Neural mechanisms of postural sway-related beta-band oscillations: a cortico-basal ganglia-thalamic network model of intermittent control

Electroencephalographic (EEG) studies of human quiet stance demonstrate beta-band event-related desynchronization (beta-ERD) during the micro-fall phase of postural sway, followed by event-related synchronization (beta-ERS; post-movement beta rebound) during the micro-recovery phase. These modulations correlate with intermittent ankle muscle inactivation that exploits the stable manifolds of an unstable upright equilibrium; however, the underlying neurocircuit mechanisms remain elusive. Here, we investigated this rhythmogenesis using an embodied spiking neural network model of the cortico-basal ganglia-thalamic (CBGT) circuitry integrated with a physical inverted pendulum. In this closed-loop system, continuous sensory feedback is integrated into the striatum, while the motor cortex executes decisions via drift-diffusion-like population competition, where the decision time (DT) represents the intermittent control-off period. We demonstrate that simulated cortical LFPs exhibit characteristic sway-phase-locked beta-ERD and beta-ERS exclusively when corticostriatal synaptic weights are functionally balanced to implement intermittent control. Conversely, forced-choice continuous control that ceaselessly generates feedback torque fails to replicate these modulations, sustaining flat network states devoid of control-off periods (DT). Structural dissections reveal that while sensory drive remains continuous, sway-phase-locked beta modulations are an emergent property generated fundamentally by bidirectional thalamocortical loops and the intrinsic dynamics of the GPe-STN pacemaker circuit. Our findings suggest that CBGT-mediated, sway-phase-locked beta activity serves as a hallmark of healthy intermittent motor selection. This computational framework provides a crucial bridge linking pathological alterations in basal ganglia dynamics and the loss of behavioral intermittency to the postural impairments observed in clinical populations such as Parkinsons disease. Significance StatementDuring quiet standing, human cortical beta oscillations dynamically modulate in phase with postural sway. Although this phenomenon is heavily linked to healthy motor control, the underlying neural mechanisms have remained unknown. This study resolves this ambiguity by developing a closed-loop computational model combining physical body dynamics with a cortico-basal ganglia-thalamic network. We demonstrate that human-like cortical beta modulations naturally emerge as an architectural property under an intermittent control strategy, driven fundamentally by the GPe-STN pacemaker circuit. Crucially, transitioning to a continuous control regime completely abolishes these oscillations. This framework establishes a direct neurocomputational link between the loss of behavioral intermittency and the pathological degradation of beta-band dynamics observed in patients with Parkinsons disease.