Cerebral vasospasm after subarachnoid hemorrhage.
Chronic cerebral vasospasm remains the most important cause of subsequent morbidity in patients who survive the first 48 to 72 hours after a subarachnoid hemorrhage. Prolonged arterial narrowing compromises cerebral hemodynamics and results in cerebral ischemia. Among patients in whom symptomatic chronic cerebral vasospasm develops, almost half die or have a serious residual neurologic deficit. Present evidence indicates that sustained vessel narrowing results from structural changes within the arterial wall rather than from active contraction of vascular smooth muscle. The mechanism (or mechanisms) responsible for these changes is unknown, but damage from prolonged active arterial contraction, depression of vessel wall respiration, and an inflammatory response have all been proposed as explanations. Despite more than 30 years of intensive study, an effective treatment program for chronic cerebral vasospasm remains elusive. Recent therapeutic trials, however, based on efforts to interrupt the mechanisms responsible for these structural changes hold some promise.
D000818:Animals; D001488:Basilar Artery / Q000503:physiopathology / Q000648:ultrastructure; D002536:Cerebral Arteries / Q000503:physiopathology / Q000648:ultrastructure; D004285:Dogs; D006439:Hemodynamics; D006801:Humans; D002546:Ischemic Attack, Transient / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D013345:Subarachnoid Hemorrhage / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D013718:Tensile Strength