Pathophysiology of Spontaneous Intracerebral Hemorrhage

Kim, Bum Tae; Lee, Chul Woo; Hwang, Sun Chul; Im, Soo Bin; Shin, Won Han

Abstract

Chronic hypertension causes pathologic changes within the tunica media, termed lipohyalinosis. The most prominent changes were seen at bifurcation point within the vessels and middle and distal portion of the vessels. The role of microaneursyms in spontaneous intracerebral hemorrhage (ICH) secondary to hypertension is not well understood. A cerebral amyloid angiopathy is associated with fibrinoid necrosis and affects the small to medium sized vessels and it may account for a higher percentage of spontaneous ICH in the elderly. Neurologic dysfunction secondary to ICH is caused by initial hemorrhage with its associated mass effect, and tissue destruction with hematoma enlargement. Consequently, the further deterioration may be due to cerebral edema. The exact role of CBF changes is not unproved in the pathogenesis of neuronal injury. However, much has been learned about the mechanisms involved the brain edema formation after ICH. A number of components of blood are capable of inducing brain injury and brain edema formation. The hematoma exerts its effects not only by mechanical but also by chemical influences.