Overcoming the neuroleptic-induced deficit syndrome: clinical observations with remoxipride.
Remoxipride is a selective dopamine D2 antagonist with virtually no activity on other transmitter receptors. It antagonizes dopamine agonists within a wide dose range in animals when it does not cause sedation or akinesia. Clinical studies with remoxipride have demonstrated antipsychotic efficacy apparently equal to classical neuroleptics in short- and long-term treatment of schizophrenia. Remoxipride has a low extrapyramidal syndrome (EPS) profile, and it is generally well tolerated. In clinical practice remoxipride has been reported to differ from classical neuroleptics with regard to subjective side effects. On switching to remoxipride, patients report improvement in cognitive, conative, affective and emotional functions. In many cases the reports are supported by family members and/or caregivers. Although anecdotal, such reports are in line with the low EPS profile of remoxipride and its weak sedative properties. It may indicate that remoxipride does not elicit the neuroleptic-induced deficit syndrome, commonly experienced with classical neuroleptics, or that remoxipride improves the deficit syndrome (or primary negative symptoms) of schizophrenia. These and other hypotheses need to be confirmed by formal clinical studies.
Lewander
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Astra Arcus AB, CNS R & D, Södertälje, Sweden.
D014150:Antipsychotic Agents / Q000009:adverse effects* / Q000627:therapeutic use; D001143:Arousal / Q000187:drug effects*; D003071:Cognition / Q000187:drug effects; D004409:Dyskinesia, Drug-Induced / Q000209:etiology / Q000517:prevention & control*; D006801:Humans; D009042:Motivation; D017330:Remoxipride / Q000009:adverse effects* / Q000627:therapeutic use; D012559:Schizophrenia / Q000188:drug therapy*; D012565:Schizophrenic Psychology
D014150:Antipsychotic Agents; D017330:Remoxipride