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PubMed2006

Sleep deprivation and pain perception.

Chronically painful conditions are frequently associated with sleep disturbances, i.e. changes in sleep continuity and sleep architecture as well as increased sleepiness during daytime. A new hypothesis, which has attracted more and more attention, is that disturbances of sleep cause or modulate acute and chronic pain. Since it is well-known that pain disturbs sleep the relationship between the two has since recently been seen as reciprocal. To fathom the causal direction from sleep to pain we have reviewed experimental human and animal studies on the effects of sleep deprivation on pain processing. According to the majority of the studies, sleep deprivation produces hyperalgesic changes. Furthermore, sleep deprivation can interfere with analgesic treatments involving opioidergic and serotoninergic mechanisms of action. The still existing inconsistency of the human data and the exclusive focus on REM sleep deprivation in animals so far do not allow us to draw firm conclusions as to whether the hyperalgesic effects are due to the deprivation of specific sleep stages or whether they result from a generalized disruption of sleep continuity.

Animals↗

PubMed1978

The effects of sleep deprivation on the circadian rhythm of plasma cortisol levels in depressive patients.

The circadian rhythm of plasma cortisol levels was studied in 20 endogenous depressive patients who received one-night sleep deprivation therapy and 10 normal controls who were also deprived of sleep together with patients by estimation at four-hourly intervals over 36 hours. The mean values at each sampling time were compared. The result can be summarized as follows: The mean values of depressive patients tended to be higher than those of controls on the day following sleep deprivation. In depressive patients the mean values on the following day were higher compared to those on the preceding day. In the patients who responded well to sleep deprivation therapy, the circadian variation of mean values which was obscure the preceding day showed an evident rhythm the following day. These findings suggest that sleep deprivation may cause a different effect between depressive patients and normal subjects, and that the possible mechanism of the anti-depressive efficacy of sleep deprivation may be to normalize the disturbed rhythm of the physiological function in depressive patients.

Adolescent↗

PubMed2005

Partial REM-sleep deprivation increases the dream-like quality of mentation from REM sleep and sleep onset.

STUDY OBJECTIVES: Sleep onset (SO) is cognitively and physiologically similar to rapid eye movement (REM) sleep, supporting the notion that REM sleep-related processes are 'covertly' active at this time. The objective was to determine if SO mentation is sensitive to REM sleep deprivation. DESIGN: Two-group cross-sectional design; sleep recordings for 3 nights. SETTING: Standard sleep laboratory with 24-channel polysomnography recording. PARTICIPANTS: Fourteen female, 13 male healthy volunteers (18-41 yrs, mean=24.8 +/- 6.07). INTERVENTIONS: On Night 2, half were and half were not partially REM sleep-deprived (REMD), recalled REM mentation, and rated it for dream-like quality (DLQ), sleepiness, and sensory attributes. On Night 3, all were awakened from SO substages 4 and 5 for mentation reports and further ratings. REMD measures were derived from scored sleep tracings. MEASUREMENTS AND RESULTS: REMD produced increases in DLQ for both REM and SO reports (P < .05); DLQ scores were higher for REM than for SO mentation (P < .001). Covarying sleepiness preserved the (REMD) effect but abolished the REM/SO difference. Whereas 2 sensory attributes (presence of self, visual intensity) tended to distinguish the REM-mentation reports of REMD and control subjects, only 1, self-movement, distinguished their SO mentation reports (P < .06). Multiple regression revealed that increased DLQ of both REM and SO mentation was associated with increased sleepiness and decreased REM sleep time on Night 2. CONCLUSIONS: SO mentation responds to REMD much like REM mentation does, a finding consistent with other work supporting the notion of covert REM-sleep processes at SO. DLQ may be mediated by both increases in REM-sleep propensity and a circadian process indexed by sleepiness ratings.

Adolescent↗

PubMed1989

REM sleep deprivation increases early morning pineal melatonin in castrated rats.

Recently nighttime melatonin levels have been shown to be attenuated in depressive patients or patients with dementia of the Alzheimer type. On the other hand, depression can be transiently relieved by deprivation of rapid eye movement sleep. Since exogenous melatonin administration increases rapid eye movement sleep and slow wave sleep in the rat, could rapid eye movement sleep deprivation then inversely influence endogenous melatonin production? We found indices that in castrated Wistar rats 4 days of rapid eye movement sleep deprivation by the cuff pedestal method elevates the pineal content of melatonin by a factor of two at 1 to 2 h after light onset. Rapid eye movement sleep is thus suggested to influence pineal activity. This mechanism might be involved in the human depression-alleviating effect of rapid eye movement sleep deprivation.

Animals↗

PubMed2001

Effects of one night of sleep deprivation on hormone profiles and performance efficiency.

This study examined the effects of one night of sleep deprivation on melatonin and cortisol profiles, as well as performance efficiency of military service members. Sleep intervention consisted of total lack of sleep (N = 7) or 8 hours of sleep (control group; N = 7) during the night. All parameters were measured at selected time intervals before (day 1), during (only in sleep-deprived individuals), and after (day 2) sleep intervention. Rotary pursuit scores and handgrip strength data were used as indices of psychomotor and physical performance, respectively. In sleep-deprived individuals, more salivary melatonin, but not cortisol, was secreted than in subjects who slept adequately. Significant increases in melatonin and cortisol were noted, especially at 1:30 p.m. on the day after nighttime sleep deprivation. In contrast, the tracking scores for rotary pursuit and grip strength among sleep-deprived and rested individuals were comparable. Across a normal working day (day 1), all parameters studied revealed time-specific fluctuations in both control and sleep-deprived groups. Irrespective of nighttime sleep schedule, the patterns of performance on day 2 differed from those on day 1. The tracking performance improved on day 2, whereas grip strength worsened, which may reflect inherent learning and muscle fatigue, respectively. During the night of sleep deprivation, performance declined. In conclusion, the present study showed that one night of sleep deprivation (8 hours) resulted in significant hormonal changes on the next afternoon but did not modify tracking and muscular strength performance.

Adult↗

PubMed2001

Effects of rapid eye movement (REM) sleep deprivation on pain sensitivity in the rat.

The relationship between pain and sleep seems to be reciprocal: if pain may interrupt or disturb sleep, poor sleep can also influence pain perception. However the influence of sleep disturbances on pain sensitivity remain poorly investigated. The aim of this study was to assess the effect of REM sleep deprivation on the reaction of rats subjected to different noxious stimuli. In each experiment 16 Wistar male rats were randomly assigned to two groups: controls (n=8), and REM sleep deprived rats (n=8). REM sleep deprivation was elicited using the 'inverted flower pot' technique. Four different experiments were performed to assess the sensitivity to mechanical (vocalization threshold in paw pressure), thermal (tail withdrawal latency in hot water immersion), electrical (envelope of 2nd peep in tail shock test) and chemical (analgesic behavior in formalin test) noxious stimuli. All experiments were performed over a 5-day period with baseline (day 1, day 2) in a dry environment and REM sleep deprivation (day 3, day 4 and day 5) in a wet environment. Under wet conditions, vocalization threshold in the paw pressure test (-20%, P=0.005), and tail withdrawal latency in the hot water immersion test (-21%, P=0.006) were significantly lower, and the envelope of 2nd peep in the tail electrical shock was significantly greater (+78%, P=0.009), in REM sleep deprived rats compared to controls. However, under wet conditions the mean duration of nociceptive behaviors in the formalin test did not differ between the two groups. In conclusion, REM sleep deprivation induces a significant increase in the behavioral responses to noxious mechanical, thermal and electrical stimuli in rats.

Animals↗

PubMed2002

Sleep deprivation does not affect seizure frequency during inpatient video-EEG monitoring.

OBJECTIVE: To determine whether acute sleep deprivation facilitates seizures during inpatient monitoring in a controlled protocol. METHODS: Eighty-four patients with medically refractory partial epilepsy undergoing inpatient monitoring were assigned in consecutive blocks to either sleep deprivation every other night or to normal sleep. In both groups, subjects were requested to stay awake during the day, from 6 AM to 10 PM. In the sleep deprivation group, patients also stayed awake between 10 PM and 6 AM every other night beginning with Day 2. Patients were removed from sleep deprivation if they had two or more secondarily generalized seizures within 24 hours. Patients were removed from the normal sleep group and were sleep deprived if they did not have a complex partial or secondarily generalized seizure by Day 6 of monitoring. In these patients removed from sleep deprivation or from normal sleep, data were analyzed up to and including the day of removal from the protocol. RESULTS: The sleep deprivation and normal sleep subjects did not differ in age, sex, seizure localization, or percent dosage reduction in antiepileptic drugs from baseline at days 1 to 3 of monitoring. Protocol duration was 6.5 +/- 2.4 days (mean +/- SD) for the sleep deprivation group and 5.8 +/- 2.0 days for the normal sleep group. Seizures per day for complex partial, secondarily generalized, and combined complex partial and secondarily generalized, calculated from admission until end of protocol, did not differ significantly between the two groups. CONCLUSION: Acute sleep deprivation did not affect seizure frequency during inpatient monitoring in our patients with intractable complex partial seizures with secondary generalization.

Adult↗

PubMed2006

Effects of modafinil on cognitive performance and alertness during sleep deprivation.

The performance- and alertness-sustaining/restoring effects of modafinil during sleep deprivation in normal, healthy adults were reviewed. Results indicate that modafinil is efficacious for sustaining/restoring objective performance and alertness during sleep deprivation with few adverse effects. At appropriate dosages, modafinil restores performance and alertness to non-sleep deprived levels. Modafinil also impairs post-sleep deprivation recovery sleep, but from the few studies available addressing this issue, it is unclear whether these sleep impairments translate into post-sleep performance impairments. Further research is needed to determine whether modafinil restores performance on simple cognitive tasks only or whether modafinil additionally restores executive functions (e.g., abstract thought, critical reasoning, planning, decision-making, situational awareness, and effective judgment) which are critical in most modern operational settings. In addition, studies are needed to determine whether modafinil use during sleep deprivation is preferable to that of other available controlled stimulants (such as dextroamphetamine) or non-controlled stimulants (such as caffeine). Such studies would be comprised of direct, head-to-head comparisons among various stimulants across a range of dosages.

Arousal↗

PubMed1998

Sleep Deprivation in social phobia and generalized anxiety disorder.

BACKGROUND: Sleep deprivation has been shown to improve depressive symptoms in some patients with major depressive disorder, but it has not been tested in patients with generalized anxiety disorder (GAD) or social phobia (SP). METHODS: To determine if sleep deprivation altered anxiety or depressive symptoms in patients with GAD (n = 7) or SP (n = 8), we sleep deprived patients and normal controls (n = 18) for one night. RESULTS: On one measure of anxiety, GAD patients improved compared with controls, but there were otherwise no significant change differences between controls and SP or GAD patients. CONCLUSIONS: The lack of benefit is consistent with previous findings that sleep deprivation provides no benefit to patients with other anxiety disorders. Sleep deprivation may be a biological intervention that distinguishes anxiety from affective disorders.

Adolescent↗

PubMed1984

[EEG with sleep deprivation in epileptic children].

The role of sleep and sleep deprivation as inducer of paroxysmal abnormalities in EEG was studies in 104 infants and children under 14 years of age. These children suffered from various types of seizures and of normal standard EEG. These children who suffered from seizures of epileptic origin, after sleep deprivation had an EEG that showed a paroxysmal activity of 70.91% of the cases (p less than 0.001). The forced lack of sleep and the sleep that follows were found to be equally important as activators of paroxysmal abnormalities. The method of activation was found to be efficient in both partial an generalized seizures. The paroxysmal abnormalities were noted as being greater in phase II sleep. The EEG in sleep deprivation can show paroxysmal abnormalities, in children with epileptic seizures, that were hidden from standard EEG.

Adolescent↗

PubMed1976

Sleep deprivation as treatment for endogenous depression.

Twenty-six depressed patients, 19 of whom suffered from an endogenous depression, were sleep-deprived for one night, and eight of these were additionally sleep-deprived for three to nine nights with two sleep deprivations per week. While the sleep deprivation was being carried through, none of the patients were treated with tricyclic antidepressants. The patients were rated before and after the sleep deprivation(s). Sleep deprivation appeared to be effective for both unipolar and bipolar depressions. According to the rating scale an improvement was registered especially when the clinical picture was characterized by depressed mood, psycho-motor retardation and anxiety. As sleep deprivation cured 25% of the patients and further incidentally improved another 20% of the patients, it can be concluded that sleep deprivation seems to be a valuable treatment, especially in retarded endogenous depressions.

Adult↗

PubMed1996

Sleep electroencephalogram in seasonal affective disorder and in control women: effects of midday light treatment and sleep deprivation.

The role of sleep regulation in Seasonal Affective Disorder (SAD) was studied in 11 female SAD patients and eight controls in winter before and after light treatment (LT, 6000 lux, 10-14h, 5 days). The sleep electroencephalogram (EEG) was recorded at baseline and after the total sleep deprivation (TSD) of a 40-h constant routine. The well-known effects of TSD on sleep parameters and on EEG power spectra were replicated, indicating normal homeostatic sleep regulation in SAD. Sleep improved after LT in both groups. Since the condition following LT was the second session, these improvements may be an order effect and/or an effect of LT itself. After LT, sleep EEG spectra of SAD patients, but not of controls, showed modifications resembling those of recovery sleep. Since only SAD patients curtailed their sleep while remitting during the LT period, these EEG modifications can be explained by normal sleep regulation alone. We conclude that the robust antidepressant effect of LT in SAD is unlikely to be mediated by changes in sleep, and that sleep regulatory mechanisms are not a crucial factor in the pathogenesis of winter depression.

Adult↗

PubMed1993

Effects of 12-h sleep deprivation and of 12-h cold exposure on sleep regulation and cortical temperature in the rat.

The predictions of the two-process model of sleep regulation were tested by 12-h sleep deprivation (SDEP) and 12-h cold exposure (cold, 4 degrees C) in the rat, both carried out in the 12-h dark period. The analysis was based on recordings of vigilance states, electroencephalogram (EEG) power spectra (0.25-25.0 Hz), and cortical temperature (Tcrt). During recovery from SDEP, slow-wave activity (SWA; EEG power density in the 0.75-4.0 Hz band) in non-REM sleep was higher and the number of brief awakenings (nBA) lower than in the corresponding baseline period. During recovery from cold, a moderate and delayed increase in SWA was present. During SDEP, Tcrt was above baseline, and in some intervals of recovery below baseline. In those intervals waking was also decreased. During recovery from cold, Tcrt and waking were not affected. It is concluded that 12-h SDEP causes an intensification of sleep, as indicated by the enhanced SWA and the reduced nBA, whereas 12-h cold has only marginal effects. The time course of SWA in both experiments could be accurately predicted by a computer simulation based on the assumption of the two-process model and the parameter values determined in a previous experiment.

Animals↗

PubMed2005

REM sleep deprivation inhibits LTP in vivo in area CA1 of rat hippocampus.

Rapid eye movement (REM) sleep deprivation has previously been shown to interfere with normal learning and memory and to inhibit long-term potentiation (LTP) in vitro. Previous studies on REM sleep deprivation and LTP have relied on in vitro analysis in isolated brain slices taken from animals following several days of sleep deprivation. LTP in the hippocampus in situ may differ from LTP in vitro due to modulatory inputs from other brain regions, which are altered after REM sleep deprivation. Here, we examined LTP in unanesthetized, behaving animals on the first and second recovery days following REM sleep deprivation to determine if similar effects are seen in vivo as previously reported in vitro. We found that LTP was significantly impaired in REM sleep-deprived animals on the second recovery day but not the first recovery day. Our results extend previous findings by showing that REM sleep deprivation continues to affect hippocampal function for more than 24h following the end of deprivation. Our results also suggest the presence of a modulatory process not present in vitro. Our findings are not explained by stress during REM sleep deprivation because equivalent circulating corticosterone levels (an index of stress) were found during both REM sleep deprivation and control treatment.

Animals↗

PubMed1996

Effects of short- and long-term REM sleep deprivation on sexual behavior in male rats.

The influence of selective REM sleep deprivation on masculine sexual behavior has been a matter of controversy. In the present study, the sexual behavior of male rats was analyzed in subjects deprived on REM sleep by the island technique for 24 or 16 h daily during 20 days. When compared to control rats, both groups displayed changes in sexual performance since the first day. The effects were: an increase in mount, intromission and ejaculation latencies and in mount frequency as well; a decrease of ejaculation frequency and of the Hit rate. The effects became stronger as REM sleep deprivation progressed. Rats deprived of REM sleep for 24 h were extremely debilitated after 12 days and some of them died, whereas the rats REM deprived for 16 h remained healthy during the 20 days. These data indicate that REM sleep deprivation interferes with the mechanisms that regulate male sexual behavior.

Animals↗

PubMed2004

Distinct effects of sleep deprivation on binding to norepinephrine and serotonin transporters in rat brain.

There is evidence to suggest that the antidepressant activity of sleep deprivation may be due to an enhancement of serotonergic and/or noradrenergic neurotransmission in brain. In the present study we examined the possibility that such changes may occur at the level of the norepinephrine (NET) and serotonin (SERT) and transporters. Rats were deprived of sleep for 96 h using the modified multiple platform method and then sacrificed for autoradiographic assessments of NET and SERT binding throughout the brain. [3H]Nisoxetine binding to the NE transporter was generally decreased in 44 of 45 areas examined, with significant reductions occurring in the anterior cingulate cortex (-16%), endopiriform n. (-18%), anterior olfactory n. (-19%), glomerular layer of olfactory bulb (-18%), ventral pallidum (-14%), medial preoptic area (-16%), retrochiasmatic/arcuate hypothalamus (-18%), anteromedial thalamic n. (-15%), and rostral raphe (-17%). In contrast, SERT binding measured with [11C]DASB showed no clear directional trends in 61 brain areas examined, but was significantly reduced in subdivisions of the anterior olfactory nucleus (-22%) and substantia nigra (-18%). Thus, sleep deprivation induced widespread decreases in NET binding, and fewer and well-localized decreases in SERT binding. Significant down-regulation in one brain region, the anterior olfactory nucleus, was observed in the case of both transporters. These results suggest that mechanisms involved in the antidepressant action of sleep deprivation may involve generalized NET down-regulation as well as decreased SERT binding in specific areas. Insofar as these changes may be associated with increased levels of serotonin (5-HT) and norepinephrine (NE) in the synapse, they suggest that sleep deprivation may share some basic mechanisms of action with several current antidepressant medications.

Animals↗

PubMed2006

Sleep deprivation as a neurobiologic and physiologic stressor: Allostasis and allostatic load.

Sleep has important homeostatic functions, and sleep deprivation is a stressor that has consequences for the brain, as well as many body systems. Whether sleep deprivation is due to anxiety, depression, or a hectic lifestyle, there are consequences of chronic sleep deprivation that impair brain functions and contribute to allostatic load throughout the body. Allostatic load refers to the cumulative wear and tear on body systems caused by too much stress and/or inefficient management of the systems that promote adaptation through allostasis. Chronic sleep deprivation in young healthy volunteers has been reported to increase appetite and energy expenditure, increase levels of proinflammatory cytokines, decrease parasympathetic and increase sympathetic tone, increase blood pressure, increase evening cortisol levels, as well as elevate insulin and blood glucose. Repeated stress in animal models causes brain regions involved in memory and emotions, such as hippocampus, amygdala, and prefrontal cortex, to undergo structural remodeling with the result that memory is impaired and anxiety and aggression are increased. Structural and functional magnetic resonance imaging studies in depression and Cushing's disease, as well as anxiety disorders, provide evidence that the human brain may be similarly affected. Moreover, brain regions such as the hippocampus are sensitive to glucose and insulin, and both type 1 and type 2 diabetes mellitus are associated with cognitive impairment and (for type 2 diabetes mellitus) increased risk for Alzheimer's disease. Animal models of chronic sleep deprivation indicate that memory is impaired along with depletion of glycogen stores and increases in oxidative stress and free radical production. Taken together, these changes in brain and body are further evidence that sleep deprivation is a chronic stressor and that the resulting allostatic load can contribute to cognitive problems, which can, in turn, further exacerbate pathways that lead to disease.

Animals↗

PubMed1985

Periodic sleep deprivation in drug-refractory depression.

For some time it has been known that total and partial sleep deprivation (in the second half of the night) produces an immediate antidepressive effect and a short-term effect of approximately 1-week duration. A 25-day trial is discussed here. 18 endogenous depressives who proved to be refractory to tricyclic antidepressive therapy were treated with periodic sleep deprivation (5 sleep deprivation treatments in the second half of the night at 5-day intervals) under continued drug therapy. The combined treatment led to a better result than would have been expected from drug therapy alone. Some of the sleep deprivation treatments effected an accelerated remission without the efficacy of treatment subsiding. In individual cases recovery occurred after one or a few partial sleep deprivation sessions. Whether in other respects sleep deprivation shortens the course of depressive phases is still unproven.

Antidepressive Agents, Tricyclic↗