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Results for “SLEEP DEPRIVATION”

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PubMed1998

Interactive effects of sleep deprivation, time of day, and driving experience on a driving task.

Performance decrements after more than 24 hours of sleep deprivation (SD) are not only a monotonic function of the duration of SD, but are the result of an interaction between SD and time of day. The major deteriorations in performance during SD are still evident throughout the night, as in the non-sleep-deprived state. Twelve experienced and 12 inexperienced drivers drove a driving simulator for 20 minutes at 0800, 1100, 1400, 1700, and 2000 hours on two testing days. One testing day was conducted after a normal night's sleep, and the other after one night of SD. Reaction time (RT) was also measured while driving. The standard deviation of both lateral position and speed were significantly higher during SD. Performance steadily improved across the day between 0800 and 2000 hours, and the absence of any sleep-by-time interactions suggests that the rhythm of driving performance across the day was similar after both normal sleep and SD. Inexperienced drivers had higher RTs than experienced drivers in both sleep-deprived and non-sleep-deprived conditions. These results have important implications for those involved in the transport industry.

Adult↗

PubMed1996

Rapid eye movement (REM) sleep deprivation in 6-OHDA nigro-striatal lesioned rats with and without transplants of dissociated chromaffin cells.

Since both REM sleep deprivation and unilateral 6-OHDA lesions induce supersensitivity of DA receptors, the purpose of this study was to determine whether the response of rats with such lesions would be modified by REM sleep deprivation. In addition, the effect of grafts of dissociated chromaffin cells was also tested. Rats with 6-OHDA lesions were subjected to 24 or 72 h of REM sleep deprivation and tested with various doses of apomorphine to determine turning behavior frequencies. At end of those experiments, the animals were transplanted with dissociated chromaffin cells and turning behavior was tested again. The results showed that REM sleep deprivation nearly doubled the turning behavior frequency, that chromaffin cell grafts decreased it, but that REM deprivation in grafted animals still seemed to produce an increase of post-synaptic supersensitivity independent of denervation. The results were discussed in terms of the possible relationship of sleep with Parkinson's disease through the DA system.

Animals↗

PubMed2006

Creatine supplementation, sleep deprivation, cortisol, melatonin and behavior.

The effect of creatine supplementation and sleep deprivation, with intermittent moderate-intensity exercise, on cognitive and psychomotor performance, mood state, effort and salivary concentrations of cortisol and melatonin were examined. Subjects were divided into a creatine supplementation group and a placebo group. They took 5 g of creatine monohydrate or a placebo, dependent on their group, four times a day for 7 days immediately prior to the experiment. They undertook tests examining central executive functioning, short-term memory, choice reaction time, balance, mood state and effort at baseline and following 18-, 24- and 36-h sleep deprivation, with moderate intermittent exercise. Saliva samples were taken prior to each set of tests. A group x time analysis of covariance, with baseline performance the covariate, showed that the creatine group performed significantly (p < 0.05) better than the placebo group on the central executive task but only at 36 h. The creatine group demonstrated a significant (p < 0.01) linear improvement in performance of the central executive task throughout the experiment, while the placebo group showed no significant effects. There were no significant differences between the groups for any of the other variables. A significant (p < 0.001) main effect of time was found for the balance test with a linear improvement being registered. Cortisol concentrations on Day 1 were significantly (p < 0.01) higher than on Day 2. Mood significantly (p < 0.001) deteriorated up to 24 h with no change from 24 to 36 h. Effort at baseline was significantly (p < 0.01) lower than in the other conditions. It was concluded that, during sleep deprivation with moderate-intensity exercise, creatine supplementation only affects performance of complex central executive tasks.

Adult↗

PubMed1995

Sleep deprivation in the rat: an animal model of mania.

The model of sleep deprivation in rats by the platform method has been extensively studied in our laboratory as a possible animal model of mania. At the end of the period of sleep deprivation, the rat does not fall asleep as soon as it is returned to its home cage, but shows a period of wakefulness of about 30 min, during which the animal presents a cohort of symptoms that appear to mimic those present in idiopathic mania. In particular, during this period the animal displays insomnia, a high degree of hyperactivity, irritability, aggressiveness, hypersexuality and stereotypy. Haloperidol (0.2 mg/kg) was effective in reducing latency to sleep, while L-sulpiride was much weaker (< 50 mg/kg). The dopamine D1 receptor antagonist SCH 23390 exhibited an extremely high potency and efficacy in reducing sleep latency, a significant effect being observed with 3 micrograms/kg. The administration of the specific D1 receptor agonist SKF 38393 markedly prolonged the period of insomnia with the correlated behavioral syndrome. When lithium was added to the diet and consumed during the sleep deprivation period in adequate amounts to produce serum lithium levels of 0.7-1.0 mEq/l, sleep latency and locomotor activity were significantly reduced. The administration of naloxone (1-10 mg/kg) reduced the latency to sleep in a dose-related manner. By contrast, morphine (1 and 5 mg/kg, i.p.), beta-endorphin and [D-Ala2,D-Leu5]enkephalin (i.c.v., 2 and 1 micrograms, respectively) markedly prolonged the insomnia. The model not only represents a confirmation in the rat that sleep loss often precedes and may trigger a manic episode in man, but suggests that an opioid-dopamine interaction may play a pathogenetic role in mania.

Animals↗

PubMed1979

[Use of sleep deprivation for the purpose of treating protracted depressive states].

Sleep deprivation therapy was used in 30 patients with protracted, resistant depressive phases within the framework of manic-depressive psychosis. All patients demonstrated some improvement, which lasted from several hours up to 3 days. Changes in the state were mainly expressed in mood swings and to a less extent to the sphere of thinking and motor acts. A course of sleep deprivation (6-8 nights without sleep with an interval of 2-7 days) was administered to 19 patients, of them 7 patients demonstrated a stable improvement. Recording depressive symptomatology by the scale of intensity showed significant positive changes according to the following parameters: mood, thinking, motor acts, interests, sociability. The highest effect was seen in patients with melancholic pictures and significantly worse in depressive-anxious and depressive-obsessional syndromes.

Adult↗

PubMed2005

Heart rate variability during sedentary work and sleep in normal and sleep-deprived states.

The possibility of using heart rate variability (HRV) as an indicator of sleepiness was investigated by analysing heart rate (HR) activity and electroencephalography (EEG) recordings from 10 individuals who performed a monotonous attention task for 120 min in both sleep-deprived and rested states. In both conditions, measurements were collected during 60 min of sleep immediately following a 120 min of non-sleep (awake phase). Although HR decreased significantly in both the rested and the sleep-deprived states during the awake phase, HR significantly changed sooner when subjects were sleep-deprived than when they were rested. No significant changes in HRV were found during the awake phase; however, HRV correlated significantly with alpha and theta power densities when rested but not when sleep-deprived. During the sleep phase, the total HRV and very low and low frequency HRV components significantly decreased approximately 40 min after sleeping in the sleep-deprived condition. These HRV components were also significantly and negatively correlated with delta power densities. HRV does not seem to be a viable indicator of sleepiness; however, HRV may be useful for determining sleep stages.

Adult↗

PubMed2003

Sleep deprivation prior to transient global cerebral ischemia attenuates glial reaction in the rat hippocampal formation.

This study was aimed to ascertain the effect of sleep deprivation on subsequent cerebral ischemia in the rat hippocampal formation. Seven days after transient global cerebral ischemia induced by four-vessel occlusion method, most of the pyramidal cells in the hippocampal CA1 subfield underwent disruption and pyknosis as detected by cresyl violet staining. With OX-42, OX-18, OX-6 and ED1 immunohistochemistry, robust microglia/macrophage reactions were observed in the CA1 and dentate hilus. The majority of reactive microglia was rod-shaped, bushy or amoeboidic cells bearing hypertrophic processes. Astrocytes also displayed hypertrophic processes, whose immunostaining for glial fibrillary acidic protein was markedly enhanced. The ischemia-induced neuronal damage and glial reactions, however, were noticeably attenuated in rats subjected to pretreatment with sleep deprivation for five consecutive days. The most drastic effect was the diminution of OX-18, OX-6 and ED1 immunoreactivities, suggesting that the immune potentiality and/or phagocytosis of these cells was suppressed by prolonged sleep deprivation prior to ischemic insult. It is postulated that sleep deprivation may have a preconditioning influence on subsequent lethal cerebral ischemia. Hence, sleep deprivation may be considered as a therapeutic strategy in brain ischemic damage.

Animals↗

PubMed2006

Consequences of subchronic and chronic exposure to intermittent hypoxia and sleep deprivation on cardiovascular risk factors in rats.

Since studies suggest that both hypoxia and sleep fragmentation are related to cardiovascular alterations induced by obstructive sleep apnea, the present study was designed to evaluate the effects of hypoxia, sleep deprivation, and their combination on biochemical blood parameters in rats. In subchronic experiments (4 days), rats were exposed to intermittent hypoxia (IH) during the light period (2min room air-2min 10% O(2) for 12h/day) and/or paradoxical sleep deprivation (PSD, 24h/day). Consequences of chronic intermittent hypoxia (CIH) exposure were examined after 21 consecutive days of hypoxia protocol from 10:00 to 16:00 followed by a sleep restriction (SR) period of 18h (16:00-10:00). Rats were randomly assigned to seven treatment groups: (1) control (2) IH (3) PSD (4) IH-PSD (5) SR (6) CIH and (7) CIH-SR. PSD reduced triglycerides and very low-density lipoprotein (VLDL) cholesterol concentrations and increased total cholesterol and high-density lipoprotein (HDL) cholesterol. IH did not alter any of these parameters. The combination of IH-PSD did not modify the values of total cholesterol and HDL compared to control group. In the chronic experiment, the animals exposed to CIH displayed a reduction of Vitamin B(6) and an increase of triglycerides and VLDL. Our findings show a duration-dependent effect of hypoxia on triglycerides. Rats in the SR and CIH-SR groups showed a diminished concentration of triglycerides and VLDL. SR rats showed a reduction in the concentration of homocysteine but the animals in the CIH-SR treatment condition did not display any alterations in this parameter. In this latter group, an augmentation of cysteine concentration was observed. These results suggest that sleep deprivation and hypoxia modify biochemical blood parameters in distinct ways.

Animals↗

PubMed1976

The effect of sleep deprivation on depressed patients.

In this paper an account is given of the effect of single-night sleep deprivation (SD) therapy in 124 depressive patients of different diagnostic groups. Phasic depressives showed a marked improvement after treatment by sleep deprivation. Because these improvements were often of short duration, we repeated the treatments and combined them with thymoleptic drugs. In the group of neurotic depressives the therapeutic effect of sleep deprivation varied; on the whole, however, the improvement was less marked. It is pointed out that the vital symptoms and "critical time" are of importance. Sleep deprivation can be explained as a resynchronization of disturbed circadian rhythms brought about by interrupting these rhythms.

Adjustment Disorders↗

PubMed1995

The effect of sleep deprivation on motor impairment and retinal adaptation in Parkinson's disease.

1. Sleep deprivation has previously been reported to result in a temporary improvement of motor deficits in Parkinson's disease patients. 2. The mechanism of this action is unclear but may involve an activation of dopamine pathways. 3. Other studies suggest that light adaptive changes in the retinal pigment epithelium may serve as a model of dopamine sensitivity. 4. The present study examined the effects of one night of total sleep deprivation on RPE potentials and motor abnormalities in Parkinson's patients. 5. Sleep deprivation significantly improved motor deficits and these changes were strongly correlated with increases in light adaptive RPE potentials.

Adaptation, Ocular↗

PubMed1981

Effect of sleep deprivation on dopamine receptor function in normal subjects.

Twenty-four hours sleep deprivation significantly decreased the growth hormone response to the dopamine receptor agonist, apomorphine HCl, in five normal men (0.5 mg s.c.) and one woman (0.75 mg s.c.) but had no effect on basal or post-apomorphine prolactin concentrations. These results suggest that sleep deprivation decreases the sensitivity of certain central dopamine receptors. The relevance of this finding to the antidepressant effect of sleep deprivation is unclear.

Adult↗

PubMed1989

Paradoxical sleep deprivation does not affect neuronal excitability in the rat hippocampus.

Before, during and after paradoxical sleep deprivation, field potentials, evoked in the CA1 region and in the fascia dentata of the hippocampus by means of paired pulse stimulation, were measured. Paradoxical sleep deprivation was applied for 3 days, using the platform and the pendulum technique. No changes were observed on evoked field potential amplitude, population spike or paired pulse depression during and after the deprivation period. These results suggest that the neuronal excitability in the rat hippocampus, measured with the evoked potential technique, does not change as a result of paradoxical sleep deprivation.

Action Potentials↗

PubMed1997

Temperature circadian rhythms during the menstrual cycle and sleep deprivation in premenstrual dysphoric disorder and normal comparison subjects.

The aim of this study was to test the hypothesis that the circadian rhythm of core body temperature is altered in premenstrual dysphoric disorder (PMDD) subjects compared to that in normal comparison (NC) subjects and that it is normalized in PMDD subjects after treatment with early night partial sleep deprivation (ESD) or late night partial sleep deprivation (LSD). A total of 23 subjects meeting DSM-IV criteria for PMDD and 18 NC subjects had 24-h core body temperature recordings taken during the following conditions: (1) baseline midfollicular (preovulatory) and (2) late luteal (postovulatory) menstrual cycle phases and after a randomized crossover trial in subsequent luteal phases of (3) ESD, in which subjects slept from 03:00 to 07:00 h, followed by (4) a night of recovery sleep (ESD-R: sleep 22:30 to 06:30 h), and (5) LSD, in which subjects slept from 21:00 to 01:00 h, also followed by (6) a night of recovery sleep (LSD-R: sleep 22:30 to 06:30 h). Temperature amplitudes were significantly decreased in the luteal phase compared to those in the follicular menstrual cycle phase and increased after nights of recovery sleep. Compared to the baseline late luteal phase, during LSD, temperature amplitude increased in PMDD subjects but decreased in NC subjects. During ESD, the temperature acrophase was delayed in PMDD subjects but was advanced in NC subjects; during LSD, the temperature acrophase was advanced in PMDD subjects but was delayed in NC subjects compared to the late luteal baseline. Nocturnal temperature and temperature maxima and mesors tended to be higher in PMDD subjects than in NC subjects; when not reduced during sleep deprivation interventions, these were not associated with therapeutic effects. Alterations in both phase and amplitude of temperature circadian rhythms characterize PMDD subjects as contrasted with NC subjects in response to sleep deprivation. The changes in phase reflected more shifts in temperature acrophase in response to shifts in sleep in PMDD subjects. This realignment of the timing of sleep and temperature in addition to the enhancement of blunted amplitude rhythms during recovery nights of sleep may provide corrective mechanisms that contribute to the therapeutic effects of sleep deprivation.

Adult↗

PubMed1995

Antidepressant responses and changes in visual adaptation after sleep deprivation.

The effects of 1 night of total sleep deprivation on mood state and visual light-dark adaptation were studied in 15 patients with major depression and nine normal comparison subjects. Mood improvements were evident in all but one patient, although responders (n = 9) could be easily distinguished from nonresponders (n = 6). No significant group differences were found in ocular responses before treatment. After treatment, however, light-adapted peak corneofundal potentials increased in patient responders and decreased in patient nonresponders and normal subjects. Moreover, changes in peak values were closely correlated (r = -0.74) with changes in scores on the Hamilton Depression Rating Scale. In contrast, dark-adapted trough potentials did not distinguish between diagnostic groups and were not correlated with clinical responses. The results indicate that sleep deprivation induces changes in light sensitivity that are proportional to improvements in depressive state.

Adult↗

PubMed2004

Glucocorticoids influence brain glycogen levels during sleep deprivation.

We investigated whether glucocorticoids [i.e., corticosterone (Cort) in rats] released during sleep deprivation (SD) affect regional brain glycogen stores in 34-day-old Long-Evans rats. Adrenalectomized (with Cort replacement; Adx+) and intact animals were sleep deprived for 6 h beginning at lights on and then immediately killed by microwave irradiation. Brain and liver glycogen and glucose and plasma glucose levels were measured. After SD in intact animals, glycogen levels decreased in the cerebellum and hippocampus but not in the cortex or brain stem. By contrast, glycogen levels in the cortex of Adx+ rats increased by 43% (P < 0.001) after SD, while other regions were unaffected. Also in Adx+ animals, glucose levels were decreased by an average of 28% throughout the brain after SD. Intact sleep-deprived rats had elevations of circulating Cort, blood, and liver glucose that were absent in intact control and Adx+ animals. Different responses between brain structures after SD may be due to regional variability in metabolic rate or glycogen metabolism. Our findings suggest that the elevated glucocorticoid secretion during SD causes brain glycogenolysis in response to energy demands.

Adrenalectomy↗

PubMed1997

Accelerating response in geriatric depression: a pilot study combining sleep deprivation and paroxetine.

Elderly depressed patients often require an average of 12 weeks of pharmacotherapy before attaining remission. The delay between treatment initiation and remission may decrease compliance and prolongs suffering; hence, interventions that decrease the time to onset of antidepressant activity are needed. Our objective was to evaluate, in an open trial, the use of one night of total sleep deprivation combined with paroxetine to accelerate antidepressant response in elderly patients. Thirteen elderly patients with major depression were sleep-deprived for one night and started paroxetine on the night of recovery sleep. Patients were followed for twelve weeks, and clinical improvement was rated using the 17-item Hamilton Depression Rating Scale and a version of the Hamilton modified for sleep deprivation studies. 8/13 (62%) patients experienced significant improvement of depressive symptoms by 2 weeks. Within 12 weeks 11/13 (85%) patients responded to the combination of sleep deprivation and paroxetine. Median response time was 2 weeks. Clinical response at 12 weeks was correlated with changes in Sleep Deprivation Depression Rating Scale Scores between baseline and recovery sleep. In an open trial, the combined use of total sleep deprivation and paroxetine appears to be an effective method for speeding the onset of clinical antidepressant activity in geriatric depression and for improving early recognition of non-response.

Aged↗

PubMed1997

Effects of sleep deprivation with reference to military operations.

This review discusses the need for sleep, effects of sleep deprivation on behaviour and performance in the military, and sleep management recommendations to optimise combat effectiveness. Most people, regardless of sex or race, prefer 7 to 8 hours of sleep each night. Sleeping during the day is less recuperative. Continuous sleep is more effective than multiple short naps-even when the total hours for naps is more. Ten to 20 minute naps are useful when continuous sleep is not possible. Sleep inertia is the 5 to 30 minute period of sluggishness after awakening and important military tasks should be avoided. Previously, continuous work episodes (CWEs) duration was restricted by limited night vision, unreliable equipment and reduced endurance of military personnel. With improved technology, CWEs are now restricted primarily by endurance which is affected by sleep deprivation. This was one of the experiences noted in recent conflicts (e.g. Desert Storm) by personnel in the air force, army and navy. Since there will be changes in operational requirements, several work-rest-sleep plans must be prepared. Sleeping the preferred 7 to 8 hours per 24 hours the week before an operation may help prepare for optimal performance. Personnel should be familiarised with conditions under which they may sleep. During combat, sleep management should ideally avoid situations where all personnel are exhausted at the same time. As sleep debt accumulates, a person's mood, motivation, attention, alertness, short-term memory, ability to complete routines, task performance (errors of omission more than errors of commission) and physical performance will become more negatively affected. Counter measures must then be taken (e.g. time for sleep or naps, changing routines or rotating jobs). Drugs like caffeine and amphetamine can help personnel stay awake. However, they may also keep them awake when they need to sleep- and on awakening, they could suffer from "hang-overs" and are less efficient. Sleep lost need not be replaced hour-for-hour. Therefore, after operations, personnel need continuous sleep for only 10 to 12 hours as longer sleep increases sleep inertia and delays getting back to normal schedules.

Humans↗

PubMed1983

[Sleep deprivation and dexamethasone suppression test in healthy volunteers].

One night sleep deprivation in 10 healthy volunteers was performed: none of them presented an abnormal dexamethasone suppression test (DST) during the following afternoon. In this experimentation, a short deprivation of sleep does not alter DST. Etiopathogenic hypothesis of DST abnormalities (and other factors) have been discussed.

Adult↗