Letter to the Editor
Sir: Tardive dyskinesia (TD) remains a significant clinical problem for which there is no uniformly effective therapy. The rationale for its treatment with cholinomimetic drugs derives from the conceptualization of TD as the result of an imbalance between cholinergic and dopaminergic systems in the basal ganglia. Unfortunately, the response of TD to treatment with acetylcholine precursors has been inconsistent. However, precursors may not increase acetylcholine activity if neurotransmitter synthesis is impaired in presynaptic neurons. In fact, Miller and Chouinard reviewed data which suggest that striatal cholinergic neurons are damaged in patients with TD.
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