Abstract
Spontaneous and “event-related” motor cortex oscillations in the beta (15–30 Hz) frequency range are well-established phenomena. However, the precise functional significance of these features is uncertain. An understanding of the specific function is of importance for the treatment of Parkinson's disease (PD), where attenuation of augmented beta throughout the motor network coincides with functional improvement. Previous research using a discrete movement task identified normalization of elevated spontaneous beta and postmovement beta rebound following GABAergic modulation. Here, we explore the effects of the gamma-aminobutyric acid type A modulator, zolpidem, on beta power during the performance of serial movement in 17 (15M, 2F; mean age, 66 ± 6.3 years) PD patients, using a repeated-measures, double-blinded, randomized, placebo-control design. Motor symptoms were monitored before and after treatment, using time-based Unified Parkinson's Disease Rating Scale measurements and beta oscillations in primary motor cortex (M1) were measured during a serial-movement task, using magnetoencephalography. We demonstrate that a cumulative increase in M1 beta power during a 10-s tapping trial is reduced following zolpidem, but not placebo, which is accompanied by an improvement in movement speed and efficacy. This work provides a clear mechanism for the generation of abnormally elevated beta power in PD and demonstrates that perimovement beta accumulation drives the slowing, and impaired initiation, of movement. These findings further indicate a role for GABAergic modulation in bradykinesia in PD, which merits further exploration as a therapeutic target.
Highlights
Spontaneous beta frequency (15–30 Hz) oscillations are a prominent electrophysiological signature of the primary motor cortex (M1) in humans [1, 2] and animal models [3]
This study expands upon previous observations that postmovement beta rebound (PMBR) is elevated in Parkinson’s disease (PD) patients to demonstrate a progressive accumulation of beta power during the course of a serial tapping task
Perimovement Beta as an Inhibitory Signal in PD. These experiments demonstrate an important mechanism by which abnormally elevated beta power following movement may impair the ability of patients to perform subsequent and serial movements in PD
Summary
Spontaneous beta frequency (15–30 Hz) oscillations are a prominent electrophysiological signature of the primary motor cortex (M1) in humans [1, 2] and animal models [3]. Beta oscillations have been posited as an “idling” rhythm of the motor system [4], in line with the conceptual need for a carrier signal to facilitate temporal binding of functional performance [5]. Beta power in M1 modulates in a task-dependent manner in relation to various phases of movement. There appears to be an increase in beta power associated with static postural maintenance [12,13,14]
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