Motor Cortical Network Excitability in Parkinson's Disease

Area of Science:

• Neuroscience
• Movement Disorders
• Clinical Electrophysiology

Background:

• Parkinson's disease (PD) motor impairments stem from basal ganglia-thalamocortical circuit dysfunction.
• Previous studies on PD motor cortex excitability used TMS-evoked EMG; TMS-evoked EEG offers broader network insights.

Purpose of the Study:

• To investigate motor cortical network excitability in Parkinson's disease using TMS-evoked EEG.
• To compare cortical excitability between PD patients (off and on medication) and healthy controls.
• To correlate cortical excitability measures with bradykinesia severity.

Main Methods:

• Compared TMS-evoked cortical potentials (TEPs) from primary motor cortex (M1) and pre-supplementary motor area (pre-SMA).
• Included 20 PD patients (off/on medication) and 19 healthy controls (HCs).
• Assessed TEPs (P30, N40 amplitudes) and their correlation with bradykinesia.

Main Results:

• Off-medication PD patients showed reduced M1 P30 amplitudes (contralateral and ipsilateral) and increased pre-SMA N40 compared to HCs.
• Dopaminergic therapy normalized M1 P30 and pre-SMA N40 amplitudes.
• A positive correlation was found between M1 P30 amplitude and bradykinesia in off-medication PD patients.

Conclusions:

• PD is associated with reduced M1 excitability and increased pre-SMA excitability.
• Dopaminergic therapy and clinical correlations suggest these changes reflect basal ganglia-thalamocortical pathway dysfunction.
• TMS-EEG provides valuable insights into motor cortical network alterations in Parkinson's disease pathophysiology.