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Updated: Jan 30, 2026

Measuring Contralateral Silent Period Induced by Single-Pulse Transcranial Magnetic Stimulation to Investigate M1 Corticospinal Inhibition
Published on: August 23, 2022
Changes in the cortical silent period during force control
1a Faculty of Rehabilitation , Shijonawate Gakuen University , Daitou City , Japan.
Purpose:
The contribution of gamma-aminobutyric acidergic inhibitory neural circuits in the primary motor cortex, as estimated by the cortical silent period, during weak and strong force output has not been defined. The aim of this study was to investigate whether cortical silent period is modulated with change from weak to strong force control.
Materials And Methods:
Eleven healthy right-handed adults participated in this study. With the aid of visual feedback, participants were asked to control the force of abduction of the right index finger to 10%, 20%, 40%, 60%, 80%, and 100% of the maximum voluntary contraction. Single pulse transcranial magnetic stimulation was delivered to the left primary motor cortex region during force control tasks. The averaged actual force output level, background electromyography amplitude, and cortical silent period duration were compared between conditions, and correlation analysis was conducted.
Results:
There were significant main effects of target force on background electromyography, and cortical silent period duration; with increased force, the actual force output level and background electromyography gradually increased, while cortical silent period duration gradually decreased. There were significant negative correlations between cortical silent period and force and cortical silent period and background electromyography.
Conclusions:
These findings indicate that the excitability of gamma-aminobutyric acidergic inhibitory neural circuits in primary motor cortex decreases in response to increased force output, mediated via increased corticospinal and motoneuron excitability. These results may facilitate understanding of the role of the gamma-aminobutyric acidergic circuit in primary motor cortex in force control, as well as of the mechanism underlying motor dysfunction in stroke-induced palsy, dystonia, and cerebellar ataxia.
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