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Biomedical subjects

J Gerlach

Publications and source records attributed to J Gerlach.

At least 163 records · Page 9Linked to original sources
PubMed1981

Effect of des-tyrosine-gamma-endorphin in tardive dyskinesia.

The endorphin neuropeptides may have neuroleptic-like effects on dopamine function and may be antischizophrenic. Ten chronic psychotic patients with neuroleptic-induced tardive dyskinesia and parkinsonism received placebo and des-tyrosine-gamma-endorphin (DT gamma E). Drug effects on movement disorders and eye-blinking rates were assessed by blind evaluations of randomly sequenced videotapes made during standardized examinations before and 30, 60, and 120 minutes after each injection and at 24 hours postinjection on days of consecutive treatment. Changes in schizophrenic symptoms were evaluated openly with the schizophrenia subscale of the Comprehensive Psychiatric Rating Scale. There were no significant effects of DT gamma E on any parameter and no side effects. This suggests that DT gamma E, within the tested dose range, does not influence the pathophysiology of neuroleptic-induced dyskinesias or chronic schizophrenia or have neuroleptic properties. However, DT gamma E is well tolerated and should be tested with higher doses during prolonged treatment.

Blinking↗
PubMed1981

Vasopressin in anergic schizophrenia. A cross-over study with lysine-8-vasopressin and placebo.

Sixteen out of 19 patients suffering from chronic anergic schizophrenia completed a placebo-controlled cross-over study with lysine-8-vasopressin (LVP), following a schedule of 1 week of placebo, 3 weeks of LVP, starting with 22.5 IU/day, gradually increased to 67.5 IU/day, and finally 4 weeks of placebo. The psychic state was evaluated with the Brief Psychiatric Rate Scale (BPRS), during weekly live interviews, and following videotaped BPRS interviews at the beginning and end of the LVP period, and at the end of the final placebo period. Symptoms of parkinsonism and tardive dyskinesia were also videotaped during a standardized examination at the same intervals. The videotapes were subsequently randomized and evaluated blindly. The results of liver interviews showed a significant (P less than 0.05) decrease in the BPRS anergic factor after 2 and 3 weeks of LVP treatment, but there were no changes in any single item, other BPRS factors, or the BPRS total score. The results of the videotape evaluations showed that the BPRS thinking disorder factor was significantly (P less than 0.05) decreased after 3 weeks of LVP, whereas the BPRS score was unchanged. No consistent changes in parkinsonism or tardive dyskinesia were found. Although side effects were few, six patients became agitated or aggressive during the LVP treatment. The beneficial effect on thought disorder and anergia, but the absence of global effects on the schizophrenic syndrome, illustrates the need for further research with other vasopressin analogues. The advantages and disadvantages of live and videotaped psychiatric interviews are also discussed.

Adult↗
PubMed1981

Bromocriptine and imipramine in endogenous depression. A double-blind controlled trial in out-patients.

Among 33 out-patients with endogenous depression, 16 were treated with bromocriptine (10-60 mg/day, mean 34) and 17 with imipramine (75-250 mg/day, mean 143). The total score on the Hamilton Rating Scale decreased during 6-week treatment from 19.9 to 7.8 in the bromocriptine group (P less than 0.001) and from 20.1 to 6.1 in the imipramine group (P less than 0.001). There was no significant difference between the two groups. The main side-effects were for bromocriptine: nausea, dizziness, and headache; for imipramine; dryness of mouth, dizziness, and sweating. This study suggests an antidepressant effect of bromocriptine although, due to the possibility of Type II error, it may not necessarily be equal to that of imipramine.

Adolescent↗
PubMed1981

Prevention/treatment of tardive dyskinesia.

Tardive dyskinesia (TD) is a syndrome of involuntary hyperkinetic movement associated with long-term neuroleptic treatment. The syndrome depends on 1. predisposing factors, especially high age and an unknown constitutional vulnerability, and 2. a postsynaptic dopamine receptor hypersensitivity and/or a cholinergic hypofunction developed during prolonged antidopaminergic (neuroleptic) treatment. TE is easily kept in check by continued and intensified neuroleptic treatment, which on the other hand presumably involves an aggravation of the underlying pathological process. On this account the importance of prevention can hardly be exaggerated. The most important prophylactic measures are: 1. narrowing the field of indications for the use of neuroleptics, 2. taking particular measures in predisposed subjects, 3. limiting the antidopaminergic influence by the use of neuroleptics with slight striatal antidopaminergic effect, lowest possible dose, shortest possible time of treatment, as well as increased intervals, and 4. paying close attention to the possible development of TD (early detection). The significance of anticholinergics is still not clarified. Apparently anticholinergics accentuate TD at the time of treatment, with contributing to the development of the underlying primary defect.

Aging↗
PubMed1980

[Clozapine].

Explore the source record for details and available documents.

Clozapine↗
PubMed1980

gamma-Acetylenic GABA in tardive dyskinesia.

Brain gamma-aminobutyric acid (GABA) has been proposed to play a role in the modulation of extrapyramidal motor function. The effects of increasing brain GABA with gamma-acetylenic GABA (GAG), a drug that inhibits GABA transaminase, were evaluated in ten patients with stable tardive dyskinesia during a blind placebo-controlled trial. Drug effects during active treatment and two placebo periods were evaluated by scoring randomly sequenced videotapes of tardive dyskinesia and parkinsonian symptoms recorded weekly during a standardized examination. Tardive dyskinesia was significantly reduced, and preexisting parkinsonism increased slightly. The largest decrease in tardive dyskinesia symptoms occurred in patients receiving higher neuroleptic doses, suggesting an interaction between GABA and dopamine. Prolactin values increased but growth hormone values were unchanged. Psychiatric symptoms were also unchanged during GAG treatment.

4-Aminobutyrate Transaminase↗
PubMed1980

Enkephalin, morphine, and naloxone in tardive dyskinesia.

Eight psychiatric patients with tardive dyskinesia (TD) were treated with single doses of the synthetic met-enkephalin analogue FK 33-824 (1, 2, and 3 mg IM) morphine (10 mg SC) and naloxone, an opiate receptor antagonist (0.8 mg IM). The drug effects were assessed by blind evaluation of randomly sequenced videotapes made before and during treatment. FK 33-824 (1, 2, and 3 mg IM) slightly reduced TD (P < 0.05) and increased preexisting bradykinesia. The effect on TD, however, was pronounced only in patients concurrently treated with neuroleptics in relatively high doses. Morphine had a similar although weaker antihyperkinetic effect, whereas naloxone had no effect. Side effects of FK 33-824 included dizziness, heaviness in the extremities, slurred speech, and dryness of mouth. Morphine caused drowsiness, dizziness, ataxia, and nausea, and naloxone had no side effects. The results do not point to a primary role of enkephalin in the pathophysiology of TD, but enkephalin may interact with dopamine functions and potentiate some of the effects of neuroleptic drugs.

Aged↗
PubMed1980

Dopamine, acetylcholine, and GABA effects in acute dystonia in primates.

Neurological side effects associated with neuroleptic drugs result from a complex interaction of multiple neurotransmitters. To clarify the etiology of neuroleptic-induced acute dystonic reactions, monkeys (Cercopithecus aethiops) were treated with haloperidol at doses sufficient to evoke dystonia, and the effects of agents that influenced dopaminergic, cholinergic, or GABAergic neurotransmitters were evaluated. Apomorphine, a dopamine (DA) agonist, and biperiden, an acetylcholine (ACh) antagonist, decreased acute dystonia, whereas alpha-methyl-p-tyrosine (AMPT), an inhibitor of DA synthesis, and physostigmine, an ACh agonist, agonist, increased the symptoms. Muscimol, a GABA agonist, increased the dystonias in a dose-dependent way, and GABA inhibition with picrotoxin also aggravated dystonia, complicated by systemic intoxication and seizures. The reciprocal interaction between DA and ACh influences is consistent with clinical findings and animal models of dyskinesias. Dystonia may also be modulated by GABAergic substrates, but the results suggest complex interactions among DA, ACh, and GABA neurotransmission. Symptoms involving the orofacial, limb, and trunk regions, and purposeless overactivity are discussed in comparison with acute and tardive neuroleptic-induced movement disorders.

Acetylcholine↗
PubMed1980

Antidepressant drugs in anergic schizophrenia. A double-blind cross-over study with maprotiline and placebo.

Seventeen out of 20 inactive and emotionally withdrawn schizophrenic patients under long-term neuroleptic treatment completed a double-blind cross-over investigation of the possible activating effect of maprotiline, a relatively specific noradrenaline-reuptake inhibitor, compared with that of placebo. Each treatment phase lasted 8 weeks. No significant differences with respect to either the level of activity or schizophrenic symptoms were found between maprotiline (mean dose 138 mg/day) and placebo. Maprotiline provoked a slight psychotic exacerbation in one patient and sedation in another, four patients developed orthostatic hypotension, and two patients had an epileptic seizure. In the light of this and other studies, it must be concluded that antidepressant drugs do not represent any therapeutic advance in the treatment of inactive schizophrenic patients receiving neuroleptics.

Adult↗
PubMed1980

Oxiperomide in tardive dyskinesia.

Tardive dyskinesia can be suppressed by dopaminergic receptor blockers, but often at the cost of a reciprocal increase in Parkinsonism. Oxiperomide, a dopaminergic antagonist that has been shown to reduce levodopa-induced dyskinesias without producing an equal aggravation of Parkinsonism, was evaluated in a blind placebo-controlled trial in 10 patients with tardive dyskinesia. It decreased tardive dyskinesia significantly (p less than 0.01) without significantly provoking or increasing Parkinsonism. There was no relationship between either tardive dyskinesia or Parkinsonism and eye blinking rates. These results can be interpreted as additional evidence for the existence of more than one population of dopamine receptors involved in controlling extrapyramidal function. Although oxiperomide is only a palliative suppressing agent in tardive dyskinesia, as the symptoms returned when the drug was stopped, it is an interesting agent in the search for selective dopaminergic receptor blockers.

Aged↗
PubMed1980

Gamma-Acetylenic GABA in tardive dyskinesia.

gamma-Acetylenic GABA, a drug that increases brain GABA via GABA transaminase inhibition, was evaluated in a blind placebo-controlled trial in 10 patients with stable tardive dyskinesia. Drug effects during active treatment (75 to 225 mg/day) and pre- and post-treatment placebo periods were determined by scoring TD and parkinsonian symptoms recorded weekly on videotape during standardized examinations. GAG significantly reduced TD (p < 0.01), although the effect was moderate, in patiens concurrently taking neuroleptics and increased preexisting parkinsonism. The greatest antihyperkinetic effects tended to occur in patients receiving higher neuroleptic doses, suggesting an interaction between GABA and dopamine. There was no effect of GAG on psychiatric symptoms. Further investigations with GAG and similar agents will be important tools for investigating GABA in movement disorders and other central nervous system dysfunctions.

Adult↗
PubMed1979

Sulpiride in tardive dyskinesia.

Tardive dyskinesia can be suppressed by drugs that block dopaminergic receptors, but often at the cost of a concomitant increase in parkinsonism. Sulpiride (400 -- 2100 mg/day), a selective type-2 dopamine receptor antagonist, was evaluated in a blind, placebo-controlled trial in 11 patients with tardive dyskinesia. It significantly (P less than 0.01) reduced tardive dyskinesia without significantly affecting parkinsonism, although three patients had a increase in preexisting parkinsonian hypokinesia and tremor. During the placebo phase, the tardive dyskinesia and parkinsonian scores returned to the pretreatment values. There was no relationship between either tardive dyskinesia or parkinsonism and eye blinking rates. These results are consistent with the hypothesis that more than one population of dopamine receptors are involved in controlling extrapyramidal function. Sulpiride is an important tool for elucidating both the practical and heuristic aspects of subtypes of dopamine receptors and is a lead in the search for compounds that selectively affect dopaminergic mechanisms.

Aged↗
PubMed1979

Neuroleptic-potentiating effect of alpha-methyl-p-tyrosine compared with haloperidol and placebo in a double-blind cross-over trial.

The hypothesis that schizophrenia results from overactive dopaminergic influences suggests that reducing dopamine synthesis may increase the clinical effects of dopamine receptor blocking neuroleptic drugs. The neuroleptic potentiating role of alpha-methyl-paratyrosine (AMPT), a tyrosine hydroxylase inhibitor, was compared with haloperidol and placebo in a double-blind cross-over trial. Both AMPT and haloperidol increased the anti-schizophrenic effect of neuroleptic treatment in reduced dose compared with placebo (P less than 0.05), though two patients relapsed during the AMPT period. Both drugs slightly increased extrapyramidal symptoms, but the effect was greater with haloperidol. The limited antipsychotic effect and the potential for aggravating neurological symptoms suggest that the combination of AMPT and neuroleptics does not offer a superior advantage to treating schizophrenia. AMPT, however, may still be used as a research tool in elucidating pathogenetic mechanisms.

Adult↗