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Biomedical subjects

J Gerlach

Publications and source records attributed to J Gerlach.

At least 109 records · Page 6Linked to original sources
PubMed1988

Perseverative structuring of responses by schizophrenic and affective disorder patients.

Some theoretical implications from a CNS stimulation model of psychosis were tested by analysing the response patterns of schizophrenic (N = 34), affective disorder patients (N = 18), schizoid personality disorder patients (N = 9), neurotic patients (N = 9) and normal controls (N = 34) on a visual two-choice task with reinforcement. The subjects were required to press a left and right button in order to cause a cross (+) to appear on the monitor screen above one of the buttons. Certain subsequences of right and left presses were required in order for the cross to appear, and a coin-reinforcement was delivered on a variable-ratio schedule with respect to the cross condition. An analysis of structured responding in categories: one-side greater than 6, switching (RLRL), 2-1 switching (RRL) and double alternations (RRLL), revealed that the schizophrenic and affective disorder patients were significantly more perseverative in these response categories than normal controls, schizoid or neurotic patients. The last three subject groups were not significantly different from each other. The majority of the schizophrenics and all four manic patients showed the highest percentage of responding in one sided responses greater than 6, switching and 2-1 switching. Normal control subjects showed more varied response patterns with responses in double, triple and quadruple alternations and other combinations. The results are seen to support a CNS stimulation, behavioral competition model of psychosis.

Adult↗
PubMed1988

Tardive dyskinesia.

Tardive dyskinesia (TD) is a syndrome of involuntary movements that develops in predisposed individuals during neuroleptic drug treatment, with an average prevalence of 15%. Neuroleptic (antidopaminergic) drugs are the predominant etiological factor. Although no simple correlation can be established, both dosage and treatment duration seem to be of importance for the development of dyskinesia. It is still uncertain whether some neuroleptics carry a higher risk than others, but it appears that the atypical neuroleptic clozapine, which causes no or minimal dystonia, parkinsonism, or akathisia, also carries no or minimal risk of TD. The pathophysiological mechanisms underlying TD are unclear. The traditional dopamine hypersensitivity theory is no longer viable, whereby new hypotheses have been advanced: TD can be due to the blockade of a subset of striatal dopamine receptors, while parkinsonism is due to the blockade of another such subset, and/or can be due to a reduced GABA turnover in a subgroup of neurons connecting striatum with globus pallidus and substantia nigra. TD is best prevented by a course of neuroleptic medication involving as little antidopamine effect as possible, including minimal doses and shortest possible length of treatment. The main TD treatment principle consists of a gradual dose reduction, possibly over years. It should be added, however, that more recent investigations indicate that traditional antidopaminergic treatment in moderate doses may be safely continued over a long period without an increased risk of TD progression.

Adult↗
PubMed1988

[Not Available].

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Germany↗
PubMed1988

[Not Available].

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Germany↗
PubMed1988

Tardive dyskinesia. Pathophysiological mechanisms and clinical trials.

Recent observations from human and animal studies indicate that the traditional dopamine supersensitivity theory in tardive dyskinesia (TD) is insufficient. Instead, a new hypothesis is proposed: TD may be due to an increased D-1 receptor function or an increased ratio between D-1/D-2 receptor functions in the brain, maybe associated with a diminished activity in certain striatofugal GABA neurons. This hypothesis is based on experiments with selective D-1 and D-2 drugs in rodents and monkeys, but has not yet been tested clinically due to lack of D-1 agonists and antagonists for human use. In a Nordic multicenter study, various neuroleptics (haloperidol, perphenazine, chlorprothixene) were given to 33 elderly psychiatric patients with TD. The main result of this study was the demonstration of 1) an inverse relationship between parkinsonism and TD, and 2) an inconsistent response to withdrawal of various neuroleptics. Following withdrawal, 38% of the patients had a TD aggravation, 27% a TD reduction, and 35% no TD change, all compared with the TD level before the neuroleptic test period and independent of the neuroleptic given. This observation speaks against the dopamine hypersensitivity theory and is more in accordance with the new hypothesis proposed above. The GABA part of the TD hypothesis has been tested with different GABA agonists such as gamma-acetylenic GABA, gamma-vinyl GABA and THIP, but most studies suggest that the therapeutic effect of these drugs in TD is limited and maybe secondary to parkinsonism and sedation. Clinicians are eagerly awaiting new GABA agonists with selective affinity to subgroups of GABA receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Suriclone and diazepam in the treatment of neurotic anxiety. A double-blind cross-over trial.

Suriclone is a new anxiolytic drug belonging to the family of cyclopyrrolones. Although chemically entirely different from the benzodiazepines, it acts as a benzodiazepine agonist with very high affinity for the benzodiazepine receptors. In the present cross-over study, 33 out-patients with a diagnosis of neurotic anxiety were treated with suriclone (mean dose 2 mg/day) and diazepam (25 mg/day) in two 6-week periods. Both drugs had a significant anxiolytic effect, but diazepam appeared to have a better effect within the first 2 weeks of treatment, while no significant difference was seen after treatment, while no significant difference was seen after treatment for 6 weeks. Suriclone and diazepam had a different side effect profile: suriclone produced mainly dizziness, while diazepam caused sedation. This may reflect the fact that suriclone and benzodiazepines bind to distinct sites or different allosteric conformations of the benzodiazepine receptors.

Adult↗
PubMed1987

Selective D1 and D2 receptor manipulation in Cebus monkeys: relevance for dystonia and dyskinesia in humans.

Selective D1 and D2 dopamine (DA) antagonists and agonists were given to 4 Cebus monkeys who had previously received haloperidol treatment for 4 years. SCH 23390 (a selective D1 antagonist) and raclopride (a selective D2 antagonist) induced identical syndromes consisting of dystonia and oral dyskinesia. Biperiden (an anticholinergic drug) and LY 171555 (a selective D2 agonist) completely antagonized the dystonia and dyskinesia induced by SCH 23390 as well as raclopride. The combined treatment with LY 171555 and SCH 23390 (but not LY 171555 and raclopride) caused pronounced sedation. LY 171555 induced repetitive movements of head, legs and trunk, but no oral dyskinesia. SKF 38393 (a partial D1 agonist) caused slight sedation, minimal oral dyskinesia and a significant reduction in D2 agonist-induced repetitive movements.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1986

Effects of citalopram, a specific serotonin uptake inhibitor, in tardive dyskinesia and parkinsonism.

Serotonin (5-HT) has been proposed to exert an inhibitory effect on central dopamine activity, so increased brain 5-HT would be expected to reduce tardive dyskinesia (TD). Therefore a new antidepressant, a selective 5-HT uptake inhibitor, citalopram, was evaluated in 13 psychiatric patients with TD, 11 of whom also had neuroleptic-induced parkinsonism. Drug effects during active treatment (20-40 mg/day for 3 weeks) and pre- and posttreatment placebo periods were scored blindly from videotapes recorded weekly. TD, parkinsonism, and eyeblinking rates were unchanged. Psychiatric symptoms showed no significant changes, and no side effects were reported. The data suggest that increasing 5-HT activity by 5-HT uptake inhibitors has no significant beneficial effect in TD, but citalopram may be advantageous in the treatment of depressed patients who also have TD, as this drug does not aggravate TD as do tricyclic antidepressants.

Adult↗
PubMed1986

Effects of serotonergic and anticholinergic drugs in haloperidol-induced dystonia in Cebus monkeys.

In rodents, serotonin (5-HT) antagonists counteract behavioral and biochemical effects of neuroleptic drugs. Therefore, we have studied the effect of different 5-HT drugs and one anticholinergic drug in acute dystonia in five cebus monkeys chronically treated with haloperidol. Acute dystonia induced by subcutaneous injections of haloperidol was slightly reduced by the 5-HT antagonist methysergide (4.0 mg/kg), while mianserin, ketanserin, and ritanserin (R 55 667; a new selective and potent 5-HT receptor blocker) had no effect. This was contrasted by the marked antidystonic effect of the anticholinergic drug biperiden (0.05-1.0 mg/kg). The 5-HT agonist citalopram, a specific 5-HT uptake inhibitor, had no significant effect. It is concluded that 5-HT antagonists have no useful effect in neuroleptic-induced dystonia.

Animals↗
PubMed1986

Antipsychotic effect of remoxipride, a new substituted benzamide with selective antidopaminergic activity.

Ten of 14 schizophrenic patients completed a 6-week pilot study with a new substituted benzamide, remoxipride. The final median dose was 600 mg/day (range 300-1200) corresponding to a plasma concentration of 5.16 mumol/l (1.55-11.50). Remoxipride reduced the psychotic symptomatology, especially hallucinations and delusions. The total Brief Psychiatric Rating Scale score decreased from 33.5 to 13.0 (P less than 0.01). Few side effects occurred; four patients had weak extrapyramidal symptoms, and four were slightly sedated. No cardiovascular side effects occurred. Prolactin increased, but apparently less than during sulpiride treatment.

Adult↗
PubMed1986

[Not Available].

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Germany↗