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(Stroke. 2004;35:2690.)
© 2004 American Heart Association, Inc.

Articles

Recovery and Rehabilitation in Stroke

Introduction

From the Landon Center on Aging and Department of Molecular and Integrative Physiology (R.J.N.), University of Kansas Medical Center, Kansas City, Ks; and the University of Florida Brooks Center for Rehabilitation Studies and Department of Veteran Affairs Rehabilitation Outcomes Research Center of Excellence (P.W.D.), Gainesville, Fla.

Correspondence to Dr Randolph J. Nudo, Director, Landon Center on Aging, Professor, Dept of Molecular and Integrative Physiology, Landon Center on Aging, Mail Stop 1005, KU Medical Center, 3901 Rainbow Blvd, Kansas City, KS 66160.

An extract of the first 250 words of the full text is provided, because this article has no abstract.

A large proportion of individuals who survive stroke are chronically disabled, making stroke a leading cause of serious, long-term disability. Although our society has made great strides in improving stroke awareness and survivability, until recently, the prospects for long-term improvement in sensorimotor disability and function were bleak. It is widely recognized that spontaneous recovery accounts for a significant portion of the functional improvement that occurs in the first several weeks after stroke. However, a number of new approaches, spurred by advances in the neurosciences, especially in the field of neuroplasticity, have provided hope that further improvement in function can be spurred by specific manipulations of the neural and behavioral environment.

The long-term consequences of ischemic damage on neuronal structures are beginning to unfold. An increasing number of studies in rodents, nonhuman primates, and humans have now demonstrated the potential for sensorimotor regions of the brain to undergo structural and functional alterations as a function of use and injury. After neuronal death, such as occurs in stroke, spared neural structures in the adjacent tissue, and remote structures in the ipsilesional and contralesional (intact) hemisphere undergo significant functional changes. For example, GABAa receptors are downregulated in widespread regions of the spared cerebral cortex for long periods of time after the initial infarct. Dendrites proliferate, are subsequently pruned, and substantial synaptogenesis occurs. Hemodynamic changes occur throughout the spared tissue. New blood vessels are formed, at least in the peri-infarct zone.

It is becoming clear that one of the most potent modulators of neural . . . [Full Text of this Article]

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