Apomorphine and schizophrenia. Treatment, CSF, and neuroendocrine responses.
Previous studies have variably reported the efficacy of apomorphine in treatment of schizophrenia and tardive dyskinesia. Stimulation of dopamine neuron autoreceptors is the presumed mode of action. Low-dose apomorphine (0.75 mg subcutaneously) and placebo were administered to 25 male schizophrenics to evaluate the drug's effect on psychotic and tardive dyskinetic symptoms. No significant improvement or deterioration was seen. Concomitant measurements of plasma prolactin and growth hormone levels and CSF homovanillic acid level indicated that the dose used was centrally active. These results indicate that an active though nonsedating dose of apomorphine does not ameliorate symptoms of schizophrenia or tardive dyskinesia.
D000328:Adult; D001058:Apomorphine / Q000494:pharmacology / Q000627:therapeutic use*; D002986:Clinical Trials as Topic; D004409:Dyskinesia, Drug-Induced / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D013006:Growth Hormone / Q000097:blood; D006719:Homovanillic Acid / Q000134:cerebrospinal fluid; D006801:Humans; D008297:Male; D010919:Placebos; D011388:Prolactin / Q000097:blood; D011569:Psychiatric Status Rating Scales; D011954:Receptors, Dopamine / Q000187:drug effects / Q000502:physiology; D012559:Schizophrenia / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D012565:Schizophrenic Psychology
D010919:Placebos; D011954:Receptors, Dopamine; D011388:Prolactin; D013006:Growth Hormone; D001058:Apomorphine; D006719:Homovanillic Acid