Pathophysiology of parenchymal injury in ischemic stroke

Abstract

“Stroke” is rapidly developing clinical signs of focal (or global) disturbance of cerebral function, with symptoms lasting 24 hours or longer, or leading to death, with no apparent cause other than of vascular origin. Stroke clinic may occur in two ways: “ischemic” as a result of vessel (arterial or venous) occlusion and “hemorrhagic” (intraparenchimal or subaracnoid) as a result of distruption of vascular integrity. Treating a disease requires an understanding of its mechanism of occurrence. As a matter of fact, much progress has been made over the years in elucidating the patophysiology of ischemic stroke. Current treatment trials have concentrated on breaking these mechanisms from various places, restoring circulation and protecting the surviving neurons (neuroprotection) (5,6). In this review, hemorrhagic events were excluded due to the breadth of the subject, and current information on the pathophysiology of ischemic stroke and suggestions for the use of said information in treatment were brought together.