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| Journal of the New Zealand Medical Association,
02-March-2007, Vol 120 No 1250
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Snakes alive! Caput medusae due to cerebral venous
angioma
Hu Liang Low, Brian Simpson
The increasing sophistication and availability of modern
cranial imaging techniques has resulted in the detection of incidental lesions
in greater numbers. Caution needs to be exercised when deciding whether these
lesions are responsible for the patient’s symptoms and whether treatment
is merited. We present a case where two coincident brain lesions led to a
referral for possible neurological surgery.
Case reportA 45-year-old man presented to the emergency department of a
Welsh district hospital with a 1-week history of persisting headaches and
dizziness after hitting the top of the right side of his head forcefully against
an overhead lamp. On examination, no abnormal neurological findings were found.
In view of his lingering symptoms, an un-enhanced computer
tomographic (CT) scan of his brain was performed. This showed a small,
superficial right-frontal haematoma (Figure 1). He underwent a magnetic
resonance imaging (MRI) scan which was unremarkable except for the haematoma.
The patient subsequently had a digital subtraction cerebral angiogram which
revealed a leash of vessels converging onto a dilated central vessel which
drained into the superior sagittal sinus (Figure 2).
At this stage, the patient was referred to the neurosurgical
team for consideration of surgery. When we reviewed the angiograms we found that
the vascular lesion was consistent with a cerebral venous angioma. Moreover,
this anomaly was distal to the location of the haematoma. There were no other
vascular abnormalities. The frontal haematoma was a contusion secondary to the
patient’s head injury. He was treated conservatively and made a full
recovery.
DiscussionThe actual prevalence of cerebral venous angiomas (CVA) is
probably higher than the quoted 3% of the
population1—as this figure has been
derived from brain imaging and autopsy studies.
CVAs are developmental anomalies composed entirely of venous
structures interspersed with normal brain parenchyma and are found mainly in the
posterior fossa, cerebral cortex, and the deep white
matter.2 The pathogenesis of CVAs is unknown
but may represent attempts at establishing a collateral venous circulation
following an ischaemic insult during the development of medullary veins and
their tributaries.3 CVAs therefore drain normal
brain tissue.
CVAs are usually discovered incidentally during
investigations for unrelated neurological disorders. They have a characteristic
angiographic appearance which has been likened to the head of the Medusa (caput
medusae).2 They appear as stellate structures
on contrast-enhanced MRI scans unless obscured
by the presence of haematoma.2 The incidence of
second cerebrovascular malformations in patients with known CVAs is as high as
19%.4
The majority of these coincident vascular malformations are
cavernous haemangiomas and there is a possibility that the development of both
these malformations may be related.5 CVAs had
previously been associated with various neurological symptoms and haemorrhage.
However, there is increasing evidence to suggest that venous angiomas rarely, if
ever, bleed.2,4
Most recent studies suggest that neurological symptoms
attributed to CVAs (especially haemorrhage) are probably due to associated
cavernous malformations, arteriovenous fistulas, or unidentified vascular
malformations.2,4
Patients found to have a CVA should ideally have at least an
MRI to exclude concurrent vascular malformations as these are more likely to
give rise to symptoms. Due to the low morbidity associated with bleeding (if it
was actually due to a CVA) and the high complication rates when these lesions
are treated with either surgery or radiosurgery, the majority of neurosurgeons
now treat cerebral venous angiomas
conservatively.2,4
Author information: Hu Liang Low, Fellow in
Stereotactic and Functional Neurosurgery, University of British Columbia;
Vancouver, Canada; Brian A Simpson, Consultant Neurosurgeon, University Hospital
of Wales, Cardiff, UK
Correspondence: Dr HL Low, Surgical Centre
for Movement Disorders, 8105-2775 Laurel Street, Vancouver, British Columbia V5Z
1M9, Canada. Fax: +1 604 8754882; email: lowhli@hotmail.com
References:
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