The broad objective of this project is to understand the pathophysiology of dopa-induced dyskinesisas in Parkinson's disease. By defining the functional brain abnormalities in patients with dopa-induced dyskinesias, pharmacological and surgical treatment techniques for Parkinson's disease can be more rationally developed and refined. In addition, these results will have implications for current models of basal ganglia-thalamocortical physiology. Using functional neuroimaging (PET) and pharmacological activation techniques, we have identified specific abnormality in the activation of the ventrolateral thalamus in patients with dopa-induced dyskinesias. By examining these patients' cerebral blood flow responses to levodopa before and after surgical lesion to the internal pallidum (performed for clinical purposes entirely unrelated to this study) specific hypothesis regarding the inputs responsible for this thalamic over-activation can be tested.