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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↗
PubMed1979

Plasma levels of d-amphetamine in hyperactive children. Serial behavior and motor responses.

Amphetamine has been clearly documented to be an efficacious treatment for hyperactive children. The pharmacokinetics of amphetamine have been studied in adults, but not in children. Sixteen male children who scored greater than 2SD from norms on Factors I and IV of Conner's Teacher Rating Scale and who were not excluded for reasons to do with medical or psychiatric conditions, intelligence, or age, had a plasma d-amphetamine apparent elimination half-life of 6.8 +/- 0.5h. Peak plasma level occurred between 3 and 4h (62.7 +/- 3.8 and 65.9 +/- 3.6 ng/ml, respectively). Six of these children had a repeat study and there were no significant differences within subject in apparent elimination half-lives and attained peak blood levels. The variation in plasma levels was greater during absorption than during elimination. Both behavioral and motor activity responses as analyzed by differences between amphetamine and placebo days (by paired t-tests) indicate significant responses between hours 1--4; however, these responses do not correlate with plasma amphetamine levels; they occur during the absorption phase. The decreased response to later similar plasma levels of d-amphetamine may be related to depletion of catecholamine stores, to replacement by a 'false neurotransmitter' metabolite of amphetamine, or to alteration in receptor sensitivity.

Child↗
PubMed1979

Predicting drug-free improvement in schizophrenic psychosis.

In a sample of 22 psychotic schizophrenic patients, eight improved substantially during a 30-day drug-free period. The drug-free improver group differed from the nonimprover group in demonstrating a later age of onset, briefer psychotic episodes, shorter hospitalizations, and better prognostic scores on the Phillips Scale, Strauss-Carpenter Modified Prognostic Scale, and the Vaillant Scale. After drug withdrawal, drug-free improvers frequently demonstrated further improvement when treated with doses of neuroleptic drugs that were substantially lower than the clinically recommended doses. The authors raise the question as to whether the drug-free improvers may represent a subgroup of schizophrenic patients who are being overtreated presently by standard neuroleptic practice.

Adolescent↗