Pathogenesis of cerebral vasospasm.

Cerebral arteries have been shown to react to experimental subarachnoid hemorrhage with a nonspecific arterial injury reaction characterized by endothelial cell desquamation, adherence of platelets to the exposed collagen, subendothelial edema, and medial necrosis. This injury reaction is followed by a reparative process with intimal proliferation and medial fibrosis. We have postulated that the arterial narrowing seen by angiography in patients after subarachnoid hemorrhage may be a manifestation of this injury reaction. Because it is likely that the platelets adherent to the damaged endothelium play a major role in the propagation of the process, it is possible that therapy directed at preventing platelet accumulation may interrupt the cycle.