Reorganisation of cerebral circuits in human ischemic brain disease.
Animal experiments suggest that reorganisation of cerebral representations is the neurobiological basis of post-lesional recovery. In human ischemic brain disease recovery is a dynamic and sustained process beginning after stroke manifestation. The mechanisms underlying recovery can be investigated non-invasively in the human brain using functional neuroimaging and transcranial magnetic stimulation (TMS). In the acute stage, the mismatch area of the perfusion deficit and the impaired water diffusion as assessed by magnetic resonance imaging (MRI) shows the brain tissue that potentially can be rescued by thrombolysis or emergency carotid endarterectomy. Since spontaneous motor recovery is a function of the corticospinal tract integrity, early reperfusion of ischemic tissue is critical. In the subacute and chronic stage after stroke, recovery of motor function was shown to take place irrespective of a concomitant affection of the somatosensory system. Functional MRI with simultaneous recordings of the electromyogram provides evidence that the abnormal activation of motor and premotor cortical areas in both hemispheres related to finger movements has a large interindividual variability. As evident from TMS, recovery results from regression of perilesional inhibition and from remote intracortical disinhibition. Repetitive training, constraint induced training and motor imagery can augment recovery promoting a re-emerging activation in the affected hemisphere. Evolution of altered local perilesional and large-scale bihemispheric circuits appears to allow for post-lesional deficit compensation.
Seitz
Rüdiger J
RJ
Department of Neurology, University Hospital Düsseldorf, Moorenstrasse 5, 40225 Düsseldorf, Germany. seitz@neurologie.uni-duesseldorf.de
Bütefisch
Cathrin M
CM
Kleiser
Raimund
R
Hömberg
Volker
V
D002545:Brain Ischemia / Q000503:physiopathology* / Q000534:rehabilitation; D006801:Humans; D009415:Nerve Net / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology*; D020127:Recovery of Function / Q000502:physiology*