Brain Advance Access originally published online on January 28, 2004
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Brain, Vol. 127, No. 4, 747-758, 2004
© 2004 Guarantors of Brain
doi: 10.1093/brain/awh082
Reorganization of the human ipsilesional premotor cortex after stroke
1 Human Cortical Physiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA, 2 Department of Neurology, FLENI, Buenos Aires, Argentina,
3 Kyoto University Graduate School of Medicine, Human Brain Research Centre, Kyoto, JapanCorrespondence to: Dr. Leonardo G. Cohen, Human Cortical Physiology Section, NINDS, NIH, Bldg. 10, Room 5N226, 10 Center Drive, MSC-1430, Bethesda, MD 20892-1428, USA E-mail: CohenL{at}ninds.nih.gov
The substrates that mediate recovery of motor function after stroke are incompletely understood. Several primate and human studies proposed the involvement of the premotor cortex of the lesioned hemisphere. Here, we studied four chronic stroke patients with focal subcortical lesions affecting the corticospinal outflow originating in the primary motor cortex (M1) and good motor recovery. We tested the hypothesis that, in these patients, disruption of activity in the premotor cortex of the lesioned hemisphere by transcranial magnetic stimulation (TMS) would result in degraded behaviour in the paretic hand. TMS was applied to the primary motor cortex, dorsal premotor cortex (PMd) and ventral premotor cortex (PMv) of the affected (M1AH, PMdAH, PMvAH) and intact (M1IH, PMdIH, PMvIH) hemispheres of patients and healthy controls in the setting of a simple reaction time (SRT) paradigm performed with the hand contralateral to the stimulated hemisphere. TMS applied to M1 led to substantial contralateral SRT delays in both groups. TMS applied to PMdAH of patients elicited clear delays in contralateral SRT in the paretic hand, whereas TMS applied to PMdIH of patients or healthy volunteers did not. Motor evoked potentials after stimulation of PMdAH were, on average, larger and had, on average, shorter latency than after stimulation of M1AH. These results indicate that PMdAH participates as a substrate mediating functional recovery of executive motor function in patients with focal lesions of corticospinal outflow originating in M1 and good motor recovery. Our results are consistent with the hypothesis that the dorsal premotor cortex of the affected hemisphere can reorganize to control basic parameters of movement usually assigned to M1 function.
Key Words: stroke; motor cortex; rehabilitation; pre-motor cortex; reaction time
Abbreviations: BA= Brodmann area; CS = corticospinal fibres; FDI = first dorsal interosseus; LICI = long-latency intracortical inhibition; M1 = primary motor cortex; MEP = motor evoked potential; ns = not significant; MRC = Medical Research Council; PMd = dorsal premotor cortex; PMv = ventral premotor cortex; RMT = resting motor threshold; RT = reaction time; SP = silent period; SRT = simple reaction time; TMS = transcranial magnetic stimulation
Received May 14, 2003. Accepted November 22, 2003.
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