TY - JOUR
T1 - Metamorphosis of subarachnoid hemorrhage research
T2 - From delayed vasospasm to early brain injury
AU - Sehba, Fatima A.
AU - Pluta, Ryszard M.
AU - Zhang, John H.
N1 - Funding Information:
Acknowledgments This work was supported by the American Heart Association grant number GRNT4570012 (FAS), and the National Institutes of Health, grant numbers RO1 NS050576 (FAS) and NS053407 (JHZ), and by the Intramural Research Program (RMP) of the National Institutes of Stroke and Neurological Disorders, NIH.
PY - 2011/2
Y1 - 2011/2
N2 - Delayed vasospasm that develops 3-7 days after aneurysmal subarachnoid hemorrhage (SAH) has traditionally been considered the most important determinant of delayed ischemic injury and poor outcome. Consequently, most therapies against delayed ischemic injury are directed towards reducing the incidence of vasospasm. The clinical trials based on this strategy, however, have so far claimed limited success; the incidence of vasospasm is reduced without reduction in delayed ischemic injury or improvement in the long-term outcome. This fact has shifted research interest to the early brain injury (first 72 h) evoked by SAH. In recent years, several pathological mechanisms that activate within minutes after the initial bleed and lead to early brain injury are identified. In addition, it is found that many of these mechanisms evolve with time and participate in the pathogenesis of delayed ischemic injury and poor outcome. Therefore, a therapy or therapies focused on these early mechanisms may not only prevent the early brain injury but may also help reduce the intensity of later developing neurological complications. This manuscript reviews the pathological mechanisms of early brain injury after SAH and summarizes the status of current therapies. © 2010 The Author(s).
AB - Delayed vasospasm that develops 3-7 days after aneurysmal subarachnoid hemorrhage (SAH) has traditionally been considered the most important determinant of delayed ischemic injury and poor outcome. Consequently, most therapies against delayed ischemic injury are directed towards reducing the incidence of vasospasm. The clinical trials based on this strategy, however, have so far claimed limited success; the incidence of vasospasm is reduced without reduction in delayed ischemic injury or improvement in the long-term outcome. This fact has shifted research interest to the early brain injury (first 72 h) evoked by SAH. In recent years, several pathological mechanisms that activate within minutes after the initial bleed and lead to early brain injury are identified. In addition, it is found that many of these mechanisms evolve with time and participate in the pathogenesis of delayed ischemic injury and poor outcome. Therefore, a therapy or therapies focused on these early mechanisms may not only prevent the early brain injury but may also help reduce the intensity of later developing neurological complications. This manuscript reviews the pathological mechanisms of early brain injury after SAH and summarizes the status of current therapies. © 2010 The Author(s).
KW - Cerebral ischemia
KW - Delayed vasospasm
KW - Early brain injury
KW - Subarachnoid hemorrhage
KW - Therapeutic interventions
KW - Humans
KW - Stroke/etiology
KW - Treatment Outcome
KW - Cerebrovascular Circulation
KW - Clinical Trials as Topic
KW - Brain Injuries/etiology
KW - Regional Blood Flow
KW - Subarachnoid Hemorrhage/complications
KW - Animals
KW - Time Factors
KW - Cell Death
KW - Vasospasm, Intracranial/etiology
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UR - https://www.mendeley.com/catalogue/24e280ae-4e61-36e9-96ce-35ce3375c218/
U2 - 10.1007/s12035-010-8155-z
DO - 10.1007/s12035-010-8155-z
M3 - Article
C2 - 21161614
SN - 0893-7648
VL - 43
SP - 27
EP - 40
JO - Molecular Neurobiology
JF - Molecular Neurobiology
IS - 1
ER -