Abstract
Recordings from Parkinson's disease (PD) patients show strong beta-band oscillations (13-35 Hz), which can be modulated by deep brain stimulation (DBS). While high-frequency DBS (>100 Hz) ameliorates motor symptoms and reduces beta activity in the basal ganglia and motor cortex, the effects of low-frequency DBS (<30 Hz) are less clear. Clarifying these effects is relevant for the debate about the role of beta oscillations in motor slowing, which might be causal or epiphenomenal. Here, we investigated how subthalamic nucleus (STN) beta-band DBS affects cortical beta oscillations and motor performance. We recorded the magnetoencephalogram of 14 PD patients (nine males) with DBS implants while on their usual medication. Following a baseline recording (DBS OFF), we applied bipolar DBS at beta frequencies (10, 16, 20, 26, and 30 Hz) via the left electrode in a cyclic fashion, turning stimulation on (5 s) and off (3 s) repeatedly. Cyclic stimulation was applied at rest and during right-hand finger tapping. In the baseline recording, we observed a negative correlation between the strength of hemispheric beta power lateralization and the tap rate. Importantly, beta-band DBS accentuated the lateralization and reduced the tap rate proportionally. The change in lateralization was specific to the alpha/beta range (8-26 Hz), outlasted stimulation, and did not depend on the stimulation frequency, suggesting a remote-induced response rather than entrainment. Our study demonstrates that cortical beta oscillations can be manipulated by STN beta-band DBS. This manipulation has consequences for motor performance, supporting a causal role of beta oscillations.