Reorganization of the human ipsilesional premotor cortex after stroke.

TitleReorganization of the human ipsilesional premotor cortex after stroke.
Publication TypeJournal Article
Year of Publication2004
AuthorsFridman, Esteban A., Hanakawa Takashi, Chung Melissa, Hummel Friedhelm, Leiguarda Ramon C., and Cohen Leonardo G.
JournalBrain
Volume127
IssuePt 4
Pagination747-58
Date Published2004 Apr
ISSN0006-8950
KeywordsAged, Aged, 80 and over, Chronic Disease, Electromagnetic Fields, Electromyography, Evoked Potentials, Motor, Female, Humans, Magnetic Resonance Imaging, Male, Motor Cortex, Neuronal Plasticity, Psychomotor Performance, Reaction Time, Recovery of Function, Stroke
Abstract

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.

DOI10.1093/brain/awh082
Alternate JournalBrain
PubMed ID14749291

Weill Cornell Medicine Consortium for the Advanced Study of Brain Injury 520 East 70th Street New York, NY