[Psychological changes and cerebrospinal catabolites of monoamines after total sleep deprivation and after selective REM sleep deprivation].
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Results for “SLEEP DEPRIVATION”
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Platelet serotonin and interleukin-1 beta after sleep deprivation and recovery sleep in humans.
Sleep deprivation (SD) represents a well-established therapy for major depression. Recent findings suggest that the antidepressive effects of sleep deprivation are mediated at least in part by pro-serotoninergic mechanisms. Furthermore, SD has been demonstrated to modify different host defense activities. We therefore investigated the serotonin (5-HT) content in platelets, platelet density distribution and 5-HT-induced IL-1 beta release from platelets in 10 healthy men before and after total SD (TSD) as well as after recovery sleep. Blood samples were drawn on 3 consecutive days at 7.00 h, 13.00 h, and 19.00 h, respectively. In addition, the psychophysiological parameters tiredness and wakefulness were assessed. After TSD the normal daily variation of IL-1 beta release with high morning levels and low evening levels was found to be significantly inverted. The release of IL-1 beta corresponded positively to the subjectively experienced tiredness of the probands. Analysis of platelet density distribution indicated a significant daily variation of low density platelets with low levels in the morning and high levels in the evening, which was absent after TSD. Our findings favour an increased pro-serotoninergic effect after TSD, which comprises respective variations of the host defense system, but is abolished by consecutive recovery sleep.
Adult↗
Systemic bacterial invasion induced by sleep deprivation.
Profound sleep disruption in humans is generally believed to cause health impairments. Through comparative research, specific physical effects and underlying mechanisms altered by sleep deprivation are being elucidated. Studies of sleep-deprived animals previously have shown a progressive, chronic negative energy balance and gradual deterioration of health, which culminate in fatal bloodstream infection without an infectious focus. The present study investigated the conditions antecedent to advanced morbidity in sleep-deprived rats by determining the time course and distribution of live microorganisms in body tissues that are normally sterile. The tissues cultured for microbial growth included the blood, four major organs, six regional lymph nodes, the intestine, and the skin. The principal finding was early infection of the mesenteric lymph nodes by bacteria presumably translocated from the intestine and bacterial migration to and transient infection of extraintestinal sites. Presence of pathogenic microorganisms and their toxins in tissues constitutes a septic burden and chronic antigenic challenge for the host. Bacterial translocation and pathogenic sequelae provide mechanisms by which sleep deprivation appears to adversely affect health.
Animals↗
Sleep deprivation worsens obstructive sleep apnea. Comparison between diurnal and nocturnal polysomnography.
Daytime polysomnography (DPG) has been suggested for diagnosis of obstructive sleep apnea syndrome (OSAS), because it is less expensive than whole-night polysomnography investigation (NPG). To ensure sleep during day recordings, patients are often instructed to stay awake the night preceding DPG. This procedure has been validated against NPG, and also against apnea mattress recordings combined with ear oximetry (AMO). Twenty patients with OSAS symptoms were examined with NPG and simultaneous AMO and 2 to 3 weeks later with DPG 3 to 4 h in the morning after 1 nights sleep deprivation. Median apnea-hypopnea index (AHI) of DPG was 37 (95% confidence interval [CI], 19 to 44), significantly higher than median AHI of NPG (14; 95% CI, 12 to 27), whereas median nocturnal oxygen desaturation index (ODI) (11; 95% CI, 9 to 25) did not differ significantly from median AHI of NPG. Sensitivity values for DPG increased from 81 to 100% when the criteria AHI greater than 5, greater than 10, greater than 15, and greater than 20 were used, respectively. Specificity values also increased with the AHI used as cutoff point, from 50% (AHI>5) to 75% (AHI>20). In AMO, there were one false-negative case and four nonclassifiable borderline cases. If these types of simplified tests for OSAS are used for diagnosis, the risk of both false-negative and positive results (DPG) or nonclassifiable borderline cases (AMO) must be considered. Since there was a significant increase in AHI in DPG after sleep deprivation in comparison to conventional NPG, the former procedure should not be used for staging of the disease. These results also stress the importance of advice to OSAS patients concerning regular sleeping habits.
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Sleep deprivation in prion protein deficient mice sleep deprivation in prion protein deficient mice and control mice: genotype dependent regional rebound.
We have previously reported a larger and more prolonged increase of slow wave activity (SWA) in NREM sleep after sleep deprivation (SD) in prion protein deficient mice (PrP) compared to wild-type mice. Regional differences in the SWA increase were investigated by comparing the effect of 6 h SD on a frontal and occipital derivation in PrP deficient mice and wild-type mice. The larger increase of SWA after SD in PrP deficient mice was restricted to the occipital derivation. The difference appeared after the waking-NREM sleep transitions, making it unlikely that PrP is involved in the mechanisms enabling the transition to sleep. Our findings may reflect differences between the genotypes in the need for recovery in this particular brain region.
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Comparison of the effects of sleep deprivation, alcohol and obstructive sleep apnoea (OSA) on simulated steering performance.
Patients with obstructive sleep apnoea (OSA) are reported to have an increased risk of road traffic accidents. This study examines the nature of the impairment during simulated steering in patients with OSA, compared to normal subjects following either sleep deprivation or alcohol ingestion. Twenty-six patients with OSA and 12 normal subjects, either deprived of one night's sleep or following alcohol ingestion [mean (SD) alcohol blood level 71.6 mg dl(-1) (19.6)], performed a simulated steering task for a total of 90 min. Performance was measured using the tendency to wander (SD), deterioration across the task, number of 'off-road' events and the reaction time to peripheral events. Control data for OSA, sleep deprivation and alcohol were obtained following treatment with nasal continuous positive airway pressure (nCPAP), after a normal night of sleep, and following no alcohol, respectively. Patients with untreated OSA, and sleep-deprived or alcohol-intoxicated normal subjects performed significantly less well, compared to their respective controls (P<0.01 for all tests), with untreated OSA lying between that of alcohol intoxication and sleep deprivation. Alcohol impaired steering error equally throughout the whole drive, whilst sleep deprivation caused progressive deterioration through the drive, but not initially. Untreated OSA was more like sleep deprivation than alcohol, although there was a wide spread of data. This suggests that the driving impairment in patients with OSA is more compatible with sleep deprivation or fragmentation as the cause, rather than abnormal cognitive or motor skills.
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The relationship between tiredness prior to sleep deprivation and the antidepressant response to sleep deprivation in depression.
Recently it was hypothesized that the antidepressant response to total sleep deprivation (SD) results from a disinhibition process induced by the increase of tiredness in the course of SD. In the present study, the role of tiredness in the antidepressant response to SD is further investigated. Seventy-two depressed patients scored subjective tiredness and depressed mood three times daily (in the morning, afternoon, and evening) on the days preceding and following SD. It was found that averaged tiredness on the day prior to SD was related to the SD response, when the severity of depression prior to SD had been held statistically constant. Also, when both severity of depression and diurnal variation of mood prior to SD were partialed out, tiredness showed a positive correlation with the SD response: patients who reported a relatively low degree of tiredness on the day preceding SD improved by SD. This result suggests that tiredness has an influence on SD effects, and that this influence is independent from that of the severity of depression. The findings are in accordance with current ideas on the role of tiredness as a mediating factor in the induction of the therapeutic effects of SD.
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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.
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The clinical response to total sleep deprivation and recovery sleep in geriatric depression: potential indicators of antidepressant treatment outcome.
The clinical response to antidepressant treatment in late-life depression is often delayed and highly variable. Better indicators of antidepressant efficacy are needed early in the course of treatment, so that augmentation strategies or alternative treatments may be initiated. The goal of this study was to evaluate whether the change in the Hamilton depression rating scale (HDRS) after 36 h of total sleep deprivation (TSD) and recovery sleep predicted clinical outcome after 12 weeks of antidepressant treatment, and whether greater predictive value was observed in certain aspects of depressive symptomology. Fifteen elderly patients diagnosed with major depression underwent combined treatment with an initial 36 hours of TSD and a 12-week trial with the antidepressant paroxetine. Six HDRS subscores were evaluated with respect to how the changes after TSD and after one night of recovery sleep correlated with HDRS scores after 12 weeks of treatment. A significant correlation was obtained between the change in the core depressive symptomology subscale from baseline to recovery sleep and the HDRS score at 12 weeks, but the correlation was not significant when evaluating the change from baseline to TSD. These results indicate that the decrease in symptoms after recovery sleep compared with baseline levels (indicating the persistence of the antidepressant response), rather than the symptom reduction after TSD, has greater predictive value with respect to treatment outcome.
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Sleep deprivation combined with consecutive sleep phase advance as a fast-acting therapy in depression: an open pilot trial in medicated and unmedicated patients.
OBJECTIVE: The authors' goal was to test the hypothesis that the antidepressant effect of total sleep deprivation can be maintained by initially avoiding sleep during a supposedly "critical" time period in the early morning. METHOD: They studied 33 inpatients with major depression, melancholic type, all of whom responded positively to total sleep deprivation. Twelve of the patients were men and 21 were women; their mean age was 46.7 years (SD = 13.7). After total sleep deprivation, the patients started a sleep schedule from 5:00 p.m. to 12:00 midnight, which then was shifted back by 1 hour each day until a sleep time of 11:00 p.m. to 6:00 a.m. was reached. RESULTS: Twenty (61%) of the 33 patients who responded to total sleep deprivation with an improved state of mood maintained this improvement during sleep phase advance therapy. Drug-free and medicated patients did not differ from each other. CONCLUSIONS: The rapid amelioration of mood observed with total sleep deprivation can be preserved with a succeeding phase shift of the sleep period.
Antidepressive Agents↗
Impact of sleep deprivation and subsequent recovery sleep on cortisol in unmedicated depressed patients.
OBJECTIVE: One night of sleep deprivation induces a transient improvement in about 60% of depressed patients. Since depression is associated with abnormalities of the hypothalamic-pituitary-adrenal (HPA) axis, the authors measured cortisol secretion before, during, and after therapeutic sleep deprivation for 1 night. METHOD: Fifteen unmedicated depressed inpatients participated in a combined polysomnographic and endocrine study. Blood was sampled at 30-minute intervals during 3 consecutive nights before, during, and after sleep deprivation. Saliva samples were collected at 30-minute intervals during the daytime before and after the sleep deprivation night. RESULTS: During the night of sleep deprivation, cortisol levels were significantly higher than at baseline. During the daytime, cortisol levels during the first half of the day were higher than at baseline in the patients who responded to sleep deprivation but not in the nonresponders. During recovery sleep, cortisol secretion returned to baseline values. CONCLUSIONS: This study demonstrated a significant stimulatory effect of 1 night of sleep deprivation on the HPA axis in unmedicated depressed patients. The results suggest that the short-term effects of antidepressant treatments on the HPA axis may differ from their long-term effects. A higher cortisol level after sleep deprivation might transiently improve negative feedback to the hypothalamus or interact with other neurotransmitter systems, thus mediating or contributing to the clinical response. The fast return to baseline values coincides with the short clinical effect.
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[Sleep deprivation: temporal aspects of partial sleep deprivation in the treatment of depression].
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Sleep deprivation in the rat: XIII. The effect of hypothyroidism on sleep deprivation symptoms.
Previous studies of rats subjected to total sleep deprivation by the disk-over-water method had shown a large increase in energy expenditure (EE) and an initial increase followed by a later decrease in body temperature (Tb). It had been proposed that the increase in Tb resulted from regulation toward a higher temperature or setpoint, that the later decline in Tb resulted from excessive heat loss, and that the increase in EE supported both of these thermoregulatory changes. To evaluate this proposed role of the increase in EE, we examined whether blunting the EE rise in sleep-deprived rats by making them hypothyroid attenuated and/or shortened the initial increase in Tb and accelerated the later decline in Tb. Rats made hypothyroid by propylthiouracil administration (TxD rats) were totally sleep deprived and compared to hypothyroid yoked control (TxC) rats and to previously studied, untreated, totally sleep-deprived (TSD) rats. Neither TxD nor TxC rats showed large increases in EE like those of TSD rats. TxD rats did not initially increase Tb, as TSD rats had. Presumably, TSD rats had been able to support an initially elevated Tb, in spite of excessive heat loss, by large increases in EE, although even these increases were eventually insufficient. TxD rats showed much earlier and greater declines in Tb than TxC and TSD rats, eventually becoming severely hypothermic. These results support the interpretation that the large increase in EE previously seen in TSD rats had been compensatory for deprivation-induced thermoregulatory deficits. TxD rats survived an average of 17.1 days, which was not significantly different from survival time in TSD rats. However, there were differences in mortal processes between the two groups. TxD rats died or were sacrificed after chronic, severe hypothermia without observable signs of other morbid pathology. TSD rats had not shown similarly low Tb until just prior to death, but had shown signs of severe pathology, including severely debilitated appearance, disheveled fur, and severe lesions on their tails and on the plantar surfaces of their paws. These signs were diminished or absent in TxD rats, possibly due to blunted EE, lower Tb, or other effects of hypothyroidism. Because the skin changes seen in TSD rats were minimal in TxD rats, they could not have been responsible for the excessive heat loss.
Adipose Tissue, Brown↗
Vasoactive intestinal polypeptide (VIP) and cerebrospinal fluid (CSF) of sleep-deprived cats restores REM sleep in insomniac recipients.
In the past few years a steadily increasing number of substances have been suggested to qualify as sleep-inducing factors. Most 'sleep factors' appear to exert their effects on slow-wave sleep. Recently, however, it has been shown that the cerebrospinal fluid (CSF) of sleep-deprived cats may contain a rapid eye movement (REM) sleep factor, and that vasoactive intestinal peptide (VIP) may be a specific REM sleep inducer. The purpose of this study is to determine whether the CSF of sleep-deprived cats and VIP can reverse insomnia produced by parachlorophenylalanine (PCPA). Donor cats were sleep-deprived for 24 h and their CSF extracted. Some donor cats were additionally pre-treated with chloramphenicol, and some extracted CSF was heated. Recipient cats were injected with 400 mg/kg i.p. of PCPA on two consecutive days. Twenty-four h after the second injection, the recipient cats were intraventricularly injected with a 100-microliters of the various CSF types or 200 ng of VIP. The results showed that only CSF from sleep-deprived cats and VIP were capable of restoring REM sleep in the otherwise PCPA insomniac cats. Since the return of REM sleep was through an increase in its frequency, it is suggested that the CSF of sleep-deprived cats contains a VIP-like sleep factor possibly involved in triggering REM sleep.
Animals↗
Region-specific changes in immediate early gene expression in response to sleep deprivation and recovery sleep in the mouse brain.
Previous studies have documented changes in expression of the immediate early gene (IEG) c-fos and Fos protein in the brain between sleep and wakefulness. Such expression differences implicate changes in transcriptional regulation across behavioral states and suggest that other transcription factors may also be affected. In the current study, we examined the expression of seven fos/jun family member mRNAs (c-fos, fosB, fos related antigen (fra)1, fra-2, junB, c-jun, and junD) and three other IEG mRNAs (egr-1, egr-3, and nur77) in mouse brain following short-term (6 h) sleep deprivation (SD) and 4 h recovery sleep (RS) after SD. Gene expression was quantified in seven brain regions by real-time reverse transcription-polymerase chain reaction (RT-PCR). Multivariate analysis of variance revealed statistically significant variation in cerebral cortex, basal forebrain, thalamus and cerebellum. Levels of c-fos and fosB mRNA were elevated during SD in all four of these brain regions. In the cerebral cortex, junB mRNA was also elevated during SD whereas, in the basal forebrain, fra-1 and fra-2 mRNA levels increased in this condition. During RS, the only IEG mRNA to undergo significant increase was fra-2 in the cortex. C-jun and junD mRNAs were invariant across experimental conditions. These results indicate that the expression of fos/jun family members is diverse during SD. Among other IEGs, nur77 mRNA expression across conditions was similar to c-fos and fosB, egr-1 mRNA was elevated during SD in the cortex and basal forebrain, and egr-3 mRNA was elevated in the cortex during both SD and RS. The similarity of fosB and nur77 expression to c-fos expression indicates that these genes might also be useful markers of functional activity. Along with our previous results, the increased levels of fra-2 and egr-3 mRNAs during RS reported here suggest that increased mRNA expression during sleep is rare and may be anatomically restricted.
Analysis of Variance↗
Changes in postural control during a 48-hr. sleep deprivation period.
Sleep deprivation has detrimental effects on cognitive abilities; however, there has been limited investigation into the effects of sleep deprivation on postural control or influence of time of day on postural control measures. Therefore, we measured postural control on a force plate every 6 hr. in 24 subjects (11 women, 13 men; M age 20 +/- 2.1 yr.; M height 1.68+/-0.29 m; body mass 63.3 +/- 28.7 kg) participating in a 48-hr. dance marathon. During the first 24-hr. period, postural control significantly worsened. Rather than a steady decrease in postural control, during the second day of the event a repeating oscillatory trend of fluctuations in postural control was observed for both days of the event. We hypothesize that the repeating oscillation of postural control followed a circadian rhythm pattern, suggesting that sleep deprivation for 48 hr. does not influence measures of postural control in a consistent manner. The apparent influence of time of day on postural control measures warrants consideration of this factor when conducting studies with repeated measures of postural control across different days.
Adult↗
Selective and total sleep deprivation: effect on the sleep EEG in the rat.
Although sleep deprivation is known to exert an antidepressant effect in depressed patients, the involvement of sleep regulation is still unknown. Selective sleep deprivation experiments were performed in the rat to investigate the interactions between non-REM sleep (NREMS) and REM sleep (REMS) in an animal model. A12-h total sleep deprivation (TD) period ending at lights on was followed by one of the following protocols: (1) recovery sleep (TD12); (2) 4-h total sleep deprivation (TD16); (3) 4-h slow-wave deprivation (SWD); (4) 4-h REMS deprivation (RD). In the SWD protocol, the reduction of EEG slow-wave activity (SWA; power density in the 0.75-4.0 Hz band) was obtained by curtailing NREMS episodes to 20 s. During RD the number of interventions required to prevent REMS increased during the first 2 h and then remained constant. While RD caused only a minor reduction of NREMS, it increasingly suppressed SWA in NREMS. The rebound of SWA occurred later and was less prominent after RD than after SWD. Whereas an REMS rebound occurred after all three 4-h sleep deprivation protocols, a persistent increase in the dark period was present only after TD16. It is concluded that (a) SWA in NREMS is inhibited by an increased level of REMS propensity; (b) the hypothesis that REMS propensity increases only during NREMS is not supported; and (c) the results are compatible with the hypothesis that the suppression of NREMS intensity is the common denominator of different antidepressive sleep manipulations in depressive patients.
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Evaluation of drowsiness during prolonged sleep deprivation.
Prolonged sleep deprivation is a relatively frequent situation during military training or warfare. A 60-hour sleep deprivation experiment was carried out on eight healthy volunteers of the French Air Force to assess drowsiness. Parameters used to assess drowsiness were questionnaires on behavior, measurement of sleep latency (MSLT), continuous electroencephalogram recording, and number of response failures or control losses observed during repeated psychomotor tests. Results showed a gradual decrement in arousal in all subjects and for all tests. These results, consistent with the literature, confirm the emergence of drowsiness after the 24th hour of uninterrupted wakefulness. This phenomenon had an increasingly negative effect on performance due to "micro-sleep" episodes which substantially reduced psychomotor performance.
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