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Biomedical subjects

W E Bunney

Publications and source records attributed to W E Bunney.

At least 19 recordsLinked to original sources
PubMed1992

Effect of sleep deprivation on brain metabolism of depressed patients.

OBJECTIVE: Sleep deprivation is a rapid, nonpharmacologic antidepressant intervention that is effective for a subset of depressed patients. The objective of this study was to identify which brain structures' activity differentiates responders from nonresponders and to study how metabolism in these brain regions changes with mood. METHOD: Regional cerebral glucose metabolism was assessed by positron emission tomography (PET) with [18F]deoxyglucose (FDG) before and after total sleep deprivation in 15 unmedicated awake patients with unipolar major depression and 15 normal control subjects, who did the continuous performance test during FDG uptake. RESULTS: After sleep deprivation, four patients showed a 40% or more improvement on the Hamilton Rating Scale for Depression. Before sleep deprivation the depressed responders had a significantly higher cingulate cortex metabolic rate than the depressed nonresponders, and this normalized after sleep deprivation. The normal control subjects and nonresponding depressed patients showed no change in cingulate metabolic rate after sleep deprivation. CONCLUSIONS: Overactivation of the limbic system as assessed by PET scans may characterize a subset of depressed patients. Normalization of activity with sleep deprivation is associated with a decrease in depression.

Adult↗
PubMed1991

The effect of sleep deprivation on cerebral glucose metabolic rate in normal humans assessed with positron emission tomography.

This study is the first report on the effects of total sleep deprivation (about 32 h) on regional cerebral glucose metabolism during wakefulness in man, using positron emission tomography (PET) with F-18 deoxyglucose (FDG). Sleep deprivation leads to a significant reorganization of regional cerebral metabolic activity, with relative decreases in the temporal lobes and increases in visual cortex. Absolute glucose metabolic measurements indicate a decrease in thalamus, basal ganglia, white matter, and cerebellum. No overall decrease in whole brain metabolism was noted after sleep deprivation. As expected, sleep deprivation significantly reduced visual vigilance as assessed by the continuous performance test and this decrease was correlated significantly with reduced metabolic rate in thalamic, basal ganglia, and limbic regions.

Adult↗
PubMed1990

The biological basis of an antidepressant response to sleep deprivation and relapse: review and hypothesis.

Sixty-one papers involving over 1,700 subjects have documented that over half of depressed patients experience an antidepressant response to sleep deprivation. Eighty-three percent of unmedicated depressed patients who had an antidepressant response to sleep deprivation relapsed after one night of sleep. Short naps can also activate severe relapses. The authors suggest that these phenomenological observations concerning relapse with a night of sleep or with naps after successful sleep deprivation would be compatible with the existence of a sleep-associated depressogenic process.

Circadian Rhythm↗
PubMed1989

Repeated naloxone administration in schizophrenia: a phase II World Health Organization Study.

In the context of a previous WHO collaborative study, six research centers reported that naloxone (0.3 mg/kg) produced significant improvement in symptomatology in neuroleptic-treated patients. In the current Phase II WHO study, repeated (4 days) naloxone (0.3 mg/kg) administration was performed in schizophrenic patients (n = 43) from five WHO collaborating centers using a double-blind, placebo-controlled design. Both naloxone and placebo administrations were associated with significant reductions in symptoms. Naloxone, however, was not superior to placebo. These data are discussed in relation to endorphin hypotheses of schizophrenia.

Adult↗
PubMed1989

Regional cerebral glucose metabolic rate in human sleep assessed by positron emission tomography.

The cerebral metabolic rate of glucose was measured during nighttime sleep in 36 normal volunteers using positron emission tomography and fluorine-18-labeled 2-deoxyglucose (FDG). In comparison to waking controls, subjects given FDG during non-rapid eye movement (NREM) sleep (primarily stages 2 and 3) showed about a 23% reduction in metabolic rate across the entire brain. This decrease was greater for the frontal than temporal or occipital lobes, and greater for basal ganglia and thalamus than cortex. Subjects in rapid eye movement (REM) sleep tended to have higher cortical metabolic rates than waking subjects. The cingulate gyrus was the only cortical structure to show a significant increase in glucose metabolic rate in REM sleep in comparison to waking. The basal ganglia were relatively more active on the right in REM sleep and symmetrical in NREM sleep.

Brain↗
PubMed1988

S-adenosylmethionine treatment of depression: a controlled clinical trial.

The antidepressant properties of S-adenosylmethionine, an endogenous methyl donor, were studied in inpatients who met the DSM-III criteria for major depression. Nine patients given intravenous S-adenosylmethionine and nine given low oral doses of imipramine were compared in a double-blind design for 14 days. The S-adenosylmethionine produced superior results by the end of the first week of treatment. By the end of the second week, 66% of the S-adenosylmethionine patients had a clinically significant improvement in depressive symptoms, compared to 22% of the imipramine patients. Side effects appeared to be fewer with S-adenosylmethionine than with imipramine during the last 5 days of the study.

Administration, Oral↗
PubMed1986

Biological markers in depression.

This paper presents a brief review of markers and their potential uses in the study and treatment of affective illness. Some of these include the use of markers as aids in: diagnosis, selection of medication, prediction of relapse, and prediction of suicide. The use of combinations of markers to improve accuracy and the use of markers during the well-state will be discussed. A review of the literature suggests some promising candidates as markers of affective illness including the serotonin metabolite, 5 HIAA; 3H-imipramine platelet binding; REM induction using M-1 muscarinic agonists; and melatonin. Finally, a strategy using gene mapping techniques as a possible method of detecting additional markers is presented.

Depressive Disorder↗
PubMed1985

Lithium attenuates the activation-euphoria but not the psychosis induced by d-amphetamine in schizophrenia.

d-Amphetamine (20 mg) was administered intravenously in a double-blind design to 17 schizophrenic patients with and without concurrent 3-week lithium carbonate pretreatment to evaluate the lithium attenuation of d-amphetamine effects which we had observed in affective disorder patients. Lithium significantly attenuated the acute d-amphetamine-induced changes in an activation-euphoria cluster and in the mannerisms and posturing item of the Brief Psychiatric Rating Scale. Because the psychosis-increasing effects of d-amphetamine were not significantly decreased, it is conceivable that the d-amphetamine-induced changes in activation and euphoria and in psychosis are regulated by different dopamine mechanisms. The small clinical effects seen at 3 weeks of lithium treatment in schizophrenic patients could be mediated by dopamine.

Adolescent↗
PubMed1984

Endocrine effects of the cold pressor test: relationships to subjective pain appraisal and coping.

Blood was drawn from 14 normal volunteers twice before, immediately after a 1-minute immersion of the nondominant hand in ice water (cold pressor test), and twice during recovery. Serum levels of beta-endorphin, cortisol, prolactin, growth hormone, and opioid activity were determined, and measures of subjective pain appraisal and coping styles were obtained. Cortisol was the only variable to show a significant increase as a function of noxious stimulation. Correlational analysis yielded relationships between neuroendocrine variables and subjective pain appraisal as well as coping styles, suggesting complex interactions between neuroendocrine and psychological processes in human pain.

Adult↗
PubMed1984

CSF 5-hydroxyindoleacetic acid levels in suicidal schizophrenic patients.

Concentrations of 5-hydroxyindoleacetic acid (5-HIAA) in the lumbar CSF were measured in a group of suicidal schizophrenic patients and in a matched group of nonsuicidal schizophrenic patients. The suicidal group had a significantly lower level. This finding is consistent with reports of low levels of CSF 5-HIAA in suicidal patients with other psychiatric diagnoses and suggests that low CSF 5-HIAA may be a generalized marker of aggressive behavior against the self and others.

Adult↗
PubMed1983

CSF dopamine beta-hydroxylase in schizophrenia.

Dopamine beta-hydroxylase (DBH), the enzyme that converts dopamine to norepinephrine, was measured in the CSF of 30 schizophrenic patients and 27 normal controls. The CSF DBH activity in the patients was not significantly different from that in controls. Levels of CSF DBH activity in individual patients were highly constant over time and were not influenced by clinical state or neuroleptic treatment. Low levels of DBH in CSF did significantly relate to good social and sexual functioning, good prognosis, less symptoms between hospitalizations, and excellent clinical response to neuroleptic treatment. We speculate from these data that low brain DBH activity may produce a type of vulnerability to psychotic decompensation and thereby influence the clinical course, although it does not cause schizophrenia, in general. Low CSF DBH activity may delineate a "reactive" subgroup from the heterogenous population of patients with diagnoses of schizophrenia.

Adolescent↗
PubMed1983

A risk factor strategy for investigating affective illness.

A "risk factor" approach to affective illness is outlined. Characteristics which are correlated with vulnerability to depression (or mania) should be sought and attempts made to either modify them or elucidate a pathophysiologic link between the characteristic and the illness. Genetic factors, biochemical factors, life events, demographic variables, and behavioral factors may be examined under the assumption that affective illness is multifactorially determined. Identification of these risk factors by a prospective epidemiologic study in a geographically delimited area is discussed; the risk factor model is compared with the high-risk model.

Bipolar Disorder↗