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Post-movement beta rebound inhibits future movement

E. Rhodes, A. Kharko, W. Gaetz, S. Hall (Plymouth, United Kingdom)

Meeting: 2017 International Congress

Abstract Number: 1465

Keywords: Bradykinesia, Electroencephalogram(EEG), Transcranial magnetic stimulation(TMS)

Session Information

Date: Thursday, June 8, 2017

Session Title: Parkinson's Disease: Neuroimaging And Neurophysiology

Session Time: 1:15pm-2:45pm

Location: Exhibit Hall C

Objective: To evaluate the potential inhibitory effect of post-movement beta rebound (PMBR) on future movement production.

Background: Changes in the cortical power of beta oscillations within the primary motor system have been shown to correlate with various stages of movement production. During the preparation and execution of an action there is an event-related desynchronisation (ERD) of cortical beta power, then, following the cessation of movement there is a resynchronisation of the motor networks resulting in PMBR (Jurkiewicz et al., 2006). Previous research has shown that during serial movement there is an abnormal augmentation of PMBR within Parkinson’s Disease (PD) patients not seen in healthy individuals. We suggest that this cumulative increase in beta power inhibits and impairs future movement, driving bradykinesia. Therefore it is a vital step to investigate whether PMBR inhibits future movement even in healthy individuals.

Methods: EEG was recorded from 50 healthy subjects as they performed a simple single-digit, isometric button-press task. For each individual, the EEG data was then analysed to find peak PMBR latency allowing us to design our follow-up study and time our TMS stimulation. Subjects performed the same button-press task in the follow-up study whilst motor evoked potentials (MEPs) were generated using single-pulse TMS at peak PMBR, 100ms pre-peak PMBR and 100ms post-peak PMBR. MEPs for each timepoint were compared to an average of MEPs collected during a period of rest.

Results: Preliminary results suggest that average MEP amplitude is greatly reduced during PMBR. MEPs timed during peak PMBR exhibit the greatest reduction in amplitude.

Conclusions: These data suggest that PMBR does indeed inhibit future movement production. This adds weight to our suggestion that abnormal augmentation of PMBR drives the bradykinesia exhibited by PD patients during serial movement.

References: Jurkiewicz, M. T., Gaetz, W. C., Bostan, A. C., & Cheyne, D. (2006). Post-movement beta rebound is generated in motor cortex: evidence from neuromagnetic recordings. Neuroimage, 32(3), 1281-1289.

To cite this abstract in AMA style:

E. Rhodes, A. Kharko, W. Gaetz, S. Hall. Post-movement beta rebound inhibits future movement [abstract]. Mov Disord. 2017; 32 (suppl 2). https://www.mdsabstracts.org/abstract/post-movement-beta-rebound-inhibits-future-movement/. Accessed June 14, 2025.
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