Controversies and evolving new mechanisms in subarachnoid hemorrhage.
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.
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.
Sheng
S
Chen
Department of Neurosurgery, Southwest Hospital, Third Military Medical University, Chongqing, China.
Hua
H
Feng
Department of Physiology & Pharmacology, Loma Linda University, Loma Linda, CA, USA.
Prativa
P
Sherchan
Department of Physiology & Pharmacology, Loma Linda University, Loma Linda, CA, USA.
Damon
D
Klebe
Department of Neurology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shanxi, China.
Gang
G
Zhao
Department of Neurosurgery, First Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Xiaochuan
X
Sun
Department of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Jianmin
J
Zhang
Department of Physiology & Pharmacology, Loma Linda University, Loma Linda, CA, USA.
Jiping
J
Tang
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.
John H
JH
Zhang
D000818:Animals; D001808:Blood Vessels / Q000502:physiology; D001930:Brain Injuries / Q000453:epidemiology / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D018450:Disease Progression; D049671:History, 18th Century; D049672:History, 19th Century; D049673:History, 20th Century; D049674:History, 21st Century; D049690:History, Ancient; D049691:History, Medieval; D006801:Humans; D009457:Neuroglia / Q000502:physiology; D009474:Neurons / Q000502:physiology; D013345:Subarachnoid Hemorrhage / Q000150:complications* / Q000453:epidemiology / Q000266:history
Delayed brain injury; Early brain injury; Subarachnoid hemorrhage; Vasculo-neuronal-glia triad model; Vasospasm