Movement disorders are categorized as hypokinetic (Parkinson's disease) or hyperkinetic (Huntington's disease, hemiballism, or dystonia). Neuroscience research over the last several years, using data obtained in animal models for these disorders and data from patients undergoing stereotactic surgery, has greatly advanced the knowledge of the pathophysiologic basis of these diseases. This article offers a summary and critique of current models of the pathophysiology underlying hypokinetic and hyperkinetic diseases and a discussion of the implications of these models for neurosurgical procedures as treatment for these disorders.