Permanent neurologic injury and death remain common outcomes following aneurysmal subarachnoid hemorrhage. Although many sophisticated techniques are evolving for securing intracranial aneurysms to prevent rebleeding, progress is lagging in the management of posthemorrhagic complications, particularly cerebral vasospasm. Vasospasm can be defined either angiographically, by visible reduction in arterial lumen diameters, or clinically, with signs of focal or regional cerebral ischemia. The relationship between angiographic and clinical vasospasm is not straightforward. The most important known risk factors for developing posthemorrhagic vasospasm include volume and distribution of subarachnoid blood, and no preventive measures have proven effective. Established treatment strategies for vasospasm include hyperdynamic therapy, angioplasty, and selective intra-arterial injection of vasodilators. The vasodilatory approach has been called into question by recent data suggesting that reduction of arterial luminal diameters may be due largely to a proliferative arteriopathy. Novel treatment strategies have focused on protecting the cerebrum, targeting components of the inflammatory cascade, and identifying genetic factors predisposing toward vasospasm, all of which may soon yield new treatment modalities.