The importance of early brain injury after subarachnoid hemorrhage

• Published in: Progress in neurobiology Vol. 97; no. 1; pp. 14 - 37
• Main Authors: Sehba, Fatima A, Hou, Jack, Pluta, Ryszard M, Zhang, John H
• Format: Journal Article
• Language: English
• Published: England 01-04-2012
• Subjects: Age; Age Factors; Aneurysm; Animal models; Arteries; Attention; Autopsy; Brain Injuries - etiology; Brain injury; Humans; Ischemia; Nervous system; Stroke; subarachnoid hemorrhage; Subarachnoid Hemorrhage - complications; Time Factors; Translation; Vasoconstriction
• ISSN: 0301-0082; 1873-5118; 1873-5118
• DOI: 10.1016/j.pneurobio.2012.02.003

Aneurysmal subarachnoid hemorrhage (aSAH) is a medical emergency that accounts for 5% of all stroke cases. Individuals affected are typically in the prime of their lives (mean age 50 years). Approximately 12% of patients die before receiving medical attention, 33% within 48 h and 50% within 30 days of aSAH. Of the survivors 50% suffer from permanent disability with an estimated lifetime cost more than double that of an ischemic stroke. Traditionally, spasm that develops in large cerebral arteries 3-7 days after aneurysm rupture is considered the most important determinant of brain injury and outcome after aSAH. However, recent studies show that prevention of delayed vasospasm does not improve outcome in aSAH patients. This finding has finally brought in focus the influence of early brain injury on outcome of aSAH. A substantial amount of evidence indicates that brain injury begins at the aneurysm rupture, evolves with time and plays an important role in patients' outcome. In this manuscript we review early brain injury after aSAH. Due to the early nature, most of the information on this injury comes from animals and few only from autopsy of patients who died within days after aSAH. Consequently, we began with a review of animal models of early brain injury, next we review the mechanisms of brain injury according to the sequence of their temporal appearance and finally we discuss the failure of clinical translation of therapies successful in animal models of aSAH.