Presentation Title

Hyper-connectivity despite pathologically-reduced beta activity in the motor cortex of patients with Parkinson’s disease

Advisor Information

Tony Wilson

Location

UNO Criss Library, Room 107

Presentation Type

Oral Presentation

Start Date

7-3-2014 11:30 AM

End Date

7-3-2014 11:45 AM

Abstract

Parkinson’s disease (PD) is a progressive debilitating neurodegenerative disorder clinically manifested 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 activity throughout the basal ganglia-thalamic-cortical motor network in PD. Notably, suppression of this pathological beta activity 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 connectivity 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 in the bilateral 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 connectivity 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 also 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.

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Mar 7th, 11:30 AM Mar 7th, 11:45 AM

Hyper-connectivity despite pathologically-reduced beta activity in the motor cortex of patients with Parkinson’s disease

UNO Criss Library, Room 107

Parkinson’s disease (PD) is a progressive debilitating neurodegenerative disorder clinically manifested 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 activity throughout the basal ganglia-thalamic-cortical motor network in PD. Notably, suppression of this pathological beta activity 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 connectivity 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 in the bilateral 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 connectivity 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 also 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.