Sulpiride in Tardive Dyskinesia

Abstract The pathogenesis of tardive dyskinesia (TD) appears to consist of a combination of a predisposing vulnerability of the patient and an antidopaminergic (neuroleptic) treatment. This combination may result in 1) a relative dopamine hyperreactivity associated with an increased number of dopamine receptors and/or a cholinergic hypo‐function (reversible TD), and 2) in long‐term treatment, degenerative phenomena leading to a decreased threshold for expressing dyskinetic symptoms (irreversible TD). Sulpiride, a selective D‐2 dopamine receptor blocker, is able to suppress TD without producing a reciprocal aggravation in parkinsonism, although in vulnerable patients it may induce/aggravate parkinsonian symptoms. Animal data suggest that sulpiride has less TD‐inducing effect than traditional neuroleptics, but long‐term clinical studies are still needed to prove this suggestion.