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Hyper-synchrony despite pathologically-reduced beta oscillations in patients with Parkinson's disease: A pharmaco-magnetoencephalography study.

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J Neurophysiol 2014 Jul;

Authors: Elizabeth Heinrichs-Graham, Max J Kurz, Katherine M Becker, Pamela M Santamaria, Howard E Gendelman, Tony W Wilson

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

PMID: 25008416 [PubMed - as supplied by publisher]

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