Seventeen opiate-dependent subjects accepted for methadone maintenance treatment were housed in a closed metabolic ward. They stayed drug-free for 3 weeks before methadone treatment was started. One sample of cerebrospinal fluid was taken immediately before the first methadone dose and another sample was taken after the patient had received methadone daily for 3 weeks. Fraction I and II endorphin levels were frequently pathological on both occasions, either elevated or reduced when compared with 19 healthy volunteers. Subjects with pathological pre-treatment levels of both fractions seemed to respond better to the methadone treatment that those with at least one pre-treatment value within the normal range.
Gamma-hydroxybutyrate (GHB) was administered to seven chronic schizophrenic patients in the first double-blind, placebo-replacement trial of this compound. No significant drug effect in this group was obtained. Two patients became nonpsychotic during the drug trial, three got worse and two patients did not respond. The two patients who responded with improvement were augmenters, as measured by average evoked potential (EP), had low platelet MAO activity and high cerebrospinal fluid (CSF) homovanillic acid (HVA). A number of patients developed akathisia and dystonia during the trial, especially after receiving probenecid for lumbar puncture. Further study is warranted, possibly in a selected patient group.
Fifty-nine chronic schizophrenic patients received one year of treatment with either fluphenazine enanthate or pipothiazine palmitate IM. Both long acting neuroleptics significantly decreased serum albumin, total protein and creatinine values. Triglycerides were decreased only early in treatment. Pretreatment findings from therapy responders, as compared with those who failed to respond to treatment, included higher albumin values and to a lesser extent, lower lactic dehydrogenase values and greater height. These results were discussed with an eye toward the hepatocellular effects of long acting phenothiazines and the effect of liver function on the pharmacokinetics of these medications.
26 patients with affective psychoses, 11 with the unipolar and 15 with the bipolar form of the disease, 102 first-degree relatives and healthy controls matched for age and sex were examined for their platelet MAO activity. For evaluation of enzyme activity kinetic parameters as well as activities under saturation conditions were determined. The degree of depression was estimated by two standard self-rating depression scales. Intrafamilial correlation of MAO was found. MAO activities of patients did not differ from controls, and there was no consistent difference in MAO between the relatives and their controls. Neither among patients nor among relatives or controls were there indications for a relationship between MAO and the degree of depression. Reduced MAO activity cannot be regarded as a genetic marker of vulnerability to affective psychosis.
Neuroendocrine test were carried out to study effects of clomipramine treatment in 24 unipolar depressed women. Clomipramine (50-150 mg/day) increased the response of prolactin and thyrotropin to stimulation by thyrotropin-releasing hormone (TRH), while no response of growth hormone (HGH) to TRH was seen. Clomipramine decreased the response of HGH to insulin, while the responses of prolactin and cortisol to insulin were not affected. The findings suggest that the neuroendocrine and antidepressant effects of clomipramine cannot be accounted for entirely on the basis of monoaminergic mechanisms.
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