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The term “tardive dyskinesia” (TD) applies only to abnormal involuntary movements resulting from chronic treatment with agents that block central dopamine receptors. In most instances, these drugs are antipsychotic neuroleptic agents. Nonetheless, other dopaminergic receptor blockers such as metoclopramide are associated with the same disorder.1 Schoenecker associated oral–facial dyskinesia with chlorpromazine treatment in 1957, yet three decades later a cause-and-effect relationship between neuroleptic therapy and involuntary movements was still questioned.2,3 The controversy persisted in part because neuroleptics are most commonly used to treat psychosis and agitated senile depression; mannerisms resembling the movements of TD can occur spontaneously in some persons with psychosis and in normal elderly patients.4


Nonetheless, the unequivocal occurrence of involuntary movements after chronic neuroleptic therapy in nonpsychotic young adults without other cause for movement disorders5 leaves no doubt that TD does occur. The 1980 American Psychiatric Association Task Force provided a useful definition of TD as “an abnormal involuntary movement, not including tremor, resulting from treatment with a neuroleptic drug for 3 months in persons with no other identifiable cause for movement disorder.”6 New descriptions add the possibility that tremor might need to be included as a form of TD. This discussion focuses on four topics: phenomenology, epidemiology and natural history, pathophysiology, and treatment of TD.

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A variety of movements occur in TD. Most common are rapid unsustained movements variously described as choreic or stereotypic.7,8 The former term refers to movements that are unpredictable and flow from one body region to another, whereas stereotypic movements are reproducible and regular, remaining generally restricted in their anatomic distribution. Controversy exists currently as to which term is best for most rapid TD movements and the authors have personally seen instances of both, sometimes in the same patient. Any body area may be affected, but the mouth is commonly involved, producing lip-smacking, tongue protrusion, or grimacing. In addition to facial movements, rapid movements of the fingers, hands or more proximal arm, nodding or head-bobbing, pelvic rocking motions, fine movements of the toes, or a nonrhythmic motion of both legs may develop. TD may involve the trunk and diaphragm, sometimes leading to speech disorders9,10 or even respiratory distress,11,12 which may rarely be life-threatening.13,14


Dystonic movements also occur in TD, either alone or in combination with choreic or stereotypic movements. Dystonic movements are sustained abnormal postures of a body part or parts, induced or increased with use of the affected part, often with superimposed spasm. Although axial dystonia was first reported as a sequel of chronic neuroleptic treatment in 1962,15 the term “tardive dystonia” was only recently applied to a series of neuroleptic-treated patients,16 most suffering primarily from axial dystonias.


“Tardive akathisia” is an unpleasant sensation of internal restlessness that is partially ...

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