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Increasing evidence identifies the possibility of restoring function to the damaged brain via exogenous therapies. One major target for these advances is stroke, where most patients can be left with significant disability. Treatments have the potential to improve the victim's quality of life significantly and reduce the time and expense of rehabilitation. Brain Repair After Stroke reviews the biology of spontaneous brain repair after stroke in animal models and in humans. Detailed chapters cover the many forms of therapy being explored to promote brain repair and consider clinical trial issues in this context. This book provides a summary of the neurobiology of innate and treatment-induced repair mechanisms after hypoxia and reviews the state of the art for human therapeutics in relation to promoting behavioral recovery after stroke. Essential reading for stroke physicians, neurologists, rehabilitation physicians and neuropsychologists.
Plasticity after injury to the CNS
Randolph J. Nudo, Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS, USA,
Ines Eisner-Janowicz, Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS, USA,
Ann M. Stowe, Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS, USA
Animal models have been especially useful in understanding the role of neuroplasticity in recovery of sensorimotor skills after brain injury. The type of injury and the method of induction vary with the specific purposes of the experiment. Typically, injuries are of two types: those designed to mimic traumatic brain injury (TBI) and those designed to mimic cerebral ischemia (or stroke). Studies conducted in cortical sensory areas over the past several years have revealed that representational maps are alterable as a function of the integrity of their sensory inputs, and as a function of experience. Changes in two neurotransmitter systems, gammaaminobutyric acid (GABA) and glutamate, have been implicated to play a role in functional recovery. New strategies for promoting recovery that were derived from basic studies in preclinical models are being tested in clinical trials. Approaches employing neurotrophins, neuromodulators, stem cells, magnetic stimulation, and electrical stimulation are currently under development.
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