Abstract
Deep brain stimulation of the subthalamic nucleus (STN) is an increasingly prevalent treatment for advanced Parkinson's disease (PD). Its main mechanism of action is thought to be a reduction in the inhibitory outflow from basal ganglia to cerebral cortex. However, recent animal experiments have led to the suggestion that high frequency stimulation of the STN also acts by promoting dopamine release. We tested this hypothesis by performing [11C]raclopride PET on and off stimulation in six patients with PD and implanted STN stimulators. There was no difference in tracer binding in the striatum between the two testing conditions. We conclude that high frequency stimulation of the STN does not act by increasing dopamine release.
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