The complexity of neurobiological processes in acute ischemic stroke

被引:478
作者
Brouns, R. [1 ,2 ,3 ,4 ]
De Deyn, P. P. [1 ,2 ,3 ]
机构
[1] Univ Antwerp, Lab Neurochem & Behav, Born Bunge Fdn, B-2610 Antwerp, Belgium
[2] Middelheim Hosp, Dept Neurol, Antwerp, Belgium
[3] Middelheim Hosp, Memory Clin, Antwerp, Belgium
[4] Vrije Univ Brussel, Univ Brussels, Dept Neurol, Brussels, Belgium
关键词
Acute ischemic stroke; Pathophysiology; Bioenergetic failure; Excitoxicity; Oxidative stress; Microvascular injury; Post-ischemic inflammation; Hemostatic activation; Blood-brain barrier dysfunction; BLOOD-BRAIN-BARRIER; FOCAL CEREBRAL-ISCHEMIA; CARBOXYPEPTIDASE-U TAFIA; ACTIVATABLE FIBRINOLYSIS INHIBITOR; INTERCELLULAR-ADHESION MOLECULE-1; TISSUE-PLASMINOGEN ACTIVATOR; NITRIC-OXIDE SYNTHASE; PLATELET-LEUKOCYTE INTERACTION; CORONARY-ARTERY THROMBOSIS; EARLY CLINICAL PROGRESSION;
D O I
10.1016/j.clineuro.2009.04.001
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
There is an urgent need for improved diagnostics and therapeutics for acute ischemic stroke. This is the focus of numerous research projects involving in vitro studies, animal models and clinical trials, all of which are based on current knowledge of disease mechanisms underlying acute focal cerebral ischemia. Insight in the chain of events occurring during acute ischemic injury is essential for understanding current and future diagnostic and therapeutic approaches. In this review, we summarize the actual knowledge on the pathophysiology of acute ischemic stroke. We focus on the ischemic cascade, which is a complex series of neurochemical processes that are unleashed by transient or permanent focal cerebral ischemia and involves cellular bioenergetic failure, excitotoxicity, oxidative stress, blood-brain barrier dysfunction, microvascular injury, hemostatic activation, post-ischemic inflammation and finally cell death of neurons, glial and endothelial cells. (c) 2009 Elsevier B.V. Ail rights reserved.
引用
收藏
页码:483 / 495
页数:13
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