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2nd edition
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'High-Yield Neuroanatomy
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Jarnes D. Fix, Ph.D.
Emeritus of Anatomy
Marshail University School of Medicine
Huntington, \V'est Virginia
LIpPINCOTT WILLIAMS &
.. A Wolters Kluwer Company
Philadelphia Baltimore New York london
Buenos Aires Hong Kong Srdney Tokyo
,.'
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. "'"'
rean'mmm--
., ,," .... J' ........ - ...... -
Acquisicions Editor: Eli:abelh A.
Edirori:ll Dirtcror of Dt!t'o!lotllTltmc: Julie Martinez
DewL.'fttnnlt Ediror: Karla M. Schrlledcr
Senior Ediror: A111\' G. Dinkel

__ Copyright by L.irrincott Willinms Wilki!ls.
Copyright C> 1995 by Wjlliams &. Wilkins.
All rightS This is pr ... by copyright. No r:lrt of it may be rr ... storeJ
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terials provided by the rublisher .to schools that have its lIccompanying textbook.
Printed in the United States of America. For information. \\Tite lippinc"tt Williams &
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Materials appearing in this book prepared br individuals as r<lrt ortheir official duties as U.S.
GO\'emment employees are not cO\'ered by the at-o\'e-mentioned copyright.
9 S 7 6 5 4 3 2 1
library ofCc.:1gress Cataloging-in-Pub!ication D.1[2.
Fix. ]3.lnes D.
High-yield ''''"r 0anatom}' I James D. Fix.-2nd ed.
p. ; cm. - (High-yield series)

Includes index.
ISBN 0-633-30721-5
L !'Jeuroanatomy--Outlines, syllabi. etc. 2. Neuroanatomy-Examinations. questions.
etc. I. Tide. II. Series.
1. Nervous System-anatomy & histology-Examination Questions. 2.
Nervous System-anatomy & histology--Oudines. 3. Nen'ous System
DL<eases--Examination Questions. 4. Nen'ous System Diseases-Outlines. \VL 18.2
F566h 2(\,'\1]
.F588 2000
611'.S'076--dcZl 99-051352
Care has been taken to confirm the accuracy of the infomlation presented and to describe
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fer errors or omissions or for an}' comequences from application of the information in this book
and make no warranty, express or implied. with respect to the of the publication.
The authors, editors, and publisher ha\'e exerted e\'er/' effort ro ensure that drug selecrion
and dosage set forth in this text-are in accordance with current recommendations and practice
at the time of pubiication. Howe\er. in \'iew of ongoing research. changes in gO\'emmem reg-
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Preface
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The second of Hi?0-Yield Nellroa'n{1comy is still ne.uroanatamy at its irreducible minimum,
raining most, if not all, of the 'national board themes, The sole purpose of the book is to get you
through the nen'ous system topics cO\'ered on the United Scates Medical Licensing Examination
(USMLE) Step 1. Substantial ha\'e been made to accommodate' student requests and sug-
gestions.
NEW TO THIS EDITION
of nuclear magnetic imaging scans
Carotid and \'enecral digital subtraction angiography
Nuclear magnetic angiography
Additional figures of cranial nerye function componems
Chapter on aphasia. apraxia. and dysprosody
Index
TO THE STUDENT
To make the most of this book, stud), the illustrations, computed tomography scans, and magnetic
images carefully, and read the legends. Many board-type questions come from this source.
In fact, the answers to at least 20 common USMLE questions are found within this preface. Finally,
remember these tips as you scan the chapters:
Chapter 1: The mini-atlas pro\'ides you with the essemial examination structures labeled on com-
puted tomography scans and magnetic resonance images.
Chapter 2: Cerebrospinal fluid pathways are well demonstrated in Figure 2-1. fluid is
produC'ed by the choroid plexus and absorbed by the arachnoid villi t.hat jut into the venous sinuses.
Chapter 3: The essential arteries and the functional areas that they irrigate are shown. Study the
carotid and vertebral angiograms and the epidural and subdural hematomas in computed comography
scans and magnetic resonance images. ,/
Chapter 4: The neural crest and its derivatives, the dual origin of the pituitary gland, and the differ-
ence between spina bifida and the Amold-Chiari malformation are presented. Study the figures that
ill.ustrate the Arnold-Chiari and Dandy-Walker malformations.
Chapter 5: What is the difference between Lewy and Hirano bodies'? Nen'e cells contain Nissl sub-,
stance in their perikarya and dendrites, but not in their axons. Remember that Nissl substance (rough
endoplasmic reticulum) plays a role in protein synthesis. Study Figure on the localization and
prevalence of common brain and spinal cord tumors. Remember that, in adults, glioblascoma multi-
forme is the most common brain tumor, followed by astrocytoma and meningioma. In children, as-
trocytoma is the most common brain tumor, followed by medulloblascoma and ependymoma. In the
spinal cord, ependymoma is the most common tU\;10r.
Chaptt!r 6: The adult spinal cord tcrminiHcs (conus terminalis) m the lower border of the first lumbar
\'crtebra. The newborn's spinal cord extends to thc third lumbar vcrtebra. In aduIes, the cauda equina
extends from \'crtcbr<ll IC\'cls L-2 to Co. .
Clw/w)' 7: The tracts of the spinal cord arc rcduced to four: corticospinn\ (pyramidal), dorsal
!,;lin ;md tcmpcr;uurc, and Horner's. Know thcm cold.
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ChatHa 8: Study (he eight nmillllall'oard Idkms of (Ilt! spinal cord, Four hc,wy hiners
Rrl.lwn-Sequard syndrome. BI:! ;wit,\Inino:;is <,sllbnclItt! dcgcncmtion). syringomyelia, and
al1lyotwphic btewl sClerosis (LI.)lI Gehrig':; di::c:1sc).
Chapc!!!' 9: Study the trans\'crse st!ctions l)f (he brnin stt!tn, and k)cali:e the cranial nerve nuclei. Scudy
. the surface llf (he stem, nnd the exiting and eprering crani:11 nen'cs. On thc
dorsal s\,rfac'c \')f the brain stem, identify the only exiting cranial nerve, the trochlear ner\'e.
Chaprer JO: Cr.mial ner\'e.(CN) V-I is the nfferent limb oftht! corneal reflex, CN V-I, CN V-2', eN
III, CN IV, CN VI, and the postganglionic sympathetic fibers are all found in the cavernous sinus.
Chapter 11: Figure 11-1 shows the auditory pathway. \Vhm .1re the cau:;es of conduction and sen-
$l)rineuml deafness? Describe the \Veber and Rinne tuning fl.)rk Remember that the auditory
ne,r\'e and the organ of corti nnd derived the otic placode.
'Chaprer 12: This chapter the of \'e$[ibubr n'ystClgmus: rostrotational and caloric'
(CO\VS acronYl'n). Vestibl.Jlo-ocular reflexes in the 'unconscious pntiem are also discussed (see Fig-
ure 12-3),
Chapter 13: This chapter on the cranial nen'es "is pi\'oral. It spawns m.ore neuroanatomy examination
questions than any other chapter. Carefully study all of the figures and legends. The seventh cranial
nerve desen'es special consideration (see Figures 133 and 13--f). Understand the difference between
an upper motor neuron and a lower .motor (Bell's palsy).
Chapter 14: The three important lesions of the brain stem are occlusion of the anterior spinal
arceI')' (Figure 14-1), occlusion of the posrerior inferior cerebellar artery (Figure 14-1), and medial
longitudinal fasciculus syndrome (Figure 14-2). \Veber's syndrome is the most common rnidbrain le-
sion (Figure 14,3).
Chapter 15: Figure 15-1 shows the most important cerebellar circuit. The inhibitory -y-aminoburyric
acid (GABA)-ergic Purkinje cells gh'e rise [0 the cerebellodentatochalamic cract. What are mossy
and climbing fibers? .
Chapter 16: Figure 161 shows e\'eI')'thing you need to know about what goes in and what comes out
of the thalamus. Know the anatomy of the internal capsule; it will be on the examination. \"X1hat is
the blood supply of the internal capsule {stroke}? "-
Chapca 17: Know the lesions of the \"isual system. How'are quadrantanopias created? There are t\\'o
major lesions of the optic chiasma, Know them! \Vhat i$ Meyer's loop? .
Chapcer 18: The imporra;1t anatomy of the auror,lOmic nervous system is clearly seen in Figures 18- 1
and IS2. .
Chaprer 19: Figures 191 i1nd 19-2 show that the para\'entricularand supraoptic nuclei synthesi:e and
release antidiuretic hormone and oxytocin. The supraehiasmatie nucleus receives direct input from
the redna and plays a role in the regulation of circadian rhythms.
Chapter 20: Bilateral lesions of the amygdala result in Kluver-Buey syndrome. Recall the triad hyper-
phagia, hypersexuality, nnd psychic blindness. Memory loss is associated with bilateral lesions of the
hippocampus. \Vernicke's encephalopathy results (rom a deficiency of thiamine (vitamin B). Lesions
are found in the mamillMy bodies, th:-\1C1InlIS, and midbrnin tegmentum (Figure 20-3). Know the Pa
pez circuit, a common board question.
Chapur 21: Figure 21 -) shows the circuitry of the basal ganglia ;1I1d their associatcd neurotransmit
ters, Parkinson's disease is C'lssociated with a depopubrion of neurons in the substantia nigra. Hunt
ingcon's disease results in a 105s of ncn'c cells in the caud:1[e nuclell'> nncl put;ll11en. Hcmiballism rc'
suits frl)Jn infarction of the contTC'I\;ltl'T.)1 suhthnlC"lInic nucleus.
Clw{Jtc'r 22: In this chnprer, the l';uh\\'OIYs of the m;)jor neuflltr;lll\illittC'lS ;1[(: :;]10\\'11 in br:)in
! 11 : 1 p S C; l '-I :': 111 ; 1 t cis the 1\):' j 0 r c :\ cit ;l ((\ r)' tr; m S III itt t: r (l the l)f : Ii: : . ( ;. '\ ; \. \, : : ; i""' ;:'. i (': :;' h ; : .' (j.' 1 . , ; 1 '
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Preface .xl
..... _ .................. " ............ " .... "",, .................... " ......................... " ......... " .. ---- ..: ....... ,t.................. " .............. : ......... " ..... " .. ,,:.; ......... " .. ,," .. " ........... "II ........... .; .................... " .... _
PurHnje celh-; of the cl;.rrbelium are GABA*ergic. In Alzheimer's disease, there .is a loss of
neurons in basal nucleus of Meynerr. In Pnrkinson's disease, there is a loss of
dllpmninergic nelJrons in the nigra. ..
23: This chapter' rhe cl.."Irricnllocalbuion of functional of br;in. How d\."Ies
rhe d')l1\inant hem.isphere differ fn."Im the nondominant hemisphere? Figure 23-4 shows the effects of
"'arh"us major henlispheric lesions', \Xlh;u: symptoms result from a lesion of the right inferior parietal
. lobe! \'Vllat is Gerstmann's syndrome?
,,-... .. . .
Chaprer 24: This chapter describes apraxia. aphasia, and dysprosodr, .Be,able to,differentiate J?roca's
fromWemicke's aphasia, '\Vhar is conduction aphasia? This is board-relevant.material.
I "'ish rou good luck,
James D, Fix
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Acknowledgments.
.............................................................................................................................................................................................................. -
I wish [Q th;mk my ll1:edical studen.ts. and members of the staff of \Villiams &
. \Vilkins for their ,-alual:-le comments. suggestions. and help. Thanks also go [Q Elizabeth Nieginski
for her editorial direction.
xiII
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. Contents
. . .
................................................................................................... _ ............................................................................................... .
.. .
.1. .. Anatomy of the .. ' .............
I. 1
2
3
II. scctkln
III. Coronal section thrl'ugh che chiasm 3
IV. Coron"l section thf\,'\ugh the mamillary bodies 4
V. A.xial image through che chalamus and internal cClpsule 5
VI. A.xial iinage through 1l1<1rnillary bodies, and optic mict 6
. ;--:-.. -
Meninges, \Tentricles, and Cerebrospinal Fluid ........ :
I. fenihges 8
II. Ventricular system 10
'". Cerec.r\."Ispinal tluid It
IV. Herniation 11
. . . . . . .
Blood Supply .............. .- ........................ .
(.
The srinal cord and lower brain stem 1 =
<J
II.
The internal carotid system
16
III.
The \'en:ebrobasilar system
17
IV.
The blood supply of the internal <;:apsule
18
V.
Veins of the brain
18
VI.
Venous dural sinuses
18
VII.
Angiography
18
VIII.
The middle meningeal artery
19
4
Development of the Nervous System
I. The neural tube 24
5
. . . . . . . . . . . . . . . .
. . . . . . .
II. The neural crest 25
III. The anterior neuropore 26
IV. The pOsterior neuropore 26
V. Microglia 26
VI. Myelination 27
VII . Positional changes of the spinal cord 27
VIII. The optic nerve and chiasma 27
IX. The hypophysis 27
X. Congenital malformations of the CNS 27
Neurohistology ......... .
I. Neurons 30
II. N substance 31
III. Axonal transport 31
IV. Wallerian degeneration 3 r .
V. ChromacolYSis 31
VI. Regeneration of nerve cells. 31
VII. Glial cells 31
VIII. The bloodhr<lin harrier 32
IX. The hloodCSF harrier 32
. . . . . . . . . . . . . . . . . . . . .
.f ."""',-.
. . . . . . . . . .
1:
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mses"pS:? I; 3M
nB,
vi Contents I
........................................................................................................................................................................................................
X. Pigment:: ;tnJ' .32
I
XI. The! '-It' iil'l.'r:: 32
XII. Tum('r$ rNS .'3'
XIII. reCI.'l'Wf:; 33

6 Spinal Cord ......... . ........
I. Omy "nJ Whitl.' c,-'mmuni,atit1g rami 36
. . . . . . . . . . . . . . .
II. Tcnninaci..
1
rl c.,f the C,-'tHIS 36
III. ,'f chI.' seml'ry l1uciei of che spinal c,-,rd
IV. The C<lUJ;l c:quina ) I
V. 111e my,'c.ltic retlex 3 j
7 Tracts of the Spinal Cord' .......... .
I. Incrodu .... ckm 35
. . . . . . . . .
II. Dl'r$(ll c ......lumn-mediallemnisclls pachway 38
III. Lateral :orinoch:llamic tract 40
IV. Laceral c .. 'n:ic('$rinal cracc 40
V. Hn., .... tract .. H
37
8 Lesions of the Spinal Cord ............ .
I. Disease:, .. ,t the motor neurons and corticospinal craccs 4j
. . . . . . . . .
II. Sensory pthway lesions 47'
'". Combinc:d mOWr and sensory lesions 47
IV. Peripher.'!.l ner\"ous system (PNS) lesions 48
V. lnt:ervene'tra.l disk herniation 4S
. . . . . . .
9 Brain Stem ............... ' ............................
I. O\'erview 49
11. Cros5-section through the medulla 49
III. Cross-section through the pons 51
IV. Cross-section through th:: romal midbraill 52
V. Corticol:-ulbr fibers 52
1.0 Trigeminal System
I. O\'ervicw 53
II. 11le trigeminal ganglion 53
III. Trigeminothalamic pathways 53
IV. Trigeminal ret1exes 55
V. The cavernous sinus 57
. . . . . . . .. . . . . . . . ..
','
. . . . .
:1.1. Auditory System ...
I. Overvic\\" 58
. . . . .. . . . . . . . . . . . . . . .. . . . .. .. . . . .. . . . .
II. The auditory pathway 58
'". Hearing defects 58
IV. Auditory ((:.m 59
:12 Vestibular System ...... .
I. Overview 61
". The labyrinth 61
III. The pathways 62
IV. Vescihulo-cJCulnr reflexl's 63
.13 Cranial Nerves ..... .
I. ll)c (,I(act(Jry ncn'C ())
l\. The (Jptir: :1t:J\T ()b
. . . . . . . . . . . . . . . .. . . . . . . .. .. . . . .
.. . .. . . .. .. . .. .. . .. . . . .. .. .. .. . .. . .. . . .
36
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61
65
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Contents vII
............ : ........ ; ....................... ; ........ , ............ ....... --.................. -.. --., ...................... -............................................................ : .....
tv. The nerve (eN IV) 67
V. The tri!:!cmin"l"ncT\'e (eN V) 67
VI. The al-Jucenr (eN V1) 6S
VII . The t;ltial (eN VII) 69
VIII. The \'e,::riblll,.'c('chicar (eN VIII) 71
IX. The nerve (eN IX) . n ..
X. The vagal nem! (eN X) i-t
. XI. llle accc:,sory nerve (eN Xl) i5
XII. llle, (eN 77
, 1.4 Lesions of the Brain Stem ..............................
I. Lesions of the medulla 7S
I L Lesions of the i9
III. Lesions of the midbrain S(I
IV. A.coustic nellwma(schw<llll1oma) 81
V. Jugular foramen syndrome
VI. "Locked,in" syndrome' -83
VII. Centtal rontine myelinolysis 8-1-
VIII. 'Top ot' the syndrome 84
IX. Subcla\'ian steal syndrome $4
X. The cerebellorontine angle 84
78
i5 Cere bellum .............. -. ....... ; . . . . . . . . . . . . . . . . . . 85
I. Function 8j
II. Anatomy 85
III. llle major cerebellar pathway 86
IV. Cerebellar dysfunction 87
V. Cerebellar syndromes and tumors 87
:1.6 Thalamus ............................ .
I. Introduction 88
II. thalamic nuclei and their connections 88
1If., Blood supply 90
IV. The internal capsule 90
. . . . . . . . . . . .
88
,.
:1. 7 Visual System . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 91
I. Introduction 91 /
II. The visual pathway 91
III. The pupillary light ret1ex pa,thway 93
IV. The pupillary dilation pathway 93
V. 'The near reflex and accommodation pathway 94
VI. Cortical and subcortical centers for ocular motility 94
VII. Clinical correlation 96
:18 Autonomic Nervous System ............................... 98
I. Introduction 98
II. Cranial nervcs with parasympathetic components 98
III. Communicatin.,: rami 98
IV. Neurotransmitters 98
V. Clinical correlatioll 101
:19 Hypothalamus ........................................ 103
I. lntrouuction 103
II. Functions 105
III. Clinical corrclation 106
. 'all

vIII
.................................................................................................... 0: ..................................................................................... ;
. 20 Limbic System
. .
.................. -.....
I. 11..";
II. 1.."\.'mpl)IlI..'IlC:: .U1J 107
III. The circuit
IV. Clinic.,1 corrcbCi ... 'n h.'9
. . . . . . . . .
....
10
2:1. . Basai and Stdatal1viotor System
I. Bnsal ganglia '111 . "" .
. . . . .
. 11
II. The ::crbral 111\.'Wr 112
III. Clinic'll correlaci...'n 113
22 Neurotransmitters
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
I. Impl'rc<'lnt and rach\\"ays 115
. II. Funccil..'nal and dini.:al..:onsidcer.ltions 120
23 . Cerebral Cortex ...................... .
. . .. 11:
I. Introduction 121
. . . .
. . . . . . . . . . .
12)
II. The 121
/II. FuncriL'nal area:' 1: i .
IV. Focal descrucri\"ce and srmrcoms 127
V. Cere hal dominance 1::: 7
VI. Split-l:-rainsyndron1C 128
VII. Other of the cOTj:'US callosum 128
VIII. Brain and spinal cor.i rumors 128
24 Apraxia, Aphasia, and Dysprosody ......................... 129
I. Apra:da 129
II. Aphasia 129
III. Oysprosody 131
AppendLx
Index ....
-. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
< . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
133
137
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1.
- of the Brain
I. INTRODUCTION. The illustrations in this chapter are accompanied by corresponding
magnetic resonance imaging (MRl)" scans. Together tl}ey' a of brain
slices in the three orthogonal planes (i:e., midsagittal, coronal, and axial). An insert on
each'figure shows the le\'el of the slice. The most commonly tested structures are labeled.
II. MIDSAGITTAL SECTION (Figures i-:1., :1.-2,and :1.-3). The location of the :muc-
tures shown in the figures should be known'.
Interventricular foramen
Septum pellucidum
Anterior commissure
Lamina tenninalis ,;:---.::::....----...-J
Corpus callosum
Thalamus
Motor strip
ntraJ sulcus
Sensory strip
Third ventricle --.:b-----"'\/f::1.
Superior and inferior colliculi
.
Calcarine sulcus
Fourth ventricle
Cerebellum (vennis)
Medulla oblongata
Figure :1-:1.. scction (I( the hwin anJ hrain stem shOWing the structures sllrrounding the third allJ
(nurth vcntricles. The hr;lin :.tell) incluJes the miJbrain (M), pons 0), and meJulb oblongata.
1
1
2 Chapter i
I
....... : '" ............... " # ............ ............................. ,. .......................................... -._ ................................................................... "' ....... ......................... ..
Paracentral lobule .
US
I
Cingulate gyrus
'Superior frontal gyrus
Superior sagittal sir I
Parietooccipital fiss
I
Anterior cerebral artery
Crista gal/i
Basilar artery -.;I""'-J.o
Sphenoid
Clivis
Nasophar.ynx
C2
Veifl of
Calcarine fissure
Lingual gyrus
Cerebellar vermis
Cisterna
cerebellomedullaris
Figure .1.-2. magnetic resonance imaging secrion through the brain and brain stem showins: IT
iml:'orram structures surroundinll the third and fourth ventricles. This is a Tl-weif!hced imae. The IZra\' m:'nt
is gray (hypoimense), whereas the white matter is white (hyperimense). - - _.
Fornix
Thalamus
.... r
Corpus callosum --..;;..... __ _
lateral ventricle ----...-..:0
Anterior cerebral artery ___ --"'!'.
Optic chiasm -"'----==0:--':"
Hypophysis/inrundibulum
Mamillary body
Cisterna cerebellomedullaris
Cerebral aqueduct ---::.::-....;;
Spinal cord
'-'::---'-- Subarachnoid space
Figure 1-3. !11:1gn<:tic rCS\lllancc imagint.: scction Ihrollgh til(! hrain :.rem :lIlJ Note
the tract: lateral vcnHick" infcr\'cnrricular (oramen o(Monro, third ventricle, cerehrnl aque-
duct, (L1unh vcntricle, (ora men (,( M<1I;\'IIII;e, cercbcll(IIll('duii;u}' cistern. ;md sp;!Cc, r..:(\(C'
;d",l rill' fl'htioll die optic chi;!'l". in(ul1ddH;{UIll. ;111:1 h)'l'(11,11\,\I.' (,'"rllll;,,1.' '11\<1.\.
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" Cross-Sectional Anatomy of the Brain
........... ........ '" ........... ............................................... ;. ......... -.. , ............................................. ; .................... : ....... -.................. .
CORONAL SECT,ON THROUGH THE OPTIC CHIASM (Figures :1.-4 and 1.
The k"lcution of [he in the figures should be known.
Caudate nucleJs
In:emal
Corpus callosum
Lateral ventricle
Septum pellucidum
Pu:ame.,
Insula
Figure :1.-4. Coronal secck'n of the brain at the b'el of the anterior commissure, optic chiasm, and amn
dala. Note that the internal carsule lies between the caudate nucleus and the lentifonn nucleus (globus pallidl
an.:3 putamen).
fissure
Septum pellucidum
Cingulate gyrus
Corpus callosum
....... Lateral ventricle

Internal capsule ___ _
Amygdala ___ ::----_____
Hypophysis
Cavernous sinus
Sphenoid sinus
Nasopharynx
Caudate nucleus
Third ventricle
:......,;,---,- Optic chiasm
Infundibulum
Interior carotid artery
Figure :1.5. CCJronal Inilgn('tic rcsonancc im;lt:inj.! :<cction throllgh thc mnygJa!a, (.1ptic chiasma, infundihu-
lum, find intcrn;]l capsulc. Till' Ci\\"crnous ("ncirdcs the sella !orcien and contains thc following structures:
cranial nerves (eN) fll, IV. V/. V-I, ;lnJ V-2; posIl,;anJ.,:lionic syml':lIhcric fibers; nnd thc internal cnrotiJ anery.
This is a TI-wcightcd image.
.1
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mc' ,
'.r.
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4 Chapter 1 1
" .... , ............................................. .., ............... .............................................................................................. , .................................. .
IV. CORONAL SECTION THE MAMflLARY BODIES (Figures" 1.6 am
1 7). The Illcntion of the shown in the hures should be
lateral
ventricle
Internal capsule
Third
ventricle
Subthalamic
nucleus
Substantia
nigra
Mamillary bodies
Fornix
Caudate nucleus
Thalamus
Insula
Putamen
Optic tract
Hippocampus
Figure 1-6. Coronal section of the brain at the b'el of the thalamus. mamillary bodies. and hippocampal
formation. Note thac the internal capwle lies between the thalamus and the lentiform nucleus.
Corpus callosum ---::':=.:.AIII
Caudate nucleus
Putamen
Globus pallidus
Hippocampus
Crus cerebri
Thalamus
Internal capsule
Substantia nigra
Interpeduncular foss;)
Base of pons
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Cross-Sectional Anatomy of the Brain 5
y ................................. "' ............ - _ -'--, . - -: - .................. ... : ............. __ ............................ : ...................... ,._ ............ ..
v. AXIAL ,IMAGE THROUGH THE THALAMUS AND INTERNAL CAPSULE
(Flgures :1.-8 and 1-9). The Jocation of the srruccures shown 'in the figures should be
known: " . .
Corpus callosum
,
Septum pellucidum
Fornix
Third ventricle
Corpus callosum
(splenium)
Superior colliculus
,lateral ventricle
I Q!UCl'atanucleus
Intemal capsule
. (anterior limb)
Pineal gland
Internal capsule
(poslerior limb)
Thalamus
nucleus (Iail)
Figure :1-8. Axial section of the brain at the bd of the internal capsule and basal ganglia. Note that the
internal capsule has an anterior limb, a genu, and a posterior Note also that the corpus callosum is sec-
tioned through the genu and splenium.

Lateral ventricle
Septum pelludicum
and fornix

Putamen
Globus pallidus
Insula --+.;;'"
External capsule -.-.,..,-
Velum inlerpositum
Superior sagittal sinus ___ ':":'-:-__ ---.

.........
Corpus callosum (genu)
Caudate nucleus
Internal capsule
(anterior limb)
""""--Internal capsule (genu)
capsule
(posterior limb)
---..,--'--.. Thalamus and third
ventricle
Trigone
Corpus callosum
(splenium)
Visual radiations
cortex
Figure Axial mag-netic resonance imaging scctiollllt the b'd of the internal capsule nnd bas;' ganglia.
Note thac the caud,lte nucleus hulges imo the frontal horn of the lateral ventricle. In Hunringwn's disease, there
:-: :-:::::':;;"c loss of -y-arninohutytic acid (GABA)'crgic ncurons in the caudate nuclclIs that results in h).clro.
ccrhalus cx vacuo. A ICliion Clf the S;Clllllli the internal cap:;ulc resu!rs in a contralaccrnl wcnk lower face with
sparing of the upper face. This h a TI-wdghll'd image.
. ... ' .. , .... ... '" .
::: .... '
6 Chapter 1
...................................................................................... __ ....... -.................................................................................................... -
VI. AXIAL IMAGE THROUGH THE MIDBRAIN, MAMlLLARY BODIES; AND OP-
TIC TflACT (Figures 1-1Q, 1-11, 1-12, 1-13):Thc!ocncion of the
shtl\\"l'\ in the :;hl..)uIJ be known.
Substantia nigra
Red nucleus
lateral ventricle
Cerebellum
Hippocampus
Trochlear nucleus
Nucleus 01 inferior cOlliculus
Figure :1.-:1.0. .-\xial section of the l.-rain at the le\'e! of the midbrain. mamillary bodies, and amygdala.
that the substantia nigra separates the crus cerebri from the tegmentum of the midbrain.
Interhemispheric fiss.Ire
Gyrus re<;!us
Optic t:'act
Mamillary nucreus
Red nucleus
Trigone
Sup<;rior colliculus

Middle cerebral artery
Uncus/amygdala
Crus cerebri
Substantia nigra
Straight sinus
Superior sagitlal sinus
Figure :1-:1:1. Axial magnC:tic reson;\nce imaging section the levcl o( (he l\\idh
r
;\ill ;1:1d m;lmil];lr\'
l""lie; lkC<III\C o( thl: Li.':h ire)!) COntl'lI!, the rcd nuclei, mil',,:!I:,,\, l,,;di,c, lnd ""I".: " ".1 , :1 'i ,!., ,'.\' ;: ,", l!Jcl'c
l
",iI.' i,':';.;; 1i!1 I-WI :"':' ,J ':,,.i:,( ,i.",\ .. '1: 1..)(>("j .,.,.:, '.',.
,'I "';'1,
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.. - ........................................................ -..
Optic nerve _:.-...,.,.
Optic chiasm
Optic tract
Mamillary bodies
Cerebral
Superior sagittal sinus
:Closs-Sectional Anatomy of the Brain 7
-----_ ...... _ ................................................ _ ....... : ......... : ..... -
Optic nerve
Am.ygdala
Infundibulum
cerebri
Substantia nigra
Lateral ventricle
;, (temporal horn)
Lateral ventricle
(occipital horn)
Figure. 1.-1.2. Axial magnetic resonance imaging section at me level of the optic chiasm, mamillary bodies,
and midbrain. This patient has neurofibromatis type 1 and an optic nerve glioma. Note the size of the right: cp-
tic nerve. 11le infundibulum is poscflxed. This is a Tl-weighted image.
Optic nerve
Sphenoid sinus
Infundibulum
Oculomotor ne rve
Crus cerebri
Posterior cerebral artery
Quadrigeminal cislern
Cerebral aqueduct
Cerebellar vermis
Straight sinus
Superior sagillal sinus
FIgure 1.-1.3. Axial magncric rc!;onancc imaging H'ctioll at the le\'eI of the uncal incisure, oculomotor nerve,
anJ inferior colliculus. Is thcre pathology within ,he ()rhit?
, .
Meninges, .V.entricles,
anQ
. .
[' . 5
I. are three mem.brnnes 'that surround. the spinal cord Clnd
brain.
A. They consist L'If the pia mater, arachnoid, and dura mater.
1.. The pia mater is a delicate, highly vascular layer of connective tissue. It closely
covers the surface of the !:-rain and spinal. cord.
2. The arachnoid is a delicate, nonvascular connecth'e tissue membrane, It is located
between the dura mater and the pia mater.
3. The dura mater is the outer layer of meninges. It consists of dense connective tis-
sue.
B. Meningial spaces
1.. The subarachnoid space (Figure 2-1) lies between the pia mater and the arach-
noid. It terminates at the level of the second 'sacral \ercebra. It: contains the cere-
brospinal t1uid (CSF).
2. Subdural space
a. In the cranium, the subdural space is traversed by "bridging". veins.
b. In the spinal cord, it is a clinically insignificant potential space.
3. Epidural space
a. The cranial epidural sp;lce is a potential space. It contains the meningeal ar-
teries and veins. ...
b. The spinal epid':lral space contains fatty areolar (issue, lymphatics, and \'enous
plexuses. The epidural space may be injected with a local anesthetic to pro-
duce a paravertebral nerve block.
C. Meningial tumors
:1. Meningiomas are benign, well-circumscribed, slow-growing tumors. They accoum
(or 15% o( primary intracranial tumors and are more common in women (han in
men (3:2). ,Ninety of are supratentorial.
2. Subdural and epidural hematomas
a. Subdural hematoma is calls<;d by bceration of [he superior cerebral (bridging)
veins.
b. Epidural hematoma. is CCluscJ by Inccration of the middle meningeal artery.
D. Trauma
E. Meningitis is infbmm;Hion o( the pi;Hlr;lChnoiJ :1;"(';1 of the bLlil1. til:' spin;-t1 cord, or
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.: :;,: .. ! :-"';.
. . . '
: .:f',,,:;'Y::\'."
, 'I .....
",
Meninges, Ventricles. and Cerebrospinal Ruid 9.
" - 0: _ .............. __ _ " ........................................... : ;
Superior sagIttal sinus
Interventricu
foramen (of Monro)
Third ventricle
cistern
Cerebral aqueduct
Ponti:'le cistern
Pia mater
Arachnoid
Dura mater
Central canal --ir;r---f
S;linal cistern --....;...;;;)
Arachnoid granulahon
Velum interpositum
Great cerebral vein of Galen
Superior cistern
Straight sinus in
tentorium
Confluence of the
sinuses
Fourth ventricle
(magna) cistern
" ". Suba"rachnoid space
Subdural space
Epidural space
Conus medullaris
Filum terminale
Figure 2-1.. The subarachnoid spaces and cisterns of the brain and spinal cord. Cerebrospinal tluid is pro-
dilCed in the choroid plexuses of the ventricles. It exits the fourth ventricle. cir-culates in the space,
and enrers the sagittal sinus through the arachnoid granulations. Note that the conus medullaris ter-
minates at L-l_ The lumbar cistern ends at S-2. (Reprinted with pemlission from Noback CR, Scrominger NL.
Demarest R: The Human NenxJl(s System. 4rh ed. Baltimore, Williams & Wilkins. 1991, p. 68.)
:1. Bacterial meningitrs is clinically by fever, headache, nuchal rigidity,
and Kcrnig's sign. (With the patient supine, the examiner flexes the pntienc's hip,
but cannot extend the knee without causing pain. It is a sign of meningeal irriw-
cion.) [Rcmemher: == knee.] More th;m 70% of cases occur in children
younger thlln 5 years of age. The disease may cause cranial nerve palsies Ilnd hy-
drocephalus.
'!: ... " ......
'.,. . '')-
... ...: :,"
t
I
10 Chapter 2 .'
...................................... .... .. ............................... _...................................................................... ................. I
(1) In 'newborns, bacterial meningiris is most frequendy ea'used by Group E
agalactiae) ClnJ Escherichia coli." I
(2) In older infants and young children, it is most frequenrly causeJ
injlltt!llzat!. .
(3) In young adults, it is most frequently caused .by Neisst!r;a mell;ngitidis. I
(4) In older adults, it is most frequently 'Clused by Streptoc.occliS pnewlloniae.
b. CSF findings .
(1) Numerous polymorphonuclear leukocytes
(2) Decreased glucose le\'els
(3) Increased protein le\'e!s
,
2. Viral meningitis is also known as aseptic meningiris. Ie is characreri:ed clinically
by fe\'er, headache, nuchal rigidity, and Kemig's'Sign. ..
a. Common causes. \'iruses are with viral
ing mumps, echo\'irus, Coxsackie virus, Epstein-Bart virus, and herpes sim-
plex tyre 2.
b. CSF findings
(1) Numerous lymphocytes
(2) Nonnal glucose levels
(3) Incre.ased le\'els'
. . . - '.-
II. VENTRICULAR SYSTEM
A. 111e choroid plexus is a specialized structure that projects into the lateral, third, and
fourth yenrricles of the brain. It consists of infoldings of blood \'essels of the pia mater
that are cO\'ered by modified ciliated ependymal cells. It secretes the CSF. Tight junc-
tions of the choroid plexus cells form the blood-CSF barrier.
B. Ventricles contain CSF and choroid plexus.
. .'
:to The twO lateral \'entricles communicate with the third ventricle through the in-
tefyenrricular foramina of Monro.
2.' The third ventricle is located between the medial walls of the"cliencephalon. It
communicates with the fourth \'enrriele through the cerebral aqueduct.
3. The cerebral aqueduct connects the third and fourth ven'trides. It has no choroid
plexus. Blockage of the cerebral aqueduct results in hydrocephalus.
4. The fourth ventricle communicates with the subarachnoid space through three
ourlet foramina.
C. Hydrocephalus is d,ilation of the cerebral ventricles caused by blockage of the CSF
}'i1thways. It is characterized by excessh'c accumulatiol) of CSF in the cerebral ventri-
cles or subarachnoid srace.
1. Noncommunicating hydrocephalus results from obstruction within the ventricles
{e.g., congeni[;)1 stenosis).
2. Communicating resulrs from blocbgc within (he subarCichnoid
sp:lce (e.g., adhcsions after mcningitis). .
3. hydrocephalus occurs when thc CSF is not absorbed by thc
arachnoiJ villi. It may occur sccondmyto posttf:lullwtic Illcning/?;1! hemorrhage.
Clinically. it is ch:nDctcrizeJ by thc (riC'ld of progrcssivc dCll1cnri:1, ataxic gait, :1I1d
IIrin;lry incontinence. (Rememher: wacky, wobbly, :md wct.)
4. Hydrocephalus ex V;ICt!O (rllm;1 lu:;s o( (tlls ill ti,,: 1;I)C],:l!': ((,I:.
" , .. ';. ,:'>(,ll "f ' ,
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Ventricles. andCerebrosplniil Auld
...................................................................................... _ .. _ ...................... _ ............................................................................. .
'to CSF outflow at the ;lmchnoid 'iIli.-Ie occurs in obese young women
and is ch .. \mcteri:eJ by p.lpillcdemn withollt mass. elevated CSF pressure, and de'
o rerio'rnting ,encricles may be slit,!ike.
1If. CEREBROSPINAL FLUID is oil colorless acellular fluid. It tlows through the ventricles
nndinto the sulxu-.lChnc..)id space.
A. Function
i. CSF- supporfs the central nervous system (CNS) and 'protects it against' con'
. cussi,e injury.
2. It transports hormones and hormone,releas(ng facrors.
3. It remo\-es waste produEts 'through absorption.
B. Formation and absorption. CSF is formed by the choroid plexus. Absorption is pri,
marily through the arachnoid villi into the superior sagittal sinus_
C. of CSF i,s cli
o
nica11)ftelevant (Ta):>le 2-: 1 ).
1. :rhe nomlal number of mononuclear cells is less than 5h-d.
2. Red blood cells in the CSF indicate subar?chnoid hemorrhage (e.g., caused by
trauma L"r a ruptured 1:-err)' aneurysm).
3. CSF glucose are normaHy 50 to 0 75 mg/dl (66% of the blood glucose level).
Glucose le\-els are nonnal in patients with viral meningitis and decreased in pa,o
tients with bacterial meningitis.
4. Total protein levels are normally between 15 mg/dl in the lumbar cistern.
Protein le\'els are increased in patients with bacterial meningitis and normal or
slightly in patients with yiral meningitis.
5. Normal CSF pressure in the lateral position ranges from 80 to 180 mm
H
2
0. Brain tumors and meningitis elevate CSF pressure.
Table 2i
Cerebrospinal Fluid Profiles in Subarachnoid Hemorrhage, Meningitis, and Viral Encephalitis
o 0
Cerebrospinal Subarachnoid Bacterial Viral
Fluid Nonnal Hemorrhage Meningitis Encephalitis
..
Color Clear Bloody Cloudy Clear. cloudy
Cell countjmm
3
< 5 lymphocytes blood cells > 1000 poly 25-500 lymphocytes
. present morphonuclear
leukocytes
Protein < 45 mg/dl Normal to slightly Elevated 100, Slightly elevated
elevated mgjdl < 100 mgjdl
Glucose - 66% > 45 mg/dl Normal Reduced Normal
of blood (80-
120 mgjdl)
Cell counts in infants < 10 cells/mm
3
; protein in infants = 20-170 mgjdl.
IV. HERNIATION (Figurcs 2,2,2,3,24.2,5. clOd 2,6)
A. Transtentorial (uncal) herniation is protrusion of the brllin through rhe tcneorial in-
cisure.
B. Transforaminal (tonsillar) herniation is protrusion of the brain stem and cerebellum
through the {orClmcn magnum.
C. SubfCllcial herniation is hcrniatitl\\ below the falx cc:rcbri.
'.:' ,.- .: '
2.2 . Chapter 2
.............................................................................................. -._ ........................................................................................... .
Figure 2-2. Coronal section of a cumor in the surrarencorial COl11partmenc. (1) Anterior ceret-ral artery; (2
wbfalcial hemiation; (3) shifting of "etmicleSi (4) arter)' results irr..C.ontralacer .. ,
hemiclUopia): (5) uncal (cranscencorial) herniation; (6fRernohan's notch, with damaged corticospinal and Cor
ticobulbar fibers; (7) tentorium cerebelli; (8) prramiditl cells that give rise to rhe COrticospinal traCt; (9) tonsil.
lar (transforaminal) herniation, which damages viral medullary cencers. (Adapred with pennission from Leed-
R\V. Shumann RM: J\'eilropatholog)" New York, Harper & Ro\\". 1982, p.16.)
Figure 2-3. Axial section through midbrain nn.lthc hcmi(l(ing parahippocnmpal grrus. TI1C left oculo-
motor nCITC is b<:ing !ltr<:tchcd (dilated 1'
1I
1'il). The left cerebral nTtery is resulting in a con-
trClhltcral hemianopia. The right crus cerebri is dam;lbC'\ (Kcrnoh"l)'s notch) b)' thc (rec edge of the tentorial in-
churc, rcsulting in a contr<llarcral KCnll'han's 1)0tch re:\\Ilts in il ("Isc localizing sign. TIle caudal
"';;'I,:/u.:rnent ot" the hrain !>tern rllJ'lItrc of the I\Ir,l1n('.1i;1I) "Ttcrics of the h;lsibr ;lTlcry. H
c
rnorrh:1{.:c into
the rniJhrain and pontine usuall)" (Ha! (Durct hCl1)orrh:l/;cS). The ior (ercbr;,! arterics
f ic rior 10 the: oculomotor nCf\TS. (I) r;\f:lhi)'l'PC;11l1i\1! ):ynl': (2) en:, l'c'l ',+:i; (J) I'll;,! (' I;' 'I C Ilrc! ,r;" i1f, c ry.
(';\'HHic
n
<:rv(:;(5)oPticc'I:\,m:l;"qdl
1
Ilh\(llr:'.(\\\,(I)i:' ',i .:'" (\ii',::,.,! !. , [ .. l
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......... ............. .............. , ....... ................. -.. _--...;
Meninges. Ventricles. and Cerebrospinal Auid 13
_--_ ..................................... , .................. _.-
B
c
A
D
E
Figure 2-4. resonance imaging scan showing brain trauma. (A) Internal capsule; (B) subdural
hematoma; (C) 5ul:-Jural hematoma; (D) thalamus; (E)'epidural hematoma. Epidural hematomas may cross dural
2t:eachmems. Subdural hematomas do not cross dU'rnl attachments. Tne hyperintense signals are caused by
methemoglobin. This is a Tl,weighted image.
A

B
FIgure 2-5. COIll(,lIteJ colOographr scan axial section showing an intwparcllchrmal hClllllrrhngc in the lefr
frcJntallClhc. (A) Inrraparenchyrnal hClllmrhas.;c; (I) larcn" v{,lltricle; (e) jll[ernal capsule; (D) calcifieJ glomus
in the trigone rcgilln II the lareral \(Iltriclc .
, t a.n.m
.7'75 .. m " , lZS
..
14 Chapter 2
.................................................. , ................................................................................ _ ................................................................ .
A
8
. Figure 2-6. Computed tomography axial section showing an epidural hematoma and a skull fracture. (A)
Epidural hematoma; (B) skull fracture; (C) calcified pineal gland; calcined glomus in the trigone region of
. the I "ern I ,emric/e. The epidural hemaroma is a (i
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II
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.. .;;
.. -.. -----.:...:...: .
..... ...... : .. .. -.-... -
. . . .
3
..
Blood Supply
I. THE SPINAL CORD ANP LOWER BRAIN STEM are supplied with blood through
. the anterior spinal ax:tery (Figure 3.t}.. . .. . .....
. . -.". .... .
A. The spinal artery supplies the anterior of the spinal cord.
B. In the medulla, the anterior spinal artery supplies the pyramid, medial lemniscus, and
root fibers of cranial nen'e (eN) XII.
Ant. cerebral a.----------I
Ant. communicating a. -------..
Medial striate a.-------,_

carotid a.
Middle cerebral , .....
Lat. striate aa .. Post. communicating a.
Ant. choroidal a. .,;
\I( .
Sup. cerebellar a. --------::6 .......... .."..""- cerebral a.
Basilar a. N V
Transverse pontine
CN
CN VIII----------'"
CN VI--------.,-
Ant. info a.------I
Post. info cerebellar
Vertebral a .. ----------H
Ant. spinal a.----------4--\
Labyrinthine a.
Figure 3-1. Arreries of the hase (,( the I1min and hrain Mem, incluJing the .medal circle of \'Villis.
1.5
.,.;.:, ..... -.... ..... ..... -. ____ lIIIrr_1I7 ______ .lism.'
. ':',' ..
:16 Chapter 3
....................................................... : ................................................................................................................................................... .
A
II. THE INTERNAl,. CAROTID SYSTEM (see Figure 3,1) consists of the internal carot
a rtery and its branches ..
.', ".:"
.. : ...
A. The ophthalmic artery emers rhe. orbit with the optic nerve (eN II). The centl
artery of the is'a 1::-[",1I1ch of the orhthnlmic mtery. Occlusion results in blindne:
B. The com.municating irrigmt's. and th:ll
mus. An aneurysm of this mrery is t11e second most common aneurysm of the drc
of\Villis. It commonly results in third,nerve palsy.
choroidal ar.tery_arises from the internal carotid Ie is not pan:
\ the circle of \Villis. lr rerfuses the lateral geniculate body, globus pallid liS, and post,
rior limb of the incemal capsule.
D. The ant.erior cerebral artery (Figure ,3-2) supplies rhe medial surface of the hem
the frontal pole to the pariero-occipital sulcus.
. . -
i. The anterior cerehral artery irrigates [he paracentral lobule, 'which contains d
leg .. foot area of the motor and sensory cortices.
2. The anterior communicating artery connects the twO anterior cerebral arterie
t It is most of t11e circle of \Villis, \yhich may cau:
bitemporal lower quadraJ:ltanopia. ,
"'-_. ---- .- .' " ....
3. The medial striate arteries Figure 3,1) are the penetrating arteries'of rhe ar.
terior cerebral artery. They supply the anterior portion of the putamen and cau
date nucleus and the anceroinferior parr of the internal capsule.
E. The middle cerebral artery (see Figure 3,2)
,
i. This artery supplies rhe 'lateral comexity of the hemisphere, including:
a. Broca's and \Vemicke's speech areas
b. The face and ann areas of the moror aqd sensory cortices
c. The frontal eye field
B
I Anterior cerebral artery
_____ -'I cerebral artery Posterior cerebral artery
!. A
Figure 32. C"rticaJ territories (Jf the three cerebral ;merics, (A) Lmcral aspect oi the hemisphere. Most (l:
[hc latcral Ct)Il, .. :-;ity is supplieJ by the l1liJll/e ccrehml ancry. (lJ) Medial amI inferior of the hemisphere
TIH: ;1n(crit'f (cr .. +r,d :tnery the medial 5I1r(;1(e of rhe frolll the l:\lnin:1 tcrrnin;dis en the
cuneus. The I',':r.:rio( (c_rchr,d ;H!UY the ,vistl,d ,',:ld rl;c I'f':.rrrior illfcri(l( "I d'.",rc'!I!;)')
r;)ll()h
c
, (\1(\11rcJ f(ni{l 1 j:) f ,\:1\, :l d,: ,\1(}; ff' '
(: c ... ) j r: i i ;, . <, ' / !
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Blooct Supply 1.7
. .
......................................................... , ......... __ ................... _ .... _ ..................... _ ........................................... ,. ................................ -
. .'" '. ". . .
2. The lateral :;triate arteries (Figure 3-3) are rhe penetrating branches of rhe mid-
dle cerebr."l "reery: Ther me the areeries of stroke, and they supply the internal.
: caps.ule, caudate nucleus, putamen, anJ globus pallidus.
III. THE VERTIBROBASILAR SYSTEM (see Figure 3-1)
Il.
The vertebral artery is a br.lOch of the suFclavi;lIl llrtery. Ie gives rise to [he anterior
spinal artery (see 1) nnd the posterior inferior cerebellar artery .(PICA), which sup-
plies the dorsohueralquadnlOt of the medulla. This quadrant includes the nucleus ::un-
biguus (eN IX, X. Xl) and the inferior surface of the cerebell.um.
B. The basilar artery is fonned by the n .... o vertebral mteries. It gives rise to the follow-
ing arteries.
:1.. . The paramedian branch.es of the pontine arteries supply [he base of the pons,
which includes the corticospinal fibers and the exiting root fibers o(the abducent
nerve (eN Vo. .
2. The laoyrinthirie artery the basilar artery in 15% of people. It arises
from the anterior inferior cerebellar artery in 85% of people.
3. The anterior inferior cerebellar artery (AICA) supplies the caudal lateral pon-
tine tegmentum, including CN VII, d;e spinal trigeminal tract of eN V. and the
inferior surface of the cerebellum.
4. The supe'rior cerebellar artery supplies the dorsolateral tegmentum of the rosa-al
Medial side
Anterior cerebral artery -1111
Caudate nucleus ",
Lateral ventricle "
Posterior cerebral artery -
Subthalamic
nucleus - - - - - - --
Substantia nigra - - -
Basis pedunculi - -
D
Anterior choroidal artery - -'

D
, Penetrating branches
,/ of middle cerebral
artery (lateral striate
arteries) ':
_,- Internal capsule
" Putamen
_,-Globus pallidus
1////1
_-Miqdle
cerebral artery
__ Caudate nucleus
___ - - - Lateral ventricle

fiiij
- - - Posterior
cerebral artery
- - - - - - - - - Optic tract
'- - - - - - - - - - Amygdala
J:1gure 3-3. COHlnal section through {he cerehral helllisphere at the le"e1 of the internal c:1psule and thala-
mw. the maj(lr vascular rcrriwrics.
. , ..
.. '
--.
-,
.
_."! .... ,.,-'--... ' .. -- .'''' '..,-.: --.
-. , . - :.- -.
, ... : .. ;. .. .' <:1
18 Chapter'3
........................................................ -........................................ , ................................................................................................ .
rans (j.e., rllsrrnl to the motor nuclells of CN V), the sureric.)r cerebdbr
the superior of [he cerel--ellulll nnd cerebellar nuclei. m1d [he cc.'lChlear nuc
5. The posterior cerebral (sec Figures 3-1 t 3-2. and 3-3) is connected to
.carotid artery through the posrerior communicacing artery. It provides the r
jor blood supply to the midbrain. It also supplies the thalmnus. bteral nnJ r
dial geniculate bodies, and occipital lobe (which includes the \'isual cortex r,
die inferior surface of [he temporal lobe, including the hipl-"ocampal fonnntio
Occlusion of this artery results in':1 contralateral' hemianopia withmacu
sparing.
IV. THE BLOOD SUPPLY OFTHE INTERNAL CAPSULE comes primarily the I
eral striate arteries ofthe middle cerelmll artery and the anterior choroidal artery.
V. VEINS OF THE BRAIN':
A. The superior cerebral ("bridging") veins drain into the superior sagittal sinus. Lc:
eratiOil results in a subdural hematoma.
B. The great cerebral \'ein of Galen drains the deep cerebral veins into the straight sim
VI.YENOUS DURAL SINUSES_.
A. The superior sagittal sinus receh'es the bridging veins, and through the arachne
\illi, the cerebrospinal fluid (CSF).
B. The cavernous sinus contains CN III, IV, V-I and V-2, VI, and the postganglionic syr
pqthetic fibers. It also contains the siphon of the internal carotid artery (Figure 3-4).
VII. ANGIOGRAPHY
A. Carotid angiography. Figures 3-SA and B the internal carotid 2rrery, anreric
cerebral artery, and middle cerebral artery.
Superior sagit1al Si.1US
Cavernous parI 01 ICA
Petrosal part 01 ICA
Basilar artery
Sigmoid sinus
.......
Superior cerebral veins
Superior sagil1al sinus
Branches of MCA
peA' ---
Slraight sinus
Confluence of the
sinuses
Transverse sinus
iiiiiiiiiiiiiiiiiiiiiii- Veri ebr a I a r I e ry
Figure 3-4. projccti(II). the 111;lj<,lr \,CI)('ll'i Si!l\lV:S :lnd ;':lC:
i (: S, () l c: the hr i d i; i I1g \'C i II' l'l H c:r i 111: (he in r if(;) I \ i Ii II s. ! C .\ i, ,,',' t 1 , .,' {,,,,, l i' i '.l'."" ",. ,\! . '\ : ,:.
CF.'I,-l ',d :;c(,-r y; [\ 'l/\ j{::- (i'!ch:-;11 :If[C:'/"
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Blood Supply 1.9 .
. ' ..... ........... -.# ................................................. __ .. _ .......... _-............................... __ .-: ............ -.............................................................. -
B. Yt!rtebra( angiography. 3-5C and D ::lll)W tht! vcrrebral artery, PICA and
AICA, b"silar artery, sUl'erior aner)" nnJ cerebral artery.
C. Veins dural sinuses. 3-6 rhe \'ein .. superior cerebral
great cerebml \'ein, ophrhalmic vein, and major dural sinuses.
D. Digital subtraction angiogrnphY"See Figures 3-7,38.39, and 3- 10.
. VIII. THE MIDDLE MENINGEAL ARTERY, a bmnch of the maxillary artery, {he cm-
nium throl,lgh [he foramen spinQSu!ll. It supplies most of dura, including its cakarial por-
rion. Laceration resuics in epidural hemorrhage (henl<ltoma) {Figures 3-11 and 3-iZ].
List of structures:
1. Anterior cerebral artery
2. Anterior choroidal artery
3. Anterior inferior cerebellar artery
4. Basilar artery
5. Calcarine artery (of posterior cerebral artery)
6. Callosomarginal artery (of anterior cerebral artery)
7. Callosomarginal and perica/losal arteries' .
(of anterior cerebral artery)
B. Internal carotid artery
9. Laieral striate arteries (of middle cerebral artery)
10. Middle cerebral artery
11. Ophthalmic artery
12. Peri.callosal artery (of anterior cerebral artery)
13. Posterior cerebral artery
14. Poslerior choroidal arteries
(of posteior cerebral artery)
15. Posterior communicating artery
16. Posterior inferior cerebellar artery
17. Superior cerebellar artery
. 18. Vertebral artery
F!gure 35. (A) Carmi .. 1 angiogram, latcral PfI,J\.\.,iull. \u/ Carmiu angiogralll, ;lIlt<:wpt'$cerior projection.
(e) Vcrccbral (tngi(lgr;ull, 1;1fcral prnjt'ctinn. (D) Vcrrehr,,1 ,lIlgi(lgrnm, I'rl1jcction.
o.:'::Siiasih"; ."., "1 Y . "'..'".- ... 5," - &-"! ...... SVSCr=rrssrrr:;:;m:sp,
". ... ......
'.
nzr-rm
mom
. ,
20 Chapter 3
I
..................................................................... _ ............................................... __ .......................................... -........................... '1
Inferior sagittal sinus \ :Internal cerebral vein
\_-----,
, Superior sagittal sinus
Superior ophthalmic vein,
"SUperior cerebral veins (bridging veins)
- -:"--.. -
- Great cerebral vein (of Galen)
- - Confluence of sinuses
Cavernous sinus - -- -
, Transverse sinus
- -..
Figure 36. Ca.rotid angiogram, \'enous'phase, showing the cerebral veins and \'enous sinuses.
Callosomarginal artery
of ACA
Pericaliosal artery
of ACA
Frontopolar branch -- ,
OfACA ___
Ophthalmic artery
Cavernous ICA -----=--"'j.-r.
Petrous ICA
'.
.. .,;
.; .. -'

MCA M1 segment
PCoM

Cervical ICA
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Figure 3-7. C::lwrid angiogram, I'Heral projecrion, Idcntify rhe cortical branches of the [Interior cerchr I
artery (ACA) and middle ccrebral artery (?-.fCA), Folio\\' the Course of thc internal carotid <lrtcry (leA). R.
Il1cmher chat aneurhms of the posterior communknring M(Cry may resulr in third,ner\,e p:lls},. TI1C par:lcelltr.
ld'ulc is irrig:ltcd hy the ca\losoln:1rginal artery, Conical branches of [he arc tksignntcd with dots. reo!' I
= communicating anery, '
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.' .. .' :' .
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......
....
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Blood Supply 21
............. : ........................................................................................ _ .... _-.............. -... -.-................ : .... -.............. ............................ .
A"\ segment of ACA = ...... ,..,.,"""
Cortical branches of MCA
Lateral striate branches
ofMCA
M1 segment of MCA
Cavernous part of ICA
Supraclinoid part of ICA
Petrous part of ICA
'. .
-:.
,," .T .
-. '. .-
.'.-. . ...
1'!!'''''---"""7-- Cervical part of ICA
Figure 3-8. Carotid angiogram, anteroposterior projection. Identify the anterior cerebral artery (ACA).
dIe cerebral artery (i\fCA), and internal carotid artery (lCA). The horizontal branches of the MCA perfuse the
basal ganglia and internal capsule. ACo:\i = anterior'communicating
Posterior choroidal
arten..es
.... --:."';7 .... -c--.-:, .. - .
PCA. P1

Thalamoperforating

PCoM-===
Superior cerebellar
Basilar
Vertebral artery
Parietoocd'tpital
b,anches of PCA
Calcarine branches
of PC A
=:::::;--- Hemispheric branches
of SCA
PICA
Vertebral artery
Figure 3-9. Vertebral angiogram, lateral projection. Two S[rliClUrcs arc founJ between the posterior cerebral
.: artery (PCA) and the !)up<:rior cerebellar artery: the tentorium and the thiiJ cranial nerve. PCoM = po!)terior
c()llllllunicating artcry; PICA = postcrior inferior cerehellar artery; SCA = superior cerebellar nrtery-
_
I
... .'. .. .. a; .. .. .. __ . .... II .. IIII ..
""'"4 :""" _
;22 Chapter 3
I
........ ;0 ; .... ; .... ; ; ; ; ............................. ;0 ..... ; ....... , ......................... _ .................................. ;; ; ; ; 50.; .... : ................... ;
I
;--
I
I
Calcarine artery of peA
t
t

Superior cerebellar--+
artery
Temporal branches
of PCA
I
PICA
Basilar artery - ____ -
I
Vertebral artery I
Figure 3,1.0. Vertebral angiogram, anteroposterior projection; Which artery surrlies the visual cortex? 11 I
calcarine artery, a !::-ranch of the cerebral arrery (peA). Occlusion of the PC";' (calcarine artery) resul
in a con-cralateral homonymous hemianopia, with macular sparing. PICA = Fosterior inferior cerebellar aLter
t
Diploe
t
.. ,
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1
FIgure 3-:1.1, An epidlJral hematoma rcsults (mill bcer;l[ion ofthc l1lidd!.: artery. Arterial blccl; 1
in" into the cpiJur"I.\p;ICC forms" hicol)\'cx clot. The ch:,\ic "I\lci,l inlc\,,;1\" sccn in 50% o( C;lses. Skull (r;l(
arc ((lund. Epidllr;tl ri
1
rcly cr(\,;s .,l)lur;d lillt''; i1\('i,li"ICJ with pUIlli\\jcl[) ;'(:"11 (""hi;. I
AG, Tong KA: HW\{!I)(,{jl-: 1(/ ,"! '!nllf,:r!;,f,. . ;;f"'" (,;:,: l.",. '!" ". i ;):
1,--;
;'J.'
..
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................................................................................................. .................. _. __ ..................................................... : .............................. -
Blood Supply
23
.. --
___ Dura
__ Arachnoid
Figure 3-j.2. .-\ subdural hem,l[oma (SOH) results from lacerated br-idging yeins. SDHs are frequently ac-
comranie..:i by traumatic :5ubarachnl)iJ hemorrhages and cortical contusions. Sudden deceleration of the head
causes tearing of the superior cerebral veins. The SOH o\er the crest of the convexity into the inter-
hemisrheric fissure. r-Ut does not cross the dural attachment of the falx cerebri. The clot can be crescent-shaped.
biconyex. or multi loculated. SOHsare more common than epidural hematomas. SDHs always cause brain dam-
age. (Reprinted with permission from Osbum AG. Tong KA: Handbook of Ne1!roraciiology: Brain and Skull. St.
Louis. 1996. p. 192.)
./
'
t- -.
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". ..:' .....::'; . .. .-. .., .. ,.... . ................... -_' ......... _. y= .. ziOlo3;,;:;'... )IM';Q;P?Rmiill ........ ,,:AI??I11 . .-'--.J
4
Development of the Nervous System
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1
1
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I. TH E' N EU RAL TUBE (Fi,iure 4 i) gi rise ro the cen tra I ne,,'ou s -s l'stem (eNS) [i., I
brain and spinal cord}.
A. The brain stem and 5Final cord ha\'e;
:1.. An alar plate that gi\'es rise to the sensory neurons
2. A basal plate that gi\"es rise co the motor neurons (Figure 4.2)
B. The neural tuce gives rise to th:ree primary vesicles, which develop into five sel
ondary vesicles (Figure +3).
C. Alpha.fetoprotein (AFP) is found in the amniotic r1uid and maternal serum. Ie is a
indicator of neural tut-e defects (e.g., spina binda, anencephaly). AFP levels are n
duced in mothers of fetuses with Down syndrome.
Surface ectoderm
,":
/
Dorsal root ganglion
Alar plale (sensory)
Sulcus limilans
Basal plate (motor)
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FJgure 4-:1.. [X:\e!nprntnt (J( the ncural whe and cre.'r. The abr pl.irc- !;i,'cs: ill' (.' .\cr,,()! llllurol1.< .. Th . : ,)';
":,, '- ,- "I,," ," '" ,,,,,w, ''''''',,''- -I he "',,,,,01 ",,, ,1,-" "',' "" h, 1'-' lih" " ", , ,'-', _ I
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Development of the NelVous System 25
...................... : ................................ ..................... ........................... : .... :; ....... -..-.... : ..................................................... ; .................. : ...... .
. Roof plate (ep.endymallayer)
Pial blood vessels -----.
fourth.ventricle ---.,
SSA nuclei ----+J.-
GSA column
SVA column ---"""\
GVAcolumn---
!3VE column -----
SVE column ------
GSE column - __ _
Floor plate -----
choroidea
Semicircular
. ducts
Ampullae
-1---- Cochlea
1"'--___ . Skin
g-- Taste bud cell
of tongue
Somatic striated muscle
(tongue)
-1--- Visceral epifhelium

Branchial striated muscle
(larynx)
'----- Smooth muscle
Figure 4-2. The brain stem showing the cell columns derhed from the alar and basal plates_ The seven cra-
nial nen-e modalities are shown_ GSA. ::: general somatic afferent; GSE = general somatic efferent; GVA = gen-
eral dsceral afferent; GVE = general \-isceral efferent; SSA ::: special somatic afferent; SVA = special visceral
afferent; SVE = special visceral (Adapted with pennission from Patten BM: Hwnpn Embryo log)' , 3rd
eJ. New McGraw-Hill, 1969, r- 298.} . ':
II. THE NEURAL CREST (see 4-1) gi\'es rise to:
A. The peripheral nervous system (PNS) [Le., peripheral nerves and sensory and auto-
nomic ganglia}
B. The following cells:
.. '
i. Pseudounipolar ganglion cells of the spinal and cranial nerve ganglia
2. Schwann cells (which elaborate the myelin sheath)
/
3. Multipolar ganglion cells of ganglia
4. Leptomeninges pia-arach.noid) envelop the brain and spinal cord
5. Chromaffin cells of the suprarenal medulla (which elaborate epinephrine)
6. Pigment cells (mclanocytcs)
7. Odontoblasts (which elaborate predentin)
B. AOfticopulmonary septum of the heart
.1Ia
Dar n
..
26
Chapter 4
I
-.... ........... ' ................... -: ... -.............................. ......... I
vesicles vesicles . Walls Cavities
Telencephalon
Cerebral
hemispheres
Lateral
ventricles
--r;- L Diencephalon __ -+-1--
(prosencep.hcilon)
Thalamys
Third
ventricle
--;-;-- Midbrain Mesencephalon
(mesencephalon)
Midbrain
Aqueduct
Pons
Upper part of
Cerebellum
fourtn
MetencephaJon_-H_
-H--Hindbrain _"'--_--.
(mombencephalon) '._
....... _
Medulla ..
0 Lower part of
fourth ventricle
Spinal cord
-.
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1
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4.
Figure 4-3. TIle t-rain vesicles indicating the adult derivatives of their walls and cavities. wi; J
rennission from }.ojoore KL: The Del'eloping Human: Clinically Orienting El7lbT)ology, 4th ed. Philadelphia. \\'
Saunders. 1988. p. 380.)
9. Parafollicular cells (calcitonin,producing C-celIs)
:1.0. Skeletal and connective tissue components of rhe pharyngeal arches
- .
Ifl. THE ANTERIOR NEUROPORE. The closure of the anterior neuropore gives rise to rl-
lamina renninalis. Failure to close results in anencephaly (i.e., failure of the brain to &
\e!op). ,.
IV. THE POSTERIOR NEUROPORE. Failure to close results spina bifida (Figure +4
V. MICROGLIA arise from [he mOl}ocrres.
Dura
Hairs
process
A. Spina blflda occulta
Subarachnoid
space
8, Meningocele
C. Menlngomy"/,,rn',:,
Neuralotissue
Rachischisis
Figure 4-4. Tht: \'HilHIS {H'c\ hifida (nl'l)riIHCcl with pcrlllissi,\/l (Will S:Hlkr T\X/: Lallgnwil'., At,
iced Em/nO)O,,/!):,;'! ("i,do !\ Iii :,,\,;,. \,(iilii:!rm '<'0 :';1''.., Y;:o)
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.................................... : ................... : ........ .......................................................... .. -.................... ; ............. ; ........................... : ..... :' .... ..
'.:: . :-: '. '-.
.-:.' .
.' \"'
......
"
Development of the Nervous System 27
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VI. MYELINATION in the fourth month of gestation. Myelination of the corti-
cospinnl tnlcrs is norcornpleted until the end of the second rostnaml yeM, when the tracts
become function.,l. Myelination in the cerebral cortex continues into the rhirJ
decnde.
A. of the eNS is which ;-Ire not found
in the retina. '
B. of the PNSis accomplished by Schwann cells.
VII. POSITIONAL OHANGES OF THE SPINAL CORD
A. In the the conus medullaris ends at the third lumbar vertebra (L,3).
B. In the adult, the conus medullaris ends at L,l.
VIII. THE OPTIC NERVE AND CHIASMA are derh'ed fron) the diencephalon. The optic
nerye fibers OCCUP): the choroid of this fiss.ure .close results in coloboma
iridis.
,
IX. THE HYPOPHYSIS (pituitary gland) is derh'ed from t\\'o embryologic substrata (Fig-
ures +5 and 4,6).
. ,
A. Adenohypophysis is from an ectodennal diverticulum of the primitive mouth
ca\'it)" (stomodeum), which is 'also called Rathke's pouch. Remnants of Rathke's
rouch may gh-e rise co a congenital c)'stic rumor, a craniopharyngioma.
B. Neurohypophysis de\'elops from a \'entral evagination of the hypothalamus (neu,
roectoderm of the neural tube).
X. CONGENITAL MALFORMATIONS OF THE CNS.
A. Anencephaly (meroanencephaly) results from failure of the anterior neuropore to
close. As a result, the brain does not de\elop. The frequency of this condition is
1:1000.
, .
Third ventricle
Pars tuberalis
of adenohypophysis --t---'--....
Adenohypophysis
(anterior lobe)
Infundibulum of hypothalamus
Diaphragma sellae
Pars intermedia
of anterior lobe
-+--f-''F.+-- Neurohypophysis
. (posterior lobe)
Dura
Sphenoid bone
Craniopharyngeal canal Remnant at Ralhke's pouch
Figure 4-5. Midsagittal section thwlIgh the :IIlJ sella turcica. The :lJcnohypophysis, including
the p<Jrs tuhcralis and pars intermedia, is ,ll:ri\'ed (rom Rathke's pouch (oroecwderm). The neurohypophysis
arises frelln the infundihulurn ()f the hyp'llha!amus (m'ur"l'clOJcnn).
' .
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28 Chapter 4
'-............ ......................................... : ................................... : ............... .. 1
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Figure 4-6. section through the brain stem and diencephalon. A craniopharyngioma (arroU'!
lies suprasellar in the midline. It compresses the optic chiasm and hypothalamus. This tumor is me most corr I
mon supratentorial tumor that occurs in childhood and the most common cause of hypopituitarism in childrer
This is a Tl,weighted magnetic re..-onance imaging scan.
Figure 4-7. ArnoldChiari mal({lrlll:lti()Il. Midsagittal (A) Normal cerebellllm. fourth \'cntricle. an,
brain stem. (B) Ahnormal ccrchcllullI. (ollnh \'cntricle. _lnt! hrain stem 5ho\\'ing the COllllllon congcnital anom
(I) be;lking o( the rcclill plate. (2) aqlleJlIccal (3) kinkin!,: and tr:1m(omlllinal herniation o( th
rncdldh into the \"(.:rtchral cana\. ;J1l,1 (4) hcrni:ltiol1 ;lId Ilmnlling of (he ccrchclhr \'eflnis into rhe ,'crtcbr;l
cZln;d. An ;lccnrnpanyiTlf! f11("llillgolllyclncI'!" ii, (",1'!:1\,:;, \\1[;, : ,-,,";"')'.", ({(;In Fiy if""
, I
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Development of the Nervous System 29
...................................... .................. : .. : .................................. __ ....... : ......... -........ ......................................................................... .
Corpus callosum Polymicrogyria
Superior s'agittal sinus
Straight sinus
Confluence of
Lateral ventricle
sinuses
Massa intermedia
Third ventricle
+----------,fH- Cerebellar vermis
Pons --''<''-':='''+-i- , ,
Posterior fossa cyst
Medulla -->t'r'.-
Figure 4-8. Dandy-\Valker. malfdrmation. section. An enormous dilation of the fourth ventricle
results from failure of the foramina of Luschka and Magendie co open. This condition is associated with occipi-
tal meningocele. elevation of the confluence of the sinuses {torcular Hero"phili}, agenesis of the cerebellar \'er-
mis. and splenium of the corpus callosum. (Rerrinted with permission from Dudek RW. Fix JD: BRS Embryology.
Baltimore. \Villiams & \Vilkins. 199i. r. 9i.) .
B. Spina bifida results from failure of the posterior neuropore to form. The-:defect usually
occurs in the sacrolumbar region. The frequency of spina bifida occulca is 10%.
C. Cranium bifidum resuirs from a defect in the occipital bone through which meninges,
cerebellar tissure, and the fourth may herniate.
/
D. malformation (type 2) has a frequency of 1:1000 (Figure 4-7).
E. \Valker malformation has a frequency of 1 :25000. It may result from riboflavin
inhibitors, posterior fossa trauma, or viral infection (Figure 4-8).
F. Hydrocephalus is most comnl9.nly caused by stenosis of [he cerebral aqueduct during
de\'elopment. Excessive fluid accumulates in the ventricles and sub-
arachnoid space. This condition may result from maternal infection (cytomegalovirus
and toxoplasmosis). The frequency is 1: 1000. .
G. Fetal alcohol syndrome is the most common cause'of menml retardation. It includes micro-
cephaly and congenital heart Jisease; holoprosencephaly is the most severe manifestation.
H. Holoprosencephaly resuJts frolll of miJline cleavage of [he embyonic forebrain.
The telenceplalon contain's a singllim ventricular c",ity; is seen is trisomy 13 (Patau
syndrome); the corpus callo$lIlll may be nbsclH; holoproscnccphaly is rhe most severe
manifestation of the fetal nlcohol syndrome.
I. H ydranencephaly results from biiarcral hcmispheric infnrction secondary to occlusion
of the carotid Clrtcries. The hClllbl'lH.'rcs arc replaceJ by hugely dilated vcntricles.
I
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< .... 1
. .
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5
I
Neurohistology
I
I
1
I
I. NEURONs 'are classified by of processes (Figure 5#1).
A. Pseudounipolar neurons are located in the spinal dorsal roOt ganglia and sensory g I
glia of cranial neIves (eN) V, VII, IX, and X.
Olfactory
Dendrite zone
Axon origin ____ _
Axon
T
Telaxon
1.
Sensory (receptor) neurons
Motor neuron
Auditory
Cutaneous
Synaptic endings (boulons terminaux)
Nerve endings in muscle (myoneural junction)
Figure 5-:1. Types of ncn'c cells. Ol(ac(ory ncurons flrC hirobr and lllllll\'dinarcd: Auditory neurons arc hil
I;)r nnJ myelinated. Dorsal root ganglion cells (cllt,mcous) are ,lnd myelin.ncd. Motor ncur<
;He 1l111ltipo/;lr :lnd rnr(.'lin;l[cd. ATTOW5 indicntc input through tile aX0HS o( p{her I1ClIrnllS. Nervc cclls ;"Ire eh
;IClcri:cd hy the prC\('I)CC o( ;I1\J HIlIg" cndopl;\<mic r(,{jculu\I, (H",jifil"d with l'l'fmi"sic:ll (.
(';\rlP'fiier )I.if1. illl!1on NCllrol/rlOlo'71Y H:ilrim()[c, \'1/111;.1111' {". \Vii',: I .,'., 'i" \
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Neurohistology 31
...... --: ..................................... ....................... , ............................................................................................................................................ .
. '. .." .
Bipolar nrc found in ,he anj \'c:\tihuJar I.lf eN VIII, 'in the
I.)lfac[l.)ry nerve (CN I), ;lIlJin the rerina.
C. Multipolar neuron:; me rhe lmgc$t I.\f nerve cells in rhe nervous sY:'tem. This
grl.'lIP incluJes motor neurolls, ncuronsl.\f the autonomic'nervous sY:'tem, intcmeUn)llS,
pyramidal cells of the cerebrcll cortex, Purkinjc's ce,lIs of the cerebellar correx.
D. There me 1011'n'cufoll$ in r.rain and approxim:ltely neurons in
rhe
II. NISSL SUBSTANCE is characteristic of neurons. It consists of rosettes'of polrsomes apd
< .. "Iugh endoplasmic reticulum; therefore, it has a role in protein symhesis. subsmnce
found in the nerve cell body (perikaryon) dendrites, not in the axon hillock or axon.
III. AXONAL TRANSPORT mediates the intracellular distribution of secretory proteins. or-
:;.lOelles, and cytos,keletnl elements. It is inhibited by colchicine, which depolymerizes mi- .
.:r\.'lcut-ules.
," _ .... _ J ,
Fast'an'terograde axonal transport is re'sponsible for all newly synthesi:ed
.' organelles (vesitles) and precursors of neurotransmitters. This process
occurs at the rate of 200 to 400 mm/day. It is l!1ediated by neurotubules and kinesi.!'t.
\Fast transport is neurotubule-dependem.} '. .::.=.:",.- '''" .... , ... 0,,,.
,-) '" '-,' '-, .
responsible for ,rransporting fibrillar cyroskeletal and
rroroplasmic elements. This proce6s occurs at the rate of 1 to 5 mm/day.
retrograde transporfreturns used materials from the axon tenninal to the cell
body for"'de-g"faaatiOi1'anci'recycling at a rate of 100 to 200 mm/day. It transports nerve
growth factor, neurotropic viruses, and toxins, such as herpes simplex, rabies, po-
liovirus, and tetanus toxin. It is mediated by neurotubules and dynein.
-..-...... -- .. .... .". . .. _ .. --_.--.-..
IV. WALLER IAN DEGENERATION is characterized by the dis-
;Fpearance ofaxons and myelin sheaths and the secondary proliferation of Sch\\'ann cells.
It occurs in the central nervous system (CNS) and the peripheral nervous system (PNS).
',..
V. CHROMATOLYSIS is the result of retrograde in the neurons of the CNS
3,Ild PNS. There is a loss of Nissl substance 'after axoromy.
VI. REGENERATION OF NERVE CELLS
.. /
A. eNS. Effective regeneration does not occur in the eNS. For example, there is no re-
generation of the optic nen'e, which is a tract of the diencephalon. There are no base-
ment membranes or endoneural investments surrounding the axons of the CNS.
B. PNS. Regeneration .. the PNS. The proximal tip 'of a severed axon grows
into the ei1doneuraltube, \Vh-ich consists of Schwann cell basement membrane and
endoneurium. The axon sprout grows at the rate of 3 nun/day.
VII. GLIAL CEllS nre the nonnellfnl cells of the neh'ous system.
A. Macroglia consist of astroc)'tes and oligodendrocytes .
.
:t. Astroc)'tes perform the following functions:
a. Thcy project foot p'roccsses that envelop the basement membrane of capillar-
ies, neurons, and synapses.
b. Thl'y form the external and internal membranes of the eNS.
c. They playa role in the metabolism of certain ncurotransmitters [e.g., -y-
:tlllinobutyric aciJ ;t\';llJl'Jllill, giul<JInaej.
.: -,.l
. , h:. " b' $01f0
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32 Chapter 5
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I
d. Ther butrc:r the pomssium cOllcemr:ltion of the space.
e. fl\pllJ;IJnLs91Q in Jmfinged.areas of the (Le . nsrrogliosis).
f .. Ther which is a marker (\.'r I

g. They cOllC<lin glutamine synthetase. another biochen1ical
h. l-e identified with monoclonal (e.g.! AZB
j
). "
2. Oligodendroc'tes are the myelin-((lrming cells of the eNS. One oligodendmcy
can myelinme as m:my ClS 30 a;,:o11$. . .
. '-"---_.,.-_ .. "
B. Microglia nrise twm moi1Ocyres and function as the scavenger cells (rhagocyres) ( 1
the eNS.
c. Ependymal cells are ciliated cells that line the central canal and "enrricles of rh
brain. They also line the luminal surface of the' c-horoid plexus. These cells produc .
cerebrospinal fluid (CSF). .. . .
D. 'Janycytes are that contact cnpillaries and TI1ey med
ate cellular traruron bet\\;een \'enrricles and the neuropil. They rroject to hyrotha:
amic nuclei that regulate the release of gonadotropic honnone from the adenohypophY$i:
E. Schwann are.deriyed neural crest. They are tJ1e myelin-forming celis. c
the inre61gde. Schwann cells itwe5
all myelinated and unmyelinated axons of the PNS and 'ire separated from-each othe
by the nodes of Ranvier.
VIII. THE BLOOD-BRAIN BARRIER consists of the tight junctions of nonfenestrated en
dorhelial cells; some authorities include the astrocytic foot processes. Infarction of brair
tissue destroys the tight junctions of endothelial cells and results in vasogenic edema
which is an infiltrate of plasma into the extracellular space.
IX. THE BLOOD-CSF BARRIER consists of the tight junctions between the cuboidal ep
ithelial cells of rhe choroid plexus. The barrier is permeable to some.circulating repride:
plasma proteins (e.g.; prealburi11fi). " --:
X. PIGMENTS AND INCLUSIONS
}
; .
. ,; .'-
... ..,.. ..
A. Lipofuscin granules are pigmented cytoplasmic inclusion's that commonly accumu
late wiih aging. 1lley are considered that are derh-ed from lysosomes .
..... . . ... .
B. Melanin (neuromelanin) is blackish intracytoplasmic pigment found in the subsran
tia nigra and locus coeruleus. It disappears from nigral neurons in patients who h3\'(
Parkinson's disease.
C. Lew)' bodies are neuronal inclusions that are chaf(lcteristic of Parkinson's disease.
D. Negri bodies are intracytoplasmic inclusions rhm me pathognomonic of rabies. ll1ey arc
found in the pyramidal cells of the hippocampus Clnd the Purkinje cells of the cerebellum.
E. Hirano bodies (lrc inrr;lIieurol1al, eosinophilic, roJlike inclusions that arc found in the
hippocampus of patients with discnse.
F. Neurofibrillary tangles consist of intracytoplasmic degenerated neurofilaments. They
mc seen in pnrients with Alzheimer"s disease.
type A inclusion bodics arc'intral1ucidr ancillsions th;l( arc found in neu-
rons and glin in h.TCS i (is.
_._ _. .. ... - __ _ , __ r ____
XI. THE CLASSIFICATION OF NERVE FI8ERS i:-; shown il) 'hhk ')'!.
I
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Neurohistology 33
........................................................... , ............................................... .. -................................................................................................ -
Fiber
-.
Table s.:L
Classinca[ion u( Nerve
Diameter
(I1m)*
Conduction -_
Velocity
(m/sec) Function
Sensory axons
la (A-af
Ib (A-a)
1/ (A-J3)
I" (A-S)
12-20
12-20
5-12
2-5
70-120 'Proprioception, muscle spindles
70-120 Proprioception, Golgi tendon organs
30":70 Touch, 'pressure', and vibration '.
12-30 Touch, pressure, fast pain, and
temperature
IV (C) 0.5--1 0,5-2 Slow pain and temperature,
unmyelinated fibers
Motor axons .
- ,
Alpha (A-a) 12-20 15-120 Alpha motor neurons of ventral hQrn _
(innervClte extrafusal muscle fibers)
Gamma (A--y) 2-10 10-45 Gamma m'otor neurons of ventral horn
(innervate intrafusal muscle fibers)
Preganglionic autonomic fibers (8) <3 ' 3-15 Myelinated preganglionic autonomic
ftbers
Postganglionic autonomic fibers (C) 1 2 Unmyelinated postganglionic
autonomic fibers
"Myelin sheath included if present.

XII. TUMORS OF THE CNS AND PNS are shown in Figure
A. of brain tumors are metasratic, and are primary, In metastatic
rumors, the primary site of malignancy is the lung-in 35% of cases, the breast in 17%,
in the gastrointestinal cract in 6%, melanoma in 6%, and the kidney in 5%.
B. Brain rumors are classified as glial (50%) or nonglial (50%).
C. According to national board questi.ons, the five most common brain rumors are:
"muldfc)rme-;-rh{nll)st common and most fatal type
"-...----..... -.-.... .. ----'" ........ " .-,-
2.,. Meningioma,- a benign noninv<lsi\'e tumor of the falx and the convexity of the
hemisphere
- - .. -
3. Schwannoma, a benign rumor derived (rom Schwann cells
which is (ound in rhe ventricles and accounts (or 60% of spina I cord
"'g1T6mas--' . .
'-' ....... -- ---.
which is the mc;>sl: common posterior fossa tumor seen
in'chi-Idren and may metastasi:e through the CSF craces
XIII. CUTANEOUS RECEPTORS (Figure are divided into cwo large groups: free nerve
endings and encapsulated endings.
A. Free nerve endings are nociccprors (,,_lin) and thermorecepcors (cold and hent).
B. Encapsulated endings are touch H.'Ct.'prors (Meissner's corpuscles) and pressure nnd
bration rec<:ptors (Pacininn corplIscks).
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34 Chapter 5
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A . derived from arachnoid cap cells and represent the second most
Germlnomas
germ cell tumors that are commonty
seen in the pineal region (>50.,)
overlie the tectum of the midbrain
cause obstructive hydrocephalus due to
aqueductal stenosis .'
the common cause of Parinaud's syndrome
Brain abscesses --'---....
may result from sihusitis,
mastoiditis,
hematogenous spread
location: frontal and
temporal lobes. cerebellum
organisms:
staphlococci. and
pneumococci
result in cerebrat edema'
and herniation
Colloid cysts of third ventricle
comprise 2% of intracranial gliomas
are of ependyr:-:al origin
found at Ihe in:erventricular foraminia
ventricular obs!ruction results in increased
intracranial pressure, and may cause
positional headaches, attacks;
or sudden dea!h
8
Choroid plexus papillomas
'. historically benign
represent 2% of the gliomas
common primary intracranial brain tumor atler astrocytomas (15%
are not invasive; they indent the brain; may produce hyperostosis
pathology: concentric whorls and bodies
location: parasagitlal'and convexity --_.:. ..... -. .
gender: females> men
. associated witli (NF2)
Astrocytomas
'represent 20\' of the glioma9
historically benign
diffusely infiltrate the hemispheric white matte
most common glioma found in the posterior
fossa of children
ro-+--- Glioblastoma multiforme
Oligodendrogliomas
represent of all
the gliomas
grow slowly and !'Ire
relatively benign
. represents 55% of gliomas
malignant; rapidly fatal
astrocytic tumor
commonly found in' the frontal and
temporal lobes and basal ganglia
frequently crosses the midline via the
corpus callosum (butterfly glioma)
most common primary brain tumor
histology: pseudopalisades,
perivascular pseudorosertes
most common in the frontal lobe
. calcification in 50% of cases
cells look like "fried eggs (perinuclear ha!os)
Craniopharyngiomas
represent 3% of primary brain tumors
derived from epithelial remnants of Rathke's pouch
one of the most common brain tumors in patients < 2 years of age location: suprasellar and inferior to the optic chiasma
occur in decreasing frequency: fourth, lateral, and third ventricle cause .bitemporal hemianopia and hypopituitarism
calcification is common
J Cerebellar astrocytomas' Pituitary adenomas (PA)
most common tumors of the pituitary glane
CSF overproduction m:y cause hydrocephalus
/[ . -:-6enign tumors of with prognosis
; . _---<:---_
contain piJocy.ic astrocy1es anC! Rosenthal fIbers
prolactinoma is the most common (PA)
derived from the stomodeum
'" Medulloblastomas -------'" "R
, ''- represent of primary brain tumors
(Rathke's pouch) .
represent 8% of primary brain tumors
.;...--. represent a primitive
neuroectodermal tumor (PNEn
second most common posterior fossa
tumor in children
responsible for the posterior vermis syndrome
can metastasize via the CSF tracts
highly radiosensitive
Hemangioblastomas
characterized by abundant capillary blood vessels
and foamy cells; most otten found in the cerebellum
when found in the cerebellum and retina,
may represent a part of the von HippelLinc!a.usyndrome
2% of primary intracranial tumors;' 10% of posterior fossa
tumors
may cause hypopituitarism, visual
field defects (bitemporal hemianopia
and cranial nerve palsies CNN III, IV,
VI, V1 and V2, and postganglionic
sympathetic fibers to the dilator
muscle ot the iris)
Schwannomas (acoustic neuromas)
consist of Schwann cells and arise from the
veslibular divis:on of CN VIII
compromise approx. 6% of intracranial neoplasms
pathology: Antoni A and B tissue and Verocay bodies
bilateral acoustic neuromas are diagnostic of NF2
'----
Brain stem glioma
usually a benign pilocylic astrocytoma
. Intraspinal tumors
_ I=ri .. nd . .' usually causes cranial nerve palsies
/',' mav cause the
represent 5% 01 the gliomas .=-.. -.. ----.. -...
.J . histology: benign, ependymat tubules.
.; Schwannomas 30%
Meningiomas 25%
Gliomas 20%
perivascular pseudorosettcs
Sarcomas 12% 40% are supratentoriat; 60% are inlratenlorial (posterior lossa)
most common spinal cord glioma (60%)
third most common posterior fossa tumor in children and adolescents
Ep'QQ..d.ymQrna.5. .
60% Of.
Ffgure 5-2. Tumors o( the ccnu;ll ;lnJ peripheral t\l'[\'(lll-' (;\) Sllpr all'n ((lfi;)l tu!l)(lrs. (3) In (r:1tCll
((Iri;d (posterior (ossa) and intra.\pin;-t! tUl11ors. In chililrel'. 'Ie)';.:, (,f ;,;" ;1'lr:1[('!)(,,, i;d. ]1) (0';:,
[\"l1l1r:; ;Irc \upraccncori:d, Ci,j ,-, C/;mi;til\C[\'I'; c:;r - , .. ' .. ".;,\ ,; ,1"
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Neurohistology 35
.......... _ ............................................... - ................................... .:......................... __ ........................................................................................... -
Free nerve endings Meissner corpuscle
} EPiderm;,
Schwann cells
r
Pacinian corpuscles
Dermis
o
o
-0
, l
A-P fiber Adipose tissue
Cutaneous nerve
Figure 5-3. Three important cutaneous receptors. free ner\'e endingsmediate pain and temperature sensa-
tion.0eissner corpuscles of the dermal papillae mediate cactile discrimination. Pacinian corpuscles
of the:dermis mediate touch, pressure, and vibration sensation.
-'
.-J
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6
'Spinal Cord
.
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I. GRAY AND WHITE COMMUNICATING RAMI (Figure 6.1) I
A. Gray communicating rami contain unmyelinated postganglionic sympathetic til"'er
They are found at all le\'e1s of the spinal cord.
fibers
B.
\Vhite communicating rami contain myeliI)ated preganglionic sympathetic tiber.
The\' are found from 1 to (the extent of the lateral hom and the inrermediolat
eral column). .
II. TERMINATION OF THE CONUS MEDULLAR.S (see Figure 2-1) OCcurs in the ne\\
born at the le"el of the bod\' of the third lumbar "errebra In the adule, it Occurs ,;
the le\'e I of the lower borde; of the first lumbar vertebra (L-l).
Paravertebral ganglion
(sympathetic trunk)
Prevertebral ganglion

Alpha motor neuron
of ventral horn (GSE)
Figure 6-:1. The (our (unctional of the thoracic .\pin;ll ner\'(,: gCl1er:d \'jsccr;l! :lffcrcl1t (GVA
gcncr<ll ;dfcr<:nr (C;:;;\). 50rnatic efferent (GSE). :md \'i.<cer;il d(l'IC"H iVF). l'n'pri
! . '(] I TI I ' .. . , .
ClTli',c, CliL1Il('()IJ.';, ,:Iflr (l.l'", flfC'> )01\'11. ,,"" ;:;:i.',(' :':".:: I) I "I:;" II;, ;., " .. " iiI', '\
!:i /", .. ;'1 1.'
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Spioal Cord. 37
.... ; ............... , .. : ......... ,. ....................................................... : ............................ : ....................... -..... -................ : ............................................ : ........ -.. .. " ... '" .............. ". ............................. '"'
Tabre 6-:1..
Till..' Fiw h:r C\llllll\\.,nh Tested Muscle Stretch Reflexes
. .
stretch Reflex . Cord Segment Muscle
Ankle jerk
Knee jerk .
Biceps jerk.
Forearm jerk
Triceps jerk
$-1
L2-L-4
CS and C-6
C-S-C6
C7 and C-8
Gastrocnemius
Quadriceps
BicE;!ps
Brachioradialis
Triceps
III. LOCATION OF THE MAJOR MOTOR AND SENSORY NUCLEI OF THE
SPINAL CORD
A. The ciliospinal centt!r of Budge, (rom C-8 to 1',2, mediates the s)'mpathetic innex-va
til.:'ll1 of che eye.
B. The,intermediolateral cell column, from C-8 to L-3, mediates the entiresympatheric
innernlrion l)( rhe bl.'ldy.
C. The nucleus of Clark, from C-8 [0 L;3; gives rise r:o the dorsal spinocerebel,
br tmer. ..' .
D. The parasympathetic nucleus, {rorp $-2 to S-1.f
E. The spinal accessory nucleus, from C-l r:o C6
F. The phrenic nucleus, 'from C,3 to C,6
.IV. THE CAUDA EQUINA. Motor and sensory roots (L,2 r:o Co) that are found in the sub-
arachnoid space below the conus medullaris form the'cauda equina. They exit the \-erre-
bral canal through the lumbar intervertebral and sacral foramina.
V. THE MYOTATIC REFLEX (see Figure 61) is a monosyr:taptic ipsilateral muscle
stretch reflex (MSR). Like all retlexes. the myotatic reflex has an afferenrand an efferent
limb. Interruption of either limb results in .areflexia. -
A. The afferent limb includes a muscle spindle (receptor) and a dorsal root ganglion neu
B.
C.
ron and its Ia fiber.
The efferent limb includes a veil.'tral hom motor neuron thut innervates striared mus-
cle (effector).
The four most commonty tested MSRs are listed in Table 6-1.
",-:
p,.r. __
'3
nsr.
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Tract$ of the Spinal Cord
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. I. INTRODUCTION. Figure 7-1 sho',:s theascending and descending tracts of the srina
cord. TI,;S chap ter CO\,,, I,'ur of the maj<'rtmw. I
II. DORSAL COLUMN-MEDIAL LEMNISCUS PATHWAY (Figure 7-2; see also Figurt
8-1) I
A. Function. The dorsal column-mediallemniscus'pathway mediates tactile discrirnina.-
tion, yie-ration sensation. fonn recognition, and joint and muscle sensation (consciou: I
proprioception).
B. Receptors include Pacini's and Meissner's tactile corpuscles, joint: receptors, muscle
spindles, and Goigi tendon organs. I
C. First#order neurons are located in the dorsal root ganglia at all levels. They project
axons to the spinal cord through the medial roqt entry zone. First-order neurons gin
rise to:
:1. The gracile fasciculus from the lower extremity
Ascending tracts
Gracile fasciculus "
Cuneate fasciculus
Dorsal spinocerebellar tract
Lateral spinothalamic tract
Ventral spinothalamic tract
Descending tracts
Lateral corticospinal tract
Hypothalamospinal tract
Rubrospinal tract
VestibulospInal tract
FIgure 7.1. The rn;1jor ;i:'C""
din
c: ;Int! descendil)l; 1': It hll"; ,\ .. , p{ rh<: c(lrd. The :1:;('n<i::1,l! :r;iU'
; \ :' J i 0 \ \ '1') '" 1\"\ I t'\ ,'; l c (c I ;\t 1 c.l : h ,. \ ;, 'C (" \ \ [ 1: n \ t :', i \. : r .; '(. (" :';-',' : \;., ! 1 , : \ i I \: I
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... , " ..
\ '" ' .
. .
, .. ..;:; ...
. .
Trc;tcts of the Spinal Cord
39 . . .
........................................................................................................ _ ...... _ ....................................................................... , .................... -
Thalamus
Internal capsule
Lentiform nucleus
Trigeminal nerve ----___ _
Nucleus gracilis
N ucl eus cun ea tu s -------,,4----:'
Internal arcuate fibers
(neuron II)
Cuneate fasciculus
Dorsal root ganglion cell
Postcentral gyrus
,..-------- Leg area
::::....---- Trunk area
""":;::"'"+-- Arm area
Head area
Face area
Ventral posterolateral
nucleus of thalamus
(neuron III)
Medial lemniscus
Midbrain
._.'!-:r------- Medial lemniscus
Pons
Medulla
'.)--------- Medial lemniscus
. . ..
-+--+---- Spinal trigeminal nucleus
"----H----- Decussation of
medial lemniscus
Gracile fasciculus
(neuron I) ---------..(';1
..r.-rv""?"l"-------- Cuneate fasciculus
Pacinian
Cervical cord
Meissner's
=>--,------;---- Gracile fasciculus
./
cO'Puscie _______ --
Lumbosacral cord
Figure 7-2. The dorsal column-mediallcmniscus pathway.llllpubcs conductcd by this pathway mediate dis-
criminawry tactilc sense (e .. g., touch, vibration, pressure) and kinesthetic sense (c.g., posiril)ll, movemcnt). Thc
d()rsal column system mediates conscious proprioccption. (Adapted with permission (rom Cmpcllter MB, SlItin
J: Human Neuro(ln(ltomy. Baltimorc, Williams & Wilkins, 1983, p. Z66.)
: ..
'Pm' Fa W'
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40 Chapter 7,' . . . I
...................................................................................................................... -...................................... , ..................... " ............................. ..
. . 2. The 'cunent'e frtllll 'rhe upper .
.... ...
3. The c(,llhuemls for spinnl reflexes (e.g., mrornric reflex) I
4. The l'lx(,'lns that ascend in the dorsnl columns nnd terininme in the .md
cuneate nuclei of the cnudnl medulla
,
D. Second-order. neurons' nre locnred in the nnd nuclei of the cauLbl
medu.lIa'. They gh'e rise to nxons and inremal arcuate fibers that Jecussme and f('lrm ;l
(i.e., medinllemnisclls), The medial lemniscus ascends chnJugh 1
the cl,ntrnlatemll:-rain stem nnd terminates in the \'cntral posterolarer<11 (VPL) nu-
cleus of the thabm.us. .
E. Third-order neurons are locmed in the VPL nucleus of the thalamus. They rmject I
through the limb of the internal cnpsule to the rosrcentral gyrus; which. is
the som:u('isenroT)' 3, 1, a.i1d 2).
F. Transection of the dorsal column-inediallemniscus tract
:l. Abo\'e the sensory decussation, transection resulrs in contralateral loss of the dor-
sal column modalities.
2. In the spinal cord, transection resulrs in !pilateral loss of the dorsal column
modalities.
I
I
III. LATERAL SPINOTHALAMIC TRACT (Figure 7-3; see also Figure 8-1)
I
A. Function. The lateral spinothalamic tract mediates pain and temrerature sensation.
B. Receptors are free nen'e endings. The lateral spinothalamic tract recei\'es input from
fast- and slow-conducting pain fibers (i.e., A-S and C, respecti\'ely).
C. First-order neurons are found in the dorsal roocganglia at all le\:e!s. They project ax-
ons to the spinal cord through the dorsolateral tract of Lissauer {lateral root entry
:one} to second-order neurons.
D. Second-order neurons are found in the dorsal horn, They gi\'e rise. to axo115 that de-
cussate in the \'entral white commissure and ascend in the com:ralareral lateral fu-
niculus. Their axons terminate in rhe VPS nucleus of the thplamus.
E. Third-order neurons are found in the VPL nucleus of the thalamus. They project
through the posterior limb of the internal capsule to the primary somatosensory cor-
tex (Brodmann's areas 3, I, and 2).
F. Transection of the lateral spinothalamic tra'et results in contralaceralloss of pain and
tcmperature belo\\' [he lesion.
IV. LATERAL CORTICOSPINAL TRACT (Figure 7-4; see- also Figure 8-1)
A. Function. The latcml corricospinnl tract meJiatcs voluntary skilled motor 8cti\'it)',
primarily of the uprcr limhs. It is not fully myelinarcJ until the end of (he second year
(Babinski's sign). . /
B. fiber caliber. Arrroxilll:lccly 90% of the fibers lie between I and 41-1-111, ;Jnd 4% lie
.... bo\e (from the giant cells Q( Bctz).
C. Origin and termination
1.. Origin. The brcml corticospinal tract arises (rom layer V of (he ccrcbr;JI cortex
(rom three conic;!1 areas in equal aliql1o(s:
a. The premotor cortex (nwdm:mn's (,)
I). 'fhc I"oric-: L:Lt::1 \ .
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i. -i
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, ,
r-'
! '
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"'-'
: j
! ,
1._J
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',:.' - ' .. -
;".-- : .. ::>: .. ..
of the Spinal Corq 41.
...................... , .................................................................... _ .................... ; ................................................................. , ............................. .
\.e9
'lIIII Corpus callosum
. Thalamus
Internal capsule ------'9'7--"..."..--..:..---./
Cerebral cortex
(postcentral gyrus)
Axons of n'eurons'
in limb of
iriternal capsule '
Ventral posterolateral
nucleus (VPL)
Neuron III
Medial lemniscus
Crus cerebri __________
Medial lemniscus ____ ---:-__ +-___
Neuron I
(dorsal root ganglion cell)
Free nerve
endings
Neuron"
-b4---;'--"--Jf------ Red nucleus
--=:-",
Lateral
tract
Ventral white commissure
Figure 7-3. The 1:11cral !>pinothalarnic tract. Impulses COlh\uC(eJ hy this tract mc\\iatc pain .",d thCrm31
senc,e. Numerous c.ollatcrals arc JistrihutcJ to the hrail\ stem reticular formati<\n. with permission
(rnm Carpenter Sutin J: I-ftOnctll NcuJ"(JalUltmn-y. [hltimorc, Williams & Wilkins. 1983. p. 274.)
n . -- .. --.- - "'"'-"
42 Chapter 7 .
.... : .............. ; ............................................................ -............. _ . .,._ ................................................................................................ .
. Pos!erior lim9
internal capsule
Lenticular m;cleus
Motor cortex
(precentral gyrus)
large pyramidal
cells <)f Betz
Genu of
intemal capsule
Anterior limb of
intemal capsule
Caudate nucleus (head)
tract
Crus cerebri
CNIII
Midbrain
Pons
longitudinal fibers in
basilar portion of pons
CNVI
CN XII ----.n.......",><:::
Pyramid
Laleral corticospinal tract
(crossed axons of neuron I)
Motor end
plates

-r
ee
Medulla
Medulla
'-0'-----.1--_____ Pyramidal decussation
of"I:s2::::o-------_ Venlral corticospinal tracl
(uncrossed axons of neuron I)
./
Spinal cord
_______ Venlral white commissure
Figure 7-4. The Lueral anJ \'L'lllralwrticmpinal (l'yrallliJ;d) tracts. These 1l1;ljnr motor p;!th-
.\ay\ mediate \'.,liti.'I1.11 ll1(llor acti\'it\,. TIleccllso(oril;in:lrc located ill rhe prell1(l(or, the !llut():. :n,d the serl-
"'CJ['y cortier:'. C.'J '" (ullial nCf\'C !;'('pi:ucd with \x'[mi\<i(l11 ([('Ill C;Ir;'(,l1('[ .. ". , .....
.. { " \ \ .' 1;', , \\ Ii / I j -, 1 \ '\ r:, \ (.' ;: \. , ;:"J 1
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1----
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. Tracts of tl)e Spinal Cord 43
" ... .. .
..................................................................................................................................................................................................................
Ophthalmic artery
Muller's muscle
. of
Superior
omital
Hypo.thalamus
'Long V.;3
ciliary nerve
Internal carotid artery
Subclavian artery
Ciliospinal center
(in lateral hom)
Sympathetic trunk
Figure 7-5. 1l1e oculosympathetic pathway. Hypothalqmic fibers project to the ipsilateral ciliospinal center
of the intennediolateral cell column at T-!. The cilfospinal center projects preganglionic sympathetic fibers to
the ceIYical ganglion. The cer;ical ganglion projects perivascular postganglionic sympathetic
fibers through the tympanic c8,\'ity, ca\'emous and superior orbital fissure to the dilator muscle of the iris.
Interruption of this pathway at any le\"el results in Homer's syndrome. eN = cranial nerve.

;.-
c. The primary sensory cortex (Brodmann's areas 3, 1, and 2) .
d. Arm, face, and foot areas. The arm and face areas of the motor homuncu-
lus arise from the lateral com'exity. The foot area arises from the paracen-
tral lobule.
./
2. Termination. The lateral corticospinal tract terminates contralaterally, through
intemeurons, on horn motor neurons.
D.' 'Course of the lateral corticospinal tract
1.. Telencephalon. The laterarcorricospinal tract run{in the posterior limb of the in-
ternal capsule in the telencephalon.
2. Midbrain. The lateral corticospinal trace runs in the middle three-fifths of the crus
cerebri in the midbrain. /
3. Pons. The lateral conicospinal tract runs in the base ef the pons.
,
4. Medulla. The lateral corticospinal cract runs in the medullary pyramids. Between
85% and 90% of the cOrticospin:-.1 fibers decussate in (he pyramidal decussation as
(he lateral corticospinal tract. The remllining 10% to 15% of the fibers continue
as the anrerior corticospinat (rllcr. .
5. Spinal cord. The bteral trilct runs in the Jorsill quadranr of the lat-
Crill funiculus.
-- ---
44 . Chapter 7 I
...................... ... .. ........ -.................................................................. I
:1. Above the motor results in spastic parC!'is
and (upgoing toe).
I
2. In the spinal cord, cmn!>cction in .ipsilnceral and Babinski's
:oign. -
V. HYPOTHALAMOSPJNAL TRACT (Figure 7-5)
I
A. Anatomic location. The hYJ)othahullospinal tract projects without int.;!rruption (rom I
the hypothalamus to the ciliospinaI center of the intermediolateral cell column nc T-
1 to T- 2. It found in the sJ)inal cord m T-l or abo\'e in_ the dorsolateral quadmnt of
the bten-d funiculus. It is also found in the lateral tegmentum_of the. medulla, pons,
and midbmin.
B. Clinical features. ImerruJ)-tion of chis tract at any"le\'el results hi Homer's syndrome
(Le .. miosis. ptosis. hemianhidrosis, and apparent enophthalmos). The signs are al-
ways iJ:'silareral.
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8
of th'e Spinal Cord
I. .DISEASES OF THE MOTOR NEURONs AND CORTICOSPINAL TRACTS (Fie>-
-' . -
A. l..;rr
er
nl,-"'tor n.euron (UMN) lesions are caused by trllnsecrion of the corticospinal
lr.1..::r \.'r of the cordcnl cells of origin. They result in spastic paresis with
fvr:\lni ... bl (Babinski's sign). .
B. Lower nwtor neuron (LMN) lesions are caused by damage to the motor neurons.
They re.:'lIlr in flaccid paralysis, areflexia,- atrophy, fascicularions, and fibrillmions. Po-
liomyelitis or \\lerdnig-Hoffman disease (see Figure 8-2A) results from damage to [he
111\.. ... ror neurons.
Gracile fasciculus
j
lPsilaterallOSS of taco tile discrimination and '
position and vibration sensation from leg
I Ipsilateral loss of tactile discrimination and
Cuneate fasciculus
position and vibration sensation from arm
Lateral
corticospinal tract
;..
Lateral
spinothalamic tract
Ventral white commissure
./
Ipsilateral spastic paresis
with pyramidal signs
Contralateral/oss of pain and
temperature sensation one
segment below lesion
/psilateral flaccid paralysis in aNected myotomes
Bilateral loss of pain and temperature
sensation within dermatomes of involved segments
Figure 8-:1. Transverse section of rhe ct:r\"icnl spinal cOld. The clinically imporl:llH ascending and descend.
ing rathways arc shown on the left. Clinical Jdicits that H';o;l!lt from the intcrrupti(\n of these p;nhways are shown
on -thc ri.c:ht. Destructive lesions of the dorsal horns ill nIH) mc:l1cxia. Destructioll of the veneral
whitc commissure interrupts the ccntrnl of !,ain nnd tcmpt:f;1[trrc impuhcs bilatcrally through the
later:.! !'Irinothainll1ic tracts.
45
. '; .:.. .
>., .. <
'A:i;>
a
'mr uW?ec"lWZM=_Gill' I
..

46 Chapter S
..................................................................................................................................................................................................
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Figure B-2. CIa"k Ie,;on, o( ,he 'p;n.1 co,d. CA) Po!;om)"";,;, 'nJ PlOg.essh'e ;nr.,mHe muscul., .IIoph I
(Wdn;g.Ho((m,mn d;,e.,e). (B) Muh;ple "lelO';'. (C) Do".1 colu",n d;,e"e (mhe, do",!;,). (O) Amy
atrorhic l<l(cr<ll sclerosis. (E) Hemisection of rhe spinal cord (Brown-Scquard syndrome). (F) Complete I
sp;n.1 '"1' oec/"';,,n o( ,he sp;nal cOld. (G) Sul"" .. e com[,;ncdj'eg,n"",;on (v;"",;n B" n",,,op .. hy). (H
Sy,; l'cI;". . .
C. Combined UMN and LMN diseasc. An cX;Hllplc or a combined UMN nnd LMN dis.
e;)sc is nmyotrophic bteraf sclerosis (ALS, or Lou Gehrig':> disC;1SC) (see Figure 8.
21)1. ALS is caused by Jamage to (he COr(iCl)Spinal ([;1((5, with pyr;Hnichl signs, and hy
to the LMNs, with Uvil'-J \ynl)'[\)I1)S. wit!\ /\1;'; ';1)
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'w
. .
. .
, ..
"
. ' .
Lesions of the Spinal Cord 47
..................... ............ ... ....................................... _ .. _ ..... -............................... _ ... -............................................................................................... -
. ,
II. SENSORY PATHWAY LESIONS. An cxmnple of a condirion caused by these lesions
is dorsal column disease (tabes dorsalis) {see Figure-B-2CJ.This disease is seen in patients
with neurosyphilis, Ie is ch;uncreri:edby n loss of nctile discriminmion and position and
\"(brnrion lrritnth'e im'oh'ement of the dorsal rootS results in pain and pares-
thesia:,. Patients hn\'e a sign. (Subject srnnds wirh his feet together. When he
closes eyes, he loses his This is a sign of dorsnl column ataxia.)
. .
III. COMBINED MOTOR AND SENSORY LESIONS
. .."
A. Spinal cord hemisection (Brown-Sequard syndrome) [see Figure 8-2E] is caused by
damage the following structures:
The dorsal columns [gracile (leg) and cuneate (arm) fasciculi]. Damage results
in ipsilareralloss of ractile discrimination and position and vibration sensation,
2. Tl]e lateral corticospinal tract. Damage results in ipsilateral spastiC paresis with
Fytamidal signs below the lesion.. .'
3. The lateral spinothalamic tract. Damage results in contralateral loss of pain and
temperature sensation one segment below the lesion,
4. The hypothalamospinal tract at T-l and above. Damage results in ipsilateral
, Homer's syndrome {i.e., miosis, ptosis, and aFparent enoph-
thalmos}.
5. Tl1e ventral (anterior) horn. Damage results in ipsilateral flaccid paralysis of in-
neryated muscles. .
B. Ventral spinal artery occlusion (see Figure 8-2F) causes infarction of the anterior two-
thirds of the spinal cord, but spares the dorsal columns and horns. I t results in damage
to the following structures:
1.. The lateral corticospinal tracts. Damage results in bilateral spastic paresis with
pyramidal signs belo\\' the lesion.
2. The lateral spinothalamic tracts. Damage results in bilateral loss of pain.ansi tem-
perature sensation below the lesion. <
3. The hypothalamospinal tract at T-2 and above. Damage results in bilateral
Homer's syndrome.
4. The ventral (anterior) horn!:' Damage results in bilateral flacCid paralysis of the
innervated muscles.
5. The corticospinal tracts to the sacral parasympathetic centers at S-2 to S-4.
Damage .r.esults in bilateral damage and loss of voluntary bladder and bowel
control..
C. Subacute combined degeneration {vitamin B12 [see Figure 8-20] is
caused by pernicious {megaloblastic} anemin. It results from damage to the following
structures:
./
:t. The dorsal columns (gracile and fasciculi). Damage results in bilateral
loss of tactile discrimination and position and vibration sensation.
2. The lateral tracts.' Damnge results in bibteral spastic paresis with
pyramidnl signs',
3. The spinocerebellar tracts, Dnmage results in bilateral arm and leg dystaxia.
D. Syringomyelia (sec Figure 8-2H) is a central cavitation of the cervical cord of un-
known etiology, 1 t results in damage to the following structures:

.....
1
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48 Chapter 8
..................................................................... ' ...................... ................................................................................................................ .
:1.. The vc!n'tr"l white ccmtmissure. Damage to Jecussating lateral spinothalamk I
...:wis" l'ilarcral 10$s o( {':lin and remperarure sensntion.
2. The "c!ntral horns. UvtN lesions in flaccid paralysis of the intrin::ic tllll::dt I
of rhe h;md::. '
E. Fric!drdch's <lhlXia has same spina"} cord'pnthology and symp"toms ps CO\1"
bined degelleratk1 n.
. "." , ..
F. Multiple sdc"rosis (see Figure 8-28). Pbques primarily involve the white mmter (If th
I
tV.
cerdcal segments of the spinal cord. The lesions nre random and asymmetric"
PERIPHERAL NERVOUS SYSTEM (PNS) LESIONS. An example of a PNS lcsio.
is Guillain-Barre syndrome (acute idiopathic polyneuritis. or postinfectious polyneuritis:
It rrimarily affects '(he motor fibers "of the "enrral roots and peripheral ner\es. Clnd it pre
duces LMN symptoms (Le., muscle. ascending flaccid paralysis. and areflexia"
Guillain-Barre" syndwille has the following features: "
A. It is characteri:ed by demyelination and edema.
B. cen'ical root (C4) il1\"oh'emenr and respiratory paralysis are common"
C. "Caudal cranial i'cn'e ltwoh-emenr with facial" diplegia is present in 50% of cases"
" . "
D. Elevated protein le"els may papilledema.
E.
F.
To a lesser degree, sensory fibers' affected. resulting in paresthesias"
The protein le\"el in the cerebrospinal fluid is elevated. but without pleocytosis (albu
minocytologic dissociation).
V. INTERVERTEBRAL DISK HERNIATION is seen at the L-4 to L-S or L-5 to S-l inter
space in 90% of cases. It appears at the C-5 to C-6 ro C,7 inrerspace in 10% of
A. Inten"errebral disk herniation consists of profapse, or herniation, of the nucleus pul
posus through the defective anulus fibrosus and into the vertebral canal.
B. The nucleus pulposus impinges on the spinal roots, re'sulting in sp1hal root symptom
(i.e., paresrhesias. pain. sensory loss, hyporeflexia, and muscle weakness).
VI. CAUDA EQUINA SYNDROME (SPINAL ROOTS L3 TO CO) results usually fron
a nerve roor rumor, an ependymoma, a dermoid tumor, or from a lipoma of the rennin;:;
cord. Is characreri:ed by:
A. Severe radicular unilateral pain
B. Sen.sory distribution in unilateral saddle,shapcd area
C. Unilateral muscle atrophy and absent quadriceps (U) <lnd :mkle jerks (S1)
D. Incontinence and sexual functions are not marked
E. Onset gradual and
/
VII. CONUS MEDULLARIS SYNDROME (CORD SEGMENTS 53-CO) usually result
(rom an intramedullary tumor, e.g .. ependymoma. Is characrerized by:
A. Pain usually hilateral and not severe
B. Sensory distrihution in bilatcwl !'addlc-sh:lpcd arca
C. Muscle changes not marked; qU;1driccps and ankle rcflt':'\c$ l1urmal
D. Incontinence ;I!"\d SL':\u:d (unctions SC\Trly
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_,!" .... .... --;.-. -. -.. .
. '<.. : ;. . '. . -
.. '. . - :.( ......... : ,- ...... ",'- .
'. " #' .... :.'- .. '. '. ". --
'.'
'"
9
Brain Stem
I., OVERVIEW. The stem medulla, pons, and midbrain. Ir from
the. pyramidal dec.us:mtion.to the posterior-cotnll1is5ure. The brain stem receh'es its blo<?d
supply from the \'crtehobasilar system. Ir contains cranial nerves (CN) III to XII (except
the spinal parr I."lf CN Xl). Figures 9#1 and 9-2 sho\\' its surface anatomy.
II. THE MEDULLA 9-3)
A. MedialstructuJ;es
1.. The hypoglossal nucleus of eN XII
2. The medial lemniscus, which contains crossed fibers from the gracile and cuneate
nuclei
3. The pyramid (corticospinal tracts)
Superior
colliculus
Third ventricle
Lateral geniculate body
Medial geniculate body
Crus cerebri
Superior cerebellar peduncle
Middle cerebellar peduncle
Inferior peduncle
medullares
Cuneate .tubercle
+-''+-- Gracile tubercle
Cuneate 'fasciculus
Gracile fasciculus
Rgure 9-:1. The d(lrs,,1 (l the hrain Mem, The three cerehellar peduncles ha\'e heen remo\'ed to cx-
r("l!-l: the rh(llllhoiJ The trochlear nl:(\'C is the UIlI} IlCr\'C to exit thc hrain :;rcm from the dors;!1 surfacc.
TIll: facial C(,lIiclIllls the gelill (II (ile ;Olclai nt'f\'C anJ the nhllucclH eN = craninl ncrve,
49
'--
jhn
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SO Chapter 9 . ,' .
................. , ....... : .......................................................................... -:-..................... _ .... : ........ , ... : ........................ 1
: : Olfactory bulb (CN I)
Olfactory trigone
Anterior perforated
substance ---:----:07+
Optic chiasm' '.
Olfactory tract
Infundibulum
Tuber cinereum
Mamillary body
Crus cerebri
(cerebral peduncle)
__ --u......... ........-10--- Optic tract
__
Middle cerebellar
peduncle ___ -+
CN VIII
Olive
Pyramid
CN V (motor root)
CN V (sensol)' root)
CNVI .
CN VII
eN VII (intermediate)
eN VIII '

CNX
CNXI
Cervical nerve I -""""N decussation
Figure 9-2. The \'emral :1urface of ehe brain seem and ehe actached cranial nerves (eN).
Hypoglossal nucleus of CN XII
SOlitary tract and nucleus
Vestibular nuclei
Hypothalamospinal tract
Dorsal motor nucleus at CN X
>:
Spinal trigeminal nucleus
Inferior cerebellar peduncle ----0,..-
Spinal trigeminal tract
Nucleus ambiguus (CN X) ._
Spinal lemniscus
Inferior Olivary nucleus
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FIgure 93. Trnn.w<:rsc of the medulla at the rnidllli\'<lrv le\'el. The vagal nerve [cranial nerve (eN)
XL hypoglo!'>sal ner\'c (eN XIl), anJ ner\'e (eN VIII) arc prominent in this section. Thc nuclells am- I
higuus g;\'cs ri.\c to special \'bccral <:(<:r<:nr tillers to eN IX. X, and XI.
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Brain Stem, 51
'. , ..........................................................................................................................................................................................................................................
B. Lateral structures
1.. The nucleus amhiguus (eN IX, x, XI)
, ,
2. The vestibular nuclei (eN VIII)
. ,
3. The inferior cerebellar peduncle, which contains the dorsal spinocerebellar.
'neocerebellar. and ,l1li\'ocerebellar trnc(s
4. The lateral spinothalamic tract {spinal lemniscus)
.'. ..
5. The spinal trigeminal nucleus and tract of eN v
III. CROSS-SECTION THROUGH THE PONS (Figure 9-4), The pons has a d(lrsal
tegmentum and a ventral base.
A. Medial structures
1.. Mediall0l.1gi[udinal fasciculus,
2. ,Abducent nude us of CN V[ (underlies facial
3. Genu (internal) of CN VII (underlies facial nerve) [facial colliculus]
4. Abducent fibers of CN VI
,5. Mediallemni5cus
6. Corticospinal tract (in the of the pons)
B. Lateral structures
1.. Facial nucleus (CN VII)
. 2. Facial (intraa,=ial) nerye fibers
3. Spinal trigeminal nucleus and tract (CN Y)- ,
4. Lateral spinothalamic tract (spinal lemniscus}
5. Vestibular nuclei of CN VIII
6. Cochlear nuclei of CN VIII
Abducent nucleus (eN VI)
Vestibular nerve (eN VIII)
Facial nucleus (of eN VII)
./
Fourth
ventricle
Trapezoid body
".
Middle cerebellar peduncle
Figure 9-4. Transvcrse of the pons;J( the Icvcl of the "hdllcent Illlcll'lIS of cranial nerve (eN) VI and
the f<Jcin\ of eN VII. MLF = rnedia\\ongitudiIlOlI
'. ,:.'
52 Chapter 9
..................................................................... ,' .............................................. : ................... .-........................................................... .
Cerebral aqueduct
Superior collicuJus .
Medial geniculate body
Periaqueductal gray
Oculomotor nucleus
Medial lemniscus
Dentatothalamic tract
Substantia nigra.
eNI.!1
Cerebral peduncle (crus cerebri)
Corticospinal tract
. Red nucleus' .-
C'?rticobulbar tract
Figure 9-5. Trans\'erse section of the midbrain at the level of the superior colliculus. oculomotor nucleus
cranial nerve (eN) III, and red nucleus. MLF = medial longitudinal fasciculus.
IV. CROSS-SECTION THROUGH THE ROSTRAL MIDBRAIN (Figure 9,5). The mil
brain has a dorsal tectum, an intermediate tegmentum, and a base. The aqueduct lies b
tween the tectum and the tegmentum.
A. Dorsal structures include the superior colliculi.
B.
Tegmentum
:1.
Oculomotor nucleus (eN III)

2.
fediallongitudinal fasciculus
3.
Red nucleus
4.
Substantia nigra
,:
5.
Dentatochalamic tract (crossed)
6.
;\fedial lemniscus
.'
7. Lateral tract (in the spinal lemniscus)
C. Crus cerebo (basis pedunculi cerebri. or cerebral peduncle). The corticospinal trae
lies in the middle three-fifths of the crus cerebri.
,. ..
V. CORTICOBUlBAR FIBERS (see also Figure 13-4) project bilaterally to al( motor crC.
nial nerve nuclei except the facial nucleus. The division of the facial nerve nucleus th8
innervates the upper (ace (the orbicularis oculi muscle and above) receives bilateral COr
ticobulbar input. The division pf the facial nerve nucleus that innervares the lower be
receives only contralateral corticobulbar input.
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1.0
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. Trige'minal System
,,'
.. , . ,; ..
.: .....
.'
J. OVERVIEW. The trigeminal sysrem'pro\'ides innervation to the face, oral cav-
ity, and supratentorial dura throu'gh general somatic afferent (GSA) fibers. It alsb inner-
vates tpe muscles of mastication through special visceral efferent (SVE) fibers.
II. THE TRIGEMINAL GANGLION (semilunar or gasserian) contains pseudounipolar gan,
glion cells. It has three dh'isions:
A. The ophthalmic nen'e [cranial nerve (eN) V-I] lies in the wall of the C3\'emous si,
nus. It enters the orbit through the'superior orbital fissure and innervates the forehead,
dorsum of the nose, upper eyelid, oiuit (cornea and conjunctiva), and cranial dura.
The ophthalmic nerve mediates the afferent limb of the corneal reflex.
B. The maxillary nerve (eN V-2) lies in the wall of the cavernous sinus and innervates
the upper lip and cheek, lower eyelid, 'anterior portion of the temple, oral mucosa of
the upper mouth, nose, pharynx, gums, teeth palate of the upper jaw, and cranial
dura. It exits the skull through the foramen roturidum.
C. The mandibular nerve (eN V-3) exits the skull through the foramen ovale. Its sen-
sory (GSA) component innervates the lower lip and ,chin, posterior portion of the
temple, external.audicbry meatus, and t):mpanic membrane, extern,il ear, teeth of the
lower jaw, oral mucosa of the cheeks and floor of the mouth, anterior two,thirds of the
tongue, temporomandibular joint, and cranial dura.
D. The motor (SVE) component of CN V accompanies the mandibular nerve (CN
Y,3) through the foramen Ie innervates the muscles of mastication, mylohyoid,
anterior belly of the digastric, and tensores tympani and veli palatini. It innervates the
muscles that move the jaw, the lateral and medial pterygoids (Figure 10,1).
III: TRIGEMINOTHALAMIC PATHWAYS (Figure 10.2),.'
A. The ventral trigeminothalamic tract mediates pain and temperature sensation from
the face and oral cavity.
:1.. First-order neurons are located in the (gasserian) ganglion. They give
rise to axons that descend in the spinal trigeminal tract and synapse with second,
order neurons in the spinal nucleus.
2. Second-order neurons are located in the spinal trigeminal nuclells. They gi\'e rise
to decussating axons that terminate in the contralateral \'enrral posteromedial
(VPM) nucleus of [he thalamus. . .
3. Third-order neurons are 10CIl{cd in the VPM nuclells of the thal;n.nus. They pro'
53
.": :
54 Chapter 10
..................................................................................................................... -................................................................................. .
" . .
UMN'
c'erebella'r peduncle 4th ventricle
Chief sensory nl,Jc/eus CN V
Motor nucleus eN v
--+--Pons
Medial lemniscus
Corticospinal tract
Lateral pterygoid muscle
Condyloid process
""1
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Figure 1.0-1.. Function .and innervation of [he la.teral pterygoid muscles (lPMs). The lPM receives its in- i
nervation from the motor nucleus of the trigeminal found in the rostral pons. Bilateral innervation of the
lPMs results in protrusion of the tip of the mandible in the midline. The LPMs also open rhe jaw. Denervarion
of one lPM results in deviation of the manaible to the ipsilateral or weak side. The trigeminal motor nucleus I
receives bilateral corticobulbar input. eN = crani<ll nerve; lMN == lower motor neuron; UMN = upper motor
neurOn.
jecr through the posterior limb of the internal capsule to the face area of the so-
matosensory correx. (Broqmann's areas 3 . 1. and 2).
B. The dorsal trigeminothalamic tract mediates tactile discrimination and pressure sen-
sation from the and oral cavity. receives input from Meissner's and Pacini's cor-
puscles.
:1.. First-order neurons lire loented in the trigeminal ganglion. They
synapse in [he principal sensory nuclells of eN v.
2. Second-order neurons are locHce! in the princip:11 sensory tlt;c1c:::-; or eN v
They proj,u rn the ipsihtCL11 \li't\! :;l:(lcII'; o( rill. [h:1I;:! '
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.;,.'
": .!...... --::;,::: . ';,. .. .. :.. . ;.
.. Trigeminal System 5S
............................ : ...... :: ................... : ............ :.-....... ; .. .............. .... -;.-............. __ ............................................................. : ................ ...
Ventral
nucleus 9f thalamus
Face area of
. postcentral gyrus_
Ventral trigeminothalamic tract - - - -
.
Midbrain
/
Motor nucleus of eN V""
/
""
Spinal trigeminal nucleus ""
. ,:Caudate nucleus
'Internal capsule
(posterior limb)
- - - - Dorsal trigeminothalamic tract
""
""
""
""
/.
/
/
Mesencephalic nucleus of CN V
""
:, Principal sensory nucleus of eN v
"" / Sensory branch oLCN V-1
Sensory branch of CN V-2
Sensory branch of CN V-3
"-
"-
Motor branch of CN'V-3
Spinal trigeminal tract

Figure 1.0-2. The ventral (pain and temperci'ture) and dorsal (discriminati(:e touch') trigeminothalamic path-
ways. eN = cranial nerve.
./
3. Third,order neurons are located in VPM nucleus of the thalamus. They
project through the posterior. limb of the internal capsule to the f<fee area
of the cortex. '(Brodmann's areas 3, 1, and 2).
IV. TRIGEMINAL REFLEXES
A. Introduction (T.,ble 10- J)
:1.. The cornea!:-:::!,!,:;..: ;:; u disynaptic reflex.
am s
x
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56 Chapter 10
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. .
Reflex
Corneal reflex
jaw jerk ..
Tearing (lacrimal) reflex
Ocu/ocardiac'reflex .
.. Table 10-1.
Trigeminal
Afferent Umb
Ophthalmic nerve (CN V-i)
Mandibular nerve (CN V-3)*
Ophthaimic nerve (CN V-l
Ophthalmic nerve (CN V-l')
*The cell bodies are found in the mesencephalic nucleus of eN V.
CN = cranial nerve.
I
Efferent Limb I
Facial nerve (eN VII)
Mandibular nerve (eN V-3)"
Facial nerve (eN VII) 'I
Vagal nerve (CN X)
,
. . .
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- 2. The jaw jerk refle.x is a monosynaptic myotatic reflex (Figure 103) .
. 3. The tearing (lacrimal) reflex.' "
4. The oculocardiac reflex occurs when pressure on the globe results in bradycardia. I
B. Clinical correlation. Trigeminal neuralgia {tic douloureux} is characterized by
rent paroxysms of sharp. stabHng pain in one or more branches of the trigeminal nerve I
on side of the face. It usually occurs in peo"pl.e o,lder than 50, years of age, and it is
more common in women than in men. Carbamazepine is the drug of choice for
pathic trigeminal neuralgia. . I
Mesencephalic nucleus
with primary neuron
V-3
Muscle spindle
from masseter muscle
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Motor nucleus eN v
with secondary neuron
Masseter muscle
'------ Molar division eN v
Principal sel'}sory nucleus of eN v
Spinal trigeminal nucleus
./
Figure :1.0-3. Thc jaw jerk (massc(er) reflex.TIlc a((('rem limb is V-3, and the c(ferent limb is the mOWr root
(h;lt ;lCCOl1lpan il's V- 3. Fi rst-ordcr sensory neurons :lrc locHed in the I11csencephal ic noc ICllS, The ja w jcrk reflcx,
like 0111 mllscle r<:flcx<:.,, is a mOllmY!1J[1tic rnyo(:l(tic reflex. lIH'crrcfle:xi:1 indiclccs ;1:1 Ill'per 1ll()tCJr nell
r(,!1 lesio!). C,I\! C,.- (:;ll1i:1I ncr I'C',
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;, ..... . :". . .. ' ....
......
;
Trigeminal. System 57
: ....................................... : . : ................... - : : . : .. : . ! ............................................ :
, Cavernous
Pituitary gland
(hypophysis)
Sphenoid sinus
Optic. chiasm.
Internal carotid artery
t>Rt'\\-__ CN IV
"'-- CN V-I
eN VI and
postganglionic
sympathetic.s
Figure :1.0-4. The coritents of the cavernous sinus. ll1e wall of the caverrl'OUs sinus contains the ophthalmic
cranial ner,e (eN) and maxillary (CN divisions of the trigeminal nerve (CN V) and the trochlear
(eN IV) and oculomotor (eN III) neryes. The siphon of the internal carotid artery and the abducent nerve (eN
VI), al(lng with postganglionic symrachetic fibers, lies within the ca\"eroous sinus.
V. THE CAVERNOUS SINUS (Figure 1O-4) contains the follo\ving structures:
A. Internal carotid artery (siphon)
B. eN III, IV, V,l, V,2, and VI
c. Postganglionic sympathetic fibers en route to the orbit
"
./
: .' .! ' ... 72 ... .. --erQ''',.,zn "Itf SEWS SF
...
1.1.
Auditory "System
I OVERVI EW. The auditory system "is. at"} exteroceptive special somatic afferent tha
can detect sound frequencies from 20 Hz to 20,000 Hz. It is derived from the otic vesicle
which is a derh'ative of the otic placode, a thickening of the surface ectoderm.
II. THE AUDITORY PATHWAY (Figure 11#1) consists of the following structures.
A. The hair cells of the organ of Corti are innerVated. by the peripheral processes of bipo"
lar cells of the spiral ganglion. They are stimulated by vibrations of the basilar membrane
1. Inner hair cells are the chief sensory elements; they synapse with dendrites Oi
myelinated neurons whose a"ICons comprise 90% of the cochlear nerye.
2. Outer hair cells synapse with dendrites of unmyelinated neurons whose a.-xom
" comprise 10% of the cochlear nen'e. The OHCs reduce the threshold of the IHCs.
B. The bipolar cells of the spiral (cochlear) ganglion project peripherally to the hair cells
of the organ of Corti. They project centrally as c9Chlear nerve to the cochlear nuclei.
C. The cochlear nerve [cranial nerve (CN) VllI] extends from the spiral ganglion [Q
the cerebellopontine angle, where it enters the brain stem.
D. The" cochlear nuclei receive input from the cochlear nerve. They pi-oject
ally to the superior olivary nucleus and lateral lemniscus.
E. The superior olivary nucleus, which plays a role in sound localization, receives input
from the cochlear nuclei. Ie projects co the laeerallemniscus.
F. The trapezoid body is located fn ehe pons. Ie contains decussating fibers from the ven#
tral cochlear nuclei.
G. The lateral lemniscus input from the contralateral cochlear and
rior olivary nuclei.
H. The nucleus of inferior colliculus receives input from the lateral lemniscus. Ie
jects through the brachium of the inferior colliculus CO the medial geniculate pody. "
I. The medial geniculate body receives input from the nucleus of inferior colliculus. Ie
projects through the internal capsule as the radiation to the primary auditory
cortex, the rransvcrse tcmporal gyri of Hcsch!.
J. The transverse temporal gyri of lieschl contain the primary auditory cortex
mann's areas 41 and 42). The gyri:'lre locmed in the depths of the lateral sulcus.
III. HEARING DEFECTS
A. Conduction deafness is cnused by interruption of the PZlSS;t(:,C of sound chrou!;h
t}le external or rniddlc It be c8uscd hy .. t '.
"r otitis r1lr:dia. "
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.. " ......
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".". ;" ... ;>;-.: ...... "
Auditory System . 59
..................................................... " ..................... ----.. .............. __ ................................................................................................. ..
Thalamus
Brachium of
inferior colliculus ----<
Midbrain ---1<--
Dorsal and ventral
cochlear nuclei:---I'-
Superior
oliva ry n ucl e u s -----''''-<'<-+-
Trapezoid body
Pyramidal tract
Base of pons
Caudate nucleus
Internal capsule
putamen::r .
Lentiform nucleus
Globus pallidus
. "TT-- Transverse gyrus
of temporalfobe
Auditory radiations ;n subfenticu/ar
part of internal capsule
'------ Medial geniculate body
r---i-------- Commissure of
inferior colliculus
Nucleus of inferior cotliculus
crD-------Laterallemniscus
}--.----- Nucleus and commissure
of lateral lemniscus
Spiral
Cochlear nerve (CN VIII)
/
,,'.
Figure 1.1.-1.. Peripheral and central connections of the auditory system. This system arises from the hair cells
of the organ of Corti and terminates in the transverse temporal gyri of Heschl of the superior temporal gyrus. It
is characterized by the bilaterality of projections and the tonoropic localization of pitch at all levels. For exam-
ple, high pitch (20,000 Hz) is locillized at the base of the cochlea and in the P9sterol!ledial part of the trans\erse
temporal gyri. eN = cranial nerve. .
B. Nerve deafness (sensorineural, or perceptive,. deafness) is caused by disease of the
cochlea, nerve (acoustic neuroma), or central audiwry connections. It is usu-
ally caused by presbycusis that results from degenerative disease of the organ of Coni
in the first few milJimecers of the basal coil of the cochlea (high-frequency loss of
4000-8000 H:).
IV. AUDITORY TESTS.
A. Tuning fork tests (T.1ble
. '... " ,
_ _ .. _ ...... _ _ ., r _.... . .... _. !.:, .. _'. .- - ...... ... L _ " -.. _, .4.
60 Chapter
............................................................................................................................................................................................................... ' .............. ...
OtologIc Finding
, Conduction deafness (left ear)
Conduction (right
Nerve deafness (left ear)
Nerve deafness (right,ear)
Normal ears
Table 11-1.
Tuning Fork Test Results
_
Lateralizes to left ear
Later.atizes to right ear
Lateralizes to right ear
Lateralizes to left ear
No laterlization
Rinne Test
, BC > AC on left
AC :>' BC on right
BC > AC on right
AC > Be on left
AC > BC, both ears
AC > BC, both ears
AC > BC, both ears
" Condl,lction deafness = middle ear deafness (e.g . otosclerosis. otitis media); (lerve deafness = sensorineural deaf-
ness (e.g . presbycusis; AC = air conduction: Be = bone conduction.
1.. \Veber's test is performed by placing a dbrating tuning fork on the \'ertex of the
skull. Normally, a patient hears equally on both sides.
a. A padent who has unilateral conduction deafness hears the vibration more
loudly in the affected ear.,
. . .
b. A patient who has unilateral partial nerve deafness hears the vibration more
loudly in the normal ear. "
2. The Rinne test compares air and bone conduction. Ie is Ferformed by placing a vi,
brating tuning fork on the mastoid process until the vibration is no longer heard;
then the fork is held in fronc of the Normally, a paciene hears the vibration in
the air after bone conduction is gone.
a. A patient who has unilateral conduction deafness does not hear the 'libra'
tion in the air after bone conduction is gone.
b. A patient who has unilateral partial nerve deafness hears the vibration in che
air after bone conduction is gone.
B. Brain stem auditory evoked potentials (BAEPs)
',"
:1. Testing method. Clicks are presented [0 one'ear, then (0 the o;:her. Scalp elec,
trodes and a compurer generate a series of seven waves. The waves are associated
with specific areas of the auqitory pathway.
2. Diagnostic value;. This method is valuable for diagnosing brain stem lesions (mul,
tiple sclerosis) and posterior fossa tumors (acoustic neuromas). It is also useful for
assessing hearing in infants. Approximately 50% of patients with multiple sclero-
sis have abnormal BA.EPs.
/

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1.2
Vestibular System
I. OVERVIEW. Like systeql. the \'estibuhlr system is derh'ea fro;n'the otic vesi,
cleo The otic vesicle is a deri\'mi\'e of theotic placode, which is a thickening of the sur,
face This system maintains posture and equilibrium and coordinates'head and
eye movements.
II. THE LABYRINTH
A. Kinetic labyrinth
i. Three semicircular ducts lie \\'ithin the three semicircular canals (Le., superior,
lateral, and posterior).
2. These ducts respond to angular acceleration and deceleration of the head.
a. They com.ain hair cells in the crista ampullaris. The hair cells respond to en,
dolymph flow.
Vestibular
nuclei .......
Inferior
cerebellar
peduncle -.-
MLF,
Inferior
olivary
nucleus- .-
'\
'\
Medial lemniscus /
/ Nodulus
/
'\
'\ Pyramid
Semicircular ducts
t
1\'
Flocculus
/ .
- - -Juxtarestiform
body
\ /
I \
I \
I \
'v
1 \
I \
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\ / .,'
- nerve and
ganglion in internal
auditory meatus
,Ampulla ..
/ / and crista
. /. Utricle .
" ,,/ and macula
\
Endolymphatic
I duct
Cochlear duct
Saccule and macula
Figure 1.2-1.. Peripheral connecrions llf the \'cstihJlar system. The hair cells of rhe cristae ampullares and
the lIl:lculae of the utricle and saccule l'Tl'ject, through the vestihular nerve, to the \'esribul;u nuclei of the
medulla and pons and the flocculonodubr lobe of the cl'rcbcllum (vcstibuloccrchcllulIl). l\tLF = mcdiallongi-
ti.iJinal fasciculus.
61.
FE $
.f"
''''''''''''':1
. .
. .
. .
62 Chapter 12
.................................................................................................... _ ....................................................................................... : .......... .
b. flow roward the ampulla (nmpulll'lpcral) or utricle (utricu!t,peral)
,is n tll.\n is endolymph flow in the opposite direction.
B. Static labyrinth
i. Thl! nnd saccule to the positiono( the with respect: to linear
acce1ernti.on an.d rhe pull of gravity.' .
2. Thl!utr:icle nnd. sncclile contain hair cells whose cilia are embedded .the
otoiithic membrane. When hair cells are bent toword the longest cilium (kinocil-
ium), the frequency of discharge increases.
III. THE VESTIBULAR PATHWAYS (Figures 12-1 and 12,2) consist of the follow'ing s(ruc,
(ures,
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A. Ha"ir of the semicirCular ducts, utricle are i';nerva,ed by periph. "I
eml rrocesse$ of bipolar cells of t.he \'estibular ganglion.
Vestibular area of
cerebral cortex ___
v sntral posterior
inferior nucleus
Vestibulothalamic tracts
Midbrain --______
Abducent nucleus
cf CN VI of pons
Vestibular nuclei
MlF--r-q.>/
Thalamus
-{---+---- Oculomotor nucleus of CN II I
--,--t----Trochlear nucleus Qf CN IV
----t"---;--;;n- Nodulus of cerebellum
-:--------- Vestibular ganglion
r-.-- Cochlea
Clh;--- lateral vestibulospinal (Deiters') tract
Figu re 12-2. The major cClHr:l1 connections o( the vestibular system. Vestibular nuclei project, through the
ascending rncdinllongitudinal (MLF), to the ocular motor nuclei anJ vcstibllJu-ocubr rc!1cxcs.
Ve:< ( j hu /;1 r (Hie Ie j ;dso rroj cc t. through the dcscc ndi ng I\ff.F ;1 nd !:teer;1! \'CS( i hl tin.,!, ill;,) U;IC[S, to [h c v (' n [nl h () rI1
1\1()(()1 nCtlrCl'."S {he cor!l flH'\I\:iti: (--"'I\) --:: 1"1) :: ,:
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Vestibular
...................................................................................... .;... -................................................... .......................... : ................................................................................... ..
The vestibular ganglion is locnccJ in the fundus of internal i1uJitory meacus.
':1.. Bipolar neUf(Il\$ prl\jeC[ through their periphernl processes to the hnir cells.
2: Bipolar neurolH prl1ject their cemr,,} processes <1S [he vestibular [cr.lnial
nerve (eN) Vlll) .t'-, {he \'estibubr nu.c!ei and to the flocculonodubr k'be of the
cerebellum. . . '
C. Vestibular nuclei
.:1.. These nudei receh'e input from: .
a. The semicircular ducts, saccule, and utricle
b. The flocculonodubr lobe of [he cerebellum ..
2. The nuclei project fibers to:
a. The t1occulonodular lobe o'f [he cerebellum
b., eN III, IV. and VI through [he mediallongirudinalfasciculLls (MLF)
c. The spinal cord through the lateral \'estibulospinal truCt
d. The \"entr.,l rO$teroinferior and 'posterolateral ,nuclei of the thalamu$, both of'
which project t(' the postcentral gyrus
IV. VESTIBULOOCULAR REFLEXES are mediated by the \'estibular nuclei, ocular
moror nuclei, and eN III, I\: and VI.
A. Vestibular (horizontal) nystagmus
:1.. The fast phase of nystagmus is in the direction of rotation.
2. The slow phase of nystagmus is in the opposite direction.
8. Postrotatory (horizontal) nystagmus
:1. The fast phase of nystagmus is in the direction of rotation.
2. The slow phase of nystagmus is in the direction of rotation.
3. The patient rast,points and falls in the direction of pre\-ious rotation.
C. Caloric nystagmus (stimulation of horizontal ducts) in normal sul;>Jects
:1. Cold water irrigation 'of the external audito.,: meacus results in nystagmus to the
opposite side.
2. \Varm water irrigation of the external auditory meacus results in nystagmus to the
same side. ./
Normal conscious subJect BrainstEtm intact . MLF (bilateral) lesion Low bralnstem lesion
Figure 123. Cold caloric in thc I';lticnt. \'Vhcn the hmin stcm is intact, the cyes dc-
\"i:ltc [(lw:lrd thc irrigated side; with hilateral \If rhl' IIlcdbllnngiC\l\linal f:1sciculi (MLF), thc eye de,
vi,He;'; to thc ahJucteJ siJc. Dc!>truction ()f thc cauJall>rain :;t(,111 rcsulcs in no of the eyes, DOllb/.c-headcd
(ITTfJW$ indicatc nystagmus; arTfJWS indica!\.' dc\"brillll of (hc eyes [\1 (Inc side.
. ., .... ';' . , '1
... -. ..,. .. 'd
l
64. Chapter 12
................................................................................................................. : ............................................. , ..................................... .
3. Reme,mber the mnemonic.CO\YS: Ccrld Opposite, \Ynnn Same ..
D. Test re::ults in unconscious subjects (Figure 12-3)
I
:1. N\.) nystngtnus is seen. J
2. \Vhenthe brain stem is there is deviation of the eyes to the side of the C(,){,
irrigation.
I
3. \Vith bilaterallv1LF transection, there is deviation of the abducting eye to the sid,
of the cold irrigation. . .
4. \Vith lower brain stem damage to the vestibular nuclei, there is no deviation of thl
eye5.
.
__ __ r ". _ . __
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- "
:13
'Cranial NerveS
. .
the first cranial nerve (eN 1) [figure mediates 01
(smell). It is the only sensory s}'stem that has no precortical relay in the thalamus
The olfactory nerye is a special visceral afferent (SVA) nerve. It consists of unmyelinacec
axons of bipolar neurons that are located in 'the nasal mucosa, the olfactory epithelium. 1 (
enters the skull through the cribriform plate of the ethmoid bone (see appendix).
A. Olfactory pathway
1. Olfactory receptor cells are.first.order neurons that project to the mitral cells of
the olfactory bulb.
2. Mitral cells are the principal cells of the olfactory bulb. They are excitatory and
glutaminergic. They project through the olfactory tract and lateral olfactory stria
to the primary olfactory cortex and amygdala.
Olfactory trigone
Anterior periorated
substance
Olfactory bulb (eN I)
Optic chasm
Olfactory tract
Infundibulum
Tuber cinereum
Mamillary body
Interpeduncular fossa
tract
Crus cerebri
(cerebral peduncle)'
Pons - ........
Middle cerebellar
peduncle
... CN V (motor root)
CN.v (sensory root)
CNVr'
CNVII .
CN VII (intermediate)
CNVIII
CNIX
CNX
LA,,-n--CN XI
Pyramid
Cervical nerve V'+-+-,hIfI--Pyramidal decussation

Figure :13:1. The of [he hrnin wirh aewehed cranial /lcn'cs (eN). (Reprillfl,.1 with permission (rom
Tru<::< Re, Kellncr CE: f)cUli/cd Atlas of the Hcaclllnd Neck. New York, Oxford Prl'ss, 1958, p. 34.)
f; 5
.,',,;.,;;;: " . " .
:", .
_mr' zzwm'RTiYC1"RCem:n,'

I
66 Chapter 13
. ,
....... :-
B. Lesions of the olfactory pathway result from rrnllln.a skull fracture), and, ofter 1
from 'olfactory gro,-we meningiolllCls. These lesions cause ipsilateral anosmia
ing .".due). Lesions th:lt invoke the p:lmhippocampal uncus may olfactory
ludnarions'[uncimue fits (sei:ures) wirh deja \u}. . " 1
c. Foster Kennedy s'y:nl:irome (FKS) consists of ipsilClteral anosmia, ipsilateral optic atro
phy, and contralateral papilledema. It is usually cClused by nn anterior fossa meningiomc::
1
J.!!. is a somatic efferent (GSE), general \is
ceral efferent (GVE) nerye. ,
A. General characteristics. The oculomotor nerve moves the eye, constricts the pupil,
accommodates, and con"erges. It exits the brain stem from the interpeduncular fossa
of the midbrain, Fasses through the ca\'emous '.Sinus, and enters the orbir through the
superior orbital fissure. . -
:1.. The GSE componenrarises from the oculomotor nucleus of the rostral midbrain. I
It innervates four extraocular muscles and the levator palpebrae muscle. (Re,
member the mnemonic SIN: superior muscles are intorters of ehe globe.)
a. The medial rectus muscle adduces the eye. With its opposite partner; it con, ,
\'erges the eyes.
b. The superior rectus muscle elevates, intorcs, and adduces the eye.
c. The inferior rectus muscle depresses, extorts, and adducts the eye.
d. The inferior oblique muscle elevates, and abducts the eye .
e. The levator palpebrae muscle elevates the upper eyelid.
2. The GVE component consists of preganglionic parasympathetic. fibers.
a. The nucleus projects preganglionic parasympathetic fibers
to the ciliary ganglion of the orbit through CN III. .
b. The ciliary ganglion projects postganglionic parasympathetic fibers to the
sphincter muscle of the iris (miosis) and the ciliary muscle (accommodation).
B. Clinical correlation
:1. Oculomotor (palsy) is seen with rranstentorial herniation (e.g., tumor,
subdural or epidural hematoma);
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a. Denervation of the levator palpebrae m,:!scie ptosis (Le., drooping of
the upper eyelid). '
b. Denervation of the extraocular muscles causes the affected eye to look "down
and out" as a result o( the unopposed action of the lateral rectus and superior
oblique muscles. The superior obliql!e' and bternl rectus muscles are inner'
"aced by eN IV and CNVI, rcspccti\;ely. Oculomotor palsy results in diplopia
(double vision) when the p:1cienr looks in rhe direction of the pareric muscle.
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c. Interruption of paras),mp:lt!lctic innervation (internal ophthnlmoplegia) re,
suits in a dilated, fixcd pupil and paralysis of accommodation (cycloplegia).
2. Other conditions associ:ltcd with eN III imp;lirmcnt
a. Transtentorial (uncal) herniation. IncreascJ supratentorial pressure (c.g.,
(rom;) [urnor) (orces the hi!1pOclmp:1l11nCtIS through the [cnrori;d !I(l[{:: "'ld
or srr('lc!V?:\ the '. ::
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. ,':' .. " ,
. . : .... ......... '. . .... -........ ,"
"
.' 0
. Cranial Nerves ,,67
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(:1) Pupilloconstrictor fibers nre nffected first. resulting in a dilated, fi'\:ed pupil.
(2) Somatic efferent ,fibers are affected later. resulring in externnl,strabis-
, mus (exotropb). ,"
b. Aneurysms of the c;uotid and posterior communicntiI;g arteries often
press CN III within rhe cavernous sinus or interpeduncular cistern. They
ally affect the'periphernt pupilioconstricror fibers first {e.g . uncal hemiation}.
c. ' Diabetes mellitus (diabetic oculomotor palsy) often affects the oculomotor
" nerve. Ie damages the central fibers a11d spares the pupillOconstricto'r fibers.
IV. THg IROCHLEAR..NER.\lE..(-CNJV) is a GSE nen'e.
.' , "
-
A. General characteristics. The trochlear nerve is a pure motor nerve thm innervates
5urerior oblique muscle. This 111uscle depresses, intorrs, and abducts the eye. (See

. . . .
:1. It arises from the contralater?l trochlear nucleus of the caudal midbrain.
2. It aecussates beneath the superior medullary velum,of ti1e midbrain and exits the
. brain stem on its dorsal surface, caudal to the inferior colliculus.
3. It encircles the midbrain within the subarachnoid space, passes through
ernous sinus. and enters the orbit through the superior orbital fissure.
B. ,Clinical, correlation. eN IV paralysis resulcs in follo\ving conditions:
:1. Extorsion of the eye and weakness of downward gaze
2. Vertical diplopia, which increases when looking down
3. Head tilting to compensate for extorsion (may be misdiagnosed as idiopathic
ticollis) ,
4. Head trauma. Because of its course around the midbrain, the trochlear nen'e is
particularly vulnerable to head trauma. The,trochlear decussation underlies the
rerior medullary velum. Trauma at this site'often results in bilateral
ralsies. Pressure against the free border of the tentorium (herniation) may injure
the nerve. '
v. IHETRIGEMINAL NERVE (eN V) is? special visceral efferent (SVE), general somatic
, "afferent (GSA) 'i1'er\'e (see Chapt'erTO) ..
A. General characteristics. The trigeminal nen'e is the nen'e of pharyngeal (brachial)
arch 1 (mandibular). It has three divisions: ophthalmic (CN maxillary (CN
and mandibular (CN V,3) [see Chapter 10].
:1. The SVE component arises from the moror trigeminal nucleus that is found in the
lmeral midpontine tegmentum. It of mastication (i.e.,
temporalis, masseter, lateral. and medial pterygoids), the [ensores tympani and veli
pabtini. the myelohyoid muscle. and the belly the digastric muscle.
2. The GSA component provides sensory inne;vation to the face, mucous membranes
of the nasal and oral cavities and frontaltinus, hard palate. and deep structures of
the he:1J (proprioception from muscles and the temporomandibular joint). It
\'iues the dura of the anterior and middle cranial fossae (supratentorial dura).
. .
B. Clinical correlation. Lesions result in the following neurologic deficits:
:1. Loss of general sensation (hemianesthesia) from the face and mucous membranes
II (he oral and nas:11 cm'itics
2. Lllss of the corneal t' ... [!I.OA ( .. [[I.'II':11l :iIlIU, eN V-}} (Figure
mag wrm mrS'7m
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.68 Cha.pter 13
................................................................................................. _ ................................................................................................ ,
sensory
nucleus (eN V)
Primary neuron
V2

/"
,
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Tertiary neuron .
Decussating
corneal reflex fiber
Secondary neuron.
Spinal trigeminal nucleus
Spinal trigeminal tract
Trigeminothalamic
pain fiber
Figure :1.3-2. The corneal retlex pathway showing the three neurons and decussation. This reflex is consen-
sual. like the pupillary light reflex. Secondorder pain neurons are found it:l the caudal division of the spinal
trigeminal nucleus. Second-order corneal reflex neurons are found at more rostralle\'els.

3. Flaccid paralysis of the muscles of masticati.0r'l.
4. Deviation of the jaw to the weak side as a result of the unopposed action of the
opposite lateral pterygoid muscle
5. Paralysis of the tensor mu.scle, which leads to (parcial
ness to low.pitched sounds)
6. neuralgia (tic douloureux), which is characterized by recurrent parox-
ysms of sharp, stabbing pain in one or more branches of the nerve (see Chapter 10)
VI. THE ABDUCENT figBVE:(.CN VI)
... , ..... ,-,." ,'""._., .. ,_ ....... -. - ....... .
A. General characteristics. The abducent nerve is a pure GSE nerve that innervates the
lateral rectus muscle, which abducts the eye.
.'
:1. It arises from the abducent nucleus that is found in the dorsomedial tegmentum of
the caudal pons.
2. Exiting intrllaxial fibcrspa.ss through thc c9tticospinal [Tact. A lesion results in al-
ternating abducent .'
3. It passes through the pontine cistcrn :md cavcrnous sinus and enters the orbit
through the superior orbital fissure.
B. Clinical correlation. eN VI paralysi" .. Iv:.l cominon isolntcd palsy that results
from the long peripheral course oCtile nervc.lt is seen in patients with meningitis, sub-
nrachnoid hcmorrh;1gc, brcstage syphilis, ;1nd rr;\Umn. Abducent nerve p;lralysis re-
in the following
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. Cranial Nerves 69
" .
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1.. Con\'ergent (medial) (esotropia) 'yithinnbility to "bJlIct the eye
2. Hori:ontal with n\Clximum sep:lrCltion o(the double illl;1ges when k'lok-
, ing toward the I:\teml rectus muscle '
E FACIAL '. . . . 0
,1(. characteristics. The facialner\"t! is'" GSA, general visceral afferent (GVA),
SYA, GVE, and SVE nen'e (Figures 13-3 nnd 13-4). It mediates facial movements,
taste, salivation, lac'riniation, 'and general'sensation from the external ear. It is the
nerve I?f the rharyngenl (brachia\) arch 2 (hyoid). It includes the fncial ner\'e proper
{motor division), which contains the SVE fibers that: innervate the of facial
{mimetic} expression. eN VII includes the intermediate nerve, which contains GSA,
5\ '.-\. and GVE fibers. All first-order sensory neurons me found in the geniculate gan-
glkm within the temporal bone.
i,. Anatomy. The facial. nerve exits. the. brain in d{e cerejJellcit
1
0nrine angle. It
enrers the internal auditory meatus and the facial 'canal. It then exits the facial
. canal and skull through the stylomastoid foramen.
2. The GSA component has cell bodies located in the geniculate ganglion. lr inner-
\'ates the FoSterior surface of the external.ea: through the posterior auricular
branch of eN VII. It projects ,centrally, to the spinal trigeminal tract and nucleus.
3. The GVA component has no dinical significance. The cell bodies are located in
the geniculate ganglion. Fibers innervate the soft palate and the adjacent pharyn-
geal wall.
4. The SVA component (taste) has cell bodies located in the geniculate ganglion. It
CNII
Trigeminal ganglion

Major petrosal nerve
Nasal and
palatine' glands
Superior salivatory
nucleus (GVE)
Tongue
(taste, anterior
two-thirds)
Submandibular gland
Motor nucleus of eN VII (SVE)
Nucleus of solitary tract
Solitary tract (SVA)
.",- Motor root nerve of eN VII
in stylomastoid foramen
Figure 1.3-3. fllnctional c\'\Ilp\lm:nlsofthc (acial ncrvc Icrilnialncr\"c (eN) VII),
.... ";.-: ,-.
; .... .," ...
,.;:
70 Chapter 13
.................................................................................................................................................................................................................
.--
UMN lesion of
corticobulbar tract
.(e.g., stroke of
. internal capsule)
Facial nucleus of pons
Upper face division
Lower face division
Muscles of facial expression:
Frontalis - _____ -+-+-_
LMN lesion of eN VII
(e.g., BeU's palsy)
....-...
Orbicularis _O_C_UI_i I
Buccinator
C'-..r")
Orbicularis oris ------'-r--<
Platysma
Figure 13-4. Corcicobulbar innervation of the facial nerve (cranial nerve (eN) VII] nucleus. An upper rno-
cor neuron (UMN) lesion (e.g., stroke im'olving the internal capsule) results in contralateral weakness of the
lower f;1CC, With sparing of the upper face. A lower mororneuron (LMN) lesion (e.g., Bell's pa Isy) result:s in paral-
YSis of the facial muscles in both the upper and lower face.
p'rojects centrally [0 the solitary tract and nucleus. It innervates the taste buds from
the anterior two-thirds of the tongue through: .'
a. The intennediate nerve
b. The chorda tympani, which is loc:lted in the tympanic cavity medial to [he
tympanic and malleus. It coritains the SVA and GVE
thetk) fibers.' ./
c. The lingual nerve (n branch ofCN
d. The central gustatory (see Figure 13-3). Taste fibers from CN VII,
CN IX, and CN X project through the soliwry tract to the solitary nucleus.
The solitary nucleus' projects through the central tegmental tract to the ven-
tral posteromedial nucleus (VPM) of the thnl:lmus. The VPM projects to the
gustatory cortex of the pilrirlallobe (parieral operculum).
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.. .. ::. :-=
Cranial. Nerves 71.
'. .. .. .. .
.............................................................................................. _ ....................................................... , .............. : ........................................ .
sublll.mdibular, and sublingual glands. I t contains rreganglionic parasym-
pathetic;- neurons "that are I(.lcared in thc superior sa Ii va cory' nuclct,Js of the calldal
" l'l)l\S.
a.' Lacrimal pathway (sec Figure 13-3). The salh'atory nucleus pn)jects
through the imermeJinre and greater perros.ll nerves rothe pterygopalnrine
(sphenopabdne) ganglion. The ganglion projects to the'
lacrimal gbnd of the orbit.
b. Submandibular" (see Figure" 13-3). The'surerior salivatory 'nucleus
projects through the intermediate nerve and chorda tympani to the
mandibular ganglion, The submandibular ganglion projects to and imi.ernues
the submandibular and sublingual glm1ds.
6. The SVE component arises from the facial nucleus, loops around the abducent nu-
cleus of the caudal pons, and exits the brain stem in the cerebellopontine angle. Ie
enters the internal auditory meatus. tra\'erses the facial'canal, sends a branch 'to.
the stapedius muscle of the midd.le ear, and exits the skull through the stylomas-
toid fommen: It innervates [he muscles offacial expression. the stylohyoid r11uscle,
. the posterior belly of the digastric muscle. and the stapedius muscle.
B. Clinical correlation. Lesions (see Figure 14-2) cause the following conditions:
:1.. Flaccid paralysis of the museles of facial expression (upper and lower face)
2. Loss of the corneal reflex (efferent limb), which may lead to corneal ulceration
3. Loss of taste (ageusia = gustatory anesthesia) from the anterior two-thirds of the
tongue, which may result from damage [0 the chorda tympani
4. Hyperacusis (increased acuity to sounds) as a result of stapedius paralysis
5. Bell's palsy (peripheral facial paralysis), which is caused by trauma or infection
and im'oh'es the upper and lower face
6. Crocodile tears syndrome (lacrimation eating), which is a result of aber-
rant regeneration after trauma
:j Supranuclear (central) facial palsy, which results in contralateIClI weakness of the
. lower face, with sparin'g of the upper face (see Figure 13-4)
8. Bilateral facial nerve palsies, which occur in Guillain-Barre syndrome (see Chap-
ter 14)
9. Mobius' syndrome, of congenital facial diplegia (eN VII) and con-
\'ergent strabismus;( eN VI)
VIII." THE VESTIBULPCOCHLEAR NERVE (CN VIII) is;m SSA nerve. It has twO tunc-
. ti,onaldivisions: the vestibular nerve. which maintains equilibrium and balance, and the
cochlear nen'e, which mediates hearing (see Chapters 11 and )2), It exits the brain stem
at the cerebellopontine angle ilnd enters the auditory meatus. Ie is confined to the
temporal bone, ./
A. Vestibular nerve (see Figure 12- 1)
:1.. General characteristics
a. It is associated functionally with the cerebellum (flocculonodular lobe) and
ocular motor nueld. "
b. It regulates compensatory eye movements,
c. Its first-ordcr sCll$llry biPl,lar neurons me located in the vestibular ganglion in
the (unuus of the internal nudirory meatllS.
.
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72' Chapter 13 . .
.............................................. _.-.................................................................................. .................................................. , ....................... .
d.' It projects its processes to !he hnir cells of the crisrne of the
drcularducts ;md the hair cells of the utricle nnd,saccule. ,
It projects its central 'processes to the four vestibular nuclei \.)( the brain stt!ll' ,
and the Oocculon ... 1dular lobe of rhe cerebellum.
f. Ie conducts effert!nt fibers to the hair cells from the brain stem.
,2. Cliriic;tl correlation. in disequilibriu'm; vertigo, and nystagmus.
B. Cochlear nerve (see Figure 111) .
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:1.. General characteristics ,
a. Its firstorder sensory bipolar neurons nre located in the spiral (cochlear) gnn
glion of the modiolus of the cochlea, within the temporal bone.
b. It projects its peripheral processes to die hair cells of the organ 'of Corti.
c. Ic projects its central processes to the dorsal and ven'cral cochlear nuClei of tht -I
brain stem.-.
d. Ir conducts efferent fibers tp cells from- the brain stem.
2. Clinical correlation. Destructh'e lesions cause hearing loss (sensorineural deaf
ness). Irritatiye lesions can cause tinnitus (ear ringing). An acoustic neuroma
(schwannoma) is a Schwann cell tumor.of the cochlear Derye that causes deafness
(see Chapter 14).
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GLOSSOPHARYNGEAL (eN IX) is a GSA, GVA, SVA, SVE, and
}:-_----------:- ,-- __ d
A. General characteristics. The glossopharyngeal nerve is primarily a sensory nene.
Along ,with CN X, CN XI, and CN XII, it mediates taste, salivation, and swallowing.
It mediates input from the carotid sinus, which contains baroreceptors that moniwr
arterial blood pressure. It also mediates input from the carotid body, which contains
chemoreceprors thC\t monitor the CO
2
and 02 concentration of the blood.
" ..
:1. Anatomy. eN IX is the nerve of pharyngeal '(branchial) arch 3. Ie exits the brain
stem (medulla) from the postolivary sulcus with eN x and CN XI. It exits the skull
. through the jugular foramen with CN X and CN XI..
2. The GSA component innervates part of the external ear and the external audi
tory meatus through the auricular branch of the vagus nerve. It has cell bodies in
the superior ganglion. It projects its central processes co the spinal trigeminal tract:
and nucleus. ,,'
3. The GVA component innen'ares structures that are deri\'ed from the endodern1
(e.g., pharynx). It innervates the mucous membranes of the posterior onethird
of the upper pharynx, tympanic cavity, and auditory tube. It also
nervates the carotid sinus (baroreceptors) carotid body (chemoreceptors)
through the sinus nerve. It has cell bodies in the inferior (petrosal) ganglion. It is
rhe afferent limb of the gag reflex and the carotid sinu's reflex.
4. The SVA component innervates the taste btids of the posterior one,third of the
tongue. It has cell bodies'in the inferior (petrosal) ganglion. It projects its central
processes to the solitary tract rind nucleus (for a discussion of the central path\vay,
see VII A 4 d).
5. The SVE component innervates' only rhe stylopharyngeus muscle. I t arises from
[he nucleus ambiguus of [he lateral medulla.
6. The GVEcomponcnt is a pnrasymp;lthctic component tklt inncrv;]tcs the parotid
gbnd. Prcg;-mglionic neurons :1rC loclter! in saliv;uory
nucleu-; o( rlw I\wdulb, Thc)' pro;l''-' r!':f.l'.:,:l, :1,,',,:"; , :,;!, ;,' ,:
,
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".1, ':'
.' '-
Cranial Nerves
........................................... :: .. ............... --... ........... ; .............................. _ .. _ ... : ................................................................ .
Motor cortex
---':"':.-UMN
J..--_-'-- Corticobuloar tract
Medulla
-'1---;...,:...,..- Nucleus ambiguus
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COl1icobular tract
I - UMN lesion
Medial lemniscus
)LMN
Pyramid
A
LMN
Levator veH palatini
and palatal arches
.,/
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Figure :1.3:5. Inneryation of the palatal arches Clnd uvula. Sensory is mediated by the glos-
sopharyngeal nerve (cranial ner::;:-(CN) IXJ. Motor of the palatal arches and uvula is mediated by
the vagus nen'e (CN X). (A) A normal palace and in a rerson who is saying "Ah." (B) A patient with an
upper motor neuron (Ul'v{N) lesion (lefc) and a lower Illotor neuron (LMN) lesion '( light). \V'hcn this patient says
"/\h." the pillaral arches sag. The uvula deviates toward the incact{lefc) side .
./
nerves to [he otic ganglion. Postganglionic fibers from the uric ganglion project [0
the parotid gland through the nen'e (eN
B. Clinical correlation. Lesions cause the {ollowing conditions:
.:1. .. Loss of the gag (pharrngeal) reflex (interruption of the'afferent limb)
2. Hypersensitive carotid sinus reflex (syncope)
3. Loss of general sensation in the pharynx, tonsils, fauces, nnd back of the tongue
:-.1;,"'"
... :' ..<, -'.

74 Chapter 13
...............................................................................................................................................................................................................
4. Loss of the posterior llne.th.ird of the
5. Glossopharyngeal neuralgia, which is ch:lr:\cte.ri:eJ by severe stabbing pain in the
root eJf t\)i1gUC
x. THE VAGAL N;RVE (eN X) is GSA, GVA, SVA, SYE, and GVE nen'e {see .Fig.
.. .' .. ,
A. General charncteristics. The vagal nen'e mediates phonation, swallowing (with CN
IX, eN XI, and eN XII). elevation of the palate, taste, and cutaneous sensation from
the ear. It innervates the viscera of the neck, thorax, and abdomen.
:1.. Anatomy. The vagal nen'e is the nerve of pharyngeal (brachial) arches 4 and 6.
Pharyngeal arch 5 is either absent or rudimentary.lt exits the brain stem {medulla}
from the rostolivary sulcus. Ic-exirs the skull through the jugular foramen with eN
IX and eN XI.-- -- .....
2. The GSA infratentorial dura, external ear, external au
ditory meatus, and tympanic membrane. It has cell bodies in the superior (jugular)
ganglion. and it projects its centr:ll processes ro the spinal trigemimil tracr and nu
deus.
3 . The GVA component the mucous. of the pharyn.x.; l?-rynx,
esophagus. trachea, and thoracic and abdominal viscera (to the left colic flexure).
It has cell bodies in the inferiodnodose) ganglion. It projects its central processes
to the solitary tract and nucleus.
4. The SVA component innervates the taste buds in the epiglottic region. It has cell
bodies in the inferior {nodose} ganglion. It projects its central processes to the soli
tary tract and nucleus. For a discussion of the central pathway, see VII A 4 d.
5. The SVE component innervates the pharyngeal (brachial) arch muscles of the
yn..x and pharynx, the striated muscle of upper esophagus, the muscle of the
U\'ula, and the levator veli palatini and palatoglossus muscles. It receives SVE in
Fut from the cranial division of the spinal accessory nerve (eN Xl). It arises from
the nucleus ambiguus in the lateral medulla. The SVE component provides the ef
ferent limb of the gag reflex.
6. The GVE component innervates the 'viscera of the neck and the thoracic (heart)
and abdominal cavities as as the left colic flexure. Preganglionic parasympa-
thetic neurons thar are located in the dorsal mowr nucleus of the medulla project
to the terminal (intramural) ganglia of the visceral organs (see Figure 18-2 and
Table 18-1). .
B. Clinical correlation. Lesions and reflexes cause the following conditions:
:1.. Ipsilateral paralysis of the soft palate, pharynx, and larynx that leads to dyspho-
nia (hoarseness), dyspnea, dysarthria, and dysphagia
2. Loss of the gag {palatal} reflex (efferent
. I
3. Anesthesia of the pharynx and larynx chat leads (0 unilateral loss of the cough
reflex .
4. Aortic aneurysms and tumors the neck and thorax rhllt frequently compress
(he vagal nerve .
b. L"omplctc laryngeal paralysis, which c;m be r;1pidly (awl i(it is bibtcral (asphyxia)
6. Parasymp:1thetic (veget:1tive) irlcluding t'r;ldyc;m!i,1 (irrit;Hi\'C lc-
(dr'qructi\" I.'l')"), ,1::::,)"" ,,( !:1 1,' " ,'11',
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, " ..
-. " ' ... "":\'. :, .. '
Cranial Nerves '1
, ..... : ...................................... "; ......... ; .................. : ............ : ........... -.... :-.-.. --........ : .. ............... :; ...................... ....................................... .
7. The reflex, in whkh on the eye slows t.he heart rate (affel
.limb of CN V-I .mJ limb of CN. X) .. _ -
_ 8. The carotid sinus reflex, in which pressure on the carotid sinus slows the hear
{br.ldycardia) (efferent 11mb oreN XJ
XI;....THE .. QBJ or spinal accessory is an SVE nerve (Fig
_ lire 13-6). _ . _ . _. ..
A. General ("haracteristics. The nerve mediate's head and movemenl
and innervates the laryngeal muscles. It has the following divisions:
:1.. The cranial division (accessory portion), which arises from the nuCleus ambigum
of the medulla. It exits the medulla (rom the-postolivary sulcus and joins the va-
gal nerye (CN X). It exits the skull through the jugular foramen with eN IX and
eN X. I rinnervates the intrinsic muscles of rhe larynx through the inferior
current) laryngeal nerYe, with the exception of the cricothyroid muscle.
. ..
2. spinal division (spinal portion), which' arises from the ventral horn of cervi-
cal segments Cl through C6. The spinal roots exit the spinal cord laterally be-
tween the \"entral and dorsal spinal roots, ascend through the foramen magnum,
and exit the skull through the jugular foramen. It innervates the sternocleido-
mastoid muscle with the cervical plexus (E-2-) and the trapezius muscle with the
i:en'kal plexus (C-3 and C-4).
B. Clinical correlation. Lesions cause the following conditions:
I----t-Facial nucleus in pons
Ambiguus nucleus
in medulla ----f--f-

CN IX--7'
-f---t--- Accessory- nucleus
CN X ---'---1---(1 _ in spinal cord (C1-CS)
CNIX---<",I
CNXI
/
Figure :13-6. Thc cranial and spinal divisions tlj the accessory nerve (cranial nerve (eN) IX). Thecranial
Ji\'isi{11l hitchhikcs a ride.: with thc lICCCssory ncrvc,thcn joins the vagal ncrve to become the inferior (recurrent)
bryngcal nervc. Thc rc:curn::nt laryngcal nervc innervatcs the intrinsic muscles of the larynx, except for the
cricothyroid musclc. The spinal division inncrvilles rhe trapewid :mJstcrnocleidomastoid muscles. Three nerves
I'a:.s throll!.!h thc jugular (c}ram<:n (glomus jugularc [UIlHlr).
=
.
.".,: Cd "Yi_' 'C n "S.MtM.',
76 Chapter 13
I
1. Paralysis of sterm.'lcleidomastoid muscle (har in difficulty in [uming I
the heaJ to the contralateral side .
2. Paralysis of the trnpe:ius muscle thm in shoulder droop nnd inability to I
............................................................................................................................................................................................................
.
::hrug th.e shoulJcr .
3. Paralrsis of the larynx if [he crClninl root is in\'ol\'ed
Motor cortex
. .
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Corticobulbar traC;.t I'
Hypoglossal
nucleus
Medulla
Pyramid
A
LMN
.....
\/
.. 1
-UMN
C!>-- CorticobuJar tract
UMN lesion

(spastic paralysis)
Decussation
I
8
I LMN
LMN lesion'
(
fla
9ci d paralysis)
Figure 13-7. Motor inncrvalil11l of the longue. COJlicohulhar fibers projcCll'redoll1in;lntiy to the contralat-
eral hYl'_'gloss:11 An upper llluCOr Ileuron (U,\1N) Icsi(ln C<lllses deviatiol1 (l( the protruded tongue to the
\\'c"k (c,'!\trnlatcral) r\ lower tt\(lt(lr l\l'lIrOI1 (UdN) dc\"i;ltiol1 pf the- \"": fuded t\\) :;;,1:' 10 tht:
\\':lk (i!"U;llcr:d) (/\) Norllul ([3) 11"1[11 ::Iid L\H'! !:.,i",:,
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. z ... ': ..:- .. "
" . : .
Cranial 77 .. . . ..
................................... : .............. : ............................. "' ................. : ........................................................................................................ .
XII. THE HYPOGLOSSAL NERVE (eN a GSE nerve (Figure 13.7).
F .1.", d' . .
eneral characteristics. The hypoglo.::.::nl nerve me lates tongue movement. It ames
from the hypogloSsal. nucleus of the nnd exits [he medulla in the preolivary
sulcus. Ie exits the skull through the hn"\oglossnl cC1nnl, nnd it innervates the intrinsic
and extrinsic muscles \.,f the. Extrinsic muscles are the genioglossus, Sty.
loglossus, and hyoglossus.
. ,
B. Clinical correlation
:to results in hen1ipamlysis of the tongu'e.
2. Protrusion causes the tongue to point toward the weak side because of the unop.
posed action of the opposite genioglossus muscle,
,"
./
.. '--, _.' .. __ .. IIIIJIJ!II.!
14
Lesions of the Brain Stem
I. LESIONS OF THE .
A. medullary syndrome (anterior spinalaner), syndrome). Affected structures
and re$ultant deficits include:
:1.. The corticospinal tract (medullary pyramid). Lesions result in conrralarernl spas,
tic hemiparesi5.
2. The-medial lemniscus. Lesibnnesu1c"in of tactile and \1bracion
semation frOhl the trunk and
3. The hypoglossal nucleus or root fibers [cranial nerve (eN) XII]. Le-
sions result in ipsilateral t1accid hemiparalysis of the tongue. \Xlhen protruded, the
rongue points ro the side of the lesion (i.e., the weak side). See Figure 13,7.
Vestibular nuclei
Inferior cerebellar peduncle
Spinal trigeminal tract and nucleus _-;----<:::!:.:
CNX
Nucleus ambiguus
Lateral spinothalamic tract
'. Nucleus of SOlitary tract
Dorsal motor nUCleus of eN x
.--
B
FI gu r e :1.4-:1.. V"" u ,., b;o", oi .I" """b '" 'n; ;>, 'he levd or, he hI"""''''';>' n .. clem or c '" n;;>' nen'e (eN)
XII ;",d the dors;1/ motor nltc!CU\ p(eN X. (A) Il1cdu!hry syndrome hl(cri,t/ 'lr(ery). ([3) Latern!
mcdllllary in(cri()r (<:r<:h<:ll:lr artl'ry (f'iC_\)) S)"IHlroI11c.
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lesions of the Brain Stem 79
l : ................................................ : ......... _ .............. ..: ......... :._ ................................................................. :
B. Lateral medullar)' syndrome [posterior inferior cerebellar artery (PICA) syndrome]
is by dissociated sensory loss (see I.B 6-7). Affecred strllC.tllres nnd re.
sulcanc.deficits include: .
:1. The vest.ibular nuclei. Lesions re!lult in nystagmus, nausea, vomiting, andverrigo.
2'. The inferior cerebellar peduncle. Lesidns result ipsilateral cerebellar signs [e.g.,
dystaxia, dysmetria (pasc.pointing). dysdiadochokinesia]. '
. .
. .
3. The nucleus ambiguus of CN IX, CN X, and eN XI. Lesions result in ipsilateral
laryngeal. pharyngeal; and palatailleqiiparalysis [Le . loss of the gag reflex (effer.
enc limb), dysarthria, dysphagia, and dysphonia (hoarseness)].
4. The nerve roots. Lesions result in loss of the gag reflex (afferent
limb).
5. The vagal nerve roots. Lesions result in the same deficits- as seen in lesions
\'oh'ing the nucleus ambiguus (see I B 3).
6. The tracts (spinal lemniscus). LeSIons' result contralateral loss
of pain and temperature sensation from the trunk and extremities.
7. The spinal trigeminal nucleus and tract. Lesions result in ipsilateral loss of pain
and temperature sensation from the face (facial hemianesthesia).
8. The descending sympathetic tract. Lesions result in ipsilateral Homer's syndrome
(i.e., ptosis, miosis, hemianhidrosis, and apparent enophthalmos).
II. LESIONS OF THE PONS (Figure 142A)
... inferior results from occlusion of the paramedian branches
of the baSIlar structures and resultant deficits include:
i. The corticospinal tract. Lesions result in f.ontralateral spastic hemiparesis.
2. The medial lemniscus. Lesions resule in conrralateralloss of tactile sensation from
the trunk and extremities.
Spinal trigeminal nucleus and tract --'-'r--=-H-
eN VIII (vestibular nerve)
CNVII
Lateral spinothalamic tract
CNVI
Corticospinal tract
A
FIgure :14-2. Vascular lesions of the caudal pOllS at the level of the nhduccnt nucleus of cranial nerve (CN)
VI and the fncinl nucleus of CN VII. (A) MeJial inferior pontine syndrome. (0) Latcrnl inferior pontine syn-
(./rome (anterior inferior cerehellar artery (AICA) syndrome}. (C) MeJial longitudinal fasciculus (MLF) syn-
:1:s:-:-::.
m
b' '7n-,,5 Oat 5
__ TZ
t _
1
80 Chapter 14 I
...........................................................................................................................................................................................................
. . .
3. The abducent nern! roots. Lesions result in ipsilaceral lateral reccus par,llysis. I
., , Lateral syndrome ("nterior inferior ccrebeUar mtery (AICA)
(Figure 14-2B). Affec:tcd nnd resultant deficits include:
j.. 'facial nucleus and intraaxial nerve fibers. Lesions restilr in:
a . Ipsilnreral f<lcial nen'e pctralysis
b. taste from [he anterior of the tongue
c. Jpsilmeralloss of lacrimation and reduced salhr.ation
d. Loss of comea1 and smpedial reflexes (efferent limbs)
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2. The cochlear nuclei and illtraaxial nerve fibers. Lesions result in unilateral cen; I
tral deafness.
3. The nuclei and intraa?,ial nerve fibers. result in nyscagmus.,
nausea,_\:Qmiting, and,ertigo. ' ... " ,,_,', .. ',' '
4. spinal trigeminai
and temperature sensation fron) the face (facial hemianesthesia).
5. The middle and inferior cerebellar peduncles. Lesions result in ipsilaceral limb
and gait dysraxia.
6. The Lesions. loss
of pain ana temperature sensation from the trunk and extremities. _.: .. _ .. " .
7. The descending s)mpathetic tract. Lesions result in ipsilateral Horner's syndrome.
c. ... (internuclear ophthalmoplegia)
._'-- [see Figure 14;2C] interrupts fibers from the contralateral abducent nucleus that
jeet, through the to the ipsilateral medial rectus subnucleus of CN Ill. It c'auses
medial rectus palsy on attempted lateral conjugate ga:e and nystagmus in the ab-
ducting eye. Con\'ergence remains intact. This syndrome is often seen in patients with
multiple sclerosis. . .
D., ... FaciaLcoUiculus syndrome usually results from a pontine glioma or a vascular acci-
_... dent. The internal'genu ofCNVII and the nucleus of CN. VI underlie the facial col-
lieu Ius. .';
i. Lesions of the internal genu of [he facial nerve cause:
a. Ipsilateral facial paralysis
b. Ipsilateral loss of the corneal reflex
2. Lesions of the abducent nucleus cause:
a. Lateral rectus paralysis
b. Medial (coO\'ergent) strabismus
c. Horizontal diplopia
III. LESIONS OF THE MIDBRAIN (Figure
A. Dorsal midbrain syndrome (sc
7
'Figurc.14-JA) is often the resulr of
pinealoma or germinoma of [he pineal region. Affected structures and rcsulrarH
defIcits include: .
.
:1. The supcrior colliculus and pretectal area. Lesions calise paralysis of upward and
downward gaze, pupillary disturbances, and absence of convergence.
2. The cerebral aqueduct. Compn.'ssion Crluses noncl)ll1ll1unicating
B. midbrain (Benedikt) syndrome Fit.:urc 1'1-313). ;\((ccrec! structures
;\nd result;mt deficit,; include:
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Lesions of the Brain Stem 81. ' .. '
........................ : ................... ........................ ............... -----....... -....... -............................................................................................ ..
Medial geniculate body -++-
Substantia nigra ---ii--+-
Corticospinal tract --T--
Corticobulbar tract
Posterior commissure and center for vertical conjugate
CN III
Superior colliculus
Nucleus of CN III
Spinothalamic tract .
Mediallemrtiscus
Dentatothalamic
tract
Red nucleus
Figure 14-3. Lesions of the midbrain at the of the superior col\iculus and oculomotor nucleus
,,'\t' cranial nen'e III. (A) Dorsal midbrain (Parinaud's) (B) Paramedian midbrain (Benedikt) syn-
.. iwllle. (C) }'1edial midbrain (\'Veber) s)ndrome.
. 1.. The .oc:ulomotor nen'e roots (intraa.xial fib.ers). Lesions cause complete ipsilateral
oculomOtor"paralysis. Eye and depression is caused by the intact lateral ..
rectus (eN VI) and superior oblique (eN IV) muscles. Ptosis (paralysis of the le-
vator palpebra muscle) and fixation and dilation of the ipsilateral pupil (complete
internal ophthalmoplegia) also occur.
2. The dentatothalamic fibers. Lesions contralateral cerebellar dystaxia with
intention tremOf.
3. The medial lemniscus. Lesions result in contralateral loss of tactile sensation from
the trunk and extremities.
C. Medial (Weber) syndrome (see Figure 14-3C). Affected structures and re-
sultant deficits include:. :--.
1.. The oculomotor nerve roots {intraaxial fibers}. Lesions cause complete ipsilateral
oculomotor paralysis. Eye abduction and depression is caused by intact lateral rec-
tus (eN VI) and superior oplique (eN IV) muscles. Ptosis and fixation and dila-
tion of the ipsilateral pupil also occur.
2. The corticospinal tracts. Lesions result in contralateral spastic hemiparesis.
3. The corticobulbar fibers. Lesions cause contralateral weakness of the lower face
(eN VII), tongue (CN XII), and palate_ (eN X)"The upper face division of me
facial nucleus receives bilateral corticobulbar input. The uvula and pharyngeal
wall are pulled coward the normal side (eN X), and the protruded tongue points
to [he weak side. ..-
,/
IV. ACOUSTIC NEUROMA (SCHWANNOMA) (Figure 14-4] is a benign tumor of
Schwann cells [hat affects the vestibulocochlear nerve (eN VllI). It accounts for 8% of
all intracranial tumors. It is a fossa tumor of the internal auditory meatus and
cerebellopontine angle. The often compresses the facial nerve (eN VII), which
accompanies eN VIIl in [he cerebellopontine a.ngle and internal auditory meatus. It may
impinge on the pons and affect the spinal trigeminal tract (eN V). Schwannomas occur
twice as often in females as in tn"les. Affected structures and resultant deficits include:
71
-'
82 Chapter 14 ,
.( .............................................................................................. _ ............................................. ................................................ : .......... .
..
.
a
Figure :14-4. resonance image of an acoustic neuromao This coronal section shows dilation of the
\Oentricleso The \Oestibulocochlear nenoe is \Oisible in the left internal auditory meatuso The tumor indents the lat-
eral Fonso Cranial nenoe palsies include CN V, VII, and VIIIo Symptoms inClude unilateral deafness, facial
anesthesia and weakness, and an absent coronal reflexo This is a Tl-weighced imageo

", .
A. The cochlear nen'e of eN VIII. Damage results in tinnitus and unilateral nerve deaf-"
ness,
B. The vestibular nen'e of CN VIII. Damage results in vertigo, nausea, vom-
iting, and unsteadiness of gait,
C. The facial nerve (eN VII). Damage results in facial weakness and loss of the corneal
reflex (efferent limb). /
D. The spinal trigeminal tract (eN V). Damage resulcs in paresthesia, anesthesia of the
. ipsilateral face, and loss of the corneal reflex (afferent limb),
E. Neurofibromatosis type 2 often occurs with bilateral acoustic neuromas.
v. JUGULAR FORAMEN SYNDROME lIsunlly results from'"n pos"terior fossa tumor (e,g.,
glomus jugu(are tumor, the most common inner em tumor) thnt compresses CNIX, X,
and XI. Affccted structures anq resultant deficits inc"lu"de: '
A. The glossopharyngeal nerve" (CN IX). Di1ll1ng{results in:
j.. IpsilCltcralloss of the gng reflex
2. Ipsilaccralloss of pain, tcmpcrature, and taste in (he tongue
B. Thc vagal nerve (eN X). Dam;)ge results in:
1. Ipsibrcri11 of rhe soft p:11:!tc ;md larynx
2. II'"iI:ltcr:1! !(Jc;s (;( ,he: ,(/;lg rcfh-x
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lesions of the Brain Stem 83
.............. : .......................... : ...................... :.-.. __ .;.: ......... ; ... .; ............................ , ............. : ................................. .. .. t ..... _
C. The nccess(.,ry (eN Xl). Damage in:
:L Pnmlysis of the sternocleidomastoid muscle,.which results in the inability to tum
the heaJ rothe side .
2. Pamlysis of the (rnre:ius muscle, which causes shoulder droop and inability to
shrug the shoulder
. .
VI. "LOCKED-IN" SYNDROrv'lE is a lesion of the of (he pons as the result of infarc-'
tion, trauma, tumor, or dem):elinad9n. The artd corticobulbar tr(l.cts are af-
. ECA
Aorta
A
n
Figure 1.4-5. Anatomy of the subclavian steal syndrome. of the proximal pare of the subclavian
artery (lefc) results in retrograde blood flow through the ipsilateral vertebral arcery and into the left subclavian
artery. Blood can be shunted from the right vertebral and down the left vertebral artery (A). Blood may
also rench the left vertebral artery througn the carotid circulation (8). ACA = anterior cerebellar arteryi ACOM
= anrcrior communicating arteryi AICA = anterior inferior cerebellar arteryi ASA = anterior spinal arteryi BA
= basii.lr arterYi BCT = brachioccphalic trunk; CCA = common carotid artery; ECA = extcrnal carotid .arteryi
ICA = internal carotid arteryi MCA = middle cerebral arteryi PCA = posterior cerebral arteryi PCOM = pos-
communicating arceryi PICA = posterior inferior cerebellar arterYi SCA = superior communicating artery;
SCLA = subclavian :uteryi VA = vcrtebral areery. .
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84' Chapter 14-
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VII.
l'ilater"lly. l'culomotl)r "nd (wi:hlenr nerves nre not injured. Pntiencs nrc cor I
::-:h.'lIs m1J mny thr\,'lIgh \'enical c)'e movements. . .
CENTRAL PONTINE MYELINOLYSIS is a lesion of the base of the pons thm nffects th
(\.,rrico:'l'inal nnd More than 75% ofcnses are \\lith nlcoholi51' ,
\,'r mpid. correct h.:'" of h)1'onacremia .. Symptoms include spastic qundripnresis. pseudobllUx1
VIII.
r.1hy. and ment.,l condition may become the locked*in ...
"TOP O'F THE BASilAR" SYNDROME fro;n embolic of the roSti.l
l:-.l:,ilar nrter,),. Neurologic sigll$ include ortic ataxia and psychic paralysis of fixntkm of
(Balines syndrome), ectork rurils. somnolence. and conical blindness, with or \\'ithou
"isual <1l1osogno:,ia (Anton's syndrome).
I
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IX. SUBCLAVIAN STEAL SYNDROME (Figure "14-5) result:s"from thrombosis of the let
sul:-cla\"inn artery proximal to the "errebtal artery. Blood is shunted retrograde down thl
left ,-ertebral artery and' into [he left sl,Ibclavian' artery. Clinical signs include transien
weakness and claudication of the left ann on exercise and "ertebrobasilar insufficienc:
i.e .. ,errigo. di::iness).
X. THECEREBELLOPONTINE ANGLE is the junction of the medulla. pons. and cere
hellum. CN VII and VIII are found there. Five brain rumors, including a cyst. are .. often 10
..:ated in the cerehllorontine angle cistern. Remember the acronym SAME: sch\\'annoIDc-
(7590), arachnoid cySt (1%), meningioma (10%), ependymoma (1 %), and epidermoiL
(5%). ll1e percentages refer to cerebellopontine angle tumors.
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--.
.' . .... :-
' .
. ' /., ....
. . -.
-. '-.
1.5
Cerebellunl
f. FUNCTION. The has primary functions:
. .
A. Maintenance of posture and balance
,
B. Maintenance of muscle tone
C. Coordination of voluntary motor activity
II. ,ANATOMY
A. Cerebellar peduncles
2. The superior cerebellar peduncle contains the major OUtPUt from the cerebellum,
the dentatothalamic tract. This tract terminates in the vent:rallateral nucleus of
the thalamus. It has one major afferent: pathway, the ventral spinocerebellar tract.
2. The middle cerebellar peduncle receives pont:ocerebellar fibers, which project to
the neocerebellum (pomocerebelIum). :.'
3. The inferior cerebellar peduncle has three major afferent tracts: the dorsal spi-
nocerebellar cract, the cuneocerebeIIar tract, and the olivocerebellar tract from the
inferior oIi\'ary nucleu.s. " . ".
8. Cerebellar cortex, neurons, and fibers
:1.. The cerebellar cortex has three layers.
a. The molecular layer is the outer layer underlying the pia. It contains stellate
cells, basket cells, and the dendritic arbor of the Purkinje cells.
h. The Purkinje cell layer lies between the molecular and the granule cell layers.
c. The granule layer is the inner layer overlying the white matter. It contains
granule cells, Goigi cells, and cerebellar glomeruli. A cerebellar glomerulus
consists of a mossy fiber rosette, granule cell dendrites. and a Goigi cell axon:
2. Neurons and fibers of the cerebellum
a. Purkinje cells conve}, the only output from the cere'bellar cortex. They pro-
ject inhibitory outPUt (i.e., 'Y-aminob.uiyric acid (GABA)J to the cerebellar
and vestibular nuclei. These cells me' excited by parallel and climbing fibers
and inhibited by GABA-ergic basket and stellate cells.
b. Granule cells ex<;ite (by of glutamrtte) Purkinje, basket, stellate, and
Golgi cells through p;1rallcl fibers. They nre inhibited by Golgi cells and ex-
cited by mossy fibers.
c. Parallel fibers (lre [he nxolls of granule cells. These fibers extend into the mo-
lecular farer.
n Mossy fibers arc the afFerent excitnrory fibers of the spinocerebellar. pomo-
R5
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:'.:'
Cerebellum 87
....................... ..t ... ....................... ........................ .-._ ...... !' , _ '! _.
C. nucleus of the. receives the dentatothalamic tract. It
r"l rht! primmr motor correx of the precentral gyrus (Brodmann's area 4).
.. . .
D. The motor cortex (motor strip, or Brodmann's area 4) receives input from the ven-
tral bteral ilUdell:> of the thabmus: Ie projects as the corticopontine tract to the pon-
tine nuclei.
E. pontint! nuclei recehe input the motor cortex. project as the pomo.-
cerebellar tract to the contralateral cerebellar cortex, where they terminate as mossy
.fiber::. thu:: the circuit.
IV. CEREBELLAR DYSFUNCTION includes rhe following triad:
A. Hypotonia is loss of the resisrance normally offered by muscles to palpation or passive
maniruiation. It results, in a floppy, ioose-jointe<J, rag-doll appearance with pendular
retlexes. The, patient arrears
B. Dysequilibrium is loss of c.haracteri:ed by gait and dystaxia.
. '.
C. Dyssynergia is loss of coordinated muscle activity. It includes dysmetria, intention
tr'emor, failure to check movements, nystagmus, dysdiadochokinesia, and dys,
rhythmokinesia. Cerebellar nystagmus is coarse. It is more pronounced when the
patient looks the side of the. lesion. . .
V. CEREBELLAR SYNDROMES AND TUMORS
A. Anterior vermis syndrome inv6ives the leg region of the anterior lobe. It results from
atrorhy of the romal vermis, most commonly caused by alcohol abuse. It causes,gait,
trunk, and leg dystaxia.
B. Posterior vermis syndrome involves the flocculonodular lobe. It is usually the result
of brain tumors in children and is most commonly caused by medulloblastomas or
ependymomas. It causes truncal dystaxia. ,',.
C. Hemispheric syndrome usually involves one cerebellar hemisphere. It is often the re-
sult of a brain tumor (astrocytoma) or an abscess (secondary to otitis media or mas-
toiditis). It causes arm, leg, and gait dystaxia and ipsilateral cerebellar signs.
D. Cerebellar tumors. In children, 70% of tumors are found in the posterior fossa.
In adults, 70% of brain tumors are found in the supratentorial compartment.
1. Astrocytomas constitute 30% of all brain rumors in children. They are most: oft:en
found in the cerebellar After surgical removal, it is common for the
child to survive fO,r many years. '
2. ?-"1edulloblastomas are malignant and constitute 20% of all brain tumors in chil-
dren. They are belleved to originate from the 5uperfici?1 granule layer of the cere'
bellar cortex. They usually obstruct the passage of cerebrospinal fluid (CSF). As a
result, hydrocephalus occurs.
3. Ependymomas constitute 15% of all tumors in children. They occur most
frequendy in the fourth ventricle. TheY usually obstruct the passage of CSF and
cause hydrocephalus.
_-,..-___ ... M"-.MlIlaioll$iilliiilliSll.III"IfiSR .. - 1iII'-._7.-.'.
-.;'" .
1
1..6
Th.alamus.
I. INTRODUCTION. The thalamus i.s the diviSion of the diencephalon. Ic-plays al
important role in the integration of thesensory and motor systems.
II. MAJOR THALAMIC NUCLEI AND THEIR CONNECTIONS (Figure 16-1)
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A. The anterior nucleus receives hypothalamic input from the. mamillary nucleu: I
through the mamillothalamic tract. It projects.ro the cingulare gyrus and is part, of lht
Pape: circuit of emotion of the limbic system. . ..
B. The mediodorsal (dorsomedial) nucleus is reciprocally connected to the prefrontal I
cortex- It has abundant connections with intralaminar nuclei. It receives input from
the amygdala. substantia nigra, and temporal neocortex. When it is destroyed, mem-
ory loss occurs (Wemicke-Kqrsakoff syndrome). The mediodorsal nucleus plays a role
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in the expression of affect, emotion, and behavior (limbic function).
C. The centromedian nucleus is the largest intralaminar nucleus. It is reciprocally con-
nected to the macor cortex (Brodmann's area 4):.The centromedian nucleus receives
input from the globus pallidus. It projects to the striatum (caudate nucleus and puta-
men) and projects diffusely to the entire neocortex.
D. The pulvinar is the largest thalamic nucleus. It has reciprocal connections with the
association cortex of the occipital, parietal. and posterior temporal lobes. It receives
input from the lateral and medial geniculate bodies and the superior colliculus. It plays
a role in the integration of visual, auditory, and somesthetic input. Destruction of
the dominant puh-inar may result in sensory dysphasia.
E. Ventral tier nuclei
:1. The ventral anterior nucleus receh-es input from the globus pallidus and sub-
stamia nigra. Ie projects diffusely to the prefrontal cortex, orbital cortex, and pre-
motor cortex (Brodmann's area 6).
" :
2. The ventral lateral nucleus receives input from the cerebellum (dentate nucleus),
globus pallidus, and substantia nigra. It proje,cts to the n.1otor cortex (Brodmann's
area 4) and the supplementary motor area 6).
3. The ventral posterior 'nucleus complex) is the nucleus of termina-
tion of general sommic afferc'nt (touch. pain. and temperature) and special visceral
afferent (caste) fibers. It h:lS twO' subnllclei.
a. The ventral posterolateral nucleus receives the spinothalamic ,tracts and the
medial lemniscus. It projects to the somesthetic cortex (Brodmann's
CHC;lS 3, 1, :lnJ 2).
b. The vcntral posteromedial (VPM) nuclells receives the trigcminoch:ll;<mic
tf:H:(<; ;md projeCTS to the (sen:,()ry) corte.; (Bnic1m:ll1n'.; ;Ii 1.
;111d /). "I'lle r,' ldl\I;;'IY ()C;j<rL (;: ':) .:
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I.. ,,'
. , . ....... : ................. ; ............................................ :: ............... __ ........................... : ................... : .................................. .......

A
Anterior
nuclear group
8
Mamillotnalamic tract}
Fomix
Globus pallidus }
Substantia nigra
Area 6 }
Diffuse frontal cortex
Dentate nUCleUS}
Globus paffidus
Substantia nigra
Cingulate gyrus
Medial lemniscus }
Spinothalamic tracts
Areas 3,1, 2
{
Amygdaloid complex
Temporal neocortex
Substantia nigra
{
Areas 18 and 19
parietal lobule
Trigeminothala(Tlic
tracts and taste pathways
Figure :16-:1. thalamic nuclei and their connections. (A) Dorsolateral aspect and major nuclei. (B)
l\1ajor afferenr and efferent connections, VA = ventral anterior nucleus; VL = venrrallateral nucleus; VPL =
"entral posterior lateral nucleus; VPM = \'entral posterior medial nucleus. .
.
projects via the central tegmental tract to VPM, and thence to the gustatory
cortex of the postcentral gyrus (Brodmann's area 3b), of the frontal operculum
and insubr cortex. The taste pathway is ips!lateraL ..
F. Metathalamus
:to The lateral geniculate body is a visual relaY,11ucleus. It receives retinal input through
the optic tract and projects to the cortex (Brodmann's area 17).
2. The medial geniculate body is an auditory relay nucleus. It receives auditory in-
put through the brachium of rhe inferior colliculus and projects to the primary au-
ditory correx (Brqdmann's nre;-.s 41 and 42).
G. TIle reticular nucleus of thalamus surrounds the thalamus as a thin layer of -y-aminobu-
tyrie rlcid (GABA)ergic neurons. It lies between the external medullary lamina and the
internal capsule. Ie receives excitatory collateral input from conieothalamic and thala-
mocortical fibers. It projects inhibitory fibers to thalamic nuclei from which it receives
input. Ie is thoughr to playa role in norm:1l c1ectroencephaolgram readings.
,0',- S't a UN.t
90 Chapter 16
.............................................................................................................................................................................................................
III. BLOOD SUPPLY. The thalamlls is ir:rigmeJ: 1:-r three arreries (sec Figure
A.
B.
c.
The posterior communicating. artery
cerebral artery
The anterior choroidal artery (bteral geniclilate body)
. .
1
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IV. THE INTERAL CAPSULE (Figure 162) is a layer of white matter (myelinated axons) [h;1 I
[he caudace nucleus and che tl}alamusmedially froll-i the lentiforin nucleus lacerally
A. The anterior limb is locaced between [he caudnce nucleus and the lentiform nudeu I
(glol:-us pallidus and putamen).
B. The genu contains the corticobulbar fibers.
nle posterior limb is located between the thalam'us and' the lentiform micleus. It con .1
rains corticospinal (pyramid) fibers well as sensory (pain, temperature, and touch)
c.
visual. and auditory radiations. .
D. Blood supply
I
:to TIle anterior limb is irrigated by the medial striate branches of the anterior cereera:
artery and the lateral striate (lenticulostriate) branches of the middle cerebral artery.
2. The genu is perfused either by direct branches from the internal carotid artery or
/:-Y'pallidall-ranches of the anterior choroidal artery.
3. The posterior limb is supplied by branches of the anterior choroidal arrerJ'
lenticulostriate branches of the middle cerebral arteries.
Caudate nucleus --.'--
Genu
Corticobu!bar fibers
Posterior limb --f----+-t--
Thalamus --t------'
Sensory radiations from
VP nucleus to areas 3, 1, 2
Medial geniculate body
(audition)
Lateral geniculate body
(vision)
Globus pallidus
Pulamen
Corticospinal fibers
Auditory radiation tv transverse
.' temporal gyri of Heschl
. (areas 41 and 42)
Visual radiation to
sl.riate cortex of occipital lobe (area 17)
Figure 1.62. Hnri:OlHal scctil'll d the right intcrnal the major fiber projections. Clinically
impnrt<lnt lic in the genu ;md limh. (/ (he intcrn;d C\I':ilJ!e C\lISC CL'nrraiater;!1 hcmi-
;lnd c{)(\tr,d:1(cr:d hcrni:\I\<.I!'i;\. \T c .. .-:"r;': I',';:",; Ie ","Ic",.
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.. ".:. " .. I ... -'.
, ,

- .!
-.-: ,1" -,'
1.7
Visual System
I.. INTRODUCTION. The visual ::y::tem is sen'ea by the optic nerve, which is 'a ::pecial so-
matic afferent nerve.
II. THE VlSUAL PATHWAY (Figure 171) includes the following structures,
A. Ganglion cells of the retina fonn the optic nerve [cranial nerve (eN) IIJ. They pro-
ject from the nasal hemirerina to the contralarerallateral geniculate body and from
the temporal hemiretina to the ipsilateral lateral geriiculate body.

Nasal' Nasal Temporal
00



-+-+-H-4-- Lateral geniculate
body
Visual radiation to lingual gyrus
Visual radiation to cuneus
Visual cortex area 17
Flgure 17-1. The visual pathway from the retina to the visual conex showinl:: visual field defects. (I) Ipsilat-
eral blindness. (2) Binasal hemianopia. (3) Bitemporal hemianopill. (4) Right hemianopia. (5) Right upper quad-
ranranopia.(6) Right lower quadrantanopia. (7) Right hemianopi:t with macular sparing. (8) Left constricted field
as a result of end-stage glaucoma. Bilateral constricted may be seen in hystcria. (9) Left central scotoma as
: {rctrobulb:tr} neuritis in multiple sclerosis. (10) Upper aititudinal hcmianopia as a rcsulr of bilateral
dc.!>tnJc(ion of the lingual gyri. (11) Lower nltitudinal hemianopia as n rc:\ult (If hiLHer,,1 destruction of the cunei.
I
--
.m
PSZ _em 7!"'N'!t '1
. '.
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92 Chapter 17 . .
................................................................................................................................................................................................................
B. The optic nen'e rrojec(s from the l:nnina cribrosa (,{the scleral canal, through the t
c.
tic chiasm. .
Transection callses ii'silatcral blindness, with no direct pupillary light reflex.
2. The section ,-,f the \.lptic nCr\'e "nhe optic chiasm transects all fibers (roin the i
:;ilmeml as weI.! as fibers from the contralateral inferior nasal qundmnt t!.
loop into the \."Irtic nerve. This lesion cnuses ipsilateral blindness and a COntra\;
era} temroral quadrant defect (junction sc.otoma).
The optic chiasm conrnins decussating fibers from the two nasal hemir.etinas. It co
rains noncrossing fibe:s from the c\\'o temporal hemirecinas and projects fibers t:O ti
suprachiLlsmatic nucleus of the hypothalamus.
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1.. lvlidsagittal transection or pressure (often from a pitu itary tumor) causes bi ten .1
poral hemianoria. . . .
2. Bilateral lateral compression causes binasal hemianopia{calcified internal carot:
arteries). . . I
D. The optic tract contains fibers from the ipsilateral temporal hemiretina and th
contralateral nasal hemiretina. Ie projects to the ipsilateral lateral geniculate bod- I
pretectal nuclei. and superior colliculus. Transection causes contralateral hemi
E. The lateral geniculate body is a si;<-Iayered nucleus. Layers 1,4, and 6 receive crosse(
fibers; layers 2. 3. and 5 receh'e uncrossed fibers. The lateral geniculate body receive
input from layer VI of the striate cortex (Brodmann's area 17). It also receives fiber
from the ipSilateral temporal hemiretina and the contralateral nasal hem ire tina. I
projects through the geniculocakarine tract to layer IV of the primary visual
(Brodmann's area 17).
I
F. The geniculocalcarine tract (vi;uar radiation).. projects through two divisions to the
visual cortex. I.
:to The upper di"'ision (Figure 17-2) projects to the upper bank of the calcarine suI
cus, the cuneus. It contains input from the superior retinal quad1"ants, which rep
resent the inferior visual field quadrants.
a. Transection causes a contral.aterallower quadrancanopia.
b .. Lesions that involve roth cunei cause a lower altitudinal hemianopia (alti
tudinopia).
2. The lower division, (see Figure 17-2) loops from rhe lateral geniculate body anre-
riorly (Meyer's loop), then posteriorly, to terminate in the lower bank of the cal-
carine sulcus, the lingual gyrus. It contains input from the inferior retinal quad-
rants, which represent the superior visual field quadrants.
a. Transection causes" contralateral upper quaCIrantanopia ("pie in the sky").
b. Transection of both lingual gyri causes an upper altitudinal hemianopia {al-
titudinopia}. . .
G. The visual cortex area 17) on the banks of the calcarine fiS-
sure. The cuneus is the upper b.lnk. The lingual gyrus is the lower bank. Lesions 'cause
contralateral hemianopi;l with m:1:lIlar sp:uing. The visllal cortex h<ls a rctinotopic
organization:
1.. The posterior area rcccin:s macul:lr inrut (c('ntral vision).
2. The intermediate arca recein's paro1lll;Ktd:1f input (pcriphef:11 inptlr).
3. The anterior area I1lClI1()cuhr !:'i".!r.
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'... i: . ->' ...
Visual System 93
.. : ..................... ..................................... ..... -.. -.. -.... - ................... ........................ ..... ....................................................... ..
La!: genicurate body,
loop of - --
Lesion A 01 visual radiations to'

I
/
I
/
I
I
I Field defects
Lower r. ho"monymou5 quadrantanopia

sulcus
B
Upper r. homonymous quadrantanopia
Lesion B of visual radiations to
int. bank of calcarine sulcus
Figure :1.7-2. Relations of the left upper and left lower divisions of the geniculocalcarine tract to the 12.cera:
\'erltricle and calcarine sulcus. Transection of the upper'division (A) results in right lower homonymous quae-
ramanopia. Transection of the lower division (B) results in right upper homonymous quadranta.rlOpia.
(Reprinted with pennission from FLx jO: BRS Neuroanatomy. Baltimore, Williams & Wilkins, 1997, p 261,)
III. THE PUPILLARY LIGHT REFLEX PATHWAY (Figure 17-3) has an afferenc lim'=
(eN II) and an efferent limb (eN III). It includes the following structures:
A. Ganglion cells of the retina, ,,,,hich project biiaterally to the pretectal nuclei
B. The pretectal nucleus of the midbrain, which projects (through the posterior com-
missure) crossed and uncrossed fibers to ,the Edinger-\Vestph3.l nuclel!s
. .
C. The Edinger-\Vestphal nucleus of eN III, \\lhich gives rise to preganglionic parasym-
pathetic fibers. These fibers exit the midbrain with eN III and synapse with postgan-
glionic parasympathetic neurons of the ciliary ganglion.
/
D. The ciliary ganglion, which gi\;es rise to postganglionic parasympathetic fibers. Tnes::
fibers innervate the sphincter muscle of the iris.
IV. THE PUPILLARY DILATION PATHWAY (Figure 17-4) is mediated by the sympa-
thetic division of the autonomic nervous system. Interrupt:ion of this pathway at an y level
causes ipsilateral Homer's syndrome. Ir includes the following structures:
A. The hypothalamus. Hypothal:llllic neurons of ,the paraventiicular nucleus project di-
rectly to the ciliospinal center (Tl-T2) of Yie intermediolateral cell column of the
spinal cord. ,-
B. The ciliospinal center of Budge (TI-T2) projects preganglionic sympathetic fibers
through the sympathetic trunk [0 the superior cervical ganglion.
C. The superior cervical ganglion projects postganglionic sympathetic fibers through the
perivascular plexus of the cmotiJ system to the dilator muscle of the iris. Poscg<ln-
glionic sympathetic fibers through the tympanic cavity and cavernous sinus and
enter the orbit through the superior orbital fissure.
Br"Ws


rzry , ? rrZz'?'-A?tsmS'N"!". 1 5 n
94 Chapter 17
.....................................................................................................................................................................................................................
Brachium of
superior colliculu:> ----."
Edinger-Westphal
nucleus of eN III
.Red nuclaus
Posterior
Medial geniculate
nucleus
Lateral geniculate
nucleus
Crus cerebri
Optic tract

Retinal ganglionic cell
muscle of iris
Figure :1.7-3. The pupillary light rathway.light shined inco one eye causes boch pupils co constrict. 111e re-
sr..:-
nse
in the stimulated ere is called the direct pupillary light reflex. The in the opp'osite eye is called
the consensual rupillary light reflex. C)J = cranial nerve. '.
V. THE NEAR REFLEX AND ACCOMMODATION PATHWAY
A. The cortical visual pathway pr9jeCts from the visual cortex (Brodmann's area
17) to the visual aS50Ciacion cortex (Brodmann's area 19).
8: The visual association 'cortex (Brodmann's area 19) projects through the cortico-
tee tal tract to the superior colliculus and pretectal nucleus.
C. The superior coHiculus and pretectal nucleus project.to the oculomotor complex of
the midbrain. This complex includes the following structures:
i. The rostral Edinger,Westphal nucleus, wl)ich mediaces pupillary constriction
through the ciliary ganglion /.
2. The caudal Edinger-\Vcstphal nucleus, medintcs contrnction of the ciliary
muscle. This contmction increases the refractive powcr of the lcns.
.
3. The medial rectus subnucleus of eN III, which mediares cOlwergcnce
VI. CORTlCAl AND SUBCORTICAL CENTERS FOR OCULAR MOTILITY
A. The front;)l eye flcld is locared in the posterior p:Hr o( the middle (ronrZ11 gyrus (Brod-
m;![lll\ ;Ire;l 8). it \,olunr;l:Y (:;;lcc!(lic) eyl'
. ... ,
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Visual System 95
.................................................... ........................................ ;"' ........................ -...................................................... : .............................................. : .......... ........... ...
B
Flashlight swung from right eye to left eye Looking straight ahead
o
-tifu.
Looking right Looking lett Eyes converged Looking straight ahead
,- F
I t. zt;D
E' G
Looking right'
I
i Looking up Eyes converged Looking lett and down
i
I
H J
No to light Eyes converged Eyes of a comatose Looking straight ahead
Figure j,. 7-4. Ocular mowr palsies and pupillary syndromes. (A) afferent (Marcus Gunn) pupil, left
eye. (B) Homer's syndrome, left eye. (C) Internuclear right eye. (D) Third-nerve palsy, Iefr
eye. (E) Sixth-nerve palsy, right eye. (F) Paralysis of upward gaze and com'ergence (Padnaud's syndrome). (0)
Fourth-nerve palsy, right eye. (H) Argyll Robertson pupil. (I) Destructive lesion of the right frontal eye field. U)
Third-nerye palsy with ptosis, right eye.
. -
:1.. Stimulation (e.g., from an irritative lesion) causes contralateral deviation of the
eyes (i.e., away from the lesion).
2. Destruction causes transient ipsilateral conjugate deviation of the eyes (i.e., to-
ward the lesion).
B. Occipital eye fields are located in Brodmann's areas 18 and 19 of the occipital lobes.
These fields are cortical centers for involuntary (smooth) pursuit and tracking move-
ments. Stimulation causes contralateral conjugate of the eyes.
C. The subcortical center for lateral conjugate gaze is locafed in the abducent nucleus
of the pons (Figure 17 -S). Some authorities place the "center" in the paramedian pon-
tine reticular fonnation. / '
:t. It receives input from the contralateral eye field.
2. It projects to the ipsilaterallate(al rectus muscle and, through the mediallongitu-
dinal fasciculus (MLf), to the contralateral medial rectus subnucleus of the ocu-
lomotor complex.
D. The subcortical center for vertical conjugate gaze is located in the midbrain at the
level of the posterior commissure. It is called the rostral interstitial nucleus of the MLF
anu is associated with Parinaud's syndrome (see Figures 14--3/\ and 17-4F).
-'I
,... w elB
src
7 'NIL :1
96 Chapter"17
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. " "
- Lateral rectus muscle-"
.. i

Bilateral MLF syndrome
-
Left .
"A


.. , ......

Right
-
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Midbrain
B
'" ..
I
I . -+-
Convergence
C

"
Patient with MLF syndrome cannot
Pons
adduct the eye on attempted latera:
conjugate gaze, and has nystagmus
in abducting eye. The nystagmus is
in the direction of the large arrow-
head. Convergence remains intact.
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Figure :1.7-5. Connections of the poncine center for lareral conjugate gaze. Lesions of the mediallongitudi.
nal fasciculus (]-"(LF) between [he abducent and oculomocor nuclei result in medial rectus palsy on anempteJ
lateral conjugate ga:e and hori:ontal nystagmus in abduccing eye. Convergence remaim intact {inser}. A uni-
lateral MLF lesion would affect only the ipsilateral medial rectus. eN = cranial nerve. "
I
VII. CLINICAL CORRELATION
I
A. in MLF syndrome, or internuclear ophthalmoplegia,(see F;igure 174), there is dam- I
age (demyelination) to the tv1LF between the abducent: and oculomoror nuclei. It
causes medial rectus palsy on attempted lateral conjugate gaze and monocular hori
:ontal nystagmus in the abducting eye. (Convergence is This syndrome is I
most commonly seen in"multiple sclerosis.,./
B. One,and,a,h,,1f syndrome consists ofbilllteralicsions of the MLF lind a unilateral Ie
sion of the abducent nucleus. On ,,(tempeed lateral conjugate gaze, the only muscle I
that (unctions is the intact lateral rectus.
C. Argyll Robertson pupil (pupillary light-ncar dissociation) is the absence of a miotic
reaction to light. borh direct lind consellSunl, with the prcscrvnrion of a miotic rcnc- I
tion to nc;)r stimulus (nccoll1l11olhrion-cor1\'crgcncc). J r occurs in syphilis ;)nd
diabetes.
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Visual System 97
, ,
............... , ........................................................................................................ ................................... .................... , ......................... -
'.. .-
D. Horner's syndrome is by (rnnsectk"l" of the oculosymparhetic pathway at any
ll!\'el (see IV). Thh; consists of miosis, ptosis, apparent enophthalmos, and
.
E. Gunn) pupil resuits from n lesiori o(the optic nene. the
afferent limb of the pupillary light reflex (e.g., retrobulbar neuritis seen in multiple
sclerosis). The diagnosis can be 111ade \\'ith the swinging flashlight test (see Figure
4A).
F. Tra,nstentorial (uncal) herniation occurs as a result of increased supratentorial pres-
sure, which is commonly by a bmin tuinoror hematoma (subdural or epidural).
:1. The pressure cone forces the parahippocampal uncus through the tentorial
cisure.
2. The impacted uncus forces [he' contralateral crus cerebri against the tentorial edge
(Kernohan's notch) and puts pressure on the ipsilateral eN III and posterior
bral artery. As a result. the folto}ving neurologic defects occur.
a. Ipsilateral hemiparesis occurs'as a -result ofpressure on the' corticospinal tract.
which is located in the contralateral crus cerebri.
b. A fi.'ed and dilated ptosis, and a eye are caused by
pressure on the ipsilateral oculomotor nerve.
c. Contralateral homonymous hemianopia is caused by compression of the
terior cerebral artery, whi<;h_ the visual cortex. -
G. 'Papilledema (choked disk) is noniriflammatory congestion of the optic disk as a
sulr of increased intracranial pressure. It is most commonly caused by brain tumors.
subdural hematoma, or hydrocephalus. It usually does not alter visual acuity, bur it
may cause bilateral enlarged blind spots. It is often asymmetric and is greater on the
side of the supratentorial lesion.


';':"'"':;':'.'<';";"\"-,i,;:;'.':"""',.,.,.;,,;:,;;:,,;:-, ... .. " . .. __ II?IIZiliil.7_1
1.8
Nervous System
I
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,
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I. INTRODUCTION.)he autonomic nen'ous system (ANS) is a general visceral effen
motor system that controls and regulates smooth muscle, cardiac muscle, and glands I
A. The Ai'S consists of twO types of projection neurons:
I
. i. Preganglionic neurons
2. Postganglionic neurons. Sympathetic interneurom.
I
B. Autonomic output is controlled .by the hypothalamus.
C. The Al'S has three dhisions: '.
:1.. Sympathetic. Figure 18-1 shows the sympathetic innervation of the ANS.
2. Parasympathetic. Figure 18-2 shows the parasympathetic of the AN: I
Table 18-1 compares the effects of sympathetic and parasympathetic activity c
organ systems.
. I
3. Enteric. The enteric division includes the intramural ganglia of the gastroimest
nal cract, submucosal plexus, and myemeric plexus. .
II. CRANIAL NERVES (eN) WITH PARASYMPATHETIC COMPONENTS includ I
the follo\ving:
I
A. eN III (ciliary ganglion)
B. eN VII (pterygopalatine and-submandibular ganglia)
C. eN IX (otic ganglion)
D. eN X [temlinal (mural) ganglia]
III. COMMUNICATING RAMI of the ANS include:
-'
A. \Vhite communicating rami, which are found between T-l and L-3, are myelinated.
B. Gray communicating rami, which me found :111 spinal lc'vcis, are unmyelinated.
. /
IV. NEUROTRANSMITTERS of the ANS includl::
A. Acetylcholine, which is the neUfO!f;'msmittcr orthe preganglionic neurons
B. Norepinephrine, which is the neliTOrransminer of the postganglionic neurons, with
the exception of swcnr glanJs nnt! some blood \'csscls that receive cholinergic sympa-
innervation
C. Dopamine, which is the neurocr:msmictn :he sinall ir\t{'nsclv i1\!()[(.';CCl1t (SIr)
cells, wllleh arc intcrncurons (If the '::,:\(,Ii.
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Nervous System
99
. .
a _ _ ..................................... 6
en
'0
c:
co
en
iii
Cll
:=
en
'0
c:
co
fI'i
Cll
13
en
:J
E
'5.
'-
0
(3
Cll
'-
'-
co
fI'i
03
en
en
Cll
>
'0
0
0
:a
0
r-
Superior
cervical ganglion.
\
\
\
\
L-3
,
\ ,
\ Sympathetic trunk'
. . .
..
__ - Tarsal muscle
....
....... -: .... Lacrimal gland .

Inferior
plexus
..
....... Eye: dilator of pupil
. Submandibular and
sublingual glands
.Parotid gland
Heart
Bronchial tree
Stomach
Small intestine
Large intestine
Ductus deferens
Figure :1.8-:1. The sympathetic {thoracolumhar} innervation of the autonomic ncrvous systcm. The entire
sympathetic innervation of the hcaJ is through the superior cervici11 ganglion. Gray cOl11munic;\ting r;1mi arc
found lit all cord le\"(:ls. White communicating rami nrc (ound only in spinal segmcnts T-l through L-3.
wwerem! z 75 S' 7
7S"P
aWMm?WMMo/
7'5
<I
:100, Chapter 18
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........................................... : ............................. : .................................................................................................. : ............................ .
Midbrain
. Superior __
' nucleus - __ ...; ___ { ...

. , . '-./'
Inferior salivatory {
nucleus - - - - - - -
Dorsal motor ,,' I - - --7
nucleus of ,,' \
vagal nerve>' " \
S-2
S-3
S-4
!
i
!
i
i
Pelvic
, splanchnic
nelVes
Ciliary ganglion
-Pterygopalatine' ganglion
Submandibular ganglion
Eye: constrictor
of pupil and '
Ciliary body
Lacrimal and
nasal glands
Submandibular'
and sublingual
glands -
Parotid gland
Heart
Bronchial tree
Stomach
Small intestine
Large intestine
Urinary bladder
Genital erectile tissue
Figure 1.8-2. TIle (cr;mios:tcr"l) inllcr"'Hiol1 o( the autonomic system, S;1cral Ollt-
flow inclllJcs segments S-2 through 54, Cr:1nbl OlHtlO\\' is 1l\C\.li;\{cd IIm)\I,:" cr;lnial !l"r\',,:; (eN) Ill, VII, IX,
,md X,
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. . .. Autonoll)ic Nervous.Sstem. 101
................................................................................. _ ....... '! ................................................. _ ........................... _ ......................... ......... ................. e .... ..
Table 18-1
Sympathetic and Parn$ympathetic.Acrivity on Organ Systems .
Structure
. Eye .
Radial muscle of iris
.'. Circular mvsc.le C?f iris
Ciliary muscle of ciliary body
lacrimal gland.
Salivary glands
Sweat glands
Thermoregulatory
Apocrine (stress)
Heart
Sinoatrial node
node
Contractility
Vascular smooth ITluscle
Skin, splanchniC vessels
Skeletal muscle vessels
Bronchiolar smooth muscle
Gastrointestinal tract
Smooth muscle
Walls
Sphincters
and motility
Genitourinary tract
Smooth muscle
Bladder wall
Sphincter
Penis. seminal vesicles
Adrenal medulla
Metabolic functions
Liver
Fat cells
Kidney
Function
Dilation of pupil (mydriasis)
Viscous secretion
Increase
Increase
Acceleration
Parasympathetic Function
. Constriction of pupil (miosis)
Contraction for near vision
Stimulation of secretion
Watery secretion
InGrease in conduction velocity
Increase ".
. Deceleration (vagal arr'est)
Decrease in conduction velocity
Decrease (atria)
Contraction'
Relaxation
Relaxation
Relaxation
Contraction
Decrease
Little or no effect
Contraction
Ejaculation *
Secretion of epinephrine and
norepinephrine

Gluconeogenesis and
glycogenolysis .
lipolysis
Renin release
'. . Contraction
Contraction
Relaxation
Increase
Contraction
Relaxation
Erection'"
Note erection versus ejaculation: Remember point and shoot: p = parasympathetic. s = sympathetic.
Reprinted with permission from Fix J: BRS Ne.uroanatomy. Media, PA, Williams & Wilkins, 1991.
D. Vasoactive intestinal polypeptide (VIP), a vasodilator Jhat is colocaljzed with acetyl-
choline in some postganglionic parasympathetic fibers
E. Nitric oxide (NO), a newly disco\'ered neurotrarysmitter that is responsible for the re-
laxation of smooth muscle. It is also responsible'for penile erection (see Chapter 22).
/
"
V. CLINICAL CORRELATION
A. Megacolon or congenital aganglionic megacolon) is char-
ncteri:ed by extreme dilation and hypertrophy of the colon, with fecal retention, and
by the nbsence of ganglion cells in the myenteric plexus. Ie occurs when neural crest
cells do not migrate into the colon. .
B. F:llnilial dysautonomia (Riley-Day syndrome) predominantly nffccts Jewish chil-
dn:n. Ie is an autOsomal reccssivc Hait that is charactcrized by abnormal swcaring, un-

I
zsmr ron ro=.'7
u
o RSS72rsCFIrmnw
102 Chapter 18
I
...... , ................................................................ __ ............................................................................................................................... .
(e.g., orthl,stntic in (as r.-rcH.lb I
of inadequate- muscle tlme in rhe gnstrointestinal rrilcd. nnd progressive sensory 10:::'
It results in the ,,-,SS of neurons it, the autonomic imd sensory ganglia. '
I
c. Raynaud's disease is a painful disorder of the terminal, aneries of the extremities. It i:
ch.-\racteri:ed 1:-)' idiopathic pnrl)xysmaI bilateral cy;mosis of the digits (as n result l'lf ar-
terial an9 nrreri.olar cold or emotion). It mn}' be'treared by prt!- .
s);mpathectomy.. . - . I
D. Peptic ulcer disease results (rom excessive production of hydrochloric acid because \..'\1
increased parasympathetic (tone) stimulation.
E. Horner's syndrome (see Chapter 17) is oculosympmhetic paralysis.
F. Shy-Drager syndrome itwoh"es preganglionic sympathetic neurons from the inter
mediolaternl cell column. It is characterized by orthostatic hypotension. anhidrosiS'.
impotence: and bladder
G. Botulism. The toxin of Clostriciiuln botulinum blocks the release of acetylcholine and
results in paralysis of all striated muscles. Autonomic effects include dry eyes, dry
mouth. and gastrointestinal ileus (bowel obstruction).
. H. Lambert-Eaton myasthenic syndrome (see Cl:apter 22)

,,-
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:', . " :,,!.:" ",:" .
..... :"/
1.9
'Hypothalamus
I. INTRODUCTION
. .
A.
General and function. The hypothalamus is a division of the diencephalon
that subsen'es three systems: the autonomic ner\'ous system, endocrine system, and
limbic system. The hyporhalal1lUs helps to maintain homeostasis.
B. Major hypothalamic nuclei and their functions.
:1.. The medial preoptic nucleus (Figure 19-1) regulates the release of gonadotropic
hormones from the adenohypophysis. It contains the sexually dimorphic nucleus,
the de\"elopment of which depends on testosterone l.:n:ls.
2. The suprachiasmatic 'nucleus receh'es direct input from the retina. It plays a role
in the regulation of circadian rhythms.
Paraventricular and supraoptic nuclei
regulate water balance
produce ADH and oxytocin
destruction causes diabetes insipidus
paraventricular nucleus projects to
autonomic n\lclei of brainstem and
spinal cord
Anterior nucleus
thermal regulatibn
(dissipation of heat)
stimulates parasympathetic ,NS
destruction results in hyperthermia
Preoptic area'
contains sexual dimorphic nucleus
regulates release of gonadotropic
hormones
Suprachlasmatic nucleus
receives input from retina
controls circadian rhythms
Dorsomedial nucleus
stimulation results in obesity and savage
Posterior nucleus
thermal regulation of heat)
destruction results ininability'to thermoregulate
stimulates the sympathetic NS
Lateral nucleus
stimulation induces eating
destruction results in starvation
Mamillary body
receives input from
hippocampal formation
via fornix
projects to anterior nucleus
of thalamus
c9!1tains hemorrhagic lesions
in Wernicke's encephalopathy
Ventromedial nucleus
satiety center
destruction results in obesity
Arcuate nucleus and savage behavior
produces hypothalamic releasing factors
contains DOPAergic neurons thaI inhibit prolaclin release
Figure 19-1. hypothalamic nuclei and their fUllctions. ADH :::: antidiuretic hormone; eN = cranial
lIeJ\'c; DOPA = dopamine; NS = nervous system.
1.03
d'.
rs ??'WtzUSN'7zsrrrcw'
:1.04 'Chapter 19
I
.................................................................................................................................................................................. ........................ -
. 3. The anterior nucleus pln)'s n role in tcn'ipermure regulation. It stilllul.ues tht' I
neryous system. Dcstfl.Jctilln results in hyperthermia.
4. The par.\\"entricularnudeus (Figure synthesi:es antidiuretic hOnl\\.'nt' I
(ADH), oxytocin, .... sing' hormone, It gives rise to tht'
tract, which to the neurohypophys.is. It
water babllce (conser\,ation) nnd projects directly to the llutonomic nudei of the I
brain seem and nil k\'e1,s of the spinal cord. resules in diabetes
slpidus, . .
5. The suprnoptic n.1cleus synthesi:es ADH <lnd oxytocin (similar to the para\'en-
trieular nucleus),
I
6. The dorsomedial nucleus. In an'imnls, su\'age behavior re'suIts when this
is stimulated.
7. The ventromedial nucleus is considered a satiety. center. \\lhenstimulated, it in-
hibits the urge to eat. Bilateral i:lestruccion results in hyperphagia, obesity, and sm'-
age beha\'ior,
Supraoptic nucleus
Superior hypophyseal artery
Anterior lobe (adenohypophysis)
Paiaventricular'nucleus
Third
ventricle
Arcuate. (tuberal) nucleus
Tuberohypophyseal tract

Supraoptifohypophyseal tract
Sinusoids of infundibular stem
Oxytocin
ADH
Posterior,lobe (neurohypophysis)
.'
/Hypophyseal vein
"
Inferior hypophyseal artery
Figure 19-2. The hypophyseal ponnl systcm.TI,c para,'cntricubr .md s\Jpraoptic nuclei produce nnticliurctic
hormone (ADH) and oxytocin and lranspore them rhr0ugh the suprnopticoh),l'0physcal trace to [he cnpitJary
I:<:d (I( the neurohypophysis. The nreuatc nucleus of thc infundibulum transports" ypor hOI lam ie-st irn u la [i ng hor-
m()nf.:S dH(\ugh [he traer to rhe SinU$tlids of die in(undib\lhr ::(:1\\. These si nu:;oid s the n d r;\ i [\
into die ;c'c"fHhry clpill:Jry ['\ext!' in (he ;1<kll(.fll'pol'hy.,is.
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:: :: ......
. Hypothalamus 105
................................................................... .: .......................................... -................... _ ................ : ....................................................................................................... -
8. The nrcuate (infundibular) cOllmins neurons that produce rh;,t
stimllhle or inhibit the action of This nucleus gh'es rise to
the tul-erohn'oph\'$eal tmcc, which in the hypophysl!i11rortal system
(see Figure 19-2) of the infundibulum (medium eminence). It cpnmins neurons
that rroduce dl)pamine (i.C;., prolactin-inhibiting factor).
9. The mamillary nucleus.recehes input from the hippocampal formation through
the rostcommissural fornix. It projects to the anterior ilucleus of the thalanllis
through the .tract (pare of the Papez circuit). Patients with
\X1ernicke's encephalopathy, which is a thiamine (\'itarnin B
1
) deficienc)" ha,-c
lesions in the mamillary nucleus. Lesions are also assodated with alcoholism.
:10. The posterior hypothalamic nucleus plays a role in thermal regulation (Le.,
consen'ation ,1nd increased production of heac). Lesions result in poikilother-
mia (i.e., inaHlity to thermoregulate).
1.1.. 1l1e induces eating when stimulated. Lesions
cause anorexia and starvation. .
c. 1 .... 1ajor fiber systems of the hypothalamus
:1. The fornix is the largest projection to the hypothalamus. It rrojects from the hi!=,-
pocampal fortnation to the mam.ilIary nucleus, anterior nucleus of the thalamus.
and septal area. The fornix then projects from the septal area to the hippocampal
fonnation. .
2. The medial forebrain bundle cra\'erses the entire lateral hypothalamic area. It in-
terconnects the orbitofrontal cortex, septal area, hypothalamus, and midbrain.
3. The rnamillothalamic tract projects from the mamillary nuclei to the anterior nu-
cleus of the thalamus (part of the Papez circui.t)-
4. The stria terminalis is the major pathway fr9.rr\ the amygdala. It interconnects the
septal area, hypothalamus, and amygdala.
5. The supraopticohypophysial tract conducts fibers from the supraoptic and par-
a\Oencricuiar nuclei to the which is the release she for ADH and
oxytocin.
6. The tuberohypophysial (tuberoinfundibular) tract conducts fibers from the ar-
cuate nucleus to the hypophyseal pomil system (see Figure 19-2).
7. The h ypothalamospinal tract contains direct descend ing ClDtOnOm ic fi bers. These
fibers influence the preganglionic sympathetic neurons of the intennediolateral
cell column and preganglionic neurons of the sacral parasympathetic nucleus. In-
terruption abo\'e the first thoracic segment (T-1) causes Homer's syndrome.
.. .
II. FUNCTIONS
A. Autonomic function
/'
:1. The anterior hypothalamus has nn effect on the rnrasympathetic ner-
vous system.
2. The posterior hypoth:llamus an cxcitlltory effect on the sympathetic nervouS
sys[(:m.
B. Temperature regulation
:1.. The anterior hypothalamus rL'gllhtes nnd m;)int:Jin" h0dy (L'mpcrnrurc. Destruc#
tion causes hrpcrthcrmia.
F 'W"'Tsr F7? 3M R? 7 ;; 5 7. 5 r\1;b!!:IilfW'ZiY-WW,*WST
106 Chapter 19
.......................................................................................................... __ .................................................................................................... ..... -
2. Thl! posterior hypothalamus helps to produce nnd conserve Destruction
Ciluses the tll thermoregular.e.
C. \Vater balance regulation. The paraventricular nucleus synthesizes ADH, which
controls ",<'rer excrerion by (he kidneys.
D.' Food intake regulation. Two hypoth;'llamic role in the control of ap-
petite .
. 1.; When stimulated, the,entromediaI inhibits the urge to eat.'Bilnteral
struction results in hyrerphagia. obesity. and savage behavior.
2. When stimulated, the lateral hypothalamic nucleus induces the urge to eat. De-
smlction caU5es starvation and emaciation.
, .'
III. CLINICAL CORRELATION
A. Diabetes insipidus, whicn is charaqeri:ed by 'polyuria and polydipsia. is the best
known hyrothalamic syndrome. It results from lesions of the ADH pathways to the
rosrerior lobe of the pituitary gland.
B. The syndrome of inappropriate ADH secretion is usually caused by lung rumors or
drug tI-ierapy (e.g., carbama:epine, chlorpromazine).
. .
c. is a congenitaf tumor that originates from remnants of Rathke's
pouch (see Chapter 4). This cumor'.is usually calcified. It is the most common surra-
tentorial tumor in children and the most common cause of hypopiruitarism in chil-
dren.
:1.. Pressure on the chiasma results in bitemporal hemianopia.
2. Pressure on the hypothalamus causes hypothalamic syndrome (i.e., adiposity, di-
abete.s iI)sipidus. disturbance of and somnolence).
D. Pituitary adenomas account for 15% of cliniCal symptomatic intracranial tumors.
They are rarely seen in children. \YJhen pituitary adenomas are endocrine,acche, they
cause endocrine (e.g., amenorrhea and galactorrhea a prolactin-
secreting adenoma, the most common type). .
:1.. Pressure on the chiasma re?ults 'in bitemporal hemianopia.
2. Pressu're on the hypothaIam""s may cause hypothalamus syndrome .
..'
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20
Limbic .System
L INTRODUCTION. The lil'nbic S\Hem is considered the anatomic substrate that
lies beha.'"ioral and emotional js expressed thtough the hypothalamus by way
of the autonomic nen'ous systern.
II. MAJOR COMPONENTS AND CONNECTIONS
A. The orbitofrontal cortex mediates the conscious pe.rception of smell. It has
cal connections with the mediodorsal nucleus of the thalamus. It is interconnected
through the medial forebrain bundle .with the septal area and hypothalamic nuclei.
B. The mediodorsal nucleus of the thalamus has reciprocal connections with the
bitofrontal and prefrontal cortices as well as the hypothalamus. It receives input: from
the amygdala and plays a role in affective behavior and memory.
C. The anterior nuCleus of the thalamus receives inpuc from the mamillary nucleus
through the mamillothalamic tract and fornix. It ptojects to the cingulate gyrus and
is a major link in the Papez circuit. . .
D. The septal area is a telencephalic structure. It has reciprocal connections with the
pocampal formation through the fornix and with the hypothalamus through the
dial forebrain bundle. It projects through the stria medulIaris (thalami) to the
nular nucleus.
E. The limbic lobe includes the subcallosal area, paraterminal gyrus, cingulate gyrus and
isthmus, and parahippocampal gy}Us, which includes the uncus. It c<?ntains, buried in
the parahippocampal gyrus, the hippocampal formation and amygdaloid nuclear
plex.
F. The hippocampal formation is a sheet of archicortex that is into the
parahippocampal gyrus. It functions in learning, and recognition of no\elty.
It receives major input through the enrorhinal cortex and projects major output
through the fornix. Its major structures include the following:
1.. The dentate gyrus, which has a archicortex. It contains granule cells
that receive hippocampal input and projecr/output to the pyramidal cells of the
hippocampus and subiculum. .
2. The hippocampus (cornu Ammonis), which has a archicortex. It
contains pyramidal that through the fornix to the septal area and
pothalamus.
3. The subiculum, which receives input through the hippocampal pyramidal cells. It
projects through the fornix to the mamillary nuclei and the nnterior nucleus ofehe
rhnlnmus.
:1.07

'.' ..
we ,,"=xv' 'D ma:nwr 'T' r;

I
:108 Chapter 20
.......................................................................................................... : .............................. : .............................................. I
G . The'nmygdak'id (amygdala) (Figure 1; see also Figure Z 1,1] is a b;lsal gat)
glion chm: the p.lmhiprocampal unclIs. In humans . stimuhuion causes
and signs M =,ymp;lthcdcll\ernctivicy. In other anill1:1ls. stimulation results in I
tion of nctiviry and atrenciwness. Lesions C:1use placidity nnd hypcrsexu;l
l:-ch:,wior. . . . .
1. Input is the' senSl't)' nssocitltion' cortices. olfact<;>ry bulb cmd conex, liYPl)'
thalamus and septal mea. "nd formatio.n. . .
I
2. Output is through the stria terminalis to the hypotha'lamus and septal area. Ther(
is also output [0 rhe mediodorsal nucleus of the thalamus. 1
H. The hypothalamus has reciprocal connections with the am}:gdala.
I. The limbic midbrain nuclei mid associated neu.rotransmitters include .the ventI:,,! I
tegmental 'mea (dopamine). raphe nuclei (serotonin), and locus ceruleus (nore-F'i.
nephrine).
III. THE PAPEZ CIRCUIT (Figure includes the following limb.ic structures:
I
A. The hippocampal formation, which projects through the fornix to the mamillary nu-
cleus and serral area .
B. The mamillary nucleus
Hippocampal
formation
:. "
f
-: - ' Stria terminalis
Septal area Hypothalamus

Diagonal band of Broca - - _. - -
VAFP/VAPP,
,
.
" .
Olfactory bulb and
olfactory cortex
Autonomic centers
Amygdaloid nucleus') of brain stem
Sensory association .'
and limbic cortices/
,
,
,
VAFP/VAPP
,. .

Figure 20-1.. Major conneccions of the amygdnloiJ ill/cleus. TI,is nuclells recei\'cs input frorn three major
sources: the olfactory system, semory llSsocimion and limbic cortices, and hyporhnlamus. M"jor output is through
two ch'lImcls: the (erminalis projects to the hy!'l'th:llamu5 nnJ the septal area, and the ventral <l/nyg-
dabfug,,1 p:Hhwny (VAFP) projects co the brain stem. :md spinal corJ. A smaller e(ferent bundle,
the diOl!,:(lIl:ll hand o( BrocOI, pr(ljccts co rhe sepral area. /\"(crcnr fihers (rom rhe hypo!h:il<lll)lIs ;lt1d br;lin seem en
tn the :1Illn:ch1()je! l1ucleus through the '.'cntral ;ll1lYi;lhlppct;ll [1:1thl'(;l), (\1/\[>1').
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. "" .. ;',. .;:.", ,
".',.. .',"'
",.' .... ,. to .
" .
limbic
......................................................................................................................................... -............................................................................. ..
Septal area
Mamillary body
- - - - - - - Mamillothalamic
tract
Figure 20-2. 1\tajor atT'erenc ,md efferent
cc.nnections ,,"'If the 11irpocampal f\."'ImlatiC'!\. TIl is (orma-
tion has. three c\."'ImponentS: the (cornu
Am.monis \. :,ut-iculum ... m.:l .:lemme TIle hip-
!=,ocampus rr\"'\ject:S to the seFc".l.uea. the suc-iculum pro-
jects to the mamillary nuclei. and the dencace gyrus does
not project beyond the hirr.xamral t"onnatk
1
n. TI,e
cuit of Pare: follows this route: hirrocampal (OnllatiOn
co mamill8.0 nucleus to anterior thalamic nucleus to
cingulate gyrus to emorhinal cortex to hiprocampal for-
mation.
c. The anterior thalamic nucleus
Anterior nucleus
of thalamus
!--------AnteriOr limb of
. internal capsule
Cingulate gyrus
t ----------Cingulum
Entomirial cortex
..
f -. --- ---. Perforant
pathway
Hippocampal
formation
!,
D. The cingulate gyrus (Brodmann's areas 23 and 24)
E. Ihe'entorhinal area CBrodmann's 28)
IV. CLINICAL CORRELATION
, -
--
,----- Fornix
A. Kli.iver-Buc), syndrome results .. from bilateral ablation of the anterior temporal lobes,
including the amygdaloid nuclei. It causes psychic blindness (visual agnosia), hyper'
phagia, docility (placid.ity), and hypersexuality.
B. Amnestic {confabulatory} syndrome results from bilateral infarction of the ,hip-
pocampal formation (Le., hippocampal branches of th,e posterior cerebral arteries and
anterior choroidal arteries of the internal carotid arteries). It causes anterograde am-
. nesia (Le., inability to learn and retain new information). Memory loss suggests hip ..
pocampal pathology. " ,
C. Foster Kennedy syndrome results from of the olfactory groove. The
meningioma compresses the olfactory tract and optic nerve. IpSilateral anosmia and
optic atrophy and contralateral pap,illedema occur as a result of incrensed intracranial
pressure.
D. The hippocampus is the most epileptogenic pan of the cerebrum. Lesions may cause
psychomocor attncks. Sommer's sector is very sensitive to ischemia,
E. Bilateral transection of the (ornix may cause the acute amnestic syndrome (Le., in-
ability to consoliJme short'term memory into long-term memory).
, '--
ME

110 Chapter 20
....................................................................................................................................................................................................................................
-. -'-----r--t-
B ----l.o7'--+
c-----
D------J

Figure 20-3. Midsagittal section through the
brain stetn and diencephalon showing the distri1:>u-
tion of lesions in \Vemicke's encephalopathy. (A)
lediodorsal nucleus of the thalamus. (8) Massa in-
cennedia. (C) Peri\'entricular area. (D) Mamillary
nuclei. Midbrain and pontine tegmentum. (F)
Inferior coIli<;ulus. Lesions in the mamillary nuclei
are associated with \Vemicke's encephalopathy and
thiamine (vitamin B
1
) deficiency.
F. \Vernicke's encephalopathy results from a thiamine (vitamin B
1
) deficiency. The clin-
ical triad includes ocular disturbances and nystagmus, gait ataxia, and mental dys-
function. Pathologic features include mamillary nuclei, MD nuclei of the thalamus,
and periaqueductal gray and pontine 20-3).
G. Strachan's syndrome results (rom high-dose thfa'mine (vitamin B
1
) therapy. 111e clin-
ical triad includes spinal optic atrophy, and nerve deafness.
H. Bilateral destruction or removal of the cingulate gyri causes loss of initiative and in-
hibition as well as dulling of the emotions. Memory is unaffected. Lesions of the an-
terior cingulate gyri cause placidity. Cingulectomy is used to 'treat severe anxiety and
depression.
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Basal Ganglia and Striatal Motor Syste-m
I. BASAL GANGLIA (Figure 21,1)
A. Components
:1.. Caudate nucleus
Corpus callosum
Lateral
ventricle
Caudate
nucleus
Thalamus
Internal
capsule
Claustrum
Third
Optic tract
Substantia nigra Mamillary
body
Fornix
putamen}
Globus Lentiform
pallidus nucleus
+-""",,,;;.,p..;.;.:.;,;...:,.......:;,.- Ins ul a
Subthalamic
nucleus
Lateral ventricle
Figure 21.,1.. Coronal section through the midehalalllus He the level of the mamillar}' bodies. The basal gan-
gli" me "II prominent at this include the striatum and lentiform nucleus. The :illbthnlCllnic nucleus anJ
suh:-.wntia nigra arc import"IH components of IHn(()r svstCIll. Cl\t. = centwtneJian nuclemj VA =
ventral anrerior nucleusj VL = \'cntrallatcrnl nuclells.
sa .rrr; '1W 'E" .,PXsWM'?zC"S?HwfpwtCR'sannn
I
1.:1.2 Chapter 21
............................... ... ....... :.......................................................................................................................................... I
Globus pnllidus
B. Grouping of the basal
1. The striatum consists ,-'If the caudate nucleus nnd putamen.
2. The lentiform nucleus consists of the globus pallidus an'd putamen.
3. The corpus striattim consists of rhe lentiform nucleus and caud;-t'te nucleus.
4. The claustrum lies l:-etween the lentifonn nucleus and the insular cortex. I t has
reciprocal connections between the sensory corrices (i.e., visual cortex).
II. THE STRIATAl:- (EXTRAPYRAMIDAL) MOTOR SYSTEM (see. Figure 21-1) plays
a role in the nnd execution of somatic motor nctivity, willed move-
memo It is also im'oh'ed in auromatic,stereotyped postural and retlex motor acth'ity (e.g.,
normal subjects swing their anns when they walk).
A. Structure. The :miaral motor system includes the foHowing structures:
i. Neocortex
2. Striatum (caudatoputamen, or neostriatum:)
. .'
3. Globus pallidus
I
I T
VA. VL eM
Thalamus
J. J.
T
Subthalamic -
nucleus
Neocortex
...... ,: ..... .
I
,.
Globus
paUidus

I
- Substantia
nigra
"
/
Brain stem and
spinal cord
Figure 2:1.-2. ;., lajm afferent and effcrent conncction; of the striatal systcm. The striatum receivcs In;-ljor in
put from Ihrcc :,\\urccs: the thaL"l\lIs, ncocortex, ;mJ .... !,,;., .. ,;., lIigl . Till: projects to the globus pal.
lidus and nigra. TIlc globus p"lIiJus is thc effector nuclcus of the striatal systcm; it projects to the thal-
amw; and suhth.tI<llIlic nucleus. The nigra also projects to the The striatal motor system is
rhn'lI!.:h rhe corricohllll';)f ;1Ilt! cortico.'r,in:ll tracts. ("':I\j c,i1trnll1c,li:1Il nucleus; GADA o=: -y-
;l(i-i; V/\ =, \":!lU;t! ;ulterior VI. c. "c:lf'.': '-"" .. , .. : .. -
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: ..
:'.,
. .. .... , "
..
. .....
. ,- .
.. .
.:.',
. Basal GangHa and Striatal Motor System' U3
. .
..................................... , ........................................... _._ .................................................................................. .................... ........................... -
4. Subthalamic nucleus
5. Substantia nigra . pars compacrn :lIld rericularis)
6. Thalamus \'cmmllateml, and centromedian nuclei)
B. Figure 21-2 shows the major afferent and efferent connections of rhe striatal system.
C. Neurotransmitters (Figure 21-3)
.
III. CLINICAL CORRELATION
A. Parkinson's disease is a degenerati"e disease that affects the substantia nigra and its
projections to [he striatum.
1.. Results. Parkinson's disease a depletion of dopamine in the substantia ni-
gra and striatum as well as a loss of melanin-containing dopaminergic neurons in .
the substantia nigra. .
2. Clinical signs are Fradykinesia: srooped posture, shuffling gait, cogwheel rigidity,
,pill-rolling tremor, and masked facies. Lewy bodies are found in the melanin-
containing neurons of the substantia nigra. Progressive supranuclear palsy is
associated with Parkinson disease.
. 3. Treatment has been successful with L-Dopa. 'Surgical inten'entlon includes palli-
dotomy (rigidity) and \'entral t?alomotomy (tremor).
Thalamus
GLU
Neocortex
GLU
Brain stem and
1-----_1
spinal cord
1 // results in Huntington's disease)
T,
r--""":"'---;r' S. nigra:
GLU .. ... .-. Dopamine
.. :. Compacta "1-- (Destruction restJltsin
ACh--:-.,:::, .. ,.: ... ,. Reticularis t--Parkf':'son's disease)
G)
r-
e:.
Subthalamic
GLU
c;) c;) \ GABAISP
):.):. \
\
sg ./ \
, "
.. - - - (Lesions found here
in Wilson's disease)
.. ,
nucleus
GJ.obus
pallidus
GABA '-----.--...,',.....,
(Destruction results
in hemiballism)
.
,
(lesions found
in kernicterus),
Figure 2:1-3. M,lj(lr neurmransmicters of the srriacnl motor systelll. \Vithin the srriaCllIl1, globus pallidus, and
pars rcticularis (.\f the nigra (5. nigra), -yaminohutyric aciJ (GADA) is the predominant neurotrans-
miner. GABA may c(lcxist in the samc neuron with enkerhalin (ENK) or slIhswncc P (SP). Dopamine-
containing nellWn5 arc fi.lllnJ in the pars compacta of the substantia nigra. Acetylcholine (ACh) is found in the
)(}Cal circuit nCliWIlS oi the MriaCllm. Thc subthalnmic nuck-lls projects excit:Hl'ry glllt:lminergic fibers to the
globus palliJlIs. GLU = gllltamate.
-
. {. r',: .
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114 . Chapter 21
I
...... ................................ ......................................................................... _ ......................................................................................... ...
B. parkinsonism. MPTP is nn anakll-! I
of destrors neurons in ,the subscmlcia nigm.
C. Huntington's .'10 inherited autosomal dominant movement dis-
that is traced tl) .. l single gene Jeect 01\ chromosome -to I
:1.. Ie is associated with degeneration of the cholinergic and y-aminobutyric acid
(GABA)-ergic neurons of the striatum. It is'accompanied by gyml mrophy ill the I
fronml and temrl..'\t"".lliobes.
. .
2. Glutamate excitotoxicity. GLU is released in the strintum and'binds tO,its recercors
on srrinml neurons resulting in an action rotenral. OLU is removed from the extra- I
cellular space by astTocytes. In Huntington's disease OLU is bound to the N-methyl-
O-asrartate recertorresulting in nn influx of cakium ions and subsequent
cell de.ath. This cascade of e\'ents with neuronal death most likely occurs < I
bro\'ascular accidents (e.g., stroke).
3. choreiform mm:ements, hypotonia, progressive de-
mentia.
D. Other choreiform dyskinesias
:1.. Sydenham's chorea (St. Vitus' dance) is the most common cause of chorea over-
all. It occurs primarily in girls, typically after a' bout of rheumatic fever. ' H.
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2. Chorea gravidarum usually occu,rs during the second trimester of pregnancy. Many
patients have a history of Sydenham's chorea.
E. Hemiballism is a movement disorder that usually resuh:s from a vascular lesion of the
subthalamic nucleus. Clinical signs include violent contralateral flinging {ballistic}
movements of one or both e'xtremities.
F. Hepatolenticular degeneration {\Vilson's disease} is an autosomal recessive disorder
that is caused by a defect in the metabolism of copper. The gene locus is on chromo-
some 13. /. .
:1.. Clinical signs include choreiform or athetotic mqvements, rigidity, and wing-
beating tremor. Tremor is (he most common neurologiC sign. .....
2. Lesions are found in the lentiform nucleus. Copper depQsition in the limbus of
the cornea gi\'es rise to the corneal Kayser-Fleischer ring, which is a pathogno-
monicsign. Deposition of copF'er in the liver leads to cirrhosis.
3. Psychiatric symptoms include psychosis, personality disorders, and dementia.
. 4. The diagnosis is base'd on low ::erull1 ceruloplasmin, ele\'ated urinary excretion of
co}:,per, and increased copper cLw\cenu(ltion in a Ihoer biopsy specimen.
S. Treatment includes penicillamine. a .. .':'
G. Tardive dyskinesia is a syndrome l1( repetitive choreic movement that affect the face
and trunk. It results from treatment with phen9thi:lZines, blir.yrophenones, or meta-
c1opramidc, ,,/
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22
Neurotransmitters
I. IMPORTANT TRANSMITTERS AND THEIR PATHWAYS
A. Acetylcholine is the l"najor of peripheral system, neuromus-
cular junction, parasympathetic nervous system, preganglionic sympathetic fibers, and
postganglionic sympathetic fibers that inneryate sweat glands and some blood vessels
in the ske letal muscles {Figure 22-1}. Acetylcholine is found in the neurons of the so-
matic and visceral motor' nuclei in the briin- steni and spinal cord. It is also found in
the basal nucleus of Meynert; which degenerates in Alzheimer's disease.
B. Catecholamines. Figure 22-2 shows [he biosynrher.ic pathway for catecholamines. Epi-
nephrine, although a catecholamine, plays an insignificant role" as a central nen'Ous
system neurotransmitter. In the body, epinephrine is found primarily in the adrenal
medulla. In the central nen'ous system, ic is restricted to small neuronal clusters in che
brain stem (medulla),
1.. Dopamine (Figure 22-3) is deplered in with Parkinson's disease and in-
creased in patients with schizophrenia. Dopainine is found in the arcuate nucleus
of the hypothalamus. It is the prolactin-inhibiting factor. Its two major receptOrs
are DI and D
2

Acetylcholine (ACh)
Nucleus basilis of Meynert in forebrain
(Alzheimer's disease)
Cranial nerve, motor neurons, and
preganglionic parasympathetic neurons
Spinal motor neurons
Autonomic preganglionic neuro'ns
Local circuit neurons
in striatum (caudatoputamen)
Hippocampal formation
Figure 22-1. of acetylcholine-containing neurons and their ;lxona\ projections. The basal nu-
cleus of Mcynert project!; to the entire cortex. This nuclells degenerates in patients with Alzheimcr's Jisease.
Striatal acetylcholine local circuit neurons Jegcncratc in p;tticnts with HlIntington's disease.
-..
116 Chapter 22
.......................................................................................................................... _ ............................................................................... .
Phenylethanofamine N-methyl transferase
Figure 22-2. Synthesis of catecholamines from
rhenrhllanine. Epinephrine, which is derh'ed from nc'r-
epineFhril)e, is found primarily in the adrenal medulla.
Epinephrine
. - ..; -'
a. Dl receptors are postsynaptic. They activate adenylate cyclase and are exci-
taton.
b. D., are both postsynaptic and presynaptic. They inhibit adenylate
q:Clase and are inhibirory. Antipsychotic drugs block D2 receptors.
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2. N ore'pinephrine (Figure 22-4) is the transmitter of most postganglionic sympa- I
therie neurons. Antidepressant drugs enhance its transmission.
a. Norepinephrine plays a role in'anxiety states. Panic attacks are belie,-ed to re-
sult from paroxysmal discharges from the, locus ceruleus, where norepineph- I
rinergic neurons are found in [he highesc'concemration. postsynaptic re-
ceprors of the locus ceruleus pathway are /3
1
or /3z receprors that activate
adenylate cyclase and are excitatory. -,' I
Dopamine
Limbic cortex (cingulate gyrus
Mesoliriibic tract (mesocortical tract)
Septal nuclei
Arcuate (tuberal) nucleus of hypothalamus
Substantia nigra of midbrain
Corpus callosum
Striatum (caudate
nucleus and putamen)
Nigrostriatal tract
Ventral tegmental
area ot midbrain
r:;r..,.....-:::.....- Cerebellum
Pons
Medulla
Figure 22-3. Distrihutioll o( dopamine-containing neurons anJ t".ir projectiolls. Two major nsecnding
dopnminc pathways nrbe in the midhrnin: the trnct (rl111l the nigra and thc Il1csolirnhie
traer (rom the tcglllcllt;d are:l, [n patients with Parkinson's disea>c, of dOp'1fllillcrgic neurons occurs
in the nij;r;, ;llld the \'(:l1tr;d ;l/C;], 1\')p;lfI1incq;ic (rum ,he ll\lC!cUS of ,he
1 I' f - ,- 1! -- - I I '
ttl 1,\\: r'l;!r.d (d r I il1.)!O!r
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Neurotransmitters
, ,
...... " .. .,. .............................................................. - ....................... __ ...................................................................................................... .
Norepinephrine (NE)
Thalamus
Hippocampal formation
Septal nuclei
i
r-i--f--4_
-
Cerebellar cortex
Locus ceruleus of pons and midbrain
Figure 22-4. Distributi,-'n ,-,f n,-'rerinerhrine-colltaining neurons and their projections. The k..,cus
\ :-.'caced in che and is [he chief $(lurce of noradrenergic fibers. The locus ceruleus rrojeccs c,-"\ ;;;11
;:- "rrs of the central :\'Hem.
b. catecholamine hypothesis of mood disorders scates thac reduced noreFi-
neFhrine acth'iry is related to depression. and that increased norepinephrine
activiry is related to mania.
C. Serotonin [5,hydroxytryptamine (5-HT)] is an indolamine (Figure 22-5), Serotonin-
containing neurons, are found only in the raphe nuclei of the brain stem,
i. The permissh'e serotonin hypothesis that when 5-HT activity is reduced,
decreased le\'els of catecholamines cause-,depression and insomnia. In addition.
when 5-HT activity is increased, elevated levels of catecholamines cause mania,
Dysfunccion of 5-HT may underlie obsessive-compulsh'e disorder.
2. Certain antidepressants increase 5-HT availability by reducing its reuptake. 5-HT
agonists that bind 5-HTI.A. and those that block 5-HT
2
ha\'e antidepressant
erties. Fluoxerine is a selective serotonin reuptake inhibitor (SSRl).
D. Opioid peptides (endogenous opiates) induce responses similar to those of heroin and
morphine. '
i. Endorphins incluqe l3-endorphin, which is the major endorphin found in the
brain. It: is one of the most powerful analgesics known (48 times more potent than
morphine). Endorphins are found exclusivelr in [he hypothalamus.
.. .,' ";."
2. Enkephalins are the most widely distributed and abundant opiate peptides. They
are found in the highest concentration in the globus pallidus. Enkephalins coex-
ist with dopamine, ),-aminobutyric acid (GABA), norepinephrine, and acer:'I-
choline. They arecolocalized pallidal neurons, and they playa role
in pain suppression.
3. Dynorphins follow the oistribtftion map for cnkephalins.
E. Nonopioid neuropeptides
1.. Substance P plays a role in pain transmission. It is most highly concentrated in
the substantia nigra. It is lllso found in the dorsal root ganglion cells and substan-
tia gelatinosa. It is colocalizcJ with GABA in the striaronigr:11 tract and pbys a
role in movement dIsorders. Substance P levels nrc reduced in patients with
Huntington's disease.
.
".,0=5'
-"1
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118 Chapter 22 .
.................................................................................................... _ ................ : ............... ;............................................................ ,
Serotonin (S-HT)
Hippocampal formation'
Cerebellar cortex
Septal nuclei
Hypothalamus,
Raphe nuclei in
midbrain, pons, and medulla
Tryptophan
+ Tryplophan-5-hydroxyJase
, 5Hydroxytryptophan
+ .Aromatic L-amino acid decarboxylase
Serotoniri '.
Figure 22-5. Distritution of j.hydroxytryptamine (seroronin).containing neurons and their projections.
Serotonin'comaining neurons are found in the nuclei of the raphe. They project widely to the forebrain. cere
,bellum. and spinal cord. The inset shows the synthetic pathway of serotonin.
2. Somatostatin (somatotropin-release inhibiting factor), Somatostatinergic neu
rons from the anterior hypothalamus project,c.heir axons to the median eminence,
where somatostatin enters the hypophyseal portal system and regulates the release'
of growth honnone and thyroid-stimulating honnone. The concentration of so-
matostatin in the neocortex and hippocampus is significantly reauced in patients
with Alzheimer's disease. Striaml levels are increased in patients
with Huntington's disease.
F. Amino acid transmitters
1.. Inhibitory amino acid transmitters "
a. GABA (Figure 226) is the major inhibitory neurotransmitter of the brain. Pur
kinje, stellate, basket, and GoJgi cells of rhe cerebellar cortex are GABA-ergic.
(1.) GABA,ergic striatal neurons project (0 rhe globulus pallidus and sub-
stantia nigra. , .' .
(2) pallidal neurons project to "the thalamus.
(3) GABA,ergic nigral neurons project ,to the thal;lInus.
(4) GABA receptors (GABA-A :md ,GABA.B) are intim(l[ely associated
with bemodiazcpincbinding sitci'Bemodimepines enhance GABA ac
, -
tivir}'.
(a) GABA-A receptor:; open chloride channels.
(b) GABA,B receptorS ;ue found on the terminals of neurons that usc
another transminrr(Le., dopnmine, serotonin).
Activntion of GAllAB receptors decreases (he release of the other
transmitrer.
b. Glycine is the m:ljor nClirorr:lmmiHcr of! he spin:'!! cord. I ( is used
hv th(: fZen')h;)w cells of thf:!,iln! corel.
,
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," . ..': .
.' ..
. : . .,
Neurotransmitters' 11.'
............................. ........................................................................................................................................................................................... .
-y-Aminobuty.ric acid (GABA)
local circuit GA8A neurons local circuitGABA neuron
Pallidothalamic traCt
Striatum
Globus pallidus
HypothaIamocortical tract
StriatonigraJ tract
circuit GABA neurons
....... Nigrothalamic tract
Cerebellar nuclei
Hypothalamus
. Substantia nigra (pars reticularis)
. . ,
Lateral vestibular nucleus
,,-=-- Cerebellar cortex
Purkinje cells of
cerebellar cortex
Figure 22-6. DistributiL'll1 ot' -y-aminobutyric acid (GABA)-containing neurons and their projections.
GABA-ergic neurons me the maj0r inhibitory cells of the central nervous system. GABA local circuit
are found in the neocortex. hipF0.::ampal formation. and cerebellar cortex (Purkinje cells), Striatal
neurons project (0 the 'thalamus and subthalamic nucleus {not sho\\n}.
2. Excitatory amino acid transmitters
. Glutamate
a. Glutamate (Figure is the major excitatory transmitter of the brain.
Neocortical gluramatergic neurons project to the striatum, subthalamic nu-
cleus. and thalamus.
(:1) Glutamate is the transmitter of the cerebellar granule cells.
(2) Glutamate is also the transmitt:er'of nonnociceptive, large, primary af-
ferent fibers that enter the spinal cord and brain stem.
(3) Glutamate is the transmitter of the corticobulbar and corticospinal
tracts .
Pyramidal neurons of neocortex
Cortieostriatal fibers --f-----\
Fornix
Pyramidal cell of
. hippocampal formation
Granule cells of
Septal nuclei
cerebellar cortex
Cortieobulbar and corticospinal
Proprioceptive fibers in dorsal roots
Figure 22-7. Disniblltion o( glutamate,containing neurons and their projections. Gllltamate is the major
c;o;ciwtory transmitter of rhe central nervous sysrcm. Cllrricalghumn<lccrgic neurons projecr to the striatum. Hip-
pocampal and 5uhiclll"r glutumatcrgic neurons project through th!: fornix to the septal arca and hypothalamus.
The cdls o( the cerehellllrn arc

- - - I
775 T "N'
120" Chapter 22
....................................................... ................................................... -......................................................... : .................................... -.
b. 'llll.tjl'r excit:1{I.
'
ry transmitter of the bmin. is the transmitter of the:
climbing hl--ers the ,erd't;lIl1lll. Neurons of climbing fibers are fopnd il1,[h\! .
inferh..)f l,li\'at), nudell$.
c. Beha\'ior.ll corrdation .. GIUt:lllli1te, through. its N-methyl-D-a5parrare
(NMDA) receptors. plays a rule in .Iong-term potentiation (n memory
process) .. otlltnmatc plays n .role in kindling and sub'-
sequent sei:ure ncti\'ity. Under certain conditions. glutamate and its analogs
are neurotoxic. '.. .
d. Glutamate excirotoxicity. GLU is re1ensed in the striatum nnd binds ro its re-
ceptors t,)t\ $triaml resulting in an action potential. GLU 'is removed
from the extracelluhlr space by asrrocyres. In Huntington's disease GLU
bound to the N-methyl-D-aspartate (NMDA) receptor resulting in nn influx
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. of calcium ions.and subsequent cell death. This cascade of events with neu- .1
ronal demh most occurs in cerebrovascular accidents (stroke).
. .-
3: Nitric 'oxide is a rece'ntly discQ\'e.red gaseous neurotransmitter thai: is' produced
when nitric arginine to citrulline.
a. It is located in the olfactory system, striarum, neocortex, hippocamral forma-
tion. supraoptic nucleus of the hypothalamus, and cerebellum"
b. -Nitric oxide is resronsible for smooth Il!uscle relaxation of the corpus ca\'er-
nosum and thus renile erection. It is also believed to playa role in memory
formation because of its long-tenn potentiation in the hippocampal forma-
tion. In addition. nitric oxide functions as a nitrovasodilator in the cardio-
vascular system.
II. FUNCTIONAL AND CLINICAL CONSIDERATIONS
A. Parkinson's disease results from degeneration of the dopaminergic neurons that are
round in the pars compacta of the substantia nigra,. It causes a reduction of dopamine
iIl the striatum and substantia nigra (see 21 III A).
B. Huntington's disease {chorea} results from a loss of acetylcholine- and
containing neurons in the suiatum (caudatoputamen). The effect is a loss of GABA
in the striatu'm and substantia nigra (see Chapter 21 III C). <
C. Alzheimer's disease'result:; from the degeneration of cortical neurons and cholinergic
neurons in the basal nucleus of Meynert. It is associated with a 60% to 90% loss of
choline acetyluansferase in the c,erebral cortex. Histologically, disease is
characterized by the presence of neurofibrillary tangles, senile (neuritic) plaques,
. amyloid substance, granulovacuolar degeneration, and Hirano bodies.
D. gravis results (rom autoantibodies against the nicotinic acetylcholine re-
ceptor on skeletal muscle. These ant:bodies block the postganglionic acetylcholine
binding site. Thymic cells augment B-ccll producdon of autoantibodies. The cardinal
manifestation is fatigable weakness of the skeletal muscle. The extraocular muscles,
including the levator palpebrae, are usually invoh'.ed. Edrophonium or neostigmine
jection is used (or diagnosis. .
/
E. Lambert,Eaton myasthenic syndrome is CC1\JSCJ by n prcsynaptic defect of acetyl-
choline release. It causes weakness in the limb muscles, but not the bulbar muscles.
Fifty percent of cases are associated :with neoplasms (i.e., lung, brc<1st, prostatc). In
these paticnts, muscle strength imprm'cs wirh lISC. ]n contrast, in patients with my3s-
thenia gn\\'is, muscle usc results in muscle fatiguc, and autonomic dysfunction includes
Jry mouth. constipation, impotcnce, and urinary incontinence.
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... '
. ... ',
.. "",
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23
Cerebral Cortex
I. INTRODUCTION. TIle cerebral cortex. the thin. gray co\'ering of both hemispheres of
the brain. has two the neocortex (90%) [he allocortex (10%). Motor cortex is
the (4.5 mm): visual cortex is the thinest (1.5 mm).
II. THE SIX-LAYERED NEOCORTEX. Layers II and IV of the neocortex mainly af-
ferent (i.e., receidng). Layers V and VI are mainl); efferent (i.e., sending),
A. Layer I is the molecular layer.
B. Layer II is the external granular layer.
C. III is the external pyramidal layer. Ie gives rise to association and commissural
fibers and is the major source of corricocortical fibers.
D. Layer IV is the internal granular layer. It receives thalamocortical fibers from the
thalamic nuclei of the ventral tier (i.e., ventral posterolateral and ventral posrerome-
dial). In the visual cortex (Brodmann's area 17-),',layer IV receh'es input from the lat-
eral geniculate body. '".
E. Layer V is the internal pyramidal layer. It gh'es rise to corricobulbar. corticospinal.
and corticostriatal fibers. It comains the giant pyramidal cells ofBeq, which are found
only in the mowr cortex (Brodmann's.are'a 4), .
F. Layer VI is the multiform layer. It is the major source of corticothalamic fibers. It
gi\'es rise to projection, commissural, and association fibers.
./
III. FUNCTIONAL AREAS (Figure 23-1)
A. Frontal lobe
i. The motor cortex (Brodmann's area 4) and premotor cortex (Brodmann's area 6)
are somalOtopically organized (Figure 23-2). Destruction of these areas of the
frontal lobe causes contralateral spastic paresis, Contralateral pronator drift is as-
sociated with frontal lobe lesions of the tract.
2. Frontal eye field (Brodmann's area 8). Des'truction causes deviation of the eyes to
the ipsilateral side. ,/
3. Broca's speech area (Brodmanll's areas 44 and 45) is located in the posteribr part
of the inferior frontal, gyrus in the dominant hemisphere (Figure 23-3). Destruc-
tion results in expressivc, nonfluent aphasia (Broca's aphasia). The patient under-
stands both writcen and spoken Iangu:lge, but cannot articulate spcech or write
normally. Broc"a's aphasia is lIsually associated with contrnlaternl facial and arm
wcakness bccause of the in\,ohcmcnc of the motor strip.
4. Prefrontal cortex (f3rodmann's areas 9-12 anJ 46-47). Destruction of the ante-
:l21
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'. . . ';',; .. , ...
:0',:' ": : ".; :-to: . ,
. .
, :1.22 Chapter 23
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A
Primary motor cortex ,(4)
. ' . \
\
Frontal eye field (a) ,
Broca's speech area of
left hemisphere (44, 45)
B
Secondary somatosensory ;'
and gustatory cortex,
I
Primary auditory cortex (41, 42) I
Prefrontal cortex
(9, 10, 11,12)"
Primary motor cortex (4h
\
\
Septal area"''''
limbic lobe I I
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Primary olfactory cortex (34)
,
,
,
I.
. .
,Primary somatosensory cortex (3, 1, 2)
I
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" ",Vestibular cortex (2)
'"
..;, Visual association
J cortex (39, 19, 18)
- Primary visual cortex (17)
'Auditory association cortex (Wernicke's
speech area of left hemisphere) (22)
I Primary somatosensory cortex (3, 1, 2)
I .

" / Somatosensory association
I cortex (5, 7)
I
- Limbic lobe
?' Visuarassociation
cortex (19, 18)
"Uncus (28)
Primary visual cortex (17)
, ParahipP:>campal gyrus
/
Figure 23-1. Some motor ;and semory areas of the cerebral corcex. (A) lmeral com'ex surface of the hemi-
sphere. (B) surt:lCC of the hemisphere. The refer (0 the Brodmann brain map (I3rodrnann's areas).
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....... .. ..
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-;'\0,. "'''
'.
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. ., .. .....
Cerebral Cortex :12:
... , ............................................ ; ................. " .............................. ...:. .................. __ ................................................................................... .
A Sensory homunculus
r
J
Figure 23-2. The sensory and motor homunculi. (A) Sensory representation in [he postcentral gyrus. (8)
representation in the precentral gyrus. (Reprinted with permission from Penfield W, Rasmussen T: The
Cerebral Coreex o{l'dan. New York, Hafner, 1968, pp. 44, 57.)
rior of the frontal lobe conv.exity results in deficits in concentration,
orientation, abstracting ability, and problem-solving ability. Other
frontal lobe deficits include loss of initiative, inappropriate behavior, release of
sucking and grasping reflexes, gait apraxia, and sphincteric,. incom:inence .. De-
struction of tb:! orbital (frontal) lobe results in inappropriate social behavior (e.g.,
use of obscene language, urinat'ing in public). Perseveration is associated with
frontal lobe lesions.
B. Parietal lobe
:1.. The sensory cortex (Brodmann's areas 3, I, and 2) is somacotopically organized
(see Figure 23-1); Destruction results in contralateral hemihypesthesia and aster-
eognosis.
2. The superior parietal lobule (Brodmann;s areas 5 and 7). Destruction results in
contralateral astereognosis and sensory neglect.
3. The inferior parietal lobule of the donlinant hemIsphere. Damage results in
Gerstmann's syndrome, which following deficits:
a." Right and left confusion ,-
b. Finger agnosia .
c. Dysgraphia and dyslexia
d. Dyscalculia "
e. Contralateral hemianopia or lower quadrantanopia
4. The inferior parietal lobule of the nondominant hemisphere. Destruction results
in the following deficits:
a. TopogrClphlc memory loss
n

---
124 23
........................................ : ............................................. : ............................................... , ..................................................................... .
.- -...
- ..
Motor cortexyocalization (6, 4)
Broca's speech area (44, 45)
(Broca's aphasia)
Arcuate (superior longitudinal) fasciculus
aphasia)
gyrus (39)
Visual association
cortex (18, 19)
Primary visual cortex (17)
We micke's speech area (22)
(Wernicke's aphasia)
Figure 23-3. Cortical areas of the dominant hemisphere that play important role in language production.
The image! of a word is projected from the \'isual cortex (Brodm:mns area 17) to the visual association
cortices (Brodmann's areas 18 and 19) and then to the angular gyrus (Brodmann's area 39), Furtherprocessing
occurs in \\1emicke's speech area (Brodmann's area 22), \\:here the auditory form of the word is recalled, Through
the arcuate fasciculus, this information reaches Broca's speech area (Brodmann's areas 44 and 45), where moror
sFeech Frograms control the \'ocali:ation mechanisms of the precentral gyrus. Lesions of Broca's speech area,
\Vemicke's sFeech area, or the arcuate fasciculus result in dysphasia, ,
b. Anosognosia
c. Construction apraxia (Figure 234)
d. Dressing apra.,<ia
e. COI.1tralateraI sensory neglect
f. Contralateral hemianopia or lower -quadrantanopia ,,"
C. Temporal lobe
", '
+-
,
/
A B.
C
Figure 23-4. Testing (or construction apraxia. (A) TIle patient was askcJ (0 copy the (ace 0(" clock. (8)
The paticnt was a!'>kcd to bisect a horiwll(:11 linc, (C) TIle patient W;JS llskeJ to copy a cross. Tllcse drawings
contr;dareral neglect. The rc.\ponsih1c lesion is (OUI10 in the nondOlllill;mt (righe) p;Hiecnl lobe. A left
IWlT1i;lI1()pia, hy itself. docs not in C(IIHLlhceral !!t'!:l--cr_
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\.,
.
.
. ," .:. ..
"!.., , ..... " ...,.
. ..
... ...
, .
\ .1: . :.,-: .... :: . ..
I ,"

.;. " .. .. -,
". Cortex, l.25 .
........ : ........................................................................................ _ ..................................................... ,: ....... -.............. _ ..................................... ; ................. -
A
Right Mmiplegia
,
Head and eyes tumed to t,he kllt ,
Frc:>ntallobe syndrome:
Inappropriate
social behavior
Loss of initiative
Release,o/sucking
and grasping
reflexes
Gait apraxia
Sphincteric
incontinence
Broca's .-
expressive aphasia ", I
Anosmia (left side) I
Right upper
,
B Lett hemihypesthesia, and astereognosis,
and agraphesthesia. '.
Left astereognosis, astatognosis,
and sensory neglect._
\ --
of nondominant \
inferior parietal lobule: \
Topographic
memory loss
Anosognosia
ConstnJetion
apraxia
Dressing apraxia
Contralateral
sensory neglect
Left hemianopia
Left hemianopia'"
Auditory inattention to / ,./'
the left (hemineglect)" Prosopagnosia
(bilateral leSions)
\
I
',Right hemihypesthesia, .
I astereog!,oSis, and agraphesthesia
'" Right astereognosis, astatognosis,
and sensory neglect
!\
Gerstmann's syndrome:
_ _ {Rightlleft confusion
, - - Dysgraphia
- -..., _' _ . Finger agnosia
- - Dyscalculia
, " 'Right hemianopia
,Lett hemiplegia
I
- Visual agnosia
(dyslexia)
- Right hemianopia
I Head and eyes tumed to the right
. '
Frontal lobe syndrome:
Inappropriate
social b9havior
Loss of
ReleaSe of sucking
and grasping reflexes
Gait apraxia
Sphincteric incontinence
'\
... Motor dysprosodia
. 'Anosmia (right side)
'Left upper quadrantanopia
\ Sensory dysprosodia
c
9on!ralateral spastic paresis in leg area
1\
Inappropriate
social behavior .----
Uncinate fits.
with olfactory hallucinations" I
K1UverBuey I
, syndrome ..
I
"Contralateral hypesthesia in leg area
" Contralateral sensory neglect
Contralateratlower
quadrantanopia
_. Contralateral upper
quadrantanopia
I Defective memory
consolidation (usually bilateral lesions)
Figure 23-5. Focal destructivc hemispheric lesions ,lIllllhe re,mlting symptoms. (A) Laternl convex surface
of the dominant left hemisphere, (0) Lateral wnvex surfi\(c ll( thc nOllllOlllinant right hemisphere. (C) Medial,
,,( the nondominalH
" EX en :eXlm"" 'm = -Wee=
zs en am
126 . Chapter 23 .
.......................................................................................................................................................................................................................
Stereognosis \

language center
Calculation
t.;x2 =8
R-
Major hemisphere
. Field 01. vision
Simple language
comprehension ../
Temporal crescent
Minor hemisphere
Transected corpus cailosum
.-
,/
Figure 23-6. Functions of the split brain afcer minseccion of the corpus callosum. Tactile and visual percep-
ti .. 'n is projected w the contralateral hemisrhere, olfaction is perceived on the S<1me side, and audition is per-
c<!ived predominancly in the opposite hemisphere. 1l1e left (L) hemisphere is dominant (or language. The right
(R) hemisphere i$ dominant for spatial construction and nonverb:l! ideation. (Reprinted with permission from
:\"'t-ack CR. Demarest R): The HI/man Nen'ollS System. Malvern. PAt & Febigcr. 1991, p. 416.)
, ,.-' ,"0'"
1. The primary auditory cortex (Brodmann's areas 41 and .12). Unilateral destruc-
tion results in slight loss of hearing. BilateraL loss results in cortical deafness.
. /
2. \Vemickc's speech area dominant h{misphere is found in the posterior
of the superior temporal g)'rus (Brodmnnn's aren 22). Dcstruction resulcs in recep-
tive, fluent aphasia (Wernicke's aphaSia), in which the pmicnt cannot understand
any form of bnguage. Spcech is sponrancous, fluent, and rnpid, but makes
sensc.
3. Meyer's loop (sec Chapter 17 II F 2) consists of the visual radiations that project
to the inferior o;)nk of the cnlc;)rine sulcus. Interrupt ion Cluses COn t r;) Ia rer;) I up-
qu"Jrant:mopi" ("pic in the sky").
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.. ':)
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-. j, '"
" " .' Cerebral (:ortex 1.27
......................................................................................... : ........................ , .................................................................................................. -
.4. Olfa<:tory bulb, t&.lct, and primary cortex (Brodmann's area 34). Destruction re-
su.lt:s in ipsilmt'ral nn.,)s\l,ia. An.irrimtivc lesion (psychomotor epilepsy). of the .un-
cus in ,-,If'lct\)ry anJ gustnrory hallucinations. .
a. Olfactory groove men"ingionms comrress the 'olfactory tract and bulb result-
ing in nn'-':Hnia. See Kennedy syndrome Chapter 13 I C,
b. Esthesioneuroblastom.l$ (olfactory neurobl"stomas) arise from bipolar sen-
sory cells \-"If the (llfacrory mucosn; they can extend through the cribriform plate
imo the at"lterk"lr crn"nial' fossa. Presenting symptoms are similar to Foster
Kennedy syndrome ..
5. Hippocampal cortex -(archicortex). Bilateral lesions result in the inabiiiry to con-
solidate shorr-teml memory into memory. Earlier memories a're retrievable.
6. The anterior temporal lobe, including the amygdaloid nucleus. Bilateral damage
resulrs in syndrome, which consists of psychic blindness (visual ag-
-nosia), hyperphagia, docility, and hypersexuality.
7. Inf.eromedial occipitotempo'ral cortex. Bilareral.lesions result in the in.ability to
recogni:e faces (prosopagnosia). .
.
D. Occipital lobe. Bilateral lesions cause cortical blindness. Unilateral lesions cause con-
tralateral hemianopia or quadrantanopia.
IV. FOCAL DESTRUCTIVE HEMISPHERIC LESIONS AND SYMPTOMS. 23-
5A shows the symptoms of lesions in. the -dominant hemisphere. Figure 23-5B shows the
symptoms or lesions in the nondominam hemisphere.
V. CEREBRAL DOMINANCE is determined by the Wada test. Sodium amobarbital
(Amy tal} is injected into the carotid artery: If the patient becomes aphasic, the anesthetic
was adminiscered to the dominant hemisphere.'
A. The dominant hemisphere is usually the left It is responsible for propo-
sitional language (grammar, syntax, and semantics), speech, and calculation.
B. The non dominant hemisphere is usually the right hemisphere. It is responsible for
three-dimensional, or spatial, perception and nonverbal ideation. It also allows supe-
rior recognition of faces. . ....
. ,"
Figure 23-7. Chimeric (hybrid) figure of n
used to examine the hemispheric function of COlll-
missurotomized patienrs. The patient is" instructed to
fixate on [he Jot nnd is asked to describe what he sees.
If he says that he sees [he fnce of a man, then the left
hemisphere predominates in vocal tasks. Ifhe is nskcJ
to point to the fnce nnd he points to the womnn, then
the right hemisphere predominates in pointing tasks.
: .-.-
'; "". . I
".'e
W
] eO OW12'.$
'PP'
1.28 Chapter 23
......................................................................................................................................... , ..................................................................... .
VI. SPLIT-BRAIN SYNDROME (Figure 23-6) is a syndrome ihm. results
(rom transection of .the corpus .callosum. .
A. The dominant hemisphere is better :It vocal naming. .
B., The mute hemisphere is bener at pointing to a stimulus. A person can,
not name objects thm are presented to the nondominant visual c-ortex. A blindfolded
person carmot n'ame' objects that are presented to the nondominant sensory
through touc.h.
C. Test (Figure 23-7). A subject views a composite picture of two half,faces (Le., a
chimeric. or hybrid. figure). The right side shows a man; the left side shows a woman,
The picture is remO\ed. and the subject is asked to describe what he saw. He may re-
spond that he saw a man, but when asked to point to ,,,hat he he points to the
, .. .
woman.
D. In a patient who has alexia in the.left visual field,.the verbal symbols seen in the right
Yisual cortex have no access to the' language centers of the left hemisphere,
VII. OTHER LESIONS OF THE CORPUS CALLOSUM
A. Anterior corpus callosum lesion may result in mutism or tactile anomia.
B. Posterior corpus callosum (splenium) lesion may result In alexia'without: agraphia,
C. Callosotomy has been successfully-used to treat "drop attacks" (colloid cyst of third
\'entricle).
BRAIN AND SPINAL CORD TUMORS (see Chapter 5)
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'. " . . '. .. .
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.24
Apraxia, Aphasi'a, and Oysprosody
I. APRAXIA is the inability to rerfonn.motor acti\'ities in the 'presence of intact and'
sensory systems and normal cl)n1rrehensh::m.
A. Ideomotor apraxia is the inal-ility, in response ro a \'erbal command, ro perfonn
tor acti\'ity thm can rerformed with ease spontaneously (e.g . sticking oue the
rongue). This condition is associated with a les;ion in the dominant hemisphere.
B. Ideational apraxia is the inal-ility to rerform a n1ulristep activity or demonstrate the
use of a real object (e.g .. rool): This condition is associated with a lesion iri the
inant hemisphere. .
C. Construction apra.'Xia is the inability to draw or construct a geometric figure (e.g . the
face of a clock). If the patient draws only the right half of the clock. this condition is
called hemineglect. and the lesion is located in the right inferior parietal lobule (see
Figure .
D. Gait apraxia is the inability to use the lower properly. The patient has difficulty
in lifting his feet from the floor. a frontal lobe sign seen with normal pressure
cephalus (gait apraxia, dementia, incontinance) .

II. APHASIA is impaired or absent communication by speech, writing, or signs .(Le., loss
of the capacity for spoken language). The lesions are located in the dominant
sphere. Associate the following symptoms and lesion sites with the appropriate aphasia
(Figure
A. Broca's (motor) aphasia
:L Lesion in frontal lobe. in the inferior frontal gyrus (Brodmann 44.45)
2. Good comprehension
3. Efforrfu I speech
,
4. Dysarthric speech
5. Telegraphic speech
/
,
6. Nonfluent speech
7. Poor repetition
8. Contralnrerallower facial and upper limb weakness
B. \Vcrnicke's (sensory) aphasia
1. Lesion in posterior tempor:lllobe. in rhe superior temporal gyrus (Brodmann 22)
2. Poor comprehension
1.29
1.30' Chapter 24
..................................................................................................................... ..................................................................................... .
. Fluent
speech
Nonfluent
speech
. Good
comprehension .
Conduction
. aphasia
Broca's

Transcortical
motor
aphasia
Poor
comprehension
Wernicke's
aphasia
Transcortical
sensory
aphasia
Mixed
transcortical
aphasia
Figure 24-:1.. ll1e "aphasia square" makes it easy to differentiate the six most common "national board"
aphasias. Broca's, conduction, and Wernicke's aphasias are all characterized by poor repetition. (Adapted with
rermission from Miller], Fountain N: Neurology Recall. Balrimore, \Villiams & \Vilkins, 1997, p. 35.)
3. Fluent 5I='eech
4. Poor reI='eririon
5. Quadrantanopia
6. Paraphasic errors
a. Non sequiturs (L. does not follow) are statements irrelevant to the question
asked. .
b. Neologisms are words with no meaning.
c. Driveling speech
C. Conduction aphasia
1.. Transection of the arcuate fasciculus; the arcuate (asciCLI Ius interconnects Brod-
mann's speech area with \Vernicke's
2. Poor repetition
3. Good comprehension
4. Fluent speech
D. Transcortical motor aphasia
:1. Poor comprehension
2. Good repetitinn
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';/---: .
" ..
. :. :: ' .. :. . ....
. .
. .
. ,
'.. . .. .
. .. '. Apraxia, .Aphasia, and Oysprosody 1.31.
............. .." ............................... ;, ................................................ : .................................................................................. ; ............................. -
3. N\.lntluenr spc\.'ch
. E. Transcortic<ll mixed <lphasia
1.. ' comprehension
2. Good repetition
3. Nl1nt1uenr speech
F. Transcortic<ll sensory aphasia
:1.. PI.Xlr comprehension
2. Good repetition
3. Fluent speech
G. Global aphasia results from a lesion of the-perisylvian area, which contains Broca's and
Wernicke's areas. Global aphasia combines all of the symptoms of Broca's and \Ver- .
nicke's aphasias. : . .
H. Thalamic aphasia is a dominant thalamic syndrome. It closely resembles a thought
disorder of patients with schizophrenia and chronic drug-induced psychosis. Symp.-
tOms include t1uent paraphasic speech with nonnal comprehension and repetition.
. .
I. Basal ganglia. Diseases of the basal ganglia may cause aphasia. Lesions of the anterior
basal ganglia result in nontluent aphasia. Lesions of the posterior basal ganglia result
in fluent aphasia.
J. \Vatershed infarcts are areas of infarction in the boundary :ones of the anterior, mid-
dle, and posterior cerebral arteries. These areas are vulnerable to hypoperfusion and
thus may separate Broca's and Wernicke's speech areas from the surrounding cortex.
These infarcts cause the motor, mixed, and sens<;>ry transcortical aphasias.
III. DYSPROSODY is a nondominanr hemispheric language deficit that serves propositional
language. Emotionality, inflection, melody, emphasis, and gesturing are affected.
A. Expressive dysprosody results from a lesion that to Bros:a's area, but is lo-
cated in the nondominant hemisphere, Patients cannot express emotion or inflection
in their speech.
. B. Receptive dysprosody results from a lesion that corresponds to \V'ernicke's area, but is
located in the nondominant hemisphere. Patients cannot comprehend the emotion-
alityor inflection in the speech they hear.
/
,.
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Cranial Nerve
I-::-Olfactory
II-Optlc
II/-Oculomotor
Parasympathetic
Motor
IV-Trochlear
V-Trigeminal
Motor
Sensory
VI-Abducent
type.
SVA
SSA
GVE
GSE
GSE
SVE
GSA
GSE
'.
Appenc;fix: Table o(Cranial Nerves
Origin
Bipolar olfactory
neurons' (in
olfactory
lium in roof of
nasal cavity)
Retinal ganglion cells
EdingerWestphal .
nucleus (rostral
midbrain)
Oculomotor nucleus
(rostral midbrain)
Trochlear nucleus
(caudal midbrain)
Motor nucleus CN V
(mid pons)
Trigeminal ganglion
and mesencephalic
nucleus CN V
(rostral pons and
midbrain)
Abducent
(caudal pons)
.. Function
Smell (olfaction)
Vision
Sphincter muscle
of iris; ciliary
muscle
Superior, inferior,
and medial recti
muscles; inferior
oblique muscle;
levator palpebrae
muscle
Superior oblique
muscle
f!1uscles of masti-
cation and tensor
tympani muscle
Tactile, pain, and
thermal sensation
from the face; the
oral and nasal
cavities; and the
supratentorial dura
Lateral rectus
muscle
Course
Central axons
project to the
olfactory bulb via
the cribriform plate
of the ethmoid bone.
Central axons con-
verge at the' optic
disk and form the
optic nerve, ...... hich
enters the skull via
the optiq canal. Optic
nerve axons terminate
in the lateral
geniculate bodies.
Axons exit the
midbrain in the
interpeduncular
fossa, traverse the
cavernous sinus,
and enter the orbit
via the superior
orbital fissure.
. Axons decussate in
superior medullary
velum, exit dorsally
inferior to the
inferior colliculi,
encircle the mid-
brain, traverse the
cavernous sinus,
and enter the orbit
via the superior
orbital fissure.
Ophthalmic nerve
exits via the
superior orbital
fissure; maxillary
nerve exits via the
foramen rotundum;
mandibular nerve
exits via the fora-
men ovale; ophthal-
mic and maxillary
nerves traverse the
cavernous sinus;
GSA fibers enter the
spinal trigeminal
tract of eN V.
Axons exit the pons
from the inferior pon-
tine sulcus, traverse
the cavernous sinus,
and enter the orbit
via the superior
orbital fissure.
(appendix cont.)
:1.33
. " ~ ~ " ' ' ' - , 4 ... 4'
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.--
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. _ l.3S
........................................................................... _--_._ ........................................... -..................... __ ............................................. _ .. ..
Cranial Nerve TyP!!
X-Vagal .
Parasympathetic GVE
Motor SVE
Sensory- GSA
Sensory
Sensory
XI-Accessory
Motor (cranial)
Motor (spinal)
XI I-Hypoglossal
GVA
SVA
SVE
GSE
. Orfgln
Dorsal nucleus of
CN X (medulla)
Nucleus ambiguus
(mid-medulla)
Superior ganglion
(jugular forameD)
Inferior (nodose)
ganglion (in
jugular foramen)
Inferior (nodose)
ganglion (in
jugular foramen)
Nucleus ambiguus
(medulla)
. Ventral horn
neurons Cl-C6
Hypoglossal nucleus
(medulla)
Function.
Viscera of the
thoracic and
abdominal cav-
ities to the left
colic flexure
(via terminal
(mural) ganglia]
Muscles of the
larynx and
pharynx
Tactile sensation
to the external ear
Mucous membranes
of the pharynx,
larynx, esophagus,
trachea, and
thoracic and
abdominal viscera
to the left colic
flexure
Taste from the
epiglottis
Intrinsic muscles
of
(except the crico-
thyroid muscle)
via recurrent
laryngeal nerve
Sternocleidomastoid
and trapezius
muscles
Intrinsic and extrinsic
muscles of the
tongue (except the
palatoglossus
muscle)
Course
Axons exit (motor)
and enter (sensory)
medulla fr9m the.
postolivary sulcus;
axons exit and
enter the skull via
the jugular for&
men; GSA fibers
enter the spinal
trigeminal tract
of CN V; GVA and
SVA fibers enter
.the sotitary tract.
Axons from the cranial
division exit the
medulla from the
postolivary sulcus
and join the vagal
nerve; axons from
spinal division exit
spinal cord,
ascend through the
foramen magnum,
and exit the sKull
via the jugular
foramen_
Axons exit from the
preolivary sulcus
of the medulla
and exit the
skull via the hypo-
glossal canal.
SVA = special visceral afferent; SSA = special somatic afferent: GVE/= general visceral efferent; GSE = general so-
matic efferent: SVE = special visceral efferent; GSA = general somatic afferent; GVA = general visceral afferent;-CN
= cranial nerve.
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.. '.
Illdex
, ,


.. .'
.0 ........................................................................ 0 ......................... 0 .......................................... ofO" 0 ............................................ 0 .......... .
lwlic page numb$!rs Je$ignatl! tlgurl:!:': p.1gs: folkm'ed by "t': designate cables; (see also) refers to relate
topics or more demiled c\'"'\pic Tl'pics h,l\"ing more than one subentry nre listed under the noun [e,g
BoJy (bodies): carociJ]" - _
Abducent nerve (CN \'1) (see linda Cr.mial nerves)
nerye (CN Xl) (see IInd.:r Cranial nen'es)
Accommodation, ocular. 66-67' --
Acetylcholine. 98, 113-. 115
Acoustic neuron)a (5chw,mn0111a). 33. 34. 60,
81-82
Agnosia
linger, 123
\'isual (dyslexia), 125
Alar (sensory) Flate, 24. 2-1, 25
:\b:heimer's disease, 32. 115, 115, lIS
-y-Aminobutyric acid (GABA), 85. 89. 113, 114,
117, 118, 119
Amyotrophic lateral sclerosis (ALS, Lou Gehrig's
disease),46
Anencephaly (meroanencephaly), 26. 27
Aneurysm, 67, 74
Angiography
carotid, 18, 19, 20,21
cerebral blood suprly. 18-19.20.21.22
digital subtraction, 19. 21-22
"ertebral. 19, 21
Anosmia, 66, 125
Anosognosia, 124
Aphasia, 129-131, 130
basal ganglionic, 131
Broca's. 121,125, 129 ,-
conduction, 125. 130
global, 131
thalamic-, 131
transcortical mixed, 130
transcortical mocor, 130-131
transcortical scnsory, 131
Wernicke's, 125, 125, 129
Apraxia, 129
construction, 124, 124. 129
dressing, 124
ideational, 129
ideomotor, 129
Al\ueJlIcr.II stcnosis, 28, 29
Arachnoid granulation, 9
ArgyllRobcrtson pupil, 95,96
ArnlllJChiari malformation, 28, 29
125
Asrrocytes, 31-32
Astrocytoma, 34, 87
cerebellar, 34
Ataxia, Fr(edreich's, 48
Auditory 58-60
auditOry pathway, 58, 59
-hearing defects, 58-59
Autonomic nervous system, 98-102, 99, 100,
, (see also Hypothalamus; Limbic
system)
Axonal transport, 31
Basal ganglia, 111-112, 131
Basal (motor) plate, 24,25
Bet! pyramidal cells, 42
Bloodbrain barrier, 32
BloodCSF barrier, 32
Blood 15-23 (see also Angiography and
-,.- specific \'essels)
of internal capsule, 18, 90, 90
internal carotid system, 15, 16, 16-17
middle meningeal artery, 19,._22,23
spinal cord and lower brain stem. 15, 15
thalamic, 90
\'eins, 18
venous dural sinuses, 18
\'ertebrobasilar system, 15, 17-18
Body (bodies) (see also Nucleus [nuclei])
carotid,72
Co\\'dry type A inclusion. 32
geniculate
lateral, 49, 89,89,90, 91, 93 (see also Cranial
ner\'es: II (optic) 91)
medial, 49, 89,89, 90
Hirano, 32 --
ju)taresti(orm, 61, 62"
Lcwy, 32, 113
mamillary, 1,2.6,7,50, 103, 105,109
medial geniculate, 52, 58, 59, 81
Negri,32
pinellI, 1, 49
trapezoid, 51, 58, 59
Botulism, 102
l3rain rumors. 28. 33-34, 82, 84, 87
1.37
M"
:1.38 Index
,,,-el
'tc'r 7 nu.mOM' ....
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I
Brolin tlllmlT:l-CC;l1Iil1f(cJ
.l.: .. 'u:ttic "euwllla ,U-_H. $1-82
. 34, 87
"hltterfly glil,ma"
rr;lin 'lhl'ccss. 34
c:h .. 'roiJ plexus parillolllil:l. 33
C:l,lIl.)iJ cyst l,f third ventricle, 33
cr&li,iophnryngiomas. 2S. 34
33-34.87
genninomct pineal region. 34, S0
di .. "lblnscoma mulciforme, 33, 34
rontine. optic. 7, 34
34
33-34
33-34'
l"lligodendroglioma. 34
pituitary adenoma. 34
34
Broca's aphasia. 121. 129
Brodmann's areas, 122
Cauda equina. 37
Ca\-emous sinus. 57
Central pontine myelinolysis. 84
connections. 85-86
syndromes, 87
rumors. 87
Cerec-ral coreex function, 121-127
fronrallobe, 121-123
limbic. 107-110
parietal lobe. 123-124
temporal lobe. 124
oCcipitai lobe, 127
sFlit-brain sydrome. 127-128
Cerehospinal fluid (CSF), II, 11 t, 31
Chorea
gra\'idarum, 114
Huntington's, 113. 114. 117, 118
Sydenham's (Sc. Vitus' dance), 114
Choroid plexus. 34
Cortex
allocortex, 121
archicortex, 127
encorhinal, 109
neocortex, 121
piriform, 66
Corti, organ of, 58, 59
Cranial nen-es, 65, 133-135
alx!ucent (VI), 65,67,68-69, 133
acccssory (Xl). 65, 68. 69,135
acoustic (VIII), 58-60,65, 134
cochlear (VlII), 58.60,65, 134
facial (VII), 65, 69-71, 133
(IX), 65, 72-74, 133
hypoglossal (XII). 65.76-77,135
inccrlllcJiacc (VII), 65, 69,70
()culolll(lwr (III). 65. 66. 67. 133
(J!/'ac[ory (I). 65. 66.13,
'lJlfic (II). 65-66,91. 97. 133
:-l'in.,1 accessory (XI). 65, 75, 135
trigcn\in;,[ (V). 53. '55"':'57,67.63. 133
rrochleM (IV). 65. 67. 133
\-aeal (X). 65. 74-75. 135
\cstibulilr (YJIl). 61. 64-65.71.72,134.
\mibull"ICochlear (Vlll) .. S8, 64-65, 71. 134
Cnmiopharyngoll\<l. 27. 28. 34
Crest, neural, 24, 25-26
Crista amrullaris. 61
D.mdy,Willker malformation, 29, 29

conduction, 58
nerve'(sensorineural, 59,68
Diabetes 104, 106
Dura mater, 8, 9, 22, 23
Duret hemorrhage, 12
Dynorphins. 117
DyscaI01lia, 123
Dysdiadochokinesia. 87
'. Dysequilibrium. 87
Dysgraphia, 123 -
. Dyskinesia. cardh-e, 114
. Dysle.'ria.I23, 125
D),smeuia, 87
Dysphasia, 88
Dysprosodia (dysprosody), 125. 131
Dysmymmokinesia. 87
DySS)nergia. 87
Oys[a.da, SO.' 7
Endorphins; 117
Epend)"tnoma, 33,87
Eye fields
trontal,94-95, 121
occipital,95
, -
Facial nerve (CN VII) (see Hnder Cranial nerves)
Fetal alcohol syndrome, 29
Filum cemlinale, 9
Finger agnosia, 123
Foster Kennedy syndrome. 66, 109
Friedreich's awxia, 48
Gait apraxia (dyscaxi;1). 86 '
),aminobutyric acid (GABA), 85, 89, J 13, 114,
117,118,119
Gcnninomi 34, 80
GlanJ{s)/
pineal. 1.2,5
pituitary (hypophysis). 2, 3. 27. 27, 28,57
'Gliohbstoma Inultiforme. 33, 34
Glomus. calcified. 14
ncrve (CN IX) ,Older Cr;lIlial
nerves)
Glut;lIll:JCC, 119. 119, 120
118
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Br
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." .
. ., .. '
.> .". ,-
.. ... '. "::'
'. :
........
lndex 139
.......................................................................................................................................................................................................... -
HenJ tilting: 67
He.tring dcfc-ccs, 58-59
/
criJuml,8, 13, 14. 2Z
suWuml, 8,13, 23
Hemianeschesi;l, 67, 73-74, 80
97
Hemianopia
91
bitemporal. 91, 106
with macular sparing, 18,91
Hemiballism, 113, 114
Hemihypesthesia. 125
Hemiparesis (hemiplegia), 125
'alternating a1:-ducent, 68
ipsilaterial, 97
spastic, 82 .
Hepatolenticular degeneration (\Vilson's disease).
113, 114 .
Herniation
cerebral. 11-14
hippocampal gyrus. 12
interyertebral disk. 48
suHalcial. 12
tonsillar (transforaminal). 12
transtentorial (uncal), 12, 66. 97
Hippocampal formation. 107. 108, 109,115, 117.
118
Hippocampus (cornu Ammonis). 4. 6.107
Sommer's sector of, 109 )"
Hirschsprung's disease (megacolon), 101
Holoprosencephaly. 29
Hydranencephaly. 29
Hydrocephalus. 10. 29
Hyperacusis, 71
Hypesthesia, 125
Hyperphagia. 109.127
Hyperreflexia, 56
Hypersexuality. 109, 127

Hypoglossal ner\'e (CN XII) (see under Cranial
ner\,es)
Hypophysis (pituitary gland), 3.27,27.28. 104
anterior lobe, 104
posterior loc-e. 104
Hypopituitarism. 106

Hypothalamus, -H. 93.98,103. 103-106.104, 108.
117. 118
Hypotonia. in cerebcllar disease. 87
Internal capsule. 90
anterior limb of. 90
genu of, 90
posterior limb"t)f .90
jugular foramen $yndromc, 82-83
Knyscr-Fleischer ring. 114
(nucle.lr j;llIndicc), 113
Kerl\n!t:m's notch, 12, 97
LlInina tcn.nin"lis, 1
Lentiform nuclells, 112
limbicsY$tcm,107-11O,lOS,L09
Lipofuscin granules, 32
LMN (lower mowr neuron) lesions, 45,45-46,
46
Ll'lCUS ce.ruleus. J 16. 117. .
Medial forebrain brnin bundle. 105
Megnco\on (Hirschsprung's disease), 101
Meninges. 8-10
8-10
bacterial. 9-10
viral. 10
. 28
Methylphenyltetrahydropyridine (MPTP) induced
parkinsonism, 113
Meyer's loop. 9/, 92. 125
cells}. 26, 32
Mulciple sclerosis, 48, 80
Myasthenia gravis. 120
Myelination, 26
M yot:l.ctic reflex. 37
Neural crest, 24,25-26
Neuropathy
vitamin B
1
, 105, 110. 110
vitamin 47
Neuropore ..
anterior; 26
posterior, 26, 26
Neurotransmitters. 115-120 (see also specific sltb-
stances) " :.:
. acetylcholine. 115
aspartate, 120
dopamine, 116
dynorphins. 117
endorphins. 117
enkephalins. 117
GABA,IIS
glutamate. 119
glycine. lIS
nitric oxide (NO). 101. 120
norepinephrine. 117
serotonin, 117
somatostatin. 118
substlnce p. 117, 118
incestinal polypeptide (VIP). 101
N issl substance, J 1
Nucleus (nuclei)
abducent. ofCN VI. 51. 79
ambiguus.50. 51,73. 75. 78,79
amygdaloidclIs. 3, 6,108. LOS. 127
arcuate (infundihular). 103. 105
arcuatc (tuberal) hypoth;'damic, 104, 116
h;lsal o( Ml'YIll:rt, 115. 115
':140 Index
.............................................................................................................. _,--_ ........................... : ....................... -.................... ,.
(nudd)-Concinuc:J
vestibular (hori:ontal), 63
3. 4, 5, Ii. 42. 55. 90, III, III, il6
cr""h,l nerve nuclei
"",fCN III
94
m"'[,,'r. 52, 66
",fCN IV, 50
l,fCN V.51, 54
:tensory, 54
mesencephalic. 55-56
111(1[\."lr. 54
spinal,55
",fCN VI. 51
VII, 51,68-70
l'fCNVIII' .
59
\'es[i!:-ular, 50-51. 61-61 .
IX
ambiguus, 75

ambiguu:s, 50, 73
ofC;-.J XI
'ambiguus, 75
spinal accessory, 75
of XII
hypoglossal, 76, 7S
cuneate. of medulla, 39
dentate, 86, 89
globus Fallidus, 111-111
gracile, of medulla, 39
of inferior colliculus. 1
hYFOthalamic, 116
lentitonn, III
mamillary, 6, IC8 (see also Body; mamillary)
niger. III
olivary
interior. 50, 61
superior, 58,59
para\'entricular of hypothalamus, 104
phrenic, 37
preOFtic, 103
pretectal of midbrain, 94
putamen, 111
raphe, 116, 117
red, 6, 52, 81,86,
ruber, 6, 52,81,86
septal, 109, 116-118
solitarius (of solitary cract),
subthalamic, 4. 17. 113, J J 3
$uprachiasmiatic. 103
supraoptic, J 04
thalamic, 88-89, 107, 109
Nlllethyl.D-asparcate (NMDA) receptors, 120
Nystagmus, 72,80
caloric, 63.63
87
I'ostrot;ltory (horizontal), 63
in 64
Oculomotor nen'e'(CN Ill) (see under nerws)
. Oltaaorynen'e (CN I) (see underCmnial nerves)
65, 66
Oligodendrocyees. 32 .
.. Opeicncn'e (eN 11) (see undcrCmninl nerves)
Otic pbcoJe, 61 .
Otieis media. 58
Ocosdcrosis.58
Oxrtocin. 104, 104
Pa Ilidocomy, 113
Pape: cirt:uie, 109
Papillcdc:ma (ch:oked disk). 97
Parkinsoosdisease, 113. 115. 116
rersevttation,123 .
Pia.arachnoid, 8
Polyomyditis, 45--46
PolYncurltis, acute idiopathic (Guillain Barre syn.
drome),48
Postinfectiouspolyneuritis (Guillain.Barre syn.
drome). 48
Presbycusis,59
Prolactin-inihibiting factor, I1j
Pronator drifr, 121
ProsopagIlOSia, 125
Pseudorumor cerebri, 30
Ps},chicblindness, 109, 127
Ptosis. 66, 82, 95,97
Pupil
Argyll.RobertSon, 95, 96
fixed dilated, 97
relam'e afferent (Marcus Gunn), 95, 97
Purkinje cd!, 85-86
Pyramidal tract, 42-44
Quadrantanopia ("pie in the sky"), 91,123,124,
125, 130
93
RllffiUS (rami)
communicating. of autonomic nervous system, 98
graymJ whiCe:communic<lting, 36, 36
Raphe nuclei; 118 .'
Rathkespooch,27:27
Raynaufs disease, 102
Retlex{cs} .-
carociJ sinus, 73, 75
como( 55, SSe, 67, 6S, 71,80
gag (faucial), 73
, jaw j<:tt (masseter), 56,56, 56t
myotxlic, 36, 37
pupilbty light (.\('I! emnial nerves; II (optic)
91 )
Redn.1.91
Rinne tcSf, 60
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Index 1.41
: " : ............................ -:................................. " ............................. ': ; - : "! ::
S.tccuic. ('II. 62
Schwanl\ 3.!
Schwann\.lma (ClCllll:'[ic "J3. _,4, 60
SCllcllm.t. 91
(5-hydrl'xycrYrmmine, 5-HT), 117, i 1 S
Signs
"Babinski's, 44
Kemh:s.9 .
- t- I d . 70 --
.. Inu:'es. ,-l c le ura, _ J I
Srina l->itlJa, 26-28
Spinal c,-"rJ. 2,8,36-48. 1I6, U7
supply, 15, 15
COIUF'-"nems, 36-37
lesk",:,. 45-48 (sa also sp<!dfic encici.:s)
l)f Olllcor neurons .1n..:1 corticosrinal rraers. 45,
, 45-46,46. .
l111)tl..
l
r/sensory comHned, 47--f8
reripheral ner .... ous. syscem (PNS), 47
senSllr)' pachway. 46. 4 I .
!-,ositional changes in de\-elopmem. 27
tracts of. 38-44 (see dso Tract[s])
Stral:-i:m1ll.:S. 69, SO
Striae medullares, ..;9
Stria terminalis,1C5, lOS
Striatum. 112-113. 115-116, 118-120
Subdrural hematoma, 8, 13,23
Substance P, 113, 117
Substantia nigra, 4,6,7.17,52,81,89,112,113,
113,116, 119
Sydenham's chorea (St. Vitus' dance), 114
Syndromes
amnestic (confabular)-)' 109
anterior spinal arter)', 46-47
anterior \"ermis, 87
Anton's, 84
Arrroid-Chiari, 28
Argyll-RobertSon pupil. 95, 96
Balint's, 84
Benedikt's, 80-81
Brown Sequard (spinal cord hemisection), 46-47
Central pontine myelinolysis, 84
crocodile tears, 71
\V'alker, 29
dorsal midbrain (Parinaud's), 80, 95, 95
facial colliculus, 49, 80
fetal alcohol, 29
Foster Kennedy, 66, 109
{rontal lobe, 125
Gerstmann's, 125
Guillain Barre, 48, 71
Horncr's, 47, 79,80,93,95,97,102,105
of inappropriace ADH secretion (SIADH), 106
internuclear ophthalmoplegia, 80, 96
jugular (oramcn, 82-83
Kluvcr-Buey, 109, 127
bmhcrc-E.icon myaschenic, 102
lateral inferior pontine, 80
later"l medullary (PICA), 78,79
.,-
"locked-in," 83-84
medial inferior pontine, 79, 79-80. .
Illedial longitudinal fasciculus (MLF, internuclear
ophthalmoplegia), 80, 96, 96 . .
incJial inedulbry, 78
medial midbrain (Weber's), 82
Mobius, 71
.Illyesrhenia gravis, 120
. of nondominant inferior parietal lobule, 125
one-and-a-half, 96
paramedian midbrain (Benedikt's), 80:-81
PICA, 78 .
poliomyelitis, 45-46
posterior vermis, 87
pupillary light, 95
Riley-Day (familial dysautonomia), 101-102
Shy-Drager,I02 .
.' . Strachan's, 110
subclavian steal, 83., 84
"cop of che basilar," 84
Weber's, 81
Werdnig-tIoffinann, 46
Wernicke-Korsakoff,88
Wernicke's encephalopathy, 110
. Syringomelia, 47-48
Tabes dorsalis, 46
Tanycytes,32
Tardi\'e dyskinesia, 114
Thalamus, 1, 2,4,5,13, 17,39,41,42,49,62,
113,113, 117, 119
blood supp,ly, 90
internal capsule, 90, 90 (see also Capsule: internal)
major nuclei and connections, 89
Thiamine (vitamin B
1
) deficiency, lOS, 110, 110
Tic douloureux (trigeminal neuralg\.a), 56, 68
Tracts (see also Pathway[s]) - .
corticobulbar, 52,73,76,81, 119
corticospinal, 12, 38, 42,45,45-46,46,47,51,
51,54,78,79,82,86,119
dentochalamic,81
descending sympathetic, 79
dorsal column-medial lemniscus pathway, 38-40, 39
geniculocalcarine {see also Cranial nerves: II (op-
tic) 91)
Homer's, 78
mamillorhalamic, 89, 105
o!(acrory, 50,65, 127
optic, 4, 6, 7, 17, 89, 91 (see also Cranial nerves:
II (optic))
solitary, 50, 69
nucleus of, 78
spinocerebellnr, dors;l\, 38
spinothnlamic, 38, 47, 51, 79, 80, 81 , 89
Iareenl,78
spillocrigcrnin:ll, 50, 51,5 J , 68, 79, 79, 80
:;upral'pticohypophyscal, 104, 105
lrigcminoth:1lamic, 53-55,55, 89
. ". " . '.
"
.142. Index
...................................................................................................................................................................................................................................
Tmccs-Canrinl,c:J
wherohYlXlph)'$clll, 104
vcsribulo$pinal. lateral. 38
Tmnsp<Jrt. mCl.lll'll, 3 I "
Trigcminal nervc.(CN V) (see linda CranialnC'n"c:;)
Trigeminal neum)gia, 56
Tremor. intentic:lO $i
staric. resting (Parkinson). 113 .
Trochlear nen'e (CN V) (see lI11d("T Cmninl ner"e:;)
Tuning fork tests. 59, 60t
Ulcer. reptic, 102
Uncal (transtemorial) hemiation. 11. 66, 9i
Upcinate fits. 125 .
Uncus. 6.7 "
UPMN (upper motor neuron) lesi(lm. 45.45-46.46
Urinan" bladder: 100
61. 62
Uvula. i3
Vagus ntn'c (CN X) (see Imder Cranial nerves")
Vasoacrt\"e intestinal peptide (VIP), 101

V,-,ntric1e$. 8, 9
thnlnmocomy.llJ
V""nico, n. 80
VC$(ibular "ystem, 61-64
VC'$cibuk'IC(lchlenr nerve (CN VllI) (see under
Cntninl nerves)
Vi$\I;l1 91-92 "
Vi::ual system, 91, 9-1-97, 93-96
Yit;llllin Bb neuropathy, 47" ,
Vic.lmin BI (thiamine) deficiency, 105. 110.
110
Wallerian degeneration. 31
W:uershel.finfarccs, 131
\X'er-er's re:lt. 60 .
\Vernicke's encephalopathY.- 103. 105
,Wernicke's (fluent) aphasia. rz5
Wernicke's speech area, 125
Wernig-Hof{man disease. 46
\\lllite and gray communicating rami, 36, 36
\Vilson's disease (hepatolenticular degeneration),
lB. 114
,-
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