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Biomedical subjects

R H Mindham

Publications and source records attributed to R H Mindham.

At least 37 records · Page 2Linked to original sources

A controlled trial of prostaglandin E1 precursor in chronic neuroleptic resistant schizophrenic patients.

The postulated deficiency of prostaglandin E1 series (PGE1) in schizophrenia has been investigated in a controlled therapeutic trial. Twenty-one inpatients with a schizophrenic illness resistant to neuroleptic drug treatments were randomly assigned to one of three treatment conditions in a blind controlled trial of dihomo-gammalinolenic acid (DHLA), a PGE1 precursor. Patients received depot neuroleptic medication and DHLA capsules, placebo depot medication and DHLA capsules, or placebo depot medication and placebo capsules. No marked treatment effects were noticed on ratings of the patients' behaviour or symptomatology, though some clinical effects were noted in dyskinetic patients. Abnormalities in red blood cell lipids were observed in the patients entering the trial, suggesting that further investigation of an EFA/prostaglandin deficiency hypothesis in schizophrenia is worth pursuing.

8,11,14-Eicosatrienoic Acid↗

Identical twins discordant for presenile dementia of the Alzheimer type.

In genetically proven identical female twins, discordant for presenile dementia of the Alzheimer type, the affected twin began to dement at the age of 49, and died 15 years later; the diagnosis was confirmed at post-mortem. The surviving twin remains clinically unaffected 20 years after the onset of dementia in her sister. Environmental aetiological factors are postulated to account for this discordance.

Alzheimer Disease↗

A comparison of the frequency of major affective disorder in Huntington's disease and Alzheimer's disease.

Matched groups of patients suffering from Huntington's disease and Alzheimer's disease were compared for psychiatric morbidity prior to the onset of dementia. The Huntington's disease group showed twice the incidence of major affective disorder. This finding suggests a specific relationship between Huntington's disease and major affective disorder rather than the latter being a non-specific prodromal feature of dementia.

Affective Disorders, Psychotic↗

A controlled study of dementia in Parkinson's disease.

Tests of cognitive functions were carried out in a group of patients with Parkinson's disease and repeated after a three-year interval. Comparison was made with a control group drawn from a population of psychiatric patients, matched for age and sex. No differences in cognitive functions were found between the groups, either initially, or between those surviving for three years. Deaths among the index group included a high proportion of patients with cognitive impairment and there was an increasing prevalence and severity of dementia in the index group which exceeded that observed in the control group. Requirements for a methodologically sound study of dementia in Parkinson's disease are discussed.

Aged↗

Continuation therapy with tricyclic antidepressants in relapsing depressive illness.

Patients who have suffered a depressive illness frequently relapse when treatment is stopped. A controlled study of continued medication after clinical recovery was carried out. Of 92 patients studied, 22% of those who received amitriptyline or imipramine relapsed during 6 months of observation, compared with 50% of those who received placebo. Patients who experienced persistent residual symptoms derived more benefit from the active drug during continuation treatment than those who made a complete recovery from their illness.

Adult↗

A comparison of piribedil, procyclidine and placebo in the control of phenothiazine-induced parkinsonism.

A double-blind, cross-over trial of the effectiveness of piribedil, procyclidine and placebo in the control of parkinsonism induced by fluphenazine decanoate was conducted in sixteen cases of chronic schizophrenia. Procyclidine was shown to be more effective and piribedil less effective than the placebo. Piribedil produced a number of unpleasant effects, including headache, vomiting and malaise.

Chronic Disease↗

Psychiatric symptoms during l-dopa therapy for Parkinson's disease and their relationship to physical disability.

Fifty patients attending a neurological outpatient clinic for Parkinson's disease were assessed by standardized methods for both physical and psychiatric symptoms. The patients then received treatment with L-dopa with carbidopa or anticholinergic drugs and/or amantadine. During the following six-month period the subjects were assessed at intervals, both physically and psychiatrically. Forty patients were followed up for the full six-month period. The severity of physical signs and affective symptoms was shown to be significantly related at several stages of the investigation. Initially, the patients showed a high psychiatric morbidity. During treatment, 22 patients developed a depressive disorder, 12 or which had a history of previous depressive episodes. By contrast, of the 11 patients who showed very few affective symptoms during follow-up, none had a history of depression. Of the 22 patients with a depressive disorder, only two were in the anticholinergic/amantadine group, compared with nine and 11 in the other groups. L-dopa was not an effective antidepressant agent. The probable relevance of the findings of the study to the management of patients with Parkinson's disease is outlined.

Aged↗

Assessment of drugs in schizophrenia. Asessment of drug-induced extrapyramidal reactions and of drugs given for their control.

I have tried to bring out some of the important methodological problems found in examining the effectiveness of drugs used in the control of druginduced parkinsonism by referring mainly to studies in which I have taken part. I hope I have shown that the whole topic is far less well understood than is often assumed. The main points may be summarized as follows: there is doubt as to whether many of the drugs used in controlling drug-induced parkinsonism are really effective; the results of many studies are conflicting; many studies contain serious flaws in design; methods for assessing extrapyramidal signs are not well developed; we are ignorant of the way in which drug-induced extrapyramidal signs change spontaneously. There is a clear need for further research in this area to improve techniques of assessment, to provide basic information on drug-induced syndromes, and to rigorously examine the efficacy of the drugs used in controlling them.

Amantadine↗