Pathophysiology of acute and delayed brain injury after subarachnoid hemorrhage: an update

Abstract

Aneurysmal subarachnoid hemorrhage (SAH) is still further complicated by a high mortality and morbidity rate related to early or delayed ischemic brain injury. Cerebral vasospasm is one of the factors associated with ischemic injury, but it usually appears with some delay. Recent experimental data are focusing on early brain injury after SAH. Several etiological factors have been suggested: changes in intracranial pressure and cerebral blood flow, microvascular vasospasm and platelet aggregation, cortical spreading depolarization, induction of apoptosis, oxidative stress, etc. The amount of blood present in the subarachnoid space causes an intense inflammatory response that involves both cellular and molecular factors (cytokines, endothelin, nitric oxide) and triggers vasospasm and delayed ischemic neurologic deficit. A better understanding of the pathophysiology of the early brain injury after SAH can lead to a more targeted therapy.