To the Editor: The hypothesis that clinical tardive dyskinesia represents a defect in the balance between cholinergic and dopaminergic influences converging on the striatum has been raised.12On the assumption that deanol increased Central-nervous-system acetylcholine, the initial trials34with this drug were encouraging. However, a summary5of further trials that did not always corroborate the initial reports led me to try drugs that might predict the response to deanol. Six patients with severe tardive dyskinesia were treated on consecutive days with challenge doses of a dopamine agonist (levodopa), an antagonist (droperidol), an acetylcholine agonist (physostigmine) and an antagonist (benztropine). No extract is available for articles shorter than 400 words.
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