Treatment of cerebral arteriovenous malformations

Even today, arteriovenous malformations (AVM) are one of the most complex conditions encountered in neurosurgical practice. The difficulty in treatment is not confined to surgical resection of the AVM, but also affects the indications for treatment and the type of appropriate therapy. Each treatment aims at complete exclusion of the AVM. Partial resection has no significant effect on the risk of bleeding. Despite ongoing attempts to devise treatment protocols, each patient presenting an AVM is different and each individual case needs to be assessed by a team familiar with this type of lesion and aware of the percentage risk to the patient in proposing a treatment. A recent evaluation of numerous surgical series demonstrated an operative mortality for AVMs of different sizes at 3.3%. Post-operative angiography only displays complete exclusion of the AVM in 97% of cases. The aim of endovascular treatment is to exclude the nidus. If this is not achieved, the AVM will revascularize sooner or later Endovascular treatment alone seldom results in complete occlusion of the AVM. Some literature reports describe a high mortality rate linked with endovascular treatment with percentages of around 1.6% with a 12.8% morbidity. In our experience, the morbidity linked to endovascular treatment is below 4%. Complications linked to radiosurgery are extremely rare. The main problem of radiosurgery with LINAC or gamma knife is the possibility of treating only small AVM successfully. From November 1991 to August 2001, AVM were found in 115 cases out of 1137 patients admitted for vascular malformations (10%). Of these, 93 (81%) had supratentorial AVM whereas 22 (19%) had subtentorial lesions. Treatment (surgery, embolisation, radiosurgery or a combination) was carried out in 94 cases (82%). Of the nine patients with non-bleeding AVM who did not receive treatment for various reasons, none experienced haemorrhage in the follow-up period of one to ten years. Of the 94 patients who had had a haemorrhage, 12 presented rebleeding of the AVM (13%). In an overall analysis of our results irrespective of the type of treatment and including untreated patients, 67 out of 115 (59%) were discharged without neurological deficit (good outcome). Overall morbidity was 29%; 14 patients died, giving a mortality rate of 12%. The decision how to treat each individual patients is taken after discussion with neuroradiologists and radiosurgeons. In general, in the cases referred to us, we acted as follows: In superficial AVM less than 25-30 cm(3) in non-eloquent brain areas, the lesion was treated surgically. In AVM on the mesial face of the hemisphere or involving the cingulate or corpus callosum regions, direct obliteration was performed in six cases whereas three were treated by radiosurgery. Deep para or intraventricular AVM or caudate nucleus or striocapsulothalamic lesions were usually treated by radiosurgery preceded by partial embolisation. Small AVM in eloquent areas were treated by radiosurgery whereas large lesions were first treated by embolisation followed by radiosurgery. AVM close to eloquent areas were usually treated surgically, possibly after endovascular therapy.