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2014 ; 115
(ä): 64-91
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Controversies and evolving new mechanisms in subarachnoid hemorrhage
#MMPMID24076160
Chen S
; Feng H
; Sherchan P
; Klebe D
; Zhao G
; Sun X
; Zhang J
; Tang J
; Zhang JH
Prog Neurobiol
2014[Apr]; 115
(ä): 64-91
PMID24076160
show ga
Despite decades of study, subarachnoid hemorrhage (SAH) continues to be a serious
and significant health problem in the United States and worldwide. The mechanisms
contributing to brain injury after SAH remain unclear. Traditionally, most in
vivo research has heavily emphasized the basic mechanisms of SAH over the
pathophysiological or morphological changes of delayed cerebral vasospasm after
SAH. Unfortunately, the results of clinical trials based on this premise have
mostly been disappointing, implicating some other pathophysiological factors,
independent of vasospasm, as contributors to poor clinical outcomes. Delayed
cerebral vasospasm is no longer the only culprit. In this review, we summarize
recent data from both experimental and clinical studies of SAH and discuss the
vast array of physiological dysfunctions following SAH that ultimately lead to
cell death. Based on the progress in neurobiological understanding of SAH, the
terms "early brain injury" and "delayed brain injury" are used according to the
temporal progression of SAH-induced brain injury. Additionally, a new concept of
the vasculo-neuronal-glia triad model for SAH study is highlighted and presents
the challenges and opportunities of this model for future SAH applications.