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Subthalamic nucleus (STN) stimulation has become an accepted treatment modality for patients with advanced Parkinson disease (PD) who, despite optimal medical management, suffer from significant dyskinesias or motor fluctuations. While the clinical effects of STN stimulation are undisputed, the mechanisms underlying the symptomatic benefit are not well understood. One possibility, suggested in early studies and based on similar effects associated with STN lesions and stimulation, is that stimulation decreases neuronal activity in the STN, leading to decreased output from this structure.1–3 Alternate hypotheses suggest high frequency stimulation may activate projection axons traversing the electrical field, resulting in increased output from stimulated structures.2,3
Resolution of the controversy surrounding the mechanisms responsible for symptomatic benefits of stimulation has been difficult due, in part, to the challenges of performing direct measurements of neuronal activity in multiple neuroanatomically related structures following implantation of stimulating electrodes in …
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