Aneurysmal subarachnoid hemorrhage (SAH) affects approximately 30,000 people each year in North America. At least 30% of these patients will develop vasospasm as a result of the initial hemorrhage, and two thirds of these develop permanent disabilities or die. Blood deposited into the basal cisterns from the ruptured aneurysm can form thick clots around the major cerebral vessels. The by-products of the hemolyzed clots are believed to be responsible for the subsequent development of vasospasm. Hypervolemic, hypertensive, hemodilution therapy (HHHT) and nimodipine may improve outcome in some cases but there is no therapy known to prevent vasospasm in all patients. One potential therapeutic agent under investigation is tissue plasminogen activator (t-PA), a fibrinolytic enzyme. Instilled into the basal cisterns at time of aneurysm clipping, t-PA dissolves the clot so spasmogenic substances may be removed, thus preventing or reducing the severity of vasospasm.