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PD 1 1 2 Hyper-synchrony despite pathologically-reduced beta oscillations 3 in patients with Parkinson ’ s disease : A pharmaco-4 magnetoencephalography study 5 6 7

39 Parkinson’s disease (PD) is a progressive debilitating neurodegenerative disorder clinically 40 manifest by motor, posture and gait abnormalities. Human neurophysiological studies recording 41 local field potentials within the subthalamic nucleus and scalp-based electroencephalography 42 have shown pathological beta synchrony throughout the basal ganglia-thalamic-cortical motor 43 network in PD. Notably, suppression of this pathological beta synchrony by dopamine 44 replacement therapy or deep-brain stimulation has been associated with improved motor 45 function. However, due to the invasive nature of these studies, it remains unknown whether this 46 “pathological beta” is actually stronger than that observed in healthy demographically-matched 47 controls. We used magnetoencephalography (MEG) to investigate neuronal synchrony and 48 oscillatory amplitude in the beta range and lower frequencies during the resting-state in patients 49 with PD and a matched group of patients without neurologic disease. Patients with PD were 50 studied both in the practically-defined drug “OFF” state, and after administration of dopamine 51 replacements. We found that beta oscillatory amplitude was reduced bilaterally in the primary 52 motor cortices of un-medicated patients with PD compared with controls. Administration of 53 dopaminergic medications significantly increased beta oscillatory activity, thus having a 54 normalizing effect. Interestingly, we also found significantly stronger beta synchrony (i.e., 55 hyper-synchrony) between the primary motor cortices in un-medicated patients with PD 56 compared with controls, and that medication reduced this coupling which is in agreement with 57 the intra-operative studies. These results are consistent with the known functionality of the basal 58 ganglia-thalamic-cortical motor circuit, and the likely consequences of beta hyper-synchrony in 59 the subthalamic nucleus of patients with PD. 60