See discussions, stats, and author profiles for this publication at: https://www.researchgate.

net/publication/49853743

Interhemispheric epidermoids - An uncommon lesion in an uncommon

location: A report of 15 cases

Article  in  Neurology India · January 2011

DOI: 10.4103/0028-3886.76874 · Source: PubMed

CITATIONS READS
3 38

5 authors, including:

Dhananjaya I Bhat Indira devi Bhagavatula

National Institute of Mental Health and Neuro Sciences National Instituteof Mental Health and Neurosciences , Bangalore
107 PUBLICATIONS   435 CITATIONS    271 PUBLICATIONS   1,786 CITATIONS   

SEE PROFILE SEE PROFILE

Sampath Somanna
NIMHANS
108 PUBLICATIONS   400 CITATIONS   

SEE PROFILE

Some of the authors of this publication are also working on these related projects:

published in neurosurgery focus june 2016 View project

Peadiatric Brain: White matter plasticity in response to direct (Brachial Plexus Injury) versus indirect (Traumatic Brain Injury) insult to Brain View project

All content following this page was uploaded by Dhananjaya I Bhat on 27 May 2015.

The user has requested enhancement of the downloaded file.

[Downloaded free from http://www.neurologyindia.com on Tuesday, May 26, 2015, IP: 14.139.159.99]

Brief Report
Interhemispheric epidermoids - An
uncommon lesion in an uncommon
location: A report of 15 cases
Dhananjaya I. Bhat, B. Indira Devi, Raghunath A., Sampath Somanna, B. A. Chandramouli

Department of Neurosurgery, National Institute of Mental Health and Neurosciences, Bangalore, India

Address for correspondence:
Dr. B Indira Devi,
Department of Neurosurgery,
NIMHANS, Hosur Road, Bangalore,
India.
E-mail: bidevidr@gmail.com
Received : 25-06-2010
Review completed : 19-08-2010
Accepted : 23-08-2010
Abstract
Of the intracranial epidermoids, interhemispheric epidermoids are extremely rare and
only about 19 cases have been reported. This is a retrospective study of 15 patients
with interhemispheric epidermoids surgically treated over a 13-year period. The age at
the time of presentation varied between 17 and 45 years and there were 9 males. The
presenting feature was seizures (focal with secondary generalization) in 12 patients,
hemiparesis in 5 and features of raised intracranial pressure in 3. On computerized
tomography scan the lesions were hypodense in the interhemispheric region. On
magnetic resonance imaging, the lesions were located in the interhemispheric region with
heterogenous signal intensities. Restricted diffusion was evident on diffusion-weighted
images and apparent diffusion co-efficient images. All the lesions were predominantly
located in the anterior interhemispheric region, with either basal or parietal extension
along the interhemispheric fissure. Eleven patients underwent frontal or fronto-parietal
craniotomies, 3 underwent bifrontal craniotomies and 1 patient underwent supra-orbital
craniotomy and endoscopic procedure. Total excision could be achieved in 11 patients;
near-total, in 3; and partial excision, in 1 patient. Follow-up was available in 10 patients.
Three patients had recurrence of lesion at 5½, 8 and 10 years, respectively.
Key words: Anterior interhemispheric, congenital, epidermoids, parasagittal, seizures

Introduction Material and Methods

Epidermoids are benign, slow-growing congenital lesions Fifteen cases of interhemispheric epidermoids were
and are most commonly located in the cerebellopontine operated between 1997 and 2010 at the National Institute
angle, followed by the suprasellar cisterns, other locations of Mental Health and Neurosciences, Bangalore, India.
include Sylvian fissure, brainstem, intraventricular, The case records were reviewed and the data analyzed
pineal regions, intradiploic space of skull, and spinal included clinical characteristics, neuroimaging findings,
cord.[1] Interhemispheric epidermoids are rare, and only operative notes and follow-up data.
19 cases have been reported.[2] We report our experience
with 15 patients, the largest series from a single center.
Results
Access this article online
Quick Response Code: Patient characteristics of the 15 cases are given in Table 1.
Website:
www.neurologyindia.com The age ranged between 17 and 45 years with mean of 28.6
years and there were 9 males. Twelve patients had history
PMID:
***
of seizures, 8 presented with focal-onset seizures with
or without secondary generalization and one had focal
DOI: sensory seizures, which later progressed to focal motor
10.4103/0028-3886.76874
seizures with secondary generalization (Case 3). Four
82 Neurology India | Jan-Feb 2011 | Vol 59 | Issue 1
 Table 1: Clinical data of all 15 patients
Case Age Presentation-duration Location Surgery Follow up Recurrence
(years)/
sex
1. 40/f Rt focal motor seizures with secondary Anterior Frontal parasagittal craniotomy and Nil NA
generalisation-7years. No deficits Interhemispheric total excision
2. 25/m Lt focal motor seizures, Lt hemiparesis - 3 Fronto-parietal Fronto-parietal parasagittal 10 years later, recurrence of Recurrence at 10 years
years interhemispheric craniotomy and near total excision seizures and hemiparesis
3. 23/m Lt lower limb sensory seizures- 1 ½ Fronto –parietal Fronto-parietal parasagittal 3months No recurrence
years, progressing to generalised motor Interhemispheric craniotomy and total excision
seizures-8 months. Papilledema +
4. 33/m Rt focal motor seizures with secondary Fronto –parietal Fronto-parietal parasagittal 3 months No recurrence
generalisation-4 years. No deficits Interhemispheric craniotomy and total excision
5. 17/m Generalised tonic clonic seizures-3 Anterior , basal Bifrontal craniotomy and total 8 years. Continued to have Recurrence seen at 8 years

Neurology India | Jan-Feb 2011 | Vol 59 | Issue 1

years. No deficits interhemispheric excision GTCS throughout ( not
compliant with medication)
6. 23/m Altered sensorium, Lt IIIrd nerve palsy, Large fronto-parietal Fronto-parietal parasagittal NIL NA
papilledema, Rt hemiparesis -1 week interhemispheric, craniotomy and partial excision.
extending to the Lt Stereotactic aspiration of the
atrium recurrence in 2months (Purulent
collection). Ventriculoperitoneal
shunt.
7. 28/f Lt focal motor seizures with secondary Anterior basal Endoscopic gross total excision 1 year. Seizure after 1 year. Residue /? recurrence
generalisation-1 year interhemispheric
8. 45/m Lt focal motor seizures -10yrs. Rt frontoparietal Fronto-parietal parasagittal NIL NA
Progressive Lt. Hemiparesis -4 years. with intraventricular craniotomy and total excision
Headache -2 years. No papilledema extension
9. 35/f 1 episode of status epilepticus. No Anterior Bifrontal craniotomy and near total Sezures 9 years later NIL
deficits interhemispheric excision. (after 5 years of stopping
epidermoid anticonvulsants).
10. 20/f Lt focal motor seizures with secondary Fronto –parietal Fronto-parietal parasagittal Seizures at 1year follow up NIL
generalisation, hemiparesis- 7 months. interhemispheric craniotomy and total excision inspite of being on regular
Bhat, et al.: Interhemispheric epidermoids

Headache, vomiting-3months. Fundus anticonvulsants.

-normal
[Downloaded free from http://www.neurologyindia.com on Tuesday, May 26, 2015, IP: 14.139.159.99]

11. 18/f I episode of Rt focal motor seizures with Lt frontal anterior Frontal parasagittal craniotomy and NIL NA
secondary generalisation with status interhemispheric total excision
epilepticus- 1½ years ago. No deficits
12. 27/m Headache, nausea vomiting-2years. Anterior Frontal parasagittal craniotomy and 4 ½ years. No seizures/deficits. NIL
Fundi-papilloedema Interhemispheric total excision
13. 25/m Generalised tonic clonic seizures since Lt Frontal Frontal parasagittal craniotomy and Recurrent seizures -5½ years Recurrence at 5½ years. Re operated.
childhood. No deficits interhemispheric total excision later. Small residue attached to ACAs left
behind. Follow up- 2 years, patient
continues to have episode of staring looks.
14. 40/m Altered behaviour, rage, assaulting wife, Large anterior and mid Frontoparietal parasagittal NIL NA
foul word usage, wandering 1 year; 1/3 interhemispheric craniotomy and near total excision
memory loss, urinary and faecal social Spanning both frontal
incontinence -1 year. Drowsiness, left and parietal regions.
upper and lower limb weakness- 3
months.
15. 30/f Episodic loss of consciousness-6months; Anterior basal Bifrontal craniotomy interhemispheric 3 years. No further seizures NIL
1-2 episodes/month. No deficits interhemispheric approach and total excision

83
NA - data not available; m - male, f - female; rt - right; lt - left
[Downloaded free from http://www.neurologyindia.com on Tuesday, May 26, 2015, IP: 14.139.159.99]

Bhat, et al.: Interhemispheric epidermoids

patients presented with generalized seizures with no focal

onset. The mean seizure duration was 4.5 years (range 6
months – 15 years). One patient presented with frontal-
and temporal-lobe dysfunction, and 2 others presented
with raised intracranial pressure. Neurologically,
papilledema was seen in 3 patients; and hemiparesis, in
5. Nine patients had no neurological deficits.

Neuroimaging
All patients were investigated with a cranial computerized
tomography (CT) and 7 patients were also investigated
with a magnetic resonance imaging (MRI). All the lesions
were frontal interhemispheric in location with varying
degrees of basal or parietal extension. The smallest and the Figure 1: CT scan, plain, showing a fronto-parietal hypodense
epidermoid with peripheral calcification (Case 4)
largest lesions were 3 and 10 cm in its maximum diameter,
respectively. On CT scan, the lesions were hypodense,
well defined, with density similar to that of cerebrospinal
fluid (CSF). Four lesions showed peripheral specks of
calcification [Figure 1]. None of the lesion had perilesional
edema or contrast enhancement. On MRI, the lesions were
located in the interhemispheric region with heterogenous
signal intensities. On T1-weighted images, they were
hypointense to gray matter and slightly hyperintense to
CSF. On T2-weighted images, they appeared hyperintense
to both gray matter and CSF [Figure 2]. Restricted diffusion
was evident on diffusion-weighted images (DWI) and
apparent diffusion co-efficient (ADC) images. There was a b
no contrast enhancement. Constructive interference in
steady state (CISS) 3-D images showed the lesions to be
heterointense with a good anatomical delineation from the
surrounding tissues. In recurrent cases, there was minimal
peripheral enhancement with contrast. The preoperative
diagnosis of epidermoid was made in all the cases.

Operative details
Eleven patients underwent appropriate frontal or
fronto-parietal parasagittal craniotomies. Three patients
underwent bifrontal craniotomies, while one basal
epidermoid was approached endoscopically through
a supra-orbital mini craniotomy. In 12 patients, an
interhemispheric approach was used. However, in
2 patients, due to large draining cortical veins and
severe adhesions between the dura and the cortex, a
transcortical approach through the superior frontal
gyrus had to be used (Cases 6 and 14). Total excision was
possible in 11 patients. In 3 patients, near-total excision
was done, and a small part of the capsule adherent to
the major branches of the anterior cerebral artery or
the cortex was left behind. In 1 patient only, a partial
excision could be done (Case 6). Before closure of the
craniotomy, the entire field was irrigated thoroughly
with hydrocortisone-saline solution.
Postoperative course
All patients were on injectable steroids for a week; and
then, on a tapering dose of oral steroids for a month.
c d
Figure 2: MRI appearance of interhemispheric epidermoids. T1-weighted
axial (a) and sagittal (b) images — the lesion is hypointense (Case 7) (c) In
T2-weighted images, the lesions are hyperintense with heterogeneity (Case
5) (d) Diffusion-weighted images — the lesion is hyperintense (Case 3)
Immediate postoperative CT scan was done for all
patients to rule out surgical complications. Immediate
MRI or an MRI at the 3-month follow-up was not done
to document the extent of excision. The patient in
whom a partial excision was done, presented within 2
months of surgery in altered sensorium. CT showed a
cystic recollection. Stereotactic aspiration revealed foul-
smelling pus. He later underwent a ventriculoperitoneal
shunt after the infection was treated. However, he
remained in a state of decortication and was discharged
against medical advice. None of the patients had
postoperative chemical meningitis or fresh neurological
deficits at the time of discharge.

84 Neurology India | Jan-Feb 2011 | Vol 59 | Issue 1

[Downloaded free from http://www.neurologyindia.com on Tuesday, May 26, 2015, IP: 14.139.159.99]
Bhat, et al.: Interhemispheric epidermoids
Histopathology
Grossly, the tumors were soft, friable, with pearly-white
flakes. Microscopic examination revealed stratified
squamous epithelium on a collagenous base, consistent
with epidermoid.
Follow-up
Follow-up data was available for 10 patients and the
follow-up ranged from 3 months to 10 years. Six patients
had 3 or more years of follow-up. Of the 8 patients with 1
year or more-than-one years of follow-up, only 2 patients
were seizures free (1 patient did not have seizures even
prior to surgery). The remaining 6 patients continued to
have seizures with reduced frequency as compared to
the preoperative state. Two patients with hemiparesis
improved after surgery to normal power.
Follow-up MRI had been done in 8 patients in the period
between 1 and 10 years following surgery [Figure 3]. The
surgical impression was total or near-total excision of
the lesion in all the 8 patients. Recurrence of the lesion
was seen in 3 patients (5½, 8 and 10 years, respectively,
following surgery), 1 of whom was reoperated (Case
13). The patient with a recurrence at 10 years was
symptomatic but refused surgery, while the other had
an asymptomatic recurrence. One more patient (Case
7) had a residue at 1-year follow-up; however, as an
immediate postoperative MRI was not done, it is difficult
to say whether it was a residual lesion or a recurrence.
Discussion
Epidermoids are benign congenital lesions and account
for 0.5% to 1.8% of all intracranial brain tumors.[3,4] During
the third to fifth week of embryonic life, the ectoderm on
the mid-dorsal region forms a neural plate, which then
infolds to form the neural tube. During infolding, if the
surrounding ectoderm (which later forms the cutaneous
structures) does not separate from the neural ectoderm
completely, nests of these cells may be entrapped along
with the neural ectoderm. These nests of cells later grow
within the central nervous system (CNS), resulting in the
formation of a spectrum of lesions, viz., epidermoids,
dermoids and dermal sinuses.[5-7] Epidermoids grow
slowly and become symptomatic during the third to
fifth decades of life (17 to 45 years, in our series), unlike
dermoids, which are faster growing and which become
symptomatic in the second decade.[5] The epidermoids
have a growth pattern similar to that of the skin. Like
skin cells, these epidermoid cells also desquamate but
into a closed cavity. Slowly as the keratin, cholesterol
and desquamated cells accumulate, the lesion grows and
becomes symptomatic either due to the mass or rupture.
[1,8,9]
In general, there is no gender preponderance,[1,10] but
in our series the male-to-female ratio was 3:2.
Neurology India | Jan-Feb 2011 | Vol 59 | Issue 1
a b
Figure 3: Follow-up MRI. (a) Apparent diffusion co-efficient images
showing no recurrence of the frontal interhemispheric epidermoid
(intensity similar to that of CSF) (Case 9) (b) CISS 3-D images showing
recurrence with a hypointense reticulated pattern (Case 2)
Epidermoids are mostly cerebellopontine angle in location
followed by the suprasellar cistern, the other sites being
the Sylvian fissure, brainstem, pineal region, petrous
apex, intra-fourth ventricular.[1,5,7,10,11] Interhemispheric
location is rare, and only 19 cases (including one reported
from our institute previously) have been reported.[2,12]
As these lesions are slow growing and “soft,” they tend
to mould according to the surrounding structures and
seep through the cisternal spaces, encasing rather than
displacing the nerves and vessels. These lesions become
symptomatic due to either the pressure effects on the
surrounding neural elements or irritation of the nerves or
cortex, presenting with ataxia, nystagmus, hemiparesis,
hydrocephalus, neuralgia or seizures. Rupture of these
cysts spontaneously or spillage of contents during
surgery can cause aseptic chemical meningitis. [7,11,13]
In our series, 80% of patients presented with seizures
of long-duration due to cortical irritation; 33% with
hemiparesis due to mass effect, and 20% with features
of raised intracranial pressure.
Radiologically, epidermoids may be seen as extra-
axial lesions in the basal cisterns growing along the
CSF spaces encasing vessels and nerves and causing a
disproportionately less distortion of the surrounding
brain. On CT scan, the lesions appear as hypodense
lesions with attenuation similar to or lower than that
of CSF. Occasional calcification of the saponified fat
contents may be seen as hyperdensities in about 10 -
25% of the cases. There is usually no enhancement on
contrast.[7,14,15,16] Four of our cases showed calcification
(27%), and none showed any contrast enhancement. In
the interhemispheric region, the differential diagnosis
include a low-grade or a nonenhancing high-grade
glioma.With the advent of MRI and the newer sequences,
preoperative diagnosis of an epidermoid can be made
in almost all cases. On T1-weighted images, epidermoid
appears hypointense to the gray matter and slightly
hyperintense to CSF. On T2-weighted images, the
lesion is hyperintense to gray matter and similar to
that of CSF. However, heterogeneity of the signals is
85
[Downloaded free from http://www.neurologyindia.com on Tuesday, May 26, 2015, IP: 14.139.159.99]
Bhat, et al.: Interhemispheric epidermoids
seen commonly.[17-19] Diffusion-weighted images show
restricted diffusion making the lesion hyperintense.
CSF and arachnoid cysts appear hypointense as there
is no restricted diffusion.[20] Fluid-attenuated inversion
recovery (FLAIR) images and constructive interference
in steady state (CISS) 3-D images are also useful in
diagnosing this condition. In the former sequence, the
epidermoid appears heterogenous and hyperintense to
CSF; while in the latter, the lesion appears heterogenous
with hypointense and hyperintense areas. The extent of
the lesion and its relation to the neurovascular structures
can also be seen clearly.[21,22] As in CT, there is usually no
enhancement on administration of gadolinium contrast.
The radiological features were similar in our series.
The interhemispheric location of the lesion and its proximity
to the anterior cerebral arteries, its branches, motor cortex
and supplementary motor cortex make surgical excision
technically challenging. Preservation of the bridging veins
must be given utmost priority. Despite this, safe radical
excision can be achieved in most of these cases. In 3 patienst,
we had left a small residue due to its attachment to the
anterior cerebral artery branches and surrounding cortex.
In 2 patients, in order to preserve the bridging veins, a
transcortical approach was used. Chemical meningitis is a
well-known complication after epidermoid surgery.[7,13] Up
to 40% incidence of chemical meningitis following surgery
has been reported.[11] In our series, none of the patients
had chemical meningitis. Intraoperative hydrocortisone
irrigation, postoperative steroids, and safe radical excision
might have helped in preventing this complication.[10,11]
Since there is not much CSF in interhemispheric region,
and there is no free communication with the CSF of the
basal cisterns, intraoperative spread of the contents of
epidermoid is less, hence incidence of chemical meningitis
is also minimal.
These slow-growing epidermoids are known to recur
during the long-term, especially when partially removed.
However, as the risk of recurrence is low for small residues,
it is better to try to achieve total excision safely and when
not possible leave behind small residues attached to vital
structures.[7,13,23] As these lesions are congenital, the time to
symptomatic recurrence following total excision may be
estimated as, age at the time of diagnosis plus 9 months.
It has been stated that due to the above reasons the
chance of symptomatic recurrence during one’s lifetime
following total excision may be negligible or practically
absent.[7,8,13,24] However, an overall recurrence rate of 24%
has been quoted in older studies.[24] On long-term follow-
up, there were 3 recurrences in our study, though the
surgical impression was near-total or total excision in
these patients. This highlights the need for a long-term
follow-up of these patients. On follow-up, all our patients
improved symptomatically, and the neurologic deficits
86
View publication stats
recovered. However, seizures still continued to occur in
majority with reduced frequency.
References
1. Lantos PL, Louis DN, Rosenblum MK, Kleihues P. In: Graham DI, Lantos
PL, editors. Greenfield’s Neuropathology. London;Arnold;2002.p.964-5.
2. Praveen KS, Devi BI. Calcified epidermoid cyst of the anterior
interhemispheric fissure. Br J Neurosurg 2009;23:90-1.
3. Ulrich J. Intracranial Epidermoids. A Study on Their Distribution and
Spread. J Neurosurg 1964;21:1051-8.
4. Guidetti B, Gagliardi FM. Epidermoid and dermoid cysts. J Neurosurg
1977;47:12-8.
5. McLendon RE. Epidermoid and Dermoid tumors: Pathology. In: Wilkins
RH, Rengachary SS, editors. Neurosurgery. New York: McGraw-
Hill;1996. p. 959-63.
6. Choremis C, Economos D, Gargoulas A, Papadatos C. Intraspinal
epidermoid tumours (cholesteatomas) in patients treated for tuberculous
meningitis. Lancet 1956;271:437-9.
7. Samii M, Tatagiba M, Piquer J. Surgical treatment of epidermoid cysts
of the cerebellopontine angle. J Neurosurg 1996;84:14-9.
8. Alvord EC Jr. Growth rates of epidermoids tumors. Ann Neurol
1977;2:367-70.
9. Berger MS, Wilson CB. Epidermoid cysts of the posterior fossa. J of
Neurosurg 1985;62:214-9.
10. Desai KI, Nadkarni TD, Fattepurkar SC, Goel AH. Pineal epidermoid
cysts: a study of 24 cases. Surg Neurol 2006;65:124-9.
11. Conley FK. Epidermoid and dermoid tumors: clinical features and
surgical management, In: Wilkins RH, Rengachary SS, editors.
Neurosurgery. New York: McGraw-Hill; 1996. p. 971-6.
12. Matsuno A, Takanashi S, Iwamuro H, Tanaka H, Nakaguchi
H, Nagashima T. Epidermoid tumour arising in the anterior
interhemispheric fissure. J Clin Neurosci 2006;13:262-4.
13. Yarasgil MG, Abernathy CD, Sarioglu AC. Microsurgical treatment
of intracranial dermoid and epidermoids tumors. Neurosurgery
1989;24:561-7.
14. Karantanas AH. MR imaging of intracranial epidermoid tumors: specific
diagnosis with turbo-FLAIR pulse sequence. Comput Med Imaging
Graph 2001;25:249-55.
15. Zimmerman RA, Bilaniuk LT. Cranial CT of epidermoid and congenital
fatty tumors of maldevelopmental origin. J Comput Assist Tomgr
1979;3:40-50.
16. Nagashima C, Takahama M, Sakaguchi A. Dense cerebellopontine
epidermoid cyst. Surg Neurol 1982;17:172-7.
17. Ishikawa M, Kikuchi H, Asato R. Magnetic resonance imaging of the
intracranial epidermoids. Acta Neurochir 1989;101:108-11.
18. Kallmes DF, Provenzale JM, Cloft HJ. Typical and atypical MR imaging
features of intracranial epidermoid tumors. AJR Am J Roentgenol.
1997;169(3):883-7
19. Tampieri D, Melanson D, Ethier R. MR imaging of epidermoids cysts.
AJNR 1989;10:351-6.
20. Tsuruda JS, Chew WM, Moseley ME, Norman D. Diffusion-weighted MR
imaging of the brain: value of differentiating between extraaxial cysts and
epidermoids tumors. AJR Am J Roentgenol 1990;155:1059-65.
21. Ikushima I, Korogi Y, Hirai T, Sugahara T, Shigematsu Y, Komohara
Y, et al. MR of epidermoids with a variety of pulse sequences. Am J
Neuroradiol 1997;18:1359-63
22. Chen S, Ikawa F, Kurisu K, Arita K, Takaba J, Kanou Y. Quantitative
MR Evaluation of Intracranial Epidermoid Tumors by Fast Fluid-
attenuated Inversion Recovery Imaging and Echo-planar Diffusion-
weighted Imaging. AJNR Am J Neuroradiol 2001;22:1089-96
23. Mohanty A, Venkatramana SK, Rao BR, Chandramouli BA, Jayakumar
PN, Das BS. Experience with cerebellopontine angle epidermoids.
Neurosurgery 1997;40:24-30.
24. Akar Z, Tanriover N, Tuzgen S, Kafadar AM, Kuday C. Surgical
Treatment of Intracranial Epidermoid Tumors. Neurol Med Chir
2003;4:275-81.
Source of Support: Nil, Conflict of Interest: None declared.
Neurology India | Jan-Feb 2011 | Vol 59 | Issue 1