Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SLEEP DEPRIVATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 757 records · Page 42Linked to original sources
PubMed2002

Non-rapid-eye-movement sleep propensity after sleep deprivation in human subjects.

The circadian modulation of occurrence of non-rapid-eye-movement sleep (NREM) was investigated in 37 volunteers under dim-light conditions after 24-h total sleep deprivation using a 26-h 10/20-min ultra-short sleep-wake schedule. The propensity of NREM showed rapid increase followed by gradual decrease during the subjective day and nocturnal bouts during the subjective night coinciding with melatonin production. The mean propensity of NREM during the subjective day was smaller than that during the subjective night, even though the sleep debt due to the 24-h sleep deprivation would have enhanced NREM more strongly during the subjective day than that during the subjective night. These results suggest that the occurrence of NREM sleep is modulated by a circadian pacemaker.

Adult↗
PubMed2003

Blunted prolactin response to fentanyl in depression. Normalizing effect of partial sleep deprivation.

There is some evidence that sleep deprivation (SD) might exert its antidepressant properties by involving endogenous opioid mechanisms. The authors investigated the effects of mu-receptor agonist administration on prolactin release in depressed patients before and after partial SD. Medication-free female depressed inpatients (N=18) were participating in two fentanyl challenge tests after partial SD and undisturbed sleep, 3 days apart in random order. Healthy volunteer women (N=10) were enrolled after full night sleep as comparison subjects. Five of them had placebo trials. Participants were given an intravenous injection of 0.1 mg/70 kg fentanyl at 9:00 AM. The prolactin secretory response to the opiate agonist was investigated for 1 h with serial blood sampling. After a night of undisturbed sleep, fentanyl administration prompted increases in plasma prolactin concentrations with blunted responses found in the depressed group. Following partial SD, the stimulated prolactin secretion of depressed patients increased significantly and was comparable to the response of comparison subjects. These findings suggest that SD acts via an opioid/dopamine-related mechanism. An alternative explanation, based on serotonin involvement is addressed in the discussion.

Adult↗
PubMed1997

Can negative self-schemes in depressives be altered through sleep deprivation?

This paper addresses the question whether negative cognitive style represents a state or trait variable of depressive patients. For this reason, it studies the influence of sleep deprivation on negative self-schemes of those patients. 10 patients suffering from DSM-III-R major depression were compared with 10 age- and sex-matched controls on a task for rating the self-descriptiveness of positive and negative adjectives as well as a subsequent word recognition task. Three sessions were involved: an initial session (baseline), the second following a night of sleep deprivation, and the third after a successive full night's sleep. During the baseline examination, depressives showed a relatively negative cognitive bias; that is, the same number of positive and negative self-scheme elements. In comparison to controls, they showed significantly more negative and significantly less positive self-scheme elements. The same pattern emerged in a word recognition task for the number of recognized self-scheme elements. These variables indicated no change in the depressive group following sleep deprivation. Depressive subjects' reaction times on self-descriptiveness rating were significantly longer for positive than for negative self-scheme elements at the baseline session. The opposite was true for controls. Here, a sleep deprivation effect was evident. There was no longer a difference in the speed of information processing for positive as compared to negative self-scheme elements. This applied to both depressive and control groups.

Adult↗
PubMed2000

Regulation of cardiac and renal peripheral benzodiazepine receptor binding in rapid eye movement sleep-deprived rats.

This study was designed to examine the effects of rapid eye movement (REM) sleep deprivation and stress on the properties of peripheral benzodiazepine receptors (PBRs). Rats were deprived of REM sleep for 96 hours by a small pedestal (water tank) method. Using radioligand assays with the selective antagonist [3H]PK11195, receptor density (Bmax) and affinity were measured in the heart and kidney in three groups: 1) REMSD group (REM sleep deprived-group), 2) TC group (tank control group; large pedestal), and 3) CC group (cage control group). REMSD group showed an increase in the density of PBRs in the heart (18%; p<0.002), but not in the kidney (-5%; p=0.058) compared to TC group, and IC group showed an increase in the density of these receptors in the heart (17%; p<0.014), and the kidney (12%; p<0.002) compared to CC group. While the cardiac Kd value was 37% (p<0.0004) and 36% (p<0.002) higher in the REMSD group than in the CC and TC groups, respectively, the renal Kd value was lower (-5%; p=0.057 and -16%; p<0.0004, respectively). The changes in PBRs observed herein are tissue- and treatment-specific, and may suggest a close functional relationship between REM sleep and PBRs.

Animals↗
PubMed1992

Sleep deprivation in rapid-cycling bipolar affective disorder: case report.

We describe a 4-month long hypomanic response to sleep deprivation in a patient with consistent (20-day cycles) rapid cycling. He subsequently reverted to very rapid cycling; however, sleep deprivation remained effective for each attack of depression. Sleep deprivation treatment, its immediate but short-lived beneficial effect, may have a role in the treatment of the ultra-short depressions encountered in very rapid cycling.

Bipolar Disorder↗
PubMed1982

The persistence of hyperresponsiveness to apomorphine in rats following REM sleep deprivation and the influence of housing conditions.

The hyperresponsiveness to apomorphine disappears after REM sleep deprivation of rats; the time course of the disappearance was investigated. When REM sleep-deprived (REMd) rats were caged individually during the recovery period the increase in ambulation and in stereotyped behaviour elicited by apomorphine subsided within 8-24 h; on the other hand, the exaggerated aggressiveness persisted up to 64 days. However, when the deprived rats were allowed to recovery in groups of 3 per cage the increase in aggressiveness subsided after 4 days. Since individual housing of non-deprived rats for 4--11 days increased the apomorphine-aggressiveness steadily, 'isolation' probably summed with REM deprivation in facilitating the effects of apomorphine on aggressive behaviour. The results also suggest that the dopaminergic systems implicated in aggressive behaviour are sensitized by REM deprivation for a longer period than those subjacent to ambulation and stereotype.

Aggression↗
PubMed2004

An event-related fMRI study of the neurobehavioral impact of sleep deprivation on performance of a delayed-match-to-sample task.

Eighteen subjects (ages 18-35) underwent event-related functional magnetic resonance imaging (efMRI) while performing a delayed-match-to-sample (DMS) task before and immediately after 48 h of sustained wakefulness. The DMS trial events were: a 3-s study period of either a one-, three-, or six-letter visual array; a 7-s retention interval; and a 3-s probe period, where a button press indicated whether the probe letter was in the study array. Ordinal Trend Canonical Variates Analysis (OrT CVA) was applied to the data from the probe period for trials with six-letter study lists prior to and immediately following sleep deprivation to find an activation pattern whose expression decreased with sleep deprivation in as many subjects as possible, while being present in both conditions. The first principal component of the OrT analysis identified a covariance pattern whose expression decreased as a function of sleep deprivation in 17 of 18 subjects (p<0.001). While overall expression of the pattern showed a systematic decrease with sleep deprivation, the brain regions that make up the pattern show covarying increases and decreases in activation. Regions that decreased their activation were noted in the parietal (BA 7 and 40), temporal (BA 37, 38 and 39) and occipital (BA 18 and 19) lobes; regions that increased their activation were noted in the cerebellum, basal ganglia, thalamus and the anterior cingulate gyrus (BA 32). The reduction in pattern expression with sleep deprivation for each subject was related to the change in performance on the DMS task. Subject decreases in pattern expression were correlated with reductions in recognition accuracy (p<0.05), increased intra-individual variability in reaction time (p<0.005) and increased lapsing (p<0.005).

Adult↗
PubMed1995

Serial partial sleep deprivation as adjuvant treatment of depressive insomnia.

1. Sleep disturbance is a prominent symptom of major depression. Despite specific treatment with antidepressants, there is a substantial number of patients who improve in depressed mood but remain sleep disturbed. 2. Polysomnographic sleep (PSG) data and self reported sleep measures were assessed at baseline and after one week in 18 patients (35-65 years) randomly assigned to treatment with either trimipramine alone 200 mg/d (group 1) or trimipramine (200 mg/d) and additional serial partial sleep deprivation in the second half of the night (3x/week) (group 2). 3. In group 1 no marked changes between baseline and after treatment were found. 4. In group 2 the PSG data showed a significant increase of slow wave sleep and a compensatory decrease in stage 1. Sleep continuity improved in terms of numbers of awakenings, sleep onset latency and total sleep time. These changes were in parallel with the subjective estimation of sleep in group 2. 5. There was no significant difference in the Hamilton rating scale scores neither at baseline nor after treatment. 6. These observed effects on sleep following additional serial PSD therapy seem to occur independent from the antidepressive effect.

Adult↗
PubMed2005

Deletion of the mammalian circadian clock gene BMAL1/Mop3 alters baseline sleep architecture and the response to sleep deprivation.

STUDY OBJECTIVES: The finding that deletion or mutation of core circadian clock genes in both mice and flies induce unexpected alterations in sleep amount, sleep architecture and the recovery response to sleep deprivation, has led to new insights into functions of the circadian system that extend beyond its role as a regulator of the timing of the sleep-wake cycle. A key transcription factor in the transcriptional/translational feedback loop of mammalian circadian genes is BMAL1/Mop3, a heterodimeric partner to CLOCK. It was previously shown that mice deficient in the BMAL1/Mop3 gene become immediately arrhythmic in constant darkness and have reduced locomotor activity levels under entrained and constant conditions. In this study, we tested the hypothesis that the mammalian BMAL1/Mop3 gene would have regulatory effects on sleep-wake patterns. DESIGN: In mice with targeted deletion of the BMAL1/Mop3 gene, EEG/EMG sleep-wake patterns were recorded under entrained and free-running conditions as well as following acute (6-hrs) sleep deprivation. MEASUREMENTS AND RESULTS: Mice homozygous for the BMAL1/Mop3 deletion showed an attenuated rhythm of sleep and wakefulness distribution across the 24-hr period. In addition, these mice showed increases in total sleep time, sleep fragmentation and EEG delta power under baseline conditions, and an attenuated compensatory response to acute sleep deprivation. CONCLUSIONS: These new data strengthen the hypothesis that molecular components of the circadian system play a central role in the generation of sleep and wakefulness beyond just the timing of these behavioral vigilance states.

ARNTL Transcription Factors↗
PubMed2000

Topography of EEG dynamics after sleep deprivation in mice.

Several recent results show that sleep and sleep regulation are not only global phenomena encompassing the entire brain, but have local features. It is well established that slow-wave activity [SWA; mean electroencephalographic (EEG) power density in the 0.75-4.0 Hz band] in non-rapid eye movement (NREM) sleep is a function of the prior history of sleep and wakefulness. SWA is thought to reflect the homeostatic component of the two-process model of sleep regulation. According to this model, originally formulated for the rat and later extended to human sleep, the timing and structure of sleep are determined by the interaction of a homeostatic Process S and a circadian process. Our aim was to investigate the dynamics of SWA in the EEG of two brain regions (frontal and occipital cortex) after sleep deprivation (SD) in two of the mice strains most often used in gene targeting. C57BL/6J (n = 9) and 129/Ola (n = 8) were recorded during a 24-h baseline day, 6-h SD, and 18-h recovery. Both derivations showed a significant increase in SWA in NREM sleep after SD in both strains. In the first hour of recovery, SWA was enhanced more in the frontal derivation than in the occipital derivation and showed a faster decline. This difference resulted in a lower value for the time constant for the decrease of SWA in the frontal derivation (frontal: 10.9 +/- 2.1 and 6.8 +/- 0.9 h in Ola and C57, respectively; occipital: 16.6 +/- 2.1 and 14.1 +/- 1.5 h; P < 0.02; for each of the strains; paired t-test). Neither time constant differed significantly between the strains. The subdivision of SWA into a slower and faster band (0.75-2.5 Hz and 2.75-4.0 Hz) further highlighted regional differences in the effect of SD. The lower frequency band had a higher initial value in the frontal derivation than in the occipital derivation in both strains. Moreover, in the higher frequency band a prominent reversal took place so that power in the frontal derivation fell below the occipital values in both strains. Thus our results indicate that there may be differences in the brain in the effects of SD on SWA in mice, suggesting regional differences in the dynamics of the homeostatic component of sleep regulation. The data support the hypothesis that sleep has local, use- or waking-dependent features that are reflected in the EEG, as has been shown for humans and the laboratory rat.

Animals↗
PubMed2005

Sleep deprivation potentiates activation of cardiovascular and catecholamine responses in abstinent alcoholics.

Alcohol dependence is associated with an increased incidence of hypertension and cardiac arrhythmias, but the triggering mechanisms are not known. Sleep loss, common in alcohol-dependent patients, causes an activation of the sympathetic nervous system. To determine whether sleep deprivation induces differential cardiovascular and sympathetic responses in alcohol dependence, we measured heart rate, blood pressure, and circulating sympathetic catecholamines in 36 abstinent alcohol-dependent men and 36 age-, gender-, and ethnicity-matched controls after a baseline night of sleep, in the morning after early night partial sleep deprivation, and again after a full night of recovery sleep. Subjects were on average normotensive and none was being treated for hypertension. Baseline heart rate, blood pressure, and sympathetic catecholamines were similar in the 2 groups. Administration of partial night sleep deprivation induced greater increases of heart rate (P<0.01) and circulating levels of norepinephrine (P<0.05) and epinephrine (P<0.05) in the alcohol-dependent men as compared with responses in controls. Even after a full night of recovery sleep, elevations in heart rate (P<0.05) and circulating catecholamines (P<0.05) persisted in the alcoholic subjects. Partial night sleep deprivation induces elevated heart rate and sympathetic catecholamine responses in alcoholic subjects as compared with controls, and this sympathetic activation is sustained after nights of partial and recovery sleep. It is possible that modest habitual sleep loss could contribute to triggering cardiac arrhythmias or other cardiovascular events in alcohol dependence.

Adult↗
PubMed1993

Therapy and prevention of affective illness by total sleep deprivation.

The therapeutic effect of total sleep deprivation (SD) given twice a week, for 4 weeks, was investigated in 16 drug-free patients with major affective disorders. The response was excellent in five patients, satisfactory in three and minimal in eight patients. Six of these patients were treated prophylactically once a week, and four had an excellent response. Additionally, out of five normothymic drug-free patients with affective illness treated prophylactically with SD, without prior therapeutic SD treatment, three had an excellent response. The majority of responders were rapid cycling patients. This method is worth applying to patients resistant to classical treatment.

Adult↗
PubMed1996

Influence of paradoxical sleep deprivation on the intermediate stage of sleep in the rat.

In the rat, paradoxical sleep (PS) is preceded by a short-lasting stage characterized by high amplitude cortical spindles and low frequency hippocampal theta rhythm. This intermediate stage (IS) is massively extended at the expense of PS by barbiturates and benzodiazepines. To further study the relationship between the IS and PS, six rats were PS deprived for 48 h by sitting on one of three small platforms surrounded by water. A control group of six other rats remained in dry cages with shavings. After 24 h PS deprivation the latency of IS occurrence increased, was unchanged after 48 h deprivation and decreased during recovery on shavings after 52 h deprivation. The total IS duration, number of episodes and mean duration per episode were unchanged during deprivation but increased during recovery. This recovery was characterized by an increase in the number of PS episodes and the total duration while the latency of PS occurrence decreased. The frequency of theta rhythm, unchanged for PS, increased for the IS during deprivation and recovery. In conclusion, the IS did not substitute for PS after selective deprivation.

Animals↗
PubMed2001

Dopaminergic augmentation of sleep deprivation effects in bipolar depression.

Total sleep deprivation (TSD) has been used in association with lithium salts and with serotonergic and noradrenergic antidepressants, leading to sustained improvements in patients affected by major depression. Current theories on the neurobiological mechanism of action of TSD propose a major role for enhanced dopamine activity. To test the clinical relevance of dopaminergic enhancement in TSD, we treated a homogeneous sample of 28 bipolar depressed patients with three cycles of TSD combined with placebo or with the dopaminergic antidepressant amineptine. Changes in mood over time were rated with self-administered visual analogue scales and with the Montgomery-Asberg Depression Rating Scale. Patients showed improved mean daily-mood scores after TSD, an effect that was highest at the first cycle and decreased with treatment repetition. Amineptine enhanced the effects of TSD on perceived mood during the first two TSD cycles, but patients in the placebo and amineptine groups showed comparable results at the end of the treatment. Despite its theoretical importance, the clinical usefulness of combining TSD with a dopaminergic agent must be questioned.

Bipolar Disorder↗
PubMed1999

Influence of a functional polymorphism within the promoter of the serotonin transporter gene on the effects of total sleep deprivation in bipolar depression.

OBJECTIVE: A functional polymorphism in the transcriptional control region upstream of the coding sequence of the 5-hydroxytryptamine transporter (5-HTT) has been reported. This polymorphism has been shown to influence the antidepressant response to fluvoxamine and paroxetine. The authors tested the hypothesis that the allelic variation of the 5-HTT-linked polymorphic region (5-HTTLPR) could influence the response of depressed patients to total sleep deprivation. METHOD: Sixty-eight drug-free inpatients with bipolar depression underwent a night of total sleep deprivation. 5-HTTLPR was genotyped in these patients. Changes in perceived mood were rated on a visual analogue scale and analyzed by using repeated measures analysis of covariance. RESULTS: Patients who were homozygotic for the long variant of 5-HTTLPR showed a significantly better mood amelioration after total sleep deprivation than those who were heterozygotic and homozygotic for the short variant. CONCLUSIONS: The influence of 5-HTTLPR on response to total sleep deprivation is similar to its observed influence on response to serotonergic drug treatments. This finding supports the hypothesis of a major role for serotonin in the mechanism of action of total sleep deprivation in depression.

Adult↗
PubMed1981

Changes of response to dopaminergic drugs in rats submitted to REM-sleep deprivation.

Three experiments were performed in order to add further support to the hypothesis that the exaggerated aggressiveness elicited by apomorphine in REM sleep deprived rats was due to a state of supersensitivity of post-synaptic dopaminergic receptors in brain. In the first experiment, REM deprived rats displayed much aggressiveness when challenged with 10 and 20 mg/kg of bromocriptine and piribedil. Thus, the intensification of responses by REM sleep deprivation is not restricted to apomorphine, as it was also obtained with two other dopaminergic agonists. In the second experiment, the association of REM deprivation with an injection of haloperidol 24 h before apomorphine administration induced still more aggressive behavior when compared to the rats that were only sleep deprived. It has been claimed that 24 h after haloperidol a state of supersensitivity to dopamine agonists occurs in the brain; therefore, it is probable that REM deprivation could also act similarly. The third experiment showed that haloperidol administered 2 h before apomorphine administration blocked the aggressive behavior in rats either submitted to REM deprivation alone or to REM deprivation plus a previous injection of haloperidol 24 h before. This also favors the proposed hypothesis. Alternative possibilities for explaining the observed hyperresponsiveness of REM deprived rats to apomorphine and other dopaminergic agonists are also analysed.

Adrenergic Agonists↗
PubMed1999

Sleep deprivation therapy in depressive illness and Parkinson's disease.

1. Sleep deprivation is commonly associated with feelings of fatigue and cognitive impairment. 2. Patients with depressive illness, however, often experience mood improvements under these same conditions. 3. Other studies now show that tremor and rigidity, in patients with Parkinson's disease, are also improved by sleep depression therapy. 4. The neural substrates which underlie these effects are unclear. Some recent evidence, however, suggests that sleep deprivation may activate mechanisms which are otherwise typical of conditions of metabolic stress. 5. A common feature of these mechanisms is the suppression of cholinergic activity which is thought to be excessive, in relation to monoamine transmission, in both depression and Parkinson's disease.

Animals↗
PubMed1988

Electro-mechanical response times and muscle strength after sleep deprivation.

This study examined the effect of 60 h of sleep deprivation (SD) on electromechanical response times (EMRT), maximal voluntary isometric contraction (MVC), rate of force development (RFD), and times required to reach various percentages of MVC, during a maximal voluntary isometric contraction of both the forearm flexors and leg extensors. Eleven male subjects were either sleep deprived for 60 h (E) or performed similar daily activities and slept 7 h per night (C). Performance variables were evaluated at the same time intervals during both conditions. No significant differences were observed between the E and C conditions for EMRT (pre-motor time, electro-mechanical delay, total reaction time) or muscular performance (MVC, RFD). The results suggest that subjects who have undergone 60 h of SD can react as fast, and with as much force, as those who have had 7 h of sleep per night.

Adult↗