Movement disorders associated with basal ganglia dysfunction comprise a spectrum of abnormalities that range from the hypokinetic disorders (of which Parkmson's disease is the best-known example) at one extreme to the hyperkinetic disorders (exemplified by Huntington's disease and hemiballismus) at the other. Both extremes of this movement disorder spectrum can be accounted for by postulating specific disturbances within the basal ganglia-thalamocortical'motor'circuit. In this paper, Mahlon DeLong describes the changes in neuronal activity in the motor circuit in animal models of hypo-and hyperkinetic disorders.

Hypokinetic disorders are characterized by significant impairments in movement initiation (akinesia) and reductions in the amplitude and velocity of voluntary movements (bradykinesia). Hypokinetic disorders are usua!! y accompanied by muscular rigidity and tremor at rest. By contrast, hyperkinetic disorders are characterized by excessive motor activity in the form of involuntary movements (dyskinesias) and varying degrees of hypotonia. In recent years, the development of primate models of these disorders (induced by systemic or local administration of selective neurotoxins) has made it possible to clarify some of the pathophysiological mechanisms underlying such diverse symptomatology as the hypokinesia of parkinsonism and the involuntary, hyperkinetic movements of hemiballismus and other dyskinesias. This range of movement disorders can be explained using a functional model of the basal ganglia-thalamocortical'motor'circuit that incorporates current data from a variety of experimental fields 1-3.