Treatment of Tardive Dyskinesia

Abstract

Abnormal movements of tardive dyskinesia are presumed to result from hyperactivity or supersensitivity of dopaminergic neurones in the brain. Methyldopa (Aldomet) is known to affect dopaminergic systems either by competitive inhibition of dopa decarboxylase or by synaptic action of its metabolite as a false neurotransmitter. Dual action of methyldopa on the dopamine receptor can then be expected theoretically to result in a somewhat equivocal response, although it was our hope that the results would be more helpful than harmful to the patients. On these theoretical grounds, methyldopa was administered to nine schizophrenics with tardive dyskinesia at daily dosages up to 1,000 mg over six weeks. Methyldopa did not show any marked clinical effect in suppressing abnormal mouth movements, while it induced considerable decrease in blood pressure. Psychotic episodes presumably due to methyldopa were observed in two patients.