Delayed vasospasm as a result of subarachnoid blood after rupture of a cerebral aneurysm is a major complication. It is seen in over half of patients and causes symptomatic ischemia in about one third. If left untreated, it leads to death or permanent deficits in over 20% of patients. The essential cause and the relative contribution of true muscle spasm and other changes in the vessel wall remain uncertain. The mainstays of treatment are careful maintenance of fluid balance, induced hypervolemia and hypertension, calcium antagonists, balloon or chemical angioplasty, and, in some centers, cisternal fibrinolytic drugs. Promising future lines of treatment include gene therapy, nitric oxide donors, magnesium, sustained release cisternal drugs, and several other drugs that are under experimental or clinical trial.