Delayed dyskinesia (DD) apparently originates in the combination of an individual susceptibility and an antidopaminergic (neuroleptic) treatment. This combination may be responsible for: 1) relative hypersensitivity to dopamine with a rise in the number of dopaminergic receptors and/or depressed cholinergic activity (reversible DD); 2) a degenerative process, in prolonged treatments, resulting in a lowered threshold for emergence of dyskinetic manifestations (irreversible DD). Dogmatil, through selective blockade of D-2 dopaminergic receptors, is capable of reversing DD without exacerbating the parkinson-like syndrome. However, in predisposed patients, parkinson-like manifestations may be induced or exacerbated by dogmatil. Findings in animals suggest that the risk of including DD is less with dogmatil than with conventional neuroleptics. Nevertheless, long term clinical trials are needed to test this hypothesis.
|Number of pages||7|
|Journal||Semaine des Hopitaux|
|Publication status||Published - 1985|
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