beta-endorphin and Dyskinesia--Drug-Induced

Topics: Affective Disorders, Psychotic; Animals; Anxiety; beta-Endorphin; Catatonia; Dyskinesia, Drug-Induced; Electroconvulsive Therapy; Endorphins; Humans; Mental Disorders; Narcotic Antagonists; Opioid-Related Disorders; Pain; Rats; Receptors, Opioid; Renal Dialysis; Schizophrenia; Stress, Psychological

The subjects were 13 psychiatric inpatients with tardive dyskinesia. Each subject participated in two sessions. Either naloxone (10 mg) or placebo was administered intravenously during each session. In a subset of subjects (n = 7), blood samples for beta-endorphin were drawn before and at 30 and 60 minutes after the injection. The Abnormal Involuntary Movement Scale was administered before and at 10, 20, 40, 60, 120, and 360 minutes after the injection. Double-blind procedures were maintained throughout the experiment. Neither naloxone nor placebo had any appreciable effect on the involuntary movements. Naloxone elicited a significant increase in the plasma beta-endorphin.

Topics: Adult; Affective Disorders, Psychotic; Aged; beta-Endorphin; Dyskinesia, Drug-Induced; Endorphins; Female; Humans; Male; Middle Aged; Naloxone; Psychotic Disorders; Receptors, Dopamine; Schizophrenia

The unilateral microinjection of ACTH 1-24 (20 nmol) into the locus coeruleus (LC) produced a long lasting (2-3 hr) posture asymmetry and movement disorder in all rats tested. This response was readily suppressed by the subsequent local microinjection of an equimolar dose of beta-endorphin or morphine or by the intraperitoneal injection of morphine sulphate (50 mg/kg). Microinjection of naloxone (20 nmol) into the LC produced the above syndrome in a lower percentage of animals. The results support the hypothesis that ACTH peptides and opioids play opposite roles in the control of different brain functions.

Topics: Adrenocorticotropic Hormone; Animals; beta-Endorphin; Cosyntropin; Dyskinesia, Drug-Induced; Endorphins; Locus Coeruleus; Male; Microinjections; Morphine; Naloxone; Posture; Rats; Rats, Inbred Strains

Severity of tardive dyskinesia (TD) and psychopathology of 36 chronic schizophrenic patients under long-term treatment with neuroleptics (NL) was rated during NL therapy and again 12 days after NL withdrawal. Both times serum levels of prolactin, norepinephrine, beta-endorphin, and cortisol were determined. In 27 of these patients ventricular-brain ratio, width of third ventricle, maximal width of anterior horns, distance between choroid plexus, and width of four largest sulci were also measured. Fifteen patients had no signs of TD; 14 had moderate, and 7 severe TD. TD was not related to age, age at onset of illness, duration of illness, dosage and type of neuroleptics, number of ECTs, or any endocrine variable. Psychopathology was barely related to TD, but after NL withdrawal, patients with TD tended to show more deterioration, particularly with regard to thought disorder and activation. With regard to computer-tomographic (CT) variables, patients without TD showed significantly less sulcal enlargement than those with TD. These results indicate that individual predisposition, which may have led to the development of TD, also seems to involve a higher risk of relapse after NL withdrawal.

Topics: Adult; Antipsychotic Agents; beta-Endorphin; Brain; Dyskinesia, Drug-Induced; Endorphins; Hormones; Humans; Hydrocortisone; Male; Middle Aged; Norepinephrine; Prolactin; Psychiatric Status Rating Scales; Schizophrenia; Substance Withdrawal Syndrome; Tomography, X-Ray Computed

Topics: beta-Endorphin; Dyskinesia, Drug-Induced; Endorphins; Female; Humans; Middle Aged; Renal Dialysis; Schizophrenia