The most common clinical manifestation of an AVM is intracranial hemorrhage. Among young patients who are normotensive and have normal coagulation, AVMs are a common cause of ICH. Most supratentorial AVM hemorrhages are lobar in location, but may also occur in the basal ganglia or thalamus. In the posterior fossa, AVMs cause most cerebellar hemorrhages in normotensive patients less than 40 years old. Brainstem AVMs causing hemorrhage often may be angiographically occult immediately post-hemorrhage. These patients require delayed angiography once the hematoma has resolved in order to define the malformation. Patients with AVMs near the ventricular surface may present with recurrent intraventricular hemorrhage and subsequent hydrocephalus from obstruction of proximal or distal cere-brospinal fluid pathways. Intraventricular hemorrhage from AVMs is often small in volume, with mild clinical manifestations. Pial-based AVMs may cause subarachnoid hemorrhage.

In most instances, however, subarachnoid hemorrhage results from the rupture of a primary intraparenchymal bleed through the pial surface. In contrast to aneurysms, basal subarachnoid hemorrhage from AVM rupture is rarely associated with vasospasm [12]. Furthermore, recurrent hemorrhage within the first 2 weeks after AVM rupture is rare and complicates only 1% of patients [12]. The overall mortality rate after each AVM rupture is approximately 10% [10].

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