Interhemispheric and ipsilateral connections in Parkinson's disease: relation to mirror movements

Jie-Yuan Li1, Alberto J Espay, Carolyn A Gunraj

  • 1Division of Neurology, Department of Medicine, Toronto Western Research Institute, University of Toronto, Toronto, Ontario, Canada.

Insights

Mirror movements in Parkinson's disease (PD) stem from contralateral motor cortex activation. Reduced transcallosal inhibition in PD patients with mirror movements (PD-MM) impacts cortical circuits.

Area of Science:

  • Neuroscience
  • Motor Control
  • Clinical Neurology

Background:

  • Mirror movements (MM) are observed in early Parkinson's disease (PD), particularly in asymmetric cases.
  • The underlying pathophysiology of MM in PD remains incompletely understood.

Purpose of the Study:

  • To investigate the neural mechanisms contributing to mirror movements in Parkinson's disease.
  • To compare corticospinal excitability and interhemispheric inhibition between PD patients with and without MM, and healthy controls.

Main Methods:

  • Studied 13 PD patients with MM (PD-MM), 7 PD patients without MM (PD-NM), and 14 healthy controls.
  • Utilized cross-correlogram analysis to assess synaptic input to motoneurons.
  • Employed transcranial magnetic stimulation (TMS) to evaluate ipsilateral motor-evoked potentials, silent periods, short-interval intracortical inhibition (SICI), and intracortical facilitation (ICF).

Main Results:

  • No common synaptic input detected in PD-MM motoneurons.
  • MM side showed altered silent period dynamics during muscle contraction.
  • Reduced interhemispheric inhibition (IHI) at long intervals observed in PD-MM compared to PD-NM.
  • IHI failed to modulate SICI in PD-MM, unlike in controls and PD-NM.
  • IHI increased ICF in PD-MM and PD-NM, but not in controls.

Conclusions:

  • Mirror movements in PD are likely caused by contralateral motor cortex activation.
  • PD-MM patients exhibit diminished transcallosal inhibition affecting cortical output and inhibitory circuits.
  • Deficits in transcallosal inhibition may be a key factor contributing to MM in Parkinson's disease.

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