Considerable evidence is now available to indicate that hypokinetic movement disorders, such as PD, and hyperkinetic disorders, such as dystonia, ballismus, and chorea, represent circuit disorders, which result from varying forms of abnormally patterned activity throughout the motor circuit of the basal ganglia. The specific clinical features of these disorders may depend on the unique combination of changes in discharge rate, pattern, and synchronization of discharge and varying degrees of involvement of individual motor subcircuits. Remarkably, these heterogeneous disorders all respond to the same surgical approaches, which either remove or modify the abnormal activity within the larger motor circuit. Such interventions may work by (nonspecifically) freeing thalamocortical and brainstem motor systems from abnormal and disruptive basal ganglia influences. Evidence indicates that the brain can compensate far better for the loss of basal ganglia output produced by ablation than for the corrupted output that characterizes the individual movement disorders and that neuromodulation (eg, DBS) is a highly effective, less invasive, and more flexible alternative to ablation.