naa a22 4500 510776086 CHVBK 20180411083230.0 cr unu---uuuuu 180411e20130801xx s 000 0 eng 10.1007/s12975-013-0257-2 doi (NATIONALLICENCE)springer-10.1007/s12975-013-0257-2 Early Brain Injury, an Evolving Frontier in Subarachnoid Hemorrhage Research [Elektronische Daten] [Mutsumi Fujii, Junhao Yan, William Rolland, Yoshiteru Soejima, Basak Caner, John Zhang] Subarachnoid hemorrhage (SAH), predominantly caused by a ruptured aneurysm, is a devastating neurological disease that has a morbidity and mortality rate higher than 50%. Most of the traditional in vivo research has focused on the pathophysiological or morphological changes of large arteries after intracisternal blood injection. This was due to a widely held assumption that delayed vasospasm following SAH was the major cause of delayed cerebral ischemia and poor outcome. However, the results of the CONSCIOUS-1 trial implicated some other pathophysiological factors, independent of angiographic vasospasm, in contributing to the poor clinical outcome. The term early brain injury (EBI) has been coined and describes the immediate injury to the brain after SAH, before onset of delayed vasospasm. During the EBI period, a ruptured aneurysm brings on many physiological derangements such as increasing intracranial pressure, decreased cerebral blood flow, and global cerebral ischemia. These events initiate secondary injuries such as blood-brain barrier disruption, inflammation, and oxidative cascades that all ultimately lead to cell death. Given the fact that the reversal of vasospasm does not appear to improve patient outcome, it could be argued that the treatment of EBI may successfully attenuate some of the devastating secondary injuries and improve the outcome of patients with SAH. In this review, we provide an overview of the major advances in EBI after SAH research. Springer Science+Business Media New York, 2013 Subarachnoid hemorrhage nationallicence Early brain injury nationallicence Cerebral vasospasm nationallicence Animal model nationallicence Fujii Mutsumi Department of Physiology, Loma Linda University, 92354, Loma Linda, CA, USA aut Yan Junhao Department of Physiology, Loma Linda University, 92354, Loma Linda, CA, USA aut Rolland William Department of Physiology, Loma Linda University, 92354, Loma Linda, CA, USA aut Soejima Yoshiteru Department of Physiology, Loma Linda University, 92354, Loma Linda, CA, USA aut Caner Basak Department of Physiology, Loma Linda University, 92354, Loma Linda, CA, USA aut Zhang John Department of Neurosurgery, Loma Linda University, School of Medicine, 11234 Anderson Street, Room 2562B, 92354, Loma Linda, CA, USA aut Translational Stroke Research Springer US; http://www.springer-ny.com 4/4(2013-08-01), 432-446 1868-4483 4:4<432 2013 4 12975 https://doi.org/10.1007/s12975-013-0257-2 text/html Onlinezugriff via DOI 1 review-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s12975-013-0257-2 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Fujii Mutsumi Department of Physiology, Loma Linda University, 92354, Loma Linda, CA, USA aut NATIONALLICENCE 700 1- Yan Junhao Department of Physiology, Loma Linda University, 92354, Loma Linda, CA, USA aut NATIONALLICENCE 700 1- Rolland William Department of Physiology, Loma Linda University, 92354, Loma Linda, CA, USA aut NATIONALLICENCE 700 1- Soejima Yoshiteru Department of Physiology, Loma Linda University, 92354, Loma Linda, CA, USA aut NATIONALLICENCE 700 1- Caner Basak Department of Physiology, Loma Linda University, 92354, Loma Linda, CA, USA aut NATIONALLICENCE 700 1- Zhang John Department of Neurosurgery, Loma Linda University, School of Medicine, 11234 Anderson Street, Room 2562B, 92354, Loma Linda, CA, USA aut NATIONALLICENCE 773 0- Translational Stroke Research Springer US; http://www.springer-ny.com 4/4(2013-08-01), 432-446 1868-4483 4:4<432 2013 4 12975 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer