{"title":"Tranylcypromine isomers in the treatment of Parkinson's disease. Biochemical effects.","authors":"G P Reynolds, P Riederer","doi":"10.1159/000468471","DOIUrl":"https://doi.org/10.1159/000468471","url":null,"abstract":"<p><p>Isomers of the monoamine oxidase inhibitor tranylcypromine were administered separately to 15 hospitalized parkinsonian patients. The activity of the platelet enzyme, the plasma and urinary tranylcypromine, were measured. While the (+)isomer inhibited monoamine oxidase to a greater extent, both isomers increased plasma phenylethylamine. Differences between the pharmacokinetics of the two isomers were substantial, (-)tranylcypromine being excreted much faster.</p>","PeriodicalId":75943,"journal":{"name":"International pharmacopsychiatry","volume":"16 1","pages":"30-3"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000468471","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18311076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Dopamine antagonist properties of atypical neuroleptics may be revealed following mesolimbic denervation.","authors":"V Nohria, B Costall, R J Naylor","doi":"10.1159/000468470","DOIUrl":"https://doi.org/10.1159/000468470","url":null,"abstract":"<p><p>A mesolimbic denervation, caused by bilateral intra-accumbens 6-hydroxydopamine, increased the potency of apomorphine in two behavioural tests of dopamine agonist activity, climbing behaviour and circling (combinations of the accumbens denervation with unilateral electrolesion of the striatum). Of a number of neuroleptics tested, haloperidol, fluphenazine, sultopride, tiapride, sulpiride and thioridazine, only the latter two showed greater effectiveness than normal to antagonize the apomorphine responses after mesolimbic denervation. Sulpiride and thioridazine cause remarkably little change in 'normal' tests for antipsychotic activity; their effectiveness in the clinic may reflect a more unique ability to act on dopamine receptor mechanisms of changed sensitivity.</p>","PeriodicalId":75943,"journal":{"name":"International pharmacopsychiatry","volume":"16 1","pages":"21-9"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000468470","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17183823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Benzodiazepine withdrawal phenomena.","authors":"C Hallstrom, M Lader","doi":"10.1159/000468500","DOIUrl":"https://doi.org/10.1159/000468500","url":null,"abstract":"<p><p>A withdrawal syndrome is described in 10 patients who claimed to be unable to discontinue benzodiazepines. A high dose group took the equivalent of a mean of 135 mg diazepam/day, and the normal dose group of 20 mg/day. Associated with the gradual reduction of medication was the emergence of severe symptoms of anxiety as well as sensory intolerance, perceptual disturbances and weight loss. The withdrawal syndrome subsided after 2 weeks and was similar in both groups of patients. EEG changes were detected on withdrawal opposite to those known to be associated with initiation of diazepam treatment. The measures tended to revert to the baseline after a drug-free period. One reason why chronic users of diazepam experience difficulty in stopping medication may be the development of a withdrawal syndrome even after moderate dosage.</p>","PeriodicalId":75943,"journal":{"name":"International pharmacopsychiatry","volume":"16 4","pages":"235-44"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000468500","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17188302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Metabolism and excretion of the neuroleptic drug perazine in healthy volunteers].","authors":"J. Schley, E. Riedel, B. Müller-Oerlinghausen","doi":"10.1159/000468497","DOIUrl":"https://doi.org/10.1159/000468497","url":null,"abstract":"The renal and faecal excretion of a single dose of 75 mg 35S-labelled perazine was investigated. The time course of the total radioactivity in plasma could not be adjusted satisfactorily to a Bateman function, whereas the renal excretion of radioactivity corresponded to an open two-compartment model. The marked interindividual variation of the metabolic profile, and of plasma half-lives reported in patients was not observed in normal volunteers. Thus, it is suggested that such interindividual variance is related to the special conditions in psychiatric patients such as individual pretreatment strategies.","PeriodicalId":75943,"journal":{"name":"International pharmacopsychiatry","volume":"16 4 1","pages":"201-11"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000468497","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65243392","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Long-term application of haloperidol: effects on dopamine and acetylcholine receptors.","authors":"G Stock, P Kummer","doi":"10.1159/000468489","DOIUrl":"https://doi.org/10.1159/000468489","url":null,"abstract":"<p><p>Rats were injected daily with haloperidol, 0.5 mg/kg i.p., or pimozide, 2 mg/kg i.p., for a period of 8 or 16 days, respectively. 24 h after the last injection of haloperidol, these rats were challenged with gamma-butyrolactone (GBL) in doses of 200-750 mg/kg i.p. In haloperidol-treated rats, higher doses of GBL are needed in order to increase the rate of dopa accumulation. This finding demonstrates the development of supersensitivity of dopamine (DA) autoreceptors towards endogenously released DA. Pimozide had no effect on the increased rate of dopa accumulation induced by increasing doses of GBL. From this data it is concluded that pimozide in our model is mainly active on postsynaptic DA receptors and haloperidol is active on pre- and postsynaptic DA receptors. In rats treated chronically with daily injections of haloperidol, benztropine, in a dose of 50 mg/kg, induced a decrease in dopa accumulation which was more marked than the decrease seen with benztropine, 50 mg/kg in animals treated with a single injection of haloperidol only. The opiate antagonist, naloxone at a dose of 10 mg/kg, had no effect on these results. Benztropine, 50 mg/kg i.p., had no effect on the increased rate of dopa accumulation induced by GBL, 400 mg/kg. The data support the hypothesis that in parallel to the development of supersensitive postsynaptic DA receptors, there is a development of subsensitivity in cholinergic receptors within the nigro-neostriatal system. Further the results show that a new DA-acetylcholine equilibrium is reached during long-term haloperidol treatment. The implications of these findings in regard to extrapyramidal side effects during long-term neuroleptic treatment are briefly discussed.</p>","PeriodicalId":75943,"journal":{"name":"International pharmacopsychiatry","volume":"16 3","pages":"144-53"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000468489","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17850799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Drug interactions in psychiatric practice.","authors":"M Ragheb","doi":"10.1159/000468482","DOIUrl":"https://doi.org/10.1159/000468482","url":null,"abstract":"<p><p>The interaction of neuroleptics, tricyclic antidepressants, monoamine oxidase inhibitors, lithium and anxiolytic sedatives with other drugs and food is reviewed with special emphasis on drug interactions commonly encountered in psychiatric practice. Clinical relevance and mechanism of action of such interactions are discussed. An update of the interaction of lithium with prostaglandin inhibitors is presented.</p>","PeriodicalId":75943,"journal":{"name":"International pharmacopsychiatry","volume":"16 2","pages":"92-118"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000468482","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17188057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Drug fever due to nomifensine treatment in patients with endogenous depression.","authors":"J L Nielsen, N O Lund","doi":"10.1159/000468476","DOIUrl":"https://doi.org/10.1159/000468476","url":null,"abstract":"<p><p>Nomifensine was introduced as an effective antidepressant drug with few side effects. However, among our patients we have seen 2 typical cases of drug fever due to nomifensine. 2-4 weeks after start of nomifensine treatment, 75-150 mg/day, for recurrent endogenous depressions the patients developed shiverings and fever. Nomifensine was withdrawn and both became afebrile within 1 day. A provocation test with 50 mg nomifensine p.o. again resulted in shiverings and fever within 6-8 h. 1 of the patients was allergic to other drugs and suffered from asthma. During the acute episode of illness the serum concentration of alanine aminotransferase was elevated and it normalized after stopping the treatment. A liver biopsy at that time showed liver cell necrosis, and a moderate grade of steatosis and fibrosis was also present. The results indicate that nomifensine may cause drug fever. It is possible that patients with allergy and/or liver diseases in particular may be susceptible to drug fever due to nomifensine.</p>","PeriodicalId":75943,"journal":{"name":"International pharmacopsychiatry","volume":"16 1","pages":"66-8"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000468476","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18311078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Follow-up study of 281 schizophrenic patients treated with high dosage fluphenazine decanoate.","authors":"S Steiner, C Nagy","doi":"10.1159/000468493","DOIUrl":"https://doi.org/10.1159/000468493","url":null,"abstract":"<p><p>281 newly admitted female schizophrenic patients were treated with high dosage fluphenazine decanoate intramuscularly, starting with 250 mg per injection together with antiparkinsonian and antidepressant drugs. On a set day the 3 groups 'with neuroleptics' (NL) (n = 54), 'without NL' (n = 152) and 'relapsed when without NL' (n = 42) were compared concerning age, diagnosis, hereditary disposition, first admission and readmissions, number of admissions and global judgement. From the differences no clear conclusion for practical clinical work could be obtained. The good tolerance is discussed using the list of side effects including tardive dyskinesia and laboratory data.</p>","PeriodicalId":75943,"journal":{"name":"International pharmacopsychiatry","volume":"16 3","pages":"184-92"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000468493","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18330329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Acute effects of disulfiram on anxiety levels of chronic alcoholics.","authors":"S Snyder, M Keeler","doi":"10.1159/000468474","DOIUrl":"https://doi.org/10.1159/000468474","url":null,"abstract":"<p><p>30 male alcoholics, who were anxious by clinical research standards, received either disulfiram (250 mg) or placebo daily for 1 week. There are claims that disulfiram has a sedative effect and that this has some useful antianxiety action, but this had not been tested in a controlled manner. There were no significant differences in the mean changes between the disulfiram and placebo groups as determined by any of the tests used. Both the Zung self-rating anxiety scale and the anxiety scale of the profile of mood states indicated ( p less than 0.05) that those receiving disulfiram were extreme reactors as compared to the placebo group; those receiving disulfiram either became more anxious or experienced the most improvement. The study suggests that disulfiram may selectively relieve or increase the anxiety level of subgroups of subjects, but does not delineate a predictor response.</p>","PeriodicalId":75943,"journal":{"name":"International pharmacopsychiatry","volume":"16 1","pages":"49-56"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000468474","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18077175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effects of long-term administration of anticonvulsant drugs on chromosomes in man.","authors":"Y Matsushima, H Hazama, R Kawahara","doi":"10.1159/000468468","DOIUrl":"https://doi.org/10.1159/000468468","url":null,"abstract":"<p><p>Effects of long=term administration of anticonvulsant drugs on chromosomes in epileptic mothers and their children were examined. Specimens from peripheral lymphocytes were prepared by incubation for 3 days and colchicine treatment. Results obtained were as follows: (1) The incidence of abnormal cells in epileptic mother group over 9 years of drug administration was significantly higher than in the group below 9 years. (2) Most of chromosome abnormalities found in subjects were of comparatively simple morphological aberrations such as gaps or breaks. The incidence of the chromosome-type abnormalities was significantly higher in the patient group than in the control group. (3) Chromosome abnormality of children showed a positive correlation with that of mothers but was not significant. (4) The incidence of chromosome abnormality in children was reduced along with aging. (5) These observations could be interpreted to suggest that chromosome abnormality appearing in children born from epileptic mothers under drug therapy was probably formed by direct effects of anticonvulsant drugs on the fetal hematopoietic system.</p>","PeriodicalId":75943,"journal":{"name":"International pharmacopsychiatry","volume":"16 1","pages":"1-9"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000468468","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18311074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}