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Myelomeningoceles and Meningoceles: A Clinicopathologic Study of 43 Cases

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J.Neurol.Sci.[Turk]

Journal of Neurological Sciences [Turkish] 31:(2)# 40; 335-345, 2014

http://www.jns.dergisi.org/text.php3?id=776
Research Article

Myelomeningoceles and Meningoceles: A Clinicopathologic Study of 43 Cases

Pinar KARABAGLI1, Tugba GURCAN1, Zeliha Esin CELIK1, Hakan KARABAGLI2
1
Selcuk University, School of Medicine, Pathology Department, Konya, Türkiye 2Selcuk
University, School of Medicine, Neurosurgery Department, Konya, Türkiye
Summary
Objective: The purpose of the study both meningocele and myelomeningocele reviewing the
clinical and pathological findings as well as to discuss the pathological diagnosis.
Material and methods: Meningocel and myelomeningocele were retrived from the
pathology files. Forty three cases with detailed clinical and radiological data were selected.
Masson's trichrome performed on original sections from paraffin blocks. All sections from
each case were reviewed.
Results: There were 34 cases of myelomeningocele, 9 cases of meningocele. F/M ratio was
1.2 to 1. The age range of patients were from newborn to 4 months. 90% of cases were in the
lumbosacral region. 31 cases of myelomeningoceles, and 3 cases of meningoceles were
hydrocephalus. Chiari II malformation was seen in 88% of myelomeningocels and in 22% of
meningoceles. Three patients had a clubfoot deformity. Microscopically, epithelial changes
included ulceration, loss of appendages. Mesodermal findings included fibrosis (90% of
cases), adipose tissue (62%), hypertrophic smooth muscle (18%), skeletal muscle (4%) and
increased numbers of blood vessels (79%). Subepidermal calcification was noted in 2 cases.
Neuroectodermal features, neuropil-like matrix and ependymal lining were noted in 34 and 15
cases respectively. Nerve fibers were identified varied from easily identifiable large
myelinated nerve trunks to slightly increased numbers of fibers in 83% of the cases.
Conclusion: Both clinical and pathological differences were seen among myelomeningoceles.
These malformations involve ectoderm, neuroectoderm, and mesoderm. Definition of the
pathological aspects of dysraphism will potentiate the understanding of these anomalies.
Key words: Myelomeningocele, meningocele, pathology, Chiari II malformation, Clubfoot
deformity

Miyelomeningosel ve Meningosel : 43 Olgulu Kliniko-Patolojik Bir Çalışma

Özet
Amaç: Çalışmanın amacı, meningosel ve miyelomeningosel olgularının klinik ve patolojik
bulgularını gözden geçirmek yanında patolojik tanıyı tartışmaktır.
Gereç ve yöntem: Meningosel ve miyelomeningosel patoloji dosyalarından elde edilmiştir.
Detaylı klinik ve radyolojik verileri bulunan kırk üç olgu seçildi. Masson trikrom boyası
olguların parafin bloklarına uygulandı. Elde edilen tüm kesitler incelendi.
Bulgular: 34 miyelomeningosel, 9 meningosel olgusu vardır. Kadın /erkek oranı 1,2-1'dir.
Hastalar yenidoğan ile 4 ay yaş aralığındaydı. Olguların % 90'ı lumbosakral bölgede
yerleşmişdi. 31 miyelomeningosel ve meningosel olgusunda hidrosefali vardı. Chiari II
malformasyonu miyelomeningosellerde % 88 ve meningosel olgularında %22 oranında
görüldü. Üç hastada içe dönük ayak deformitesi vardı. Mikroskopik olarak, epitel
değişiklikleri ülserasyon ve deri eklerinin kaybı idi. Fibrozis (vakaların % 90'ı) , yağ dokusu
(% 62), hipertrofik düz kas (% 18), iskelet kası ( % 4) ve kan damarlarında sayıca artış (% 79
) mezodermal bulguları oluşturdu. Subepidermal kalsifikasyon 2 olguda tespit edildi.

335
J.Neurol.Sci.[Turk]

Nöroektodermal özelliklerden nöropil benzeri matris ve ependimal yapı sırasıyla 34 ve 15

olguda saptandı. Sinir lifleri vakaların % 83'ünde, hafif artmasından, kolayca farkedilebilen
büyük miyelinli sinir gövdeleri oluşturmasına kadar çeşitli şekillerde görülmüştür.
Sonuç: Miyelomeningosel olguları arasında hem klinik hem de patolojik farklılıklar görüldü.
Bu malformasyonlar ektoderm, nöroektoderm ve mezoderm içermektedir. Disrafizmin
patolojik yönlerinin tanınması bu anomalilerin anlaşılmasını güçlendirecektir.
Anahtar Kelimeler: Miyelomeningosel, meningosel, patoloji, Chiari II malformasyonu, Club
foot deformitesi

subcutaneous mass(25). OSD comprises

INTRODUCTION
Dysraphic conditions of the spine resulting
from non-closure of the neural groove
consist of several different types of
malformations, are called spina bifida(2).
The lesions of spinal dysraphism (SD) are
formed by combined malformations of the
vertebral column and the spinal cords.
There is still a considerable confusion as to
their classification. Most classifications are
strictly based on the specific derangement
of embryonic development. Spina bifida
(SB) had been classified into several
types(20). (1) SB cystica which refers to
either myelomeningocele (MMC) or
meningocele (MC). MC involves
herniation of the dura and arachnoid
through a defect in the vertebral lamina,
with the spinal cord remaining within the
spinal canal. In the MMC, the spinal cord
and nerve roots become components of the
herniated cystic structure. (2) SB aperta,
which involves lesions communicating
with the environment(25). SB occulta,
which manifests as a concealed form of
spinal dysraphism with few cutaneous
stigmata of the underlying spinal
anomaly(2,20). A recent classification of
spinal dysraphism was proposed by
Tortori-Donati et al.(25). In this
classification, not only the clinico-
neuroradiological correlations but also the
importance of almost every lesion has been
linked with the embryological
(20)
aspects .Essentially, dysraphic anomalies
are divided as open spinal dysraphism
(OSD) and closed spinal dysraphism
(CSD) as the main categories and with the
latter subdivided into two further
subcategories: with or without a
MMC, myelocele,
hemimyelomeningolocele and
hemimyelocele. CSD is much more
heterogeneous than OSD and a large
number of malformations belong to this
group. CSD consist of unenclosed
vertebral arches without externally visible
cystic lesion in the back. Only four
malformations present with a subcutaneous
mass in the back: lipomyeloschisis,
lipomyelomeningocele, MC and terminal
myelocystocele. In the neck, CSD with a
subcutaneous mass is representing by
cervical MMC, MC and
myelocystocele(20,25).
MMC, the commonest anomaly of SD,
refers to a bony defect in the vertebral
column through which the meningeal
membranes that cover the spinal cord and
part of the spinal cord protrude. Contrary
the MC does not include spinal cord within
the sac(3,20,25).
We report the histopathological findings
with the clinico-radiological features in 43
cases of MC and MMC derived from the
neuropathology files of one institution. The
aims of the study were (1) to review the
clinic and pathological findings of
congenital SD and (2) discuss the
pathological diagnosis.
MATERIAL AND METHODS
All cases from October, 2009 through
February, 2014 encoded as meningocele
and myelomeningocele were retrived from
the pathology files of at the Selcuk
University Hospital. Forty three cases with
detailed clinical and radiological data were
selected. Original microscopic slides were

336
J.Neurol.Sci.[Turk]
stained with hematoxylin and eosin (H&E)
in all cases. Some of the sections were
stained immunohistochemically with glial
fibrillary acidic protein (GFAP) and
epithelial membrane antigen (EMA).
Masson's trichrome performed on original
sections from paraffin blocks. All sections
from each case were reviewed by two
pathologist over a biheaded microscope,
and data were recorded for the presence or
absence of epithelial, mesodermal and
neuroectodermal changes. The data
consisting of patient's age, sex, site of
lesion and macroscopic definition, and
clinico-radiologic features were obtained
from the archive of the neurosurgeon.
RESULTS
Clinical
Among the 43 cases, there were 34 cases
of MMC, 9 cases of MC. There were 20
males (M) and 24 females (F) with F/M
ratio 1.2 to 1. The age range of patients
were from newborn to 4 months; 77% of
patients were less than one week old. All
of the cases had cystic lesion in the back
(Fig 1a,b). Of 34 MMCs, 2 were thoraco-
lumbar, 1 cervical, 1 sacral, and 30 were in
the lumbosacral region. Among 9 MCs, 1
was cervical, and 8 were in the
lumbosacral region. All SDs with cervical
localization were female. All thoraco-
lumbar cases were male. No particular sex
predilection for lumbosacral SDs could be
discerned. 31 cases of MMCs (91%), and 3
cases of MCs (33%) were hydrocephalus.
Chiari II malformation was seen in 30
cases of MMCs (88%) and in 2 case of MC
(22%) (Fig 1c,d). Among the 34 cases of
MMC, 3 had a clubfoot deformity (Fig 2).
Malformations as dextrocardia,
syringomyelia and diastematomyelia were
seen in one of 34 MMC patients.
Pathologic
Histopathologic characteristics are
summarized in Table 1.
Epithelial changes- Epidermis was
present in 42 of 43 cases. It was usually
normal thickness but of 42,3 were
337
papillomatous and 3 were hyperplastic.
Ulceration was noted in 28 cases (66%)
(Fig 3a). İnflammation with different
severity was seen in all ulcerated and in 11
of 14 non-ulcerated cases (90%). Both
cervical cases were non-ulcerated. Loss of
epidermal appendages was noted in 40
cases (93%). 30 of them appendages were
noted to be completely absent. In most
cases the appendage loss was in the areas
directly affected by the malformation (Fig
3a).
Mesodermal changes- Fibrosis was
identified 39 of the 43 cases (90%).In 18
cases bands of dense collagen fibers were
seen (Fig 3b). In 13 cases dermal fibrosis
were more compact than would be
expected. Fibrosis mimicking
subarachnoid space was seen in 8 cases.
Mixoid changes were seen in 3 cases.
Subepithelial edema was noted in 3 cases.
Increased numbers of blood vessels were
identified in 34 of 43 cases (79%), ranging
from a massive increase in number,
mimicking an angioma (three cases) (Fig
3c). The prominent and ectatic vessels
were seen in 28 of 43 cases (65%) (Fig 3a).
In 7 cases, there were increased numbers
of vessels with leukocyte extravasation in
areas of neuropil like matrix. In 5 cases,
there were increased numbers of vessels
that mimicked papillary endothelial
proliferation in areas of pia-arachnoid
tissue (Fig 3d).
Bundles of smooth muscle fibers were
found careful search in 8 cases ( 18%) (Fig
4a). Skeletal muscle was seen in 2 cases
(4%) (Fig 4b). One case contained islands
of mature hyaline cartilage.
Mature adipose tissue was seen in 27 of 43
cases (62%). Large groups of adipocytes
were seen scattered in 12 cases. Small
adipose tissue islands were seen around
sweat glands in 8 cases, In 7 cases, sheets
of mature adipose tissue seem like lipoma
(Fig 4c).
Subepidermal calcification was noted in 2
cases (4%) (Fig 4d).
J.Neurol.Sci.[Turk]
Neuroectodermal changes- Neuropil-like
matrix (brain tissue) was noted in 34 cases
(79%) (Fig 5a,b). Typically, the neuropil-
like matrix featured gliosis with an
increased population of the fibrillary
and/or gemistocytic type. Neurons were
numerous in some cases (Fig 5b). In 2
cases, neuropil was located directly
beneath the epidermis with only basal
lamina separating these two ectodermal
structures.
Structures resembling the normal
ependymal lining of the central canal of the
spinal cord were noted in 15 of the cases
(35%).The ependyma varied from small
canaliculi formed by only a few cells to
larger collections resembling central canal-
like structures (Fig 3a,5b,c). In one of
them, the ependyma merged into structures
suggesting choroid plexus (Fig 5c).
Figure 1: Myelomeningocele. (a) External view of the sac. (b) Intraoperative view of the myelomeningocele.
(c and d) Sagittal T1 weighted MRI sections of Chiari II malformation
338
In 11 cases (25%), there were
meningothelial cells recognizable by their
eosinophilic cytoplasm, fine nuclear
chromatin, occasional intranuclear
vacuolization, and their tendency to form
sheet-like formations. EMA stain was
performed on eight cases and showed
strong membranous staining of
meningothelial cells (Fig 5d).
Nerve fibers were identified in 36 cases
(83%). These varied from easily
identifiable large myelinated nerve trunks
(19 cases) to slightly increased numbers of
fibers compared to those normally present
in the dermis (17 cases) (Fig 3a). In 5
cases, ganglion cells were also identified
by their large eccentric nuclei with open
chromatin, prominent nucleoli, and ample
cytoplasm and were located either adjacent
to or within nerve fibers or roots.
J.Neurol.Sci.[Turk]

Figure 2: Myelomeningocele with bilateral clubfoot deformity.

Figure 3: (a) Ulceration, loss of appendages, increased numbers of ectatic vessels, neuropil-like matrix with
ependymal lining and nerve fibers were seen (H&E) (b) Ependymal canal is surrounded by dense collagen
fibers (MTK). (c) Increased blood vessels mimicking an hemangioma (H&E). (d) Papillary endothelial
proliferation in areas of pia-arachnoid tissue (H&E).

339
J.Neurol.Sci.[Turk]

Figure 4: (a) Proliferation of smooth muscle fibers (H&E) (b) Proliferations of skeletal muscle fibers(H&E)
(c) Lipoma like structure with mature adipose tissue (H&E). (d) Subepithelial calcification (H&E).

Figure 5: (a) Epidermis, loss of appendages, and neuropil surrounded by pia-arachnoid tissue (H&E) (b)
Neuropil like matrix associated with ependymal canal, gliosis, and neurons (H&E) (c) The ependyma merged
into structures suggesting choroid plexus (H&E). (d) Membranous EMA immunopositivity of meningothelial
cells.

340
J.Neurol.Sci.[Turk]

Table 1. Summary of histopathologic findings

Histopathologic features % of 43 cases % of 34 MMC % of 9 MC

Loss of epidermal appendages 93% 94% 89%

Fibrosis 90% 88% 100%

Inflammation 90% 91% 89%

Peripheral nerve fibers or roots 83% 59% 67%

Abnormal or increased vessels 79% 79% 78%

Neuropil-like matrix 79% 100% -

Ulceration 66% 79% 11%

Mature adipose component 62% 62% 67%

Ependyma and/or choroid plexus 35% 44% -

Meningothelial cells 25% 32% 22%

Arrector pili hyperplasia/hypertrophy 18% 12% 4%

Mixoid changes 7% 6% 11%

Subepithelial edema 7% 3% 22%

Skeletal muscle 4% 6% -

Calcification 4% 6% -

Mature hyaline cartilage 2% 3% -

DISCUSSION occur. Almost 1% of the cases Show

Spina Bifida is one of the most common,
serious malformations of human structure.
At birth, it tends to be more common in
girls than in boys(12,20). In our study, F/M
ratio was 1.2 to 1. The majority of MMCs
are sacral or lumbosacral. Cervical or
cervico-thoracic location of MMCs are
rare(4). However purely lumbar,
thoracolumbar and thoracic MMC do
multisegmental involvement(25,4). In our
series, among 34 MMCs, 30 were
lumbosacral, 2 thoraco-lumbar 1 sacral,
and 1 was in the cervical region.
SD is not always an isolated lesion and
may be associated with other occult
abnormalities at the same or different
spinal levels(3,26). The Chiari type II
malformation is characterized by cerebellar

341
J.Neurol.Sci.[Turk]
hypoplasia and varying degrees of caudal
displacement of the lower brainstem into
the upper cervical canal through the
foramen magnum. This deformity impedes
the flow and absorption of cerebrospinal
fluid (CSF) and causes hydrocephalus,
which occurs in more than 85% of infants
with myelomeningocele(1,14). The Chiari II
malformation is seen in almost all cases of
OSD; associated hydrocephalus; and the
complications of MMC closure
(retethering by scar, dermoid, arachnoid
cyst)(1,3,25). In our series, although 91% of
MMC cases were hydrocephalus. Chiari II
malformation was seen in 88% of MMC
cases.
Spina bifida is generally accompanied by a
high incidence of foot deformities. With
thoracic lesions, the most frequent
deformity is an equinus lesion (55%), a
club foot with mid-lumbar lesion (87%)
and a calcaneal foot with sacral lesions
(34%)(5). In our series, in 3 of the 34 MMC
patients had the clubfoot deformity. One of
them was seen bilateral.
Myelomeningocele often occurs along with
multiple system congenital anomalies.
Commonly associated anomalies are facial
clefts, heart malformations, and
(14)
genitourinary tract anomalies . In the
present study, dextrocardia, syringomyelia
and diastematomyelia was detected in one
each patient.
A short review of the normal embryology
of the involved structures is essential to
understand the pathologic features of SB.
The central nervous system (CNS)
develops by two different processes-
primary and secondary neurulation. Central
nervous system development initiates in
the third week in a process known as
primary neurulation. During primary
neurulation, the notochord induces the
overlying ectoderm to differentiate into a
specialised neural plate. The lateral edges
of the neural plate soon elevate to form the
neural folds. As development continues,
the neural folds continue to elevate and
approach each other in the midline, fusing
342
to form the neural tube. This fusion begins
in the cervical region and proceeds in both
the cephalic and caudal directions.
Secondary neurulation is the process of
development of the caudal cell mass that
forms the caudal-most portion of the neural
tube, forming the spinal segments below L-
2. Following neural tube closure, the
epithelial ectoderm separates from the
neural ectoderm, a process known as
disjunction. The epithelial layers fuse to
create skin covering the neural tube, and
mesenchyme migrates between the neural
tube and skin to form the meninges, neural
arches of the vertebrae, and paraspinal
muscles. In the third month of
development, the spinal cord extends the
entire length of the embryo. However, as
development continues, the vertebral
column and dura lengthen more rapidly
than the neural tube, and the terminal end
of the spinal cord shifts to a higher
vertebral level(19,25).
It is widely accepted that OSDs are caused
by an impairment of the morphogenetic
movements taking place during
neurulation. In MMC, a segment of the
spinal placode fails to neurulate and
protrudes, together with the meninges,
through a bony defect in the midline of the
back, thus being exposed to the
environment. Because of the expansion of
the underlying subarachnoid space, the
surface of the placode is elevated above the
skin surface(25). Several types of CSDs
result from embryological abnormalities
during primary neurulation. Some of them
arise from premature disjunction result in
fusion of the spinal cord with fatty
element(19).
We wish to emphasize some of the more
unusual microscopic findings in our study.
In contrast to proliferations of some
tissues, we noted a 93% of the cases in
which there was a diminution or complete
loss of skin appendage structures. Sibley
and Cooper have reported loss or decrease
in the number of adnexal structures in 4
cases of meningoceles(21). Berry and
J.Neurol.Sci.[Turk]
Patterson similary noted diminution or
complete loss of skin appendage structures
in 95 cases of 132 SD (72%)(2). The
surface of MMC shows a characteristic
central area devoid of epithelial lining,
exposing vascular tissue, from which
cerebrospinal fluid or tissue transudate
may ooze(16,20). In our study, ulceration
was noted in 66% and the increased
number of dilated thin walled blood
vessels in 65%. Prominent vascular
proliferation in nerve tissue can be
observed are known(20). In our study, there
were increased numbers of vessels with
leukocyte extravasation in areas of
neuropil in 7 cases. Cutaneous
hemangioma was the one of the superficial
skin manifestations(2,10). In our study, three
patients showed angioma-like vascular
proliferation. However in 5 cases, there
were increased numbers of vessels that
mimicked papillary endothelial
proliferation in areas of pia-arachnoid
tissue.
Eight cases of 43 (18%) showed
proliferation and hypertrophy of pilar
smooth muscle fibers. In a study of the
Berry and Patterson have reported smooth
muscle hypertrophy and/or hyperplasia in
56 cases of 132 SD (42%)(2). Talwalker
and Pastur noted 3 of 51 cases that had
increased proliferation of smooth muscle
fibers among other abnormalities of
mesodermal tissue(23). In 2 cases, we also
noted skeletal muscle fibers. Similar
proliferations of skeletal muscle fibers
have been reported in 7 cases by Berry and
Patterson(2).
Intraspinal lipomas are commonly found in
SD(2,22,23). There is a confusion about
spinal lipomatous masses. Although the
bulk of masses consist of mature fat cells,
they have infiltrating margins and lack of
capsule, in contrast to classic lipomas
developing elsewhere in the body. In
addition, histological examinations have
revealed that they often contained other
tissue elements(22). Several labels such as
lipoma, hamartoma, choristoma, and
343
teratoma have been applied for these
lesions, and distinguishing them may
occasionally be difficult(2,6,9,11,13,19,22,23).
The presence of masses of mature adipose
tissue in 27 of 43 cases in our study.
The foci of cartilage we noted in one case (
2%) has been described by others in spinal
cord teratomas or hamartomas and some
examples associated with SB or
MMC(2,18,24).
Subepithelial calcification was seen in 2 of
our cases which resembled the
“calcification involved and ulcer base” as
described by Berry and Patterson(2). Berry
and Patterson noted dystrophic
calcification in 9 cases. In 2 of 9,
calcification mainly involved walls of
blood vessels and in 4 cases it was
associated with foreign body reactions(2).
One of their case showed a peculiar
laminated pattern of calcification which
resembled the unusual fibro-osseous
component as described by few authors,
these findings we did not observe(2,8).
Harrist and Gang described calcification of
the stroma of the choroid plexus in an
epidermal nevus with dermal astrocytic
heterotopia and coccygeal vestige(7).
Narverud and Ramli have been reported 13
cases with calcification of
pseudomeningocele(15).
Central canal-like structures were noted in
35% of the cases. In one of them, the
ependyma merged into structures
suggesting choroid plexus. Similarly, in the
literature, central canal-like structures in
dysraphic lesions of the spine have been
reported in 27% - 37%(2,17). Choroid plexus
has previously been noted in 2,3% of
meningoceles and myelomeningocele(2).
MMC in the cervical region is rare and
occur in 1-6% all SD(4,16,17). Cervical MMs
are clearly protuberant, covered at the base
by full-thickness skin and covered on
dome by a thick epithelium. Neural tissue
is not superficially exposed. These
differences are likely responsible for the
more favoruable outcome(4,16,17). There is
two (myelo)meningocele with cervical
J.Neurol.Sci.[Turk]
localization in our series. Both of them
covered by the compact skin without
ulceration. Neuropil was seen at the deep
layer of the mass. Both cases are in
excellent condition without any
neurological deficits.
CONCLUSION
SDs manifests depending on clinical,
radiological and pathological findings.
Both clinical and pathological differences
were seen among MMCs. By considering
the embryogenesis of these malformations,
which involve ectoderm, neuroectoderm,
and mesoderm. Definition of the
pathological aspects of dysraphism will
potentiate the understanding of these
anomalies.
Acknowledge
There is no conflict of interest.
Correspondence to:
Pinar Karabagli
E-mail: pinarkarabagli@yahoo.com
Received by: 02 March 2014
Revised by: 22 May 2014
Accepted: 22 May 2014
The Online Journal of Neurological
Sciences (Turkish) 1984-2014
This e-journal is run by Ege University
Faculty of Medicine,
Dept. of Neurological Surgery, Bornova,
Izmir-35100TR
as part of the Ege Neurological Surgery
World Wide Web service.
Comments and feedback:
E-mail: editor@jns.dergisi.org
URL: http://www.jns.dergisi.org
Journal of Neurological Sciences (Turkish)
Abbr: J. Neurol. Sci.[Turk]
ISSNe 1302-1664
344
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