TY - JOUR
T1 - Early Brain Injury, an Evolving Frontier in Subarachnoid Hemorrhage Research
AU - Fujii, Mutsumi
AU - Yan, Junhao
AU - Rolland, William B.
AU - Soejima, Yoshiteru
AU - Caner, Basak
AU - Zhang, John H.
N1 - Funding Information:
Acknowledgments This study was partially supported by grants from the National Institutes of Health NS 053407 to JHZ.
PY - 2013/8
Y1 - 2013/8
N2 - 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. © 2013 Springer Science+Business Media New York.
AB - 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. © 2013 Springer Science+Business Media New York.
KW - Animal model
KW - Cerebral vasospasm
KW - Early brain injury
KW - Subarachnoid hemorrhage
KW - Acute Disease
KW - Humans
KW - Rats
KW - Randomized Controlled Trials as Topic
KW - Subarachnoid Hemorrhage/complications
KW - Animals
KW - Brain Ischemia/etiology
KW - Mice
KW - Translational Research, Biomedical
KW - Vasospasm, Intracranial/etiology
KW - Disease Models, Animal
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UR - https://www.mendeley.com/catalogue/d265bac7-05f2-3543-a17d-86042f1fe3bd/
U2 - 10.1007/s12975-013-0257-2
DO - 10.1007/s12975-013-0257-2
M3 - Review article
C2 - 23894255
SN - 1868-4483
VL - 4
SP - 432
EP - 446
JO - Translational Stroke Research
JF - Translational Stroke Research
IS - 4
ER -