[Amisulpride, neuroleptic and antinegative action].

Amisulpride (Solian), a substituted benzamide derivative, is distinguished pharmacologically by its marked affinity for dopamine D2 receptors and its higher affinity for limbic and hippocampic as compared with striatal dopamine receptors. The originality of this molecule lies in its observed 2 opposed actions at 2 distinct dose levels. High amisulpride doses, antidopaminergic, inhibit, in animals, the hyperdopaminergic symptomatology considered equivalent to positive schizophrenia, whereas low doses, dopamine-releasing and activating, improve hypodopaminergic symptomatology of negative schizophrenia. The ratio of about 300 between activating and inhibiting doses demonstrates the clear dose-related dissociation of effects, this ratio being, furthermore, much higher than that of other neuroleptics possessing bipolar activity. In contrast to conventional neuroleptics, amisulpride possesses only weak sedative activity and practically lacks cataleptigenic effects. This twofold action has been confirmed in clinical practice by open and double-blind studies, demonstrating in each case the rapidity of action (by the end of the 1st week) and very good tolerance, notably neurological, of amisulpride. Clinical studies (5 open and 4 double-blind) in patients with psychosis and positive symptomatology, have demonstrated that high doses of amisulpride (Solian 200) are effective against overall positive symptomatology at doses of 600 to 1,200 mg/day, doses of less than 300 mg/day being ineffective or aggravating. Improvement is obtained without "damping effect", amisulpride being as effective as haloperidol in this indication with a significantly better tolerance. In patients with negative schizophrenia (4 open and 3 double-blind studies) the effective dosage of amisulpride (Solian 50) is about 150 mg/day, doses above 300 mg being ineffective or aggravating. Improvement is marked and occurs in all negative symptomatology.(ABSTRACT TRUNCATED AT 250 WORDS)