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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UCL, Inst Neurol, Wellcome Trust Ctr Neuroimaging, London WC1N 3BG, England
UCL, Inst Neurol, Sobell Dept Motor Neurosci & Movement Disorders, London WC1N 3BG, England
UCL, UCL Inst Cognit Neurosci, London WC1N 3BG, England
UCL, Dept Psychol, London WC1N 3BG, EnglandUCL, Inst Neurol, Wellcome Trust Ctr Neuroimaging, London WC1N 3BG, England
Bestmann, Sven
Swayne, Orlando
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UCL, Inst Neurol, Sobell Dept Motor Neurosci & Movement Disorders, London WC1N 3BG, EnglandUCL, Inst Neurol, Wellcome Trust Ctr Neuroimaging, London WC1N 3BG, England
Swayne, Orlando
Blankenburg, Felix
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UCL, Inst Neurol, Wellcome Trust Ctr Neuroimaging, London WC1N 3BG, EnglandUCL, Inst Neurol, Wellcome Trust Ctr Neuroimaging, London WC1N 3BG, England
Blankenburg, Felix
Ruff, Christian C.
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UCL, Inst Neurol, Wellcome Trust Ctr Neuroimaging, London WC1N 3BG, England
UCL, UCL Inst Cognit Neurosci, London WC1N 3BG, England
UCL, Dept Psychol, London WC1N 3BG, EnglandUCL, Inst Neurol, Wellcome Trust Ctr Neuroimaging, London WC1N 3BG, England
Ruff, Christian C.
Haggard, Patrick
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UCL, UCL Inst Cognit Neurosci, London WC1N 3BG, England
UCL, Dept Psychol, London WC1N 3BG, EnglandUCL, Inst Neurol, Wellcome Trust Ctr Neuroimaging, London WC1N 3BG, England
Haggard, Patrick
Weiskopf, Nikolaus
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UCL, Inst Neurol, Wellcome Trust Ctr Neuroimaging, London WC1N 3BG, EnglandUCL, Inst Neurol, Wellcome Trust Ctr Neuroimaging, London WC1N 3BG, England
Weiskopf, Nikolaus
Josephs, Oliver
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UCL, Inst Neurol, Wellcome Trust Ctr Neuroimaging, London WC1N 3BG, EnglandUCL, Inst Neurol, Wellcome Trust Ctr Neuroimaging, London WC1N 3BG, England
Josephs, Oliver
Driver, Jon
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UCL, Inst Neurol, Wellcome Trust Ctr Neuroimaging, London WC1N 3BG, England
UCL, UCL Inst Cognit Neurosci, London WC1N 3BG, England
UCL, Dept Psychol, London WC1N 3BG, EnglandUCL, Inst Neurol, Wellcome Trust Ctr Neuroimaging, London WC1N 3BG, England
Driver, Jon
Rothwell, John C.
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UCL, Inst Neurol, Sobell Dept Motor Neurosci & Movement Disorders, London WC1N 3BG, EnglandUCL, Inst Neurol, Wellcome Trust Ctr Neuroimaging, London WC1N 3BG, England
Rothwell, John C.
Ward, Nick S.
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UCL, Inst Neurol, Wellcome Trust Ctr Neuroimaging, London WC1N 3BG, England
UCL, Inst Neurol, Dept Brain Repair & Rehabil, London WC1N 3BG, EnglandUCL, Inst Neurol, Wellcome Trust Ctr Neuroimaging, London WC1N 3BG, England