In addition to the well-known motor symptoms, sensory symptoms are also common and sensory abnormalities have been documented in Parkinson's disease (PD). Although deep brain stimulation (DBS) of the subthalamic nucleus (STN) is increasingly being used to treat PD, it mechanism of action is unknown. In a previous study, we found that the way sensory input (produced by median nerve stimulation at the wrist) changes the excitability of the part of the brain that mediates voluntary movement known as the motor cortex is abnormal in PD patients. This will be referred to as deficient sensorimotor integration. Part of this abnormality was worsened by dopaminergic drugs while another aspect of this abnormality was unaffected by drugs. However, the functional significance of these findings are unclear. The aims of the present study are to 1) Examine the relationship between deficit in position sense, dyskinesia and abnormal sensorimotor integration in PD. 2) Determine whether STN DBS can reverse deficient sensorimotor integration and whether the effects are due to short-term or long-term effects of STN DBS. Fourteen PD patients who are scheduled to undergo STN DBS will be studied before surgery both on and off medications. The study will be repeated 2-4 weeks and more than 6 months after surgery to examine both the acute and chronic effects of STN DBS. At each study the severity of PD and dyskinesia will be rated with established clinical rating scales. Position sense will be assessed quantitatively using an electromagnetic device. Sensorimotor integration will be tested with median nerve stimulation followed by magnetic stimulation of the motor cortex. The results will clarify the functional significance of deficient sensorimotor integration in PD and the mechanism of action of STN stimulation.