British Journal of Neurosurgery, February 2014; 28(1): 110–112

© 2014 The Neurosurgical Foundation

ISSN: 0268-8697 print / ISSN 1360-046X online
DOI: 10.3109/02688697.2013.812183

SHORT REPORT

Third ventricular cavernous malformation: an unusual lesion

Mohana Rao Patibandla1, Amit Kumar Thotakura2 & Manas Kumar Panigrahi3
1Department of Neurosurgery, Nizam’s Institute of Medical Sciences, Hyderabad, India, 2Department of Neurosurgery,

NRI Medical College, Mangalagiri, Guntur, India, and 3Department of Neurosurgery, Krishna Institute of Medical Sciences,
Secunderabad, India
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Abstract brain showed an oval, well circumscribed, heterogeneous

Cavernomas constitute 5–10% of all the vascular
malformations of the CNS. They commonly present during
the 2nd and 5th decades of life. Intraventricular cavernomas
constitute rare pathological entity, constituting 2.5–10.8% of
cerebral cavernomas.1 The natural history of intraventricular
cavernomas remains undefined to some extent. Those in third
ventricle are different in biological nature and need more
aggressive therapy. These cavernomas appear to have the
ability to grow very rapidly, resulting in significant morbidity.
For personal use only.
hyperdense mass compressing the foramen of Monroe
(Fig. 1). Magnetic resonance imaging (MRI) showed T1W
and T2W heterogeneous intense lesions with hypointense
ring surrounding the lesion on T2W along with heteroge-
neous enhancement with contrast administration (Fig. 2).
A preoperative memory test done by a neuropsychologist
revealed no deficit. A right transcallosal–transventric-
ular–transforaminal approach was employed. On entry
into the foramen of Monroe into the third ventricle, an

It is not known whether waiting after acute hemorrhage from
an intraventricular cavernoma improves our ability to remove
the lesion safely or if waiting unnecessarily increases the
risk of hydrocephalus, additional bleeding, or further lesion
growth.
Keywords: cavernoma; hydrocephalus; third ventricle; tumor
Introduction
Cavernomas constitute 5–10% of all the vascular malforma-
tions of the CNS. They commonly present during the 2nd and
5th decades of life. Intraventricular cavernomas constitute a
rare pathological entity, constituting 2.5–10.8% of cerebral
cavernomas.1 The natural history of intraventricular cav-
ernomas remains undefined to some extent. Those in third
ventricle are different in biological nature and need more
aggressive therapy.
Case report
A 35-year-old man began to suffer attacks of headache
3 months before admission: holocranial with on and off
vomiting. The headaches occurred several times a day. In
between the attacks the patient was absolutely asymptom-
atic. Examination showed only papilledema. CT scan of
oval, well demarcated, mildly vascular yellowish lesion
with a smooth surface and a firm consistency was noted
attached to the walls of the third ventricle. Histopatho-
logical examination revealed cavernoma. The patient was
discharged alert, fully mobile, without any recent memory
deficit. At 3 months follow-up, postoperative MRI brain
contrast study revealed no residual lesion or recurrence
(Fig. 2). Two years postoperatively, the patient was doing
well without any symptoms.
Discussion
Cavernomas occur in both sporadic and familial forms,
and three genes have been described for the inher-
ited forms.1 De novo growth is reported in pediatric
patients with a history of radiotherapy.1 Cavernomas are
prone to bleeding due to their composition of dilated
sinusoids lined by a single layer of endothelium with
immature subendothelial interstitium and interstitial
junctions. Over time, these lesions have frequent small
hemorrhages that are often subclinical.2 There have been
24 patients reported with well-described cavernomas in
the third ventricle (Table I).1 Based on their origin and
attachment to the ventricle, third ventricular cavernomas
are divided into four types: suprachiasmatic region, lateral
wall region, foramen of Monroe region, and floor region
tumors.2

Correspondence: Dr. Mohana Rao Patibandla, Department of Neurosurgery, Nizam’s Institute of Medical Sciences, Hyderabad- 500082, Andhra Pradesh,
India. Tel: ⫹ 91-9948096369. Office: ⫹ 91-40-23489279. Fax: ⫹ 91-40-23310076. E-mail: drpatibandla@gmail.com
Received for publication 30 January 2013; accepted 2 June 2013

110

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Fig. 1. CT and MRI showing third ventricular cavernoma.
These lesions usually occur with symptoms of hydro-
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cephalus or with short-term memory loss. Other behavioral
and endocrinological disorders such as depression, diabe-
tes insipidus, decreased sexual function, and Morgagni’s
syndrome or visual field deficits or seizures may also be
present.
Colloid cyst, craniopharyngioma, meningioma, epend-
ymoma, choroid plexus papilloma, and pituitary ade-
noma are considered in the differential diagnosis of the
third ventricular cavernomas. Contrast enhancement is
associated with venous angioma, and the tendency for
multiple, small hemorrhages results in the presence of
hemosiderin.2 These characteristics help to differentiate
Fig. 2. Postoperative MRI brain sagittal section showing no residual or
recurrence.
Third ventricular cavernoma 111
the cavernous malformation from other lesions on radio-
graphic evaluation.
From the limited literature available, the natural history
of intraventricular cavernous malformations is not well
understood and they appear to have a worse natural his-
tory. The significant deficits frequently found at the time of
patient admission, the documented rapid growth of some
of these lesions, and the poor outcome of patients who
have undergone subtotal resections suggest the need to
treat these lesions aggressively.1,3 This is accomplished by
surgically removing the entire cavernoma. Transcortical or
transcallosal approaches to the third ventricle have been
used most commonly for anterior third ventricular caver-
nomas. Both of these techniques allow adequate visualiza-
tion and working area to remove the cavernoma. Particular
attention should be directed to the preservation of deep
venous drainage.
The posterior location of the lesion represents an
unusual variant of third ventricular cavernous malfor-
mations. The infratentorial supracerebellar approach or
occipital transtentorial approach has been described for
them. Lack of adjacent brain tissue in ventricular caverno-
mas may be the cause of their rapid growth. The absence of
big feeding arteries or draining veins facilitates this resec-
tion. Tumor consistency and vascularity typically permit
complete removal with suction and bipolar forceps.
These cavernomas appear to have the ability to grow very
rapidly, resulting in significant morbidity. It is not known
whether waiting after acute hemorrhage from an intraven-
tricular cavernoma improves our ability to remove the lesion
safely or if waiting unnecessarily increases the risk of hydro-
cephalus, additional bleeding, or further lesion growth.
 112 M. R. Patibandla et al.

Table I. Cases reported in literature.

Patient Clinical Total/
Authors details picture subtotal Outcome
Latterman et al. (1952) 68/F Mass effect – Died
Vaquero et al. (1980) 18/F Mass effect Total Improved
Pozzati et al. (1981) 31/F Mass effect Total Improved
Lavyne et al. (1983) 48/F Mass effect Partial Hydrocephalus,
Bleeding
Amagasa et al. (1984) 40/M Mass effect Total Improved
Harbaugh et al. (1984) 44/F IVH Total Improved
Yamasaki et al. (1986) 9/M Mass effect Partial Improved
36/M Mass effect Total Improved
Voci et al. (1989) 19/F IVH Total Improved
Ogawa et al. (1990) 16/M Mass effect Total Improved
40/M Mass effect Total DI, HH
Katayama et al. (1994) 9/F Seizures Partial Died
50/F Mass effect – –
45/F IVH – –
49/M Mass effect – –
47/F Mass effect Total Transient DI
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Sinson et al. (1995) 43/F Mass effect Total Died

36/F Mass effect Total HP, HT, HCP
52/F Mass effect Total Improved
32/F Mass effect Total Improved
Kaim et al. (1997) 64/M Mass effect Total –
Reyns et al. (1999) 42/M Asymptomatic Partial Improved
Suess et al. (2002) 36/F Mass effect Total Improved

Crivelli et al. (2002) 38/M Mass effect Total Improved

Wang et al. (2003) 62/F Mass effect Total Improved

Darwish et al. (2005) 47/F Incidental Total Improved

Milenkovic (2005) 56/M Mass effect Total Improved
Chen et al. (2006) 51/F Mass effect Total Improved
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Longatti et al. (2006) 35/M Mass effect Total Improved

Zakaria et al. (2006) 8/M Mass effect Total Improved
Sato et al. (2006) 47/F Mass effect Total Improved
Prat et al. (2008) 56/NM Mass effect Total Improved
Kivelev et al. (2010) 52/M Mass effect Total Improved
Present case 35/F Mass effect Total Improved
Total third ventricular cavernomas reported in Literature.
DI, Diabetes Incipidis; HCP, hydrocephalus; HP, hemiparesis; HT, hypothyroidism; HH, Homonymous hemianopia;
IVH, intraventricular hemorrhage; NM, not mentioned; NR, not registered.

Declaration of interest: The authors report no declarations
of interest. The authors alone are responsible for the content
and writing of the paper.
2. Sinson G, Zager EL, Grossman RI, Gennarelli TA, Flamm ES. Cavernous
malformations of the third ventricle. Neurosurgery 1995;37:37–42.
3. Reyns N, Assaker R, Louis E, Lejeune JP. Intraventricular
cavernomas: three cases and review of the literature. Neurosurgery
1999;44:648–54.

References
1. Kivelev J, Niemelä M, Kivisaari R, Hernesniemi J. Intraventricular
cerebral cavernomas: a series of 12 patients and review of the
literature. J Neurosurg 2010;112:140–9.