ABSTRACT
Cerebral vasospasm is the delayed narrowing of cerebral arteries exposed to blood. Although vasospasm typically occurs after subarachnoid hemorrhage (SAH) from rupture of a cerebral aneurysm, it can also develop after trauma ( 1,2 ) and infections ( 3 ). In humans, vasospasm presents as a biphasic phenomenon. Whereas acute vasospasm generally presents immediately after SAH and typically resolves within hours, chronic vasospasm occurs at 4 to 21 days and peaks 7 to 10 days after hemorrhage, with an overall angiographic incidence of 67% ( 4 ) and a clinical incidence of 37% ( 4 ). Chronic vasospasm causes delayed ischemic defi cits, stroke, and death.
