Reorganization of the human ipsilesional premotor cortex after stroke

 

In my case since most of my premotor cortex is dead there can be no transfer from prefrontal to premotor.  I had to figure out what died in my brain by myself since my useless doctor told me nothing on diagnosis or rehab.

Reorganization of the human ipsilesional premotor cortex after stroke

Esteban A. Fridman, Takashi Hanakawa, Melissa Chung, Friedhelm Hummel, Ramon C. Leiguarda, Leonardo G. Cohen

Brain, Volume 127, Issue 4, April 2004, Pages 747–758, https://doi.org/10.1093/brain/awh082

Published:

01 April 2004

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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 (M1_AH, PMd_AH, PMv_AH) and intact (M1_IH, PMd_IH, PMv_IH) 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 PMd_AH of patients elicited clear delays in contralateral SRT in the paretic hand, whereas TMS applied to PMd_IH of patients or healthy volunteers did not. Motor evoked potentials after stimulation of PMd_AH were, on average, larger and had, on average, shorter latency than after stimulation of M1_AH. These results indicate that PMd_AH 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.