Developmental Deficits in Adult Patients With Arteriovenous Malformations

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Abstract
INTRACRANIAL arteriovenous malformations (AVMs) are lesions composed of a coiled mass of arteries and veins, joined by arteriovenous fistulas, partially separated by sclerotic tissue, and lying in a bed formed by displacement rather than invasion of normal brain tissue.1 Arteriovenous malformations are thought to begin in some primitive form during the fetal period and appear to undergo an unclear "maturation" process for many years until some critical mass or event is reached and symptoms, usually seizures or hemorrhage, ensue.2 Recent studies show that neurologic deficits are rare before clinical presentation,3 and most neurocognitive studies for symptomatic patients have not been able to demonstrate the degree of impairment seen with comparable focal lesions from other causes.4,5 To our knowledge, neither the time course nor the underlying brain mechanisms for adaptation to AVMs have been described.