Conditions for the generation of beta band activity in Parkinson's disease

Abstract

Background The basal ganglia plays a key role in motor control, and its dysfunction is associated with various neurological disorders including Parkinson's disease. The symptoms of Parkinson's disease include bradykinesia, characterized by a general slowing of movement execution. The advance of bradykinesia is highly correlated with the presence of abnormal oscillations within basal ganglia in the beta band frequency [1]. Some evidence suggests the oscillations observed in the basal ganglia originate from the network comprised of two nuclei: subthalamic nucleus (STN) and globus pallidus pars externa (GPe) [2], while other authors attribute their source to the entire corticobasal-ganglia-thalamic circuit [3]. In this work, we attempt to address this question of the origin of beta band oscillations.