Post-Movement Beta Synchrony Inhibits Cortical Excitability

Abstract

Background/objectives: This study investigates the relationship between movement-related beta synchrony and primary motor cortex (M1) excitability, focusing on the time-dependent inhibition of movement. Voluntary movement induces beta frequency (13-30 Hz) event-related desynchronisation (B-ERD) in M1, followed by post-movement beta rebound (PMBR). Although PMBR is linked to cortical inhibition, its temporal relationship with motor cortical excitability is unclear. This study aims to determine whether PMBR acts as a marker for post-movement inhibition by assessing motor-evoked potentials (MEPs) during distinct phases of the beta synchrony profile.

Methods: Twenty-five right-handed participants (mean age: 24 years) were recruited. EMG data were recorded from the first dorsal interosseous muscle, and TMS was applied to the M1 motor hotspot to evoke MEPs. A reaction time task was used to elicit beta oscillations, with TMS delivered at participant-specific time points based on EEG-derived beta power envelopes. MEP amplitudes were compared across four phases: B-ERD, early PMBR, peak PMBR, and late PMBR.

Results: Our findings demonstrate that MEP amplitude significantly increased during B-ERD compared to rest, indicating heightened cortical excitability. In contrast, MEPs recorded during peak PMBR were significantly reduced, suggesting cortical inhibition. While all three PMBR phases exhibited reduced cortical excitability, a trend toward amplitude-dependent inhibition was observed.

Conclusions: This study confirms that PMBR is linked to reduced cortical excitability, validating its role as a marker of motor cortical inhibition. These results enhance the understanding of beta oscillations in motor control and suggest that further research on altered PMBR could be crucial for understanding neurological and psychiatric disorders.

Keywords: B-ERD; PMBR; beta synchrony; cortical excitability; motor control; movement; oscillations.

Figure 1

Experimental Protocol. (A) Schematic summary of a trial, showing the screen presentation and time course of the cue onset and duration, rest period, and overall trial length. (B) EMG measurement and response–device arrangement, showing the location of the force sensor beneath the tip of the index finger (1), locations of the FDI EMG sensor (2) and ulnar process reference (3). (C) EEG and MEP block designs, showing the arrangement of data acquisition in Experiments 1 (top) and 2 (bottom). (D) The 5 electrode EEG array centred on the functionally–localized M1.

Figure 2

Time-frequency spectrogram. Grand-averaged Morlet Wavelet time-frequency analysis output from all participants, showing the mean oscillatory power in M1 across the experimental trial, with zero time-locked to cue onset.

Figure 3

Characterisation of the beta-change time-points for TMS stimulation showing a representative single trial for an individual participant. (A) Normalised beta power at individual peak frequency, (B) Normalised EMG amplitude, and (C) Mean force production. Dashed vertical lines indicate the time-point selected for stimulation, as summarised in Table 1.

Figure 4

EMG Amplitude at beta-change time-points showing the difference from baseline in the mean peak-to-peak amplitude of MEPs induced during the four beta-change time-points. Data are normalised to the rest period, with statistically significant differences denoted as follows: ** p < 0.01; * p < 0.05.