Cerebral vasospasm is the classic cause of delayed neurological deterioration 
after aneurysmal subarachnoid hemorrhage, leading to cerebral ischemia and 
infarction, and thus to poor outcome and occasionally death. Advances in 
diagnosis and treatment-principally the use of nimodipine, intensive care 
management, hemodynamic manipulations and endovascular neuroradiology 
procedures-have improved the prospects for these patients, but outcomes remain 
disappointing. Recent clinical trials have demonstrated marked prevention of 
vasospasm with the endothelin receptor antagonist clazosentan, yet patient 
outcome was not improved. This Review considers possible explanations for this 
result and proposes alternative causes of neurological deterioration and poor 
outcome after subarachnoid hemorrhage, including delayed effects of global 
cerebral ischemia, thromboembolism, microcirculatory dysfunction and cortical 
spreading depression.