| Description |
Healthy cortical and subthalamic beta power shows a robust correlation with motor events, where increased power is associated with motor suppression. However, patients with Parkinson's disease and animal models of the disease show substantially higher beta power, and structures within the parkinsonian cortico-basal ganglia network appear coupled together, with persistently high coherence in the beta range. Furthermore, symptomatic therapies reduce beta power and coherence while alleviating motor symptoms like akinesia and rigidity. These observations have led to the hypothesis that motor impairment in PD could be related to pathological beta oscillations. However, a direct correlation between beta power and symptom severity has been elusive. We aim to elucidate a better understanding of how maladaptive changes to movement-related beta dynamics in the parkinsonian condition may be associated with akinetic symptoms. In this work, we contrast healthy and parkinsonian beta responses under different motor conditions, and we explore how symptomatic relief could be associated with changes in beta dynamics induced by DBS.We discovered that a healthy brain regulates cortical beta power roughly as a linear function of locomotive speed and that nigral dopaminergic neurodegeneration breaks this relation. We show that restoration of this linear modulation of power is a better predictor of symptomatic amelioration than average cortical beta power taken over a long period. We also found that healthy cortical beta rebound and cortico-subthalamic coherence measured during a stop are predictors of the speed of the subsequent movement. Although these dynamic responses are absent in PD, they are mostly restored by subthalamic high-frequency DBS. On the other hand, coherence at the onset of acceleration after a stop follows the same dynamics for healthy and parkinsonian animals, suggesting this mechanism is preserved, or even amplified, in the pathophysiology of the disease. Although this response is also seen in the healthy condition, we show that it is eliminated in parkinsonian animals by DBS. Our results suggest that changes in healthy beta dynamics may facilitate the generation of future movement, but that this dynamic adaptation is impaired in PD, where a more rigid beta dynamic suggests a bias for the suppression of movement. |
