Motor map plasticity as a model for studying functional improvements after stroke. The loss of neural tissue associated with stroke induces profound neurophysiological changes throughout the brain that incite a wide range of behavioral impairments. Such impairments are not solely a manifestation of the damaged brain region, but are also an expression of the ability of the rest of the brain to maintain normal function. Indeed, the capacity to maintain function is often hindered by a cascade of neuronal events within residual neural tissue after stroke including inflammation, edema and deafferentation that can occur both proximal and distal to the infarction. In some instances, behavioral improvements can be attributed to the progressive resolution of these factors that allow for the compromised brain areas to regain control of lost function. However, functional gains can be brought about that are independent of simply resolving neural dysfunction resulting from edema or inflammation. These changes can be driven by rehabilitation and are supported by structural and functional adaptation of residual neural circuits. Identifying the specific neural mechanisms underlying rehabilitation-dependent neural plasticity for any given functional impairment after stroke is not trivial. It is difficult to obtain neurobiological measures that can be directly related to specific changes in behavior and thereby targeted for therapy. For example, even in healthy subjects we do not yet have a neural measure that directly reflects linguistic ability or capacity for memory, so it is difficult to identify specific adaptations in function related to recovery from aphasia or amnesia in brain-injured patients.
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