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Prog Neurobiol. 2014 Apr;115:64-91. doi: 10.1016/j.pneurobio.2013.09.002. Epub 2013 Sep 25.

Controversies and evolving new mechanisms in subarachnoid hemorrhage.

Author information

1
Department of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China; Department of Physiology & Pharmacology, Loma Linda University, Loma Linda, CA, USA.
2
Department of Neurosurgery, Southwest Hospital, Third Military Medical University, Chongqing, China.
3
Department of Physiology & Pharmacology, Loma Linda University, Loma Linda, CA, USA.
4
Department of Neurology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shanxi, China.
5
Department of Neurosurgery, First Affiliated Hospital, Chongqing Medical University, Chongqing, China.
6
Department of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
7
Department of Physiology & Pharmacology, Loma Linda University, Loma Linda, CA, USA; Department of Neurosurgery, Loma Linda University, Loma Linda, CA, USA. Electronic address: johnzhang3910@yahoo.com.

Abstract

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.

KEYWORDS:

Delayed brain injury; Early brain injury; Subarachnoid hemorrhage; Vasculo-neuronal-glia triad model; Vasospasm

PMID:
24076160
PMCID:
PMC3961493
DOI:
10.1016/j.pneurobio.2013.09.002
[Indexed for MEDLINE]
Free PMC Article

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