Symptomatic vasospasme or delayed cerebral ischemia associated with arterio
graphic evidence of arterial constriction is currently the most important c
ause of morbidity after acute subarachnoid hemorrhage. Symptomatic vasospas
m usually develops between 4 and 12 days after subarachnoid hemorrhage. The
re is typically a gradual deterioration of the level of consciousness accom
panied by focal neurological deficits. 30% of patients who survived aneurys
mal SAH develop delayed cerebral ischemia secondary to vasospasm. Vasospasm
produces cerebral ischemia and infarction by hemodynamic mechanisms. Vasos
pasm is an important independant predictor of poor outcome after aneurysmal
SAH.
Other conditions than aneurysmal subarachnoid hemorrhage such as trauma, tu
mors, unruptured aneurysms, meningitis and ruptured AVM may be associated w
ith vasospasm.