The basic pathogenesis of TD appears to relate to chronic pharmacologic denervation of specific dopaminergic receptor sites in the striatum. The pathophysiology of the disorder relates to the resultant denervation hypersensitivity. The mainstay of treatment includes withdrawal of neuroleptics when feasible and the use of dopamine-depleting agents. Enhancement of the striatal cholinergic input offers potential ancillary benefit to the alleviation of abnormal movements. The possibility of benefit from manipulating other neurotransmitters remains experimental. Treatment of TD with neuroleptics themselves is clearly treatment with the presumed offending agent and should be avoided. This shortsighted therapy may temporarily abate the pathophysiology of the condition, but it serves to aggravate its pathogenesis.