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Effects of Small Ischemic Lesions in the Primary Motor Cortex on Neurophysiological Organization in Ventral Premotor Cortex

¹Department of Neurology, University of Rochester Medical Center, Rochester, New York; and ²Departments of Molecular and Integrative Physiology and ³Preventive Medicine and Public Health, ⁴Landon Center on Aging, ⁵Mental Retardation Research Center, ⁶Center for Biostatistics and Advanced Informatics, ⁷University of Kansas Medical Center, Kansas City, Kansas

Submitted 1 August 2006; accepted in final form 14 September 2006

After a cortical lesion, cortical areas distant from the site of injury are known to undergo physiological and anatomical changes. However, the mechanisms through which reorganization of distant cortical areas is initiated are poorly understood. In a previous publication, we showed that the ventral premotor cortex (PMv) undergoes physiological reorganization after a lesion destroying the majority of the primary motor cortex (M1) distal forelimb representation (DFL). After large lesions destroying >50% of the M1 DFL, the PMv DFL invariably increased in size, and the amount of the increase was positively correlated with the size of lesion. To determine whether lesions destroying <50% of the M1 DFL followed a similar trajectory, we documented PMv reorganization using intracortical microstimulation techniques after small, ischemic lesions targeting subregions within the M1 DFL. In contrast to earlier results, lesions resulted in a reduction of the PMv DFL regardless of their location. Further, because recent anatomical findings suggest a segregation of PMv connectivity with M1, we examined two lesion characteristics that may drive alterations in PMv physiological reorganization: location of the lesion with respect to PMv connectivity and relative size of the lesion. The results suggest that after a lesion in the M1 DFL, the induction of representational plasticity in PMv, as evaluated using intracortical microstimulation, is related more to the size of the lesion than to the disruption of its intracortical connections.

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