Considerable evidence suggests a role of beta-band oscillations in voluntary movements. However, most of the studies linking beta power to motor performance are based on data averaged across trials that ignore the fast dynamics of oscillatory activity and trial-to-trial variations in motor responses. Recently, emphasis has shifted from the functional implications of the mean beta power to the presence and nature of episodic bursts of beta activity. Here we test the hypothesis that beta bursts, though short in duration in more physiological state, may help explain spontaneous variations in motor behavior of human adults at the single-trial level. To this end, we recorded local field potential activity from the subthalamic nucleus of parkinsonian patients of both genders whose motor behavior had been normalized as far as possible through treatment with the dopamine prodrug, levodopa. We found that beta bursts present in a time-limited window well before movement onset in the contralateral subthalamic nucleus reduce the peak velocity of that movement and that this effect is further amplified by the amplitude of the burst. Additionally, prolonged reaction times are observed when bursts occur immediately after the GO cue. Together, these results suggest that the modulation of the timing and amplitude of beta bursts might serve to dynamically adapt motor performance. These results offer new insight in the pathology of Parkinson's disease, and suggest that beta bursts whose presence and nature are modulated by context may have a physiological role in modulating behavior. Beta oscillations (∼13-30 Hz) have been increasingly interpreted as transient bursts rather than as rhythmically sustained oscillations (Feingold et al., 2015). Prolonged and increased probability of beta bursts in the subthalamic nucleus correlates with the severity of motor impairment in Parkinson's disease (Tinkhauser et al., 2017a, b). However, it remains unclear whether beta bursts act to modify motor performance on a trial-by-trial basis under more physiological condition. Here, we found that, according to the time window in which they fall, beta bursts reduced the velocity of the forthcoming movement or prolonged the reaction time. These results offer new insight in the pathology of Parkinson's disease and also suggest that the modulation of beta bursts might serve to dynamically adapt motor performance.

In a recent study, Tan et al. (2014a,b) showed that the increase in ␤-power typically observed after a movement above sensorimotor regions (␤-rebound) is attenuated when movement-execution errors are induced by visual perturbations. Moreover, akin to sensorimotor adaptation, the effect depended on the context in which the errors are experienced. Thus the ␤-rebound attenuation might relate to neural processes involved in trial-to-trial adaptive mechanisms. In two EEG experiments with human participants, along with the ␤-rebound, we examine ␤-activity during the preparation of reaches immediately following perturbed movements. In the first experiment, we show that both foreperiod and postmovement ␤-activities are parametrically modulated by the sizes of kinematic errors produced by unpredictable mechanical perturbations (force field) independent of their on-line corrections. In the second experiment, we contrast two types of reach errors: movement-execution errors that trigger trial-to-trial adaptive mechanisms and goal errors that do not elicit sensorimotor adaptation. Movement-execution errors were induced by mechanical or visual perturbations, whereas goal errors were caused by unexpected displacements of the target at movement initiation. Interestingly, foreperiod and postmovement ␤-activities exhibit contrasting patterns, pointing to important functional differences of their underlying neuronal activity. While both types of reach errors attenuate the postmovement ␤-rebound, only the kinematic errors that trigger trial-to-trial motor-command updates influenced ␤-activity during the foreperiod. These findings suggest that the error-related modulation of the ␤-rebound may reflect salience processing, independent of sensorimotor adaptation. In contrast, modulations in the foreperiod ␤-power might relate to the motorcommand adjustments activated after movement-execution errors are experienced.