Brain stimulation in the awake patient was systematically used by Penfield to map cortical functions during epilepsy and tumor surgery.1 Although it was initially thought that such stimulation activated circuits much like turning on a tape recorder, electrophysiologic mapping during stereotactic surgery showed that high-frequency stimulation could temporarily disrupt normal neural activity and produce a functional lesion.2 This eventually led to the use of deep brain stimulation (DBS) to replace Vim thalamotomy for the treatment of tremor.3 Now hailed as the holy grail of treatment for advanced Parkinson disease (PD), dystonia, and tremor, but also applied to the treatment of chronic pain, Tourette syndrome, depression, Huntington disease, obsessive-compulsive disorder, and epilepsy, DBS is established as a major technique in functional neurosurgery. The pathophysiologic basis of DBS is proposed to be the induction of a functional lesion, a cancellation of error messages, or perhaps the liberation of transmitter either locally or at a distance from the point stimulated.4 Subthalamic nucleus (STN) DBS allows the reduction of dopaminergic medication by approximately 50% and provides long-term improvement of motor symptoms.5 Stimulation of other brain targets (e.g., the globus pallidus internus) is of less benefit and does not reduce the need for dopaminergic medication.6 This raises the question as to whether (and to what extent) STN DBS activates dopaminergic …