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PubMed1975

Extraction of sleep-promoting factor S from cerebrospinal fluid and from brains of sleep-deprived animals.

Sleep-promoting factor (factor S) was extracted, partially purified, and concentrated from cerebrospinal fluid and from acid-acetone extracts of brain stem anc cortex of sleep-deprived goats and sheep. 2. Solutes greater than 500 daltons were largely removed by serial ultrafiltrations through molecular sieves (Amicon membranes UM10 and UM05); solutes less than 350 daltons were largely eliminated by gel filtration through Sephadex G10 columns. Sleep-promoting activity was found in a fraction eluted prior to [14C] sucrose marker. 3. Concentrated fraction were infused intraventricularly in rats (0.1 ml in 30 min just prior to 12-h dark cycle) and in rabbits (0.3 ml in 90 min in morning). Sleep-promoting activity was assayed by decrease in nocturnal locomotor activity of rats and by duration and amplitude of slow-wave cortical EEG in rabbits.

Animals↗
PubMed2005

The effect of REM sleep deprivation on motivation for food reward.

Prolonged sleep deprivation in rats produces a characteristic syndrome consisting of an increase in food intake yet a decrease in weight. Moreover, the increase in food intake generally precedes the weight loss, suggesting that sleep deprivation may affect appetitive behaviors. Using the multiple platform method to produce rapid eye movement (REM) sleep deprivation, we investigated the effect of REM sleep deprivation (REMSD) on motivation for food reward utilizing food-reinforced operant tasks. In acquisition or maintenance of an operant task, REM sleep-deprived rats, with or without simultaneous food restriction, decreased responding for sucrose pellet reward in comparison to controls, despite the fact that all REM sleep-deprived rats lost weight. Furthermore, the overall response deficit of the REM sleep-deprived rats was due to a within-session decline in responding. REM sleep-deprived rats showed evidence of understanding the contingency of the task comparable to controls throughout deprivation period, suggesting that the decrements in responding were not primarily related to deficits in learning or memory. Rather, REM sleep deprivation appears to alter systems involved in motivational processes, reward, and/or attention.

Animals↗
PubMed1998

Efficacy of oral magnesium administration on decreased exercise tolerance in a state of chronic sleep deprivation.

We have previously reported that chronic sleep deprivation causes a deficiency of intracellular magnesium (Mg) and decreased exercise tolerance. The aim of this study was to clarify whether oral administration of Mg could be effective in restoring the exercise tolerance that is decreased by chronic sleep deprivation. A bicycle ergometer cardiopulmonary exercise test was performed by 16 healthy volunteers (mean age 21.9 years). They were divided into 2 groups: 8 received doses of 100 mg of Mg orally per day for 1 month (Mg group) and the remaining 8 received no Mg and served as the control group. The study conditions were designed as follows: (1) the usual state (good sleep); and (2) the sleep-deprived state (sleeping time up to 60% less than the usual state for 1 month). The ratio of intracellular Mg content of the sleep-deprived state to the usual sleep state was significantly higher in the Mg group (p<0.05) than the untreated control group. There was no difference between the sleep-deprived state and the usual state with regard to anaerobic threshold and peak oxygen uptake in the Mg group, whereas both of these decreased in the sleep-deprived state in the control group. These results indicate that decreased exercise tolerance observed in the sleep-deprived state could be improved by oral Mg administration.

Administration, Oral↗
PubMed2002

Dichotic listening and sleep deprivation: vigilance effects.

Twelve sleep-deprived and 13 non-deprived Navy cadets were tested with the dichotic listening procedure for effects of sleep deprivation on hemispheric asymmetry and sustained attention. Consonant-vowel syllables were presented to the subjects in three different conditions, a divided (non-forced) attention condition, a forced right ear and a forced left ear attention condition. In the two forced attention conditions the subjects were instructed to focus attention only on the right or left ear stimulus. The results showed an expected right ear advantage for both groups during the non-forced and forced right attention conditions, indicating superior left hemisphere processing. During the forced left attention condition, the sleep-deprived subjects showed no ear advantage at all, while the non-deprived subjects showed an expected left ear advantage. The results are discussed within a theoretical framework of a dual process model, where sleep deprivation disrupts the ability to sustain attention, caused by a temporary failure of the right hemisphere's top-down (instruction-driven) processing to override the left hemisphere's bottom-up (stimulus-driven) processing.

Adult↗
PubMedDate not supplied

Sleep deprivation in critical care units.

Sleep deprivation is a significant problem for patients in critical care units. Sleep is a complex, active process that is divided into 4 stages of non-rapid eye movement (NREM) sleep, and rapid eye movement (REM) sleep. Noise, lights, discomfort, pain, medications, and stress all contribute to a patient's inability to sleep. Lack of knowledge about the sleep stages, nursing routines, and frequent nursing assessment and interventions also impact the critically ill patient's ability to sleep. Education about sleep deprivation needs to be integrated into critical care courses and orientation programs. Sleep deprivation should be addressed on the multidisciplinary care plan and in health team conference, and nursing care planned accordingly. Sleep medications and their effects should be evaluated for each patient, as well as identifying medications that might be preventing or disturbing sleep.

Aged↗
PubMed1997

Absence of oxidative stress following paradoxical sleep deprivation in rats.

Paradoxical sleep deprivation was performed on rats using platform technique to investigate the oxidative process associated with it. Levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), total glutathione (GSH) and malondialdehyde production were measured in brain of rats under control conditions (C) and those on single large platforms (SLP), multiple large platforms (MLP), single small platforms (SSP) and multiple small platforms (MSP) groups. SOD, CAT and GPx brain activity and malondialdehyde production were not modified by any of the procedures. Brain GSH, however, was significantly reduced in both SSP and SLP groups. These results suggest that paradoxical sleep deprivation per se is not associated with oxidative damage. The observed alterations could be attributed to factors such as immobilization and social isolation present in the single platform techniques.

Animals↗
PubMed2004

Sleep deprivation for pediatric sedated procedures: not worth the effort.

OBJECTIVE: Sleep deprivation is commonly used to enhance the effectiveness of pediatric sedation and to decrease sedation failures. We reviewed our sedation database to evaluate the efficacy of sleep deprivation. METHODS: The entire pediatric sedation unit database (n = 5640) was reviewed retrospectively. Patients without complete data sets were excluded. The remaining patients were separated into 2 groups: 3272 patients who underwent noninvasive procedures and 1210 who underwent invasive procedures. A subgroup of noninvasive procedure patients <2 years old (n = 1398) was also analyzed. The sedation failure rate (%) and nursing care hours for both sleep-deprived and non-sleep-deprived patients were analyzed. RESULTS: In the noninvasive procedure group, the sedation failure rate was 5.7% for the sleep-deprived patients and 5.6% for the non-sleep-deprived patients, whereas the sedation failure rate for children <2 years old was 4.2% for sleep-deprived patients and 4.7% for non-sleep-deprived patients. The sedation failure rate in the invasive procedure group was 7.5% for sleep-deprived patients and 7.2% for non-sleep-deprived patients. Nursing care hours in the noninvasive procedure group were significantly longer for the sleep-deprived patients (4.5 +/- 1.6 hours) versus the non-sleep-deprived patients (3.8 +/- 1.6 hours). This finding was true also for the subgroup of children <2 years old (sleep-deprived patients: 4.2 +/- 1.4 hours; non-sleep-deprived patients: 3.5 +/- 1.4 hours). No difference was noted in nursing care hours for the invasive procedure group. CONCLUSIONS: Sleep deprivation had no effect in reducing the pediatric sedation failure rate. The patients having noninvasive procedures who were sleep deprived required significantly more nursing care hours than their non-sleep-deprived counterparts. Routine use of sleep deprivation for pediatric sedation should be critically reevaluated.

Adolescent↗
PubMed1997

NGFI-A expression in the rat brain after sleep deprivation.

The effects of total sleep deprivation (SD) on the expression of the immediate-early gene NGFI-A were studied in the rat brain by in situ hybridization. Rats were manually sleep-deprived for 3, 6, 12 and 24 h starting at light onset (08:00 h) and for 12 h starting at dark onset (20:00 h). SD performed during the day induced a marked increase in NGFI-A mRNA levels with respect to sleep controls in many cerebrocortical areas and caudate-putamen, which was most evident after 6 h SD. A decrease was seen in hippocampus and thalamus, particularly after 12 h SD. Rats sleep-deprived for 12 h during the night showed an increase in NGFI-A expression in some cortical areas while rats sleep-deprived for 24 h showed few changes with respect to controls. The pattern of NGFI-A expression after forced wakefulness showed some differences from that observed after spontaneous wakefulness [M. Pompeiano, C. Cirelli and G. Tononi, Immediate early genes in spontaneous wakefulness and sleep: expression of c-fos and NGFI-A mRNA and protein, J. Sleep Res., 3 (1994) 80-96]. These observations are discussed with respect to the functional consequences of wakefulness in specific brain areas.

Animals↗
PubMed1976

Sleep deprivation therapy in depression.

A study of sleep deprivation therapy was made in 62 females and 15 males, aged 20-72, with monopolar (60 patients) and bipolar (17 patients) types of manic-depressive psychosis. Of these patients, 30 had suffered only the current depression, 29 a maximum of five depressions, and 18 more than five depressions before the sleep deprivation therapy. Twenty-five patients had been treated with antidepressant drugs for less than 10 days, 12 patients for 10-24 days, and 36 patients for more than 24 days. Twenty-four patients were treated with one sleep deprivation, 29 patients with one sleep deprivations per week (average 1.59), and 24 patients with two sleep deprivations per week (average 2.5). The effect of the sleep deprivation therapy was evaluated clinically and by means of Cronholm-Ottosson's rating scale. The effect was found good and lasting in 29%, good but temporary in 38%, and poor in 32% of the cases. The best results were achieved with twice-weekly treatments, the poorest results with once-weekly treatment. The results were equal in monopolar and bipolar cases and were independent of the number of previous depressions as well as antidepressant drug treatment. No side effects have been observed, in particular no conversion to mania. The results of the present investigation indicate that depression and sleep disturbances are symptoms produced by a common factor which, however, it as yet unknown. Sleep deprivation therapy is seen to have at least some effect on all cases of endogenous depression. Sleep deprivation therapy has no side effects and is more quick-acting than any other treatment procedure hitherto known. It should therefore be considered the first treatment offer to all endogenously depressed patients in whom immediate ECT is not necessitated.

Adult↗
PubMed1997

The pioneering experimental studies on sleep deprivation.

The experimental studies on sleep deprivation were initiated by the Russian physician and scientist, Marie de Manacéine, who studied sleep-deprived puppies kept in constant activity. She reported in 1894 that the complete absence of sleep was fatal in a few days, pointing out that the most severe lesions occurred in the brain. In 1898, the Italian physiologists Lamberto Daddi and Giulio Tarozzi also kept dogs awake by walking them; the animals died after 9-17 days, and their survival was unrelated to food consumption. In the histological study performed by Daddi, degenerative alterations, mainly represented by chromatolytic changes, were observed in neurons of the spinal ganglia, Purkinje cells of the cerebellum, and neurons of the frontal cortex. Daddi ascribed these changes to a state of autointoxication of the brain during insomnia. In 1898, the psychiatrist Cesare Agostini, interested in the psychic phenomena caused by prolonged insomnia in humans, sleep deprived dogs by keeping them in a metallic cage in order to avoid fatigue. The dogs survived about 2 weeks, and degenerative changes were observed in their brains. In these experimental paradigms, the effect of sleep loss was confounded by motor exhaustion and/or intense sensory stimulation. In spite of the absence of adequate controls, the pioneering studies performed at the end of the 19th century represented the first experimental attempts to relate sleep with neural centers and suggested that sleep is a vital function and that the brain may be affected by insomnia.

Animals↗
PubMed2002

The sleep-deprived electroencephalogram: evidence and practice.

BACKGROUND: Sleep deprivation for the initial electroencephalogram for suspected seizures is a widespread but inconsistent practice not informed by balanced evidence. Daily practice suggests that nonneurologists are confused by the meaning and value of, and indications for, "sleep" (tracing) vs "sleep deprivation" (and other alternatives). They need specific, informed guidance from general neurologists on best practices. OBJECTIVES: To document illustratively the variability of neurologists' practices, the level of relevant information among nonneurologists, and the current state of published evidence; and to stimulate formulation of consensus advisories. DESIGN AND SETTING: I surveyed knowledge and practices of (1) nonneurologists in a community teaching hospital; (2) local and national neurologists and epileptologists; (3) electroencephalogram laboratory protocols; and (4) textbook accounts and recommendations and the relevant journal literature. National professional organizations were contacted for advisories or guidelines. RESULTS: Most nonneurologists surveyed misunderstood "sleep" vs "sleep-deprived" electroencephalograms and their actual protocols. They are unaware of evidence on benefits vs burdens. Neurologists' practices are inconsistent. Experts generally agree that sleep deprivation produces substantial activation of interictal epileptiform discharges beyond the activation of sleep per se. However, most published recommendations and interviewed epileptologists do not suggest sleep deprivation for the initial electroencephalogram because of "inconvenience" (burdens) for the patient. Evidence-based or reasoned guidance is minimal, and professional societies have not issued advisories. CONCLUSION: Confusion over sleep deprivation, disparities between evidence and recommendations, and inconsistent practices create a need for expert consensus for guidance, as well as comparative research on alternative methods of increasing diagnostic yield.

Electroencephalography↗
PubMed1966

Sleep deprivation in the rat.

Sleep deprivation, induced by injections of dextroamphetamine or by forced treadmill activity, resulted in a temporary increase in daily sleep time. However, increasing the period of sleep deprivation above 24 hours to 72 or 120 hours did not result in increased recovery sleep above that present in the 24-hour group.

Animals↗
PubMed1995

REM sleep deprivation induces galanin gene expression in the rat brain.

Rats were deprived of REM sleep for 24 h by keeping them on small platforms that were placed in a water bath (the platform method). Galanin coding mRNA was visualized using in situ hybridization, and cells expressing galanin mRNA were counted. In REM sleep-deprived animals the cell count was higher in the preoptic area and periventricular nucleus. Lesions of this area have been reported to induce wakefulness in cats and rats. Galanin administered into the lateral ventricle had no effect on sleep. We conclude that REM sleep deprivation can induce galanin gene expression in some brain areas, but galanin alone does not modify spontaneous sleep.

Animals↗
PubMed2004

Sleep deprivation induced by the modified multiple platform technique: quantification of sleep loss and recovery.

Vigilance status was continually monitored in socially stable groups of rats exposed to the modified multiple platform (MMP) technique for sleep deprivation. For comparison, sleep parameters were also monitored in socially isolated rats deprived of sleep by the single platform (SP) method. In all cases, sleep was continuously recorded during baseline, during 96 h of sleep deprivation and during 4 days of recovery. Both multiple- and single-platform techniques completely abolished paradoxical sleep (PS) during the deprivation period, but also resulted in significant decreases in slow wave sleep (SWS) (-31% and -37%, respectively). Unexpectedly, animals on large platforms, which are normally intended as controls, also showed significant reductions in PS and SWS, and these effects were more pronounced in rats deprived in groups than in animals deprived in isolation. Another control preparation, rats placed on wire-mesh grids in the deprivation tank, also showed PS reduction (-39%) but no loss of SWS during the 4 test days. Paradoxical sleep rebound was observed in the first 24 h in all groups, except for grid controls. Overall, no significant differences were found between single- and multiple-platform procedures during the 4 days of deprivation. However, sleep rebound was more pronounced in MMP-deprived rats than in SP-deprived rats. Sleep loss in both control groups may reflect residual effect of stress that remain in the platform technique. These findings indicate that the MMP technique is effective in inducing PS deprivation (PSD). However, the fact that SWS is also affected may have implications for conclusions on paradoxical sleep function based upon paradoxical sleep deprivation.

Animals↗
PubMed1998

Sleep deprivation and its effect on an index of cardiac parasympathetic activity in early nonREM sleep in normal and epileptic subjects.

The effect of 24-hour sleep deprivation on cardiac vagal tone during the first 90 minutes of sleep was studied in 16 subjects using a new real-time index of cardiac parasympathetic activity. The level of cardiac vagal tone in subjects who were sleep deprived was more than doubled that in non-sleep-deprived subjects during sleep stage 0 immediately prior to the onset of sleep stage 1. The mean cardiac vagal tone fell significantly (p < 0.01), from a high level of 19.2 arbitrary units of a linear vagal scale (LVS) to 10 units on reaching slow-wave sleep stage 4 in sleep-deprived epileptic subjects, There was a similar fall in cardiac vagal tone from 18.7 units to 12 units in the LVS in sleep-deprived normal subjects, but this was not statistically significant. There was no change in the mean vagal tone of non-sleep-deprived normal subjects. We propose that the cardiac vagal tone can be used as an objective index of sleep propensity.

Adult↗
PubMed1989

Effects of repeated sleep deprivation in the dark- or light-period on sleep in rats.

This study was designed to examine the differences between sleep duration and EEG when sleep was restricted to the rest- or activity-phase for 5 successive days, achieved by repeated sleep deprivation in the dark (DSD) or light-period (LSD). In the DSD-experiment the percentages of the vigilance states were comparable to the level of the baseline light period. In LSD, the amounts of all sleep states increased substantially relative to baseline dark. The sleep episodes were lengthened in DSD and LSD. The duration of NREM-sleep and the sleep episodes remained longer in the light than in the dark, indicating circadian influences. In the first hours after sleep deprivation the delta activity during NREM-sleep was enhanced in LSD and to a lesser extent in DSD. This effect diminished over the consecutive days in both experiments. The EEG energy gained during sleep and its accumulation pattern on each day in DSD and LSD were strikingly similar, thereby reflecting a homeostatic process. After the sleep deprivation days, small changes were observed in the distribution of the vigilance states, the delta activity and EEG energy over the light- and dark-period.

Animals↗
PubMed1985

Evaluation of the effects of antiepileptic drugs on sleep-wakefulness patterns following 1 night total sleep deprivation in epileptic patients.

Sleep-wakefulness patterns recorded following 1 night total sleep deprivation were studied in 15 normal subjects and in 252 epileptic patients. The patients were taking various types and combinations of antiepileptic medication. Sleep deprivation caused a reduction in sleep latency and an increase in NREM stage 3 + 4 sleep. This effect persisted in patients treated with valproate sodium and/or carbamazepine. In patients treated with diphenylhydantoin light NREM 1 + 2 sleep increased. In those treated with antiepileptics + chlorazepate, both an increase in NREM 1 + 2 and NREM 3 + 4 sleep was seen. The former probably reflects a benzodiazepine effect, the latter is due to a sleep deprivation effect. In patients treated with antiepileptics + clonazepam, a benzodiazepine effect predominated.

Adolescent↗