The clinical significance of acute brain injury in subarachnoid hemorrhage and opportunity for intervention

Abstract

Aneurysmal subarachnoid hemorrhage (SAH) is a devastating neurological event that accounts for 3-7% of all strokes and carries a mortality rate as high as 40%. Delayed cerebral vasospasm has traditionally been recognized as the most treatable cause of morbidity and mortality from SAH. However, evidence is mounting that the physiological and cellular events of acute brain injury, which occur during the 24-72 h following aneurysm rupture, make significant contributions to patient outcomes, and may even be a more significant factor than delayed cerebral vasospasm. Acute brain injury in aneurysmal SAH is the result of physiological derangements such as increased intracranial pressure and decreased cerebral blood flow that result in global cerebral ischemia, and lead to the acute development of edema, oxidative stress, inflammation, apoptosis, and infarction. The consequence of these events is often death or significant neurological disability. In this study of acute brain injury, we elucidate some of the complex molecular signaling pathways responsible for these poor outcomes. Continued research in this area and the development of therapies to interrupt these cascades should be a major focus in the future as we continue to seek effective therapies for aneurysmal SAH.