Deep brain stimulation for parkinson's disease induces spontaneous cortical hypersynchrony in extended motor and cognitive networks

Abstract

The mechanism of action of deep brain stimulation (DBS) to the basal ganglia for Parkinson's disease remains unclear. Studies have shown that DBS decreases pathological beta hypersynchrony between the basal ganglia and motor cortex. However, little is known about DBS's effects on long range corticocortical synchronization. Here, we use machine learning combined with graph theory to compare resting-state cortical connectivity between the off and on-stimulation states and to healthy controls. We found that turning DBS on increased high beta and gamma band synchrony (26 to 50 Hz) in a cortical circuit spanning the motor, occipitoparietal, middle temporal, and prefrontal cortices. The synchrony in this network was greater in DBS on relative to both DBS off and controls, with no significant difference between DBS off and controls. Turning DBS on also increased network efficiency and strength and subnetwork modularity relative to both DBS off and controls in the beta and gamma band. Thus, unlike DBS's subcortical normalization of pathological basal ganglia activity, it introduces greater synchrony relative to healthy controls in cortical circuitry that includes both motor and non-motor systems. This increased high beta/gamma synchronization may reflect compensatory mechanisms related to DBS's clinical benefits, as well as undesirable non-motor side effects.

Keywords: deep brain stimulation; functional connectivity; magnetoencephalography; parkinson’s disease; synchrony.