Cerebral Ischemia Following Subarachnoid Hemorrhage — The Efficacy of Nimodipine as Therapy

The rupture of a cerebral aneurysm commonly results in the deposition of a large volume of subarachnoid clot which adheres to the adventitia of the basal conducting arteries. As the erythrocytes lyse over a period of several days, spasmogenic substances are released which permeate the arterial vessel wall and result in a slowly developing and sustained vasoconstriction. The likelihood of a degree of vasoconstriction developing which is observable angiographically is proportional to the volume of blood in the subarachnoid space. Severe diffuse angiographic vasospasm is commonly associated with delayed onset ischemic neurological deficit. Whether the latter develops or not is a function of many factors, including the anatomy of the cerebral vasculature, the nature of collateral vessels, associated atherosclerosis, the age of the cerebral cortex, cardiac output, arterial blood pressure, and intracranial pressure.