ABSTRACT
Cerebral vasospasm affects approximately 60% to 70% of patients after subarachnoid hemorrhage (SAH), resulting in symptomatic ischemia in approximately half of these patients (1). It reaches the peak of maximal severity between 7 and 14 days after the ictus of SAH, typically resolving spontaneously in the third or fourth week. Vasospasm causes death or serious disability from infarction in up to one-third of patients with SAH. For this reason, vasospasm constitutes the most serious threat to disability after aneurysm rupture secondary to delayed ischemic events. Although the pathogenesis is not clearly known, the risk is related to the amount of subarachnoid blood (1-3). Therefore, vasospasm can occur in the absence of a ruptured aneurysm (angiographic negative SAH) Fig. 17.1.
