PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “SLEEP DEPRIVATION”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 487 records · Page 27Linked to original sources
PubMed1995

Early versus late partial sleep deprivation in patients with premenstrual dysphoric disorder and normal comparison subjects.

OBJECTIVE: The aim of this study was to compare the clinical effects of early-night and late-night partial sleep deprivation in patients with premenstrual dysphoric disorder and normal comparison subjects. METHOD: In the premenstrual phase of two menstrual cycles, 23 subjects with DSM-IV premenstrual dysphoric disorder and 18 normal comparison subjects underwent a randomized crossover trial of 1) early-night sleep deprivation, in which subjects slept from 3:00 a.m. to 7:00 a.m., followed by a night of recovery sleep (11:00 p.m. to 7:00 a.m.), and 2) late-night sleep deprivation, in which subjects slept from 9:00 p.m. to 1:00 a.m., followed by a night of recovery sleep. RESULTS: For the subjects with premenstrual dysphoric disorder, in both partial sleep deprivation conditions the Hamilton and Beck depression ratings were significantly lower after recovery sleep than at baseline. Ratings on the day after early or late partial sleep deprivation tended to be lower than at baseline but were not statistically different. The normal comparison subjects showed no clinically important mood changes. A factor analytic approach used with the Hamilton depression scores showed that depressive retardation symptoms were the most responsive to sleep deprivation in the premenstrual dysphoric disorder subjects. CONCLUSIONS: These results are consistent with the reported efficacy of sleep deprivation for major depressive disorder. However, the premenstrual dysphoric disorder subjects improved after the recovery sleep rather than directly after partial sleep deprivation. That late-night sleep deprivation did not have greater benefit than did the hypothesized sham treatment, early-night sleep deprivation, also suggests that placebo effects cannot be ruled out.

Adult↗
PubMed1990

Effect of sleep and sleep deprivation on ventilatory response to bronchoconstriction.

To characterize ventilatory responses to bronchoconstriction during sleep and to assess the effect of prior sleep deprivation on ventilatory and arousal responses to bronchoconstriction, bronchoconstriction was induced in eight asthmatic subjects while they were awake, during normal sleep, and during sleep after a 36-h period of sleep deprivation. Each subject was bronchoconstricted with increasing concentrations of aerosolized methacholine while ventilatory patterns and lower airway resistance (Rla) were continually monitored. The asthmatic patients maintained their minute ventilation as Rla increased under all conditions, demonstrating a stable tidal volume with a mild increase in respiratory frequency. Inspiratory drive, as measured by occlusion pressure (P0.1), increased progressively and significantly as Rla increased under all conditions (slopes of P0.1 vs. Rla = 0.249, 0.112, and 0.154 for awake, normal sleep, and sleep after sleep deprivation, respectively, P less than 0.0006). Chemostimuli did not appear to contribute significantly to the observed increases in P0.1. Prior sleep deprivation had no effect on ventilatory and P0.1 responses to bronchoconstriction but did significantly raise the arousal threshold to induced bronchoconstriction. We conclude that ventilatory responses to bronchoconstriction, unlike extrinsic loading, are not imparied by the presence of sleep, nor are they chemically mediated. However, prior sleep deprivation does increase the subsequent arousal threshold.

Adult↗
PubMed2001

Effect of total sleep deprivation on the dimensional complexity of the waking EEG.

STUDY OBJECTIVES: Sleep deprivation can affect the waking EEG that may reflect information processing of the brain. We examined the effect of total sleep deprivation (TSD) on nonlinear dynamics of the waking EEG. DESIGN: Paired-group design. SETTING: A sleep disorders laboratory in a hospital. PARTICIPANTS: Twenty healthy male volunteers. INTERVENTIONS: Waking EEG data were recorded from subjects with eyes closed after (a) an 8-hour night's sleep and (b) TSD for 24 hours. The dimensional complexity (D2), as a nonlinear measure of complexity, of the EEG after a full night sleep were compared with those of the EEG after TSD. MEASUREMENTS AND RESULTS: The sleep-deprived states had lower D2 values at three channels (P4, O2, and C3) than normal states. CONCLUSIONS: TSD results in the decrease of complexity in the brain, which may imply sub-optimal information processing of the cerebral cortex. We suggest that the investigation of the relation between nonlinear dynamics of the waking EEG induced by TSD and cognitive performance may offer fruitful clues for understanding the role of sleep and the effects of sleep deprivation on brain function.

Adult↗
PubMed1998

[Sleep deprivation in inpatient treatment of depression. A report of experiences].

Sleep deprivation or "stay awake"-therapy), given in addition to drug therapy, is seen as an effective anti-depressive treatment with actually no side effects. Nevertheless, it is not regularly and systematically used. A reason for this might be doubts about its feasibility in psychiatric hospitals without specialised depression wards. Only a few reports exist on the practical aspects of sleep deprivation. The present article informs about the "stay awake"-therapy on 101 depressive patients (in the mean 25 patient-nights per month), carried out at the Psychiatric Hospital Sanatorium Kilchberg/Zurich. The patients (age between 19 and 76, mean 47 years) participated on average in 4.4 partial sleep deprivations. 72% participated at least for a set of three nights. One staff person takes care of a group of at most five patients. Indication, organisation, night programme, care and possible strains are reported. A stay awake night (three times a week) consists of breakfast, games, conversations, taking two walks, and discussions about depression and about treatment (psychoeducation), with the aim to avoid naps and to provide a pleasant social event. The experiences made with serial partial sleep deprivation are encouraging.

Adult↗
PubMed1988

Sleep deprivation and imipramine binding sites in depressed patients and healthy subjects.

The influence of sleep deprivation on 3H imipramine binding was investigated in blood platelets of 32 depressed patients and 15 healthy subjects. The effect of sleep deprivation was not statistically different in either group. Changes of Bmax associated with sleep deprivation were compensated for by reciprocal changes of Kd in the group of patients, suggesting altered regulatory mechanisms. A comparison of binding characteristics of responders and nonresponders to sleep deprivation revealed no difference between groups. If the patients were divided by a biological criterion (number of binding sites), a prediction of clinical response to sleep deprivation was possible.

Adult↗
PubMed2004

Auditory event-related potentials and psychological changes during sleep deprivation.

This study investigated the psychophysiological effects of sleep deprivation on auditory event-related potentials (AERPs) and their relationship with psychological parameters. Twenty-four subjects remained awake for 37 h under continuous surveillance. In the mornings and the evenings of 2 consecutive study days, AERPs were recorded and 4 self-rated scales (sleepiness, fatigue, anxiety, and mood) were quantified. The latencies of P300 and N200 were significantly prolonged (p < 0.001) and their amplitudes decreased (p < 0.05) as a consequence of sleep deprivation. However, the only significant change in N100 and P200 was an increase in the P200 amplitude (p < 0.05). The increase in the latencies of P300 and N200 were correlated with increased sleepiness (p < 0.05), and the increase in P200 amplitude was correlated with negative mood, anxiety, and fatigue (p < 0.05). Although the changes in P300 and N200 induced by sleep deprivation are due to sleepiness, which may slow cognitive processing and decrease the efficiency of mental processing, the increase in P200 may be related with increased anxiety, negative mood, and fatigue.

Adult↗
PubMed1978

[Psychological aspects of sleep deprivation. A controlled study on depressives and normals (author's transl)].

A study of total sleep deprivation for one night was performed on 12 patients with endogenic depression and 10 with neurotic depression, as well as a control group of 10 normals. The study was designed to answer the following questions: 1. Are the correlations between self-ratings and clinical assessments of sleep deprivation effects satisfactory? 2. Are sleep deprivation effects modified by the personality dimensions extraversion and neuroticism? 3. What effects do the interactions of rater and patient and their expectations have on therapeutic results? The findings confirmed the therapeutic effects of sleep deprivation in depressives. The correlations between self-ratings and clinical assessments were satisfactory. The therapeutic effects were not significantly influenced by psychiatrist-patient interactions or their expectations. The relevance of these results to explanations of sleep deprivation effects is discussed.

Adjustment Disorders↗
PubMed2001

Sustained attention performance during sleep deprivation: evidence of state instability.

Nathaniel Kleitman was the first to observe that sleep deprivation in humans did not eliminate the ability to perform neurobehavioral functions, but it did make it difficult to maintain stable performance for more than a few minutes. To investigate variability in performance as a function of sleep deprivation, n = 13 subjects were tested every 2 hours on a 10-minute, sustained-attention, psychomotor vigilance task (PVT) throughout 88 hours of total sleep deprivation (TSD condition), and compared to a control group of n = 15 subjects who were permitted a 2-hour nap every 12 hours (NAP condition) throughout the 88-hour period. PVT reaction time means and standard deviations increased markedly among subjects and within each individual subject in the TSD condition relative to the NAP condition. TSD subjects also had increasingly greater performance variability as a function of time on task after 18 hours of wakefulness. During sleep deprivation, variability in PVT performance reflected a combination of normal timely responses, errors of omission (i.e., lapses), and errors of commission (i.e., responding when no stimulus was present). Errors of omission and errors of commission were highly intercorrelated across deprivation in the TSD condition (r = 0.85, p = 0.0001), suggesting that performance instability is more likely to include compensatory effort than a lack of motivation. The marked increases in PVT performance variability as sleep loss continued supports the "state instability" hypothesis, which posits that performance during sleep deprivation is increasingly variable due to the influence of sleep initiating mechanisms on the endogenous capacity to maintain attention and alertness, thereby creating an unstable state that fluctuates within seconds and that cannot be characterized as either fully awake or asleep.

Adult↗
PubMed1993

Simple reaction time event-related potentials: effects of alcohol and sleep deprivation.

The effects of two levels of alcohol intoxication and 30 hr of sleep deprivation on visual event-related potential (ERP) waveforms concomitant to simple reaction time (RT) were examined in 54 normal male subjects. In a previous study, we reported that alcohol and sleep deprivation each increased RT. At a 0.05 breath alcohol concentration (BAC), the combined treatments produced an additive increase in RT, whereas at a 0.08 BAC the combined treatments produced no increase beyond that seen with each alone. In this study we present the ERP findings. Sleep deprivation alone increased the latency of a 150 msec negative component (N1) of the ERP. Alcohol increased the latency of a 250 msec negative component (N2), but only in the absence of sleep deprivation. Furthermore, this increased latency of N2 was correlated with RT measures. These results suggested that sleep deprivation slowed initial stimulus detection, whereas alcohol slowed later processing and response activation.

Adult↗
PubMed1996

Amitriptyline in combination with repeated late sleep deprivation versus amitriptyline alone in major depression. A randomised study.

Only few systematic studies are available on the status of sleep deprivation therapy in the overall treatment regimen of depressive patients. 51 patients suffering from a major depressive episode (ICD-10) were randomly allocated to 4 weeks' treatment with amitriptyline (150 mg/day) or to a combination of amitriptyline with six partial-sleep-deprivation treatments late in the night (at 4-5 day intervals). According to observer rating (Hamilton Rating Scale for Depression, 21- and 10-item version), a highly significant amelioration was recorded in both groups until the 14th day of treatment. A further improvement occurred, however, only in those patients treated with both antidepressants and sleep deprivation. Hence the response rate ( > or = 50% HAMD reduction) after 4 weeks' treatment was distinctly more favourable in this group than in those patients under pharmacotherapy alone. The superiority of the combined therapy cannot be confirmed statistically by self-rating (Befindlichkeitsskala: von Zerssen; Visual Analogue Mood Scale). The immediate antidepressive effect of sleep deprivation diminished in the course of the sleep deprivation series. The response to the first sleep deprivation was a predictor neither for the response to further sleep deprivation treatments nor for the overall treatment outcome.

Adult↗
PubMed2002

Correlation between the fighting rates of REM sleep-deprived rats and susceptibility to the 'wild running' of audiogenic seizures.

Sleep-deprived rats exhibit defensive fighting as well as explosive flights very similar to the wild-running of audiogenic seizures. In order to determine why sleep deprivation is a common factor that facilitates both panic and convulsive manifestations, the present study was undertaken to investigate whether rats that display sleep deprivation-induced fighting (SDIF) are the same as those that are susceptible to audiogenic wild-running (WR). Twenty-eight male adult Wistar rats were divided into two groups assigned to two experimental schemes. In the first, 18 subjects were submitted to REM-sleep deprivation for 5 days and had their SDIF evaluated in social grouping. After 1 week for recovery, their susceptibility to WR was tested in an acoustic stimulation trial (104 dB, 200 Hz, 60 s). Rats that did not present WR received a lactate infusion and were tested again by acoustic stimulation 40 min later. In the second experimental scheme, 10 subjects were initially evaluated for WR susceptibility and the number of SDIF was recorded in social grouping after 1 week. Three categories of WR-susceptibility were determined: WR-sensitive rats, intermediate WR-sensitive rats and WR-insensitive rats. The number of SDIF in each category was significantly different and there was a high positive correlation (r=0.89; Spearman test) between the number of SDIF and the level of WR-susceptibility. We conclude that the reasons why sleep deprivation exerts facilitatory effects on both panic and convulsive manifestations are due to overlappings of neural pathways responsible for both behavioral patterns and for the property of sleep deprivation to increase neuronal excitability.

Acoustic Stimulation↗
PubMed1998

Effect of night exercise on the following partially deprived sleep.

Six trained male athletes (aged 24.3+/-2.9 years) performed cycling exercise from 23.00 to 23.50 h. From 00.30 to 07.00 h, the subjects followed a schedule that consisted of 30 min trying to fall asleep in bed and 60 min of being awake outside the bedroom. The control experiment was conducted without exercise under the same time schedule. An increase in rectal temperature induced by exercise was 1.9+/-0.4. After exercise, prolongation of sleep onset latency was observed only in the sleep period fron 00.30 to 01.00 h compared with the control night. Time spent in slow wave sleep throughout the night was significantly longer after exercise.

Adult↗
PubMed1975

Altered growth of hormone secretory pattern following prolonged sleep deprivation in the rhesus monkey.

Plasma concentrations of growth hormone (GH) were determined in samples obtained sequentially at 15-min intervals during the last 4 h in monkeys deprived of sleep for 76 h and the first 8 h of ensuing recovery sleep. Electroencephalographic (EEG), electro-oculographic (EOG), and electromyographic (EMG) activities were recorded. Stages 3-4 sleep occurred rapidly after sleep onset and were of long duration. Plasma GH secretion was markedly elevated during sleep recovery, without apparent relationship to stage of sleep.

Animals↗
PubMed1992

The effect of sleep deprivation and sustained military operations on near visual performance.

A group of military servicemen were deprived of sleep for 65 h while they carried out a simulated military mission with a high visual workload. Their performance in a series of near vision tests was monitored. In general, the visual system was found to be resilient to the stress of sleep loss, the subjects experiencing mild symptoms of asthenopia (eyestrain). However, after 48 h without sleep there was a reduction in amplitude of convergent fusional reserves and a decrease in contrast sensitivity to a spatial frequency of 6 cycles/degree. A disruption in diurnal rhythms for these parameters was suggested. The results are considered in terms of the maintenance of visual efficiency and comfort with loss of sleep, and have implications for both the military and civilians involved in shift work and long work schedules.

Accommodation, Ocular↗