Vicarious function of remote cortex following stroke: recent evidence from human and animal studies.
Following a lesion, the adult central nervous system undergoes dramatic structural and physiological reorganization in diverse subcortical and cortical areas. Our knowledge of the events that parallel recovery within the tissue surrounding the lesion and other distant cortical areas has evolved greatly in the past few years. Particularly, recent efforts have increased our understanding of the potential implication of premotor areas in recovery from lesions disturbing the primary motor cortex (M1) and its corticospinal outputs. Because these areas share extensive connections with M1 and have direct access to the spinal cord through corticospinal projections, they are particularly well positioned to take over the role of M1 in a vicarious manner and thus compensate for the neuronal loss resulting from M1 lesions. The impressive postlesional reorganization known to occur in many areas of the CNS including the premotor cortex traditionally has been assumed to play a beneficial role in recovery. However, recent experiments suggest that in some cases, reorganization of distant cortical areas correlates with poor recovery, raising the concept of maladaptive vicarious process. This concept might be particularly critical in the development of new treatment approaches favoring postlesion plasticity and even more so for interventions targeting specific area(s). Here, the author reviews human and animal studies that show the plastic potential of the adult CNS after stroke, highlighting the vicarious role of the premotor cortex in the recovery of motor control.
Dancause
Numa
N
Department of Neurology, University of Rochester, Rochester, NY 14642, USA. numa_dancause@urmc.rochester.edu
D000818:Animals; D001931:Brain Mapping; D002540:Cerebral Cortex / Q000473:pathology / Q000503:physiopathology*; D007839:Functional Laterality / Q000502:physiology*; D006801:Humans; D009473:Neuronal Plasticity; D020521:Stroke / Q000473:pathology / Q000503:physiopathology*