Stephen D. Hall

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.

Neurofeedback (NF) is a promising intervention for improvements in motor performance in Parkinson’s disease. This NF pilot study in healthy participants aimed to achieve the following: (1) determine participants’ ability to bi-directionally modulate sensorimotor beta power and (2) determine the effect of NF on movement performance. A real-time EEG-NF protocol was used to train participants to increase and decrease their individual motor cortex beta power amplitude, using a within-subject double-blind sham-controlled approach. Movement was assessed using a Go/No-go task. Participants completed the NASA Task Load Index and provided verbal feedback of the NF task difficulty. All 17 participants (median age = 38 (19–65); 10 females) reliably reduced sensorimotor beta power. No participant could reliably increase their beta activity. Participants reported that the NF task was challenging, particularly increasing beta. A modest but significant increase in reaction time correlated with a reduction in beta power only in the real condition. Findings suggest that beta power control difficulty varies by modulation direction, affecting participant perceptions. A correlation between beta power reduction and reaction times only in the real condition suggests that intentional beta power reduction may shorten reaction times. Future research should examine the minimum beta threshold for meaningful motor improvements, and the relationship between EEG mechanisms and NF learning to optimise NF outcomes.

Background: Neurofeedback has been proposed as a treatment for Parkinson’s disease (PD) motor symptoms by changing the neural network activity directly linked with movement. However, the effectiveness of neurofeedback as a treatment for PD motor symptoms is unclear. Aim: To systematically review the literature to identify the effects of neurofeedback in people with idiopathic PD; as defined by measurement of brain activity; motor function; and performance. Design: A systematic review. Included Sources and Articles: PubMed; MEDLINE; Cinhal; PsychoInfo; Prospero; Cochrane; ClinicalTrials.gov; EMBASE; Web of Science; PEDro; OpenGrey; Conference Paper Index; Google Scholar; and eThos; searched using the Population-Intervention-Comparison-Outcome (PICO) framework. Primary studies with the following designs were included: randomized controlled trials (RCTs), non-RCTs; quasi-experimental; pre/post studies; and case studies. Results: This review included 11 studies out of 6197 studies that were identified from the literature search. Neuroimaging methods used were fMRI; scalp EEG; surface brain EEG; and deep brain EEG; where 10–15 Hz and the supplementary motor area were the most commonly targeted signatures for EEG and fMRI, respectively. Success rates for changing one’s brain activity ranged from 47% to 100%; however, both sample sizes and success criteria differed considerably between studies. While six studies included a clinical outcome; a lack of consistent assessments prevented a reliable conclusion on neurofeedback’s effectiveness. Narratively, fMRI neurofeedback has the greatest potential to improve PD motor symptoms. Two main limitations were found in the studies that contributed to the lack of a confident conclusion: (1) insufficient clinical information and perspectives (e.g., no reporting of adverse events), and (2) limitations in numerical data reporting (e.g., lack of explicit statistics) that prevented a meta-analysis. Conclusions: While fMRI neurofeedback was narratively the most effective treatment; the omission of clinical outcome measures in studies using other neurofeedback approaches limits comparison. Therefore, no single neurofeedback type can currently be identified as an optimal treatment for PD motor symptoms. This systematic review highlights the need to improve the inclusion of clinical information and more robust reporting of numerical data in future work. Neurofeedback appears to hold great potential as a treatment for PD motor symptoms. However, this field is still in its infancy and needs high quality RCTs to establish its effectiveness. Review Registration: PROSPERO (ID: CRD42020191097)

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.