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A Unifying Pathophysiological Account for Post-stroke Spasticity and Disordered Motor Control.

Sheng Li1, Yen-Ting Chen1, Gerard E Francisco1

  • 1Department of Physical Medicine and Rehabilitation, McGovern Medical School, University of Texas Health Science Center - Houston and TIRR Memorial Hermann Hospital, Houston, TX, United States.

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Summary

Contralesional motor cortex hyperexcitability via the reticulospinal tract may cause post-stroke spasticity and abnormal movements. This pathway, disinhibited after stroke, warrants further investigation for potential therapeutic targets.

Keywords:
motor controlreticulospinal tractspasticitystrokesynergy

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Area of Science:

  • Neuroscience
  • Rehabilitation Medicine
  • Motor Control

Background:

  • Stroke-induced motor impairments involve complex cortical and subcortical reorganization.
  • The role of the contralesional motor cortex in motor recovery after stroke is not fully understood.
  • Reticulospinal tract (RST) hyperexcitability is implicated in post-stroke spasticity and abnormal motor control.

Purpose of the Study:

  • To propose a unifying account for the role of contralesional motor cortex plasticity in post-stroke motor impairments.
  • To highlight the potential contribution of ipsilateral PM/SMA-cortico-reticulospinal tract hyperexcitability to spasticity and disordered movement after stroke.

Main Methods:

  • Review and revision of existing theoretical frameworks based on animal and human stroke studies.
  • Analysis of corticoreticular projections, particularly ipsilateral projections from contralesional premotor cortex (PM) and supplementary motor area (SMA).

Main Results:

  • Evidence suggests upregulation of RST excitability in the contralesional hemisphere post-stroke due to disinhibition.
  • Animal studies show compensatory roles for RST hyperexcitability in motor recovery, but human studies link it to abnormal synergy and control.
  • Upregulation of ipsilateral corticoreticular projections from contralesional PM/SMA to medial reticular nuclei is highlighted.

Conclusions:

  • Ipsilateral PM/SMA-cortico-reticulospinal tract hyperexcitability from the contralesional motor cortex offers a pathophysiological basis for post-stroke spasticity and movement disorders.
  • This pathway may not contribute to normal motor recovery but underlies abnormal motor synergy and control.
  • Further research in stroke survivors is needed to validate this pathway's role in muscle strength and motor recovery, potentially guiding neuromodulatory interventions.