Methods of treatment (contd)
Embolization: Skilled catheterisation permits selective embolisation of feeding vessels with isobutyl-cyanoacrylate, although this technique is not without risk. Embolisation alone is unlikely to produce complete obliteration, but used preoperatively, it may significantly aid operative removal.
Occlusion of feeding vessels: Repeat investigation shows that occlusion of feeding vessels, whether by direct operation or by an endovascular balloon, fails to prevent persistent filling of the AVM due to dilated collaterals.
CAVERNOUS MALFORMATIONS (syn. cavernous angioma)
With the appearance of improved imaging, in particular MRI, cavernous malformations arc now identified as a source of intracranial haemorrhage in some patients with an otherwise normal CT scan and angiogram. They occur in 0.5% of the population, are occasionally multiple and in a few patients, have a familial basis. A cavernous malformation may present with epilepsy, haemorrhage or with focal neurological signs.. Once diagnosed the risk of haemorrhage is 0.7% per year. Lesions in accessible sites are readily excised with linle risk; a conservative approach is adopted for those in the basal ganglia, thalamus or brainstem, wherever possible.
This is a type of arteriovenous malformation in which arteries feed directly into the great vein of Galen causing massive aneurysmal dilatation. Patients present either in the neonatal period with severe high output cardiac failure due to the associated arteriovenous shunt, in infancy with cranial enlargement due to an obstructive hydrocephalus, or in childhood with subarachnoid haemorrhage. A cranial bruit is always evident. Cardiac failure usually develops in the neonatal period and is usually fatal. In the other groups the treatment of choice is now endovascular obliteration of the feeding vessels combined with ventricular drainage if required. As a result, the high mortality and morbidity experienced with direct operative repair has considerably reduced.
Angiomatosis affecting the facial skin, eyes and leptomeninges produces the characteristic features of the Sturgc-Weber syndrome - a capillary nacvus over the forehead and eye, epilepsy and intracranial calcification. (See page 542.)
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