A cortico-basal ganglia-thalamic network model linking intermittent postural control to sway-related beta-band oscillations

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, how such sway-related beta dynamics may arise within closed-loop brain–body interactions remains unclear. Here, we investigated a possible circuit-level account of these dynamics using an embodied spiking neural network model of the cortico-basal ganglia-thalamic (CBGT) circuitry integrated with an 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 when corticostriatal synaptic weights are functionally balanced to implement intermittent control. Conversely, a forced-choice continuous-like regime that ceaselessly generates feedback torque fails to replicate these modulations, sustaining flat network states devoid of control-off periods (DT). Structural dissections show that, within the model, disrupting bidirectional thalamocortical loops or the GPe-STN circuit abolishes sway-phase-locked beta modulation, despite continuous sensory drive. Our findings provide a computational account linking sway-phase-locked beta activity to intermittent motor selection within the proposed CBGT framework. This closed-loop modeling framework offers a testable candidate account for how alterations in brain–body dynamics may jointly affect behavioral intermittency and beta-band modulation, with potential relevance to postural impairments in clinical conditions such as Parkinson’s disease. Significance Statement Intermittent motor commands during quiet standing are accompanied by phase-specific cortical beta-band modulations, but how these neural dynamics may relate to intermittent postural control remains unclear. Here, using a closed-loop model integrating spiking cortico-basal ganglia-thalamic (CBGT) circuitry with body dynamics, we show that human-like beta modulations arise when the model implements intermittent control. Within the model, these modulations are abolished by disrupting thalamocortical or GPe-STN interactions and are absent in a forced-choice continuous-like regime. These findings provide a computational account linking intermittent postural control to sway-related beta dynamics and identify circuit interactions sufficient for their emergence within the proposed CBGT framework. The model offers testable predictions for investigating how brain–body interactions shape beta dynamics in healthy and impaired postural control.