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Experimental Models of Human Stroke

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Part of the book series: Neuromethods ((NM,volume 22))

Abstract

Stroke in humans consists of a focal neurological deficit that develops abruptly, attributable to either cerebral vessel occlusion or to the spontaneous rupture of an intracranial artery with hemorrhage into the brain parenchyma or subarachnoid space (Walker and Marx, 1981). Brain infarction, a localized lesion caused by the occlusion of a brain vessel (usually an artery), accounts for about 75% of the lesions produced by stroke, with brain hemorrhage (11%) and subarachnoid hemorrhage (5%) accounting for most of the rest (Anderson and Whisnant, 1982; Robins and Baum, 1981; Sacco et al., 1982). Thus, human stroke takes many forms depending on the etiology and spatial/temporal characteristics of the lesion. Consequently, there has been a variety of experimental stroke models developed to mimic the conditions that arise in human cerebrovascular accidents. These include many varied paradigms: in vivo and in vitro, global and focal, complete and incomplete ischemia, as well as hemorrhagic and nonhemorrhagic insults. In addition, these models may be adapted to study the events that occur upon recirculation following an ischemic episode. Two of these models will be described in detail: the bilateral common carotid artery occlusion model of global ischemia in the gerbil, and the middle cerebral artery occlusion model of focal ischemia in the rat.

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Seta, K.A., Crumrine, R.C., Whittingham, T.S., Lust, W.D., McCandless, D.W. (1992). Experimental Models of Human Stroke. In: Boulton, A.A., Baker, G.B., Butterworth, R.F. (eds) Animal Models of Neurological Disease, II. Neuromethods, vol 22. Humana Press. https://doi.org/10.1385/0-89603-211-6:1

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