[Psychological changes and cerebrospinal catabolites of monoamines after total sleep deprivation and after selective REM sleep deprivation].
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Effects of sleep deprivation on sleepiness, sleep intensity, and subsequent sleep in the rat.
The effects of 24 hr of sleep deprivation on cortical EEG and ventral hippocampus EEG recordings, ventral hippocampus spike rates, sleep stages percentages, and bout length measures were studied in rats. Two groups, differing only in the rate and distance they were forced to walk during deprivation by the water wheel method, were recorded continuously (23 hr per day) for one baseline, one deprivation, and two recovery days. During deprivation, microsleeps, increased hippocampal spike rates, and increased amplitude of the EEG recordings all suggested the intrusion of sleep processes. Nonetheless, there was no evidence to support the idea that these animals were not substantially deprived of sleep. No important differences were found in the recovery data of the two groups, even though one group walked three times as far as the other during deprivation. This supports the idea that, in conjunction with large amounts of sleep deprivation, changes in exercise and energy depletion may have little effect on sleep measures. During recovery, increased hippocampal spike rates and bout lengths, as well as increases in EEG amplitude, were interpreted in terms of increased sleep "intensity." High amplitude NREM sleep rebounded first, followed by rebounds in both paradoxical sleep and low amplitude NREM sleep. This pattern was compared to patterns previously reported for humans, cats, and rats. Finally, the tendency for some measures to fall below their baseline levels after an initial rebound was discussed in terms of "sleep inhibition" and servomechanism theory.
Animals↗
The diagnostic value of the short sleep EEG and other provocative methods following sleep deprivation.
One hundred and eighty-five EEGs recorded after deprivation of sleep for 24 h were evaluated. Valuable diagnostic information was found in 59% of the EEG recordings; 24% of the EEGs contained seizure activity. The duration of the stages of sleep and the frequency of seizure activity, paroxysmal sharp wave groups and localizing findings were analyzed. The sleep stages A to C (based on the Loomis scale) were reached for about equal duration by an EEG recording of 30--40 min; sleep stage D was reached only shortly and stage E was not observed. Pathological EEG findings appeared for the most part in the sleep stages A and B. Localized findings were pronounced in stage C. No significant differences pertaining to the occurrence and form of EEG patterns were found between patient groups with primary generalized seizures, psychomotor seizures or those with unclarified disturbances of consciousness. The combination of the short sleep EEG following 24 h of sleep deprivation with subsequent use of the additional provocative methods of hyperventilation, photostimulation and hydration, yielded, in all, new information in 50% of the patients. Each of these additional methods contributed nearly equally to this information.
Adult↗
Homovanillic acid and 5-hydroxyindoleacetic acid in lumbar cerebrospinal fluid after total and REM sleep deprivation in humans.
Lumbar CSF HVA and 5-HIAA levels were assayed in 3 groups each of 10 subjects, which were respectively deprived of sleep for 30 h, deprived of REM sleep and disturbed with several awakenings during SW sleep for two consecutive nights. HVA levels after total sleep (39 +/- 20 ng/ml) or REM (35 +/- 11 ng/ml) deprivation as well as after SW sleep awakenings (32 +/- 26 ng/ml) were not different from controls (42 +/- 14 ng/ml). 5-HIAA levels after REM deprivation (32 +/- 15 ng/ml) appeared increased when compared with controls (21 +/- 7 ng/ml), total sleep-deprived subjects (21 +/- 10 ng/ml) or subjects with SW sleep awakenings (27 +/- 13 ng/ml). Possible increase in 5-HT turnover after REM deprivation and possible 5-HT role in REM sleep regulation in humans are discussed.
Adult↗
[Y-maze learning in two strains of mice. Effects of instrumental and pharmacologic sleep deprivation].
Effects of instrumental and pharmacological deprivation of sleep on Y-maze learning have been studied in two inbred strains of mice (C57BR/cd/Orl and C57BL/6/Orl), having identical sleep rhythms, but mainly differing in their ability to learn. Administration of alpha-methyl-DOPA (100 mg/kg) provokes complete suppression of paradoxical sleep (PS) for 9-11 h. Injection immediately after each training session over the first 5 days caused a delay in acquisition of an active avoidance task in C57BR mice. Treated C57BL/6 mice exhibited a significant facilitation of acquisition. Similar results were obtained by instrumental deprivation of sleep for 10 h.
Animals↗
Recovery sleep following different visual conditions during total sleep deprivation in man.
The findings of visual impairment during total sleep deprivation were used as a basis for a possible link between vision and sleep. It was proposed that the level of visual load imposed during sleep deprivation was an important variable, and would have a substantial effect upon recovery sleep. Six young male subjects underwent two conditions of 64 h of sleep deprivation on separate occasions. One condition incorporated a high visual load, and the other a low load. Exercise and sound were balanced. All night sleep EEGs were taken for two baseline nights, and also for two recovery nights following each condition. There was a significant increase of stage 4 on all recovery nights and a REM rebound on the second recovery night. SWS, particularly stage 4, TST and REM density, were significantly greater following the high load. Implications of these findings for sleep theories and for sleep deprivation research are discussed.
Adult↗
Potentiation of ketamine effects on the spiking activity in the lateral geniculate nucleus by rapid eye movement (REM) sleep deprivation.
In cats prepared for chronic recording of sleep, an investigation was made on the effects of an anaesthetic agent, ketamine [cl-581, 2-(O-chlorophenyl)-2-methylaminocyclohexamine HCl] and rapid eye movement (REM) sleep deprivation on spiking activity recorded from lateral geniculate (LGN) nucleus. In normal cats most of the LGN spikes occurring during sleep are found in REM sleep. Follwoing injection of 10 mg/kg of ketamine a substantial increase of slow wave sleep (SWS) spikes occurred. While selective REM sleep deprivation had the same effects, combined influences of ketamine and REM-sleep deprivation led to a marked potentiation of their individual effects probably by simultaneous stimulation of the neurone system which determines the endogenous electrical activity of LGN cells.
Action Potentials↗
A review of REM sleep deprivation.
Studies on the behavioral consequences of rapid eye movement (REM) sleep deprivation in animals and humans are critically reviewed. In animals, converging evidence--some reasonably well controlled--indicates that REM sleep deprivation probably heightens central neural excitability and increased motivational behavior, but has nuclear or inconclusive effects on learning. In humans, evidence indicates that REM sleep deprivation is not dream deprivation and is not harmful to schizophrenic, depressed, or healthy subjects. Controversy continues about whether or not (some) schizophrenic patients respond abnormally to REM sleep deprivation by having no REM rebound. Controlled but unconfirmed work indicates that that endogenous, but not reactive, depressive patients are improved by REM sleep deprivation, a finding consistent with the animal behavioral consequences of the procedure and with the unique REM-depriving properties of efficacious antidepressant drugs.
Adjustment Disorders↗
An attempt to influence by drugs recovery sleep after sleep deprivation.
Rats were deprived of sleep by placing them for 36 hours in a slowly moving drum. After this procedure, during recovery sleep, the latency of onset of the first rhombencephalic - paradoxical sleep period decreased and the proportion of telencephalic/rhombencephalic - slow wave sleep reversed (during the first hour of recovery sleep). Repeated administration during the deprivation period of physostigmine (0,5 mg/kg i. p. in 30 min intervals 20-30 times) inducing in waking animals in EEG pattern close to that of rhombencephalic sleep, or atropine (1 mg/kg i. p. in 60 min intervals 10-15 times) evoking an activity resembling telencephalic sleep, did not change the above measures of recovery sleep. Pharmacologically induced sleep-like patterns did not substitute for the sleep the rats were deprived off.
Animals↗
Lymphocyte and granulocyte reactions during sleep deprivation.
The possible influence of 48 hr of sleep deprivation on in vitro DNA synthesis of blood lymphocytes and on the adhesiveness and intracellular, stainable activity of alkaline phosphatase in blood granulocytes was studied in twelve young male volunteers. Following the sleep deprivation, all 12 subjects showed marked reductions of DNA synthesis after stimulation with phytohemagglutinin. Pre-exposure levels were regained 5 days after terminating the vigil. No changes were noted in granulocyte adherence or alkaline phosphatase activity. The results suggest that sleep deprivation may decrease cell-mediated immune reactions and thereby impair some aspects of host defense.
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Rapid eye movement (rem) sleep deprivation: effect on acid mucopolysaccharides in rat brain.
The effect of rapid eye movement (REM) sleep deprivation on the total content and proportion of different mucopolysaccharides (AMPS) containing uronic acid in rat brain was studied. REM sleep deprivation was induced by the water tank methods. Five experimental groups of animals were used: control, stressed, REM sleep deprived, post-stress sleeping and post-deprivation sleeping rats. No changes of AMPS were observed in any of the experimental groups when the whole brain was analysed. A significant increase of AMPS was found in the cerebral hemispheres of stressed and REM deprived rats. A significant decrease of AMPS was observed in the cerebellum and brain stem. A further increase of AMPS was found in the cerebral hemispheres after the rebound of REM sleep following its deprivation, and after the recovery sleep following the stress. A significant increase of AMPS was found in the brain stem of rats allowed to recuperate after REM deprivation or stress as compared with the stressed and REM deprived animals. Recovery sleep induced a significant increase of AMPS in the cerebellum in previously stressed rats, while previously REM deprived rats exhibited a further decrease of AMPS from control values. The possible functional meaning of these results is discussed in relation to the role of REM sleep in protein synthesis and learning and memory processes. Intriguing, well-controlled positive findings and the fact that no experimental design is known where stress is minimal while REM deprivation is 100 per cent, justify and encourage continued efforts in studying the biochemical state of the brain during sleep and/or its alterations.
Adrenal Glands↗
Enzyme activity in sleep and sleep deprivation.
Liver tyrosine transaminase activity is low during the day when the rats are mostly asleep and high during the night when they are awake. When wakefulness was imposed for 8 hr during daylight on the day of the experiment and the rats were allowed to sleep for the following 3 hr during darkness, the tyrosine transaminase activity became high during the day and low at night. That this reversal in enzyme activity is not mediated by the pituitary-adrenal axis is demonstrated by the fact that in adrenalectomized rats tyrosine transaminase activity increased during the day in the sleep deprived rats. However, in these rats the enzyme activity did not become low in the sleep-deprived-sleeping condition. Changes in tryptophan pyrrolase activity during sleep deprivation were demonstrated to be mediated by the pituitary-adrenal axis.
Adrenal Glands↗
Thyroid and adrenomedullary reactions during sleep deprivation.
The possible influence of a 48 h period of sleep deprivation on the serum concentrations of total and unbound 3,5,3',5'-thyroxine (T4) and 3,5,3'-triiodothyronine (T3), and of total 3,3',5'-triiodothyronine (reverse T3, rT3) was studied in 12 young male volunteers. In addition, plasma concentrations of TSH and the urinary excretion of noradrenaline and adrenaline were examined. Both total S-T4, S-T3 and S-rT3, and unbound S-T4 and S-T3 (unbound rT3 was not calculated) were significantly enhanced following sleep deprivation. P-TSH showed a numerical but statistically not significant increase, while the catecholamines remained unaltered. The results suggest that sleep deprivation provokes enhanced secretion of thyroid hormone(s), supposedly via increased secretion of TSH.
Adrenal Medulla↗
Clinical Performance in Critical Care Simulation under Sleep Deprivation: Effects of Power Napping in the Recovery Napping Protocol for Anesthesiologist Performance (R-NAP) Randomized Controlled Trial.
BACKGROUND: Sleep deprivation is common among anesthesia residents and impairs both technical and nontechnical skills such as leadership. Napping is recommended in fatigue management across healthcare and other safety-sensitive sectors, yet its effectiveness for healthcare providers remains underexplored. This study evaluated whether a 30-min nap opportunity improved simulated crisis performance after a 24-h shift. METHODS: Residents were tested twice: once rested and once using a 24-h shift to induce partial sleep deprivation. Between sessions, they were trained in fatigue management. In the sleep-deprived condition, they were randomized to a nap opportunity or a control condition. Actigraphy objectively assessed sleep and nap duration. The primary endpoint was overall simulated clinical performance (0 to 200; combined technical and nontechnical scores). Secondary endpoints were technical and nontechnical subscales. Group effects were primarily tested using intention-to-treat regression models adjusted for rested performance, previous sleep, and critical care experience. RESULTS: Thirty-five residents were enrolled (nap opportunity, n = 19; control, n = 16). In the primary analysis sample (n = 27), clinical performance was 14.8 points higher after the nap opportunity compared with controls (95% CI, 2.8 to 26.9; P = 0.018), corresponding to a 7.4% improvement. Technical skills did not differ significantly between groups, although more sleep was associated with better technical performance. Nontechnical skills were higher in the nap opportunity condition (+11.0 points; 95% CI, 2.2 to 19.8; P = 0.016), including significant effects of leadership and resource utilization. Exploratory analyses suggested associations between longer nap duration and multiple performance domains, strongest for technical skills ( P = 0.010). CONCLUSIONS: Napping appears to enhance clinical performance, while the nap opportunity, nap duration, and previous sleep deprivation each influenced technical and nontechnical performance in distinct ways. These findings support integrating napping and recovery into medical education and scheduling.
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[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↗
Electrophysiological changes induced by paradoxical sleep deprivation and lithium chloride poisoning in rats.
In an attempt to analyze the disruption of conditioned taste aversion (CTA) caused by pre-acquisition paradoxical sleep deprivation (PSD), the effect of poisoning (0.15 M LiCl, 4% body weight) on the sleep--wakefulness pattern was studied in 12 rats with chronically implanted electrodes. The polygraphic recording showed that poisoning reduced the total sleep time in the subsequent 3 h from 57 to 42% and REM sleep from 6 to 2%. The lithium chloride effect was still more pronounced after 24-h REM sleep deprivation: the total sleep time decreased from 67 to 46% and REM sleep from 13 to 2%. The change of sleep--wakefulness pattern, most pronounced during the first hour of poisoning, gradually returned to normal but REM sleep was significantly reduced even 3 h after poisoning. It is concluded that 24-h PSD does not alleviate the subsequent poisoning. On the other hand, the lithium chloride induced reduction of post-acquisition REM sleep many enhance the learning impairment caused by pre-acquisition PSD.
Activity Cycles↗
[The value of EEG after sleep deprivation (author's transl)].
Seventy seven adult epileptics and 30 patients with clinically non epileptic seizures were subject to a 24 hours sleep deprivation. The waking records of these patients were normal or unspecific abnormal. After sleep deprivation 29 (37%) of epileptics had abnormal EEG with epileptiform or focal activity, more often in cases with frequent (26 (60%) patients out of 43) epileptic seizures. Patients with sporadic attacks only exceptionally showed specific EEG changes (3 patients (8,8%) out of 34). Drug induced sleep emerged to be diagnostically less helpful. Twenty nine out of 30 patients with clinical nonepileptic seizures had no additional abnormalities in the EEG after sleep deprivation.
Adolescent↗
Sleep deprivation deficits and their reversal by d- and l-amphetamine.
Vigilance performance, waking EEG patterns and mood were studied before and after one night of sleep deprivation in normal males. The effects of d-amphetamine 10 mg, l-amphetamine 10 mg and placebo on these measures were compared. Changes were found in all three measures after one night of sleep-deprivation. d-Amphetamine was more powerful than l-amphetamine in reversing sleep deprivation effects on vigilance and on waking EEG.
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