Balance impairment is a common and disabling symptom of Parkinson's disease, but the brain mechanisms underlying individual differences are poorly understood. Beta oscillations (13–30 Hz) in the sensorimotor cortex are enhanced both in aging and in Parkinson's disease. They are thought to 'lock in' the current motor state, preventing flexible responses to changes. The work sits at the intersection of research on EEG markers of Parkinson's disease and the neurophysiology of postural control, where it has already been shown that the N1 evoked potential from the supplementary motor cortex reflects the processing of balance perturbations. However, the link between background beta activity and clinical balance in older adults with and without Parkinson's disease remained unclear.
Participants stood on a movable platform that unexpectedly shifted forward or backward with varying force. EEG was recorded from 32 electrodes, then an independent component maximally related to the N1 potential (the brain's response to perturbation at 100–200 ms) was extracted. From this component, a power spectrum was constructed for the second before the push and decomposed into periodic (oscillatory) and aperiodic components using the FOOOF algorithm. Balance was assessed with the Mini-BESTest clinical scale. Groups were compared and correlations between beta rhythm parameters and balance scores were sought, including regression models with group-by-beta-parameter interactions.
The groups did not differ in average or peak beta rhythm power. However, in people with Parkinson's disease, higher beta power significantly correlated with worse balance (r = -0.67 for average power, p = 0.003; r = -0.64 for peak power, p = 0.006). In healthy older adults, no such correlations were found. The interaction between group and beta power was significant (β = -1.37, p = 0.003, η²p = 0.25), confirming the specificity of the effect to Parkinson's disease. In healthy older adults, a link emerged between a higher central frequency of the beta peak and worse balance (r = -0.53, p = 0.02). Aperiodic parameters did not correlate with balance.
The work shows that background beta activity in the supplementary motor cortex may be not just a marker of Parkinson's disease but a factor limiting the sensory perception and motor updating needed to maintain balance. Unlike neighboring studies that examined evoked potentials or resting-state beta activity, this one for the first time links pre-perturbation beta power from a localized source to clinical balance. This shifts the focus from averaged power to the dynamics of beta bursts as a potentially more sensitive marker.
It would be promising to study beta bursts (short episodes of enhanced beta rhythm) instead of averaged power: their frequency and duration may better distinguish Parkinson's disease from aging. Longitudinal studies will help understand how changes in beta activity relate to the progression of balance impairments. Experiments with separate manipulation of sensory and motor demands will clarify which aspect of information processing is disrupted.
The results could influence the development of neurophysiological biomarkers for balance impairment in Parkinson's disease and approaches to neuromodulation (for example, adaptive deep brain stimulation targeting beta activity).
Check whether the characteristics of beta bursts before perturbation correlate with balance in patients with Parkinson's disease. Conduct longitudinal monitoring of beta activity and balance as the disease progresses.
The work addresses an unresolved problem: why some people with Parkinson's disease have more severe balance impairment than others despite similar motor symptom severity. It also raises the question of the specificity of the beta rhythm as a marker: whether to distinguish pathological enhancement from age-related changes.
The supplementary motor area (SMA), the region from which the signal was extracted, is involved in movement planning and was first described in monkeys in the 1950s. Damage to it in humans causes alien hand syndrome.
Not published on arXiv. Here are its page, the PDF and the formalization: you can check it yourself, not only read our account.