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Results for “SLEEP DEPRIVATION”

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PubMed1999

Sleep EEG studies during early and late partial sleep deprivation in premenstrual dysphoric disorder and normal control subjects.

In this study of 23 patients with premenstrual dysphoric disorder (PMDD) and 18 normal comparison (NC) subjects, we examined sleep EEG measures during baseline midfollicular (MF) and late luteal (LL) menstrual cycle phases and after early sleep deprivation (ESD), in which subjects slept from 03.00 to 07.00 h, and late sleep deprivation (LSD), in which subjects slept from 21.00 to 01.00 h. Each sleep deprivation night was followed by a night of recovery sleep (ESD-R, LSD-R) (sleep 22.30-06.30 h) and was administered in the late luteal phase of separate menstrual cycles. During baseline studies, sleep EEG measures differed significantly by menstrual cycle phase, but not group. Both PMDD and NC groups showed longer REM latencies and less REM sleep (minutes and percent) during the luteal compared with the follicular menstrual cycle phase. PMDD subjects, however, did not show sleep architecture changes similar to those of patients with major depressive disorders. Sleep quality was better during recovery nights of sleep in PMDD compared with NC subjects. REM sleep measures changed in association with clinical improvement in responders to sleep deprivation. Both early and late sleep deprivation may help to correct underlying circadian rhythm disturbances during sleep in PMDD, although differential sleep changes during ESD vs. LSD did not correlate with clinical response. Further sleep studies addressing additional circadian variables may serve to elucidate mechanisms mediating the therapeutic effects of sleep deprivation in PMDD.

Affect↗

PubMed2001

Clinical neurochemical implications of sleep deprivation's effects on the anterior cingulate of depressed responders.

The antidepressant and cerebral metabolic effects of total sleep deprivation (TSD) or partial sleep deprivation (PSD) for one night has been studied with functional neuroimaging in seven publications from five different groups. Despite the variations in methods and techniques, the over-all findings were relatively consistent. First, before sleep deprivation, responders have significantly elevated metabolism compared with non-responders and normal controls, in the orbital medial prefrontal cortex, and especially the ventral portions of the anterior cingulate cortex. Second, after sleep deprivation, these hyperactive areas normalize in the responders. One functional imaging study suggested that synaptic dopamine release was associated with the antidepressant effects of TSD. The neurochemical implications of these findings are explored. Possible dopaminergic and serotonergic mechanisms are discussed.

Cerebral Cortex↗

PubMed1990

Sleep deprivation in depression: pattern of relapse and characteristics of preceding sleep.

The pattern of relapse following therapeutic response to 40-hr sleep deprivation (SD) was examined in nine depressed patients. On the night ending SD patients were awakened from polygraphically recorded sleep on one or more occasions, in order to assess the clinical state. All subjects were found to demonstrate a precipitous and full relapse over this night, the timing of the relapse varying considerably between individuals. No association was found between deterioration in the clinical state and characteristics of preceding sleep. These results are consistent with the notion that, in predisposed individuals, some process associated with sleep has a depressogenic effect. However, they necessitate revision of theories of SD and depression that emphasize the infrastructure of sleep.

Adult↗

PubMed2006

Sleep deprivation inhibits adult neurogenesis in the hippocampus by elevating glucocorticoids.

Prolonged sleep deprivation is stressful and has been associated with adverse consequences for health and cognitive performance. Here, we show that sleep deprivation inhibits adult neurogenesis at a time when circulating levels of corticosterone are elevated. Moreover, clamping levels of this hormone prevents the sleep deprivation-induced reduction of cell proliferation. The recovery of normal levels of adult neurogenesis after chronic sleep deprivation occurs over a 2-wk period and involves a temporary increase in new neuron formation. This compensatory increase is dissociated from glucocorticoid levels as well as from the restoration of normal sleep patterns. Collectively, these findings suggest that, although sleep deprivation inhibits adult neurogenesis by acting as a stressor, its compensatory aftereffects involve glucocorticoid-independent factors.

Aging↗

PubMed2002

Sleep deprivation reduces total plasma homocysteine levels in rats.

Hyperhomocysteinemia has been associated with pathological and stressful conditions and is a risk factor for cardiovascular disease. Since sleep deprivation is a stressful condition that is associated with disruption of various physiological processes, we investigated whether it would also be associated with increases in plasma homocysteine levels. Further, since hyperhomocysteinemia may promote oxidative stress, and we had previously found evidence of oxidative stress in brain following sleep deprivation, we also searched for evidence of systemic oxidative stress by measuring glutathione and thiobarbituric acid reactive substance levels. Rats were sleep deprived for 96 h using the platform technique. A group was killed after sleep deprivation and another two groups were allowed to undergo sleep recovery for 24 or 48 h. Contrary to expectation, plasma homocysteine was reduced in sleep-deprived rats as compared with the control group and did not revert to normal levels after 24 or 48 h of sleep recovery. A trend was observed towards decreased glutathione and increased thiobarbituric acid reactive substance levels in sleep-deprived rats. It is possible that the observed decreases in homocysteine levels may represent a self-correcting response to depleted glutathione in sleep-deprived animals, which would contribute to the attenuation of the deleterious effects of sleep deprivation.

Animals↗

PubMed1987

Effect of sleep deprivation on the performance of surgical residents.

Surgical residents were tested under sleep-deprived and nonsleep-deprived conditions. Three performance domains were tested: factual recall, the ability to concentrate, and manual dexterity. Sleep deprivation was defined as less than 3 hours of sleep in a 24 hour period. A randomized, repeated measures design was used. Split-plot analysis of variances was used to analyze the mean scores, and it revealed that there were no significant differences in performance in the sleep-deprived condition compared with performance in the nonsleep-deprived condition in any of the three domains tested. Moderate sleep deprivation appeared to be well tolerated by the surgical residents studied in this investigation.

Adult↗

PubMed1998

Biochemical effects induced by REM sleep deprivation in naive and in D-amphetamine treated rats.

The neurochemical dysfunction present in patients showing self-mutilating behavior (SMB) is not well understood. In animal models, rapid eye movement (REM) sleep deprivation enhances the SMB induced by the chronic administration of d-amphetamine. To understand the mechanism underlying these effects the levels of dopamine (DA), noradrenaline (NA) and serotonin (5-HT) were measured in REM sleep deprived only, and in REM sleep deprived and d-amphetamine treated rats. DA levels were elevated (31%) after REM sleep deprivation (48 h) in the neostriatum and the cerebral cortex (33%), while the levels of NA and 5-HT remained constant. A 6-day treatment with d-amphetamine (7.5 mg/kg; i.p.) failed to affect, in REM sleep deprived rats, DA, NA and 5-HT levels. It was also found that REM sleep deprivation had no effects on the d-amphetamine induced [3H]DA release from slices of the same regions. Our results suggests that dopaminergic mechanisms are involved in the effects of REM sleep deprivation on SMB.

Animals↗

PubMed1996

Brain distribution of vasoactive intestinal peptide receptors following REM sleep deprivation.

Vasoactive intestinal peptide (VIP) has been shown to increase rapid eye movement (REM) sleep in normal and insomniac animals, while the administration of anti-VIP antibodies or an antagonist of VIP receptors decreases REM sleep. In addition, recently, it has been suggested that a VIP-like substance accumulates in the CSF during waking and that it may be involved in the production of the REM rebound normally seen following REM sleep deprivation. This evidence suggests that VIP may be important in modulating REM sleep in normal conditions and during REM sleep rebound. To determine whether VIP is involved in REM sleep homeostasis, VIP receptors of discrete brain areas was determined by autoradiography after 24 and 72 h of REM sleep deprivation (REM SD) by the water tank technique. Since this procedure has been suggested to produce some stress, an additional group adapted for 7 days to the sleep deprivation situation was tested. The results showed that REM SD produces an increase in the density of VIP receptors in several brainstem and forebrain structures at 24 h of REM SD and more so at 72 h of REM SD. Interestingly, results showed that habituation to the REM SD procedure decreases the density of VIP receptors in some areas of the brain of the REM sleep-deprived rats. The results are discussed in terms of the possibility that waking induces an increase of VIP receptors in several structures, which in turn are responsible for modulating REM sleep, but that stress contributes in part to VIP receptor changes.

Animals↗

PubMed1987

Role of brain monoaminergic systems in the increased ethanol drinking caused by REM-sleep deprivation.

The central monoaminergic neuronal effects of REM-sleep deprivation, and the effect of different monoamine uptake blocking agents on the REM-sleep deprivation-induced increase in ethanol intake were studied. The levels of 5-HT and 5-HIAA in the hypothalamus were increased both in the REM-sleep deprived rats and the stressed control rats, but the hypothalamic level of MHPG was decreased only in the REM-sleep deprived animals. Two daily injections (5-20 mg/kg/d) of citalopram or GBR-12909 (uptake blocking agents for 5-HT and dopamine, respectively) did not modify the increased level of ethanol intake. The noradrenaline uptake blocking agent, talsupram (5-10 mg/kg/d), however, decreased ethanol intake to the levels seen prior to deprivation. This effect of talsupram could be antagonized by blocking alpha-1-adrenoreceptors with prazosin (1 mg/kg/d).

3,4-Dihydroxyphenylacetic Acid↗

PubMed2001

EEG arousals in normal sleep: variations induced by total and selective slow-wave sleep deprivation.

STUDY OBJECTIVES: Aim of the present study was to assess changes in arousal rates after selective slow-wave (SWS) and total sleep deprivations. DESIGN: Two-way mixed design comparing the arousal index (Al), as expressed by the number of EEG arousals divided by sleep duration, in totally or selectively sleep deprived subjects. SETTING: Sleep laboratory. PATIENTS OR PARTICIPANTS: Nineteen normal male subjects [mean age=23.3 years (S.E.M.=0.55)]. INTERVENTIONS: Al was measured in baseline nights and after selective SWS (N=10) and total sleep deprivation (N=9). MEASUREMENTS AND RESULTS: During the baseline nights AI values changed across sleep stages as follows: stage 1 > stage 2 and REM > SWS, but did not present any significant variations as a function of time elapsed from sleep onset. The recovery after deprivation showed a reduction in EEG arousals, more pronounced after total sleep deprivation; this decrease affected NREM but not REM sleep. During the baseline nights Al showed a close-to-significance negative correlation with REM duration, while during the recovery nights a significant positive relation with stage 1 duration was found. CONCLUSIONS: The present results suggest that recuperative processes after sleep deprivation are also associated with a higher sleep continuity as defined by the reduction of EEG arousals.

Adult↗

PubMed2000

The value of partial sleep deprivation as a routine measure in pediatric electroencephalography.

For more than 50 years it has been known that in patients with epilepsy, sleep markedly increases the diagnostic yield of the electroencephalogram (EEG). Sleep deprivation could have an additional activating role. Many laboratories do not use these methods routinely but reserve them for a second EEG if equivocal or negative findings are present in the initial EEG. We studied a regime of routine partial sleep deprivation without the use of hypnotic agents in 396 children younger than age 17 years who were referred for EEG with a diagnosis of epilepsy or suspected epilepsy. Sleep was achieved for the EEG in 77% (96% in the 1 month to 2 year age group, 78% in the 2 to 8 year age group, and in 64% of those more than 8 years old). In a comparison group of 72 children who had not been sleep-deprived, sleep was achieved in 44% (69% of those less than 2 years old, 27% of those between 2 and 8 years of age, and 33% of those older than 8 years). The differences were highly significant. The regime was well tolerated. Routine partial sleep deprivation is a practical and effective method of obtaining sleep and thus maximizing the information obtained from a single EEG.

Adolescent↗

PubMed1996

Alterations in c-fos expression after different experimental procedures of sleep deprivation in the cat.

In the present study, we sought to examine the expression of the c-fos proto-oncogene in the cat brain after two different procedures of 24 h sleep deprivation. A first group of cats was gently sleep-deprived; they were awoken by a gentle touch of the hand (n = 5). A second group was sleep-deprived by the water tank technique which is a stressful deprivation (n = 4). A third group was placed 2 h on the water tank and was therefore stressed but not sleep-deprived (n = 2). A fourth group (control group of basal and unspecific Fos expression) was not sleep-deprived (n = 5). These four groups allowed us to separate Fos expression due to stress from Fos expression due to sleep deprivation. On the one hand, compared with controls cats, an important increase in Fos expression, detected by immunohistochemistry, was observed in the preoptic area of sleep-deprived cats by both gentle and stressful methods. On the other hand, there was a significant increase in Fos expression in the lateral hypothalamus of gently deprived cats as compared with control cats. These data indicate that c-fos expression can be employed as a marker of some putative homeostatic mechanism regulating sleep. The only sites in which there was a significant increased number of c-fos expressing neurons were located in the preoptic area which is known to be involved in sleep and in the lateral hypothalamic area.

Animals↗

PubMed2003

Sleep regulation in the Djungarian hamster: comparison of the dynamics leading to the slow-wave activity increase after sleep deprivation and daily torpor.

STUDY OBJECTIVES: Emerging from daily torpor, Djungarian hamsters (Phodopus sungorus) show an initial increase in electroencephalographic slow-wave activity (power density between 0.75 and 4.0 Hz) during sleep that gradually declines. This feature is typical for sleep following prolonged waking and supports the hypothesis that sleep pressure increases during daily torpor. After hamsters were subjected to sleep deprivation or partial non-rapid eye movement sleep deprivation immediately following torpor, slow-wave activity remained high and decreased only when sleep was allowed. An analysis of the dynamics of the process underlying the build-up of sleep pressure during episodes of waking and torpor may provide insights into the regulation of normal sleep and wakefulness. We have analyzed in more detail the timecourse of the process that is common for waking and daily torpor and that could account for the subsequent increase in slow-wave activity. DESIGN: Continuous 24-hour recordings of electroencephalography, electromyography, cortical temperature, and electroencephalographic spectral analysis were performed. Torpor data of 28 hamsters and sleep-deprivation data of diverse durations collected previously in 15 hamsters were analyzed. SETTING: N/A. PATIENTS OR PARTICIPANTS: N/A. INTERVENTIONS: Sleep deprivation. MEASUREMENTS AND RESULTS: Slow-wave activity invariably increased as a function of the duration of both prior waking and torpor. However, the time constant of the build-up of slow-wave activity was approximately 2.75 times slower during torpor compared to sleep deprivation. Brain temperature recorded during the torpor bouts was 10 degrees to 12 degrees C below euthermic brain temperature. Therefore, the temperature coefficient of the time constant for the slow-wave-activity increase is between 2.3 and 2.8, a range typical for biochemical processes. CONCLUSIONS: We conclude that the processes occurring during daily torpor in the Djungarian hamster are similar to those occurring during sleep deprivation, but the build-up of sleep pressure during torpor appears to be slowed down by the lower brain temperature.

Animals↗

PubMed1992

The P300 event-related potential. The effects of sleep deprivation.

We monitored 15 healthy young adults during 18 hours of sleep deprivation. Subjects were repeatedly tested on measures of the P300 (P3) event-related potential, reaction time, body temperature, and a subjective rating of fatigue. Statistically significant decreases in P3 amplitude (P < or = .01) and increases in P3 latency (P < or = .0001) were found during sleep deprivation. These changes correlated with body temperature and fatigue and were not due to circadian variation. Reaction time did not show a significant change over time. We conclude that the P3 potential is a more sensitive cognitive measure of sleep deprivation than reaction time, a measure commonly used in previous studies. We provide a review of the literature on the P3 and recommend the use of the P3 as a marker to examine sleep deprivation in health professionals.

Adult↗

PubMed2002

How sleep deprivation affects gene expression in the brain: a review of recent findings.

The identification of the molecular correlates of sleep and wakefulness is essential to understand the restorative processes occurring during sleep, the cellular mechanisms underlying sleep regulation, and the functional consequences of sleep loss. To determine what molecular changes occur in the brain during the sleep-waking cycle and after sleep deprivation, our laboratory is performing a systematic screening of brain gene expression in rats that have been either sleeping or spontaneously awake for a few hours and in rats that have been sleep deprived for different periods of time ranging from a few hours to several days. So far, ~10,000 transcripts expressed in the cerebral cortex have been screened. The expression of the vast majority of these genes does not change either across behavioral states or after sleep deprivation, even when forced wakefulness is prolonged for several days. A few hours of wakefulness, either spontaneous or forced by sleep deprivation, increase the expression of the same small groups of genes: immediate-early genes/transcription factors, genes related to energy metabolism, growth factors/adhesion molecules, chaperones/heat shock proteins, vesicle- and synapse-related genes, neurotransmitter/hormone receptors, neurotransmitter transporters, and enzymes. Sleep, on the other hand, induces the expression of a few unknown transcripts whose characterization is in progress. Thus, although the characterization of the molecular correlates of behavioral states is not yet complete, it is already apparent that the transition from sleep to waking can affect basic cellular functions such as RNA and protein synthesis, neural plasticity, neurotransmission, and metabolism. The pattern of changes in gene expression after long periods of sleep deprivation is unique and does not resemble that of short-term sleep deprivation or spontaneous wakefulness. A notable exception is represented, however, by the enzyme arylsulfotransferase, whose induction appears to be proportional to the duration of previous wakefulness. Arylsulfotransferase in rodents plays a major role in the catabolism of catecholamines, suggesting that an important role for sleep may be that of interrupting the continuous activity, during wakefulness, of brain catecholaminergic systems.

Animals↗

PubMed1991

Green light attenuates melatonin output and sleepiness during sleep deprivation.

Melatonin output covaries with sleepiness, with both peaking early morning. Bright white light suppresses this output, but it is not known if such treatment ameliorates nighttime sleepiness during sleep deprivation. However, sleep-deprived subjects find such light irritating. Humans are particularly sensitive to green light, and melatonin output is more readily suppressed by this hue. A pilot study using different green light regimens showed that sleep-deprived subjects well tolerated 2,000 lux green light given 10 min hourly, and that this dose reduced nighttime melatonin output. The main study gave this light treatment vs. a low intensity red/green light control, from 1900 hr for 11 hr, to two groups of subjects (n = 6 each) sleep deprived for 36 hr. Urine was collected at 6-hr intervals during sleep loss and on a baseline day. Vigilance performance, subjective sleepiness, and oral temperature were monitored during sleep loss. The experimental condition suppressed urine 6-hydroxymelatonin sulfate (aMT6s) output between 0000 hr and 0600 hr, and increased it 0600-1200 hr; but there was no change in total 24-hr values. The control condition had no such effects. The oral temperature rhythm remained unchanged. Vigilance and subjective sleepiness were improved significantly relative to control values during 0000-0600 hr; these improvements were maintained somewhat over the 0600-1200-hr period, contrary to what one might expect if the delayed melatonin surge at this time was increasing sleepiness. Although the bright green light helped counteract sleepiness, any causal link with changes in melatonin output seem tenuous.

Adult↗

PubMedDate not supplied

Partial sleep deprivation reduces natural killer cell activity in humans.

Sleep disturbance, measured by either subjective report or electroencephalographic (EEG) assessment of sleep, correlates with a reduction of natural killer (NK) cell activity in major depression. To test whether sleep loss independent of mood disturbance alters daytime values of cellular immune function, the effect of late-night partial sleep deprivation on NK cell activity was studied in 23 medically and psychiatrically healthy male volunteers. After a night of sleep deprivation between 3 and 7 AM, NK cell activity was reduced in 18 of the 23 subjects with average lytic activity reduced significantly (p < .01) to a level 72% of the mean of three separate baseline values. After a night of resumed nocturnal sleep, NK cell activity had returned to baseline levels. These data implicate sleep in the modulation of natural immunity and demonstrate that even modest disturbances of sleep produce a reduction of NK cell activity.

Adult↗

PubMed2006

Hormone treatment gives no benefit against cognitive changes caused by acute sleep deprivation in postmenopausal women.

The objective was to evaluate whether hormone therapy (HT) gives any benefit against the possible impairment of cognitive performance when challenged by acute sleep deprivation. Twenty postmenopausal women volunteered (age range 59-72 years, mean=64.4 years, SD=4.4): 10 HT users and 10 nonusers. Eleven young women served as a control group for the cognitive age effect (age range 20-26 years, mean age 23.1 years, SD=1.6). The subjects spent four consecutive nights at the sleep laboratory and were exposed to acute sleep deprivation of 40 h. Measures of attention (reaction speed and vigilance), alertness, and mood were administered every 2 h during the daytime and every hour during the sleep deprivation night. Postmenopausal women performed slower than young controls, whereas young controls made more errors. In HT users, the recovery night did not fully restore the performance in the simple and two-choice reaction time tasks, but in nonusers it did so. Sleep deprivation had a detrimental, yet reversible effect on vigilance in all groups. In all groups, sleepiness started to increase after 15 h of sleep deprivation and remained elevated in the morning after the recovery night. Prolonged wakefulness or HT had no effect on mood. In conclusion, sleep deprivation impaired cognitive performance in postmenopausal as well as young women. Postmenopausal women kept up their performance at the expense of reaction speed and young women at the expense of accuracy. One night was not enough for HT users to recover from sleep deprivation. Thus, HT gave no benefit in maintaining the attention and alertness during sleep deprivation.

Adult↗