Vasospasm is one of the leading causes of morbidity and mortality following 
aneurysmal subarachnoid hemorrhage (SAH). Radiographic vasospasm usually 
develops between 5 and 15 days after the initial hemorrhage, and is associated 
with clinically apparent delayed ischemic neurological deficits (DID) in 
one-third of patients. The pathophysiology of this reversible vasculopathy is 
not fully understood but appears to involve structural changes and biochemical 
alterations at the levels of the vascular endothelium and smooth muscle cells. 
Blood in the subarachnoid space is believed to trigger these changes. In 
addition, cerebral perfusion may be concurrently impaired by hypovolemia and 
impaired cerebral autoregulatory function. The combined effects of these 
processes can lead to reduction in cerebral blood flow so severe as to cause 
ischemia leading to infarction. Diagnosis is made by some combination of 
clinical, cerebral angiographic, and transcranial doppler ultrasonographic 
factors. Nimodipine, a calcium channel antagonist, is so far the only available 
therapy with proven benefit for reducing the impact of DID. Aggressive therapy 
combining hemodynamic augmentation, transluminal balloon angioplasty, and 
intra-arterial infusion of vasodilator drugs is, to varying degrees, usually 
implemented. A panoply of drugs, with different mechanisms of action, has been 
studied in SAH related vasospasm. Currently, the most promising are magnesium 
sulfate, 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors, nitric oxide 
donors and endothelin-1 antagonists. This paper reviews established and emerging 
therapies for vasospasm.