Abstract
Tardive dyskinesia has been studied and reported with increasing frequency since the initial paper by Schönecker 1 in 1957. The classical symptoms of tardive dyskinesia (TD) are involuntary movements of the lips, jaws, and tongue. In addition, there may be choreiform (quick, jerking) movements or athetoid (arhythmic, wormlike) movements of the extremities. Characteristically, these movements are inhibited by self-conscious awareness; 2 they are aggravated by anxiety and disappear during sleep. 3,4 In 1973, after several years of controversy, the American College of Neuropsychopharmacology declared that TD was unquestionably linked to neuroleptic administration and suggested that prolonged use of these drugs must be approached with caution. 3 It is postulated that the etiological mechanism is a hyperdopaminergic state resulting from dopamine receptor supersensitivity induced by long-term receptor blockade by neuroleptics. 5 Clinically, symptoms become manifest after neuroleptic withdrawal or dose reduction; symptoms disappear for a time when neuroleptic dose is increased; anticholinergic drugs worsen the symptoms. 3,5 Prevalence of TD in neuroleptic-treated patients varies with the population studied and depends on several factors, notably age. 6,7 Once TD has been discovered in a chronic schizophrenic patient, the clinician needs to make a difficult decision. Should maintenance therapy be continued? 8 What is the natural progression of TD under conditions of clinically appropriate neuroleptic maintenance? In order to answer this question, we did a 2-year follow-up of patients whose TD had been diagnosed in an outpatient survey 2 years previously. 6
Published Version
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