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Biomedical subjects

S A Checkley

Publications and source records attributed to S A Checkley.

At least 73 records · Page 4Linked to original sources
PubMed1983

Suppression of bulimic symptoms with methylamphetamine.

Eight patients with bulimia nervosa were given methylamphetamine or placebo intravenously under double blind controlled conditions. In every patient, methylamphetamine reduced self-ratings of hunger and amount of food eaten as measured under laboratory conditions. This shows that the food intake of patients with bulimia nervosa can be modified by experimental drugs. The symptom of bulimia (rapid, excessive and distressing eating) which may be followed by self-induced vomiting or purgation was seen in four patients after receiving placebo but in none after receiving methylamphetamine. These findings suggest that the severe symptom of bulimia may be amenable to drug treatment. Further studies are needed to explore the mechanism by which methylamphetamine appears to prevent bulimia.

Adult↗
PubMed1982

Changes in noradrenergic neuroendocrine responses following repeated seizures and the mechanism of action of ECT.

To investigate the mechanism of action of ECT in depression, functional changes in central noradrenergic systems, resulting from a series of electroshock- or photic-induced seizures have been evaluated in baboons. The plasma growth hormone (GH) response to IV infusion of an alpha 2-noradrenergic agonist clonidine (0.02 mg/kg) or a beta 2-adrenergic antagonist, ICI 118,551 (0.02 mg/kg) has been measured before, during and up to 15 days after the series of seizures. Electroshock (ECS) or sham ECS was given with standard clinical premedication (atropine, methohexital, suxamethonium and oxygen ventilation) seven times over 15 days. Plasma GH responses were unchanged 24 h after one or seven ECS. An enhanced GH response occurred 7 and 15 days after the seventh ECS. Sham ECS (seven times in 15 days) produced no changes in GH response to clonidine. The plasma GH response to ICI 118,551 was apparently decreased 1 and 7 days after the seventh ECS. Photic seizures were induced seven times in 15 days in baboons which were primed with a subconvulsant dose of D,L-allylglycine (180 mg/kg), but were otherwise drug-free. Plasma GH responses to clonidine were enhanced 1 and 7 days after the seventh photically induced seizure. It is concluded that in the primate there is an enhancement of a central alpha 2-noradrenergic response during 1-15 days after a sequence of generalised seizures. The time course of this enhancement appears to be influenced by drugs given directly before the seizures.

Adrenergic beta-Antagonists↗
PubMed1982

The effect of desipramine upon central adrenergic function in depressed patients.

Eleven drug free patients meeting Research Diagnostic Criteria for Major Depressive Disorder have been treated with desipramine and given a clonidine infusion after 0, 1 and 3 weeks of treatment. The sedative and hypotensive effects of clonidine were significantly inhibited after three weeks of treatment with desipramine: a similar interaction was seen after one week of treatment although this just failed to reach statistical significance. The growth hormone (GH) response to clonidine was initially impaired, but increased significantly after one week of treatment. A significant reduction in the GH response occurred during the second and third weeks of treatment with desipramine. This last finding is interpreted as evidence of adaptive change of alpha 2 adrenoceptors: the other changes can be explained by the known ability of desipramine to block the re-uptake of noradrenaline.

Adult↗
PubMed1981

Growth hormone and other responses to clonidine in patients with endogenous depression.

The growth hormone response to clonidine was significantly less in 10 drug-free patients with endogenous depression than in 10 normal subjects who were individually matched with the patients for age and sex. The hypotensive and sedative effects of clonidine in the two groups were similar. The findings may indicate a defect at central alpha adrenoceptors at least in neuro-endocrine systems.

Adult↗
PubMed1981

A pilot study of the mechanism of action of desipramine.

To test the hypothesis the desipramine alters alpha adrenoceptor function in depressed patients, the effects of clonidine upon growth hormone sedation and blood pressure have been measured in depressed patients before and after treatment with desipramine. After three weeks of treatment the hypotensive and sedative effects of clonidine were inhibited in all patients even though plasma desipramine concentrations at this time varied from 42 to 560 micrograms/l. Growth hormone responses to clonidine were enhanced in five of the six patients but this effect was not statistically significant. These findings are consistent with the hypothesis that in these patients desipramine altered alpha adrenoceptor function: other explanation are discussed.

Adult↗
PubMed1980

Neuroendocrine tests of monoamine function in man: a review of basic theory and its application to the study of depressive illness.

Neuroendocrine tests are now available for studying monoamine function in the brains of patients with mental illness. Great care is required in the selection of drugs which act upon specific monoamine receptors to produce specific hormonal responses. Equal care is required in the control of biological variables which may influence hormonal release. Recently reported neuroendocrine studies of depressive illness are assessed in these terms. The results of these studies support the hypothesis that there is defective noradrenergic function in the brains of some patients with depressive illness.

Adrenocorticotropic Hormone↗
PubMed1980

Cushing's syndrome, tryptophan and depression.

Fifteen patients with active Cushing's syndrome have been compared with 15 other patients who had been treated successfully for Cushing's syndrome and with 13 patients with other pituitary tumours. Depression was the main psychiatric diagnosis made by the CATEGO programme after Present State Examinations. Patients with active Cushing's syndrome were significantly more depressed (Hamilton Rating Scores), than were the other patients. Compared with the control patients, those with active Cushing's syndrome had slightly lower plasma concentrations of total tryptophan, though the concentrations of freely diffusible tryptophan were not significantly changed.

Adolescent↗
PubMed1980

A neuroendocrine study of the mechanism of action of ECT.

To test the possibility that the antidepressant action of ECT is due to an enhanced responsiveness to the stimulation of monoamine receptors, we have measured pituitary hormone responses to test doses of clonidine and methylamphetamine in depressed patients before and after a course of ECT. There was no enhancement of the growth hormone response to either drug following a course of ECT. Cortisol responses to methylamphetamine were enhanced, but probably this was secondary to the partial or complete recovery of the patients. Further neuroendocrine studies of the mechanism of action of ECT in man are needed.

Adult↗
PubMed1980

A longitudinal study of urinary excretion of N,N,-dimethyltryptamine in psychotic patients.

The excretion of N,N,-dimethyltryptamine (DMT) has been measured in longitudinal studies of five patients with schizophrenic illnesses and in four patients with rapidly or slowly cycling manic-depressive illness. The excretion of DMT was frequently raised in patients when they were psychotic but was usually normal when they had recovered. However, rapid changes in the severity of illness or sudden switches from one mood state to another were not accompanied by changes in the excretion of DMT. These findings contrast with the immediate hallucinogenic effects of an injection of DMT, and suggest that the extracerebral production of DMT (as measured by its urinary excretion) does not provoke the experience of hallucinations in psychotic patients.

Bipolar Disorder↗
PubMed1979

Corticosteroid and growth hormone responses to methylamphetamine in depressive illness.

It is suggested that, if depressed patients have deficient noradrenergic function at central alpha-adrenergic receptors, then they will also have impaired corticosteroid responses to methylamphetamine but unaltered growth hormone responses. This prediction has been confirmed when the responses of a group of patients with endogenous depression were compared with the responses of a group of patients with other functional psychoses, a group of patients with reactive depression, and a group of patients with other psychiatric diagnoses. These findings support the hypothesis that there is a functional deficiency of noradrenaline at some central alpha-adrenergic receptors.

Adjustment Disorders↗
PubMed1979

Urinary excretion of dimethyltryptamine in liver disease.

The urinary excretion of N,N-dimethyltryptamine (DMT) was higher in patients with severe liver disease than in normal subjects. This difference remained significant when patients with all grades of hepatic encephalopathy were excluded. Patients with liver disease whose mental states were normal excreted amounts of DMT similar to those of patients with a hospital diagnosis of schizophrenia.

Acute Disease↗
PubMed1978

Thyrotoxicosis and the course of manic-depressive illness.

The effect of thyrotoxicosis upon the recurrence of manic-depressive psychoses has been studied by the use of a routine follow-up system. In this system 267 patients had three or more affective illnesses. Five of these patients had eight well-documented episodes of thyrotoxicosis. Only three of these eight episodes coincided with an affective illness, and in each case an alternative explanation for the association was available. These findings suggest that thyrotoxicosis has little effect upon the occurrence of a manic-depressive episode.

Adult↗
PubMed1978

A new distinction between the euphoric and the anti-depressant effects of methylamphetamine.

The psychological effects of an injection of methylamphetamine have been measured in 22 drug-free patients with endogenous depressive illness and in 9 patients with other psychiatric illness. A new distinction between the time course of the euphoric and anti-depressant effects is described. The euphoric effects were seen in the first hour after the injection, but the anti-depressant effects were delayed for 1--3 hours and then lasted for as long as 36 hours. These findings are at variance with the noradrenaline depletion hypothesis of depressive illness which (in its simplest form) predicts an immediate alleviation of depression as a result of an immediate rise in the concentration of noradrenaline at central receptor sites.

Adolescent↗