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Biomedical subjects

G Chouinard

Publications and source records attributed to G Chouinard.

At least 19 recordsLinked to original sources
PubMed1979

Ineffectiveness of deanol in tardive dyskinesia: a placebo controlled study.

In a double-blind placebo-controlled study, deanol acetamidobenzoate, administered in doses up to 1.5 g q.d. for three weeks to chronic schizophrenic patients presenting moderate to severe tardive dyskinesia, failed to alleviate the dyskinetic movements. However, there was a tendency for a significant increase in the schizophrenic symptoms of the deanol-treated group relative to the control group. The ineffectiveness of deanol in alleviating tardive dyskinesia is consistent with its inability to enhance brain acetylcholine synthesis. The worsening of the schizophrenic symptoms may possibly result from an interference by deanol with central cholinergic function.

Adult↗
PubMed1979

Tryptophan-nicotinamide, imipramine and their combination in depression. A controlled study.

In a double-blind controlled study lasting 4 weeks 25 newly admitted severely depressed patients were randomly assigned to tryptophan-nicotinamide or imipramine or tryptophan-nicotinamide-imipramine combination. Nicotinamide was given to reduce peripheral breakdown of tryptophan. Although there were no substantial differences between the three treatments, the efficacy of tryptophan-nicotinamide tended to diminish after 2 weeks when the dose of tryptophan was increased from 4 g/day to 6 g/day and that of nicotinamide from 1.0 g/day to 1.5 g/day. The therapeutic response of patients treated with tryptophan-nicotinamide was significantly correlated with the rise in plasma tryptophan. For the tryptophan-nicotinamide-imipramine group, however, therapeutic response and rise in plasma tryptophan were negatively correlated, implying that tryptophan levels were too high in some patients. The data suggest that tryptophan-nicotamide may be as effective as imipramine in unipolar patients providing the dose is kept within the therapeutic window, and that at low doses it could also potentiate the action of tricyclic antidepressants. Bipolar patients seem to require higher doses of tryptophan than unipolar patients.

Adult↗
PubMed1979

Factors related to tardive dyskinesia.

The authors found a 31% incidence of tardive dyskinesia among 261 schizophrenic outpatients treated with neuroleptics. Multiple linear logistic regression analysis revealed a higher incidence of tardive dyskinesia among elderly patients, those with longer records of hospitalization, those for whom neuroleptic medication had little therapeutic effect, and those treated with fluphenazine. Patients manifesting tardive dyskinesia tended to have fewer parkinsonian symptoms than those without the disorder, especially when tremors and akathisia were excluded from consideration. Multiple linear regression analysis indicated that brain-damaged patients and male patients were more susceptible to severe forms of the disorder, even though these factors were not implicated in its initial appearance.

Adult↗
PubMed1979

Evidence of brain dopamine deficiency in schizophrenia.

It is proposed that the increased dopamine function suggested by the dopamine hypothesis of schizophrenia is a dopaminergic postsynaptic receptor supersensitivity resulting from a dopamine deficiency. In support of this, three double-blind controlled studies conducted on drugs which alter brain dopaminergic activity in a manner different from that of classic neuroleptics are reported. 1) alpha-methyldopa-neuroleptic interaction proved efficacious for schizophrenic positive symptoms but only on a short-term basis. 2) Rubidium improved negative symptoms rapidly, and in contrast has a late onset of action on positive symptoms of schizophrenia. 3) Tryptophan-benserazide was efficacious in controlling both negative and positive symptoms of schizophrenia (although less so than chlorpromazine). It is concluded that currently accepted modes of pharmacological therapy (classical neuroleptics) are in the short-term controlling the dopamine supersensitivity secondary to a deficiency, but contributing in the long-term to increase the dopamine deficiency, and so exacerbate the supersensitivity. More effective forms of treatment may involve the use of agents which alter dopamine activity without inducing dopamine supersensitivity.

Benserazide↗
PubMed1979

Ethopropazine and benztropine in neuroleptic-induced parkinsonism.

In a 12-week controlled study ethopropazine was compared to benztropine in the treatment of parkinsonism induced by fluphenazine enanthate in 60 schizophrenic outpatients. Ethopropazine and benztropine were found to be equally effective in controlling parkinsonian symptoms and were as efficacious as procyclidine, their previous antiparkinsonian drug. However, benztropine treated patients had a significant increase in tardive dyskinesia compared to their condition during procyclindine treatment, and significantly more anxiety and depression than ethopropazine treated patients. This suggests that benztropine is not the anticholinergic drug of choice in the treatment of neuroleptic-induced parkinsonian symptoms, because of its more toxic central and peripheral atropinic effect.

Adult↗
PubMed1978

Death attributed to ventricular arrhythmia induced by thioridazine in combination with a single Contac C capsule.

Phenothiazines are known to produce electrocardiographic repolarization abnormalities. Thioridazine and mesoridazine appear to induce such changes more frequently than other neuroleptics and are also known to induce fatal ventricular arrhythmia. The woman described in this article died after taking her usual dose of thioridazine, 100 mg/d, in combination with a single capsule of Contac. C, a decongestant-antihistamine containing phenylpropanolamine and chlorpheniramine. Phenylpropanolamine, an ephedrine-like drug, was thought to have favoured the initiation by thioridazine of the ventricular arrhythmia that led to the woman's death. It is therefore suggested that ephedrine-like medications not be given to patients receiving thioridazine.

Adult↗
PubMed1977

Phenothiazine-induced ECG abnormalities: effect of a glucose load.

A total of 54 schizophrenic patients, 27 male and 27 female, satisfying study criteria, were randomly assigned to one of three treatments: placebo; perphenazine, 20 mg/day; or the combination of amitriptyline, 125 mg/day, with perphenazine, 20 mg/day. Medication was administered under double-blind conditions for 12 weeks, after which ECGs were taken following an overnight fast and again following a 600-calorie meal. Among patients receiving perphenazine or amitriptyline-perphenazine, there was a statistically significant increase in repolarization abnormally after eating, whereas placebo-treated patients incurred no such increases. This supports the hypothesis that phenothiazine-induced ECG changes may be caused or facilitated by the glucose load. The incidence of increase in repolarization abnormality after the meal was higher among female patients than among male patients. The findings are of practical significance for readings of abnormality in the ECG of phenothiazine-treated patients.

Adult↗
PubMed1977

A controlled study of a dopa decarboxylase inhibitor (benserazide) in the treatment of schizophrenic patients.

In a double-blind controlled study lasting 6 weeks, 32 schizophrenic patients were randomly assigned to one of two treatments: chlorpromazine or benserazide, a dopa decarboxylase inhibitor. Results on each measure were subject to multifactorial analysis of covariance. Benserazide did not appear to be as effective an antipsychotic medicaiton as chlorpromazine. In fact, chlorpromazine was significantly better on measures of tension, excitement, hallucinatory behavior, thinking disturbance, social interest, and drop-out rate. At the relatively low dosages used in this study, it would seem that benserazide had little effect on the cerebral dopa decarboxylase, and it would be worthwhile trying higher dosages.

Adult↗