HUMAN MOTOR CORTEX ORGANIZATION: HOMUNCULAR PLASTICITY AND ITS MECHANISM

Abstract

The primary motor cortex (M1) contains a somatotopic progression with highly overlapping areas outputting to muscles of the upper limb. This organization is modified by muscle activity and neurological injury such as spinal cord injury (SCI). To date, bilateral M1 organization in controls and SCI has been minimally explored, and no study has examined the cortical territory that directs output to multiple muscles thought to be involved in movement synergies. An initial study was conducted to characterize the bilateral organization and representational overlap for muscles of the upper limb in incomplete spinal cord injury relative to uninjured individuals. Differences in symmetry and amount of overlapping territory were observed between groups, possibly reflecting differences in synergistic muscle use. The second study examined transcallosal communication between the two motor cortices and its role in dynamically modulating motor representations during unilateral contraction. The depth of interhemispheric inhibition (IHI) was examined in a muscle of the right hand by delivering a conditioning stimulus to ipsilateral M1 followed by a test stimulus to contralateral M1. Reduced IHI corresponded to larger cortical territory, a relationship that existed for both contralateral and ipsilateral contraction. These data demonstrate that the magnitude of IHI in a hand muscle predicts the size of the cortical territory occupied by that muscle. We present a mechanistic model to explain these findings that further elucidate the role of interhemispheric communication in shaping motor output. This interaction between transcallosal inhibition and motor output may act as a component to experience-dependent plasticity within M1. By targeting this interaction, it may be possible to facilitate motor learning and performance or promote recovery of function following neurological injury. Further study examining the role of various intracortical circuits on representational plasticity and modulation of these interactions may yield advances in both basic and clinical neuroscience.