Introduction: Excessive beta (13-30 Hz) oscillatory activity in the basal ganglia thalamocortical network has been proposed as a biomarker for the parkinsonian state, based on the finding that reduction of beta oscillations in the basal ganglia by levodopa and deep brain stimulation (DBS) correlates with motor symptom improvement. Two prior studies comparing pallidal local field potentials (LFPs) between Parkinson’s disease (PD) and non-parkinsonian conditions supported a relative increase in beta band oscillatory activity in PD, but it is not clear how these differences affect cortical function.
Methods: In 20 PD and 14 isolated dystonia patients undergoing pallidal DBS lead implantation, we recorded LFPs from the globus pallidus (GP) and in a subset of these, recorded simultaneous sensorimotor cortex electrocorticography (ECoG) potentials.
Results: PD patients had higher pallidal resting low beta (13-30 Hz) band power compared to dystonia patients, whereas dystonia patients had higher theta (4-8 Hz) resting power compared to PD. We show that this results in disease-specific patterns of interaction between the pallidum and motor cortex: PD patients demonstrated relatively elevated phase synchrony with the motor cortex in the beta band and this synchrony was reduced by pallidal DBS. Dystonia patients had greater theta band phase synchrony.
Conclusions: Our results support the hypothesis that specific motor signs of movement disorders are associated with elevated network oscillations in specific frequency bands, and that DBS in movement disorders acts in general by disrupting elevated phase synchrony between basal ganglia output and motor cortex.
Patient Care: Our study identifies disease-specific physiological biomarkers for Parkinson's disease and isolated dystonia in the globus pallidus, and describes a mechanism for DBS in movement disorders by disrupting these excessive pallido-cortical oscillatory interactions.
Learning Objectives: By the conclusion of this session, participants should be able to: 1) Describe the different patterns of pallidal oscillatory outflow in Parkinson's disease and isolated dystonia, 2) Identify disease-specific patterns of interaction between the pallidum and motor cortex in Parkinson's disease and isolated dystonia, and 3) Understand the effect of pallidal DBS on pallidal beta oscillations and pallido-cortical beta frequency interactions.