Abstract
Movement related beta band cortical oscillations, including beta rebound after execution and/or suppression of movement, have drawn attention in upper extremity motor control literature. However, fewer studies focused on beta band oscillations during postural control in upright stance. In this preliminary study, we examined beta rebound and other components of electroencephalogram (EEG) activity during perturbed upright stance to investigate supraspinal contributions to postural stabilization. Particularly, we aimed to clarify the timing and duration of beta rebound within a non-sustained, but long-lasting postural recovery process that occurs more slowly compared to upper extremities. To this end, EEG signals were acquired from nine healthy young adults in response to a brief support-surface perturbation, together with the center of pressure, the center of mass and electromyogram (EMG) activities of ankle muscles. Event-related potentials (ERPs) and event-related spectral perturbations were computed from EEG data using the perturbation-onset as a triggering event. After short-latency (<0.3 s) ERPs, our results showed a decrease in high-beta band oscillations (event-related desynchronization), which was followed by a significant increase (event-related synchronization) in the same band, as well as a decrease in theta band oscillations. Unlike during upper extremity motor tasks, the beta rebound in this case was initiated before the postural recovery was completed, and sustained for as long as 3 s with small EMG responses for the first half period, followed by no excessive EMG activities for the second half period. We speculate that those novel characteristics of beta rebound might be caused by slow postural dynamics along a stable manifold of the unstable saddle-type upright equilibrium of the postural control system without active feedback control, but with active monitoring of the postural state, in the framework of the intermittent control.
Highlights
Supraspinal contributions to postural stabilization during human upright stance have been demonstrated by postural instability in patients with neurological disorders such as Parkinson’s disease (PD), multiple sclerosis, and stroke (e.g., Horak et al, 1992; Frzovic et al, 2000; Geurts et al, 2005; Visser et al, 2008; Perera et al, 2018; Suzuki et al, 2020)
Based on preceding numerical simulations of the intermittent postural control model in section “Theoretical Background,” it was expected that the late phase of the postural recovery, which is characterized theoretically by slow dynamics along a stable manifold of the saddle-type unstable upright equilibrium point in the absence of active feedback control, might be accompanied with the sensorimotor information processing
We showed that neural responses for re-stabilizing upright posture lasted over a relatively long periods of time, which is consistent to our hypothesis
Summary
Supraspinal contributions to postural stabilization during human upright stance have been demonstrated by postural instability in patients with neurological disorders such as Parkinson’s disease (PD), multiple sclerosis, and stroke (e.g., Horak et al, 1992; Frzovic et al, 2000; Geurts et al, 2005; Visser et al, 2008; Perera et al, 2018; Suzuki et al, 2020). Electroencephalogram (EEG) activity and/or motoneuronal responses to transcranial magnetic stimulation (TMS) during standing are more direct methods to characterize electrical activity of the cerebral cortex associated with postural control. There is relatively limited knowledge on how activities of the cerebral cortex, those measured by EEG, encode sensory information processing and motor control during stabilization of upright stance (Jacobs and Horak, 2007; Bolton, 2015; Wittenberg et al, 2017)
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