ABSTRACT
Arteriovenous malformations (AVMs) of the brain consist of abnormal primitive connections between the arterial and venous systems, single or multiple. They can occur throughout the brain with a predilection for the cerebral hemispheres supplied by branches of the middle cerebral artery (MCA) (1-4). AVMs are congenital lesions that develop most likely between the fourth and the eighth weeks of embryonic life (5,6). The lesion is characterized by a persistent direct connection of the arterial inflow and venous outflow without an intervening capillary bed. The primordial vascular plexus first differentiates into afferent, efferent, and capillary components. The more superficial plexus forms large vascular channels destined to be arteries and veins, while the deeper part develops into the capillary component associated with the brain surface. Perfusion of the embryonic brain starts at week four. AVMs arise from failure to develop an intervening capillary system. There is no genetic predisposition. Most AVMs are diagnosed initially in individuals between ages 20 and 40 who typically present with seizures, hemorrhages, and progressive deficits. In children, hemorrhage is the presenting symptom in approximately 80% of cases, and is about seven times more likely than seizure (7,8). This proportion is significantly higher than that found in adults. The reasons for the propensity of pediatric AVMs to hemorrhage are not understood. The mortality rate for AVM hemorrhage in children (25%) (9) is higher than that in adults, which approaches 6% to 10% (7). This may be due to the fact that AVMs in children are more prevalent in the posterior fossa (approximately 24%), where the effects of hemorrhage are more catastrophic, as compared with the predominantly supratentorial location in adults (7,9,10).
