Based on the results of two preliminary studies, we concluded that late-developing persistent drug-induced movement disorders are pharmacologically heterogeneous, and this heterogeneity is seen between individual patients (and groups of patients) as well as within body areas of individual patients; dystonic pathology has a distinct and more consistent response to pharmacologic stimulation than does nondystonic tardive dyskinesia (TD); and, although disturbances in dopamine and acetylcholine appear to be involved in these disorders, they do not in all cases exist in functionally opposite relationships. The observed pharmacologic heterogeneity in TD response reflects the limitations of the dopamine/acetylcholine model of TD, which oversimplifies the neuroanatomy of the basal ganglia and the pathophysiology of TD. The chemical and anatomical complexity of this region suggests that other neurotransmitter systems and neuronal circuits within and extending from the basal ganglia may be disturbed in the pathogenesis of TD.