Sulpiride in tardive dyskinesia.
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.
D014150:Antipsychotic Agents / Q000494:pharmacology; D018492:Dopamine Antagonists; D004409:Dyskinesia, Drug-Induced / Q000209:etiology* / Q000517:prevention & control; D006801:Humans; D010302:Parkinson Disease, Secondary / Q000139:chemically induced / Q000517:prevention & control; D011954:Receptors, Dopamine / Q000187:drug effects; D017448:Receptors, Dopamine D2; D013469:Sulpiride / Q000494:pharmacology* / Q000627:therapeutic use
D014150:Antipsychotic Agents; D018492:Dopamine Antagonists; D011954:Receptors, Dopamine; D017448:Receptors, Dopamine D2; D013469:Sulpiride