of the
operating table tend to place the right occipital pole at the highest point of the
operating field so that during the exposure the occipital lobe is retracted and not
simultaneously forcibly elevated. At the completion of operation after retractors
are removed, when the flattened hemisphere resumes its normal contour and
position, head flexion reduces venous traction. Before dural closure, the cranial
cavity can be completely filled with fluid without leakage, preventing
postoperative pneumocephalus and decreasing the tension on bridging veins.
After finalization of position with flexion of the head the tracheal tube can be
incidentally displaced forward to the carina or even into the main stem bronchus.
Thus, after head flexion, it is necessary to check the free airway. Most
frequently, pineal operation is performed on young patients without cervical
spondylosis but, if the patient is elderly, forced head flexion should be avoided.
Positive end expiratory pressure is used, FiCO2 is continuously analyzed by a
capnograph, and arterial pressure and central venous pressure are monitored. A
free access at the patient's neck is preserved to be able to compress the jugular
veins at each step of the operation, checking the quality of hemostasis and
enlarging venous sinuses and veins when they need to be accurately recognized.
Opening
The skin flap around the right occipital pole is large enough to identify the
sagittal suture, the lambdoid suture, and the upper insertions of the neck
muscles. When a shunt is required before direct operation, it is better to insert it
on the left side to avoid the catheter crossing the skin flap. Operation is
performed on the right side to avoid the development of an alexia without
agraphia.
 The bone flap is lozenge-shaped. The upper lateral burr hole is situated as far laterally
and as high as possible to give room for occipital pole retraction and to prevent brain
compression against the craniotomy opening (Fig. 26.2). The upper medial burr hole is
made just tangent to the midline marked by the sagittal suture. The lower medial burr
hole at the torcular is enlarged by bone removal until the confluence is well exposed and
an area of occipital dura mater free of venous sinuses is available. The inferolateral burr
hole is less lateral than the upper one to be far from the temporal posterior veins. It is
located higher than the level of the lateral sinus located when making the medial burr
hole 1 cm above the neck muscle insertions.
A free bone flap is turned. Before dividing the dura mater it is useful to ask the
anesthesiologist to compress the jugular veins to see precisely where the dural sinuses
are located. The intradural walls of the venous sinuses are also checked. The dural
incision is blocked by a cross stitch at its end to prevent the danger of the incision
spontaneously enlarging after dural retraction and lacerating the venous sinuses. The
dural flap is turned along the midline and the dura mater is suspended. Bridging veins
between the convexity and the dural flap are never found.
 Retraction
Minimal retraction of the medial occipital cortex from the falx allows division of
posterior arachnoid granulations. At times, especially when the patient is elderly, the
dura mater sheds bloody tears at the granulation site. Laying on a piece of Surgicel is
preferable to extensive coagulation, which retracts the dura. The parietal posterior
bridging veins are not within the area of exposure. The occipital lobe is retracted.
Usually, it only has one or two small veins between it and the lateral sinus or directly to
the tentorium. They are carefully divided. The retractor is advanced until it reaches the
free edge of the tentorium. It is not necessary to retract deeper to see, for example, the
vein of Galen or even the splenium of the corpus callosum. It is adequate to appreciate
the free border of the tentorium. Some cases complicated by postoperative hemianopsia
are probably related to inappropriate use of the retractor. This happens when the
retractor is used not only to retract, but simultaneously to elevate the occipital lobe if
head position is not appropriate, or an effort is made to see the splenium. Self-retaining
retractors are used after the occipital lobe is protected with a collagen sponge. Two
retractors are usually used: (a) a larger one upon the inferior surface of the occipital
lobe, directed in a superior lateral plane, and (b) a medium-sized instrument vertical and
lateral supporting the first retractor as it advances to the tentorium.
Dissection
The operating microscope is now required. The tentorium is opened along a line
parallel and 1.5 cm lateral to the straight sinus. This opening is a key step of the
procedure. It is at least half the sagittal length of the tentorium. It is made by opening
posteriorly and advancing anteriorly toward the incisural margin. Sometimes, an
aberrant venous sinus is seen in the middle of the tentorium (Fig. 26.3B). This venous
sinus is divided after opening the dura anterior and posterior to it and closing it by a
perforating stitch on each side. The venous sinus of the free edge of the tentorium is
small and needs only to be coagulated. It is necessary to take care not to divide the
tentorium obliquely and to remain at least 1 cm lateral to the vein of Galen. The lateral
flap of the tentorium is retracted by coagulation. The medial flap is suspended by two
sutures. An incision made medially at the posterior end of the sagittal incision further
allows optimal retraction of the medial flap of the tentorium. To avoid traction upon the
vein of Galen one does not forcibly retract the anterior suture.
The posterior part of the ambient cistern or pineal cistern is examined (Fig. 26.3C). At
times with large pineal tumors that have developed posteriorly, the cistern is filled and the
tumor appears immediately. But in the majority of cases, the culmen of the cerebellum is
close to the vein of Galen and covers the pineal region. Approaching pineal tumors re-
quires separation of the upper cerebellum from the vein of Galen by dissecting arachnoid
and dividing veins crossing the cistern. Dissection of arachnoid is performed near the top
of the cerebellum, eventually slightly encroaching upon it, but never at the highest point
of the cistern close to the vein of Galen. The arachnoid sheet of the vein, firmly adherent
to its walls, is carefully preserved. Arachnoid dissection is extended far laterally around
the brain stem. Lateral dissection is easier as arachnoid is less adherent to vessels and
brain structures. Two or three veins, the precentral veins, are sagittally arranged in the
midline, crossing the cistern and joining the cerebellum and quadrigeminal plate to the
vein of Galen. All are sacrificed. Sacrificing these veins is devoid of neurological
consequences. (In our experience of 58 patients operated
on according to this technique and anlayzed for late follow-up, 32 have no cerebellar
sequellae.) Dissecting the arachnoid and dividing the veins allows the cerebellum to slip
slightly into the posterior fossa, enlarging the corridor, displacing the cerebellum away
from the vein of Galen (Fig. 26.4A), and facilitating dissection of the quadrigeminal
plate and pineal region. Pineal tumors appear under a venous arch made by the vein of
Galen (Fig. 26.4B) at the midline and the basilar veins of Rosenthal on each side. This
venous arch is well defined and must be preserved. It is the limiting margin under which
operation is performed. Pineal tumors encroach upon the rostral quadrigeminal plate
where it is impossible to recognize the structure of the posterior commissure.
Removal
Biopsies for frozen section are taken. Dissection is first performed to ascertain
whether the tumor is infiltrating and if removal is possible. Beginning at the midline,
between tumor and quadrigeminal plate, where few vessels are observed, eventual
extension to the brain stem is recognized. If dissection is possible, the floor of the third
ventricle is reached and operation can proceed. Laterally there is a groove between
tumor and thalamopulvinar mass where the posterior choroidal artery is visible (Fig.
26.5A). At this level the artery is ascending in the subarachnoid space and is never
included in the brain parenchyma or in the tumor mass (Fig. 26.5B). Tumor branches
originating along the vertical portion of the artery are also initially situated in the
subarachnoid space, where they are easily divided before disappearing into the tumor
mass (Fig. 26.5C). Even when pineal tumors fill the cistern, the posterior choroidal artery
is not displaced (Fig. 26.5D). After dividing the arteries, it is possible to perform lateral
dissection between the tumor and the lateral wall of the third ventricle and again to
determine whether the tumor is infiltrating.
If tumor is infiltrating toward the brain stem or the thalamopulvinar mass, total
removal is impossible and operation is limited to biopsy or partial removal. If the tumor
does not seem to be infiltrating at those levels, tumor removal is attempted.
Excision begins inferiorly and laterally with care taken not be retract the tumor
forcibly. One progressively works forward until the third ventricle, anterior to the tumor,
is appreciated. Generally, in approaching from the right side, the left lateral wall of the
third ventricle is better visualized than the right. If a nodule extends laterally farther than
the right wall of the ventricle, it is possible to remove it under view after venous
dissection. Displacing the retractor laterally the upper part of the basilar vein of
Rosenthal is exposed. Dissection on the external side of
the basilar vein is possible as there are no venous afferents at this level. Care is required
at the lower part of the basilar vein near the level of the tentorium where it receives
small, but functionally important, internal occipital veins. External dissection of the
basilar vein of Rosenthal gives good access to the ipsilateral wall of the third ventricle.
When the tumor is large, it is at times necessary to perform an internal decompression
to determine the extent of anterior and superior involvement. Retrograde removal of the
upper part of the tumor is then performed, separating its anterior extension from the
internal cerebral veins. Anterior dissection is relatively safe because venous afferents are
rare at this level.
Dissection of the last fragments of tumor remaining fixed under the vein of Galen is
painstaking because they are united by a dense, adhering, and thick arachnoid.
Sometimes achieving a total removal is impossible, and the fragments below the vein of
Galen are coagulated in place. When this is required, we use anticoagulant therapy
during the postoperative period.
At the completion of the removal, the cavity of the third ventricle is visualized with
the massa intermedia, the foramen of Monro, the posterior part of the floor, and
eventually the origin of the aqueduct. The space between the quadrigeminal plate and the
upper cerebellum is evaluated.
The occipital supratentorial and transtentorial approach probably gives the most
extensive view of the entire pineal region, allowing total removal
even for large tumors in 66% of cases. We consider that total removal of pineal tumors
is the most important factor for late results independent of histological findings.

Strategies
Some clinical or laboratory data may influence surgical indication.
Clinical Symptoms
Clinical symptoms are not necessarily reliable guides for outcome. The only
noticeable fact is the poor prognosis for patients with impaired consciousness not
improved by shunting and for patients presenting a complete Parinaud's syndrome
(paralyzed, dilated pupils and convergence palsy associated with the classical upward
and downward gaze palsy). These symptoms have been observed in patients with large,
malignant, invading tumors.
Preoperative diabetes insipidus does not necessarily indicate that the tumor is a
germinoma, is invading the floor of the third ventricle, or has even seeded the
optochiasmatic region. This symptom has been reported in all types of pineal tumors and
can disappear after simple surgical removal. In our experience of five patients with
preoperative diabetes insipidus, three have been cured after operation and two still
require treatment, but diabetes insipidus is sometimes observed in cases of bipolar
germinomas, simultaneously developed in the pineal and optochiasmatic regions.
Operation is not indicated in these cases.
From the literature, it is difficult to have an idea of the value of pubertas precox for
prognosis and surgical indication. We have observed two male patients with pubertas
precox. They had malignant pineal tumors, large and diffusely invading in one case and
rather small and only superficially encroaching upon the quadrigeminal plate in the other
case. Removal was partial in the first case and apparently total in the second case.
However, late results were poor in the two patients.

Etiology
Surgical indications are not influenced by the age of the patient. The same surgical
approach can be used in children and adults. The sitting position is no more difficult in
children than older patients. However, during infancy, pineal tumors are often associated
with extensive hydrocephalus, making operation in the sitting position dangerous when
the flattened hemisphere stretches the bridging veins. It is better to delay direct operation
until the ventricles become smaller after shunting or to operate with the patient in an
alternate position. We have no experience of approaching the pineal region with the
patient prone, but it probably is more difficult than with the patient sitting because there
is no spontaneous opening of the pineal cistern after dissection of the arachnoid and
division of the precentral veins. In infancy, when a pineal tumor is associated with large
ventricles, the best approach is probably through the cortex, with the patient lying
laterally.
The sex of the patient gives some indication of tumor type; pineal germ cell tumors are
extremely rare in female patients (17 male/2 female in our statistics; 1 female among 10
germinoma cases). The small probability of a germinoma is an argument for direct
operation in a female patient with a pineal tumor.
Computerized Tomographic (CT) Appearance
It is difficult to know on CT studies whether a tumor is infiltrating (Fig. 26.6). Volume
is not a good guide. Large tumors completely filling the
posterior cistern are amenable to total removal. On the other hand, small pineal tumors
theoretically suited for total removal could infiltrate the quadrigeminal plate.
The limits of tumor on CT scans are better guides than volume (Fig. 26.7). If a tumor
shape is clearly delineated, whatever its volume may be, total resection is probably
possible. The only difficult point concerns tumors that are richly vascularized. On
enhanced CT studies it is sometimes difficult to differentiate between tumor extension
toward the corpus callosum and the simple injection of numerous vessels in the roof of
the third ventricle or between tumor extension toward the brain stem and a rich vascular
network behind the brain stem extending into the tentorium (Fig. 26.8).

Laboratory Data
Normal cytology of cerebrospinal fluid (CSF) has no diagnostic value. If cytological
examination shows tumor cells, any type of malignant pineal tumor is possible, germ
cells (malignant teratoma or germinoma) as well as pineal cells (pineoblastomas) or even
others (glioblastoma, metastasis, etc.). Therefore, as only a diagnosis of malignancy is
made, surgical indications and techniques cannot be directed by this assay. The prog-
nosis of pineal tumors does not change if malignant cells are found in CSF before
operation. Tumors associated with malignant cells are limited and resectable as
frequently as others. But postoperative radiation therapy and chemotherapy are indicated
if tumor cells were observed before operation. The presence of persistent malignant cells
in spite of these treatment initiatives carries a bad prognosis. When cytology shows two
types of abnormal cells (large clear germ cells associated with small lymphocytes), the
most likely diagnosis is germinoma.
Evaluation of blood levels of alpha-fetoprotein (AFP) and beta-chorionic gonatropin
hormone (HCG) is actually routinely performed. Elevated levels of HCG alone are
observed for all types of malignant germ cell tumors (germinomas, malignant teratomas,
choriocarcinomas) whera where elevated levels of AFP would be more specific for
malignant teratomas. In our experience, elevated levels of HCG and AFP have also found
in patients with pineoblastomas. Thus, tumor markers seem more indicative of a
malignancy than a particular histological type. Tumor markers are useful during follow-
up to indicate total removal when they disappear and recurrence when they are again
elevated.
 -
Radiotherapy Test
Analysis of the preceding data indicates that the accurate clinical diagnosis of a
germinoma is rarely possible. However, this diagnosis is the critical point for surgical
indications because germinomas are very radiosensitive and could be cured without
direct operation. Other malignant pineal tumors (malignant teratomas, pineoblastomas)
are also radiosensitive, but the possibility of cure without operation is much less. If a
stereotaxic biopsy is performed, the diagnosis of germinoma is possible and radiotherapy
first is a good strategy. When stereotaxy is not available or if the tumor seems too small
or to have a rich vascular bed, thus making stereotaxy dangerous, the diagnosis of
germinoma may be suspected in relation to certain clinical variables. It is established on
variables of sex (male), clinical signs (eventually diabetes insipidus), CT appearance
(medium size tumor, nonhomogeneous, developed on the midline, spontaneously dense,
becoming irregularly hyperdense after enhancement, without calcifications),
angiographic appearance (vascular bed composed of many thin capillary vessels, with a
regular blush, without large spots injected by contrast agent), cytology of CSF
(eventually two cell types), and blood levels of tumor markers (eventually elevated
HCG, no AFP). If germinoma is suspected clinically, others have proposed abbreviated
radiotherapy or a full radiotherapy cycle.
If the tumor size distinctly diminishes after 2000 rads and if the tumor disappears after
radiotherapy is completed, the diagnosis of germinoma is proven. If the tumor size is not
modified by radiation or diminishes only slightly or even increases, the diagnosis of
germinoma is questionable. Operation is then undertaken, but time has been consumed
and operative conditions are worse than before radiation. Dissection is more difficult
because the irradiated tumor is fibrous and strongly adherent to adjacent vessels and
nervous structures. The arachnoid is thickened and
dense. Direct operation was necessary for three patients after the failure of shunting and
radiotherapy, the so-called "conservative treatment." We could achieve a total removal
in only one case (benign teratoma); the patient is still alive. Total removal was
impossible for two others (meningioma and malignant teratoma). Both patients died
later of local progression, after 7 years with meningioma and after 3 months with tera-
toma.
We do not recommend the use of a radiotherapy test. To treat malignant tumors it is
preferable to resect the tumoral mass before radiotherapy, even performing a total
removal in some cases. This strategy gives the best chance for prolonged survival for the
patient. In the event that stereotaxis is not available, we also recommend the direct
approach. The diagnosis is made by frozen section and the occipital transtentorial
approach allows for a large surgical removal without particular risks. Radiotherapy is
used after surgical resection. We have had no operative mortality and have achieved a
90% late survival for germinoma patients treated according to this strategy.

References
1. Dandy WE: Benign Tumors in the Third Ventricle of the Brain: Diagnosis
and Treatment. Springfield, Charles С Thomas, 1933.
2. Jamieson KG: Excision of pineal tumors. J Neurosurg 35:550-553, 1971.
3. Poppen JL: The right occipital approach to a pinealoma. J Neurosurg 25:706-
710, 1966.
4. Stein BM: Supracerebellar-infratentorial approach to pineal tumors. Surg
Neurol 11:331-337, 1979.
5. Van Wagenen WP: A surgical approach for the removal of certain pineal
tumors. Surg Gyncecol Obstet 53:216-220, 1931.
27
Pineal Region and
Posterior Third
Ventricular Tumors: A
Surgical Overview
Keiji Sano, M.D., D.M.Sc, FAC.S.(hon.)

So-called Germ Cell Tumors and Pineal Tumors in the Pineal-Posterior Third
Ventricular Region
Rene Descartes (1596-1650), the greatest philosopher of 17th century France, thought
that the pineal body might act as a valve or sphincter to regulate the passage of spirits
between the ventricular chambers, and this tiny organ thus gained supreme importance
as the seat of the soul. This concept is, of course, wrong. The pineal body or gland,
however, is certainly the seat of various kinds of tumors.
Tumors in the pineal region occupy 4% of all intracranial primary neoplasms in Japan
(583 of 14,672 cases) (9, 47) (Table 27.1). This is definitely a higher incidence than in
any other country (2, 45-48, 56). This high incidence is mostly comprised of the so-
called germinoma, or pinealoma, of the two-cell pattern type (PTC), which forms 2.6%
of all intracranial primary neoplasms according to the most recent Japanese statistics (9,
47). In these same statistics, pineocytoma occupies 0.2%, pineoblastoma 0.1%, and
teratoma including malignant teratoma 0.7%. In Cushing's series (10), pinealoma is
found in 0.7%, and in the Chinese statistics (8) it appears in 0.9%. Most European and
American statistics show a lower incidence of this tumor than these figures (8).
Table 27.2 shows 125 cases of tumors in the pineal region and the posterior third
ventricle (excluding falcotentorial meningiomas) treated in my clinic and its affiliated
hospitals. The pineal tumor of the two-cell pattern type, which has been called
pinealoma (17, 18, 24) or germinoma (12, 13, 42-44), is described in this table as PTC.
Pineoblastoma corresponds to medulloblastoma of the pineal of Zulch (63). Mixed germ
cell tumors are composed of two or three types of tumors such as germinoma
(seminema), teratoma, teratoma with malignant transformation, embryonal carcinoma,
choriocarcinoma, and endodermal sinus tumor (Table 7). According to the studies of
Zulch and my group (31, 40, 47), PTC can be divided into germinoma (seminoma) of
germ cell origin and pinealoma of pineal parenchymal origin. If we admit, although there
is no convincing
evidence, the germ cell theory that teratoma, teratoma with malignant transformation,
germinoma (seminoma), embryonal carcinoma, endodermal sinus tumor,
choriocarcinoma, and mixed germ cell tumors all arise from the imaginary germ cell (12,
13, 55), they can be grouped under the term "germ cell tumors." The tumors in the pineal
region and the posterior third ventricle are classified as follows: (a) germ cell tumors —
including germinoma (seminoma), teratoma (and epidermoid or dermoid), teratoma with
malignant transformation, embryonal carcinoma, endodermal sinus tumor,
choriocarcinoma, and mixed germ cell tumors; (b) tumors of pineal parenchymal origin
— including pinealoma, pineocytoma, and pineoblastoma; (c) gliomas; and (d) tumors of
the velum interpositum — including meningioma, hemangiopericytoma, angiomas, and
cysts. In this chapter, I will deal mainly with Groups a and b.
PTC, as its name implies, is composed of two distinct cell types. Groups of large,
polygonal cells with frequently clear cytoplasm are separated by fibrous strands with
perivascular lymphocytic infiltration, displaying a "mosaic pattern." Because of its
morphological similarity to seminoma or dysgerminoma, the term germinoma, which
was proposed by Friedman (12, 13) and later adopted by Russell and Rubinstein (42-44),
or atypical teratoma (Russell and Rubinstein [44]), has now received wide acceptance.
The term "pinealoma" was introduced by Krabbe in 1923 (24) in a very
casual way as "an adenoma, or more exactly, 'pinealoma'," was adopted by Horrax and
Bailey (17, 18), and has since been generally used. It is held to signify a tumor of the
pineal parenchymal cells. The tumor is likewise composed of masses of large spherical
epithelial cells separated by a reticular connective tissue containing lymphoid cells. Both
Bailey (3, 17, 18) and Zulch (63) regarded these epithelial cells as originating from the
parenchymal cells of the pineal body.
There are, less frequently, tumors composed of a homogeneous mass of smaller
epithelial cells without lymphoid cells. Bailey (3, 17, 18) called tumors of this type
"pinealoma of spongioblastic type" or "pineoblastoma." Russel and Rubinstein regarded
this type of tumor as the true pinealoma of pineal parenchymal origin and divided it into
"pineocytoma" and malignant "pineoblastoma" (44). Zulch named these two "isomorphic
pinealoma" and "medulloblastoma of the pineal," respectively, and called the two-cell
pattern type tumor "anisomorphic pinealoma" (63). These rather chaotic nomenclatures
are listed in Table 27.3.
PTC is found not only in the pineal region but also in other areas of the brain. Table
27.4 lists PTCs in various sites that have been treated in my clinic and histologically
verified. The results seem to favor the classification of PTC as a germinoma (seminoma).
For reevaluation of the histogenesis of PTC, 48 surgical specimens, a number
sufficient for detailed study, were selected and carefully reviewed by both light and
electron microscopic examinations, as was reported elsewhere (47).
Of the total 48 cases of PTC, 28 cases were located in the pineal body, 11 in the
suprasellar-hypothalamic area, and the remaining 9 in other sites (Table 27.5). They
consisted of 41 males and 7 females, indicating a marked preponderance of males over
females. Thirty-three patients were younger than 20 years of age and 15 patients were 20
or older.
 The pineal organ of lower vertebrates functions as a photoreceptor that transduces an
exteroceptive input (light) into neural signals. In birds, the pineal is not a true
photoreceptor but in response to light it changes the rate of synthesis of hormonal
products like melatonin (photoendocrine transducer). In mammals the pineal gland is an
endocrine organ with some of the properties of a "neuroendocrine transducer": one of its
major functions is to convert the input of neural signals to a hormonal output, i.e.,
melatonin and other methoxyindoles and probably Polypeptides (7).
In the normal pineal gland, lobules consisting of pineal parenchymal cells are
incompletely separated by irregular trabeculae and fibrous septae carrying blood vessels
along with them. Like all other endocrine organs, the pineal body has a very rich
capillary blood supply (sinusoids). The parenchymal cells attach closely to the sinusoidal
sheaths. The intimate proximity of the cells to the sinusoids is regarded as a common
feature of the endocrine glands. Thus, it might be expected that true tumors originating
from the pineal parenchymal cells would show a close relationship between the tumor
cells and the sinusoids as the tumor stroma.
The seminiferous tubules constitute the exocrine portion of the testes. There is no
direct interrelationship between the tubules and blood vessels from the tunica vasculosa
testis. Typical microscopic pictures of seminoma reveal regular, fibrous supporting
stromata containing capillaries and lymphocytes that divide the tumor into lobules. There
is no evidence of tumor cells attaching to the capillaries.
Based on this new criterion that in a true tumor of pineal origin tumor cells should be,
as in any endocrine neoplasm, in close proximity to the capillaries (sinusoids) without
intervening mesenchymal tissues, histological reevaluation of 48 specimens was
performed. Besides this fundamental finding of close proximity to the capillaries, the
pattern of lymphocytic infiltration is different in tumors of pineal origin and semino-mas.
In the former, lymphocytes are mainly seen along the margins of tumor nests or clusters
with occasional sparse scattering in tumor cell clustlers. In the latter, lymphocytes are
seen mainly in fibrous septa with occasional granulomatous reaction, something never
noticed in tumors of pineal origin. In addition, tumor cells in seminoma are somewhat
larger than those in tumors of pineal origin.
According to this criterion, PTC can be divided into two groups: one corresponds to a
true tumor of pineal origin, which may be called pinealoma, and the other to the
seminoma, which, according to Friedman (12), may be called germinoma.
In some parts of pinealoma, transition from the main component of
 large, ovoid cells with central, vesiculated nuclei to rather smaller cells with eccentric,
dark-staining nuclei and eosinophilic cytoplasm is frequently observed (47).
The cytological features of these smaller cells are exactly compatible with those of
pineocytoma postulated by Russell and Rubinstein (16, 42, 44). Therefore, the available
evidence strongly favors that Russell's pineocytoma be regarded as the mature type of
pinealoma here described.
Ultrastructural observations of this pinealoma (31, 47) also support the concept of its
endocrine properties. The cytoplasmic processes of the tumor cells extend into the
perivascular interstices, and the tumor cells remain closely adjacent to the fenestrated
pores of the endothelium. The tumor cells extensively show smooth-surfaced
endoplasmic reticula in the tubular and vesicular forms of cisterns, which may represent
their secretive phase. Also, microtubules, as one of the characteristics of pineal cells, are
noticed in the cytoplasm of the tumor cells.
According to the formulated criterion, 24 of the 48 cases could be assigned to the
category of pinealoma (Table 27.5). Of these 24 cases of pinealoma, 19 were found in
the pineal region, 2 in the suprasellar-hypothalamic area, and 3 in other sites. The sites of
the other 24 cases with germinoma included the pineal region in 9 cases, the suprasellar-
hypothalamic area in 9, and the other sites in 6. Of tumors involving the pineal region,
pinealoma accounted for two-thirds of the 28 cases (19 cases); in contrast, 80% of
suprasellar-hypothalamic neoplasms were germinoma (Table 27.5). In both pinealoma
and germinoma, males were predominant (83 to 88%). However, 2 pinealoma patients in
the suprasellar region and 3 of 9 germinoma patients in the suprasellar region were
female. Therefore, in pinealoma and germinoma in the suprasellar region the male
predominance was not marked.
The results found in earlier ultrastructural studies (54) supporting the close
resemblance between pineal tumors with a mosaic pattern and testicular seminomas may
have been because those specimens had been mostly obtained from suprasellar-
hypothalamic tumors. The age of predilection of patients with pinealoma involving the
pineal region ranged from 12 to 20 years, with an average of 16.4 ± 4.8. Suprasellar-
hypothalamic germinomas mostly appeared between the ages of 8 and 12, with a mean
age of 10.4 ± 2.5—slightly younger than that for pinealoma. However, germinomas of
the pineal region did not show such a predilection for younger ages. The average age of
pineoblastoma cases was 13.8 ± 10.9 (16), i.e., younger than that of pinealoma cases.
According to Herrick and Rubinstein (16), the average age of pineocytoma cases was
42.6 ± 20.6. In terms of age, therefore, pinealoma is situated between immature
pineoblastoma and mature pineocytoma. Neoplasms of endocrine organs usually appear
after endocrine functions have developed to some extent, and so the average age of 16
years for pinealoma seems compatible. In terms of sex distribution, pinealoma,
pineoblastoma, and probably pineocytoma, as well as germinoma showed a male
predominance (Tables 27.2, 27.4, and 27.5).
Table 27.6 shows cases of the so-called intracranial germ cell tumors experienced in
my clinic. All of these tumors were located in the area of the third ventricle including the
pineal and suprasellar regions. Germinoma (9 cases) is included in this list; pinealoma,
however, is excluded for the reason mentioned previously. All mature teratoma cases (16
cases), 4 cases of teratoma with malignant transformation, 15 of 30 mixed germ cell
tumor cases, and 1 case of unclassified germ cell tumor were located in the pineal region
(see Table 27.2). Table 27.7 shows the histological components of the mixed germ cell
tumors described. As seen in Table 27.7, two or three components can be noted.
 Among 84 patients with germ cell tumors, 66 (78.6%) were under the age of 20 and 18
(21.4%) were at least 20 years. There were 70 (83.3%) males and 14 (16.7%) females
(Table 27.6). This age and sex distribution for intracranial germ cell tumors is essentially
similar to that for germ cell tumors of other organs.

Therapeutic Principles and Preoperative Evaluation

Diagnosis of a medium-sized or large tumor arising in the pineal region and the
posterior third ventricle is not difficult because of the presence of increased intracranial
pressure, paralysis of the conjugate upward gaze (Parinaud's sign), pseudo-Argyll
Robertson pupil, etc. Cerebral an-
giography is useful to detect the extent and vascularization of the tumor (38).
Calcification in plain craniograms may sometimes be pathogno-monic, especially in
patients under 10 years of age. The most powerful and noninvasive diagnostic tool,
however, is computerized tomography (CT). Magnetic resonance imaging may likewise
be useful; I, however, have had no experience with its use. Before the advent of CT,
ventriculography, especially positive-contrast ventriculography, had widely been used,
but it is now used only in exceptional cases.
Examination of levels of alpha-fetoprotein (AFP), human chorionic gonadotropin
(HCG), and carcinoembryonic antigen in the serum or in the cerebrospinal fluid should
be done in all cases. The first two tumor markers (AFP and HCG) are especially
informative as to the nature of tumors.
If HCG is positive, the tumor must be choriocarcinoma or a mixed germ cell tumor
with choriocarcinomatous elements. If AFP is positive, the tumor must be an endodermal
sinus tumor or a mixed germ cell tumor with endodermal sinus elements. In both cases,
prognosis is rather poor even after surgical removal of the tumor and postoperative
radiotherapy of the whole neuraxis. Recently, chemotherapeutic agents such as acti-
nomycin D, cis-platinum, vinblastine, bleomycin, etc., or their combinations have been
reported to be worthy of use.
If AFP and HCG are negative, the tumor may be pinealoma, germinoma, embryonal
carcinoma, teratoma with malignant transformation, or mature teratoma. If 2000 rads of
local radiation effectively abolishes the tumor on CT, it may be pinealoma or
germinoma, and radiotherapy should be continued with or without a shunting procedure.
However, if the tumor is more than 2 cm or sometimes more than 1.5 cm in diameter,
direct operation and removal of the tumor followed by radiation should be
recommended. (For pinealoma and germinoma, local radiation is usually
 sufficient.) Mature teratoma can be cured only by removal of the tumor, and its
prognosis is good. Embryonal carcinoma and teratoma with malignant transformation
usually carry a poor prognosis even after surgical removal and postoperative
radiotherapy of the whole neuraxis. The previously mentioned chemotherapeutic agents
are also recommended as being worthwhile. These principles are schematically
illustrated in Figure 27.1.
Stereotaxic biopsy of tumors of this region has recently been gaining in popularity. I,
however, am not particularly enthusiastic about this procedure because different parts
of the same tumor of this region may show different histological findings so that biopsy
of a small piece of the tumor may be misleading as to the true nature of the tumor.
Therefore, I prefer exploration and partial resection (unless total removal is possible) of
the tumor.
Cytological examination of the cerebrospinal fluid is important for diagnosis. If
malignant neoplastic cells are identified at cytology, the case may develop
dissemination metastases in the cerebrospinal fluid space. For diagnostic purposes, I
recommend Millipore filter-cell culture (49) of the cerebrospinal fluid. This method is
more sensitive than conventional cytological studies. Therefore, positive culture does
not necessarily mean that the probability of dissemination metastases is high.
After treatment is finished, during follow-up, repeated examinations of the tumor
markers are useful to detect recurrence of the tumor producing these markers at the
earliest possible stage.

Historical Perspectives of Various Approaches

Horsley (19) was probably the first to try to remove a pineal tumor. He used the
infratentorial Supracerebellar approach, but with poor results. He therefore
recommended supratentorial approaches. In 1913, Krause successfully removed a huge
tumor in the region of the corpora quadrigemina from a 10-year-old boy by the
infratentorial Supracerebellar approach, which he reported with Oppenheim, who
diagnosed the case (34). The tumor was reported to be a fibrosarcoma or an
encapsulated mixed cell sarcoma, but seems, however, to have been a teratoma or
meningioma according to modern pathological designation. In 1926 (25), Krause added
two more cases operated upon by the same approach; in these two, however, he could
not remove the tumors. Practically the same approach was reported by Zapletal in 1956
(62). He reported four cases: a malignant astrocytoma in the quadrigeminal region, a
medulloblastoma of the upper vermis, an epidermoid, and a pinealoma. The last was
successfully removed.
In the era of microsurgery, Stein (51), in 1971, revived and elaborated this
infratentorial Supracerebellar approach, which has been widely used since (35, 47, 48).
The occipital or parietooccipital approach with or without splitting the splenium of
the corpus callosum or the tentorium along the straight sinus has been proposed by
Brunner (5, 41), Pratt (37), Heppner (15), Poppen (36), Kempe (23), Glasauer (14),
Jamieson (20), Lazar and Clark (29), Sano (45-48), Lapras (27), and others. Special
credit should be given to Jamieson, who established the occipital transtentorial
approach.
The parietal transcallosal approach was proposed by Dandy (11), then by Kunicki
(26), Suzuki and Iwabuchi (53), and others. In 1931, Van Wagenen (57) proposed the
posterior transventricular approach. This has, however, been used only occasionally. For
huge tumors in the pineal region or in the posterior third ventricle, Sano proposed the
anterior or frontal transcallosal approach (47).
 Other approaches such as the subchoroidal approach (28, 58) or the transcallosal
interforniceal approach (1), which are primarily for lesions in the middle or anterior third
ventricle, may be used for tumors in the pineal-posterior third ventricular region.
These various approaches and the pertinent anatomy were summarized by Rhoton and
his group (39, 61). Of these approaches, I prefer (a) the occipital transtentorial approach,
(b) the infratentorial Supracerebellar approach, and for huge tumors (c) the frontal
transcallosal approach.

Indications for Utilization of the Various Approaches

For the occipital transtentorial approach to a pineal tumor, I prefer the incision
(usually on the nondominant side) illustrated in Figure 27.2. The midline portion of the
incision can be elongated to the suboccipital region if it is necessary to open the
posterior fossa.
Craniotomy is close to the superior sagittal sinus and the transverse sinus. The patient
is either in the prone position or the lounging position, as seen in Figure 27.2. The
occipital lobe is punctured through the dura
mater, and a silicone rubber tube is inserted into the posterior portion of the lateral
ventricle and secured to the dura (Fig. 27.10). The tube drains the cerebrospinal fluid
during the operation and makes lateral retraction of the occipital lobe easier. The
tentorium is split close to the straight sinus, and the superior surface of the cerebellum is
exposed. The operating microscope is used from this stage. A pineal tumor is often
visible rostral to the vermis, underneath the vein of Galen. If the tumor is located further
rostrally, the splenium of the corpus callosum is split by suction to expose the tela
choroidea of the third ventricle. If the tumor is large, it is often already breaking through
the tela choroidea; if not, the tela is incised along the midline or close to the
nondominant occipital lobe after cauterization with a bipolar coagulator.
Therefore, this approach enables the operator to use the low (parie-to-)occipital
approach (as proposed by Poppen (36) and Jamieson (20)) and, if necessary, the high
parietooccipital approach (as proposed by Dandy (11) and others) as well.
If the tumor is a pinealoma or a germinoma (germinoma is usually slightly tougher),
the tumor is removed piecemeal. If the tumor is a teratoma, removal en bloc will often be
feasible. After removal of the
tumor, the other end of the silicone rubber tube (which has been inserted into the lateral
ventricle) is brought into the lateral cistern or the pontine cistern to secure the
cerebrospinal fluid pathway. This is done because the rostral portion of the aqueduct is
often compressed by the tumor, and even after removal of the tumor the effect of the
compression may remain for a certain period.
 The infratentorial Supracerebellar approach is utilized when the pineal tumor is not too
large. The superior surface of the cerebellum is pressed down after electrocauterizing and
severing the bridging veins between the cerebellum and the tentorium (Fig. 27.3). The
tumor can be seen beneath the vein of Galen and between the basal veins of Rosenthal.
The precentral cerebellar vein and the superior vermian vein are identified and severed.
The tumor is usually removed piecemeal. Figure 27.4 shows CT of a 7-year-old boy with
a medium-sized tumor in the pineal region that was removed by this approach. Figure
27.5 shows the tumor being removed piecemeal with the aid of the Cavitron ultrasonic
aspirator. In Figure 27.6, no tumor is visible; the normal wall of the third ventricle can
now be seen. Figure 27.7 is a postoperative CT (1 week after the operation). The tumor is
totally removed. This tumor turned out to be a
teratoma with malignant transformation. The patient is well and attending school a little
more than 3 years postoperatively.
I previously performed the infratentorial Supracerebellar approach with the patient in a
sitting position as advocated by Stein (51). However, because of the fear of air embolism
I am now using this approach with the patient in an oblique prone position as shown in
Figure 27.8. The operator stands to the left of the patient and looks down on the pineal
region through the operating microscope.
 Another point that should be mentioned and has hitherto never been described is that
in rare cases the vein of the cerebellomesencephalic fissure (30) or the superior and
inferior quadrigeminal veins are so well developed that the tumor cannot be reached
directly from behind. In that case the tumor should be approached slightly obliquely
between these veins and the basal vein of Rosenthal. Another alternative for such cases
is the occipital transtentorial approach. As shown in Figure 27.9, the tumor is attacked
from a more superior and lateral direction without touching the quadrigeminal veins.
I have experienced no operative mortality either by the occipital or the infratentorial
approach. Steroid is administered before, during, and after the operation.
Postoperative irradiation for pinealoma or germinaoma was done with Co-60 or
LINAC, the total dose being 5000 to 6000 rads (the daily dose, 100 to 200 rads). The
field of irradiation was 6 X 6 to 8 X 8 cm, centering on the pineal region. In cases of
malignant tumors, whole brain irradiation and spinal cord irradiation were added, but
even in these cases the total dose did not exceed 5000 to 6000 rads.
Several years ago, I treated two cases (4- and 7-year-old boys) of huge malignant
pineal teratoma with an endodermal sinus tumor element that showed increased serum
AFP. I thought that these were both too large to attack either by the occipital
transtentorial approach or by the infratentorial Supracerebellar approach (Fig. 27.10 and
27.11). I decided to remove the tumors en bloc by the frontal transcallosal approach.
Frontal craniotomy was fashioned, as shown in Figure 27.12A. The corpus callosum was
longitudinally split, about 4 cm in length, at its junction with the nondominant cingulate
gyrus (Fig. 27.12B). The tumor was easily identified and gently detached from the
surrounding tissues under the micro-scope and then was removed en bloc (Fig. 27.13 and
27.14). The tumors were 4.5 cm and 5 cm in diameter. After the operation, a marked
decrease of AFP was noted. The postoperative course was uneventful and the patients
returned to school. The 4-year-old boy is still healthy more than 3 years postoperatively.
The 7-year-old boy, however, later developed diffuse metastases in his body and died 1.5
years later.
 I favor the occipital transtentorial approach or the infratentorial Supracerebellar
approach if the pineal tumor is located posterior to the adhesio interthalamica. If the
tumor is too large and reaches anterior to the adhesio iterthalamica, the transcallosal,
especially the frontal transcallosal approach may be recommended.

Radiotherapy or Direct Operation

Both pinealoma and germinoma are radiosensitive (4, 6, 21, 33, 50, 52, 59, 60).
Therefore, radiation alone or radiation plus ventriculoperitoneal shunting prevails as the
established treatment. The greatest criticism against direct operation is the anticipated
significant operative mortality and the increased probability of dissemination metastases
in the cerebrospinal fluid space.
 However, there was no operative mortality in my series. I believe that meticulous
surgical maneuvers, especially microsurgical ones, do not carry a significant operative
risk. I also believe that reduction of the bulk of a neoplasm by direct operation, even if
that neoplasm is radiosensitive, is important for the effectiveness of radiotherapy.
This may be clearly demonstrated if one compares the results of treatments of pineal
pinealoma-germinoma with those of suprasellar pineal-oma-germinoma, where reduction
of the bulk of the tumor is easier and more extensive (Table 27.8). The 10-year survival
rate (calculated by the Kaplan-Meier method (22)) of suprasellar pinealoma-germinoma
cases was 100%, whereas that of pineal pinealoma-germinoma cases was 74.9% in my
series.
In the literature, the incidence of dissemination metastases of pinealoma or germinoma
in the cerebrospinal fluid space is 8 to 20% (48); in my series it was 3.7%. Therefore, one
cannot say that direct operation of the tumor will increase the probability of
dissemination metastases.
In Japan, the general trend is first to irradiate the tumor with 2000 rads. If the tumor
disappears on CT, radiation therapy is continued; if not, direct operation is performed
because in that case the tumor is most probably a neoplasm other than pinealoma or
germinoma.
However, when a pinealoma or a germinoma is of considerable size, it may recur even
if the tumor disappears on CT after radiotherapy. Therefore, I recommend direct
operation and postoperative radiotherapy for
pinealoma-germinoma cases (except for cases with small or multiple tumors).
Patients harboring mixed germ cell tumors usually have a poor prognosis even if their
tumors are totally removed and radiotherapy follows. Cases of mature teratoma, on the
other hand, show good outcome in the follow-up. Table 27.9 shows survival rates of
patients with tumors other than pinealoma and germinoma.

Summary and Conclusion

There are various kinds of tumors in the pineal-posterior third ventricular region.
Among them, the so-called two-cell pattern tumor is most frequent. These tumors can be
divided into tumors of pineal parenchymal origin (pinealoma) and tumors of germ cell
origin (germinoma or seminoma). These two-cell pattern tumors and the so-called germ
cell tumors are also found in other areas of the brain, most frequently, however, in the
area of the third ventricle. The germ cell tumors are grossly divided into two groups by
the tumor markers (AFP and HCG), with those being either positive or negative.
However, exact diagnosis can be made only by operation and histological examination of
the surgical specimens.
In treatment, mature teratoma should be surgically removed because it is not
radiosensitive. Pinealoma and germinoma (seminoma) are radiosensitive; if they are of a
considerable size, however, surgical removal and postoperative radiotherapy should be
recommended (for these tumors, local radiation may be sufficient because dissemination
metastases are not frequent). Embryonal carcinoma, teratoma with malignant trans-
formation, choriocarcinoma, endodermal sinus tumor, and their combinations (mixed
germ cell tumors) should be submitted to operation and postoperative radiation (whole
neuraxis) combined with chemotherapy. Pinealoma, germinoma, and mature teratoma
carry good prognoses, but other tumors carry rather poor prognoses.
Among the various surgical approaches to tumors in the pineal-posterior third
ventricular region, the infratentorial Supracerebellar approach and the occipital
transtentorial approach may be the methods of choice if the tumor is confined posterior
to the adhesio interthalamica. If the tumor is large and reaches anterior to the adhesio
interthalamica, the frontal transcallosal approach may be preferable.

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28
Technical Aspects of Excision of
Giant Basal Tumors with Third
Ventricular Involvement
Madjid Samii, Prof. Dr. med.

The third ventricle with its central location in the intracranial cavity can be involved by
the different pathological processes arising from structures at the skull base. Giant tumors
of the sellar and parasellar region reach the third ventricle anteriorly. They push or
invade its wall and further propagate, filling its cavity. Processes along the tentorial
margin can grow and involve the third ventricle from a caudolateral aspect. The posterior
part of the ventricle can be affected by those pathological processes originating in the
pineal region.
The planning of our operative strategy for excision of these lesions will depend on
their primary site of origin and their propagation. Now, with our increased knowledge of
the microanatomy of the third ventricle and its surrounding delicate structures as well as
the tremendous advancement of microsurgical techniques, we are able to deal with these
lesions with the least percentage of morbidity and nearly negligible mortality.
In this book all different approaches to the third ventricle are described in other
chapters. Our only concern is directed to the surgical management of giant pathological
processes that secondarily involve the third ventricle.

Giant Space-occupying Lesions Involving the Anterior Portion of the Third

Ventricle
Tumors of the sellar and parasellar region may secondarily involve the anterior wall of
the third ventricle, later filling its cavity. There they may compress its wall or obstruct
the cerebrospinal fluid (CSF) flow by closure of the foramen of Monro, producing
different neurological deficits.
The most important pathological processes in this group are Craniopharyngiomas and
pituitary adenomas. In the past, surgical excision of these giant tumors was usually
partial; total removal was accompanied by a high percentage of both morbidity and
mortality. This is due to the involvement of many important structures like the optic
nerves, chiasm, hypothalamus, and perforating vessels of the circle of Willis. Delicate
 and meticulous microsurgical techniques are required to avoid damaging these
structures.
During surgical excision the strategy for total removal will depend on whether the
tumor is compressing the surrounding neural tissues or, as in rare cases, infiltrating these
tissues, e.g., craniopharyngioma (28). Another fact that influences the ease or difficulty
of operation is how the nerves and vessels are involved in the neoplasm. In general, we
should divide all tumors into two categories. One group of tumors grows and enlarges
symmetrically, compressing and displacing the structures in all possible directions. In
such a tumor all important structures are localized around the tumour capsule. Gradual
resection and central reduction of the tumor will make the capsule collapse, giving more
and more space. The tumor capsule can then be easily dissected from the important
structures. In such cases the huge size of the tumor does not add to the gravity or risks of
total removal.
In contrast to this group we are sometimes confronted by a second group of tumors
that grow and then engulf surrounding vessels and nerves, like the carotid, anterior
cerebral, anterior choroidal, posterior communicating, and perforating arteries, as well as
the cranial nerves. The removal of these tumors can be hazardous with a high rate of
morbidity and sometimes mortality. Therefore, the strategy of microsurgical approach
and tumor excision requires a firm comprehension of the microanatomy that is altered to
a great extent by the growing neoplasm. In handling these tumors one must start at
definite anatomical landmarks, beginning where the surrounded vital structures are not
involved and obscured by the pathological process. The tumor can be removed piecemeal
and the structures dissected stepwise and freed. A direct attack into the center of these
tumors can lead to traumatization of the structures engulfed and increases the risk of
morbidity or even mortality. Fortunately these types of suprasellar tumors are only a
minority.
For the removal of giant sellar and parasellar tumors with extensive involvement of
the third ventricle, many approaches have been described (3, 17, 18, 29, 30). As the
tumor arises primarily basely and secondarily extends into the third ventricle, we prefer
subfrontal access (6, 27) compared to a transcortical (4) or transcallosal approach (10).
This approach is more direct and gives much more space than the subtemporal (5) or
transtemporal technique (31).
A giant basal tumor elevates the suprasellar structures and enlarges the suprasellar
space. This may lead to a retrofixed chiasm with opening of the angle between the optic
nerves and the chiasm (Fig. 28.1). In certain cases the tumor can separate the
supracavernous part of the internal carotid artery (ICA) from the optic nerve, giving
sufficient distance for a lateral approach to the tumor. In these situations a subchiasmatic
or a laterochiasmatic approach can be performed. If the distance between the tuberculum
sellae and the optic chiasm is not large enough for total removal, a retrochiasmatic
approach through the lamina terminalis should be performed.
The choice of the frontal craniotomy, whether right, left, or bifrontal, depends on the
additional extension of the tumor to the parasellar and retrosellar region. In the case of
midline tumors with no lateral extension a right frontal craniotomy is performed. With
extreme parasellar extension to one side we prefer a craniotomy on the opposite side.
This is important as it gives a better subchiasmatic visual access to the structures at the
tentorial margin.
In cases of bilateral extension of the tumor, which is common with giant basal tumors,
we prefer a small bifrontal craniotomy. The crani-
otomy should be quite basal, extending to the roof of the orbit without respect to the
frontal sinus. The superior sagittal sinus will be ligated and the attachment of the falx to
the crista galli will be transected. With microsurgical dissection both olfactory nerves can
be preserved (19, 26).
Case 1
A 9-year-old girl presented in a somnolent state with a history of headache and gradual
deterioration of visual acuity. Ophthalmological examination revealed central tubular
vision in the left eye, perception of light in the right eye, and bilateral primary optic
atrophy. Computerized axial tomography (CT) (Fig. 28.2) showed a large suprasellar
cystic craniopharyngioma with a small solid sellar part. The tumor filled the third
ventricle, occluding the foramen of Monro and producing obstructive hydrocephalus.
A ventriculoperitoneal shunt was done to improve the level of consciousness by
relieving the obstructive hydrocephalus. Two weeks later a bifrontal osteoclas-tic
craniotomy was carried out and the anterior part of the tumor was exposed.
The tumor was punctured and the cyst was aspirated. Gradual resection of the tumor
capsule from the left and right optic nerves and carotid arteries was done. The majority
of the capsule and the tumor could be removed subchiasmatically, but there was still a
tumor remnant left behind the chiasm and in the third ventricle. The third ventricle was
opened through the lamina terminalis and the tumor was totally excised. After total
removal we had a good view of the pons, interpeduncular fossa, and basilar artery and
its tributaries (Fig. 28.3).
During the early postoperative period the child suffered from a transient diabetes
insipidus and was for 3 days somnolent. The patient was discharged 5 weeks after
operation in a very good general condition. Her visual deficit was the same. A
postoperative control CT scan showed complete excision of the tumor (Fig. 28.4).

Case 2
A 56-year-old woman presented with a giant recurrence of a pituitary adenoma. She
had undergone operation 6 years before and postoperatively had suffered from mental
disturbances, bilateral dyskinesia, panhypopituitarism, and bitemporal hemianopsia that
did not improve. CT (Fig. 28.5) showed a giant parasellar tumor extending suprasellarly
into both lateral ventricles and compressing the third ventricle. Angiography showed
definitive displacement and engulfment of the right carotid artery and its bifurcation.
The tumor was approached through a bifrontal craniotomy. The parasellar part was
compressing the cavernous sinus and right optic nerve. The supracavernous part of the
ICA and its bifurcation were completely surrounded by the tumor. Superiorly, the tumor
extended through the frontal lobe to both lateral ventricles. Posteriorly, it indented the
third ventricle.
To avoid damaging the surrounding structures we used the first few millimeters of the
right ICA as a landmark and followed the tumor around the vessels. After exposure of
the carotid bifurcation further dissection and removal of the tumor around the anterior
and middle cerebral arteries was carried out, sparing the important perforating vessels. In
the next step the tumor in front of the lamina terminalis was removed, exposing the
cavity of the third ventricle. At the last stage the part of the tumor extending to the
lateral ventricle was removed. Postoperatively the patient made an excellent recovery
and was discharged in the same clinical condition as preoperatively. (Fig. 28.6 shows a
postoperative CT scan.)
 Giant Space-occupying Lesions Involving the Lateral Portion of the Third Ventricle
Processes arising along the tentorial margin can reach the third ventricle in a
caudolateral aspect. This region is of particular importance because of its close
relationship to functionally important cranial nerves and vessels as well as brain stem
structures (12). Pathological processes of the tentorial notch that reach a huge size and
may compress the third ventricle are usually meningiomas, chordomas, and neurinomas.
There are many operative approaches (11, 14, 16) to deal with lesions in the region of
the tentorial notch. We prefer the pterional approach modified by Yasargil (33) for
lesions in the region of the anterior and middle third of the tentorium. A curved
frontotemporal incision is made inside the hairline and running 1 cm anterior to the
tragus. In this way one secures an adequate approach to the lesser wing of the sphenoid
and the floors of the anterior and middle fossae. After raising a small frontotemporal flap
and removing the lateral part of the lesser wing, one continues intradurally along the
sphenoid wing in the direction of the anterior clinoid process by gradually opening the
cisterns and removing CSF. This procedure must not be rushed; by constant aspiration of
CSF and gentle retraction the frontal and temporal lips of the sylvian fissure can be
gradually opened without any undue pressure on the brain.
After exposure of the optic nerve and further opening of the cisterns along the edge of
the tentorium, the internal carotid, posterior communicating, and anterior choroidal
arteries and the oculomotor nerve are exposed in the anterior third of the tentorial notch.
By further dissection along the free margin of the middle third of the tentorium in a
posterior direction, the trochlear nerve and the posterior cerebral artery and its origin
from the basilar artery become visible. After incising the margin of the tentorium and
stitching it back in its middle third one has a very good view into the depth of the
infratentorial space.
Our further surgical strategy depends on the anatomical variations of the tentorial
notch (9). In some individuals the tentorial notch is narrow. In such a situation, exposure
of the tentorial margin does not permit any view to the infratentorial region. The
previously mentioned incision of the tentorium can be helpful in certain circumstances,
but would still not
be sufficient for those giant tumors that extend infratentorially in the cerebellopontine
angle and prepontine space. To avoid a second stage operation through a lateral
suboccipital approach, we coagulate and transect the superior petrosal sinus and expose
the petrous apex. This can be removed carefully up to the internal auditory meatus with a
high speed diamond drill (Fig. 28.7).
The seventh and eighth cranial nerves are now visible and can be dissected free from
the lesion. The manner in which we deal with the fifth nerve depends on the clinical
findings and morphological behavior of the tumor. If there is no functional deficit and the
nerve is only compressed by the tumor, all efforts are undertaken to preserve the nerve. In
cases of functional deficit and infiltration of the nerve fascicles, e.g., invasive
meningioma, one must sacrifice the nerve for more radical removal of the tumor. The
most important aspects of such giant tumors at the tentorial margin are their relation to
vessels supplying the brain stem and the severe adhesion of the tumor to this very delicate
area. According to my personal experience one can decompress the brain stem by gradual
resection of the tumor from lateral to medial in a piece-meal manner until the tumor is
completely removed. During dissection some small arteries can be sacrificed without
compromising the blood supply to the mesencephalon.
As the circle of Willis demonstrates a tremendous degree of variation we are not able
to determine in each individual case the exact blood supply and collateral circulation of
the brain stem (13). There are no fixed criteria to be taken into consideration for this
special problem. The
outcome of our operated cases has shown that many of those vessels that supply the
tumor and also the brain stem can be sacrificed without any postoperative consequences.
It seems that it is more dangerous to apply traction to brain stem vessels by pulling on
the tumor. Traction of any vessel at the brain stem can lead to interstitial rupture and
bleeding, which causes severe brain stem lesions and marked neurological deficits. It
seems wiser to coagulate and cut such vessels when necessary.
Case 1
A 55-year-old Italian man complained of headache, diplopia, right hemiparesis, and
regurgitation that had been progressive over 1 year. On examination the patient suffered
from bilateral papilledema, right sixth and seventh nerve palsy, diminished pharyngeal
reflexes, bilateral pyramidal syndrome (more on the right side), and a positive
rombergism sign. Plain x-ray tomography showed widening of the sella with destruction
of the dorsum sellae and clivus and parasellar calcification. CT scanning and magnetic
resonance imaging (MRI) showed a huge
space-occupying lesion in the region of the clivus, displacing the brain stem upward and
dorsally, compressing the third ventricle and mesencephalon with secondary obstructive
hydrocephalus, and extending bilaterally (more to the right side) down to the foramen
magnum. Anteriorly it extended supra- and parasel-larly, invading the right cavernous
sinus (Fig. 28.8A). Angiography showed dorsal displacement of the basilar artery (Fig.
28.8B) and opening of the carotid bifurcation.
The right pterional approach was chosen as it allows handling of the tumor in the
suprasellar, parasellar, and petroclival region. Through a right frontotemporal
osteoplastic flap, the right sylvian fissure was opened. The suprasellar part was removed
using a laterochiasmatic approach. The supracavernous part of the ICA was dissected
from the tumor up to the carotid bifurcation. Incision of the tentorium was carried out and
the superior surface of the tumor in the right middle fossa was exposed. The oculomotor
nerve was gradually exposed by piecemeal removal of the tumor. The tumor was
followed to the cavernous sinus, which was opened, excising the intracavernous portion
of the tumor and freeing the third, fourth, and sixth nerves. The last step was meticulous
dissection and piecemeal removal of the part of the tumor adherent to the mesencephalon
and brain stem, freeing the basilar artery and its branches. At the end of this procedure
complete excision of the tumor was accomplished to the contralateral side of the brain
stem. One could then have a good view of the structures on both sides of the tentorial
edge.
The patient made an excellent recovery with improvement of his paresis. The
histopathological report was chordoma. Follow-up CT scan showed complete excision of
the tumor (Fig. 28.9). Four weeks later the patient left the hospital, walking unassisted,
and flew back home.
Case 2
An Indian man, 56 years old, complained of gradually progressing left hemiparesis of
6 months' duration. This was accompanied by emotional instability and a complete fifth
cranial nerve lesion.
His CT scan showed a petroclival mass destroying the clivus and the petrous apex and
compressing the third ventricle, producing secondary obstructive hydrocephalus (Fig.
28.10). A ventricular shunt was performed in India. After verification of the benign
nature of the tumor (meningioma) through a stereotoaxic biopsy, the patient was referred
to our clinic.
The modified pterional approach was carried out for total removal of the tumor. After
removal of the supratentorial part, the tentorium was incised, the superior petrosal sinus
was coagulated and transected, and the petrous apex was drilled out to the internal
auditory meatus. Because of the previous clinical loss of
trigeminal nerve function and its infiltration by the tumor, the trigeminal as well as the
trochlear nerves were sacrificed to allow complete removal of the tumor.
The patient had an uneventful postoperative course. He left the hospital 4 weeks later
completely recovered from his hemiparesis.

Giant Space-occupying Lesions Involving the Posterior Part of the Third Ventricle
The pineal region may show a wide variety of pathological processes, ranging from the
most malignant to the most benign (21). These tumors indent the posterior aspect of the
third ventricle or infiltrate its wall, finally filling the ventricular cavity. The most
common tumors in this region are the so-called germinomas or pinealomas of the two-
cell pattern type (PTC) (23). Other lesions that may sometimes reach huge sizes are
falcotentorial meningiomas, teratomas, and pineoblastomas. The strategy for
management of these pathological processes is still a matter of controversy.
Germinomas or the two-cell pattern type of pinealom is radiosensitive. Therefore some
advocate radiation alone or radiation plus ventricular shunting as the established
treatments. The greatest criticism against direct operation is the anticipated significant
operative mortality and the increased probability of dissemination metastases in the CSF.
With the recent advances in the technology of diagnosis, improved pre- and post-
operative management, and the perfection of operative techniques, no significant
operative risk is encountered when dealing with these tumors.
It seems also that reduction of the bulk of the neoplasm by direct operation, even if
that neoplasm is radiosensitive, is important for the effectiveness of radiotherapy. Sano
(20, 22) also reported no increased incidence of dissemination metastases in his series of
operated patients with such tumors. By using the conservative line of management we
can miss patients harboring benign lesions that could be cured completely by a direct
attack.
In our clinic we manage these cases by direct surgical attack. The following treatment
(radiotherapy, chemotherapy) will depend on the pathological character of the tumor.
Usually a preliminary idea of the pathological classification of the tumor is obtained
before operation from radiography (CT scan, angiography, MRI) and hormonal assay
(alpha-fetoprotein (AFP), human chorionic gonadotropin (HCG)) in the serum and CSF.
Several approaches have been proposed for the excision of tumors in
the pineal region. These include the parietal transcallosal (2, 25), the occipital or
parietooccipital transtentorial (1, 15), the infratentorial Supracerebellar (8, 24), the
posterior transventricular (32), and the frontal or anterior transcallosal approach (20).
The infratentorial Supracerebellar approach is preferred for most tumors invading the
pineal region because the access is not obstructed by the deep venous system that caps
the dorsal and lateral aspects of pineal tumors. The occipital transtentorial approach is
used only for tumors above the tentorial edge if there is no major extension to the
posterior fossa or opposite side and for those located above the vein of Galen. In the
infratentorial Supracerebellar approach the patient is in the semisitting position. Some
surgeons prefer the concorde position (7). The head and neck is flexed to bring the
tentorium near the horizontal plane. A vertical midline incision is used. The suboccipital
craniectomy extends above the lower edge of the torcular and both transverse sinuses.
The dural incision extends up to the inferior margin of the transverse sinus. Gravity
assists the cerebellum in falling down away from the tentorium cerebelli. The straight
sinus and tentorium may be elevated with a retractor and the vermis is retracted gently
inferiorly. Bridging veins over the superior surface of the cerebellum may be coagulated
and transected without risk. Incision of the arachnoid over the quadrigeminal cistern
brings the tumor and deep venous system in view. The vein of Galen and the internal
cerebral veins are above the tumor. The precentral vein is posterior, the thalamus, the
medial posterior choroidal and posterior cerebral arteries, and the basal veins are lateral.
The superior cerebellar arteries and veins are below.

Case 1
A 15-year-old boy presented in a stuporous state. His symptoms had begun 2 years
previously with headache and diabetes insipidus followed by bilateral hearing
disturbance. On examination the patient had bilateral papilledema and a positive
Parinaud's sign. A CT scan showed a hyperdense space-occupying lesion in the pineal
region with hydrocephalus (Fig. 28.11, A and B).
A ventricular shunt was inserted. After his general condition improved, excision of the
tumor was accomplished through a Supracerebellar subtentorial approach.
Postoperatively the patient showed an excellent recovery; his follow-up CT scan
demonstrated complete excision of the tumor (Fig. 28.11С). The tumor excised was
histopathologically verified as a teratoma with malignant changes. The patient received
postoperatively deep x-ray therapy as a supplementary treatment.

References
1. Ausman J: A new operative approach to the pineal region. In Samii M (ed):
Surgery in and around the Brain Stem and Third Ventricle. Berlin, Sprin
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2. Dandy W: An operation for the removal of pineal tumours. Surg Gynecol
Obstet 33:113-119, 1921.
3. Hardy J, Vezina JL: Transphenoidal neurosurgery of intracranial neoplasm.
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4. Hirsch JF, Zouaoui A, Renier D, Pierre K: A new surgical approach to the
third ventricle with interruption of the striothalamic vein. Acta Neurochir
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5. Kempe LG: Operative Neurosurgery. Berlin, Springer-Verlag, 1968, vol 1.
6. King TT: Removal of intraventricular craniopharyngioma through the lamina
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8. Krause F: Operative Freilegung der Vierhugel nebst Beobachtungen uber
Hirndruck und Dekompression. Zbl Chir 35:2812-2819, 1926.
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DM, Chou SN: Transcallosal removal of craniopharyngioma within the third ventricle. J
Neurosurg 39:563-567, 1973.
11. Malis LI: Surgical resection of tumours of the skull base. In Wilkins RH,
Rengachary SS (eds): Neurosurgery, 1985, pp 1011-1021.
12. Michio O, Makiko O, Rhoton Jr AL: Microsurgical anatomy of the region of
the tentorial incisura. J Neurosurg 60:356-399, 1984.
13. Mitterwallner FV: Variationsstatistische Untersuchungen an den basalen
HintergefaBen. Acta Anat [Basel) 24:51, 1955.
14. Perneczky A, Horaczek A: Approaches to the tentorial edge, demonstrated by
references to 30 cases of tentorial meningiomas. Adv Neurosurg 13:186-
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15. Poppen JL, Marino R Jr: Pinealomas and tumours of the posterior portion of
the third ventricle. J Neurosurg 28:357-364, 1968.
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17. Rand R: Transfrontal, transphenoidal craniotomy in pituitary and related
tumours. In Microneurosurgery, ed 3, 1985, pp 135-145.
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Part 2. Operative approaches. Neurosurgery 8:357-373, 1981.
19. Samii M: Olfactory nerve. In Samii M, Jannetta PJ (eds): The Cranial Nerves.
Berlin, Springer-Verlag, 1981.
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21. Sano K: Pineal region tumours: Problems in pathology and treatment. Clln
Neurosurg 30:39-91, 1983.
22. Sano K, Matsutani M: Pinealoma (germinoma) treated by direct surgery and
postoperative irradiation: A long-term followup. Child's Brain 8:81-97, 1981.
23. Sano K, et al: Brain Tumour Registry in Japan, 1981, vol 3.
24. Stein BM: The infratentorial Supracerebellar approach to pineal lesions. J
Neurosurg 35:197-202, 1977.
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series of 19 cases. J Neurosurg 23:565-571, 1965.
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craniotomy for anterior communicating artery aneurysms and functional
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27. Suzuki J, Katakura R, Mori T: Interhemispheric approach through the lamina
terminalis to tumours of the anterior part of the third ventricle. Surg Neurol
22:157-163, 1984.
28. Sweet WH: Recurrent craniopharyngioma. In Edwards JMR (ed): Topical
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29
Cerebrospinal Fluid Diversion
J. Gordon McComb, M.D., and F. Miles Little, M.D.

Cerebrospinal Fluid Dynamics

The multiple functions of cerebrospinal fluid (CSF) coupled with its
fairly rapid turnover indeed make CSF "the third circulation" as first
referred to by Cushing (2). The circulation of CSF throughout the central
nervous system is maintained primarily by the hydrostatic difference
between newly formed CSF within the ventricles and parenchyma and
that at its sites of absorption. Less important factors influencing CSF
circulation are associated with pulsations of the brain and choroid plexus
from the arterial tree, respiratory variations, changes in bodily position,
and ciliary action of the ependyma and choroid plexus epithelium.
CSF is produced in all four ventricles although the majority originates
from the lateral ventricles, consistent with the larger amount of choroid
plexus tissue present in the lateral as compared with the midline ventri-
cles. The lateral ventricles are joined together at the anterior superior
aspect of the third ventricle by the foramina of Monro, each of which
measures less than a centimeter at its greatest diameter. Obstruction to
CSF flow can occur at one or both of these foramina by a fairly small
mass. The third ventricle, normally only 3 to 5 mm in width, drains into
the aqueduct of Sylvius, the diameter of which usually measures only 2
mm. The relatively long and narrow aqueduct of Sylvius is the most
frequent site of obstruction within the ventricular system. Tumors in and
around the third ventricle can either obstruct the CSF before it enters
the third ventricle from the lateral ventricles or prevent its egress from
the posterior portion of the third ventricle into the aqueduct of Sylvius.
The first step in the formation of CSF is the passage of an ultrafiltrate
of plasma through the non-tight junctioned choroidal capillary endothe-
lium by hydrostatic pressure into the surrounding connective tissue
stroma beneath the epithelium of the villus. The ultrafiltrate is subse-
quently transformed into a secretion (namely, CSF) by an active metabolic
process within the choroidal epithelium via a mechanism that is largely
speculative. Approximately 80 to 90% of CSF formation occurs at the
choroid plexus with the remainder being produced in the parenchyma,
most likely at the capillary-glial complex. The CSF formation rate is about
20 ml per hour or 500 ml per day. Because the total amount of CSF in
the ventricles and subarachnoid space (SAS) in the adult averages ap-
proximately 150 ml, a threefold turnover of CSF occurs daily. Production
of CSF is only slightly pressure-responsive and does not diminish notice-
ably until cerebral prefusion pressure is markedly reduced» interfering
with the first step in CSF production, reducing the quantity of ultrafiltrate
from the choroidal capillary.
Absorption of CSF and its constituents depends upon bulk flow in
addition to passive or facilitated diffusion and active transport of specific
solutes. With the single rare exception of CSF overproduction by a choroid
plexus papilloma, hydrocephalus results from impaired CSF absorption.
Production of CSF in hydrocephalus is either normal or nearly normal.
In compensated hydrocephalus, the rate of absorption must equal the
rate of formation, approximately 500 ml per day, and in the noncompen-
sated state only a small fraction of the total amount secreted is retained;
thus the overwhelming majority of CSF output is still absorbed. As CSF
formation is relatively constant, the change in resistance to absorption
determines CSF pressure and whether the hydrocephalus is progressive.
Impairment of CSF absorption in communicating hydrocephalus could
occur at some or all of the following sites: the arachnoid villus, the
lymphatic channels associated with cranial and spinal nerves, the lym-
phatic channels in the adventitia of the cerebral vessels, or the arachnoid
membrane. If CSF outflow from the ventricles is blocked (i.e., noncom-
municating hydrocephalus), fluid flow could still take place via the Pierre-
Robin spaces surrounding the blood vessels and the extracellular space
of the cortical mantle to reach the SAS on the brain's surface. Assuming
a complete blockage within the ventricular system, which is not always
the case, additional ways for CSF to exit the ventricles would be through
a fistulous opening created by rupture of the ventricular system into the
SAS at a location such as the lamina terminalis or suprapineal recess.
CSF drainage could then occur as if the ventricular obstruction did not
exist (15). The question of whether CSF can be absorbed by the brain has
been debated for some time. Penetration of substances into the periven-
tricular region of the hydrocephalic animal has been well documented.
With the advent of computerized tomographic (CT) scanning, periventric-
ular hypodensity may be noted in the presence of hydrocephalus and has
been shown to be the result of CSF migrating into the area surrounding
the ventricles in the face of increased intraventricular pressure (ICP).
CSF in the parenchyma, indicative of migration, does not necessarily
equate with absorption. The extracellular space in the brain, which
amounts to 15%, readily allows fluid flow in the parenchyma under
normal physiological conditions and its velocity and direction is respon-
sive to changes in hydrostatic and osmotic pressure gradients. Macro-
molecules injected into the CSF of the ventricles or SAS have been
observed to penetrate readily the extracellular space of the parenchyma
and vice versa, there being no barrier to free movement across either the
ependyma or the pial membranes. Evidence thus supports the contention
that the brain, rather than absorbing CSF, is acting as a conduit for fluid
to move from the ventricles through the parenchyma to the SAS. With
very high ICP, it is possible that absorption of CSF may also occur via the
choroid plexus. This would involve the flow of CSF (or extracellular fluid
within the parenchyma) into the stroma of the choroid plexus from the
subependymal region. Absorption of CSF into the blood could take place
via the choroidal capillaries as these capillaries are of the fenestrated
type and thus do not have tight junctions. There is no evidence to support
CSF being absorbed by the parenchymal capillary epithelium. This does
not preclude, however, net water changes between the parenchymal
extracellular fluid and blood when dysequilibrium in the blood-brain
osmotic gradient occurs as there is no barrier in this regard.
Ventriculostomy
General Considerations
The initial management of hydrocephalus associated with tumors in or
about the third ventricle often requires CSF diversion. This may be
accomplished either by placing a ventriculostomy or by inserting an
extracranial shunting system before a direct surgical procedure of the
third ventricle. We prefer a ventriculostomy to a shunt followed by an
attempt to reestablish CSF circulation at the time of tumor removal,
thereby obviating the need for a shunt if this is successful. Also, placing
a ventriculostomy and keeping the ventricles somewhat dilated by drain-
ing CSF only if the ICP exceeds 15 to 20 torr will permit further de-
compression of the ventricles interoperatively, improving exposure to the
third ventricular region. With a permanent shunting system in place, the
ventricles may come down to normal size by the time of the definitive
operative procedure and this opportunity will have been lost. In the
immediate postoperative period the presence of a ventriculostomy will
allow monitoring of ICP as well as determination of whether CSF circu-
lation has been adequately reestablished.
Operative Corridor: Anatomy and Physiological Risks
The ventriculostomy insertion site is usually the frontal or parietal
region. The right side is usually chosen as it is rarely the dominant
hemisphere. If one lateral ventricle is significantly more dilated than the
other, ventriculostomy placement should be into the larger ventricle. Our
personal preference for site of ventriculostomy insertion is the frontal
region under most circumstances because in such a location (a) the
ventriculostomy can be placed more easily in an intensive care unit (ICU)
setting; (b) the external landmarks are more readily apparent; (c) smaller
ventricles may be more easily cannulated, decreasing the risk for damage
to other structures; (d) the frontal region is easier to bandage; (e) there is
less problem with the patient lying on the bandage or tubing; and (f) if
it is necessary to insert a permanent CSF-diverting shunt, the ventricu-
lostomy in the frontal region would not be in the operative field at the
posterior parietal region, our preferred site for the insertion of a perma-
nent diverting system. Physiological risks are approximately the same
when comparing the frontal and parietal approaches, with the one excep-
tion of an increased risk of hemiparesis if the catheter is passed through
the internal capsule. A possible risk with frontal insertion is that of
damage to the hypothalamic structures if the tubing is passed through
the lateral ventricles and into the floor of the third ventricle. CT scans
have shown on more than one occasion that the tip of the catheter has
obviously gone into the hypothalamic region without any clinical evidence
of dysfunction.
Structural Definitions
Initial diagnostic studies are either CT scanning with or without con-
trast agent and magnetic resonance imaging (MRI). Angiography is not
necessary unless the mass might be vascular. If a question exists as to
whether adequate communication is present between the lateral ventri-
cles via the foramina of Monro, metrizamide can be placed into the
ventricular system once the ventriculostomy is in place. Small obstructing
lesions in the posterior portion of the third ventricle can be more accu-
rately outlined with metrizamide.
Operative Technique
To diminish the incidence of infection, which is the primary ventricu-
lostomy complication, strict attention to aseptic technique is very impor-
tant whether the ventriculostomy is placed in an ICU setting or in the
operating room. Hair is removed for a considerable distance around the
planned site of ventriculostomy insertion; in fact, in most instances it is
probably just as well to remove all of the hair as it will be necessary to do
so later at the time of the definitive procedure. The skin is scrubbed with
alcohol and a degreasing agent (such as Freon) and then well prepared
with povidone-iodine (Betadine) solution.
At the site of planned incision, the skin is injected with lidocaine
containing epinephrine. In the child or adult, a linear incision 1 cm long,
is made 1 to 2 cm anterior to the coronal suture in the midpupillary line
(Fig. 29.1 A and B). The coronal suture is used as a site of entry in the
infant. A hand or twist drill may be used to make the opening through
the skull. A hand drill is faster and easier but is less safe than the twist
drill. In the infant or young child in whom the skull is not thick, a smaller-
diameter drill can be used. In the older child or adult, a larger hole is
necessary. It is easier to make the initial hole with a smaller diameter bit
followed by a larger one rather than using the larger diameter drill at the
outset. Keeping the head in a midline position with the face exposed will
provide visualization of the external landmarks and thereby promote a
more accurate placement of the ventriculostomy (Fig. 29.1С). A #11 blade
is used to make certain that the inner table of bone has been adequately
removed and to incise the dura mater. This makes it less likely that the
dura mater will be stripped from the ventriculostomy entrance site and
decreases the chance of an epidural hematoma.
For the past several years we have been using a ventriculostomy tube
modified by Holter-Hausner (Fig. 29.1С). This tubing has several advan-
tages over the others presently available. The holes at the distal end of
the catheter are covered with another layer of tubing containing longi-
tudinal slits. The overcovering slits make it less likely that the holes will
be plugged with brain on catheter entry. In addition, if the ventricles
should collapse around the tubing, the holes are protected and have a
greater chance of remaining patent. Markers are placed on the tubing at
5-, 10-, and 15-cm intervals, allowing one to know the depth of penetra-
tion without having to resort to the use of a ruler. Tabs are bonded to the
tubing and easily pass with it when making a subcutaneous tunnel. The
tabs are sewn to the scalp to prevent dislodgment.
The tubing is passed through the twist drill hole perpendicular to a
tangent at the plane of the site of insertion with the tip directed toward
the middle of the nose. (Fig. 29.1С). Unless the ventricle is markedly
dilated, it is usually entered 5 to 7 cm beneath the skin surface, which is
often confirmed by CSF emerging from the end of the tubing. The stylette
is removed from the tubing and a curved, flanged trocar is attached to
the end of the ventriculostomy tubing and secured with a suture (Fig.
29.2A). Using the catheter entry site, one pushes the trocar under the
skin so as to exit 5 or more cm from the point of insertion, thus creating
a subcutaneous tunnel through which the tubing is pulled (Fig. 29.2B).
Care is taken not to disturb the placement of the tube tip within the
ventricular system. The trocar is removed and patency is checked again
to make certain that CSF is freely flowing from the catheter. A Luer-lok
tip is placed on the tubing along with a 1 -ml tuberculine syringe to prevent
any further loss of CSF (Fig. 29.2С). The Luer-lok tip is secured to the
tubing with a suture. At the initial site of entry, the skin is closed with a
single horizontal mattress suture. As the tube exists from the subcuta-
neous tunnel it is secured to the skin in a manner similar to that of a
chest tube by wrapping a suture affixed to the skin several times around
the tubing and tying it. The tubing is then brought anteriorly in a gentle
loop and the two tabs are sutured to the skin to provide additional security
against dislodgment (Fig. 29.2C). The wounds are covered and taped. A
tape mesentery is made for the tubing to secure the catheter to the head
(Fig. 29.2D). Using pressure (arterial type) tubing the ventriculostomy
catheter is connected to a transducer to monitor ICP and/or drain CSF.
With the ventriculostomy placed in such a location the patient has good
mobility of the head and the head does not rest upon the tubing or
dressing.
Complications
The principle complication is infection. In a pediatric series of over 250
ventriculostomies, our infection rate was between 2 and 3%. The duration
of monitoring averaged 7 days. The infection rate did not seem to be
related to the duration of placement, leakage of CSF at the catheter site,
or whether the ventriculostomy tubing was tunneled, but rather to factors
that reduced the patient's resistance to infection. Tunneling has de-
creased the incidence of CSF leakage, however. There have been no
wound infections. Approximately three-quarters of the infections were
from staphylococcal organisms (half Staphylococcus epidermidis and
the other quarter Staphylococcus aureus). Prophylactic antibiotics have
not been used routinely. Another major complication would be a hema-
toma (epidural, subdural, or intraparenchymal) at the site of the ventric-
ulostomy. This is a rare complication and most often has been associated
with a known or unsuspected coagulation disorder. Although possible,
we have not encountered either hemiparesis or hypothalamic dysfunction
associated with ventriculostomy placement. Seizures originating at the
site of insertion are another risk. As these patients often have one or
more reasons to experience seizures, it is usually not possible to ascribe
seizures to the ventriculostomy insertion site unless electroencephalo-
gram (EEG) tracings show epileptiform activity localized to the appropri-
ate site and not elsewhere.
Utilization
It is thought that a ventriculostomy can be used in the situation where
a mass in or adjacent to the third ventricle has obstructed CSF flow
resulting in ventricular enlargement and raised ICP. We prefer the place-
ment of a ventriculostomy to a definitive shunting procedure because a
permanent shunt may not be necessary if the obstruction to normal CSF
flow can be surgically removed. In addition, it is helpful to have dilated
ventricles at the time of the definitive operative procedure as deflating
them will allow further access to deep midline structures. A ventriculos-
tomy will also allow monitoring of ICP postoperatively. The ventriculos-
tomy can be placed in the ICU setting without having to bring the patient
to the operating room as would be necessary for the placement of a
permanent CSF-diverting shunt. The major complication to the placement
of a ventriculostomy is infection, the incidence rate of which should be
5% or under (this is the same as for a permanent shunt). Most infections
are fairly easily cleared with appropriate antibiotic therapy, especially if
the ventriculostomy can be removed, and are usually not associated with
any permanent sequelae.
Intracranial CSF Diversions
Historical and General Considerations
Dandy (3) performed the first operative procedure for the treatment of
hydrocephalus by fenestrating the anterior third ventricle. He had pre-
viously abandoned fulguration of the choroid plexus and cannulation of
the aqueduct of Sylvius because of their high mortality and failure rates.
He, as well as others, had also found that sectioning of the corpus
callosum or incision of the cortex to allow CSF to escape from an ob-
structed ventricular system was rarely successful. Dandy did not have
much enthusiasm for Torkildsen's procedure of using a tube to divert
CSF from the ventricles into the cisterna magna as he thought that the
rate of obstruction was higher than with third ventriculostomy. As White
and Michelsen (34) pointed out (in the pre-CT and MRI scanning era) the
Torkildsen procedure permitted the surgeon to explore the posterior fossa
before placing the shunt. An anterior third ventriculostomy could relieve
the symptoms associated with hydrocephalus and raised ICP, thereby
masking the presence of a surgically resectable mass in the posterior
fossa.
In 1932 Dandy (4) significantly modified his operative procedure for
third ventriculostomy and advocated a temporal rather than subfrontal
approach, as the former avoided sacrificing an optic nerve and diminished
the chance of CSF collecting on the surface of the brain to produce an
"external hydrocephalus." It was not until 1945 that Dandy (5) reported
his full series of 92 cases of hydrocephalus treated by an open operative
anterior third ventriculostomy. The mortality was 12% with 50% good
results; most of the failures were in infants less than 1 year of age. It
became evident that success was dependent upon the patency of the
subarachnoid drainage pathways outside the ventricular system rather
than on the technique of third ventricular fenestration. Dye circulation
studies sometimes were useful in determining such patency, but often
were not. It also became evident that the chance of reestablishing ade-
quate CSF flow in the subarachnoid pathways in congenital hydroceph-
alus was considerably less likely than in an acquired form.
Scarff (25-27, 29) for decades reminded us of the benefits of third
ventriculostomy while an ever-increasing assortment of shunting devices
carried the day as the standard treatment for hydrocephalus.
Mixter (19) was the first to report an endoscopic means of fenestrating
the third ventricle into the surrounding cisterns. This technique has more
recently been updated by Vires (32). In the last decade most third ventri-
culostomies have been accomplished by stereotaxis (9, 24) with virtually
no attention being given to an open operative procedure not associated
with an attempt to biopsy or remove a mass lesion in or about the third
ventricle. Percutaneous stereotaxic methods, which have been even fur-
ther refined with CT-guided assistance, have markedly reduced the mor-
tality and morbidity associated with third ventriculostomy, but this tech-
nique will not increase the rate of success for it is tied to the patency of
the CSF drainage pathways beyond the ventricular system, the adequacy
of which is difficult to ascertain beforehand.
Utilization
Third ventriculostomy is very appealing as it poses the chance to
reestablish physiological CSF circulation without having to insert foreign
bodies and eliminates all of the problems associated with these devices.
For a third ventriculostomy to succeed it is essential that the resistance
to CSF drainage beyond the ventricular system be within the normal
range. As the majority of cases with obstruction to CSF flow in and
around the third ventricle are acquired rather than congenital it seems
that there would be a much greater likelihood that the subarachnoid
pathways for CSF drainage would be adequate and thus a third ventri-
culostomy would be successful. Unfortunately, there is still a significant
failure rate even when an attempt is made to preselect carefully the
patients for this procedure. We are not confident that the clearance
studies using radiopharmaceuticals are all that reliable in determining the
adequacy of the CSF pathways beyond the ventricular system. We have no
experience with either endoscopic or stereotaxic procedures
for third ventriculostomy because it is our practice to insert an extra-
cranial CSF-diverting shunt if it has not been possible to reestablish
normal CSF circulation at the time of the third ventricular operative
procedure. If removing the obstructing mass has not resulted in the
reestablishment of normal CSF circulation, especially if the third ventri-
cle has been fenestrated at its floor, the lamina terminalis, or the supra-
pineal recess in the process of or in addition to tumor removal, the
likelihood of accomplishing normal CSF circulation by a subsequent
endoscopic or stereotaxic procedure is remote (Fig. 29.3). In the current
era of fairly reliable extracranial CSF shunting systems, it seems that
most attempts at third ventriculostomy are made in frustration, after
repeated shunt failures in patients with nonmalignant disease. The oc-
casional and relatively isolated enthusiasm for third ventriculostomy is
neither catching nor sustained. Even if third ventriculostomy is success-
ful in restoring normal CSF circulation it is necessary to follow these
patients routinely with CT or MRI scanning for some will subsequently
develop progressive hydrocephalus and require extracranial CSF diver-
sion.

Extracranial CSF Diversion

Historical and General Considerations
Torkildsen in 1939 (31) produced the first clinically practical method
to divert CSF past an obstruction in the ventricular system by inserting
a rubber tube between the ventricles and the cisterna magna. This type
of shunt did not require a valve but did necessitate that the hydrocephalus
be noncommunicating. Irrespective of whether or not the hydrocephalus
is noncommunicating, it is not always possible to tell beforehand whether
diverting CSF into the SAS from the ventricles will successfully control
the hydrocephalus. Although a lateral decubitus position can be used, in
the past most patients were placed prone to insert a ventriculocisternal
or ventriculocervical (VC) shunt, requiring more set-up time and incurring
more anesthetic risk than if the patient were supine. In addition it is
necessary to do an occipital craniectomy or a cervical laminectomy to
insert the distal end of the shunt into the SAS. Revision of the distal end
of the shunt is also cumbersome. For these reasons and with the devel-
opment of pressure-regulated one-way flow valves, the VC shunt is only
occasionally used today.
The modern extracranial shunting era for noncommunicating hydro-
cephalus began in 1949 when Matson introduced diversion of CSF into
the ureter (13). The subsequent development of new synthetic materials
and pressure-regulated one-way flow valves in the 1950s (20, 22, 23)
subsequently made this shunting procedure unnecessary and avoided the
sacrifice of a kidney. In addition the ureteral shunts were associated with
such severe complications as gram-negative ventriculitis and life-threat-
ening dehydration in infants (14). Steady improvement in shunting hard-
ware associated with a progressive decline in shunt-related complications
have made extracranial shunting the procedure of choice when direct
surgical removal of an obstruction is not feasible. As noted previously,
we prefer the use of a ventriculostomy to initial shunting if it seems that
CSF circulation may be reestablished by surgical removal of the obstruc-
tion in or about the third ventricle. The ideal shunt would be free of all
complications and would drain the right amount of CSF on a minute to
minute basis so as to maintain the appropriate normal physiological
intraventricular pressure at all times. Such a goal is obviously not obtain-
able with any implanted mechanical device.
 Extracranial CSF-diverting shunts commonly in use today include the
ventriculoperitoneal (VP), ventriculopleural (VP1), ventriculoatrial (VA),
and lumboperitoneal (LP) varieties. Until 10 to 15 years ago the VA shunt
was the type most frequently inserted as it had the highest degree of
success. The VA shunts have been largely supplanted by VP shunts as
the latter are technically easier to insert or distally revise; have less
severe complications, even though the incidence of such for the two types
is similar; and, although not a factor in the adult, lengthening of the
shunt can be avoided as enough tubing can be placed into the infant's
abdominal cavity to allow for growth into adulthood. VA shunts inserted
in infants and children necessitate elective lengthening of the distal end
on one or more occasions so that the tip is properly positioned in the
atrium, a consideration not relevant in the adult patient. The development
of newer silicone elastomers and the insertion of enough tubing to allow
the abdominal end to migrate freely about the peritoneal cavity have
largely eliminated the problem of distal obstruction and allowed the VP
shunt to supplant the VA variety. On our service, a pediatric one, less
than 1 % of shunt insertions or revisions are of the VA type.
The shunt that we use next most frequently after the VP variety is the
VP1 type. The technical ease of inserting the distal end into the pleural
space is very nearly equivalent to that of insertion into the peritoneal
cavity (in fact probably even easier in the obese patient), and the incidence
and severity of complications is about the same. This form of shunt,
however, cannot be used in infants and children as the absorptive capac-
ity of the pleural space is often not adequate and hydrothorax develops.
In the adolescent or adult patient this is rarely a problem. An advantage
to using a VP1 shunt is that the distance required to enter the pleural
cavity is less than that when the shunt is directed into the abdominal
cavity.
As obstruction to CSF flow in and about the third ventricle produces a
noncommunicating form of hydrocephalus, a LP shunt cannot be used
so there need be no further discussion of this type of shunt.
Whereas lesions in the posterior third ventricle rarely produce hydro-
cephalus that obstructs CSF flow from one lateral ventricle to another,
this happens with some frequency with lesions situated in the anterior
portion of the third ventricle where one or both of the foramina of Monro
can be blocked. Removal of an anteriorly located third ventricular mass
can often reestablish the communication between the two lateral ventri-
cles, but if questionable it is suggested that the septum pellucidum be
fenestrated. If it is necessary to place catheters in both lateral ventricles
at the outset to control progressive hydrocephalus, the two systems can
be connected, requiring only one distal tube. What frequently happens,
however, is that a catheter placed in one lateral ventricle initially drains
both lateral ventricles satisfactorily. Then with subsequent tumor growth
or scarring, the two ventricular systems become isolated. The patient
may be symptomatic with evidence of raised ICP or the problem may be
detected only on routine follow-up CT or MRI studies. At this point it
becomes necessary to place a second ventricular catheter in the nondrain-
ing lateral ventricle. The choice in this situation would be either to
connect the second ventricular catheter to the existing shunt or to insert
an entirely separate new shunt. The technical ease of putting in a
completely new second shunt is probably equivalent to that of connecting
it into the existing shunt in the infant or child, but most likely not for
the adult. The advantage of two completely separate shunts is that they
facilitate the diagnosis and treatment of shunt malfunction and some-
times infection.
 If the proper cephalic skin incision site is not outlined before draping,
orientation can be lost and the entry site can be placed over the superior
sagittal sinus. The superior sagittal sinus often can be just to the right of
midline in the posterior parietal area and may account for the tendency
to place the catheter entry site too far laterally. With growth of the skull
in infants it has been observed that the entry site will migrate laterally,
resulting in the ventricular catheter having a definite curve whereas
initially it was straight.
It is important that the skin incisions be placed so that they are adjacent
to and not directly over the shunt hardware, particularly in infants where
the scalp is thin, as this will lessen the incidence of wound breakdown
and resultant shunt infection. Thought must be given to the location of
the incisions and various shunt components in regard to possible future
shunt revisions.
Operative Corridor: Anatomy and Physiological Risks
Whereas we prefer a frontal location to insert a catheter for a ventri-
culostomy we advocate a posterior parietal location for the placement of
a permanent shunt. Disadvantages of the frontal approach include more
extensive hair shaving and scalp preparation and an additional skin
incision needed in the posterior parietal region as it is very difficult in
the infant and almost impossible in the adolescent or adult to tunnel the
catheter from the frontal area to the distal entry site. Minimizing the
number of skin incisions should lead to a lower shunt infection rate. If
the tubing is tunneled too close to the ear the wearing of glasses becomes
a problem. The rationale for placing the tip of the ventricular catheter in
the frontal horn, anterior to the foramen of Monro, is that the absence of
choroid plexus tissue in this region reduces the chance that the ventric-
ular catheter will be obstructed. The advantage of the frontal approach
is a shorter distance into the ventricle and less chance that the catheter
could be passed through the hemisphere without reaching the ventricle,
a problem when the ventricles are not significantly enlarged. We have
not found this to be a particular problem with the posterior parietal
approach if the projection of the frontal horn has been properly marked
to provide good intraoperative orientation showing where to pass the
ventricular catheter. The expanding use of intraoperative ultrasound will
also be of benefit in canulating the lateral ventricle at the desired site of
entry. The lateral ventricle is most easily entered posteriorly at the site
of the occipital horn projected on to the skin surface. Many published
drawings show the ventricular catheter being inserted anterior to and
often inferior to this location.
As noted in the ventriculostomy section, a risk to a frontal approach
includes passing the catheter through the lateral ventricles into the basal
ganglia or through the floor of the third ventricle into the hypothalamic
structures. The chance of producing neurological sequelae with inadvert-
ent misdirection of the ventricular catheter from the frontal approach
seems to be roughly equivalent when the entry site is from the occipital
horn.
A subxiphoid midline abdominal incision is preferred to a subcostal
incision as it is easier to reach the peritoneum without having to traverse
muscle layers. If the midline is not available a subcostal incision is used.
If it becomes necessary to reposition the catheter later in the abdominal
cavity it is easier to use a new site of entry rather than trying to trace the
established tract into the peritoneal cavity. A new entry site will also
reduce the risk of injury to a viscus.
Determining the site of entry into the pleural cavity must take into
consideration the location of the neurovascular bundle, which lies under
the rib. Staying on the superior surface of the lower rib of the intercostal
space chosen avoids this possible problem. It is also necessary to appre-
ciate the location of the internal mammary artery and vein running a
centimeter or two lateral to the border of the sternum so as to avoid these
vessels. The only other concern is not to enter the chest so low that the
diaphragm is encountered. For cosmesis, an incision just below the breast
is often used. If cosmesis is of no concern or the patient is obese, the
second-third interspace in the midclavicular line is technically easier.
The quantity of air entering the pleural cavity has not been a problem. It
is not necessary to place a chest tube.
For an atrial shunt, a neck incision is made midway between the
mandible and the clavicle. This allows ready access to the carotid sheath
and the common facial vein. The incision is made parallel to the creases
in the neck to minimize scarring. Structures at risk in the carotid sheath
are the common carotid artery, internal jugular vein, and vagus nerve. If
the common facial vein is available, it is simpler to introduce the atrial
catheter into this vein than directly into the internal jugular vein. With
atrial shunt placement it is necessary to ensure that no significant air
embolus occurs. Use of a soft pliable catheter will avoid the possibility of
perforating the vascular system and subsequent complications that this
might cause.
Structural definitions
As noted in the ventriculostomy section the diagnostic studies are either
CT scanning with and without contrast or MRI. If a question exists as to
whether adequate communication is present between the two lateral
ventricles metrizamide can be placed into the ventricular system.
Operative Technique
Ventriculoperitoneal Shunt
The patient is placed in the upper right corner of the table with the
head turned to the left. This allows the anesthesiologist complete access
to the airway (Fig. 29.4A). In infants, an esophageal stethoscope is used
to avoid placing a stethoscope over the chest in the region of the operative
field. A doughnut made of any soft material is placed under the head.
Padding is also placed beneath the neck to make the angle between the
head and chest as flat as possible, thereby making it easier to pass the
tubing subcutaneously from the head to the abdomen. It is helpful to
place a rubber button, taken from a medicine bottle, on the patient's
forehead in a position representing the anterior surface projection of the
right frontal horn (Fig. 29.6B). The patient's skin is shaved and prepared
with soap, alcohol, and a degreasing agent (such as Freon) and then is
well prepared with povidone-iodine (Betadine) solution. A thorough skin
cleansing should markedly reduce the skin bacterial count and presum-
ably lower the incidence of shunt infections as it is thought that skin
contamination accounts for a significant percentage of shunt infections.
Excess povidone-iodine is removed with more alcohol to ensure better
adherence of a barrier drape to the skin. The skin is sprayed with an
adhesive (such as Vidrape) to ensure better adherence of the barrier
drape. At this step in the procedure, the incisions are outlined with a
skin marker to ensure proper orientation before draping. Cloth towels are
placed at some distance from the incision sites to prevent the barrier
drape from sticking to the endotracheal tube, i.v.s, etc. A barrier drape
impregnated with povidone-iodine (Ioban) is placed over the exposed skin.
Care is taken to ensure that the barrier drape adheres well to the skin,
particularly at the incision sites. Paper drapes, impenetrable to liquid,
are placed closer to the proposed incision sites. A second layer of paper
drapes are then placed around the patient and operating table. The skin
is injected with 0.25% lidocaine and 1:400,000 epinephrine solution to
decrease bleeding.
A small curvilinear incision is made in the right posterior parietal area
in the region of the projection of the occipital horn to the skin surface
(Fig. 29.4). The scalp is reflected. A cruciate incision is made in the
periosteum, which is elevated enough to allow a perforator to make a hole
through the underlying bone (Fig. 29.5A). The wound is next covered
with a sponge moistened with either Ringer's lactate containing bacitra-
cin or povidone-iodine and is covered with a towel to prevent contami-
nation.
Attention is then directed to the abdomen where a subxiphoid midline
incision is made through the abdominal wall until the peritoneum is
encountered and two 4-0 absorbable sutures are placed into the perito-
neum without opening this membrane. This eliminates hunting for the
opening subsequently.
A shunt tube passer is then tunneled from the cephalic to the abdominal
incision without making any additional incisions along the pathway and
the tubing is implanted subcutaneously (Fig. 29.5B and C). The perito-
neum is opened and the remainder of the tubing is placed into the
abdominal cavity (Fig. 29.5D). We are using abdominal tubing 120 cm
long even in newborn infants to eliminate the subsequent need to
lengthen the shunt. The tubing is flushed with Ringer's lactate containing
bacitracin. The injection of this solution into the tubing lumen establishes
that the distal end is patent and that there is no resistance to flow. If a
valve is to be used, it is inserted onto the proximal end of the tubing and
affixed with nonabsorbable 3-0 sutures (Fig. 29.5E).
Pinpoint cautery is used to make a hole through the dura mater exposed
by the perforator and the underlying arachnoid and pia (Fig. 29.6A). If
the cortex is thick the dural hole size is not critical; it should be big
enough to allow the ventricular catheter to be introduced easily without
resistance. If the cortex is greatly thinned care is taken to make certain
that the dural hole is no bigger than the diameter of the ventricular
catheter to minimize the possibility of CSF leaking around the entry site
resulting in a subcutaneous collection of fluid. Cortical bleeding is occa-
sionally encountered but it can be readily controlled with bipolar cautery
or direct pressure. From the CT or MRI scan and by measuring the skull
the appropriate length of ventricular tubing needed to reach the frontal
horn can be estimated (Fig. 29.6B). In the older child and the adult, a 12-
cm-long ventricular catheter is usually appropriate. After the ventricle is
entered, CSF is obtained and sent for analysis for cells, sugar, and protein
and for culture (Fig. 29.6C). This establishes the nature of the CSF for
future reference. If indicated, CSF can also be obtained for cytology or
biological marker examination. Care is taken not to drain an excessive
amount of CSF, especially if the ventricles are large and the cortical
mantle is thin, as doing so increases the risk of subdural hematoma
formation. If desired, an antibiotic may be injected into the ventricles.
The side arm of the ventricular catheter reservoir is then attached to the
proximal end of the valve and secured with a 3-0 nonabsorbable suture
(Fig. 29.7). Attaching the sidearm of the reservoir to the valve or perito-
neal tubing immediately after placing the ventricular catheter diminishes
the CSF loss. If a separate reservoir is used rather than a one-piece
ventricular catheter reservoir unit, it is better to attach the reservoir to
the proximal end of the valve or peritoneal tubing before inserting the
ventricular catheter. Once again, this minimizes the loss of CSF from the
ventricles.
The wounds are scrubbed with povidone-iodine solution followed by
irrigation with Ringer's lactate containing bacitracin. The incisions are
then closed using either interrupted 3-0 or 4-0 absorbable sutures. The
skin edges are approximated with tape such as Steri-strips.
The technique described can be used in the infant, child, or adult. Skin
stitches are not used; the wounds heal better and there is no need to
remove the sutures, particularly a factor in the uncooperative patient. If
there is any question about the integrity of the closure in regard to
possible CSF leakage, a second layer of sutures placed in the skin is
advisable. This would also be true if difficulty exists in controlling scalp
bleeding at the termination of the procedure.
Ventriculopleural Shunt
As with a VP shunt, the cephalic incision is made first and the burr
hole is placed. The wound is covered and attention is directed to the chest
wall.
For cosmesis, an incision approximately 3 cm long is made just below
the breast and the midclavicular line (Fig. 29.4A). If the patient is obese
or the presence of an incision higher on the chest wall is not objectionable
the site may be moved up to the second-third intercostal space. The
subcutaneous tissue, deep fascia, and pectoralis muscles are divided (Fig.
29.8A). It helps to wear a headlight to see more easily into the depths of
the incision. The external and internal intercostal muscles are divided at
the superior aspect of the lower of the two ribs of the intercostal space
chosen. A self-retaining retractor placed between the two ribs opens the
intercostal space even further (Fig. 29.6B). The parietal pleura is next
visualized with the lung beneath moving with respiration. The pleura is
not opened at this point.
The tubing is passed from the cephalic to the chest incision, with no
additional incisions being necessary between. Once the tubing is in its
subcutaneous location the pleura is opened just enough to admit the
tubing (Fig. 29.8C). Twenty to 40 cm of tubing is inserted into the pleural
cavity to provide redundancy and to ensure that the tubing will contin-
ually migrate in the pleural space. If the pleural opening is small it need
not be sutured, but if larger it can be closed about the tubing with a 4-0
absorbable suture. Before the pleura is closed the anesthesiologist is
asked to expand the lung to expel as much air as possible. This step can
be repeated at closure of the first muscle layer. The remainder of this
incision is closed like the abdominal wall. There is no need to place a
chest tube. A postoperative chest x-ray film is routinely obtained.
Ventriculoatrial Shunt
The cranial portion is handled in the same manner as with a VP or VP1
shunt. An incision following a skin crease is made midway between the
mandible and the clavicle (Fig. 29.4A). The platysma muscle is divided
and the anterior border of the sternocleidomastoid muscle is identified,
dissected, and retracted posteriorly until the carotid sheath is located
(Fig. 29.9A). The internal jugular vein is then separated from the common
carotid artery and the vagus nerve. With further exposure the common
facial vein is isolated for at least 1 cm before its entry into the internal
jugular vein (Fig. 29.9B). If the common facial vein is not suitable as an
entry site, the tubing can be placed directly into the internal jugular vein
after placing a purse string suture in the vessel wall. The common facial
vein is then ligated and put on tension so as to facilitate entry of the
tubing. For control, temporary vascular clamps or silicone elastomer
vascular loops are placed about the internal jugular vein proximal and
distal to the entry site of the common facial vein (Fig. 29.9C). A stick tie
through the wall of the common facial vein is made but not tied proximal
to the vein's entry into the internal jugular vein. The length of tubing
needed to place the tip of the catheter into the right atrium is estimated
and a suture or mark is placed on the tubing for future reference (Fig.
29.9D). The tip of the tubing is cut on a slight angle to facilitate its entry.
The tubing is filled with normal saline and clamped so as not to allow air
into the atrium. The common facial vein is opened enough to admit the
tubing, which is advanced to what is thought to be the desired location.
As the necessary length of tubing is only an estimate and it is possible
that the tubing can go into other vascular channels than the one desired,
it is necessary to confirm the location of the catheter tip. A monometer
can be placed on the tubing and the pressure measured. If the pressure
is low then the tip is most likely in the right atrium. If the pressure is
over 10 cm H2O and pulsatile then the end most likely is in the right
ventricle, the tip having gone through the tricuspid valve. By pulling the
tubing back, a pressure drop should be noted, indicating that the end
now resides in the right atrium. In addition there is usually a change in
the P-wave of the electrocardiogram when the tubing tip resides in the
right atrium. To be absolutely certain that the tip is in the position desired,
it is suggested that intraoperative fluoroscopy be used to visualize the
tubing by the injection of a contrast agent. In an adult the midportion of
the atrium is a satisfactory location for the end of the tubing; in an infant
or child it is best to position the end as low as possible within the atrium
to allow for future growth of the child.
The mark or suture on the tubing is noted in relation to its entry into
the common facial vein so that final proper positioning is assured and to
indicate inadvertent movement of the tubing during subsequent steps in
the operative procedure (Fig. 29.9E).
The valve may be attached before or after the tubing is tunneled to the
cephalic incision (Fig. 29.9F). This would not be necessary if a distal slit
valve type of catheter is used. The stick tie through the wall of the
common facial vein before its entry into the internal jugular vein is now
securely tied. Previously it need only have been tied loosely if bleeding
had occurred. The remainder of the operative procedure is as described
for a VP shunt. A concern with a VA shunt is to prevent a significant
amount of air from entering the system. This is rarely a problem.
Biventricular Shunt
Biventricular shunts can be inserted in either frontal or parietal loca-
tions (Figs. 29.10 and 29.11). If the frontal region is chosen the patient
is positioned as described previously. If a parietal approach is used the
main problem is one of positioning. The patient is placed with the head
face down to assure good access to both posterior parietal regions. The
torso is rotated so as to expose the right chest wall or the right flank. In
this position it is easy to make an incision in either the lateral chest wall
for a VP1 shunt or the right lower quadrant for a VP shunt. It is not
possible to insert a VA shunt in this position. Scalp incisions are made
as before as are chest or abdominal incisions.
There are three options at this point. The two shunts can be treated
independently with two tubes tunneled to the pleural or abdominal cavity,
the ventricular catheter can be connected by a Y or T connector proximal
to a valve (if a proximal valve is used), or a valve can be placed just after
the reservoir on each side and the two shunts can be joined at a more
distal location. In the infant or child it is probably just as easy to make
two entirely separate shunting systems as it will simplify future revisions.
In the adult a single distal tube would often be technically easier. It is
also necessary to make an incision in the neck as it is not possible to
tunnel subcutaneously between the cephalic and distal incisions. When
designing the system and placing the incisions it is always best to consider
that subsequent revision of the shunt might be necessary.
Complications
As the best way to avoid shunt complications is not to insert a shunt,
it is necessary to establish beyond a reasonable doubt that the shunt is
needed. Shunt complications can be divided into those that are common to
all types of shunts and those that are unique to a particular shunt type.
All shunts are subject to obstruction, disconnection, and infection. The
frequency and location of obstruction or disconnection depend to a fair
degree on the type of shunt hardware utilized. In general, the most frequent
malfunction is occlusion somewhere within the shunt lumen. In the
pediatric age group, particularly those under 1 year of age, the most
frequent site of obstruction is in the ventricular catheter by choroid plexus or
ependymal or glial tissue, which can grow into the lumen. Another source of
malfunction is disconnection, which can occur at any point in the system but
most commonly where the various components are joined. Pressure-
regulated valves can block, drain CSF at higher or lower than the intended
pressure, and rarely allow retrograde flow, a concern only in a vascular
shunt. Although considerable apprehension has been expressed regarding
the protein content of CSF and the likelihood of valve obstruction, no
definite relationship has been established (17). It is our experience that, in
the pediatric age group, the increased protein of the CSF is usually
associated with more frequent ventricular catheter obstructions. The use of
radiopaque materials for the entire length of the shunt is advocated, making
it possible to determine the continuity of the shunting system on plain x-ray
films. It is also recommended that a reservoir be placed in the system to
allow access to the CSF. By tapping the reservoir, pressure measurements
can be made, function of the system can be ascertained, and CSF can be
obtained for examination as needed. If, after tapping the reservoir, the
adequacy of function of the shunt is still in doubt, imaging techniques
that use contrast agents or radiopharmaceuticals can determine patency.
Each type of shunting system has its own peculiarities that determine how
best to establish the adequacy of its function. Most shunting systems
contain a pumping mechanism in either the valve or the reservoir that
allegedly tests whether the shunt is functioning properly. The correlation
between response to pumping and proper functioning of the shunt may be at
variance, with some shunts that do not pump normally functioning
satisfactorily while others that pump normally are malfunctioning. If a
shunt malfunction is suspected, it is strongly advocated that response to
pumping not be the sole criterion used to make any definite conclusions in
this regard.
The use of implanted foreign materials always presents the risk of
infection. Infection prevention obviously is preferable to treatment. The vast
majority of shunt infections occur at the time of insertion, revision, or
improper tapping. The use of meticulous aseptic surgical technique and
possibly prophylactic antibiotics has steadily reduced the risk of infection so
that a per case infection rate of 5% or less should be the standard, with some
centers reporting infection rates in the 1 to 2% range (30, 33). A shunt
infection may manifest itself by swelling and redness over a portion or all of
the shunt tract and such generalized symptoms as peritonitis (with a VP
shunt) or septicemia (with a VA shunt). Skin breakdown over the hardware
and resultant shunt infection are problems that can be seen in the infant but
are rarely a consideration in the adult.
Proper incision and hardware placement and the use of low profile and
pliable materials should virtually eliminate this form of complication.
Infection can be solely confined to the CSF in the ventricles and shunt,
giving no external evidence other than a shunt malfunction. Initial infec-
tion rates for both VP and VA shunts are similar; however, the presence
of a catheter within the atrium allows subsequent colonization during
episodes of bacteremia (11). A VA shunt infection may lead to septicemia
with subsequent renal damage, lung damage, endocarditis, and septic
emboli, whereas a VP shunt infection most commonly leads only to
obstruction of the distal end of the tubing. A complication of a chronic
low grade shunt infection that is limited to VA shunts is that of nephritis,
which develops from deposition of antibody-antigen and complement
immune complexes in the glomeruli. The most reliable way to confirm a
shunt infection is to obtain multiple CSF samples from the shunting
system (28). Approximately one-half of the infecting organisms are S.
epidermidis and one-quarter are S. aureus, with the remaining one-
quarter being a wide variety of pathogens (7, 8, 28). The management of
shunt infections is still subject to considerable debate. All advocate the
use of appropriate intraventricular and systemic antibiotics. Some au-
thorities attempt to clear the infection without replacement of the shunt-
ing system, others favor immediate replacement, whereas others advo-
cate delayed replacement (7, 10, 16, 21). Our preference is complete
removal of the infected system with delayed replacement as this has the
highest chance of success with the lowest morbidity and the shortest
hospital stay (10). Delayed replacement usually necessitates drainage of
CSF intermittently via a reservoir or continuously by the establishment
of an external ventricular drainage system.
Complications unique to VP shunts are ascites, pseudocyst formation,
perforation of a viscus or the abdominal wall, intestinal obstruction,
spread of infection or neoplasm from the ventricles to the abdominal
cavity, and a higher incidence of inguinal and umbilical hernias in infants
(6). The use of a coiled spring inside the peritoneal catheter to prevent its
kinking is responsible for the majority of abdominal complications be-
cause the stiffness of the catheter tip results in its penetration of sur-
rounding structures. The length of tubing in the peritoneal cavity does
not seem to be a factor in subsequent complications. We have used an
extended length of peritoneal tubing for over 10 years even in the most
premature neonates without any complications due to the length. Use of
extended length tubing eliminates the need to lengthen the distal end of
the shunt to accommodate for growth. Complications unique to VP1
shunts are primarily those of fluid accumulation within the pleural
cavity. This is particularly a problem in the infant and child and is
considerably less a problem in the adolescent or adult. Hydrothorax is
treated by moving the distal catheter to a site outside of the thoracic
cavity. Complications unique to vascular shunts involve the heart, lungs,
and vasculature and include vena cava obstruction, mural thrombosis,
bacterial endocarditis, cardiac arrhythmias, cardiac tamponade (second-
ary to perforation of the heart wall), embolization of the distal catheter
into a pulmonary artery, and chronic pulmonary thromboembolization
that could result in pulmonary hypertension or even cor pulmonale (17).
The development of a significant subdural fluid collection after ven-
tricular shunting relates directly to the age of the patient and the size of
the ventricles; the older the patient, the bigger the ventricles, the more
likely this complication, not only at the time of shunt insertion but ever
thereafter. Even a seemingly minor head injury may produce a significant
subdural fluid accumulation. The use of a higher pressure valve helps to
reduce this problem. If the subdural collection is asymptomatic, treatment
is not necessarily indicated, but if a progressive increase in volume and
associated clinical symptoms occur the subdural fluid must be drained,
usually by the placement of a subdural peritoneal shunt without a valve
to provide a pressure gradient between the two shunting systems.
The incidence of seizures in patients with shunted hydrocephalus is
higher than can be attributed to hydrocephalus alone (1, 17). This is
substantiated by the finding of EEG abnormalities local to the site of
shunt insertion (12). Whether prophylactic anticonvulsant treatment is
needed and for how long is not clear and is probably best decided on a
case by case basis. We routinely do not advocate such for our patients.
Utilization
A CSF-diverting shunt must be inserted when there is evidence of
progressive hydrocephalus after failure to reestablish CSF circulation by
removal of a third ventricular obstruction. A second attempt at intracra-
nial CSF diversion is rarely warranted.
References
1. Copeland GP, Foy PM, Shaw MD: The incidence of epilepsy after ventricular
shunting operations. Surg Neurol 17:279-281, 1982.
2. Cushing H: The Third Circulation. London, Oxford University Press, 1926.
3. Dandy WE: An operative procedure for hydrocephalus. Johns Hopkins Hosp
Bull 33:189-190, 1922.
4. Dandy WE: Surgery of the brain. In Lewis D (ed): Practice of Surgery.
Hagerstown, MD, WF Prior Co, Inc, 1932.
5. Dandy WE: Diagnosis and treatment of strictures of aqueduct of Sylvius
(causing hydrocephalus). Arch Surg 51:1-14, 1945.
6. Davidson RI: Peritoneal bypass in the treatment of hydrocephalus: Historical
review of abdominal complications. J Neurol Neurosurg Psychiatry 39:640-
646, 1976.
7. Forward KR, Fewer HD, Stiver HG: Cerebrospinal fluid shunt infections: A
review of 35 infections in 32 patients. J Neurosurg 59:389-394, 1983.
8. George R, Leibrock L, Epstein M: Long-term analysis of Cerebrospinal fluid
shunt infections. J Neurosurg 51:804-811, 1979.
9. Hoffman HJ, Harwood-Nash D, Gilday DL: Percutaneous third ventriculos
tomy in the management of noncommunicating hydrocephalus. Neurosur-
gery 7:313-321, 1980.
10. James HE, Walsh JW, Wilson HD, et al: Prospective randomized study of
therapy in Cerebrospinal fluid shunt infection. Neurosurgery 7:459-463,
1980.
11. Keucher TR, Mealey J Jr: Long-term results after ventriculo-atrial and ven-
triculo-peritoneal shunting for infantile hydrocephalus. J Neurosurg
50:197-186, 1979.
12. Laws ER Jr, Niedermeyer E: EEG findings in hydrocephalic patients with
shunt procedures. Electroencephalogr Clin Neurophysiol 29:325, 1970.
13. Matson DD: A new operation for the treatment of communicating hydroceph
alus: Report of a case secondary to generalized meningitis. J Neurosurg
6:238-247, 1949.
14. Matson DD: Neurosurgery of Infancy and Childhood, ed 2. Springfield,
Charles С Thomas, 1969.
15. McComb JG, Hyman S, Weiss MH: Cerebrospinal fluid drainage following
acute obstruction of the fourth ventricle in the rabbit. Concepts Pediatr
Neurosurg 4:90-101, 1983.
16. McLaurin RL: Treatment of infected ventricular shunts. Child Brain 1:306-
310, 1975.
17. McLaurin RL: Shunt complications. In Section of Pediatric Neurosurgery of
the American Association of Neurological Surgeons (eds): Pediatric Neuro
surgery: Surgery of the Developing Nervous System. New York, Grune and
Stratton, 1982, pp 243-253.
18. Miller CF II, White RJ, Roski RA: Spontaneous ventriculo-cisternostomy.
Surg Neurol 11:63-66, 1979.
19. Mixter WJ: Ventriculoscopy and puncture of the floor of the third ventricle.
Boston Med Surg J 188:277-278, 1923.
20. Nulsen FE, Spitz EB: Treatment of hydrocephalus by direct shunt from
ventricle to jugular vein. Surg Forum 2:399-403, 1952.
21. O'Brien M, Parent A, Davis B: Management of ventricular shunt infections.
Childs Brain 5:304-309, 1979.
22. Pudenz RH, Russell FE, Hurd AH, et al: Ventriculo-auriculostomy: A tech
nique for shunting Cerebrospinal fluid into the right auricle. Preliminary
report. J Neurosurg 14:171-179, 1957.
23. Pudenz RH: The surgical treatment of hydrocephalus—an historical review.
Surg Neurol 15:15-26, 1981.
24. Sayers MP, Kosnick EJ: Percutaneous third ventriculostomy: Experience and
technique. Childs Brain 2:24-30, 1976.
25. Scarff JE: Treatment of obstructive hydrocephalus by puncture of the lamina
terminalis and floor of the third ventricle. J Neurosurg 8:204-213, 1951.
26. Scarff JE: Treatment of hydrocephalus: An historical and critical review of
methods and results. J Neurol Neurosurg Psychiatry 26:1-26, 1963.
27. Scarff JE: Third ventriculostomy by puncture of the lamina terminalis and
the floor of third ventricle. J Neurosurg 24:935-943, 1966.
28. Schoenbaum SC, Gardner P, Shilito J Jr: Infections of Cerebrospinal fluid
shunts: Epidemiology, clinical manifestations and therapy. J Infect Dis
131:543-552, 1975.
29. Stookey B, Scarff J: Occlusion of the aqueduct of Sylvius by neoplastic and
non-neoplastic processes with a rational surgical treatment for relief of the
resultant obstructive hydrocephalus. Bull Neurol Inst NY 5:348-377, 1936.
30. Tabars Z, Forrest D: Colonisation of CSF shunts: Preventive measures.
Kinderchir 37:156-157, 1982.
31. Torkildsen A: A new palliative operation in cases of inoperable occlusion of
sylvian aqueduct. Acta Chir Scand 82:117-124, 1939.
32. Vries JK: An endoscopic technique for third ventriculostomy. Surg Neurol
9:165-168, 1978.
33. Welch K: Residual shunt infection in a program aimed at its prevention.
Kinderchir 28:374-377, 1979.
34. White JC, Michelsen JJ: Treatment of obstructive hydrocephalus in adults.
Surg Gynecol Obstet 74:99-109, 1942.
30
Considerations and Techniques in the Pediatric Age
Group
Harold J. Hoffman, M.D., F.R.C.S.(C)

Tumors in and around the third ventricle are common in childhood.

During the years 1950 to 1984 a total of 1367 children with brain tumors
were seen at the Hospital for Sick Children. Three hundred ninety-three
of these children had third ventricular tumors (28.7%); 72 had optic nerve
gliomas, 122 had suprasellar tumors, 66 had pineal region tumors, 17
had tumors within the confines of the third ventricle, 55 had hypothal-
amic tumors, and 61 had thalamic tumors. The majority of these tumors
were benign, 110 being low grade astrocytomas and 95 being cranio-
pharyngiomas.
Optic Nerve Gliomas
Optic pathway gliomas are relatively common in children. They consti-
tuted 3.6% of all brain tumors in Matson's series (11) and made up 6% of
our series of brain tumors at the Hospital for Sick Children (4).
Davies initially described the close relationship between optic nerve
tumors and von Recklinghausen's disease (3). Thirty percent of patients
with optic nerve gliomas at the Hospital for Sick Children have evidence
of von Recklinghausen's disease.
Optic gliomas have a highly unpredictable course; in one patient the
tumor will spread and quickly become fatal, but in another it can remain
quiescent for many years (Fig. 30.1). As a result, opinion concerning the
management and treatment of this tumor has been radically divided.
Some clinicians advocate surgical intervention, others rely on radiother-
apy, and still others refuse to undertake any active form of treatment,
believing that these tumors are not true neoplasms, but hamartomas.
The tumors typically begin within the optic nerve in the optic canal
and from this point usually extend forward into the orbit as well as
backward toward the chiasm. They can infiltrate adjacent brain. Of the
72 optic pathway tumors seen during the past 25 years at the Hospital
for Sick Children, 24 lay anterior to the optic chiasm and 48 involved
chiasm and optic tracts. The tumors are usually Grade 1 to 2 astrocyto-
mas, but they may occasionally show some signs of aggressivity and have
been graded as high as Grade 3.
The vast majority of patients with optic nerve gliomas present before
the age of 6. The most common presenting symptom is visual loss, often
in conjunction with optic atrophy. Proptosis is common when the tumor
extends forward into the orbit. At first the globe protrudes forward and
then it is displaced laterally (Fig. 30.2). Visual field defects indicate
involvement of the optic tract and optic chiasm.
Papilledema is usually produced by tumors that encroach posteriorly
on the third ventricle and produce hydrocephalus (Fig. 30.3). As the
tumor extends beyond the confines of the optic system, it can involve the
internal capsule and produce hemiparesis (Fig. 30.4A).
 The diencephalic syndrome consisting of emaciation in association with
an alert hyperkinetic infant can be seen in patients with an optic nerve
glioma.
Optic nerve gliomas that involve the optic tract often produce extensive
distension of the basal cisterns and Cerebrospinal fluid (CSF) subarach-
noid pathways (Figs. 30.4B and 30.5). The resulting hydrocephalus is
frequently extraventricular and a computerized tomographic (CT) scan
may show only minimal ventricular enlargement. Rarely, the distended
 CSF pathways over the surface of the brain can rupture, producing
massive subdural effusions (Fig. ЗОЛА).
Ascites after diversionary ventriculoperitoneal shunting is a rare com-
plication seen in patients with optic nerve gliomas.
Kronlein described the operative technique for resection of the intraor-
bial portion of the optic nerve glioma in 1888 (9). However, because these
tumors involve the intracranial portion of the optic nerve, a two-stage
procedure emerged: the neurosurgeon would resect the intracranial por-
tion of the optic nerve tumor and disengage it from the optic canal through
a craniotomy approach and the ophthalmologist would remove the orbital
tumor through a Kronlein procedure.
An entirely transcranial route developed by Jackson (8) and Housepian
(7) allowed access to intracranial as well as orbital portions of the tumor
in one stage.
Optic nerve gliomas are almost always low grade astrocytomas. There
is no chance of tumor recurrence if they can be totally resected. Unfor-
tunately, total resection is only possible when the tumor is present in one
optic nerve and is well in front of the optic chiasm. When the tumor
involves the optic chiasm, optic tracts, optic radiation, and geniculate
bodies, total resection is not possible. However, a partial or sometimes
subtotal removal of such posterior optic pathway tumors can be carried
out.
When vision is compromised by an optic nerve glioma that can be only
partially removed, radiotherapy is indicated. Low grade tumors can re-
spond to radiation and may even disappear completely with such a course
of radiotherapy (Fig. 30.4). If vision is not significantly compromised,
radiotherapy can be delayed and the patient can be followed clinically
and on CT scan to see whether the tumor is aggressive and will require
radiation.
In patients in whom an anteriorly placed tumor is located in one optic
nerve, there is frequently intraorbital as well as intracranial tumor. An
attempt should be made to remove the tumor en bloc. We position the
patient face up with neck extended and head in the pin fixation headrest.
Brain relaxation is achieved by the intravenous instillation of mannitol
in a dose of 2 g/kg and hyperventilation of the patient.
A bicoronal incision is used and a front craniotomy is carried out on
the side of the optic nerve involved. A small frontal flap is turned. This
extends from the midline medially to the outer edge of the supraorbital
margin laterally and from supraorbital margin to midway between nasion
and coronal suture posteriorly. The dura mater is opened just above the
supraorbital margin and the frontal lobe is retracted, exposing optic nerve
and chiasm. Frontopolar veins in the way can be coagulated and divided.
The olfactory tract is coagulated and divided to prevent avulsion of the
olfactory bulb.
The posterior extent of the tumor is visualized. If the tumor does not
involve the chiasm, one should then prepare for total excision of the
tumor. If the tumor grossly appears to involve chiasm and vision is
severely compromised or if significant proptosis is present, resection of
the optic nerve is still indicated.
The dura mater in the floor of the anterior fossa is divided back to the
level of the optic foramen. With a retractor between the orbital fascia
and the roof of the orbit, a high speed drill is used to open the orbital
roof, which is then removed with rongeurs and punches back to the optic
canal. The optic canal is then unroofed using high speed burrs and 1-
mm punches.
This done, the dura of the optic nerve is opened and the optic nerve is
followed into the orbit. The anulus of Zinn is divided, and traction sutures
are left to hold the two cut edges in place for eventual reconstitution.
The ocular muscles are retracted and the nerve is followed directly to
the globe. The nerve is then amputated behind the globe, with care being
taken not to penetrate the globe. Such penetration can lead to irreversible
globe damage.
The entire optic nerve is then lifted out of the orbit and the optic canal
and amputated just in front of the chiasm. Care should be taken to label
its proximal and distal ends for histological examination to confirm that
there has been no histological spread of tumor beyond the posterior line
of resection. The orbital roof is repaired with tantalum mesh.
In patients with posteriorly placed tumors that do not go forward into
the orbit but extend back along the optic tract and involve the chiasm, it
is possible to remove large portions of tumor while preserving vision. The
ultrasonic aspirator is an ideal tool for removing such tumors. The tumor
can be resected partially under microscopic vision. After such an opera-
tion, the patient can be followed clinically and with CT scanning (Fig.
30.6). If there is no further evidence of tumor growth and vision is good,
a watchful wait is indicated. However, if the tumor does show evidence
of growth or if vision is bad or deteriorating, radiotherapy is indicated
(Fig. 30.4).
Craniopharyngiomas
Craniopharyngiomas are benign suprasellar tumors that are seen pre-
dominantly in childhood. Although there is great controversy on the
definitive management of these tumors, the overwhelming majority of
craniopharyngiomas can be totally resected to cure the patient (5, 12-
14).
Craniopharyngiomas can present as small tumors that enlarge the sella
and produce endocrine deficiency and headache (Fig. 30.7). These tumors
do not displace vessels on angiography. Although such tumors can be
resected transsphenoidally, I prefer a subfrontal approach. The patient's
head is positioned in anatomical position, with the nose directly upward
and the head extended (Fig. 30.8). The pin fixation headrest should be
used in patients over 2 years of age. It is essential that the brain be
relaxed when the frontal lobe is elevated. Mannitol in a dose of 2 g/kg is
given at the start of the operation and the patient is hyperventilated. I
use a small right frontal bone flap, cut low just above the supraorbital
margin and extending to the midline, with burr holes placed over the
sagittal sinus and the medial cut made just to the left of the midline. The
lateral burr hole is made at the pterion. The dura mater is opened just
above the supraorbital margin and the dural opening is extended trans-
versely to the sagittal sinus medially and to the pterion laterally. The
frontal lobe is elevated. Any frontopolar veins in the way are divided, and
the olfactory nerve is divided just behind the olfactory bulb. Self-retaining
brain retractors are used to elevate the frontal lobe, the arachnoid is
incised over the right optic nerve, and the chiasmatic cistern is opened
and emptied of CSF.
Using the operating microscope, one exposes the craniopharyngioma
and incises its capsule. Whether the contents are liquid or solid, they are
then emptied with the ultrasonic aspirator. The collapsed tumor can then
be separated from the optic nerves and internal carotid arteries and
pulled down from the hypothalamus. Frequently, the pituitary stalk ends
in the tumor and must be divided at this point. The tumor can then be
shelled out of the sella. If the diaphragma sellae is deficient, the tumor
invades the pituitary gland and, as one pulls on the neoplasm, fingers of
tumor will come out along with some adherent pituitary gland.
The larger craniopharyngiomas extend either forward between the two
optic nerves (prechiasmatic) (Fig. 30.9) or backward into the third ventri-
cle (retrochiasmatic) (Fig. 30.10). The prechiasmatic tumors typically
compress one optic nerve more than the other and the patients usually
present with severe visual loss in one eye. Endocrine problems are
commonly present in this group of patients. Angiography will show
elevation of the A1 segment of the anterior cerebral arteries with no
displacement of the basilar artery.
In much the same way as for sellar tumors, prechiasmatic tumors are
approached through a small right frontal bone flap that brings one down
on the optic nerves, the chiasm, and the tumor situated between the two
optic nerves. The tumor capsule is coagulated and incised and the tumor
contents are emptied with the ultrasonic aspirator. This procedure col-
lapses the capsule and allows it to be pulled forward and dissected free
from the optic nerves, internal carotid arteries, posterior communicating
arteries, third cranial nerves, and hypothalamus. The tumor is situated
above the diaphragma sellae unless the diaphragma is deficient in which
case the tumor invades the pituitary gland. Occasionally the pituitary
stalk can be saved but it usually comes out with the tumor when the
latter is pulled free from surrounding structures.
The retrochiasmatic tumors protrude posteriorly and extend into the
third ventricle and commonly present with ventricular dilatation. If hy-
drocephalus is present the patients will have papilledema but rarely any
other visual problem. Endocrine problems are relatively uncommon at
the time of presentation with this type of tumor. On angiography, these
tumors will show no elevation of the A1 segment of the anterior cerebral
artery, but they will show posterior displacement of the basilar artery
and stretching of the posterior communicating arteries. Retrochiasmatic
tumors frequently thin out the chiasm to a sheet that is pushed up against
the tuberculum sellae, providing a cover for the dome of the tumor (Fig.
30.10C). Despite this severely distorted appearance of the visual appa-
ratus, these patients usually have normal acuity and often have no visual
field defect.
The retrochiasmatic tumors are reached through a combination of
routes always involving an approach between the optic nerve and internal
carotid artery and frequently involving opening of the lamina terminalis.
To gain access to the route between the optic nerve and the internal
carotid artery, the right frontal flap used for both sellar and prechiasmatic
tumors is enlarged by removal of the pterion along with some temporal
bone and the outer half of the sphenoid wing. This allows one to retract
the temporal lobe posteriorly and the frontal lobe upward, thus bringing
the optic nerve, optic tract, and internal carotid artery into clear view.
 Under the microscope, with self-retaining brain retractors on the fron-
tal and temporal lobes, one can retract the optic tract medially and the
internal carotid artery laterally to expose the tumor. If only solid calcified
tumor is encountered here, the frontal lobe is elevated off the chiasm and
the lamina terminalis is exposed. This structure is greyish and can be
easily distinguished from chiasm. The lamina is incised and the third
ventricle is entered. The floor of the third ventricle is then opened to
expose the tumor cyst, which can be entered and emptied. One can then
go back to the route between the internal carotid artery and the optic
tract and shift calcified tumor forward to the space that opens up between
the two optic nerves as the collapsed tumor allows the chiasm to move
back into normal position. Once the tumor has been decompressed, it
becomes possible to remove it between the optic nerve and internal carotid
artery as well as between the two optic nerves. Occasionally, it must be
extracted through the opening in the lamina terminalis.
 The membrane of Lilliequist is always intact so there should be no fear
of damage to the basilar artery or brain stem. These structures come into
clear view once the tumor is removed (Fig. 30.11). Claude Lapras recom-
mends inserting a cotton patty into the third ventricle when the lamina
is opened to prevent the migration of tumor contents up into the third
ventricle during tumor removal (10). This can certainly happen if no
measures are taken to prevent it; one does not become aware of such
migration until the postoperative CT scan is seen.
Pineal Region Tumors
In recent years the ability to determine serum and CSF markers in the
case of pineal region tumors has allowed identification of particular germ
cell tumors (1). Choriocarcinomas lead to a marked increase in human
chorionic gonadotropin (HCG) in both serum and CSF. Endodermal sinus
tumors (yolk sac tumors) are associated with increased levels of alpha-
fetoprotein (AFP) in both serum and CSF. Embryonal carcinomas produce
increased levels of both HCG and AFP in serum and CSF. The common
germ cell tumor, the germinoma, has no effect on these markers. Among
46 verified pineal tumors treated in our institution, there were only 4
that could be identified with markers (6).
With small tumors in this region a CT-guided stereotaxic biopsy is of
value. The procedure can be done with little in the way of morbidity and
can provide diagnostic specimens of tumor in a safe fashion.
In the case of large tumors there is a significant risk of mixed histology,
and a small biopsy can therefore be misleading. Six of the 46 verified
tumors seen at our institution had mixed histology (6). Radical resection
of a malignant tumor has the advantage of leaving less of a tumor burden
to be dealt with by radiotherapy.
The approach to the pineal region, located in the center of the brain,
has always been a challenge to neurosurgeons.
There are three main approaches in current use: the transcallosal, the
supracerebellar-infratentorial, and the occipital-transtentorial. I use the
posterior transcallosal approach for tumors that extend anteriorly into
the third ventricle as well as for those that extend upward toward the
corpus callosum (Fig. 30.12). The supracerebellar-infratentorial ap-
proach is used for tumors that extend inferiorly into the posterior fossa
(Fig. 30.13). The occipital-transtentorial approach is used for tumors that
extend posteriorly above the level of the tentorium (Fig. 30.14). A sagittal
cut of a magnetic resonance imaging (MRI) scan or a sagittal reconstruc-
tion of the CT scan will show the direction of tumor growth (Fig. 30.15).
Pineal neoplasms commonly occlude the aqueduct and the posterior
third ventricle; consequently, hydrocephalus is usually manifest when
these patients present. Because many of the tumors in the pineal region
can disseminate systemically through a diversionary shunt, we utilize a
filtered ventriculoperitoneal shunt to treat the attendent hydrocephalus
as an initial step in management (15). The diversionary shunt relieves
the patient of many of his symptoms and also helps to slacken the brain
at the time of surgical exposure. Although it has been assumed best to
leave the ventricles dilated and to institute drainage at the time of
operation, we have found that diversionary shunting will create a slack
brain for several weeks after shunting, allowing one to operate on a well
patient with a relaxed brain. In addition to the use of a diversionary
shunt, patients are given mannitol in a dose of 2 g/kg during opening of
the bone flap and are hyperventilated.
For the posterior transcallosal approach the patient is positioned supine
with the body and head flexed and the head in the pin fixation headrest
in anatomical position (Fig. 30.16). A right parietal bone flap extending
from the midline to 4 cm laterally is turned. The length of the bone flap
is determined by the preoperative angiogram, which shows the draining
parasagittal veins. The bone flap never reaches as far as the motor strip
anteriorly and never goes as far back as the lambdoid suture. The medial
cut is made just to the left of the midline, thus exposing the sagittal sinus
in the operative field (Fig. 30.17).
The dural reflection starts out laterally and extends anteriorly and
posteriorly depending on the course of the draining parasagittal veins.
Every effort is made not to compromise any of these veins during the
opening of the dura mater. The dural incision is carried up to the sagittal
sinus anteriorly and posteriorly, allowing the dura to be reflected to the
left. These vertical limbs of the dural incision are made to preserve the
draining veins in safety.
The parietal lobe is then gently retracted away from the falx utilizing
self-retaining retractors, and the corpus callosum is exposed. Care must
be taken not to damage the anterior cerebral arteries. With the aid of the
microscope a 1 -cm-long incision is made in the corpus callosum just in
front of the splenium.
With most pineal tumors the internal cerebral veins will be situated
over the dome of the tumor (Fig. 30.18). These veins are venae commu-
nicantes and can be retracted to one side of the dome of the tumor. Once
this is done the tumor can be dissected from surrounding structures. In
the case of large tumors, we have found it useful to reduce the tumor
with the ultrasonic aspirator, which allows for histological examination
of all removed tumor tissue. This is particularly important in the pineal
region, where so many tumors have mixed histology.
In the case of benign tumors such as teratoma or dermoid, it should be
possible to remove the tumor totally. With infiltrating tumors such as
geminomas, pineoblastomas, and astrocytomas, a subtotal resection is
carried out.
In those cases in which the tumor surrounds the internal cerebral
veins, care must be taken not to injure these veins. Germinomas may
occasionally surround the internal veins so that one comes directly down
on tumor as the corpus callosum is divided. This is more characteristic
of glial tumors and is never seen with large benign teratomas and der-
moids, which always elevate the internal cerebral veins in this region.
In the callosal approach, the collicular plate and brain stem are not
well visualized until the tumor has been removed. Therefore, brain stem
function must be carefully monitored as the tumor is removed as there
can be serious disturbances in vital signs with traction on tumors that
infiltrate the collicular plate.
The supracerebellar-infratentorial approach is ideal for tumors that
extent inferiorly into the posterior fossa. In these cases, the tentorial
notch is large, allowing for downward protrusion of the tumor. The
patient is positioned prone, with the head flexed and fixed in anatomical
position in the pin fixation headrest.
 A midline incision is used to strip muscles off occipital bone. The bone
is removed to just above the level of the lateral sinuses and torcular. The
foramen magnum is removed. A V-shaped dural incision is made with
the two sides of the V coming together in the region of the foramen
magnum. In children there is a prominent suboccipital sinus and there
may be a falx overlying the vermis. Removing the foramen magnum and
bringing the two dural incisions together at the level of the foramen
magnum allows one to open dura mater below the level of the midline
sinus and falx.
The operating microscope is then used and the superior surface of the
cerebellum is retracted with self-retaining brain retractors. The draining
veins coming off the superior surface of the cerebellum are coagulated
and divided, allowing for inferior retraction on the cerebellum.
The arachnoid in the pineal regions is extremely thick, obscuring veins
and tumor in the region. This arachnoid is opened by sharp dissection.
The precentral cerebellar vein is coagulated and divided, allowing further
downward retraction on the superior surface of the cerebellum. Care
must be taken not to damage the basal veins of Rosenthal, which lie out
laterally. Once the tumor is exposed, it can be gutted with the ultrasonic
aspirator. If it is not an infiltrating tumor, it can then be easily separated
from surrounding structures and removed.
The occipital transtentorial approach is utilized for tumors that extend
posteriorly above the level of the tentorium. We position the patient
supine, with head flexed. A right occipital bone flap is turned. This is
hinged inferiorly and exposes the sagittal sinus medially and the torcular
and transverse sinus inferiorly. The occipital lobe is retracted superiorly
and laterally, exposing the tentorium, the falx, and the straight sinus.
Draining veins going into the tentorium and falx are divided. The tento-
rium is then incised 1 cm from the torcular, with the incision extending
laterally and anteriorly to the tentorial notch. The edges of the divided
tentorium are retracted with traction sutures and the arachnoid overlying
the deep venous system is exposed.
Under the microscope, the thinned arachnoid is opened sharply, thus
bringing the quadrigeminal plate, the superior vermis, the splenium of
the corpus callosum, and the major veins draining into the straight sinus
(including the internal cerebral veins, the vein of Galen, the basal veins
of Rosenthal, and the precentral cerebellar vein) into view.
The veins are dissected from the tumor capsule and the tumor is
dissected free from surrounding structures. In the case of a noninfiltrat-
ing tumor, the tumor is gutted with the ultrasonic aspirator allowing the
capsule to be totally removed once it has been freed from surrounding
structures. Infiltrating tumors are resected subtotally.
Thalamic Tumors
Thalamic tumors are common in childhood. About half of these tumors
are benign and almost all are glial in origin (2). Obstruction of CSF
pathways is common, and diversionary shunts will frequently be required
before the treatment of the tumor. In the case of small thalamic tumors
presenting with the classical signs of contralateral hemiplegia, we favor
a CT-guided sterotaxic biopsy. In our unit the Brown-Robert-Wells frame
is used; we think that we can safely biopsy such small tumors and obtain
representative tissue samples to guide us in subsequent tumor manage-
ment. However, in the case of large thalamic tumors, particularly those
that protrude into the lateral ventricle, we recommend an attempt at
subtotal excision. This allows the tumor to be made smaller and provides
a more reliable sample for histological diagnosis. With such a reduction
procedure, further therapy is frequently unnecessary for low grade astro-
cytomas in the thalamus.
Thalamic tumors that protrude into the lateral ventricle do so anteriorly
near the foramen of Monro, and frequently occlude the foramina of Monro
and produce hydrocephalus (Fig. 30.19).
With such patients, we use an anterior transcallosal approach. We turn
a small right frontal bone flap that is centered over the coronal suture
and extends anteriorly to the region of the hairline and posteriorly to the
pre-Rolandic region. The medial extent of the bone flap is just to the left
of midline, and the bone flap extends 4 cm to the right of midline. The
patient frequently has a diversionary shunt, is given mannitol in a dose
of 2 g/kg, and is hyperventilated. The brain is consequently slack. Every
effort is made to preserve draining parasagittal veins. The dural opening
is made so as to achieve this end. The frontal lobe is then retracted away
from the falx and the corpus callosum is exposed. The corpus callosum
is then incised with the ultrasonic aspirator over the lateral ventricle into
which the thalamic tumor protrudes. The ultrasonic aspirator is used
because it will incise the corpus callosum very gently and bring one down
to the ependymal surface of the lateral ventricle. There may be some
veins in the roof of the lateral ventricle that must be coagulated at this
point. Self-retaining brain retractors are used in the lateral ventricle and,
with the microscope in place, the tumor, which has frequently breached
the ependymal surface of the lateral ventricle, can be visualized and
partially resected (Fig. 30.20). If the ependymal surface is intact, a thin
layer of thalamus must be incised to expose the tumor.
Occasionally the cingulate gyri of the two frontal lobes are fused
anteriorly and it therefore becomes impossible to expose the corpus
callosum. In such cases an incision is made in the cingulate gyrus to
allow access to the corpus callosum.
In all cases of thalamic tumor in which this approach is used it is
relatively simple to make a large opening in the septum pellucidum so
that one ventricular shunt will drain both lateral ventricles effectively.
Thalamic tumors that expand laterally can be approached transcorti-
cally using a posterior parietal bone flap. The parietal cortex is incised,
thus allowing both access to thalamus and cytoreduction of the tumor.
Operative ultrasound is invaluable in guiding one to the tumor. Posterior
thalamic tumors can be resected through the occipital transtentorial
approach.
In the case of large benign tumors that have been satisfactorily re-
sected, radiotherapy is not used (Fig. 30.19). Radiotherapy is reserved for
histologically benign thalamic tumors that show evidence of further
growth on CT scan after resection and for histologically malignant tu-
mors.

Hypothalamic Tumors
Hypothalamic tumors that fill the third ventricle and produce hydro-
cephalus are approached through an anterior transcallosal route. The
third ventricle is entered through the foramen of Monro (Fig. 30.21). If
the tumor is large the third ventricle can be entered by dividing the
thalamostriate vein and splitting the choroidal fissure, thus gaining
access to the entire third ventricle.
 In the case of hypothalamic gliomas that present as suprasellar masses,
a combined subfrontal and transpterional route allows adequate access
to the tumor.
As long as one works in tumor, one can satisfactorily remove tumor
without disturbing normal function. In the case of hypothalamic astro-
cytomas that fill the third ventricle and are removed by the transcallosal
route, endocrine dysfunction is uncommon, particularly if the patient is
not given radiotherapy.
 When a low grade astrocytoma is resected, radiation therapy is fre-
quently unnecessary. Many such patients have now been followed for
over 10 years with no change in their residual tumor without radiotherapy
(Fig. 30.22). On the other hand, if the tumor does show evidence of
further growth after resection a course of radiotherapy is indicated; some
of these low grade tumors will disappear with radiotherapy.
The hypothalamic hamartomas present with precocious puberty. The
transpterional route allows access to the tumor between the optic nerve
and internal carotid artery. The tumor frequently hangs down from the
hypothalamus in the suprasellar cistern like a grape and can be readily
resected (Fig. 30.23).
Suprasellar Germinomas
These tumors typically occur in young girls who present with visual
and endocrine problems. The tumor is in the suprasellar area and a
subfront and transpterional route is used to expose the tumor in an
attempt to resect it subtotally (Fig. 30.24). These suprasellar germinomas
will frequently infiltrate optic nerves and enlarge the chiasm and nerves,
thus mimicking the appearance of an optic nerve glioma (Fig. 30.25). If
the tumor extends into the third ventricle, filling it and producing hydro-
cephalus, I prefer to use an anterior transcallosal approach and resect
the tumor from within the third ventricle.
Choroid Plexus Papillomas
These tumors are also approached through an anterior transcallosal
route. The third ventricle is entered by dividing the thalamostriate vein
and opening the choroidal fissure. This allows access to the entire third
ventricle. The tumor's blood supply can then be controlled and the tumor
resected.

Subependymal Mixed Gliomas of Tuberous Sclerosis

These tumors can reach enormous size (Fig. 30.26). They frequently
occlude the foramen of Monro and produce hydrocephalus. They too can
be approached through an anterior transcallosal route and frequently
require posterior enlargement of the foramen of Monro to allow resection
of the tumor. The Cavitron aspirator has proved invaluable in resecting
these tumors.
Conclusion
The advances in neuroradiological imaging of lesions in and around
the third ventricle during the past decade have allowed the neurosurgeon
to plan his approach to tumors in this region in a rational fashion. The
technological advances during the same period have allowed safe execu-
tion of a variety of routes to tumors in the region of the third ventricle
and expeditious removal of these tumors. Many of the intraaxial tumors
in the region of the third ventricle are low grade astrocytomas. In the
past these low grade tumors were frequently only biopsied and were then
treated with radiotherapy. Because of the follow-up that CT scanning
provides we now know that many of these low grade tumors do not
respond to radiotherapy. With radical resection there frequently seems
to be no further growth of the residual tumor over a follow-up of many
years.
However, there is little doubt that radiotherapy is of use for some of
these low grade tumors. Therefore, we can now reserve radiotherapy for
low grade tumors that cannot be removed subtotally and for low grade
tumors that behave in an aggressive fashion and continue showing
evidence of growth after subtotal removal.
The extraaxial tumors in and around the third ventricle can be totally
and safely removed with the technological advances that we now have
available to us, thus avoiding the risks inherent in courses of radiotherapy
to the developing brain of the child.
References
1. Allen JC, Nisselbaum J, Epstein F, Rosen G, Schawartz MK: Alphafetoprotein
and human chorionic gonadotrophin determination in Cerebrospinal fluid:
An aid to the diagnosis and management of intracranial germ-cell tumors. J
Neurosurg 51:368-374, 1979.
2. Bernstein M, Hoffman HJ, Halliday W, Hendrick EB, Humphreys RP: Thala
mic tumors in children: Longterm follow-up and treatment guide lines. J
Neurosurg 61:649-656, 1984.
3. Davies FA: Primary tumors of the optic nerve (a phenomenon of von Reck-
linghausen's disease); a clinical and pathological study with a report of five
 cases and a review of the literature. Arch Ophthalmol 23:735-821, 957-
1022, 1940.
4. Hoffman HJ: Supratentorial tumors in children. In Youmans JR (ed): Neu
rological Surgery. Philadelphia, 1982, pp 2702-2732.
5. Hoffman HJ: Craniopharyngioma: The continuing controversy on manage
ment. Concepts Pediatr Neurosurg 2:14-28, 1982.
6. Hoffman HJ, Yoshida M, Hendrick EB, Humphreys RP: Pineal tumors in
childhood. Concepts Pediatr Neurosurg 4:360-386, 1983.
7. Housepian EM: Surgical treatment of unilateral optic nerve gliomas. J Neu
rosurg 31:604-607, 1969.
8. Jackson H: Orbital tumors. J Neurosurg 18:317-439, 1912.
9. Kronlein RV: Zur Pathologie und Operativen Behandlung der Dermoid Cysten
der Orbita. Beitr Z Klin Chir 4:149-163, 1988.
10. Lapras C, Patet JD, Mottolese C, Lapras CA Jr: Results after surgery for
craniopharyngioma in 42 children. Presented at XIII Annual Meeting of the
International Society for Pediatric Neurosurgery, Mexico City, July 18, 1985.
11. Matson DD: Neurosurgery of Infancy and Childhood, ed 2. Springfield, IL,
Charles С Thomas, 1969, pp 523-536
12. Mori K, Handa H, Murata T, Takeuchi J, Nura S, Osaka K: Results of
treatment of craniopharyngioma. Childs Brain 6:303-312, 1980.
13. Rougerie J: What can be expected from the surgical treatment of craniophar
yngiomas in children: Report of 92 cases. Childs Brain 5:433-449, 1979.
14. Sweet WH: Radical surgical treatment of craniopharyngioma. Clin Neurosurg
23:52-79, 1976.
15. Wilson ER, Takei Y, Bikhoff WT, O'Brien M, Tindall GT: Abdominal metas-
tases of primary intracranial yolk sac tumors through ventriculo-peritoneal
shunts: Report of three cases. Neurosurgery 5:356-364, 1979.
31
Applications of Computerized Tomographic
Guidance Stereotaxy
Michael L J. Apuzzo, M.D., Parakrama T. Chandrasoma, M.D.,
Vladimir Zelman, M.D., Roger I. von Hanwehr, M.D., and Craig A.
Fredericks, M.D.

Refinements in the technology of radiographic imaging have revolu-

tionized the surgeon's appreciation of intracranial mass processes. From
the standpoints of localization and extent, lesions may be defined to
comprehensive limits that have previously been unappreciated. The wed-
ding of computerized tomographic (CT) radiological imaging and tech-
niques of stereotaxy allows the formulation of totally novel and improved
methods of management strategies for various intracranial disorders (9,
37) and mass processes (4, 6, 31, 41, 42, 50, 51, 53, 65). Perhaps in no
area of the brain is this more apparent than in the third ventricular
region, where the spectrum of pathology and the controversial nature of
many management strategies argue for low risk biological assays of
offending lesions and management techniques that are minimally trau-
matic in view of the physiologically fragile nature of the region and the
potential risks versus the benefits of major operative endeavors (4, 68).
Such has been the experience at the University of Southern California
Medical Center, where 500 consecutive CT stereotaxic guidance opera-
tions have been analyzed. Over 140 were studied for the definition of
management strategies of third ventricular region masses. These opera-
tions were undertaken for purposes of biopsy, culture, aspiration, per-
manent conduit placement, radionuclide implantation (4, 5, 28, 29, 38,
56, 57, 82), endoscopic visualization with biopsy (4, 6), excision, or
aspiration.
Although a number of stereotaxic instruments applicable to the tech-
niques of computerized guidance stereotaxy are available, our experience
and familiarity with the Brown-Roberts-Wells (BRW) system is presented
as the basis for point access, the guidance for point instrumentation as
defined in this chapter.
Instrumentation and Techniques
Stereotaxic Instrument
The BRW guidance system (Radionics, Inc., Burlington, MA) consists
of four major components: a head ring, a localizer unit, an arc guidance
system, and a phantom base simulator.
Head ring
This nickel-plated aluminum ring is fixed to the cranium at four points
by vertical graphite epoxy posts with plastic and steel pins (Fig. 31.1).
This component of the system acts as a stationary platform for the
localizer and arc guidance systems, which are applied during scanning
and the stereotaxic invasive procedure.
Localizing Unit
This component is comprised of six vertical and three diagonal graphite
rods and is attached to the head ring during the imaging process (Fig.
31.2). The rods act as reference markers on each scan slice and may be
mathematically related to an intracranial target point.
Arc Guidance System
This component consists of a base ring, a rotatable ring, and a perpen-
dicular arc (Fig. 31.3). The base ring is accurately and securely affixed to
the patient head ring by three mounting balls. The rotatable ring sur-
rounds the base ring and allows 360° (alpha) manipulation. Attached to
the rotatable ring is a perpendicular arc. This arc may be pivoted through
the base ring to 30° (beta). A radial slide is attached to the arc. This slide
has 180° (gamma) of movement along the arc. In addition, the slide
contains a sleeve that pivots 90° (delta) about the axis pin of the arc. This
sleeve accepts various bushings that act as carriers and direct the trajec-
tory of surgical instrumentation to the target point.
The combination of angle settings (alpha, beta, gamma, delta) are
computed in an Epson HX-20 programmable calculator and allow the
operator to design entry points to use with intracranial target points
anywhere within the sphere of the guidance arc.
Phantom Base
This device consists of a base ring (head ring equivalent) and a movable
pointed tip designated a "phantom target" (Fig. 31.4). This point may be
fixed to any x, y, and z setting. These settings are established when
calculation output coordinates for target point or entry point coordinates
are chosen with the arc system. After entry of scan coordinates and entry
point data derived from the phantom, the Epson HX-20 portable computer
provides the arc frame settings and the distance to the target. The target
coordinates are set in the phantom. Trajectory coordinates are placed on
the arc and checked on the phantom target. The arc system on the
phantom ring bears the same relationship to the phantom target as it will
to the intracranial target when it will be affixed to the patient base ring.
This provides an extracranial check of the target settings, arc coordi-
nates, and distances for the instrument placement in intracranial point
access.
Software
The software for the system uses data from x and у coordinates of the
central CT pixel of the nine localizer rods and CT target. Applying various
mathematical formulae, the two-dimensional formulae (x and y) are
transformed to three-dimensional coordinates (x, y, and z) relating the
position of the localizer rods and the targets to the plane with its vertical
height reference to the patient's base ring. With the x, y, and z coordinates
of the target derived, the design of the arc system allows a course and
distance to be plotted between any two points in space. These points are
the entry point (scalp or dura mater) and the target. Software allows for
selection of multiple targets, entry points, and parallel transits per scan
plane.
Steps in Point Access
Point access is achieved readily, rapidly, and safely with local anes-
thesia with standby utilized in all but selected pediatric cases.
Application of the Base Ring (10 Minutes)
After preparation of the scalp, selection of appropriate post and pin
position is made with the patient in the sitting position (Fig. 31.5). This
is most easily achieved on an operating room table in an anesthesia
preparation room. In most cases for lesions in the third ventricular region
the base ring is positioned in a plane defined by the tip of the nose and
the inion. Not only is the ring secured during placement fixation by a
Velcro strap, but observors at the foot of the operating table and lateral
to the patient visually monitor ring position during the placement. The
assistant lateral to the patient assesses ring position and manually main-
tains the sagittal suture in position parallel to the floor. The operator is
free to direct and infiltrate the scalp at the four points of fixation with
1% xylocaine with epinephrine. He advances the nylon drive pins to the
scalp and, adjusting the tracks, advances the four carbon fiber posts to
set the pins securely to the pericranium. This evolution requires 5 to 10
minutes to complete. Generally, intravenous contrast medium is being
infused during the early stages of this procedure. The patient is trans-
ported to the scanner with the anesthesiologist in attendance.
Scan Target (10 Minutes)
The localizer unit is affixed to the base ring in the scanner (Fig. 31.6).
Because detailed imaging studies have been previously attained, an ab-
breviated study defining desired aspects of the target region may be
obtained. Depending on the number of slices, this is generally accom-
plished in 10 minutes and the patient is returned to the operating room,
where he is prepared for the formal surgical aspect of the procedure. The
surgeons then study the scan slices, select a slice for targeting, and derive
and record pixel coordinates for the nine localizer rods and the targets.
These steps require 5 to 10 minutes.
Entry Point Selection (5 Minutes)
Entry points are selected according to the target position and may be
variable according to special elements of lesion, disposition, and extent.
Once a scalp point is selected the arc system is affixed to the base ring
and the entry point is marked in position by a probe placed to the point
and rigidly fixed in the arc (Fig. 31.7). The arc is then moved to the
phantom base where the x, y, and z coordinates are derived from three
appropriate scales and are recorded. Optimal entry point selection may
be attained within the scanning unit. If scanner software is appropriate,
an entry site may be marked during the imaging and planes of transit
may be reconstructed to the target point. This technique used concur-
rently with rapid bolus contrast infusion to define vascular structures
will increase the safety and control of the entry to target transit. This
requires 5 minutes.
Data Processing (10 Minutes)
All localization values for reference, the target values, and, finally, the
entry point coordinates are entered on the Epson HX-20 programmable
computer and appropriate alpha, beta, gamma, and delta settings are
derived for the arc system along with data describing the depth of the
target from the arc slide bushing. In addition, coordinates for localization
of the phantom are rendered (Fig. 31.8A).
Arc Settings and Phantom (10 Minutes)
The settings for the arc are entered and initially checked on the phan-
tom base against the entry point (phantom target) (Fig. 31.8, В to D). The
target coordinates in vertical, lateral, and anterior planes (x, y, z) are
then placed on the phantom as the target and the arc coordinates and
depth of transit to the phantom target point are checked, thus providing
the extracranial assessment of arc setting and transit trajectories and
distances. In addition, instrumentation to be introduced to the true target
point may be precisely calibrated to the phantom target.
In general, these preparations are usually completed in 45 minutes,
with additional time for transportation to and from the scanner.
Instrumentation at the Target Point
Biopsy
For purposes of biopsy a #13 gauge cannula with a blunt stylette is
introduced to the target site as a conduit (Fig. 31.9). In preparation for
the introduction of this instrument to the target point, a flexible bron-
choscopy cup biopsy forceps is advanced through the cannula and the
distance to the emergence of the cups is carefully marked with a Steris-
trip. The cup closure and length of introduction is determined on the
phantom base target point and marked with an adjustable sleeve in
reference to the rigid bushing and guide tube fixation of the arc system
(Fig. 31.10).
The scalp entry point is infiltrated with 1 % xylocaine with epinephrine,
and a 7- to 10-mm incision is made. The arc system is now affixed to the
base ring, and a guide tube appropriate for fixation of a long 4.5-mm
twist drill is passed and secured within the arc slide bushing. The twist
drill is then used to penetrate to the skull; the inner table is recognized
by a catch of the drill and minimal discomfort is appreciated by the
patient as the dura mater is encountered. A sharp probe is used to
penetrate the dura after the drill guide tube is exchanged for a 2.7-mm
guide tube in the slide bushing. The 13 gauge cannula is then advanced
to the target site (along the trajectory of the drill hole) in rigid fixation.
The blunt stylette is removed. The biopsy forceps is advanced to the
Steristrip marker and opened, and biopsies are obtained at various vec-
tors and, if appropriate, at various depths. An assistant opens and closes
the cups of the instrument while the operator palpates the barrel of the
flexible forceps, appreciating resistance and tissue texture changes. As-
piration for drainage and fluid analysis may be undertaken.
A number of devices for tissue retrieval have been used on our service
(Fig. 31.9 and 31.11). The flexible forceps are considered the best uni-
versal instrument for biopsy, while the slotted and coiled instruments
are dependent on minimal tissue resistance for removal of satisfactory
samples. The forceps have afforded satisfactory tissue samples with
minimal morbidity.
Permanent Conduit (Fig. 31.12)
For the placement of a permanent drainage conduit we have used a 22-
cm x 2.5-mm-diameter Silastic tubing with a rigid stylette (Radionics,
Inc., Burlington, MA). The device is available with either a single 0.5-cm
slot 0.5 cm from the tip or two 0.5-cm slots at 180° orientation 0.5 and 1
cm from the catheter tip. The catheter is fixed to a large Rickham
reservoir which is "countersunk" in the calvarium. The technique for
conduit placement is similar to that of biopsy. A 3-cm curvilinear scalp
flap is made. The arc-directed 4.5-mm twist drill penetration is then
followed by the use of a Cushing perforator to form a cone-shaped
depression in the calvarium, which will accept a Rickham device. The 13
gauge cannula is then introduced to the target point, aspiration is at-
tempted to assure entry to the cystic cavity, and the catheter is then
advanced to the target point, aspirated, trimmed, and secured to the
Rickham device, which seats in the calvarial depression.
Radionuclide Instillation (Fig. 31.12)
Colloid Beta Emitter. The use of colloid-based beta-emitting radio-
nuclides offers a plausible management option for cystic lesions in the
peri-third ventricular area. In particular, cystic craniopharyngiomas may
be approached by this technique. To avoid leaking of the colloid, we wait
7 to 14 days after the placement of a catheter-reservoir system and
perform a cystogram with metrizamide to determine cyst volume and the
integrity of the system (44). Cyst volume has been an important parameter
for our radiotherapists in calculating the quantity and distribution kinet-
ics of the colloid. The radionuclide is then infused in a single bolus
through the Rickham device.
Point Source Gamma Emitter. To assure homogeneous dose delivery
in solid tumors with strict control of the rate and dose distribution,
multiple sources of iridium-192 have been used with multiple catheter
arrays (5, 6). The rationale for this approach and elements of the tech-
nique have been previously described. It involves the transcutaneous
placement of Silastic catheters in parallel array to CT-derived target
points. The catheters are delivered through 4.5-mm twist drill calvarial
openings and are fixed to the scalp by adjustable Silastic cuffs, which
are initially secured to the catheters by Aron alpha acrylic. Later, follow-
ing afterloading with iridium ribbons, a large vascular clip is used to
consolidate the catheter ribbon and cuff complex for the 4- to 6-day
period of brachytherapy. After dose delivery, the scalp sutures are cut,
and the catheters with sources are removed at the bedside. The patients
are maintained on full dose high potency glucocorticoids and prophylactic
antibiotics intravenously by the heparin lock system during the period of
treatment. Glucocorticoids are then tapered related to patient tolerance.
Endoscopy
A 6.2-mm-diameter endoscope with a 20-cm-long barrel has been used
for both cerebroscopy and ventriculoscopy (Fig. 31.13). The instrument,
produced by Karl Storz Endoscopy (Tuttlingen, West Germany), provides
capabilities of visualization and irrigation and a port for the introduction
of point instrumentation for biopsy with either flexible or rigid cupped
forceps. In addition, specialized cannulae for cyst wall puncture and
aspiration are readily accepted (Fig. 31.14). Submersible quartz fibers for
transmission of laser energy may be likewise introduced for applications
of hemostasis or lesion coagulation.
These procedures are undertaken with local anesthesia with a neuro-
anesthesiologist in attendance. For visualization of the foramen of Monro,
a scan slice through the structure is obtained and the target point is
selected at the orifice. A 18-mm burr hole is then made 1 cm anterior to
the coronal suture in the right pupillary line, and the entry point coordi-
nate is selected from the center of the exposed dura (Fig. 31.15). After
checking of arc coordinate settings on the phantom base the dura is
opened and a 5-mm corticopial window is fashioned with bipolar coagu-
lating forceps. The endoscopy sheath with a blunt stylette in place is
then introduced through the rigid bushing (with a Teflon sleeve for ease
of passage) to the target point. The stylette is then removed and the
fiberoptic visualization package is introduced, sealing the system to the
target point. Irrigating fluid (Ringer's lactate) at body temperature is then
introduced intermittently through adjustable side ports. Visualization
may be enhanced in both clarity and scope by minor alterations of depth
and angulation within the arc system as well as employment of irrigating
fluid and instrumentation through the central port.
Cyst puncture and aspiration may be undertaken under direct visual-
ization at the foramen of Monro. A 13 gauge cannula with a blunt stylette
is introduced to approximate the cyst wall. Next, a sharp-tipped stylette
replaces the blunt one and cyst wall puncture is undertaken; the cannula is
then advanced into the cystic cavity and aspiration is undertaken.
Calvarial Entry Point Selection
Selection of an appropriate entry point is critical for the safety of transit
to individual target points. Such a selection is made based on considera-
tions of (a) the lesion's location, size, and suspected composition; (b)
intervening neural structures; (c) intervening vascular structures; and
(d) the target point and objective of the procedure.
The safety of transit is increased by using computer software that
allows real time reconstruction of transit planes or individual axial slice
presentation with cursor marking of transit points. This data manage-
ment capability, when coupled with rapid bolus infusion of contrast agent
to define neighboring and other vascular structures, enhances the safety
of transit and allows alteration of the entry point. Approximations of
entry point selection are presented in Table 31.1. Entry point and transit
trajectory are not standardized, but are selected individually related to
the four variables noted in the preceding paragraph.

Pathological Considerations
Although the technique of imaging directed stereotaxic brain biopsy
has been developed recently, the methods used for pathological interpre-
tation have been established for many years. The use of smears in the
diagnosis of nervous system lesions was first reported by Eisenhart and
Cushing and was perfected in later years (25, 40, 55, 70, 83). Many
extensive reports are available on the appearances of brain tumors on
smear preparations (2, 52, 83). Routine frozen sections and other histo-
logical techniques used are standard techniques.
The specimen obtained at stereotaxic biopsy differs from other brain
biopsy specimens in two ways, one a disadvantage and the other an
advantage.
The major disadvantage with the specimen is its size. The usual speci-
men is 1 to 2 mm in greatest diameter. Two or three such pieces are
obtained initially, with more similarly sized pieces provided if the pathol-
ogist cannot make a diagnosis. Although it seems to be restrictive initially,
as experience with the technique increases this represents an adequate
sample in the majority of cases.
A more serious limitation is the potential sampling error resulting from
the small specimen. When a neoplasm is a composite of various popula-
tions, errors may result. Differences in the degree of malignancy in
astrocytomas and variations in the appearance of pineal neoplasms in
different regions are obvious examples of such sampling problems.
The major advantage with the specimen is that it is obtained from a
predetermined CT scan target point in the lesion. With little exception,
this provides a more representative specimen than an open brain biopsy
at the edge of the lesion, where the greatest difficulty exists in establish-
ing a diagnosis.
The objective of a stereotaxic biopsy must be fully understood. It should
be used to provide a guide in terms of tissue diagnosis so that appropriate
treatment can be planned in a manner that is more rational and scientific
than without such information. When so utilized, stereotaxic diagnosis
is very successful because it provides excellent differentiation between
broad groups of lesions, e.g., inflammatory versus neoplastic. The rela-
tively minor variations between stereotaxic and final histological diag-
nosis rarely affect treatment.
Interpretation of the Stereotaxic Biopsy
Three factors are essential for the interpretation of the stereotaxic
biopsy. These are the pathologist, the neurosurgeon who performs the
biopsy, and the CT scan. In our institution, the neurosurgeon brings the
specimen and CT scan to the pathology frozen section area. For transport
from the operating room, the specimen is placed on a saline-soaked piece
of Gelfoam and is carried in a Petri dish. In rare cases where there is
difficulty obtaining a solid specimen, the pathologist comes to the oper-
ating room with fixative, stain, and microscope.
The pathologist who interprets the stereotaxic biopsy may be either a
neuropathologist with experience and interest in cytology and handling
small specimens or a general surgical pathologist with experience and
interest in surgical neuropathology and aspiration cytology. In our de-
partment the stereotaxic biopsies are interpreted by a surgical patholo-
gist. The establishment of a team of pathologist and neurosurgeon who
understand the procedure and work well together is imperative.
The neurosurgeon who performs the biopsy provides invaluable infor-
mation. The consistency of the specimen is important for two reasons.
First, it may give a clue as to the possible nature of the lesion. Second,
this information influences the way in which the specimen is processed.
The CT scan and its interpretation are critical, and a stereotaxic biopsy
should not be interpreted without this information. Discussion of the CT
scan always includes a clinical history and a differential diagnosis. If a
pathological diagnosis does not conform to the CT scan appearance, the
case is reevaluated. For example, a biopsy showing only low grade astro-
cytoma may be deemed insufficient and a request may be made for
additional sampling if the CT scan or clinical history suggests a more
histologically malignant neoplasm.
Processing the Stereotaxic Biopsy
We almost invariably prepare a smear as the first step in processing
the specimen. The only exception to this is if the neurosurgeon reports
an unusually firm consistency of the lesion at the time of biopsy. Very
firm lesions tend to smear poorly, and we proceed to frozen section
directly in this circumstance. This happens very rarely.
To make the smear, we cut out with a sharp scalpel blade a minute
piece from each biopsy specimen, lay these out in a horizontal row on a
glass slide, and smear them using a second glass slide. The best method
of smearing is to first crush the tissue between the flat surfaces of the
two slides and then draw the slides apart. With experience the amount
of pressure needed to make the optimal smear can be assessed by the
way in which the specimen crushes between the slides. All pieces are
sampled, and the smear from each piece can be separately identified by
its position on the slide. When the biopsies are less than 0.5 mm, the
entire specimen is used to make the smear.
The amount of pressure needed for making smears varies. Normal
brain smears very easily. Neoplasms vary in the way in which they smear
even within a given class of neoplasm. Low grade astrocytomas some-
times smear very easily but at other times do not smear out at all. When
a specimen does not smear out, we use maximal pressure to produce a
crush preparation. While this is not as satisfactory as a smear, it fre-
quently provides diagnostic information. Both slides used to make the
smear are stained.
The smear or crush preparation is immediately fixed in 100% methanol
and stained by a rapid hematoxylin and eosin (H & E) technique. This
takes 1 minute to perform, provides a permanent smear that can be
stored indefinitely, and gives excellent cytological detail. We initially used
air-drying and Romanowsky stain, as suggested in much of the literature,
but discarded it. Romanowsky-stained smears are associated with cyto-
logical distortion due to drying and are much less satisfactory for per-
manent storage. The latter is a major problem as the smear represents
the diagnostic material in many cases and the only diagnostic material
in a few cases. H & E staining is also much closer to what the pathologist
sees in routine sections and permits better correlation between smears
and sections. We also tried Papanicolaou stain, but discarded it as it
stained the background fibrillary material less effectively than eosin.
Currently, we use Romanowsky stains in addition to H & E only if a
diagnosis of malignant lymphoma is suspected.
Microscopic examination of the smear determines the further process-
ing of the specimen. If the initial smear is diagnostic, the remainder of
the material is placed in 10% formalin for permanent paraffin-embedded
sections. If the smear is not diagnostic, the rest of the material is proc-
essed, either by repeat smear or frozen section. If a diagnosis is still not
reached, additional biopsy material from a slightly different target point
is requested. We have never requested more than one additional series of
biopsies and have been successful in providing accurate diagnostic infor-
mation in over 90% of cases (4, 6). Where necessary, specimens may be
taken for electron microscopy or snap frozen for immunoperoxidase
studies and additional specimens may be sent for culture if an infectious
cause seems possible.
The Normal Brain Smear
It is part of training for the pathologist to examine normal brain smears.
We used autopsy brain to provide normal controls for different parts of
the brain. We found that such preparations provide more than adequate
material with surprisingly good preservation of cytological detail. Recog-
nizing normal cellularity of different areas of the brain and the appear-
ance of the normal fibrillary background of the deep cerebral white matter
is critical.
The brain around the third ventricle resembles deep white matter in
other areas of the cerebral hemispheres and does not cause confusion.
Stereotaxic biopsies of intraventricular lesions frequently show cells from
the choroid plexus. These appear as groups of columnar epithelial cells,
arranged in clusters and singly. Calcification is frequently present in the
choroid plexus. These features can cause confusion when diagnoses of
craniopharyngioma and colloid cyst are considerations.
Smears from the white matter of the cerebral hemispheres show scat-
tered glial cells in a background of fine fibers. The fibers are mainly the
long tracts passing through the area and do not originate in the glial cells.
Most of the glial cells are small, very uniform, and round to oval and
show few processes in routine smears. It is very difficult to identify
specific types of glial cells in normal brain. Such identification is possible
with special techniques (18). The thalamus and basal ganglia show the
presence of neurons in addition to glial cells. Neurons appear as large
cells with abundant cytoplasm and a central nucleus that contains a
prominent nucleolus.
Reactive Gliosis versus Astrocytoma
The differentiation of low grade astrocytoma from reactive gliosis pre-
sents fewer problems on stereotaxic biopsy than open biopsy. Delineation
of low grade astrocytoma at operation is difficult, and open biopsy spec-
imens are frequently from the periphery, where normal brain is infil-
trated by astrocytoma. We have great difficulty on such open biopsy
specimens where infiltration of brain by neoplastic astrocytes is very
difficult to differentiate from reactive gliosis. The stereotaxic biopsy
specimen is from the center of the much more accurately delineated CT
lesion, and the smear shows only neoplastic astrocytes and their proc-
esses and presents an appearance that is usually diagnostic.
Astrocytomas include the fibrillary astrocytoma and the juvenile pilo-
cytic astrocytoma. The latter occurs more commonly in the region of the
hypothalamus. These are difficult to distinguish on smear, and we use
the term astrocytoma to cover both lesions.
The majority of astrocytomas smear poorly, the cells tending to remain
in fibrillar masses (Fig. 31.16). The masses show a network of coarse
fibrillary processes in which are uniformly scattered fibrillary astrocytes.
The processes arise from and are traceable to the astrocytes, unlike in
normal brain. The cells are slightly larger than normal glial cells and
have short, spindle-shaped, often angulated nuclei with blunted ends.
More rounded cells may also be present. There may be considerable
cytological distortion. Although they smear with difficulty, the diagnosis
is easily made on smear, mainly by the greatly abnormal, coarse fibrillar
background. On frozen section, the cellularity is only slightly increased.
A minority of astrocytomas smear easily (Fig. 31.17). The increased
cellularity and the presence of coarse fibrillar processes arising from the
spindle or stellate astrocytic cells distinguishes these from normal brain.
Astrocytomas tend to be more uniform than reactive gliosis, where the
cell population seems to consist of several different cell types. Astrocy-
tomas with microcystic change appear more cellular on the smear than
on sections. Because of this, when a neoplasm with clinical or cytological
features of a low grade astrocytoma appears more cellular than usual, we
proceed to a frozen section.
The absence of significant cytological atypia, pleomorphism, endothe-
lial proliferation, mitotic activity, or necrosis is essential for a diagnosis
of low grade astrocytoma. The presence of any of these features, even in
a small area of the smear, suggests the probability of a more malignant
astrocytoma (26).
Reactive gliosis usually presents a more heterogeneous appearance,
with fibrillary, protoplasmic, and gemistocytic astrocytes and microglial
cells. These occur in a background that may have the fine granularity of
normal brain or be composed of coarse fibers. Inflammatory cells, includ-
ing neutrophils, lymphocytes, and plasma cells, foamy histiocytes, and
hemosiderin pigment may be present. We commonly encounter gliosis
when a stereotaxic biopsy is taken from the edge of a cystic or necrotic
lesion. In most of these cases, the CT scan appearance makes low grade
astrocytoma unlikely, so that differentiation of astrocytoma and gliosis
is not even a consideration.
Malignant Astrocytoma, Glioblastoma Multiforme
The diagnosis of malignant (or anaplastic) astrocytoma and glioblas-
toma multiforme is usually not difficult. Both present highly cellular
smears in the characteristic fibrillary background of astrocytic neo-
plasms (Figs. 31.18 and 31.19). There is cytological pleomorphism, nu-
clear enlargement, and abnormal chromatin distribution in the nuclei
(Fig. 31.20). These features are very prominent in glioblastoma multi-
forme. The presence of numerous gemistocytic astrocytes is also a com-
mon feature in high grade astrocytomas. Gemistocytic astrocytes are
recognizable as large cells with homogeneous eosinophilic cytoplasm and
a small, often eccentric nucleus.
Differentiation between malignant (anaplastic) astrocytoma and glio-
blastoma multiforme is possible when there is evidence of necrosis on
the smear. Necrosis is recognizable as either coagulated pink-purple
debris or better, as individual cells that have undergone coagulative
necrosis. We made a diagnosis of glioblastoma multiforme only when
necrosis is present (26). Endothelial proliferation is recognizable as col-
lections of cohesive spindle cells arranged in the linear fashion of a blood
vessel. A cellular astrocytoma that has endothelial proliferation, but no
necrosis, is reported as a malignant (anaplastic) astrocytoma. Sampling
is an important factor in the differentiation between these two astrocy-
tomas. A report of malignant astrocytoma is always accompanied by a
comment that glioblastoma multiforme cannot be excluded.
The differentiation of glioblastoma multiforme from metastatic carci-
noma can be made, usually without much difficulty, by the lack of
cohesiveness of the malignant astrocytes, the presence of numerous
gemistocytes, and, most importantly, the fibrillary background of astro-
cytic neoplasms (Figs. 31.10, 31.19, and 31.20).
The presence of extensive necrosis presents problems at stereotaxic
biopsy. A specimen composed of necrotic tissue is inadequate and neces-
sitates further sampling. Careful selection of the target point in the lesion
can avoid this problem.
Subependymal Giant Cell Astrocytoma
This neoplasm is composed of large cells with abundant pink cyto-
plasm, numerous fibrillary processes, and eccentric nuclei that resemble
gemistocytic astrocytes very closely. The clinical history of tuberous
sclerosis, the occurrence in a younger age group, and the ventricular
location of the subependymal giant cell astrocytoma should permit its
differentiation from gemistocytic astrocytoma.
Metastatic Neoplasms
Stereotaxic biopsy finds a major role in establishing a histological
diagnosis of a brain lesion in a patient with a known primary malignancy
elsewhere. In these cases, the diagnosis of metastatic carcinoma presents
few problems. Two types of smears may be seen. The first is a highly
cellular smear composed of cohesive malignant cells without a fibrillary
background from an area where the neoplasm has replaced normal brain
(Fig. 31.21). The cells vary in their differentiation. Melanin pigment of
malignant melanoma is more clearly seen in smears than frozen or
permanent sections. The second type of smear shows a small number of
cohesive cell groups in a background of necrosis or normal brain. In this
type of specimen, the smear represents a much more sensitive method of
establishing a diagnosis than a frozen section.
When a patient is not known to have a primary lesion elsewhere, the
diagnosis of metastatic tumor must be made on the features seen on the
smear alone. Carcinomas show cohesive groups of round or oval malig-
nant cells without fibrillary processes. The diagnosis of specific sites is
possible for a few distinctive tumors like oat cell carcinoma of lung and
renal adenocarcinoma. In most cases, however, the carcinoma is too
poorly differentiated to indicate the primary site.
Malignant neoplasms composed of noncohesive spindle cells are very
difficult to diagnose specifically. Metastatic sarcoma, sarcomas of the
brain, including meningeal sarcoma, and gliosarcoma are all possibilities.
Cellular, Nonastrocytic, Primary Neoplasms
Meningioma
Meningioma rarely occurs as an intraventricular neoplasm. It occurs
more commonly as a basal tumor that may extend up into the floor of the
third ventricle. The neurosurgeon frequently recognizes the firm consist-
ency of the neoplasm at the time of biopsy. On smear, meningiomas are
highly cellular and composed of meningothelial cells (Fig. 31.22). These
are easily recognizable as plump spindle cells with central nuclei and
abundant pink cytoplasm. The cells present as cohesive groups with
numerous single cells. Although they usually present a very regular
cytological appearance, considerable cytological atypia is not uncommon.
Enlargement of cells, pleomorphism, nuclear chromatin abnormalities,
and rare mitotic figures may be seen. Tight whorls are seen in most
cases. Psammoma bodies are seen in a few cases. Foamy histiocytes are
common and correlate well with xanthomatous degeneration. The back-
ground material is usually scant. In some cases, a collagenous background
is easily distinguishable from the fibrillary background of an astrocytic
neoplasm. It should be stressed that the critical diagnostic feature is the
recognition of meningothelial cells on smear.
Although we evaluate cytological atypia in meningiomas and include
these in our report, we do not attempt to predict biological behavior on
the basis of smears. In a few cases, extreme atypia on smear has corre-
lated with malignancy. We also do not attempt to classify meningiomas
according to histological subtypes.
Oligodendroglioma
Oligodendroglioma infrequently presents as an intraventricular neo-
plasm. The smear is highly cellular (Fig. 31.23). The cells are small and
dyscohesive and have very uniform round nuclei with a delicate chro-
matin distribution. The cytoplasm and cell membranes cannot usually
be seen on smears and a halo-like appearance is seen only rarely around
cells. The background is nonfibrillary and usually scant. Calcospherites
are commonly found, even when calcification is not appreciated radiolog-
ically, and are helpful in diagnosis. Another feature that is helpful is the
presence of numerous small blood vessels in the smear. These are rec-
ognizable as linear structures containing erythrocytes and lined by reg-
ular endothelial cells.
Ependymoma
Although uncommon, ependymoma frequently enters into the differ-
ential diagnosis of third ventricular neoplasms. On smear, they present
a fairly uniform population of small round to polygonal cells presenting
as lightly cohesive groupings and single cells. The cells have somewhat
hyperchromatic nuclei and scanty cytoplasm. The smear is highly cellular
and the background lacks astrocytic processes. Mild cellular atypia is
commonly present. The tendency to form rosettes varies. In one of our
cases, the smear was composed almost entirely of rosette-like cell clus-
ters. These had a central mass of fibrillar material surrounded by epen-
dymal cells (Fig. 31.24). In other cases, rosettes could not be identified on
smears, except for a tendency for the cells to group around vascular
structures.
Choroid Plexus Neoplasms
Normal choroid plexus is very distinctive, appearing as small cuboidal
to columnar cells lining a fibrovascular stroma that is frequently thrown
into papillary structures. We anticipate that cytological differentiation of
Papillomas from normal choroid plexus will probably be a matter of
quantity and accurate CT localization.
Pineal Neoplasms
Pineal neoplasms represent a very important group of lesions in the
region of the third ventricle. They are among the most troublesome at
stereotaxic biopsy because their frequent lack of uniformity make them
very prone to sampling errors.
We have encountered a number of germinomas presenting as intraaxial
para-third ventricle lesions. In one of these, the diagnosis was made with
relative ease because the smear showed the typical dual population of
germ cells and lymphocytes (Fig. 31.25). The germ cells appear as highly
active-looking, large, round cells with central nuclei. Cytological atypia
and mitotic activity are present. Although not appearing cohesive, the
cells tend not to separate extensively. Interspersed among these large
cells are numerous small lymphocytes and collagenous bands of varying
thickness. Another case presented the greatest difficulty in our experi-
ence with stereotaxic biopsies. Two separate stereotaxic biopsies showed
chronic inflammatory cells on smear and epithelioid granulomas on
sections (Fig. 31.26). Although culture was negative, the patient had an
unsuccessful trial of antituberculous therapy before the diagnosis was
made on open biopsy (Fig. 31.27). The germinoma had areas of extensive
granulomatous inflammation leading to a sampling error at stereotaxic
biopsy. Pineal germ cell tumors are frequently mixed, with teratoma,
embryonal carcinoma, and yolk sac carcinoma present in varying
amounts (12). This presents obvious sampling problems. However, bio-
chemical markers in serum and Cerebrospinal fluid may suggest such a
composite if it is overlooked because of sampling error.
 Germinomas and other germ cell tumors can occur in the floor of the
third ventricle ("ectopic pinealoma").
Pineal parenchymal neoplasms also present problems. Pineocytomas
are characterized by a uniform population of round, dyscohesive cells
with scant cytoplasm (Fig. 31.28). These resemble Oligodendroglioma on
smear. Pineoblastomas are composed of very primitive, intermediate-
sized cells that tend to form cohesive groups. The cells have hyperchro-
matic nuclei and scanty cytoplasm and tend to show nuclear molding.
Extensive necrosis and a high mitotic rate are common. In one of our
cases, two separate stereotaxic biopsies showed both of these types of
neoplasm (Fig. 31.29), representing a transitional form (33).
Pituitary Adenoma
Pituitary adenoma appears as a third ventricular lesion only when it is
large and invasive. Such tumors are usually obvious on CT scan, and
stereotaxic biopsy is rarely undertaken. On smears, cells from pituitary
adenomas appear as small, dyscohesive round cells with delicate nuclei
and variable amounts of cytoplasm. Those lesions that are invasive tend
to have greater degrees of cytological atypia.
Craniopharyngioma
Craniopharyngioma is a frequent diagnostic consideration in this re-
gion. The cytological identification of a craniopharyngioma depends on
the presence of squamous epithelial elements. Tissue from solid areas
shows large cohesive sheets of benign squamous epithelium (Fig. 31.30).
Considerable cytological atypia may be present. Smears from cystic areas
show squames. Examination of fresh smears made from the oily fluid in
polarized light for the presence of cholesterol crystals is a useful diagnos-
tic maneuver. Calcification is very common, both in smears and in
sections, and is helpful in making a diagnosis in a cystic lesion of the
third ventricle. Correlation of the CT scan and clinical features precludes
confusion with well-differentiated metastatic squamous carcinoma,
which may be suggested when cytological atypia is present. Distinction
from an epidermoid or dermoid cyst is impossible on the smear, although
the CT appearance of a solid component to the mass would suggest
craniopharyngioma (Fig. 31.31).
Colloid (Neuroepithelial) Cyst
Colloid cysts are characterized by their epithelial lining, which is usu-
ally cuboidal or columnar and may be ciliated, and its gelatinous contents
(Fig. 31.32). Stereotaxic biopsies from outside the wall show gliotic brain
and choroid plexus. Smears from the cyst wall that we have made from
excised specimens show columnar epithelium that resemble choroid
plexus epithelium. In one of our cases, there was marked cytological
atypia and increased mitotic activity (Fig. 31.33). Histological examina-
tion of these cases showed the epithelial lining to be three to four layers
thick without any invasive tendency. Smears of cyst contents do not have
any diagnostic characteristics.
Other Cysts
Epidermoid and dermoid cysts rarely occur in this region. Smears from
the cyst interior and wall show anucleate squames and squamous epithe-
lial cells. Distinction from craniopharyngioma needs clinical correlation.
Arachnoid cysts rarely enter into consideration in the diagnosis of a
cystic lesion in this region. Its content of Cerebrospinal fluid distinguishes
it from other cysts. The arachnoidal cell lining of these cysts is difficult
to identify on small biopsy specimens.
Malignant Lymphoma
Primary lymphomas of the brain may occur in the region of the third
ventricle. They are more frequently encountered since the onset of the
current epidemic of acquired immune deficiency syndrome (AIDS). In
these patients, the neurological mass lesion is frequently the first mani-
festation of AIDS. Smears from lymphomas show a monomorphous pop-
ulation of transformed lymphocytes. The most common subtype is im-
munoblastic sarcoma, the immunoblasts appearing as round, large cells
with large nuclei showing prominent nucleoli and abundant cytoplasm.
More rarely, the lymphoma is composed of small lymphocytes, frequently
showing plasmacytoid features. These cases are unusual and difficult to
differentiate from a reactive lymphocytic infiltrate associated with an
inflammatory process. Smears to establish monoclonal staining for im-
munoglobulin markers are essential for diagnosis in these cases. Air-
dried smears are optimal for such marker studies.
Inflammatory Lesions
Granulomas
Granulomas present several problems in diagnosis. First, the smear
frequently consists entirely of the central necrotic material which is not
diagnostic. Second, the epithelioid cells are difficult to recognize as such
in smears. When an admixture of lymphocytes is present, as is frequent,
the recognition of the mass as inflammatory is easier. Third, the identi-
fication of a granuloma does not provide a specific diagnosis. We have
identified Coccidiodes immitis spherules in the center of one granuloma
and acid-fast bacilli in two others. Culture, however, is essential for
diagnosis. In one case, the granulomatous inflammation was part of a
pineal germinoma.
Toxoplasmosis
Infection with Toxoplasma gondii has become common in patients
with AIDS. The lesions are difficult to distinguish from malignant lym-
phoma clinically. Stereotaxic biopsy is the method of choice in most cases
to establish a tissue diagnosis. Toxoplasmosis is usually characterized by
a necrotizing encephalitis in which Toxoplasma pseudocysts can be
identified. We have successfully identified pseudocysts on both frozen
sections and smears. Pseudocysts of Toxoplasma appear as large,
rounded structures containing numerous trophozoites. The diagnosis is
suggested on the initial smear by the presence of necrosis, a polymor-
phous inflammatory infiltrate containing lymphocytes, plasma cells, and
numerous foamy histiocytes (Fig. 31.34). If no trophozoites are identified
on the smear, frozen sections, often multiple, should be performed (Fig.
31.35). Immunoperoxidase techniques for toxoplasma pseudocysts and
trophozoites are useful.
Acute Encephalitis
Herpes simplex encephalitis rarely enters the differential diagnosis of
a mass lesion in the region of the third ventricle. It does, however, come
into consideration when the smear shows a mixed inflammatory reaction
and no infectious agent is identified. In herpes simplex encephalitis,
there are numerous transformed lymphocytes, cells with large eosino-
philic intranuclear inclusions, and bi- and multinucleated giant cells.
The binucleate cells resemble Reed-Sternberg cells. Immunoperoxidase
techniques and electron microscopy are extremely useful in confirming
the diagnosis.
Cysticercosis
Cysticercal cysts commonly occur in the third ventricle and the supra-
sellar region. In the Los Angeles County Hospital, which serves a large
Mexican population, this is a common lesion.
Stereotaxic biopsies are commonly from the gliotic inflamed brain
adjacent to the cyst. These show increased cells with astrocytes and
inflammatory cells. The presence of large numbers of eosinophils in this
area is highly suggestive of cysticercosis. Fragments of choroid plexus in
the biopsy may cause confusion with epithelium-lined cysts. The cysti-
cercal cyst is lined by a homogeneous structureless eosinophilic cuticle
that is thrown into scallops. Immediately below this are numerous small
basophilic bodies that resemble daryorrhectic nuclei. Calcification is
common. Aspiration of cysticercal cyst contents produces a watery fluid
in which small fragments of cuticle may be seen. This, however, is
difficult to distinguish from artifact, and a diagnosis is rarely made on
smears of cyst fluid.

Anesthetic Considerations
The successful outcome of stereotaxic neurosurgical procedures is, to
a large extent, dependent on the smooth relationship between analgesic/
amnestic neuroleptic local standby anesthesia and the effective mainte-
nance of a precise and reproducible stereotaxic routine. The demands
placed on the neuroanesthesiologist center around amnestic sedation,
neuroleptic analgesia, and the continuous assessment of neurological
function.
Issues governing the attainment of these objectives are: (a) the effective
preoperative priming of patient expectations and comprehension relating
to the procedure, (b) development of isolated voice recognition as a chan-
nel of communication between anesthetist and patient, (c) identification
of functional neurological implications posed by the specific abnormality,
(d) selection of adequate but judicious premedication, (e) the use of a
controlled sedation-titration technique throughout the procedure, (f)
adequate airway access for rapid intubation should the extremely infre-
quent need for induction of general anesthesia arise, and (g) monitoring
of neurological assessment including speech, cognition, sensorimotor
lateralization, and level of consciousness.
Appropriately managed local standby anesthesia permits a maximum
of operative control as well as patient comfort and safety. In over 500
cases managed by stereotaxis from 1981 to 1986 at LAC-USC Medical
Center, discrete anesthetic complications have not been encountered.
Clinically manifest seizure activity occurred in 2 patients with mass
lesions. The induction of general neuroanesthesia was electively under-
taken in 10 preoperatively obtunded patients.
There are a number of key stages to local anesthesia during a stereo-
taxic procedure that relate to the various operative, radiographic, and
transport steps described in the previous section. Before the procedure,
patient evaluation, preparation, and premedication must be established.
Once in the operating room area where the base ring is to be applied,
reliable venous access and stable physiological monitoring are attained.
Conray contrast infusion is generally instituted in all CT-guided proce-
dures at this point. Depending on the nature of the lesion, prior delayed-
dose contrast infusion may be utilized. Contrast dye hypersensitivity
reactions must of course be anticipated, and one must be prepared to
treat these appropriately. Institution of appropriate neuroleptic sedation-
titration technique along with the surgeon's delivery of generous local
cutaneous analgesia is required before application of the stereotaxic
reference base ring.
Transport of the patient to and from the CT scanner and the operating
room suite must be well planned from an anesthetic point of view to avoid
delays in the flow of the stereotaxic routine. Continuation of analgesic/
amnestic sedation as well as attention to maintaining proper physiologi-
cal monitoring are important during these stages.
Once in the operating theatre, appropriately titrated anesthesia is
continued. Before the actual operative phase when the skin incision,
twist drill hole, and biopsy are to be performed, the surgeon again applies
local cutaneous analgesia. At the conclusion of the procedure the anes-
thetist begins reversal of anesthesia about when the base ring is being
removed. Patient monitoring is continued during transport to the recovery
room area or the CT scanner for the standard postoperative CT scan.
The relevant neurological aspects underlying a patient's particular
diagnosis must be adequately ascertained preoperatively. One must con-
sider the presence of any significant intracranial mass effect, intracra-
nial hypertension, or hydrocephalus, as well as any underlying systemic
problems (cardiopulmonary and metabolic stability).
The presence of stability in the patient's psychological status as it may
be related to modification of neuroleptic anesthesia at certain points
during the procedure is of considerable importance. Patient education is
particularly relevant in relation to this last point. With repetitive and
reassuring explanations of the details of the stereotaxic technique one
will develop an operantly trained participant. Such a patient will take an
active and interested but calmly cooperative and hypokinetic role.
Pharmacological agents useful for neuroleptic sedation-titration tech-
nique during stereotaxic procedures include benzodiazepams, narcotics,
hypnotics, butyrophenones, and related agents, of which the most com-
monly employed exampes are: diazepam (Valium), meperidine (Demerol),
fentanyl (Sublimaze), droperidol (Inapsine), alphaprodine (Nisentil), and
hydroxyzine (Vistaril).
Glucocorticoids and, at times, anticonvulsants or diuretics are used in
the presence of mass lesions, cerebral edema, or elevated intracranial
pressure. Antimicrobial agents may be appropriate during endoscopy or
protracted procedures entailing multiple stereotaxic corridors or the im-
plantation of foreign bodies (interstitial stereotaxic radioisotope implan-
tation for tumor brachytherapy is one example).
If one adheres to the basic practical strategies outlined here for effective
neuroanesthetic management of the various CT-guided stereotaxic pro-
cedures, successful and efficient realization of neurosurgical objectives
may be more reliably attained. In undertaking such a procedure where
the patient plays such an active role and multiple detailed steps must be
carried out with reproducible meticulous precision, the role of the anes-
thetist is vital. Patient cooperation and responses during the transcere-
bral probe transit and target point surgical manipulations enhance the
safety of the method.

Experience and Rationale for Utilization of the Technique

With the use of these techniques in over 140 operations in the third
ventricular region, procedural objectives as described in the previous
section were realized in 98% of cases (histological and/or microbiological
verification in 94%) with a mortality rate of less than 1 % and a significant
complication rate of less than 2% (Figs. 31.36 to 31.41). Based on the
broad spectrum of abnormalities in both the anterior and the posterior
third ventricular regions as well as the generally restricted ability of
imaging and indirect diagnostic procedures to provide absolute histologi-
cal or microbiological diagnosis, the technique of imaging-guided stereo-
taxis should be considered as an alternative initial procedure to crani-
otomy in cases where midline lesions seem to be of intrinsic neoplastic
or infectious origin or potentially radiosensitive or when the diagnosis is
in doubt (15, 17, 62, 63). This stereotaxic procedure provides diagnosis
at low risk and offers a rational guide for proceeding to further therapy,
which may include craniotomy, radiotherapy (teletherapy and/or brach-
ytherapy), or chemotherapy (antimicrobial or antineoplastic).
In the anterior and mid-third ventricular regions, cystic lesions such
as colloid cysts or cysticercosis may be aspirated or excised with or
without direct visualization by using a variety of cerebroscopic techniques
(4, 6, 7, 14, 19, 39, 48, 54, 66, 69, 76, 79). In high risk patients or those
with recurrent lesions, craniopharyngioma cysts may be aspirated and
treated with colloid-suspended radionuclides (10, 11, 44).
The posterior third ventricular and pineal region provides a site for a
diverse spectrum of pathological processes and diverse neoplastic involve-
ment (21-24, 32, 35, 36, 45-47, 60, 67, 72, 74, 75).
 In spite of their complexity, the diverse spectrum of pineal region
tumors may be simply classified into four major groups: germ cell tumors
(germinomas and teratomas), pineal parenchymal cell tumors (Pineocy-
tomas and pineoblastomas), tumors of supporting (glial stroma) or adja-
cent tissues and others, and nonneoplastic cysts and vascular lesions.
Of the true pineal tumors, approximately 80% are of germ cell origin.
Of these, 70% are germinomas and 30% are teratomas (60% benign, 40%
malignant). Pineal cell tumors (Pineocytomas and pineoblastomas) ac-
count for approximately one-fifth of the lesions. Long term survival has
been reported after the excision of benign and circumscribed lesions (30%
of the entire spectrum) as well as after radiotherapy of germinomas (20,
73, 80, 81). Histologically malignant lesions in this region have a uni-
formly poor prognosis in spite of multimodality aggressive therapy. These
lesions include embryonal carcinoma, endodermal sinus tumor, and cho-
riocarcinoma in pure form or as a component of mixed lesions including
other germinal components. Approximately 35% of germ cell tumors are
comprised of mixed elements.
Computerized radiographic imaging defines the presence and general
extent of this spectrum of pathological lesions in the majority of cases.
Most commonly, masses present as high density lesions with contrast
enhancement. Although radiographic imaging is suggestive of a diagnosis
in many cases (especially teratomas and cysts), strict histological ap-
praisal is not uniformly obtainable.
The presence of biological tumor markers in the serum or Cerebrospinal
fluid may indicate a functioning cellular component of these tumors (3,
7, 8, 30, 34). In general, the functioning tumors have a poor prognosis.
Beta chain human chorionic gonadatropic hormone is considered indic-
ative of the presence of a choriocarcinoma or a mixed germ cell tumor
with choriocarcinomatous elements. Alpha-fetoprotein in spinal fluid or
serum is considered indicative of an endodermal sinus tumor or a mixed
germ cell tumor with endodermal sinus elements.
Cerebrospinal fluid cytology assessment may indicate the presence of
malignant cells, but is of limited overall practical value because of the
lack of consistency of response (less than 20% in potentially disseminat-
ing neoplasms).
With the complexity of histological types of lesions that may evolve
there is little doubt that adequate histological diagnosis should be the
initial objective in patient management. Stereotaxic biopsy provides such
data which, when combined with imaging studies and biological marker
assays, may be used to direct further therapy, which may include opera-
tion, whole neural axis radiation, or polychemotherapy (1, 13, 16, 20, 27,
43, 49, 58, 59, 61, 64, 71, 77, 78, 80-82).
Considering the histological spectrum of tumors, diagnostic capability
of imaging devices, availability of biological markers, current imaging-
guided stereotaxic methods, and effectiveness of therapeutic modalities,
it seems that direct surgical approaches should be reserved for benign
potentially excisable lesions and malignant and mixed germinal tumors,
where multimodality therapy offers the best opportunity for palliation.
With techniques of imaging-directed stereotaxis it is possible to select
patients who may derive the major operative benefit before undertaking
a direct surgical approach.

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Commentary E
Contemporary European Contributions to Neurosurgical Stereotaxy
Roger I. von Hanwehr, M.D.
Significant contributions within the field of
stereotaxic neurosurgery have emerged from the
European sector, especially since the advent of
contemporary computerized tomography (CT),
beginning in the early 1970s. The actual and
potential application of stereotaxic technology in
the diagnosis and therapeutic management of
mass lesions either impacting on deep midline/
paramedian neural axis structures within the
cranial vault or directly situated throughout the
diencephalic region has been readily apparent in
original work emanating from Sweden, France,
the United Kingdom, Spain, Italy, the Federal
Republic of Germany, and the Benelux countries.
Diverse areas of progress within the field of neu-
rosurgical stereotaxy have included: (a) devel-
opment of various CT-guided stereotaxic sys-
tems; (b) numerous diagnostic biopsy tech-
niques; (c) localization of deep-seated cystic, neo-
plastic, or vascular lesions followed by often
innovative surgical management effected via
stereotactically defined access corridors; (d) in-
terstitial radioisotope implant brachytherapy; (e)
high energy lesion radiosurgery; (f) miscella-
neous but potentially applicable adaptions of
stereotaxy ranging from cryosurgery to assess-
ment of deoxyribonucleic acid (DNA) distribution
patterns within gliomas; and (g) more recently
the utilization of precise implantation methods
intended for attempts at microtransplantation
within the central nervous system (CNS).
The evolution of CT-guided stereotaxic tech-
nology has involved the utilization and adaption
of numerous systems with individual variations
between differing national settings. The current
British contribution has centered on both the
Bennett stereotaxic frame with transfer of CT-
defined target coordinates via the Leksell method
and the Brown-Robert-Wells stereotaxic appa-
ratus, which permits direct CT-guided stereo-
taxic intervention (76, 78). In contrast, stereo-
taxic systems used in Belgium and France (Sue-
tens and Talairach methods, respectively) rely on
indirect transfer of CT-reconstructed or cerebral
angiographic data to provide multidimensional
spatial definition of target lesions, including the
potential availability of stereoscopic imaging and
simulation of biopsy probe/electrode positioning
(72). An Italian team (Colombo/Dettori) has de-
veloped reliable techniques for CT control of
diencephalic lesions in functional stereotaxis as
well as a novel adaption of the Reichert-Mundin-
ger apparatus, the Siemens Siretom 2000 CT
scanner, and a rigidly attachable calvarial coor-
dinate system, thus permitting combined or sep-
arate use of CT, angiographic, and encephalo-
graphically derived targeting data (22, 26). Var-
ious German groups have contributed toward the
innovation of more elegant stereotaxic interven-
tion, primarily relying on the Reichert-Mundin-
ger device coupled to CT imaging technology
during stereotaxic biopsy and interstitial brachy-
therapy procedures (9, 10, 47, 71). The develop-
ment of various base ring, phantom coordinate
grid, and stereotaxic coordinate assemblies has
been extensively detailed in conjunction with
computer-assisted direct axial tomography ref-
erence point and target point guidance (9, 10, 47,
50, 71). Digital radiographic systems have also
been developed in conjunction with CT-guided
stereotaxic systems (31), whereas new targeting
devices within existing stereotaxic assemblies
allow constant CT guidance during a given pro-
cedure in conjunction with universal reference
modes that facilitate multiple entry and target
points as well as varied transit trajectory settings
(32). Although the Leksell stereotaxis unit has
remained the cornerstone of the leading Swedish
impact on this subdiscipline of neurosurgery
(38), more contemporary stereotaxic instrument
systems such as that of Boethius allow direct
data interface between the surgical stereotaxic
assembly and various diagnostic neuroradiologi-
cal (CT, positron emission tomography (PET),
magnetic resonance imaging (MRI), etc.) or ther-
apeutic (linear accelerators, stereotaxic "gamma
knife" radiosurgery units, cryosurgery devices,
etc.) technology (12, 14). Other Swedish groups
have provided valuable ancillary insight into the
refinement of CT data acquisition for the pur-
poses of ensuring accurate stereotaxic coordinate
determination during surgical procedures (8, 75).
 The major impact of increasingly accurate CT-
guided biopsy techniques is apparent in the
Swedish as well as the overall European stereo-
taxic experience. Willems et al. demonstrated
highly reliable (87 to 88%) cytodiagnostic accu-
racy in 112 stereotaxic aspiration biopsies of
benign and malignant neoplasms in part located
in sellar, suprasellar, diencephalic, and pineal
locales (80). Edner similarly reported 94 stereo-
taxic puncture biopsies in cases of sellar, para-
sellar, and suprasellar lesions, of which 28 were
CT-guided (29). Various therapeutic options in-
cluding cyst aspiration (in the case of cranio-
pharyngiomas), intracystic radioisotope instilla-
tion, etc., were included in the stereotaxic series,
with the initial diagnostic impression gained
from a stereotaxic intervention guiding eventual
therapeutic action. Utilizing the Leksell stereo-
taxic apparatus, the same author detailed 345
biopsy procedures including 84 directed at
mostly deep-seated sellar, diencephalic (third
ventricular/foramen of Monro), pineal, basal
ganglia, and hypothalamic cystic lesions, as
identified with enhanced CT imaging in roughly
half of these cases (30). Twenty-two solid lesions
in the identical anatomical distributions were
also encountered. Using enhanced CT data, path-
ological diagnostic accuracy approached 90%
with a mortality of less than 1 % and a morbidity
of 2.3%. Cystic lesions encountered in the supra-
sellar/diencephalic domain included craniophar-
yngiomas, cystic gliomas, and arachnoidal as
well as colloidal cysts. Solid lesions of the third
ventricle and pineal regions included astrocyto-
mas, pineoblastomas, germinomas, and ependy-
momas as well as a rare dermoid and teratoma-
tous lesion. Other Swedish teams have developed
related issues relating to contrast enhancement
techniques/patterns and CT criteria that aid in
the effective lesion localization, definition, and
target evaluation essential in effective stereo-
taxic diagnosis of deep midline glial neoplasms
(44, 45).
In Belgium (Waltregny) and in the Netherlands
(Bosch), further experience with stereotaxic bi-
opsy has resulted in clarification of specific in-
dications (a) for serial stereotaxic biopsies where
extensive pathological and structural/anatomi-
cal assessment of tumor constituents and vol-
ume is deemed appropriate and (b) for stereotaxic
biopsies designed to establish histopathological
diagnosis permitting nonsurgical management of
extremely radiosensitive deep midline lesions
(dysgerminomas) or conversely stereotaxic evac-
uation of cystic diencephalic lesions (third ven-
tricular colloid cyst) (15, 79).
The reliability of stereotaxic biopsies from a
diagnostic standpoint has been the focal impetus
of the Italian contribution to this application of
neurosurgical stereotaxy. Scerrati et al. found a
near perfect reliability of diagnostic information
in the stereotaxic biopsy of intracranial space-
occupying lesions, whereas de Divitis cited an
accuracy of 81 to 92% in the evaluation of 64
cases including 27 neuroglial tumors represent-
ing the lower margin of diagnostic accuracy (24,
65). Broggi specifically reported a small series of
17 pediatric deep-seated neoplastic lesions (in-
cluding third ventricular, suprasellar, and pineal
masses) where a CT-guided stereotaxic Reichert
apparatus afforded a highly accurate and varied
compendium of tissue diagnoses in part obtained
through imprint cytological techniques (19). The
same author separately cited a diagnostic accu-
racy of 85% in an overall series of 200 biopsies
utilizing varied transit trajectory options, tissue
impedance, and depth electroencephalogram re-
cording techniques all aimed at maximizing ster-
eotaxic localization and three-dimensional topo-
graphic definition of the mass target lesion in-
volved (18). Lobato, from Spain, provided addi-
tional data on 28 diencephalic and deep-seated
midline lesions which, in some cases, underwent
CT-guided stereotaxic biopsy with an overall di-
agnostic accuracy of 89% (10- X 1.2-mm speci-
mens harvested utilizing a Backlund spiral
needle) and a complication rate of 8%, including
7% with transiently increased neurological defi-
cits and a 1 % incidence of postbiopsy intracere-
bral hematoma (46).
Although the French contribution to CT guid-
ance in stereotaxic biopsy procedures remains
limited because of continued reliance on stereo-
taxic angiography (Talairach system), a large se-
ries reported by Sedan (318 biopsies) detailed
criteria for limiting potential complications, in-
cluding less than 4 biopsy trajectory passes per
procedure, decreasing biopsy sampling fre-
quency, and judicious selection of patients as
well as stereotaxic entry point to target point
transit route (66). A fairly broad experience with
stereotaxic biopsy techniques was also described
by Daumas-Duport, with nearly exclusive em-
phasis on correlation between CT findings and
histological configuration, which is presented as
an important factor in the choice of successful
trajectory routes during stereotaxic biopsies (27,
28).
With reference to stereotaxic biopsies directed
at deep midline and diencephalic target mass
lesions, the German experience of the Freiburg
group (Mundinger, Birg, Ostertag, Kiessling, and
 Kleihues) remains the dominant contribution
(36, 48, 60). Direct CT stereotaxis utilizing the
Mundinger/Birg computer-compatible version of
the Reichert/Mundinger stereotaxic apparatus
has been refined to the point where, given certain
reference relationships with the stereotaxic de-
vice and patient on the one hand and the CT scan
gantry on the other hand, the CT screen and
stereotaxic apparatus coordinates are identical,
thus obviating any need for a reference frame or
conversion system (48). This permits biopsies or
implantation corridors to be effected in a given
patient at exact and reproducible targets and
trajectories. In over 600 patients, biopsies by the
Freiburg stereotaxic team yielded accurate tumor
diagnoses and approximate grading (combined
cytological/histological evaluation) in 82% of
cases (36). Immunohistochemical tumor marker
and cytoskeleton protein identification may fur-
ther enhance this rate of diagnostic accuracy. In
stereotaxic biopsies of 302 deep-seated brain tu-
mors by the same group, 30% of lesions were
situated in the basal ganglia, 36% in the deep
cerebral hemispheres, 13% in the parapineal re-
gion, and 21% in the diencephalic/suprasellar
regions (60). A wide and comprehensive scope of
pathological diagnoses cover the full spectrum of
the patient population reported, but most of the
lesions were gliomas (71%). Operative mortality
was 2.3% with a 3% incidence of transient neu-
rological deterioration within the overall series
(60). In nearly all cases of complications, an in-
tracerebral hematoma was the offending post-
biopsy development. Biopsy samples with an av-
erage volume of 1 mm3 were routinely obtained
with a special stereotaxic microbiopsy forceps
(diameter 0.8 mm), and one or more samples were
harvested at intervals of 5 to 10 mm within the
transit pathway (60). Local anesthesia was rou-
tinely utilized. Stereotaxic biopsy led to therapeu-
tic management decisions involving interstitial
radioisotope implant brachytherapy in 74% of
cases and further surgical intervention (stereo-
taxic or conventional) or external irradiation in
26% of cases (60).
Innovations in operative stereotaxis other
than biopsy-directed procedures are extensive
throughout the European stereotaxic experience.
Operative stereotaxic CT-guided management is
usually based on valuable diagnostic information
gained during the biopsy procedure. In addition,
the stereotaxic approach offers an accurate
means to localize the target lesion via a safe,
selected transit corridor, while stereotaxic data
also provide further information defining the
stereoscopic three-dimensional topography of a
given lesion if the appropriate CT-guided imaging
and stereotaxic system is utilized (64). Stereo-
taxic treatment of deep-seated diencephalic/
midline lesions may involve interstitial radioiso-
tope implantation (brachytherapy), intracavitary
Curie therapy utilizing radiocolloid agents, direct
drainage of cystic structures (arachnoid cysts,
colloid cysts, neoplastic cysts, abscesses, etc.),
stereotaxic ventriculostomy or ventriculocister-
nostomy (cystic craniopharyngioma, arachnoid
cyst), direct instillation of immunotherapeutic
agents (interstitial interferon), and combined
open-stereotaxic procedures for a direct surgical
approach to small deep-seated neoplasms or vas-
cular malformations (53). One particularly ger-
mane operative application of stereotaxy relates
to diencephalic access with a minimum of risk
in the case of colloid cyst aspiration techniques
that have been reported from Sweden (Bosch,
Rahn, Backlund) and Spain (Rivas, Lobato) (17,
62). The former group has reported four cases of
stereotaxic third ventricular colloid cyst aspira-
tion utilizing air ventriculographic or CT guid-
ance and employing cannula probes 0.6 to 1.5
mm in inside diameter (ID) for cyst puncture. The
volume yield of the viscous aspirates averaged
0.3 to 1 ml and this type of specimen allowed
accurate cytological diagnosis. Two of four cases
demonstrated no cyst recurrence on follow-up
CT evaluation, whereas the remaining two cases
demonstrated cyst remnants and a decreased
cyst size, respectively (17). The report by Rivas
et al. again cited three cases with stereotaxic
colloid cyst aspiration via a Leksell-Jernberg CT-
adapted stereotaxic frame (62). In two of these
three cases, aspirates of 1.8 and 40 ml were
obtained utilizing 1.2- to 1.8-ID probe cannulas
with an internal spiral biopsy device designed to
enter through the cyst capsule. Cytological diag-
nosis was confirmatory with periodic acid-
Schiff-positive amorphous eosinophilic colloid
cyst contents being present. Concomitant hydro-
cephalus was reduced or resolved along with the
complete disappearance of both cysts. The third
patient required repeat stereotaxic aspiration
with a 1.8-mm cannula yielding 2 ml of viscous
material, and again the postoperative course was
eventually characterized by resolution of the cyst
(62). Thus, stereotaxic approaches to third ven-
tricular cysts of this type may represent a viable
and potentially less risky alternative to conven-
tional open surgical management techniques.
Utilization of stereotaxic methods for the evac-
uation of deep-seated intracerebral hematomas
has similarly been reported by numerous authors
including Kandel (U.S.S.R.) and Broseta (Spain),
in both instances employing some modification
of the Backlund/von Hoist Archimedes spiral
cannula screw originally designed for stereotaxic
hematoma extrication (20, 34). Hematoma vol-
ume and localization is determined from the CT-
derived stereotaxic coordinate data, and multiple
evacuation access corridors are stereotaxically
planned (34). Catheters with endpoint Silastic
balloons have been used for cortical hemostasis
after hematoma removal. These are inserted
down the stereotaxic transit access and inflation
is maintained at the pressure level of CSF in the
contralateral ventricle (34). Kandel reported this
procedure with documentation for 32 patients
with deep-seated spontaneous hemorrhages in-
cluding 30 hypertensive cases with an overall
mortality of 20% and a 16% rebleeding rate (34).
With appropriate selection of patients and en-
hanced knowledge regarding optimal time for he-
matoma evacuation after the acute ictus, ster-
eotaxic hematoma evacuation may emerge as a
useful surgical adjunct to open approaches in
those cases deemed appropriate for intervention.
A major issue that remains unresolved relates to
the impact of complete versus incomplete he-
matoma removal on the risk of rebleeding after
a stereotaxic hematoma evacuation (34). Brose-
ta's experience with 16 spontaneous intracere-
bral hematomas presented similar data and
raised identical questions (17). Of interest is the
role of acute cortical edema after hematoma de-
compression and removal, as well as the pattern
of intracranial pressure dynamics, which in the
case of Brosetta's series remained decreased
compared with the uniform preoperative intra-
cranial hypertension in these patients (17). Al-
though numbers of patients studied do not per-
mit an accurate statistical assessment, Kandel
reported the majority of patients representative
of postoperative mortality (especially those re-
lated to rebleeding) underwent early operation
within 3 days of the initial insult (34). Thus,
delayed aspiration of hematomas deserves con-
sideration although complications in this cate-
gory related to pulmonary embolism were also
observed, thus clouding resolution of this issue.
This stereotaxic methodology has been adapted
for the evacuation of intracerebral clots stem-
ming from rupture of aneurysmal lesions or vas-
cular malformations. Furthermore, Kandel has
detailed experimental stereotaxic technology de-
signed for angiographically guided clipping of
arterial and arteriovenous aneurysmal lesions
(33). Of more immediate practical value is the
development of combined stereotaxic localization
and access corridor placement followed by ster-
eotaxically directed microsurgical approaches to
and excision of deep-seated midline arteriove-
nous malformations that present difficult sur-
gical challenges by virtue of small dimensions or
anatomical location in the paraventricular dien-
cephalic region. De Sola detailed such a case (25)
successfully managed with the Talairach angiog-
raphy-stereotaxy apparatus, and a substantial
potential for the utilization of combined CT and
angiographically guided stereotaxic surgery of
treacherous vascular malformations has pro-
gressively emerged.
A comprehensive survey of stereotaxic radioi-
sotope implantation brachytherapy is beyond the
scope of this review. Extensive and internation-
ally recognized innovation in this field has
emerged from Germany, as well as from France
and Sweden. Various series detailing a multitude
of clinical experiences with brachytherapy of in-
tracranial deep-seated neoplasms have emerged
in recent years, including reports of stereotaxic
intracavitary yttrium-90 and rhenium-186 radi-
ocolloid irradiation of cystic craniopharyngiomas
(Netzeband, 1984) and of active glioma cysts
(Szikla, 1984), as well as combined stereotaxic
interstitial and external radiation therapy ad-
vances directed at therapy of deep-seated glial
neoplastic lesions (Rougier, 1984; Szikla, 1984;
Mundinger and Weigel, 1984) (57, 58, 63, 73,
74). By far the most voluminous accumulation of
experience in the subdiscipline of stereotaxic
glioma brachytherapy rests with the noted Fri-
burg group of Mundinger et al. Experimental data
on the early and late sequential morphological
effects of iridium-192, yttrium-90, and iodine-
125 gamma and beta interstitial radionuclide
source implants in the brain are fairly unique in
the international literature (35, 59, 61). The sub-
stantial clinical experience with treatment of in-
tracranial glial neoplasms has been equally well
detailed (21, 49, 51-56). In one series of patients
compiled between 1965 and 1983, 329 deep-
seated midline/diencephalic region (mesenceph-
alon excluded) lesions were treated with various
stereotaxic interventions, and 168 patients re-
mained alive at the conclusion of the retrospec-
tive review period. Of these, 185 patients under-
went stereotaxic iridium-192 (91 patients) or io-
dine-125 (94 patients) curiebrachytherapy of
their neoplastic lesions, with 34 and 54 patients
respectively, remaining alive at the conclusion of
the review period (57). A related study provided
a spectrum of 28 diencephalic neoplasms sub-
jected to iridium-192 or iodine-125 interstitial
radiotherapy from among a total population of
251 intracranial tumors. Three- and 5-year sur-
vival rates with this form of therapeutic manage-
ment for diencephalic lesions are 52% and 37%,
respectively, whereas the overall 5-year survival
rate for malignant astrocytomas (irrespective of
intracranial anatomical site) is 47% in patients
receiving interstitial implant brachytherapy (53).
Various forms of high dose short range and long
term graduated dose implant techniques are uti-
lized in the treatment of hypothalamic and dien-
cephalic gliomas, and these include procedures
with stereotaxic permanent iridium-192 implan-
tation under bioptic control (51). The integration
of CT imaging with stereotaxy has permitted top-
ographic definition of tumor mass, resulting in
enhanced data useful for planning radioisotope
implantation (53). The trend of Mundinger et al.
toward the use of iodine-125 reflects the prefer-
ence for a radioisotope source with soft (28 to 35-
keV) radiation (desirable from the standpoint of
radiation protection for medical personnel) out-
put, a steep dose curve fall off permitting tightly
controlled isqdose curve configurations, a favor-
able half-life time factor of 60 days, and a suffi-
ciently high initial dose delivery to the tumor,
thus guaranteeing a sufficient cumulative focal
dose (51, 53, 56). These factors, in addition to
low intensity, long term permanent implantation
techniques, allow a dosing sequence extending
over 7 months in some cases. Under these cir-
cumstances the slow dose accumulation tends to
spare viable neuraxis tissue, while resulting in a
steady increase in radiation sensitivity on the
part of neoplastic components, where cellular
fatality is more probable in abnormal cells exhib-
iting a premitotic pause than in normal cellular
elements (51).
In contrast to the theoretical approach to tumor
radiotherapy offered by stereotaxic radioisotope
implant brachycurietherapy, stereotaxic radio-
surgery delivers a singularly decisive radiother-
apeutic/destructive impact to the neoplastic tar-
get lesion. The latter method is equally applicable
to deep-seated tumors.
Ever since the first pioneering ventures into
stereotaxic neuroradiosurgery by Professor Lars
Leksell, Sweden has remained synonymous with
state of the art stereotaxic technology (38, 41).
The development and scope of stereotaxic neu-
roradiosurgery in its evolution from the original
utilization of stereotaxic methodology for open
surgical procedures involving radiofrequency
probes (38), to synchrocyclotron and linear ac-
celerator heavy particle/proton beam closed ster-
eotaxic radiosurgery (37, 42), and finally to the
presently operational second and third genera-
tion gamma knife units (41, 40) remains beyond
the scope of this discussion. Nevertheless, with
regard to deeply situated neoplastic mass lesions
such as craniopharyngiomas, as well as small
vascular malformations, the gamma knife has
assumed an increasingly significant therapeutic
role as an adjunct to more conventional modes
of surgical treatment (3, 69, 70).
As of 1983, over 760 patients had undergone
stereotaxic radiosurgical treatment for mass le-
sions and other indications, in all cases utilizing
the cobalt-60 gamma knife unit along with var-
ious methods of stereotaxic radiological localiza-
tion (41). Twenty-two craniopharyngiomas and
204 vascular malformations were treated from
1968 to 1982 and are included in this series. In
addition, between 1966 and 1980, a larger series
of craniopharyngiomas exhibiting a predomi-
nantly cystic component (Backlund et al., 1980)
was treated with stereotaxic injections into the
tumor cyst, utilizing yttrium-90 radiocolloid in
all 54 cases (2, 41). Of these 54 patients, 34 had
not previously undergone treatment, surgically
or otherwise, and no recurrences were reported.
The overall Swedish experience with radiocolloid
treatment of cystic craniopharyngiomas has gen-
erally yielded impressive results, with gradual
shrinkage and eventual collapse of the cyst wall
(2, 4, 5, 41, 43). However, in at least 31 other
cases where a primarily solid or combined mul-
ticystic/solid craniopharyngioma was involved,
treatment with external closed stereotaxic
gamma knife radiosurgery (preceded by stereo-
taxic yttrium-90 instillation only where indicated
by the presence of a sizable partial cystic com-
ponent) was the preferred modality. The exclu-
sive use of the gamma knife was usually (but not
exclusively) employed for those cases where
small (less than 2.5-cm diameter), relatively cir-
cumscribed, deep-seated neoplastic lesions per-
mitted maximal utilization of the gamma unit's
sharply demarcated multiportal intersecting
beams providing selective, precise high intensity
irradiation of the designated target field (41).
Radionecrosis of craniopharyngiomas can oc-
cur at single dose magnitudes of only 2 to 3 Gy
(1), however, and thus more sizable lesions have
also been effectively treated with gamma knife
radiosurgery (3, 6). Among the 31 craniophar-
yngiomas cited, 9 such lesions reported by Back-
lund ranged up to 5 cm in diameter and received
target doses varying between 20 and 50 Gy (3).
Doage delivery to the tumor was dependent on
tumor size (larger lesions receive attenuated dos-
age levels at their periphery and thus require
high target dosages), the relative contributions of
cystic and solid components to the tumor volume
(solid tumors require higher delivered dosages),
and the proximity of vital neural structures (the
single dose tolerance of optic pathways is limited
to 10 Gy, thus constraining dosage levels to the
periphery of certain lesions extending into the
region of the optic chiasm) (3). In maintaining
the principle that the steepest gradient of the
radiation field (50% isodose level) should coincide
with the peripheral margin of the tumor, vital
structures surrounding tumor are spared signif-
icant radiation injury in most cases. Conversely,
the delivered dose (even in larger tumors receiv-
ing only 5 Gy to some areas of their periphery) in
the cases reported still resulted in dramatic tu-
mor shrinkage and striking clinical improvement
(3). The relative paucity of acute and delayed
radiation effects observed with high intensity
gamma knife radiosurgery relates in part to the
relatively focused area of radionecrosis and the
resultant decreased risk of generalized edema
involving the surrounding neural tissue (39), pro-
vided that the basic principles governing high
energy beam irradiation, as noted, are followed.
The contribution of Swedish neurosurgery
with regard to stereotaxic radiosurgery of arterio-
venous malformations has been equally impres-
sive. Leksell (1983) cited over 204 vascular mal-
formations treated with the stereotaxic gamma
knife unit. In 67 of these patients, follow-up
angiography 2 years after treatment demon-
strated an 83% obliteration rate, most notably in
those cases where intersecting stereotaxically fo-
cused high energy radiation beams covered most
of an entire malformation (41). Mild to moderate
residual or delayed onset hemiparesis in 5 cases
and a latency of 6 to 18 months between treat-
ment and angiographically verified obliteration
of these lesions represent another drawback in
terms of delayed bleeding risks. Best suited for
this procedure are deep-seated, small (less than
2.5 to 3 cm in diameter) lesions presenting an
otherwise high surgical risk with conventional
management.
As presented in some initial pioneering reports,
stereotaxic angiography permits accurate local-
ization through three-dimensional coordinates
that define the lesion target field when trans-
ferred to the gamma knife unit (40, 67, 69, 70).
Multiple, narrow, intersecting high energy beams
(from up to 179 cobalt-60 sources) are focused
on the lesion target field using a collimator ar-
rangement with the appropriately selected cross
sectional beam diameter, thus resulting in one or
more high intensity radiation isodose fields ster-
eotaxically centered within the target lesion (68).
Preplanned dosimetry configurations placing the
50% isodose curve at the lesion margin are rou-
tinely utilized. Single dose treatment has varied
between 3 and 12.5 krads over a period of 20 to
40 minutes, utilizing collimator diameters of 8 to
14 mm which correspond to target volume cov-
erage of 0.5 to 3 cm3 (within at least the limits of
the 50% isodose curve), respectively (68, 69).
Serial follow-up angiography in 42 of 68 pa-
tients first reported by Steiner (1979) and then
expanded to a series of 85 patients with 1-year
and 67 patients with 2-year angiographic reev-
aluation by Leksell (1983) revealed that 83 to
85% of vascular malformations are completely
obliterated at 1 year, with 6% of the lesions un-
changed and the remaining 10.5% partially ob-
literated also at 2 years posttherapy (41, 68). A
single dose of 5 krads (and possibly as little as 3
to 4 krads) seems to be a sufficient critical
threshold dose for the obliteration of most arte-
riovenous malformations under 3 cm in diame-
ter. Attendant damage of surrounding brain tis-
sue emerging as a delayed consequence of treat-
ment was noted in 5 of these cases, and this late
radiation effect appearing 3 to 9 months after
stereotaxic radiosurgery is mostly restricted to
cases where the 5-krad limit was exceeded, es-
pecially in conjunction with the use of a 14-mm
collimator. The associated delayed neurological
deficit in such cases (hemiparesis, etc.) may be
related to changes affecting regional venous
drainage surrounding the target zone (68).
Any summary or review of regional contribu-
tions to a field as rapidly changing and dynamic
as neurosurgical stereotaxy requires a preview of
impending or expected developments. The con-
temporary evolution of stereotaxic radiosurgical
technology continues, as evidenced in the devel-
opment of a radiosurgery apparatus merging
stereotaxic technique with a high energy isocen-
tric 4-MV linear accelerator radiotherapy unit
(23). Colombo et al. from Italy have begun to
investigate an original adaption along these lines
and have reported the capacity for steeper iso-
dose curve fall-off, a wider spherical dose cover-
age sector, and a significantly wider range and
maneuverability of collimator setting parameters
compared with the more conventional gamma
knife unit previously described (23). By utilizing
three-dimensional CT data and modifications in
the specially constructed linear accelerator ster-
eotaxic apparatus, the investigators may even-
tually succeed in obtaining molded radiation
emission isodose curves, thus allowing extremely
enhanced accuracy in the radiotherapeutic cov-
erage of a target lesion's topographic variance.
The fusion of stereotaxy and neurooncology is
 already apparent with reports emanating from
various European centers describing the uti-
lization of stereotaxic techniques for the inter-
stitial,intraneoplasticadministration/instillation
of chemotherapeutic agents (bleomycin) and
immunomodulating / immunotherapeutic sub-
stances (interferon) (16, 53). Therapeutic anti-
neoplastic agents could thus be chosen and uti-
lized irrespective of limitations imposed by issues
impacting on vascular delivery and neurovascu-
lar blood-brain barrier dynamics.
Stereotaxic cryosurgery as advocated by Boe-
thius and Greitz in Stockholm may entail a
potential for novel management of small, deep-
seated tumors by permitting the stereotaxic neu-
rosurgeon to create a stereotaxically defined de-
structive lesion within a given neoplastic mass
that is sufficiently large to cover the full extent
of the target mass volume (13). The diameter of
the cryoprobe determines the lesion dimensions,
and the probe is left in place 15 to 20 minutes
after creation of the lesion, primarily for consid-
erations of hemostatic tamponade during the
post-cold injury phase of transient capillary
bleeding (13). Necrotized tissue may be reduced
in volume through an outer suction cannula
within the stereotaxic apparatus; however, care
must be taken to avoid the ventricular space
because this may provide a natural egress portal
for any residual capillary oozing. No data are
available on postsurgical evaluation, patient per-
formance, and effect of the stereotaxic cryosurg-
ical lesion on arresting progression of the offend-
ing neoplastic mass.
Adaption of new cell culture techniques to the
size constraints of stereotaxic microbiopsies will
allow more extensive in vitro pathological scru-
tiny of tissue specimens within culture systems
and as an adjunct to more conventional histo-
pathological analysis (77). Related harvesting
methods can provide biopsy tissue for a variety
of sophisticated analytical methodologies, in-
cluding rapid flow cytofluorometry of tumor cell
suspensions with attempts at analysis of DNA
distribution patterns among a series of glial tu-
mors, or on a comparative basis between differ-
ent biopsy target sites within a single lesion. One
such preliminary study has demonstrated the
feasibility and potential efficacy of such inves-
tigation, although no definite correlation of his-
topathological grading and DNA distribution pat-
terns within tumor cell populations from differ-
ent tumor biopsy sites and different patients was
identified (11). Such techniques may eventually
provide objective criteria for assessing a given
tumor's biological activity and degree of malig-
nancy. If histopathological correlation is even-
tually determined with respect to assays of nu-
cleic acid distribution patterns in CNS tumors,
prognostic factors and therapeutic considera-
tions may emerge as relevant correlates of DNA
distribution analysis in tumors.
The frontier of neurosurgical stereotaxy most
likely points toward future involvement with mi-
crotransplantation techniques within the CNS.
A recent pilot clinical trial reported by Backlund
et al. from Sweden detailed the first documented
attempt at autologous adrenal to striatal cross
transplantation utilizing stereotaxic implanta-
tion in patients with severe parkinsonism refrac-
tory to pharmacological modulation (7). The the-
oretical aim of providing striatal tissue with a
new cellular template source of dopaminergic
catecholamines utilizing adrenal medullary tis-
sue simultaneously harvested from the patient
just before stereotaxic implantation is well
founded on experimental animal data on rein-
nervation of nigrostriatal 6-hydroxydopamine-
lesioned striatum with fetal substantia nigra
grafting. Initial results with the two selected pa-
tients receiving the autologous adrenal medul-
lary grafts are sufficiently intriguing to merit
further clinical trials on highly selected patients.
Undoubtedly, autograft adrenal medullary cell
populations will need to be cloned or selected out
for maximal dopaminergic/catecholamine secre-
tory capacity if more biochemically sophisticated
attempts at microtransplantation within the CNS
are entertained. This initial clinical trial of Back-
lund et al. performed in a neurosurgical stereo-
taxic setting with a deep-seated striatal target
point represents the first attempt at micro-
transplantation within the human brain.
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26. Dettori P, Colombo F, Pinna V, Benedetti A: CT
control of stereotactic surgery in the dience-
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27. Daumas-Duport C, Monsaingeon V, N'Guyen JP,
Missir O, Szikla G: Some correlations between
histological and CT aspects of cerebral gliomas
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(Wien) (Suppl) 33:185-194, 1984.
28. Dauman-Duport C, Monsaingeon V, Szenthe L,
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29. Edner G: Stereotactic biopsy in tumours of the
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57:213-234, 1981.
31. Froder M, Seitzer D, Buren G, Dieckmann G: Dig
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46:206-210, 1983.
32. Huk W, Baer U: A new targeting device for ster
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33. Kandel El, Peresedov VV: Stereotaxic clipping of
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34. Kandel El, Peresedov VV: Stereotaxic evacuation
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35. Kiessling M, Kleihues P, Gessaga E, Mundinger F,
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36. Kleihues P, Volk B, Anagnostopoulos Kiessling M:
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Neurochir {Wien) {Suppl) 33:271-280, 1984.
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1980.
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Commentary F
Role of Stereotaxis in the Management of Midline Cerebral Lesions
Erik-Olof Backlund, M.D., Ph.D.
The integration of stereotaxic operative tech-
niques into traditional, "nonfunctional" neuro-
surgery has been of great importance. For many
years some clinical research groups have tried to
follow the basic principle that surgical problems
in the deeper regions of the intracranial com-
partment should be solved, if feasible, with the
use of stereotaxic techniques, whereas superfi-
cial lesions should be attacked by the best "vis-
ual" techniques available, i.e., microsurgery (Fig.
F.1). In my experience, consistent attention to
the basic principle implied radically changed
conditions of general policy, risk, and outcome
for patients with lesions inside or near the third
ventricle. The importance of this new, stereo-
taxic approach has been proven in controversial
issues such as the management of craniophar-
yngiomas.
Since the integration of stereotaxy with var-
ious imaging techniques, the crucial value of a
stereotaxic procedure as a first choice alternative
instead of a conventional operation has been
clearly demonstrated in many more patients
than was first assumed possible. As a commen-
tary to more than one chapter in this book, I will
give some examples from my personal experience
to illustrate these considerations.
agement. New therapeutic modalities for pineal
region lesions have appeared and new policies
have been designed (2, 10). This makes tissue
diagnosis a virtual prerequisite for a proper
choice of treatment.
The possible occurrence of a benign cyst in the
pineal region simulating a tumor deserves special
attention in this context. The computerized tom-
ographic (CT) attenuation level is not always con-
clusive for a cyst and may even indicate a cystic

Biopsy
Inaccessible tumors in the central core of the
brain have been treated with radiotherapy with-
out a previous tissue diagnosis. Well-established
stereotaxic biopsy techniques are now available,
and such a policy can no longer be justified. Any
intracranial tumor can now be classified by fine
needle biopsy with reasonable safety (4, 6, 11).
In spite of continuous improvement of the diag-
nostic imaging techniques, a tissue diagnosis by
biopsy (histological sectioning or smears for cy-
tological examination) increases the reliability of
the diagnosis (8). Stereotaxic biopsy also allows
new possibilities for the characterization of a
tumor by other means, such as biological mark-
ers, immunohistochemistry, and DNA measure-
ments.
The advantages of the stereotaxic approach for
biopsy are demonstrated in particular when le-
sions in the pineal region are encountered. Here
there is a wide diagnostic spectrum, making ra-
diological diagnosis less accurate and thus tissue
classification more important for further man-
lesion to be solid. Stereotaxic biopsy always re-
veals the true condition. To perform a cystocis-
ternal or cystoventricular shunting procedure
during the same operation as the biopsy is often
feasible and the treatment of choice (Fig. F.2).
Tumors in the brain stem proper at the mes-
encephalic level or in the posterior fossa have
been considered inaccessible for stereotaxic bi-
opsy because of inherent risks related to this
region. However, with the transcerebellar ap-
proach, any conceivable region of the intracra-
nial compartment can be reached for fine needle
biopsy with reasonable risk (Fig. F.3).
Colloid Cysts of the Third Ventricle
Because of the innocent character of a colloid
cyst in the third ventricle, a conventional sur-
gical intervention for its removal may be far too
mutilating and risky. Any experienced brain sur-
geon may recall frustrating episodes during such
operations, such as difficulty keeping a hydro-
cephalic hemisphere distended or troublesome
bleeding from central blood vessels at the depth
of a keyhole operating field.
The introduction of an aspiration technique for
these lesions opened new perspectives (5). My
first such case, a colleague, has now been fol-
lowed for 16 years without recurrent symptoms.
The patient continued his academic career after
the operation and is now working as a clinical
professor.
Major operation for these intraventricular
cysts seems no longer necessary. The technique
is internationally recognized, with rewarding re-
sults reported in a significant number of patients
(8, 12).
Craniopharyngiomas
For patients with huge craniopharyngiomas
extending deeply into the central regions of the
brain, the introduction of a standardized stereo-
taxic treatment program has been of great im-
portance (1). My personal experiences prove the
definite value of an exclusive stereotaxic ap-
proach in seemingly desperate cases with cystic
tumor parts encroaching upon the third ventric-
ular area far back to the aqueductal region. Long
term results from a recent review of 15 years of
material are shown in Table F. 1. Intracystic in-
stillation of radioactive material (in a liquid state,
usually colloidal yttrium-90, a pure beta-emitter)
initiates a gradual collapse of the cystic part,
with no dramatic peroperative consequences. For
many patients, the results are dramatic (Fig. F.4).
In the majority of craniopharyngioma cases the
clinical problems are due to expanding cysts. Any
treatment program should begin with a stereo-
taxic cyst puncture in preparation for radioiso-
tope treatment. This less dramatic management
is in bright contrast to the often sadly dramatic
courses after attempts at tumor removal. Re-
warding results after stereotaxic craniopharyn-
gioma treatment reported by others have given
this approach international recognition (7, 9, 13,
14).
The range of beta-radiation, albeit very short

(50% of the dose at 1.1-mm depth) is of course a
critical factor when risks and possible compli-
cations are considered. In less than 10% of my
patients was there suspicion of late adverse ef-
fects from the radiation, most often sudden im-
pairment of the visual fields after a long symp-
tom-free interval. The side effect was disabling
in only one patient. By improvement of the tech-
nique, probably using another radiocolloid, the
complication rate may well be lower in the next
series.
Occlusion of the Aqueduct
The procedure most often used for the treat-
ment of various hydrocephalic states, ventricu-
lovenous or ventriculoperitoneal shunting, is not
a logical approach when impaired Cerebrospinal
fluid (CSF) flow through the aqueduct is the
cause of the ventricular dilatation. By stereotaxic
technique it is possible to restore the anatomical
communication between the third and the fourth
ventricles (3). The course of the aqueduct strictly
in the midsagittal plane, a seeming morphologi-
cal obstacle for the instrumental approach, is no
problem with the use of a specially designed
cannula. The technique allows shorter tubes or
catheters to be placed safely through the aque-
duct after mechanical recanalization guided by
preoperative selective stereotaxic ventriculogra-
phy.
When my first material was analyzed, it was
found in retrospect that the selection criteria
(lumbar infusion/pressure test and isotope cis-
ternography) had not been accurate. When for-
mulating these criteria I assumed that normal
findings would indicate that CSF resorption was
normal and that the subarachnoid space was
patent. In spite of fulfilled selection criteria and
a perfect "morphological" result from the opera-
tion, some patients in the first series obviously
had a component of impaired CSF resorption
capacity outside the ventricular system. The ac-
quired patency of the aqueduct did not assure a
decrease of ventricular size. If better selection
methods can be designed, stereotaxic aqueduct
reconstruction will deserve a place as a logical
treatment in selected cases of obstructive hydro-
cephalus.
References
1. Backhand EO, Johansson L, Sarby B: Studies on
craniopharyngiomas: II. Treatment by stereotaxis
and radiosurgery. Acta ChirScand 138:749-759,
1972.
2. Backlund EO, Rahn T, Sarby B: Treatment of
pinealomas by stereotaxic radiation surgery. Acta
Radiol Ther Phys Biol 13:368-376, 1974.
3. Backlund EO, Grepe A, Lunsford D: Stereotaxic
reconstruction of the aqueduct of Sylvius. J Neu-
rosurg 55:800-810, 1981.
4. Bosch DA: Indications for stereotaxic biopsy in
brain tumours. Acta Neurochir (Wien) 54:167-
179, 1980.
5. Bosch DA, Rahn T, Backlund EO: Treatment of
colloid cysts of the third ventricle by stereotaxic
aspiration. Surg Neurol 9:15-18, 1978.
6. Edner G: Stereotaxic biopsy of intracranial space
occupying lesions. Acta Neurochir (Wien)
57:213-234, 1981.
7. Kobayashi T, Kageyama N, Ohara K: Internal ir
radiation for cystic craniopharyngioma. J Neuro-
surg 55:896-903, 1981.
8. Lunsford LD, Martinez AJ: Stereotaxic explora
tion of the brain in the era of computed tomogra
phy. Surg Neurol 22:222-330, 1984.
9. Lunsford LD, Gumerman L, Levine G: Stereotaxic
intracavitary irradiation of cystic neoplasms of
the brain. Presented at the IX Meeting of the World
Society for Stereotactic and Functional Neurosur
gery, Toronto, 1985.
10. Neuwelt EA, Gumerlock MK: The challenge of
pineal region tumors. In Neuwelt EA (ed): Diag
nosis and Treatment of Pineal Region Tumors.
Baltimore, Williams & Wilkins, 1984, pp 1-30.
11. Ostertag CB, Mennel HD, Kiessling M: Stereotaxic
biopsy of brain tumors. Surg Neurol 14:275-283,
1980.
12. Rivas JJ, Lobato RD: CT-assisted stereotaxic as
piration of colloid cysts of the third ventricle. J
Neurosurg 62:238-242, 1985.
13. Schaub C, Bluet-Pajot MT, Videau-Lornet C, et al:
Endocavitary beta irradiation of glioma cysts with
colloidal 186rhenium. In Szilka G (ed): Stereotactic
Cerebral Irradiation. Amsterdam, North-Hol
land, 1979, pp 293-302.
14. Strauss L, Sturm V, Georgi P, et al: Radioisotope
therapy of cystic craniopharyngiomas. Int J Ra-
diat Oncol Biol Phys 8:1581-1585, 1982.
Commentary G
Magnetic Resonance Stereotaxy
Eric R. Cosman, Ph.D., M. Peter Heilbrun, M.D., and Trent H. Wells, Jr.
We describe here the development of a new
localizer frame and head ring assembly that en-
ables the calculation of stereotaxic targets from
virtually any magnetic resonance imaging (MRI)
scan plane, including those that are parallel to
the axial, sagittal, or coronal planes and those
that are skewed to these basic slice orientations.
The assembly is compatible with the Brown-Rob-
erts-Wells (BRW) computerized tomographic (CT)
stereotaxic system and can be used in any stand-
ard MRI head coil without image aberration or a
special means of fixation to the MRI machine.
Just as the combination of CT scanning and
stereotaxic surgery evolved into a powerful neu-
rosurgical technique (1,3), MRI stereotaxy offers
yet added potential for observing and approach-
ing intracranial targets. MRI is complementary
and sometimes superior to CT in diagnosing cer-
tain brain tumors and neurological disorders.
MRI also has the significant advantage over CT
of yielding easily coronal and sagittal images and,
in the near future, possibly chemical shift and
spectroscopic images. There are, however, sev-
eral difficult technical problems in building a
universal stereotaxic MRI localizer that makes
full use of the advantages of MRI and yet does
not degrade the MRI images themselves. We sum-
marize these problems here and describe a new
localizer design that has overcome them and
worked well in early clinical trials.
The ideal MRI localizer system for stereotaxic
surgery should enable target coordinates—an-
teroposterior (AP), lateral, and vertical positions
relative to a head ring fixed to the head — to be
calculated from any slice reconstruction,
whether it be parallel to or skewed to the axial,
sagittal, or coronal plane. This would in many
cases simplify the planning of approaches to
volumetric or functional targets in the brain. The
standard CT localizer for the BRW system allows
target calculations from any nearly axial plane
to be made by means of a set of three N-type
structures (2), each with two rods and one diag-
onal made of carbon fiber, arranged around an
axial circumference of the head as shown in
Figure G.1A. A nearly axial slice will intersect
the six rods and three diagonal elements to give
nine fiducial points on the CT image (Fig. G.1B)
from which the CT plane and any target within
it can be determined. The MRI localizer extends
this concept to include any arbitrary slice plane,
not just those that are quasi-axial. It consists of
a cubical array of N-type structures with rod and
diagonal elements in three orthogonal planes, as
shown in Figure G.2A. This assures that for any
plane oriented approximately axially, sagittally,
or coronally a sufficient number of rod and di-
agonal elements will be cut to determine fully
that plane and any target within it. Furthermore,
by making the pattern of fiducial points different
for each orthogonal cut, as shown in Figure G.2B,
the plane and parity of the cut can never be
misinterpreted.
Such a universal MRI localizer is scanner-in-
dependent in the sense that it does not have to
be fixed in any particular alignment relative to
the scanner gantry. It may be placed in the gantry
with its axis skewed to the scanner axis, yet as
long as the appropriate rods and diagonals are
cut by the scan plane, the coordinates relative to
the head ring of any target seen in the scan image
can be calculated. This is a significant feature
because clamping a head ring or localizer to an
MRI machine is made difficult by the small size
of standard head coils and the variable shape of
machine tables.
The localizer frame and head ring must not
cause distortion of the precision magnetic and
radiofrequency (rf) fields of the MRI scanner that
are required for proper imaging. Thus no ferro-
magnetic materials may be used in its construc-
tion and major eddy current pathways must be
eliminated for metallic components. Figure G.3
shows the present design, which works well for
MRI magnetic fields of 0.1 to 1.5 tesla. The head
ring, head posts, and skull screws are made of
anodized aluminum, which has no effect on the
scanner's magnetic fields. The skull screws are
pointed and hardened to penetrate the scalp di-
rectly and are self-anchored to the skull without
dulling. This simplifies applying the head ring to
the patient and eliminates making scalp inci-
sions and skull drill holes. The head ring is made
in two aluminum semicircular segments that are
connected by insulating Micarta spacers 180°
apart. This is essential to prevent a macroscopic
eddy current loop running circumferentially
around the head ring, induced by the MRI scan-
ner's rf excitation field. Such a current loop
would cause severe attenuation of the MRI sig-
nal. The design has yielded MRI images of negli-
gible distortion and attenuation.
Figure G.4 shows the MRI localizer attached to
the head ring. The localizer is made of polycar-
bonate and contains tubular channels on the
front, back, sides, and top. The channels may be
filled with a variety of paramagnetic substances
so that they will be detectable as fiducial spots
on an intersecting scan slice; however, petro-
leum jelly works well for a wide range of time
and spin-echo MRI pulse sequences and elimi-
nates the problems of replenishment. Figure G.5
is an axial MRI scan illustrating the fiducial
spots. The x and у coordinate data for each fi-
ducial spot, as well as any chosen target point or
points on the MRI image, may be extracted from
the MRI machine console software and are en-
tered into an off-line computer-calculator. The
calculator computes the actual scan plane and
the AP, lateral, and vertical coordinates of the
target relative to the head ring. This is done very
efficiently by means of a vector projection for-
malism. We note that the x and у data need only
be linear (for example, pixel number or dimen-
sions of arbitrary scale factor) and do not depend
on their origin position for the calculator to make
this computation. The resulting head ring coor-
dinates are subsequently used for the stereotax-
ically calculated approach to the target.
To fit inside standard MRI machine manufac-
turers' head coils and also to mate with the BRW
stereotaxic surgical system, the MRI head ring
and localizer were made with their outer diame-
ter less than 260 mm. The outer rim of the MRI
head ring is formed to accept the standard BRW
CT head ring (which is not MRI-compatible) and
the two head rings are clamped together in a
precise orientation during the surgical phase by
fixation points, as shown in Figure G.6. After
MRI scanning with the MRI head ring and local-
izer connected (Fig. G.4), the localizer is removed
and the CT head ring is attached to the MRI head
ring (Fig. G.6). From that point on, the BRW
system components, such as the arc system,
phantom base, etc., may be used in the usual
way, all being referenced to the BRW CT head
ring. Figure G.7 shows the BRW arc system at-
tached to the combined BRW and MRI head ring
as it would be for stereotaxic surgery.
The MRI localizer system is modular so that
individual components may be changed with
minimal effort. For example, an alternate local-
izer frame with integrated surface coils that can
also couple to the MRI head ring for high resolu-
tion and isotope imaging studies is being de-
signed. The present system itself may also be
used for CT scan imaging as well as MRI, making
possible comparative scanning without change
of the head ring.
Acknowledgments
We are indebted to Dr. M. Apuzzo and Dr. E. Ganz
for facilitating several MRI tests during the course of
this development.
E.R.C. was supported in part by the Whitaker Health
Sciences Fund, a M.I.T. Faculty Research Grant, and
the William W. Harris Children Charity Trust.
References
1. Apuzzo ML, Sabshin JK: Computed tomographic
guidance stereotaxis in the management of intra
cranial mass lesions. Neurosurgery 12:277-285,
1983.
2. Brown RA: A computerized tomography-computer
graphics approach to stereotaxic localization. J
Neurosurg 50:715-720, 1979.
3. Heilbrun MP, Roberts TS, Apuzzo ML, Wells TH,
Sabshin JK: Preliminary experience with Brown-
Roberts-Wells (BRW) computerized stereotaxic
guidance system. J Neurosurg 59:217-222,
1983.
32
Computer-assisted Stereotaxic Laser Microsurgery
Patrick J. Kelly, M.D.

Tumors in and near the third ventricle may be biopsied accurately and
safely utilizing CT-based stereotaxic techniques (1, 7). Computerized
tomography (CT) provides a precise three-dimensional data base and since
1978 various systems have been developed that allow translation of
points on CT scans into stereotaxic coordinates (2, 5, 10, 15). However,
CT scanning is also precise volumetric data which, if gathered under
stereotaxic conditions, can be utilized to reconstitute defined tumor vol-
umes into stereotaxic space (8, 9, 12). These volumes may then be treated
by interstitial radionuclides or resected utilizing computer-interactive
stereotaxic control (8, 9, 11).
We have applied the concept of volume stereotaxis to the treatment of
subcortical tumors since 1979 to resect aggressively tumors located in
the thalamus, basal ganglia, and subcortical white matter with acceptable
postoperative results (11). Our experience has indicated that the method
may be applied to all subcortical intraaxial lesions including tumors in
and adjacent to the third ventricle, which are well suited to the instru-
ments and technique.
Computer-assisted stereotaxic procedures are performed in three
stages: data acquisition, surgical planning, and the interactive surgical
procedure.
Data Base Acquisition
Stereotaxic Headholder
A CT-compatible stereotaxic head holder is applied to the patient under
local anesthesia. The head holder fixes to the skull by four carbon fiber
pins inserted into drill holes through the outer table of the patient's skull
into the diploe. Micrometer attachments to the vertical supports of the
stereotaxic head holder provide a precise means for replacing the head
holder if data acquisition and operation are performed on separate days.
Stereotaxic CT Scanning
A CT table adaptation plate secures the CT-compatible stereotaxic head
holder to the CT table. A CT localization system fixes to the head holder
during CT scanning. This consists of nine reference bars in three sets of
three rods each, which are arranged in the shape of the letter N and are
located on either side of the head and anteriorly (Fig. 32.1). The localiza-
tion system produces a set of nine reference marks on each CT slice (Fig.
32.2). The height and inclination of the plane of the CT slice with
reference to the stereotaxic instrument can be calculated from the mea-
sured distance of the middle reference mark corresponding to the oblique
reference bar to the end reference marks, which correspond to the vertical
bars. Stereotaxic coordinates for any point on a CT slice can easily be
calculated using mathematical transformations described previously (12).
Stereotaxic Positioning Device
The stereotaxic instrument is based on the arc-quadrant principle. The
patient's head is moved with 3° of freedom to place an intracranial target
into the focal point of a fixed sphere defined by arc and quadrant (Fig.
32.3). The frame consists of a three-dimensional slide system, a small
internal arc-quadrant for directing probes and retractors intracranially,
and a 400-mm horizontal arc-quadrant that holds the microscope and
laser manipulation system. The stereotaxic head holder fixes to a three-
dimensional slide system that is activated by servomotors. Stereotaxic
positions are output by optical encoders on each axis and are displayed
on digital readouts. With this system, multiple areas within the target
tumor volume may be accessed quickly and conveniently.
Surgical Instrumentation
Certain specialized surgical instruments are also used during stereo-
taxic laser craniotomies. These consist of stereotaxic retractors of 2- and
3-cm diameters that mount on and are stereotaxically directed by an
internal arc-quadrant. Dilators for each retractor are used to spread the
laser incision for advancement of the retractor during the procedure.
Tear drop and fenestrated suckers and an extra-long stereotaxic bipolar
forceps are essential. Long dissectors and alligator scissors must be
custom made at present.
Surgical Planning
Stereotaxic Volume Interpolation
The archived data tape from the stereotaxic CT scan is read into the
operating room computer system (independent physician's diagnostic
console for the General Electric 8800 and 9800 CT scanning units). The
CT slices that demonstrate the lesion are displayed. The surgeon digitizes
all slices that demonstrate the tumor as follows: First, the computer
recognizes the nine reference artifacts on the CT slice utilizing an inten-
sity detection algorithm. The surgeon then inputs a series of points on
the boundary of the tumor utilizing the cursor and trackball subsystem
(Fig. 32.4). The computer places this series of points into a three-dimen-
sional image matrix in relationship to their stereotaxic position, which
has been calculated from the nine localizing artifacts, and then connects
these points into a closed contour. All subsequent CT slices demonstrating
the tumor are similarly digitized. The computer suspends all of these
tumor outlines within a three-dimensional image matrix in relationship
to their stereotaxic position. An interpolation program then creates inter-
mediate slices at 1-mm intervals, and each of the digitized and interpo-
lated slices is filled with 1-mm3 voxels. This creates a three-dimensional
volume within the computer image matrix having the same configuration,
spatial relationships, and location in stereotaxic space as the tumor
within the patient's brain in reference to the stereotaxic localization
system. If the surgeon specifies approach angles from horizontal and
vertical planes (quadrant and arc angles, respectively), this is interpreted
as a viewline by the computer. A series of two-dimensional slices of the
tumor volume cut perpendicular to the surgical viewline may be displayed
on an operating room video monitor at the precise depths encountered
during operation.
Viewline Selection
The surgeon selects a surgical trajectory (viewline) after consideration
of several factors. First, the most direct route to the tumor is optional but
the location of important cortical and subcortical areas and the direction
of major white matter pathways that overlay the tumor must be consid-
ered. A trajectory that avoids major vascular structures may also be
selected. In addition, a surgical approach that traverses the lesion along
its major axis may be optimal as regards the efficiency with which the
procedure may be performed. The surgical trajectory is expressed in arc
and quadrant approach angles that will be set on the stereotaxic instru-
ment. The mechanical control provided by the stereotaxic frame and the
computer display of the lesion with reference to the frame will keep the
surgeon oriented to the tumor volume at all times during the procedure.
Surgical Stereotaxic Laser
The carbon dioxide laser is a convenient method for removing tissue
from the bottom of a deep cavity and is especially useful in the removal
of deep-seated intracranial tumors. In addition, its thermal effects afford
some degree of hemostasis. At high power settings its thermal damage is
limited to the spot size of the laser and a thin zone of thermal necrosis
usually no more than 200 to 300 mm. In our system the laser beam is
reflected by mirrors on the stereotaxic frame that are controlled with
precision by the computer.
A laser manipulator system (microslad) attaches to the operating mi-
croscope on the stereotaxic frame. The laser beam is delivered to the
manipulator system by an articulated arm and focusing lens. Within the
microslad, x and у mirrors deflect the laser beam toward the focal point
of the stereotaxic frame. The pitch of these mirrors is controlled by
galvanometers whose voltage input is controlled by the digital to analog
output of the computer system. The computer plots the position of the
laser beam on the operating room video monitor as a cursor that is
overlayed on reformatted tumor outlines sliced perpendicular to the sur-
gical viewline at the level at which the microscope and surgical laser are
focused (Fig. 32.5).
Surgical Procedure
The surgical approach to lesions of the third ventricular region depends
on whether the tumor is located within the third ventricle entirely or is
located primarily within the thalamus or hypothalamus and displaces
the third ventricle. The approach to anteriorly situated intraventricular
lesions is through the lateral ventricle anteriorly. On the other hand, the
surgical approach to thalamic tumors is through the frontal white matter
and anterior limb of the internal capsule. Tumors of the posterior thala-
mus are best approached through the temporooccipital junction.
Intraventricular Lesions
After the data acquisition and surgical planning phases have been
completed the patient is placed under general anesthesia and the CT-
compatible stereotaxic head frame is replaced on the patient's head
utilizing the same pin holes in the skull and micrometer settings that had
been utilized during the stereotaxic CT scan. A central point within the
tumor, selected by the surgeon, is positioned into the focal point of the
stereotaxic frame. After preparing and draping the scalp, the surgeon
makes an incision at the hairline approximately 3 in. long (Fig. 32.6).
The skull is opened by a 1.5-in. cranial trephine and the dura mater is
opened in a cruciate manner. The frontal cortex is coagulated with bipolar
forceps and a vertical incision through the pia is made with scissors. The
incision is deepened into the frontal white matter using the carbon dioxide
laser as the laser manipulator system and microscope are advanced
toward the focal point of the stereotaxic frame. The stereotaxic retractor
is inserted into the cortical opening, and further deepening of the incision
is done, directing the laser beam through the retractor as follows: The
incision is extended 1.5 cm deep to the end of the retractor with the laser.
The surgeon then inserts the dilator and the retractor is advanced over
the dilator. The dilator is withdrawn, and the incision is extended deeper
using the laser.
Upon entering the lateral ventricle, the surgeon drains ventricular fluid
with the sucker and advances the retractor to the floor of the lateral
ventricle (Fig. 32.7, A and B). The fenestrated suction is used against a
small cotton ball to keep ventricular fluid away from the surgical field.
With the laser at 10 watts with a focused spot, an incision is made in the
floor of the lateral ventricle lateral to the foramen of Monro and lateral
to the septal and thalamostriate veins (Fig. 32.7C). This incision is
deepened to the tumor. Gentle retraction is applied to the incision with
the fenestrated suction as the laser is used to dissect ependyma of the
superior portion of the third ventricle from the superficial aspect of the
tumor (Fig. 32.8). Then the dilator is inserted through the retractor into
this opening over the tumor and rotated 90° as the surgeon slides the
retractor deeper (Fig. 32.9, A to D). This creates a shaft from the surface
to the outer border of the tumor (Fig. 32.9E).
The surgeon can measure the depth of the retractor from position
calibrations in reference to the fixed radius of the stereotaxic arc-quad-
rant. At a depth corresponding to the superficial boundary of the tumor,
which has been calculated along the viewline by the computer, the first
slice of the tumor is displayed on the operating room video monitor (Fig.
32.10). The surgeon vaporizes the interior of the tumor utilizing a defo-
cused laser beam with a 1 - to 2-mm spot size and 50 to 80 watts of power.
The position of the laser within the tumor is displayed on the video
monitor in reference to tumor outlines reconstructed from the CT-defined
tumor volume (Fig. 32.11). This continues as the surgeon progresses from
the most superficial aspect of the tumor to the deepest. A thin capsule of
tumor is left attached to the third ventricular ependymal wall. This
cytoreduction process is easily accomplished by keeping the retractor
within the outlines of the tumor using the computer display as a reference
(Fig. 32.12). If the tumor is larger than the retractor, the computer image
may be translated on the screen in reference to the retractor and new
stereotaxic frame settings are calculated. In practice, a technician acti-
vates the servomotors controlling the three-dimensional slide to move the
patient's head within the stereotaxic arc-quadrant and place another
portion of the tumor under the retractor. The retractor will always be
directed at the focal point of the stereotaxic arc-quadrant.
After creating a large cavity within the tumor, the stereotaxic retractor is
withdrawn to the superficial portion of the tumor and the capsule is
drawn under the retractor. This is accomplished by grasping it with a
biopsy forceps or suction tip. The capsule may be gradually dissected
away from the ventricular ependyma using short bursts of low power (10
to 15 watts) defocused laser energy, which results in contraction of the
capsule as it separates from the ependyma (Fig. 32.13). It is advised that
the procedure not extend too deeply on one side of the tumor before the
other sides are freed. After portions of the capsule are freed, the plane of
dissection is preserved by placing a cotton ball between ependyma and
tumor capsule. This will result in the tumor capsule being directed into
the center of the stereotaxic retractor. The capsule of the tumor may then
be contracted by low power defocused laser energy and then vaporized
utilizing higher power settings on the laser. The retractor is advanced to
facilitate deeper capsule dissection as necessary. Ultimately, the entire
capsule may be removed in this manner. Throughout the procedure,
hemostasis should be meticulously maintained. An extra-long bipolar
forceps and defocused low power laser energy may be used for this
purpose. After removal or, in some cases, internal resection of the tumor
the retractor is slowly withdrawn as hemostasis is secured along the
tract.
Pre- and postoperative scans of patients who have undergone this
procedure are presented in Figure 32.14.
Paraventricular Thalamic Lesions
We have found that in stereotaxic laser resections of tumors of the
thalamus bordering on the third ventricle patients do better if the ven-
tricular system is avoided and the dorsal thalamus is left intact. A surgical
approach to thalamic lesions through the anterior limb of the internal
capsule parallel to white matter fibers is advised. In this way, only
anterior thalamus and anterior limb of the internal capsule risk injury,
which should be well tolerated in the unilateral situation. Lesions located
in the posterior regions of the thalamus can be approached from a
temporooccipital incision that is directed horizontally and traverses the
posterior temporal horn of the lateral ventricle. This may result in a
contralateral superior temporal quadrantanopsia postoperatively. With
either approach, the computer-assisted stereotaxic technique will main-
tain orientation within the lesion as tumor borders delineated by stereo-
taxic CT scanning and reformatted in three-dimensional space are por-
trayed to the surgeon interactively during the procedure.
A surgical trajectory is planned to access the thalamic neoplasm from
a trephine that will be performed at the frontal hairline in the case of
anterior thalamic tumors or at the temporooccipital junction if the ap-
proach to a posterior thalamic neoplasm is to be through the temporooc-
cipital white matter. It is desirable to have the surgical approach along
the long axis of the tumor to minimize the amount of retraction necessary
to visualize the entirety of the lesion. To obviate the possibility of intra-
operative shifts of position of the tumor in stereotaxic space, one should
perform the following step. This step is especially important in very large
or cystic lesions or in cases where there is a possibility of entering the
ventricular system. A series of stainless steel reference balls (0.5 mm in
diameter) are deposited in the lesion utilizing a biopsy cannula stereotax-
ically directed through a 1/8-in. twist drill hole in the skull. Anteroposterior
and lateral roentgenograms are then obtained before craniotomy and
dural opening. Spatial shifts of the tumor detected by movements of the
stainless steel balls on subsequent roentgenograms and resulting from
decompression of the brain during tumor removal, cyst drainage, or
escape of ventricular fluid can be corrected within the three-dimensional
computer matrix.
The scalp, bone, and dural openings and cortical and subcortical white
matter incisions are made and deepened as described in the previous
section. At the outer border of the tumor, the incision is undercut by
reflecting the laser with a stainless steel instrument. Using the dilator,
the retractor may be advanced to create a shaft through the brain. Deep
to the retractor will be found the superficial aspect of the tumor. At this
point the first slice of the tumor volume reconstructed from the stereo-
taxic CT is displayed on the operating room computer system. First, the
surgeon uses the laser to cut around the tumor to separate it from
surrounding brain tissue. The computer has displayed the position of the
laser beam in reference to the outline of the tumor at the level to which
the stereotaxic retractor has been advanced and at the level at which the
microscope and laser are focused. As the tumor is progressively separated
from brain tissue, the retractor is advanced and new slices of the tumor
are displayed on the screen. After the tumor has been isolated from
surrounding brain tissue or in the event that it fills the retractor to
obscure visualization, it may be resected down to the deepest extent of
the retractor using biopsy forceps, defocused high power laser (85 watts,
2- to 5-mm spot size), or suction. Then the process of separating deeper
levels from surrounding brain tissue continues. If the tumor is larger
than the retractor, the patient's head can simply be moved with the
servomotor-controlled stereotaxic instrument to place another portion of
the tumor directly under the retractor as described previously. The depth
of the procedure is controlled by noting the depth of the retractor in
relationship to the stereotaxic arc-quadrant and by stereotaxic teleradi-
ographs (Fig. 32.15). In addition, the stereotaxically inserted reference
balls will give an indication of the depth of the procedure as they are
encountered.
Ultimately, the final slices of the tumor are vaporized from superficial
to the deepest layer as the surgeon monitors not only the operative field,
but also the position of the laser beam represented by the cursor on the
computer display monitor in relationship to the outlines of the tumor.
Bleeding is controlled utilizing defocused low power laser energy with
a power density of less than 10 watts/cm2 or by an extra-long (150-mm)
bipolar forceps (Radionics Incorporated, Burlington, Massachusetts). He-
mostasis is secured as the stereotaxic retractor is slowly withdrawn. A
tight dural closure and double-layer scalp closure, after the trephine bone
plug is secured, is utilized. Figures 32.16 and 32.17 demonstrate pre-
and postoperative scans in two patients with thalamic pilocytic astrocy-
tomas resected by this procedure.
An 8-year-old boy (Fig. 32.16) had presented with apraxia of the right
upper extremity of 3 years' duration. The 3-cm3 contrast-enhancing
lesion in the left thalamus was approached anteriorly. Postoperatively no
worsening of his right-sided apraxia was noted and speech was normal.
He was discharged from the hospital 6 days after operation. CT scanning
18 months after operation demonstrated no evidence of residual or re-
current tumor. He continues to do well. Postoperative radiation therapy
was not administered.
The second patient is a 5-year-old girl who presented with increased
intracranial pressure and mild right hemiparesis with dyskinesia. Her
tumor in the posterior left thalamus was resected from a temporooccipital
approach (Fig. 32.17). A ventriculoperitoneal shunt had been inserted at
another institution. Postoperatively she was neurologically normal and
we were unable to document a visual field deficit. No residual tumor was
noted on postoperative CT scanning.

Discussion
Traditionally neurosurgeons have relied on knowledge of neuroa-
natomy and hand-eye coordination to guide their surgical procedures.
However, a surgeon's three-dimensional orientation decreases the deeper
a procedure extends below the cortical surface. Surgeons must therefore
depend on the identification of normal anatomy that may be distorted by
the pathological condition to avoid getting lost in their attempts to treat
deep subcortical lesions. Within the lateral and third ventricles surgeons
attempt to maintain their spatial orientation by structural landmarks
such as the foramen of Monro, thalamostriate vein, choroid plexus, and
fornix (19, 21). This may not be particularly difficult when the ventricles
are dilated and visualization is optimal. However, a surgeon may have
difficulty maintaining orientation within the lateral ventricle and indeed
may have difficulty even finding the lateral ventricle and the structures
within it in patients with normal-sized or small ventricles (3, 13, 14, 16,
18). It has therefore usually been recommended that the surgical proce-
dure should traverse the corpus callosum to gain access to the third
ventricle in patients with small or normal-sized lateral ventricles (1, 20).
The structures of the corpus callosum and branches of the anterior
cerebral artery can then spatially orient the surgeon. A callossal incision
made perpendicular to its fibers is usually well tolerated (1) although it
may be associated with some memory impairment and personality
changes (4, 7). However, because normal anatomical structures must be
identified in both the transventricular and transcallosal approaches, the
craniotomies, cortical incisions, and openings into the ventricular system
or through the corpus callosum may be more extensive than really nec-
essary to deal only with the specific lesion.
This problem is more serious for tumors located in the wall of the third
ventricle and in the thalamus. Conventionally, the transventricular ap-
proach to identify normal ventricular system landmarks has been rec-
ommended before the tumor can be approached through the inferior wall
of the lateral ventricle and through dorsal thalamic nuclei (6). Unfortu-
nately, if the tumor is found it may not be clear where tumor ends and
normal brain begins. The results of spatial miscalculations in this regard
are severe neurological complications. Therefore, most procedures listed
initially as "tumor excisions" are, in fact, usually nervous biopsies that
could have been accomplished utilizing stereotaxic techniques with less
hazard to the patient (2, 5, 10, 17). However, stereotaxic methodology
provides a means of effectively biopsying lesions of and around the third
ventricle and also may be used to guide a controlled craniotomy for tumor
excision.
The advantage of the stereotaxic approach described is that it main-
tains three-dimensional surgical orientation with respect to a computer-
interpolated CT-defined tumor volume. The surgical approach that will
minimize exposure of and injury to essential brain structures can be
selected. Aggressive resections of circumscribed tumors from neurologi-
cally important subcortical areas can be accomplished with a high degree
of accuracy. Recurrent or residual low grade lesions of the third ventricle
or thalamus may be treated by a second stereotaxic procedure utilizing
the same bone flap and surgical pathway as the first. It is probably best
to deal with especially large lesions in two separate operations performed
several months apart.
The instrumentation described in this report may seem complicated to
many and unrealistically expensive to some. Nevertheless, commercially
available stereotaxic instruments could be adapted to the procedures
described in this chapter. In addition, computer systems are becoming
more powerful and less expensive. Stock software could be adapted to
stereotaxic volumetric surgery by individuals and instructions willing to
make a commitment to the task.
References
1. Apuzzo MLJ, Chikovani OK, Gott PS, Teng EL, Zee CS, Gianotta SC, Weiss
MH: Transcallosal, interforniceal approaches for lesions affecting the third
ventricle: Surgical considerations and consequences. Neurosurgery 10:547-
554, 1982.
2. Apuzzo MLJ, Chandrasoma PT, Zelman V, Giannotta SL, Weiss MH: Com
puted tomographic-based stereotaxis in the management of lesions of the
third ventricular region. Neurosurgery 15:502-508, 1984.
3. Busch E: A new approach for the removal of tumors of the third ventricle.
Acta Psychiatr Scand 19:57-60, 1944.
4. Geffen G, Walsh A, Simpson D, Jeeves M: Comparison of the effects of
transcortical and transcallosal removal of intraventricular tumors. Brain
113:773-788, 1980.
5. Heilbrun MP, Roberts TS, Apuzzo MLJ, Well TH Jr, Sabshin JK: Preliminary
experience with Brown-Roberts-Wells (BRW) computerized tomography ster
eotaxic guidance system. J Neurosurg 59:217-222, 1983.
6. Hirsch JF, Zouaoui A, Reinger D, Pierre-Kahn A: A new surgical approach to
the third ventricle with interruption of the striothalamic vein. Acta Neurochir
(Wien) 47:135-147, 1979.
7. Jeeves MA, Simpson DA, Geffen G: Functional consequences of the trans
callosal removal of intraventricular tumors. J Neurol Neurosurg Psychiatry
42:134-142, 1979.
8. Kelly PJ, Alker GJ, Goerss S: Computer-assisted stereotaxic laser microsur
gery for the treatment of intracranial neoplasms. Neurosurgery 10:324-331,
1982.
9. Kelly PJ, Kail BA, Goerss S: Computer simulation for the stereotactic place
ment of interstitial radionuclide sources into computed tomography-defined
tumor volumes. Neurosurgery 14:442-448, 1984.
10. Kelly PJ, Alker GJ, Kail BA, Goerss S: Method of computed tomography-
based stereotactic biopsy with arteriographic control. Neurosurgery 14:172-
177, 1984.
11. Kelly PJ, Kail B, Goerss S, Alker GJ: Precision resection of intra-axial CNS
lesions by CT-based stereotactic craniotomy and computer monitored CO2
laser. Acta Neurochir (Wien) 68:1-9, 1983.
12. Kelly PJ, Kail BA, Goerss S: Transposition of volumetric information derived
from computed tomography scanning into stereotactic space. Surg Neurol
21:465-471, 1984.
13. Kempe LG: Operative Neurosurgery. New York, Springer-Verlag, 1968, vol
1.
14. Little JR, MacCarty CS: Colloid cysts of the third ventricle. J Neurosurg
40:230-235, 1974.
15. Lunsford LD, Martinez AJ: Stereotactic exploration of the brain in the era of
computed tomography. Surg Neurol 22:222-230, 1984.
16. McKissock W: The surgical treatment of colloid cyst of the third ventricle: A
report based on twenty-one personal cases. Brain 74:1-9, 1951.
17. Menezes AH, Bell WE, Perrett GE: Hypothalamic tumors in children: Their
diagnosis and management. Childs Brain 3:265-280, 1977.
18. Poppen JL, Reyes V, Horrax G: Colloid cysts of the third ventricle. J Neuro
surg 10:242-263, 1953.
19. Rhoton AL Jr, Yamamoto I, Peace DA: Microsurgery of the third ventricle:
Part 2. Operative approaches. Neurosurgery 8:357-373, 1981.
20. Shucart WA, Stein BM: Transcallosal approach to the anterior ventricular
system. Neurosurgery 3:339-343, 1978.
21. Viale GL, Turtas S: The subchoroid approach to the third ventricle. Surg
Neurol 14:71-76, 1980.
33
Radiotherapy of Pineal and Suprasellar Tumors
William M. Wara, M.D., and Philip H. Gutin, M.D.
Radiotherapy is commonly used in the treat-
ment of pineal and suprasellar tumors. Because
of the differences in histological classification of
tumors occurring in this region (i.e., germ cell
tumors, pineal parenchymal tumors, glial tu-
mors, and benign tumors) and their differing
biological behavior, selection of the appropriate
treatment regimen requires knowledge of the tu-
mors and of the value and limitations of the
various therapeutic options.
Physical Factors Pertinent to
Radiotherapy
Megavoltage irradiation (x-rays and gamma
rays with energies of 1 to 40 MeV) is clinically
used in the treatment of central nervous system
(CNS) tumors. The biological effects of these
types of radiation are due to their ability to pro-
duce charged ions and free radicals that second-
arily cause permanent deoxyribonucleic acid
damage. The distribution of energy deposited in
tissues varies with the energy of the radiation,
the size of the radiation source (60Co), the size of
the beam treatment, the use of absorbing filters,
the source to target distance, and the collimation
system. Computer dosimetry that incorporates
shape-shielding blocks, wedge filters, and indi-
vidually designed tissue-compensating filters are
used to localize the high dose volume and to
minimize irradiation to sensitive normal tissues.
In selected situations, interstitial or intracavitary
radiation sources may be used.
Biological Factors
The biological basis of radiation therapy is
complex. The success of this treatment depends
on including careful treatment planning to max-
imize the high dose region, the differential sen-
sitivity of normal and tumor cells, the total vol-
ume of tumor, the repopulation of tumor cells in
the irradiation volume, the rearrangement of
cells within the cell cycle between individual ra-
diation exposures, the differential capability of
tumor and normal cells to repair sublethal radia-
tion damage, and the amount of oxygen within
the usually hypoxic tumor cells. Experimentally,
each of these factors has been shown to be sig-
nificant but in the complex clinical situation it
is difficult to evaluate them simultaneously. In
practice, treatment is selected to provide optimal
physical distribution of radiation with minimal
risk to surrounding critical normal structures.
Radiation Tolerance of the CNS
Radiation doses utilized for the treatment of
most brain tumors carry a definite but poorly
quantitated possibility of damage. The larger the
daily dose, the total dose, and/or the volume
irradiated, the greater the risk. If damage occurs,
the functional deficit varies with anatomical lo-
cation and extent of injury. Clinical experience
has demonstrated that there is minimal risk if
the total dose does not exceed 5000 to 5500 rads
and individual fractions are 180 to 200 rads (33).
Higher doses may be utilized for very malignant
tumors where without radical treatment death is
assured. In children less than 18 months of age
the dose is usually reduced by 10 to 20%. Adverse
effects of brain radiation are generally divided
into three groups depending upon time of ap-
pearance. Acute reactions during the course of
therapy are probably secondary to cerebral
edema. With conventionally fractionated radio-
therapy, i.e., daily fractions of 180 to 200 rads,
these reactions are uncommon and usually are
reversible with corticosteroid treatment. Onset
of the acute delayed reaction varies from a few
weeks to 4 months after completion of irradia-
tion. This reaction is thought to be due to a
temporary demyelination. It tends to mimic the
original tumor and new symptoms and occurs in
approximately 25% of patients. The reaction is
usually self-limited and no therapy is required.
It is important to recognize this reaction so that
there will be no premature alteration or institu-
tion of revised treatment for this situation.
The delayed severe effects occur 6 months to
10 years posttreatment. The pathological mech-
anism is thought to be late damage of the vas-
cular supply of the irradiated area. The onset is
usually insidious and may progress to scarring
or necrosis. The complications are infrequent
and rare with doses of radiation below 5000 rads.
In children who have received low dose irradia-
tion, computerized tomographic (CT) scans have
shown ventricular dilatation, wide arachnoid
spaces, atrophy, and intracerebral calcifications
(26). Psychosocial studies of irradiated children
have shown impairment in quantitative tests and
performance with abstract material after irradia-
tion (10). The incidence of dysfunction and its
relationship to various combinations of chemo-
therapy and radiation are currently being pro-
spectively evaluated.
Radiation to the pituitary and hypothalamic
areas can produce growth hormone deficiency.
This complication can occur in the treatment of
tumors that do not involve the pituitary or hy-
pothalamic area. Shalet and coworkers have re-
ported decreased response of plasma growth hor-
mone to insulin hyperglycemia in 11 of 16 chil-
dren treated for intracranial tumors (32). Using
insulin, arginine, and L-dopa challenge our group
has documented similar growth hormone defi-
ciencies in 8 children after CNS radiation (28).
The incidence of this pituitary dysfunction is
unknown as the studies reported have been on
groups of patients with pituitary dysfunction. All
children who have been treated to the pituitary
and suprasellar areas should be followed with
serial growth curves. If a decreased growth rate
is documented a complete endocrine evaluation
should be undertaken.
Conventional Radiotherapy
Conventional radiotherapy is utilized in the
treatment of the majority of pineal and suprasel-
lar tumors. Most patients are treated with high
energy (4 to 18 MeV) linear accelerators after
simulation and computer dosimetry. In all types
of tumors the radiation is focal to the tumor bed
with a limited margin designed to spare as much
normal brain as possible. The exact treatment
recommendation is dependent on the pathologi-
cal diagnosis.
The dose of irradiation to the primary tumor
has generally ranged from 4500 to 5500 rads
given at 180 to 200 rads per day. Although ger-
minomas might be more sensitive, no trial using
a lower dose has been performed. Adjuvant ra-
diotherapy to uninvolved areas of the brain and
spine has used a dose of 2500 to 3500 rads.
The need to treat the spinal area is controver-
sial. The overall incidence of spinal seeding from
pineal tumors and suprasellar germinomas is
approximately 10% (38). Therefore, we do not
recommend routine craniospinal axis irradiation
(Table 33.1). However, there may be a subpopu-
lation of patients who might benefit, so we screen
all patients with Cerebrospinal fluid cytology and
a myelogram. A positive myelogram would neces-
sitate whole axis irradiation.
Germ Cell Tumors
Because of the operative morbidity associated
with surgery for these locations, historically
many of these tumors were often irradiated with-
out a biopsy. Now such patients may receive a
therapeutic trial of 2000 rads and if, on rescan-
ning, the tumor has markedly shrunk, an empir-
ical diagnosis of germinoma is made and the
irradiation is completed to 5000 rads. If a biopsy
is obtained we recommend a dose of 6000 rads
for all germ cell tumors other than germinomas.
Reported survival rates for patients with these
types of tumors are good. The 2-year survival
rate for various types is approximately 60 to 70%
(6, 17, 24, 27, 30, 37, 38). Germinomas seem to
have higher survival rates, but the lack of biopsy
in many cases makes it difficult to separate other
tumor types (Table 33.2).
Approximately 50% of patients experience im-
provement in symptoms after radiotherapy. With
germinomas, CT scans return to normal but the
more sensitive magnetic resonance scan shows
a stable residual lesion. Treatment failures in
our experience are usually recurrences at the
primary tumor site.
Pineal Parenchymal Tumors
Primary pineal tissue tumors can be low grade
Pineocytomas or malignant pineoblastomas. The
pineocytoma is given local irradiation to a dose
of 5000 rads. The malignant pineoblastoma is
treated like a medulloblastoma and given 5500
rads to the primary and 2500 to 3500 rads to the
remainder of the craniospinal axis. These pa-
tients do less well, with a survival rate of approx-
imately 30% (38).
Gliomas
Gliomas in the anatomical region are treated
with a regimen similar to that recommended for
a more common supratentorial location. Low
grade astrocytoma found in the posterior optic
region, the hypothalamic area, and the suprasel-
lar region is treated with focal irradiation, limit-
ing the field to the minimal normal tissue possi-
ble, to a total dose of 5040 rads at 180 rads per
day. A dose reduction of 20% is made for children
less than 2 years of age at time of diagnosis.
The rare patient's results in this group follow
the more common supratentorial astrocytoma.
The experience at UCSF was summarized by Lei-
bel et al., who reviewed the results for all astro-
cytomas treated between 1942 and 1967. Pa-
tients were divided into three groups. In 14 pa-
tients with total tumor resection, none received
irradiation and no tumor recurred. In 37 patients
with incomplete resection but no postoperative
irradiation the 5-year recurrence-free survival
was 19%. The third group was composed of 71
patients who received postoperative irradiation
after subtotal removal; they had a 46% recur-
rence-free survival. Based on this experience all
subtotally removed astrocytomas are irradiated
with the expectation of a 50% long term survival
(19).
The most difficult brain tumors to treat are the
malignant gliomas. Fortunately, in this region
they are quite rare. Data accumulated over the
past decade has indicated a 16% survival for
anaplastic astrocytoma and a 0% survival for
glioblastoma multiforme. An increase in radia-
tion dose from 5000 to 6000 rads can increase
median survival from 28 to 42 weeks in these
patients (39). Because of the lack of results in
this area new approaches are now being inves-
tigated including hyperfractionation radiother-
apy and the addition of multidrug chemotherapy
and radiosensitizers.
Craniopharyngioma
Although these tumors are histologically be-
nign, their proximity to critical structures causes
major morbidity and difficulty for complete sur-
gical removal. Repeated attempts at complete re-
moval usually result in a poor quality of life. We
have reviewed 8 patients with total removal, 12
patients with subtotal removal and irradiation,
and 8 patients with biopsy and irradiation
treated at UCSF from 1956 to 1974. The majority
of the patients received focal irradiation to doses
between 5000 and 5500 rads.
Five-year survival rates were similar in all pa-
tients. Seven of 8 patients (88%) with total re-
moval were alive, 11 of 12 patients with surgery
plus subtotal irradiation (88%) were alive, and 8
of 8 patients (100%) with biopsy plus irradiation
were alive (Table 33.3). Quality of life and com-
plications were similar in both groups (29).
Radical resection of craniopharyngiomas
should be considered but only if it can be accom-
plished safely. Based on our data we currently
recommend conservative resection followed by
focal irradiation if tumor is left behind. Our cur-
rent length and quality of survival is similar to
that in previous reports (16).
Localized Radiotherapy: Intracystic
Isotope Therapy
Background
For cystic craniopharyngiomas and thalamic
gliomas teletherapy is the principal radiation mo-
dality used in the United States. However, at a
number of European centers stereotaxic punc-
ture and instillation of radioactive isotopes is the
primary treatment for these tumors, particularly
craniopharyngiomas, replacing microsurgical
approaches and external irradiation.
Stereotaxic instillation of a radioisotope was
first performed in a patient with a cystic cranio-
pharyngioma recurrence by Leksell at the Karo-
linksa Hospital (20). This patient was treated
with colloidal phosphorus-32, and since that
time a large number of patients have been
treated with this isotope as well as colloidal sus-
pensions of gold-198, ytrrium-90, and rhenium-
186(1, 2, 23, 31, 36, 34).
Colloidal Isotopes
For maximally localized treatment and ease of
handling, pure beta emitters, like 32P and 90Y,
are preferred against cystic craniopharyngioma
(2). Although the lesser penetration of 32P might
be an advantage in thin-walled cysts, the shorter
half-life of 90Y makes evacuation of the cyst pos-
sible after a shorter interval because the pre-
scribed dose is administered more quickly (2). A
review of the recent literature seems to favor 90Y
as the superior isotope against cystic cranio-
pharyngioma (2, 23, 34). Unfortunately, only 32P
is available in the United States.
Treatment
In careful hands a therapeutic radioisotope is
delivered to tumor cysts through a clean stereo-
taxic puncture (preferably computerized tomog-
raphy-directed). The instillation is best moni-
tored by use of intraoperative gamma-camera
control (23) to assess isotope leakage from the
cyst, a potentially disastrous complication. Beta
radiation doses to the cyst wall have ranged from
5 to 100 krads (2). However, 20 krads is the dose
used in most recent series.
Szikla has favored colloidal 186Re for intracystic
therapy of craniopharyngiomas and glioma
cysts. This isotope has a combined beta and
gamma emission, the beta energy (358 kev) of
186
Re being lower than that of 90Y (2.27 MeV), and
therefore relatively limiting irradiation of
surrounding normal tissue (31, 36). However,
this lower penetration may have led to cyst re-
currence in four of seven patients treated with
186
Re by Sturm and his coworkers (23). Szikla
maintains, however, that 186Re instillation has
led to regression of cyst fluid formation in all
craniopharyngiomas and low grade gliomas
treated (31, 36).
The experience with the treatment of patients
with intracystic 90Y has been very favorable at
Karolinska ( 1 , 2 ) and at Heidelberg (23). Radio-
graphic regression of the craniopharyngioma
cyst and concomitant clinical improvement can
be expected. Radiation damage to the optic
nerves is seen in about 5% of cases (23, 34).
In the United States a small experience with
instillation of the only available colloidal radioi-
sotope, 32P, into recurrent, previously irradiated
craniopharyngioma cysts has been accrued. Sev-
eral centers around the country are now using
this modality as an experimental primary ther-
apy-
Stereotaxic Radiosurgery
Background
In 1959, Leksell and his coworkers introduced
the prospect of stereotaxically directing highly
collimated beams of radiation to destroy predict-
able and limited volumes of brain (21). By this
technique, radiation is delivered as a single nec-
rotizing dose from, as it is currently formulated,
the gamma unit, an array of 179 cobalt-60
sources. The gamma irradiation beam from each
source is directed toward the center of a colli-
mator helmet at which the target has been ster-
eotaxically positioned. The targets treated at Ka-
rolinska Hospital, where, until recently, the only
gamma units resided, have included thalamic
nuclei, arteriovenous malformations, acoustic
tumors, pineal region tumors, pituitary tumors,
and craniopharyngiomas (3). Other methods of
stereotaxic radiosurgery depend upon the Bragg
peak phenomenon for radiation dose localization
and have included the proton beam at the Har-
vard University cyclotron (18, 35) and the heavy
particle beams at the Lawrence Berkeley Labo-
ratory (7). It is thought that, with careful and
creative treatment planning, conventional linear
accelerators can also be adapted for obliterative
stereotaxic radiosurgery, and small series of pa-
tients are now being accrued (8, 14, 15). This
technique may be very useful for tumors in and
around the third ventricle.
Craniopharyngioma
Backlund has used the gamma unit to treat a
number of solid craniopharyngiomas or the solid
remnants of cystic craniopharyngiomas, dem-
onstrating reduction in tumor size with regres-
sion of symptoms and without complication (3,
4). The cystic tumors had been treated previously
with 90Y instillation. This is, in fact, the ap-
proach that Backlund now advocates for cranio-
pharyngioma. A stereotaxic puncture with radi-
ocolloid (90Y) instillation is done and followed by
gamma unit radiosurgery if there are solid por-
tions to the tumor (4).
There is a very limited experience with proton
irradiation of craniopharyngioma (18) and a di-
minishing small experience with stereotaxic lin-
ear accelerator treatment of craniopharyngioma
(14).
Pineal Region Tumors
A small number of pineal region ependymo-
mas, astrocytomas, and Pineocytomas have been
treated on the gamma unit to doses of 2000 to
7500 rads after stereotaxic biopsy. Results have
been variable (3). Tumors chosen for radiosur-
gery have been limited by size and geometry. Two
patients with pineal region tumors have been
treated with stereotaxic linear accelerator tech-
niques with good early results (less than 18
months follow-up) (8).
Interstitial Brachytherapy
Background
The history and scientific basis for the inter-
stitial irradiation of brain tumors have been re-
viewed (5). The possibility of delivering from im-
planted sources a localized dose of radiation to
tumors in and around the third ventricle, while
sparing surrounding normal brain, is attractive,
particularly in children, where such tumors com-
monly occur. However, the specter of even the
slightest brain injury in this region blunts one's
enthusiasm because the normal structures here
are so critical to neurological function. Thalamic
and optic gliomas, pineal region tumors, and, in
lesser numbers, several other tumors in this area
have been treated with stereotaxically implanted
iodine-125, and iridium-192 sources (11, 12, 22,
25, 40). Mundinger has treated a large number
of patients with low grade or anaplastic gliomas
in the region of the third ventricle by stereotaxic
biopsy and interstitial irradiation from perma-
nently implanted 125I and 192Ir sources, 125I being
preferred for the better-demonstrated lesions
(22). In some cases external beam treatment was
also given. Mundinger's group has also treated
many patients with pineal region tumors of all
varieties with permanent implants (40). As could
be predicted, tumor seeding along the Cerebro-
spinal fluid pathways was a problem in some
cases of germinoma. Pecker et al. have reported
treating two patients with germinomas similarly
(25).
As can be appreciated from the foregoing dis-
cussion of external beam radiotherapy, this mo-
dality is relatively effective against tumors in the
region of the third ventricle. For this reason, in
the United States external beam irradiation is
used as the primary treatment for these lesions.
Interstitial brachytherapy is reserved for reirra-
diating selected recurrences with the appropriate
geometry or for giving a "boost" dose of radiation
to the tumor bed after external radiotherapy.
Reirradiation of tumors in the region of the third
ventricle must be done with the full realization
that catastrophic brain injury might result.
Patients receiving interstitial implants for
brain tumor recurrences develop, in many in-
stances, focal radiation necrosis that might ex-
acerbate neurological deficit and require opera-
tion for resection of the necrotic material (12).
For tumors located, for example, in the thalamus,
the deficit might be devastating and the opera-
tion might be perilous. Our group has treated
several children and adults with recurrent
gliomas of the optic chiasm or thalamus with
permanent or removable 125I implants (11-13).
Because the interstitial radiation dose has been
reduced in these patients, response has been, in
general, favorable and injury has been limited.
Only a single patient, a 5-year-old boy with a
recurrent anaplastic thalamic glioma, has re-
quired reoperation for necrosis; and the outcome
has been excellent. He is surviving without re-
currence and only a mild exacerbation of his
hemiparesis nearly 3 years after implantation.
Figure 33.1 shows the clinical course of a 17-
year-old boy with a cystic recurrence of a thala-
mic glioma who received 5000 rads to the tumor
periphery from centrally implanted removable
125
I sources. The radionecrotic reaction resolved
spontaneously and left him with no residual def-
icit. He is off steroids and functioning normally
in college 2 years after implantation.
Clearly, for selected patients with tumor recur-
rences in the third ventricular region interstitial
brachytherapy can be of value. Cases must be
selected with rigorous attention to tumor geog-
raphy and geometry and the techniques must be
applied with the utmost care to avoid devastating
brain injury.
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17. Jenkin RDT, Simpson WJK, Keen CW: Pineal and
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18. Kjellberg RN: Stereotactic Bragg peak proton ra
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19. Leibel SA, Sheline GE, Wara WM, Boldrey E, Niel-
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34
Chemotherapy of Tumors of the Third Ventricular Region
MichaelS. B. Edwards, M.D., and Victor A. Levin, M.D.

The majority of tumors developing in the region

of the anterior third ventricle are glial in origin
(24). In general, initial treatment includes open
or stereotaxic biopsy (1) followed by local irradia-
tion and, on occasion, adjuvant chemotherapy.
At the time of tumor progression, chemotherapy
has been used to control tumor growth. In the
chapter that follows, we discuss our experience
at the University of California and the relevant
literature on treating patients with third ventric-
ular tumors with chemotherapy.

Materials and Methods

Patient Population
Using our computerized patient data base, we
found 39 of 1103 patients who were treated with
chemotherapy in an adjuvant or recurrent fash-
ion for glial tumors in the third ventricular region
(hypothalamus/chiasm/thalamus). The primary
location and histology of these 39 patients are
listed in Table 34.1. Thirty-six of the 39 tumors
were glial in origin. The age range for hypothal-
amic/chiasm tumors was 3 to 60 years (5 pa-
tients were less than 17 years of age or younger)
and for thalamic tumors was 1 to 64 years (6
were 17 years of age or younger). There were 21
males and 18 females.
A literature search revealed 10 cases of suc-
cessful (response) chemotherapeutic treatment
of pineal region germ cell tumors (21). In addi-
tion, we have successfully treated 3 other pa-
tients with pineal germ cell tumors and 2 pa-
tients harboring pineoblastomas. These patients
and their treatments are listed in Table 34.2.
Chemotherapy—Glial Tumors
Two patients with hypothalamic astrocytomas
were treated with a two-drug chemotherapy reg-
imen (actinomycin D and vincristine) at the time
of initial diagnosis. This decision was based on
a personal communication from Dr. Roger
Packer (Childrens Hospital of Philadelphia) who
had used this regimen and had observed objective
computerized tomographic (CT) scan responses.
Both patients continued to demonstrate clinical
deterioration (loss of vision) and worsening CT
scans. Treatment with local radiation therapy
produced CT and clinical tumor regression and
neither had required further chemotherapy for
up to 4 years. The seven other patients with
hypothalamic astrocytomas were treated with a
nitrosourea-based chemotherapy at recurrence.
Although this is a small population upon which
to base conclusions, the Kaplan-Meier represen-
tation (Fig. 34.1) indicates a median time to tu-
mor progression (MTP) of 35 weeks. There is not
enough information to assess the effectiveness
of adjuvant chemotherapy.
Thirteen patients with thalamic tumors were
treated with a nitrosourea-based chemotherapy
in an adjuvant fashion. The median age of this
group was 43 years (range, 22 to 64 years). Their
MTP was 32 weeks (Fig. 34.2). Seventeen pa-
tients with thalamic tumor were treated for tu-
mor recurrence (nitrosourea-based chemother-
apy) and exhibited an MTP of 51 weeks. The
median age of this group was 29 years (range, 1
to 60 years). No toxic deaths were observed in
these series.
Case Report
D.B. was 29 years old when she underwent a sub-
total resection of a gemistocytic astrocytoma of the
thalamus (July 6, 1981). She received 6500 rads of
radiation, which was completed on September 25,
1981. The tumor progressed in December 1982 and
she was started on poly-drug chemotherapy (BCNU, 5-
fluorouracil, hydroxyurea, 6-mercaptopurine) but
failed to respond. In February 1983, therapy was
changed to procarbazine (scans at start of procarba-
zine shown in Fig. 34.3). She returned at the comple-
tion of one cycle (April 1983) with clinical and CT scan
evidence of improvement despite a stable dexametha-
sone dosage (Fig. 34.4). She has continued on procar-

bazine and remains clinically stable with continued
but slight improvement on subsequent CT scans.
Chemotherapy—Pineal Tumors
Six patients with a presumed or recurrent ger-
minoma were treated with vincristine, bleomy-
cin, and cisplatinum or adriamycin (12, 18, 24).
All responded for variable periods up to 6 months
except one patient with metastatic germinoma
who has been free of disease for greater than 6
years (18). However, three of these patients de-
veloped bleomycin pulmonary toxicity, two suc-
cumbing to this complication. We have treated
two patients harboring pineal germ cell tumors
with combination chemotherapy adjuvant to ra-
diation therapy with good responses. The two
children with recurrent pineoblastoma initially
responded to combination chemotherapy but
progressed within 1 year of the initial response.
One patient with a pineal endodermal sinus tu-
mor was treated with radiation therapy in com-
bination with vincristine, adriamycin, and cy-
toxan and has remained free of disease for more
than 10 years (21).
Discussion
The majority of gliomas arising in the hypo-
thalamic/optic nerve region occur in children
with peak incidence at less than 5 years of age.
 The majority of these tumors are slow-growing,
although their biological aggressiveness is not
easily predicted (10). As a rule, when transfor-
mation to a more aggressive tumor does occur (2),
it is most commonly in older patients (11). Our
patients demonstrated this same tendency at re-
currence: the median age of our patients in the
hypothalamic/chiasmal group at recurrence was
15 years (range, 3 to 60 years).
The natural history of hypothalamic/chiasmal
gliomas and the relative benefits of surgery and
radiation therapy are well appreciated. Those
lesions confined to one optic nerve without chias-
mal involvement can be resected if proptosis and
blindness develop. If the glioma involves the
chiasm or hypothalamus, surgical treatment
consists of biopsy to confirm the diagnosis. On
rare occasions, a large exophytic portion com-
pressing the third ventricle and producing hydro-
cephalus can be removed without morbidity. The
biological behavior of these tumors is unpredict-
able, but frequently progressive visual loss or
increased size on CT scans requires further treat-
ment. Local radiotherapy can produce improve-
ment in visual acuity, decrease tumor size (2, 8,
16), and improve survival (17, 22). The place of
chemotherapy, instead of or before irradiation,
is presumptive. The use of chemotherapy alone
for lower grade astrocytomas has been only re-
cently considered (9). Our initial attempt to treat
two children with chemotherapy (actinomycin D
and vincristine) based on information from
Packer (19) failed. Both children showed signs of
progressive visual loss and required radiation
therapy. Visual loss returned within 3 months of
the completion of radiation therapy.
The use of chemotherapy adjuvant to radiation
therapy is based on our prior experience with
supratentorial tumors in adults (5, 7, 13-15) and
children (20). As a result of reviewing our data
for this chapter, we found that multiple agent
chemotherapy based on nitrosoureas produced
documented tumor response in five of our seven
patients treated at recurrence. In this limited
experience, tumor histology did not influence re-
sponse rate. Although CT-documented regres-
sion was observed, median time to tumor pro-
gression was only 35 weeks. This is similar to
the results obtained with nitrosourea-based
chemotherapy for malignant cerebral astrocyto-
mas (5, 7, 13-15).
Like hypothalamic/chiasmal tumors, thalamic
tumors are most frequently glial in origin (23).
Surgical sampling is essential to establish a his-
tological diagnosis and plan therapy (1). Approx-
imately 50% recur within 5 years of initial treat-
ment despite radiotherapy (6, 20). The use of
adjuvant chemotherapy for malignant thalamic
astrocytomas has produced a median time to tu-
mor progression (32 weeks) that is less than that
observed for hemispheric astrocytic tumors. Me-
dian times to tumor progression in the latter
groups vary by age at first treatment and histo-
logical classification: approximately 31 to 42
weeks for glioblastoma multiforme and 77 to 123
weeks for the less anaplastic astrocytomas (13-
15) in adults to 130 weeks in those under 18
years of age (20).
Tumor recurrence was generally treated with
chemotherapy. If a nitrosourea was used previ-
ously as an adjuvant to radiation therapy, other
agents were used at recurrence because of the
high likelihood of nitrosourea-resistant cells sur-
viving in the tumor. In this case the use of non-
cross resistant chemotherapy, such as procar-
bazine, would seem more rational. Otherwise,
nitrosourea-based therapy was our first choice.
Recurrent tumors treated with nitrosourea-
based poly drug chemotherapy resulted in im-
provement or stabilization in 7 of 17 patients.
The MTP for the entire group was 51 weeks (Fig.
34.1), which was quite good in comparison to
that observed in malignant hemispheric tumors
treated at recurrence (5, 7, 13-15) although the
median age of this group, 29 years, favors a
somewhat better response.
Treatment of recurrent or malignant germ cell
pineal region tumors is fraught with failure. De-
spite their occasional sensitivity to chemother-
apy (18), reported responses have been of short
duration or drug toxicity produced unacceptable
complications (i.e., pulmonary toxicity). Al-
though the literature is replete with reports of
attempts to treat these tumors with chemother-
apy, the number of documented responses are
few (3, 12, 18, 24) and the long term survivors
can be counted on one hand. It is clear that no
particular drug regimen is superior to another,
although the polydrug regimens of vincristine,
bleomycin, and cisplatinum and nitrosourea-
based multidrug regimens have been partially
effective. Single agent therapy has been of no
benefit for these tumors.
In summary, chemotherapy for hypothalamic/
optic nerve tumors, before or instead of irradia-
tion, is of unproven benefit, although recent the-
oretical considerations (9) suggest that it should
be pursued in some cases. In this regard, we have
been evaluating the use of cell cycle-specific
therapy consisting of 5-fluorouracil, hydroxyu-
rea, and 6-thioguanine in these patients with
non-contrast enhancing moderately anaplastic
astrocytomas. If patients progress on this poly-
drug regimen, standard radiation therapy is ad-
ministered. The use of adjuvant chemotherapy
for this group of patients awaits further confir-
mation. Since thalamic gliomas seem to behave
in a similar manner to supratentorial gliomas,
we believe that there is a good rationale to use
chemotherapy adjuvant to radiation therapy for
these patients. Unfortunately, our failure to use
a consistent chemotherapy treatment for these
patients leaves us in the awkward position of
being unable to quantify precisely the benefit of
chemotherapy. Nitrosourea-based chemotherapy
for recurrent malignant hypothalamic, optic
nerve, and thalamic tumors seems to have defi-
nite short term effectiveness and in select pa-
tients, particularly with thalamic gliomas, may
produce prolonged tumor stability.
Acknowledgment
These studies were supported in part by HEW
Grants CA-13525. We thank Pamela Silver for data
collection and Irene Asturias for manuscript prepara-
tion. We also thank the attending staff and previous
Neun-Oncology Fellows of the Neuro-Oncology Service
for their help in caring for these patients.
References
1. Bernstein M, Hoffman HJ, Halliday WC, Hendrick
EB, Humphreys RP: Thalamic tumors in children:
Long-term follow-up and treatment guidelines. J
Neurosurg 61:649-656, 1984.
2. Danoff BF, Kraner S, Thompson N: The radio-
therapeutic management of optic nerve gliomas
in children. Int J Radiat Oncol Biol Phys 6:45-
50, 1980.
3. deTribolet N, Barrelet L: Successful chemother
apy of pinealoma. Lancet 2:1228-1229, 1977.
4. Doworetz DE, Blitzer PH, Wang CC, Linggood RM:
Management of glioma of the optic nerve and/or
chiasm. Cancer 45:1467-1471, 1980.
5. Edwards MB, Levin VA, Wilson CB: Brain tumor
chemotherapy: An evaluation of agents in current
use for Phase II-III studies. Cancer Treat Rep
64:1179-1205, 1980.
6. Eisenberg HM: Supratentorial Astrocytoma in
Pediatric Neurosurgery: Surgery of the Devel
oping Nervous System. Section of Pediatric Neu
rosurgery of the American Association of Neuro
logical Surgeons. New York, Grune & Stratton,
1982, pp 429-432.
7. Gutin PH, Levin VA: Surgery, radiation, and
chemotherapy in the treatment of malignant
brain tumors. In Thompson RA, Green JR (eds):
Controversies in Neurology. New York, Raven
Press, 1983, pp 67-86.
8. Harter DJ, Caderao JB, Leavens ME, Young SE:
Radiotherapy in the management of primary
gliomas involving the intra-cranial optic nerves
and chiasm. Int J Radiat Oncol Biol Phys 4:681 -
686, 1978.
9. Hoshino T: A commentary on the biology and
growth kinetics of "low grade" and "high grade"
gliomas. J Neurosurg 61:895-900, 1984.
10. Hoyt WF, Baghdassarian SA: Optic glioma of
childhood. Br J Ophthalmol 53:793-798, 1969.
11. Hoyt WF, Mishel LG, Ussell S, Schatz NJ, Suckling
RD: Malignant optic gliomas of adulthood. Brain
96:121-132, 1973.
12. Kirshner JJ, Ginsberg SJ, Fitzpatrick AV, Comes
RL: Treatment of a primary intracranial germ cell
tumor with systemic chemotherapy. Med Pediatr
Oncol 9:361-365, 1981.
13. Levin VA, Wilson CB, Davis R, Wara W, Pischer
TL, Irwin L: A Phase III comparison of BCNU,
hydroxyurea, and radiation to BCNU and radiation
therapy for treatment of primary malignant
gliomas. J Neurosurg 51:526-532, 1979.
14. Levin VA, Gutin PH, Wilson CB: Brain tumors. In
Greenspan EM (ed): Clinical Interpretation and
Practice of Cancer Chemotherapy. New York,
Raven Press, 1982, pp 393-408.
15. Levin VA, Wara WM, Davis RL, Vestneys P, Res-
ser KJ, Yatsko K, Nutik S, Gutin PH, Wilson CB:
Phase III comparison of BCNU and the combina
tion of procarbazine, CCNU, and vincristine ad
ministered after radiation therapy with hydrox
yurea to patients with malignant gliomas. J Neu-
rosurg 63:218-223, 1985.
16. MacCarthy CS, Boyd AS, Childs DS: Tumors of
the optic nerve and optic chiasm. J Neurosurg
33:439-444, 1970.
17. Montgomery AB, Griffin T, Parker RB, Gerdes AJ:
Optic nerve glioma: The role of radiation therapy.
Cancer 40:2079-2080, 1977.
18. Neuwelt EA (ed): Diagnosis and Treatment of
Pineal Region Tumors. Baltimore, Williams &
Wilkins, 1984.
19. Packer R: Personal communication, 1984.
20. Phuphanich S, Edwards MB, Levin VA, Vestnys
PS, Wara WM, Davis RL, Wilson CB: Supratento
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treatment with radiation and chemotherapy. J
Neurosurg 60:495-499, 1984.
21. Prioleau G, Wilson CB: Endodermal sinus tumor
of the pineal region. Cancer 38:2489-2493,1976.
22. Roberson C, Tiel K: Hypothalamic gliomas in chil
dren. J Neurol Neurosurg Psychiatry 37:1047-
1052, 1974.
23. Russsell DS, Rubinstein LJ: Pathology of Tumors
of the Nervous System. Baltimore, Williams &
Wilkins, 1971.
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MJ, Fuks: Successful chemotherapy of recurrent
intracranial germinoma with spinal metastases.
Neurology (NY) 33:631-633, 1983.
35
Therapeutic Modality Selection in Management of Germ Cell Tumors
Kintomo Takakura, M.D., and Masao Matsutani, M.D.
Intracranial germ cell tumors are divided into
three major histological types: germinoma and
mature and immature teratoma. Immature tera-
tomas include embryonal carcinoma, choriocar-
cinoma, endodermal sinus tumor (yolk sac tu-
mor), and other teratocarcinomas. Mixed tumors
of these histological types are often encountered.
Because Choriocarcinomas produce human cho-
rionic gonadotropin (hCG) and endodermal sinus
tumors and some embryonal carcinomas produce
alpha-fetoprotein (AFP), the immature teratomas
containing components of those tumors can be
properly diagnosed without histological verifica-
tion when the levels of those tumor markers
elevate in the serum or in the Cerebrospinal fluid
of patients. Recent studies revealed that most
immature teratomas produced either hCG, AFP,
or both marker proteins.
From therapeutic points of view, germinoma is
quite sensitive to radiation and is properly
treated by radiotherapy alone. Mature teratomas
can be surgically removed completely in most
cases. Immature teratomas are, however, resist-
ant to radiation, grow rapidly, and metastasize
frequently inside ventricles, to subarachnoid
spaces, and to other organs. They require, there-
fore, multimodality treatment with surgical re-
moval, radiotherapy, and chemotherapy. Be-
cause histological findings of intracranial germ
cell tumors are heterogeneous in most cases, a
biopsied specimen of the tumor hardly clarifies
whole features of the tumor.
There is always controversy about the thera-
peutic modalities of intracranial germ cell tu-
mors. Some neurosurgeons insist that histologi-
cal verification is necessary before any treat-
ment. On the other hand, others prefer so-called
diagnostic radiotherapy before surgical removal
whenever it is required, mainly for reasons of
safer and better management of the patients.
The volume of germinoma can be decreased by
small doses of radiation (i.e., 20 Gy). Further-
more, many mixed-type teratomas contain ger-
minoma components and respond remarkably to
radiotherapy. Presurgical radiotherapy is, there-
fore, rational for reducing the size of the tumor
before surgical removal and also for diagnostic
aid. This short report describes our therapeutic
approach for intracranial germ cell tumors.
Histological Types of Intracranial Germ
Cell Tumors
The histological types of surgically removed
intracranial germ cell tumors are summarized in
Table 35.1. Of a total of 84 tumors completely
analyzed, 54 tumors showed a homogeneous his-
tological pattern in each tumor tissue (pure type)
and 30 other tumors contained mixed histologi-
cal patterns. Pure type is, however, determined
by the histological feature that more than 98%
of tumor tissue shows the same pattern of his-
tology; this does not mean real homogeneity of
the tumor. Pure types of those tumors included:
24 germinomas and 22 mature and 8 immature
teratomas. Mixed types of the tumor contained
various components of germinoma and mature
or immature teratoma in the same tumor tissue.
The precise histological pattern of each tumor is
described in Table 35.1. Of 84 tumors, 47 cases
(56%) contained germinomatous component and
25 cases (30%) contained some immature tera-
tomatous components. Forty-five tumors (54%)
were located in the pineal region, 29 tumors
(35%) were in the suprasellar region, and 10
tumors (12%) were in other sites. Although the
sex ratio of all germ cell tumors was 5 (male):l
(female), it largely differs with age and the his-
tological type of tumor. The most significant sex
difference was noted in cases of immature tera-
toma. Male patients with immature teratomas
were 10 times more frequent than females at
ages between 10 to 20 years old, and no female
patients at ages between 20 to 40 years old have
ever been encountered (6).
Therapeutic Modality and Results
The outcome of treatment for intracranial
germ cell tumors depends on the histological type
and location of the tumor. For tumors located in
the pineal region, radiotherapy with a small dose
of 20 Gy is locally given as the initial treatment
(diagnostic radiation). Ventriculoperitoneal
shunting for hydrocephalus is performed only
when the increased intracranial pressure is sus-
pected to be hazardous. When a patient is in good
condition without papilledema, headache, or
nausea, radiotherapy is generally given with glu-
cocorticoid administration without VP shunting.
If a tumor is germinoma, it shrinks rapidly and
almost disappears on CT scan during this radio-
therapy. In such a case, 30 to 40 Gy of radiation
is further given to whole brain for preventing the
recurrence and intraventricular dissemination.
When a tumor does not respond fully to the initial
radiotherapy, surgical removal of the tumor is
indicated. The approach to the tumor is deter-
mined by the location and shape of the tumor in
the third ventricle as appreciated on computer-
ized tomographic (CT) scan and magnetic reso-
nance imaging (MRI). In cases of mature tera-
toma, complete removal of the tumor is a goal of
operation. No postsurgical irradiation is needed.
In cases of immature teratoma, the total removal
of the tumor is hardly possible because the tumor
generally invades to the adjacent brain tissue.
All immature teratomas are treated with post-
surgical radiotherapy (30 to 40 Gy to whole brain
and 25 Gy to spinal cord) concomitantly with
chemotherapy using ACNU (100 mg/m2 i.v. on
Day 1) and vincristine (1 mg/m2 i.v. on Days 2
and 3) for synchronization of the tumor cell cycle
(5). The second course of chemotherapy is added
during radiotherapy whenever possible. After
finishing the whole course of radiotherapy,
chemotherapy with cisplatin, vinblastine, and
bleomycin (PVB therapy) is given for preventing
the recurrence. Cisplatin (20 mg/m2 i.v.) is given
5 times on Days 1 to 5. Vinblastine (4 to 6 mg/
m2 i.v.) is given on Days 1 and 7. Bleomycin (10
to 15 mg/m2 i.v.) is given on Days 1, 8, and 15.
These courses of chemotherapy (21-day course)
are repeated 3 times as the initial maintenance
chemotherapy. For further maintenance chem-
otherapy, the above one course of chemotherapy
is repeated every 3 to 4 months. All patients are
checked with regular examinations of CT scan
or MRI and serum tumor marker assays for de-
tection of recurrence.
When the diagnosis of a pineal region lesion is
suspected to be a tumor other than germ cell
such as meningioma, epidermoid, or gliomas by
imaging examinations before any treatment, sur-
gical removal and the establishment of a histo-
logical diagnosis are generally the first steps of
therapy.
 In cases of suprasellar germ cell tumors, sur- compared to other tumors. The 5-year survival
gical removal and histological verification are the rate was 26% and only few patients have been
initial steps of treatment because operation in able to survive more than 10 years. The response
this location is safely performed and various tu- to multimodal treatment is related to the marker-
mors other than germ cell tumors such as cran- producing function of the tumor. A serum hCG
iopharyngioma or optic nerve gliomas are quite level over 1000 mlU/ml or an AFP level over 1000
often encountered. The therapeutic modality ng/ml is a sign of poor prognosis. All long term
after operation is similar to that for tumors lo- survivors showed lower levels of markers in their
cated in the pineal region. Germ cell tumors in serum.
other locations require surgical verification be- Our Phase II group study (2) revealed that PVB
fore radiotherapy or chemotherapy because the therapy was effective to suppress the growth of
diagnosis of germ cell tumor cannot be estab- the immature teratoma and has extended the
lished without histological examination except in survival time. Thirty cases of immature teratoma
functioning tumors producing hCG or AFP. were treated with PVB therapy and 47 historical
Germinoma is sensitive and responds well to controls were accumulated in this study. The
radiotherapy. The survival rates of patients with median survival time of controls was 18.0
germinoma (n = 79) in all sites at 5 and 10 years months after operation. Only 14.0% of the pa-
after the initial treatment were 74 and 72%, tients survived more than 5 years. Of 30 patients
respectively (Fig. 35.1). The survival rates for treated with PVB therapy, 20 primary cases re-
suprasellar germinoma are much better than for ceived PVB therapy at the time of the initial
pineal region germinoma mainly because of sur- treatment. The effectiveness rate for reducing
gical morbidity. The survival rates for suprasel- tumor size appearing on CT scan was 71%. Nine
lar germinoma (n = 22) at 5 and 10 years after
operation were 91 and 84%, respectively,
whereas those for pineal region germinoma (n =
49) were both 65% (Fig. 35.2). These survival
rates included all cases treated during the past
20 years. The mortality and morbidity of opera-
tion for pineal region tumors have, however,
much improved recently. The surgical mortality
in the most recent 5 years was 0%. Therefore,
the long term survival rates of patients with
germinoma seem to be much better than the
above data indicate.
The outcome of treatment for mature teratoma
depends on the size of the tumor and the clinical
status of the patient at the time of admission.
The survival rates at 5 and 10 years after oper-
ation were 64 and 48%, respectively. The sur-
vival rate of immature teratomas was the worst
of 20 (45%) patients demonstrated complete re-
sponse (disappearance of the tumor on CT scan).
A reduction of serum tumor marker levels was
noted in 90% of the patients. In the recurrent
cases, the effectiveness rate for reduction of tu-
mor size on CT scan was 50% and the tumor
marker reduction rate was 69%. The survival
rates at 2 years after operation were 46.5% for
the patients who received radiotherapy alone and
67.7% for the patients who received PVB therapy
(Fig. 35.3). The major side effects of PVB therapy
were nausea and vomiting (52%) and myelo-
suppression (45%) and pulmonary fibrosis (1
case). Pneumonia (2 cases), temporary decrease
of auditory function (2 cases), hyponatremia (1
case), and pigmentation of skin were noted.
Discussion
In this chapter, we have described the thera-
peutic modality and results for intracranial germ
cell tumors. Other tumors in the pineal region
such as pineocytoma, pineoblastoma, various
gliomas, and others were excluded. Because al-
most 80% of all pineal region tumors in Japan
are germ cell tumors (6), the differential diagno-
sis can be quite satisfactorily established by CT
scan, MRI, angiography, and serum tumor
marker study. Although diagnostic radiotherapy
for pineal region tumors is opposed by some neu-
rosurgeons simply for lack of histological verifi-
cation, it is beneficial for almost all patients from
clinical points of view. Almost all tumors respond
to the radiotherapy to some extent and the sur-
gical management for the remaining tumor has
never been hindered by this presurgical radio-
therapy. Many patients with germinoma have
been cured by radiotherapy alone without oper-
ation.
Because the prognosis for immature teratoma
is still very poor, the therapeutic modality for
those tumors in the pineal region remains un-
solved. PVB therapy has been reported to be
effective for intracranial germ cell tumors by
several investigators (1, 3, 4); the side effects on
renal function, auditory disturbance, and pul-
monary fibrosis are limiting factors for continu-
ing this chemotherapeutic schedule. Combined
chemotherapy with cisplatin and VP-16 was re-
ported to have the same potential therapeutic
response as PVB therapy with less toxicity (7).
Inasmuch as immature teratomas demonstrate a
definite male predominance, endocrine factors
controlling tumor should be investigated to es-
tablish the hormonal treatment of these tumors
and better chemotherapies. Further studies are
required to improve the therapeutic modality for
these immature teratomas.
Acknowledgment
This work was supported by Cancer Research Grant
59-22 from the Ministry of Health and Welfare and a
Special Research Grant from the Japan Brain Foun-
dation. Aid in preparing this manuscript by Miss Ha-
ruko Ichimura is also acknowledged.
References
1. Kirshner JJ, Ginsberg SJ, Fitzpatrick AV, et al:
Treatment of a primary intracranial germ cell
tumor with systemic chemotherapy. Med Pediatr
Oncol 9:361-365, 1981.
2. Matsutani M: Cisplatin, vinblastine, bleomycin
(PVB) combination chemotherapy in the treat
ment of intracranial malignant germ cell tumor:
Phase II study. Presented at the 8th International
Congress of Neurological Surgery, Toronto, Can
ada, 1985, Abstract 127, pp 81-82.
3. Neuwelt EA, Frankel EP, Smith RG: Suprasellar
germinomas (ectopic pinealomas): Aspects of im-
munologic characterization and successful chem
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4. Siegel T, Pfeffer MR, Catane R, et al: Successful
chemotherapy of recurrent intracranial germi
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for brain tumors. Prog Nerv Res (Jpn) 26:105-
112, 1982.
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agnosis and Treatment of Pineal Region Tu
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309-322.
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