Abstract
Cerebral vasospasms with subsequent infarction have an important effect on the outcome of patients with ruptured intracranial aneurysms. Clinical and experimental studies of intravascular factors in the pathogenesis of cerebral infarctions, with particular regard to platelets and coagulation factors, were performed. In these studies, a systemic hypercoagulable state and platelet hyperactivity were observed, and in the experimental study, crenated red blood cells were seen in the course of vasospasms. These systemic changes in intravascular components are thought to accelerate cerebral ischemia through an increase in blood viscosity, microthrombosis, and reduced deformability of red cells.
