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(Stroke. 2006;37:314.)
© 2006 American Heart Association, Inc.

Advances in Stroke 2005

Brain Recovery and Rehabilitation

From the Max-Planck-Institut für Neurologische Forschung and Department of Neurology der Universitat zu Köln (W.-D.H.), and the University of Western Ontario and St Joseph’s Health Care, London (R.T.)

Correspondence to Wolf-Dieter Heiss, der Universitat zu Köln Joseph-Stelzmann-Str. 9, D-50931 Köln, Germany. E-mail wdh@nf.mpg.de

Key Words: brain recovery • rehabilitation

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

Rehabilitation after a stroke is undergoing a renaissance of sorts, with growing evidence of rehabilitation’s impact extending from cortical reorganization to its effect on health-related quality of life.

Functional Neuroimaging

Functional recovery after focal brain lesions is dependent on the adaptive plasticity of the cerebral cortex and of the nonaffected elements of the functional network.¹ For the motor system, it has been convincingly demonstrated that after cortical injury the adjacent spared cortical tissue as well as more remote cortical areas are altered resulting in a functionally modified network.^2–4 Small lesions in the somatosensory cortex lead to changes of excitability attributable to down-regulation of GABA_A-receptors and up-regulation of NMDA-receptors⁵ in remote brain areas, and these changes in both excitatory and inhibitory neurotransmission may be part of an adaptive process involved in functional reorganization.⁶ As a consequence, newly learned movements after focal cortical injury are represented over larger cortical territories,^3,4,7,8 an effect which is dependent on the intensity of rehabilitative training.⁹ Along with these changes in excitatory and inhibitory neurotransmitter systems, widespread structural changes with dendritic sprouting and synapse formation take place in spared regions of the damaged hemisphere, but also in the sensorimotor cortex of the hemisphere contralateral to the injury.^10,11 One could speculate that the change in excitability in adjacent and contralateral homotopic regions of a cortical lesion is a consequence of reduced collateral and transcallosal inhibition.

It was also convincingly demonstrated that specialized areas inhibit neighboring regions and (even contralateral) brain regions connected by fiber pathways.^12–18 Recent repetitive transcranial magnetic . . . [Full Text of this Article]