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PubMed2002

Sleep deprivation decreases superoxide dismutase activity in rat hippocampus and brainstem.

Sleep deprivation by the disk-over-water technique results in a predictable syndrome of physiological changes in rats. It has been proposed that reactive oxygen species (ROS) may be responsible for some of these effects. A variety of antioxidative enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GPx) help to regulate the level of ROS. In this study we investigated the effects of prolonged (5-11 days) sleep deprivation on the activities of SOD and GPx as well as the metabolic activity of the mitochondria (using alamar blue) in several brain regions (cortex, hippocampus, hypothalamus, brainstem and cerebellum). We show that prolonged sleep deprivation significantly decreased Cu/Zn-SOD activity in the hippocampus and brainstem, suggesting an alteration in the metabolism of ROS resulting in oxidative stress.

Animals↗

PubMed1980

Adrenocortical and gonadal steroids during sleep deprivation.

Twelve healthy males were exposed to 48 hr of sleep deprivation under conditions of strictly controlled activity and of food and drink intake. During the experiment the subjects were isolated from external time cures, i.e. no daylight, clocks, etc. Plasma samples were obtained before and at the end of the vigil, as well as after 5 days of recovery. Samples were analyzed for adrenal and gonadal steroid hormones and for follicle-stimulating (FSH) and luteinizing hormones (LH). The levels of all unconjugated steroids studied (cortisol, 17-hydroxypregnenolone, 17-hydroxyprogesterone, androstenedione, dihydrotestosterone) were significantly lower at the end of the sleep deprivation period. Self-ratings of fatigue were significantly higher at the end of the deprivation period. After recovery, all values returned to base line. No changes were observed in the levels of FSH, LH, or most conjugated steroids. It was concluded that the results were not consistent with the view that sleep deprivation induces an emergency reaction with increased activation, but rather that it results in lower levels of both psychological and physiological activation.

17-alpha-Hydroxypregnenolone↗

PubMed2006

Effect of creatine supplementation and sleep deprivation, with mild exercise, on cognitive and psychomotor performance, mood state, and plasma concentrations of catecholamines and cortisol.

RATIONALE: Sleep deprivation has a negative effect on cognitive and psychomotor performance and mood state, partially due to decreases in creatine levels in the brain. Therefore, creatine supplementation should lessen the negative effects of sleep deprivation. OBJECTIVES: The objective of this study was to examine the effect of creatine supplementation and sleep deprivation, with mild exercise, on cognitive and psychomotor performance, mood state, and plasma concentrations of catecholamines and cortisol. METHOD: Subjects were divided into a creatine group (n=10) and a placebo group (n=9). They took 5 g of creatine monohydrate or a placebo, dependent on their group, four times a time a day for 7 days, immediately prior to the experiment. The study was double blind. Subjects undertook tests of random movement generation (RMG), verbal and spatial recall, choice reaction time, static balance and mood state pre-test (0 h), after 6, 12 and 24 h of sleep deprivation, with intermittent exercise. They were tested for plasma concentrations of catecholamines and cortisol at 0 and 24 h. RESULTS: At 24 h, the creatine group demonstrated significantly less change in performance from 0 h (delta) in RMG, choice reaction time, balance and mood state. There were no significant differences between groups in plasma concentrations of catecholamines and cortisol. Norepinephrine and dopamine concentrations were significantly higher at 24 h than 0 h, but cortisol were lower. CONCLUSIONS: Following 24-h sleep deprivation, creatine supplementation had a positive effect on mood state and tasks that place a heavy stress on the prefrontal cortex.

Adult↗

PubMed1993

Caffeine reversal of sleep deprivation effects on alertness and mood.

This study assessed the ability of high doses of caffeine to reverse changes in alertness and mood produced by prolonged sleep deprivation. Fifty healthy, nonsmoking males between the ages of 18 and 32 served as volunteers. Following 49 h without sleep, caffeine (0, 150, 300, or 600 mg/70 kg, PO) was administered in a double-blind fashion. Measures of alertness were obtained with sleep onset tests, the Stanford Sleepiness Scale (SSS), and Visual Analog Scales (VAS). Sleep deprivation decreased onset to sleep from a rested average of 19.9 min to 7 min. Following the highest dose of caffeine tested, sleep onset averaged just over 10 min; sleep onset for the placebo group averaged 5 min. Scores on the SSS increased from a rested mean of 1.6-4.8 after sleep deprivation. Caffeine reduced this score to near rested values. Caffeine reversed sleep deprivation-induced changes in three subscales of the POMS (vigor, fatigue, and confusion) and produced values close to fully rested conditions on several VAS. Serum caffeine concentrations peaked 90 min after ingestion and remained elevated for 12 h. This study showed that caffeine was able to produce significant alerting and long-lasting beneficial mood effects in individuals deprived of sleep for 48 h.

Adolescent↗

PubMed2001

Slow-release caffeine as a countermeasure to driver sleepiness induced by partial sleep deprivation.

The effect of partial sleep deprivation (PSD) on driving abilities, as measured with a driving simulator, and the value of slow-release caffeine as a countermeasure to the expected performance decrements, were studied. Twelve subjects, between 20 and 25 years of age, underwent four experimental conditions, 4.5 or 7.5 h time in bed (TIB) with 300 mg slow-release caffeine or placebo, according to a Latin square design. Driving performance was measured twice by a 45-min driving task on a simulator. Subjective sleepiness/alertness and mood were assessed four times, by means of the Stanford Sleepiness Scale (SSS) and Profile of Mood States (POMS). After 4.5 h as compared with 7.5 h TIB lane drifting and speed deviation were higher, but only the effect on the first variable reached significance. In the placebo condition at 13.00 h, accident liability increased after PSD. Subjective sleepiness was higher in the 4.5 h TIB group. Caffeine intake gave rise to a decrease in lane drifting and after PSD it led to a smaller speed deviation and accident liability. The findings suggest that a lack of sleep can lead to a significant driving performance impairment, with drivers having problems to maintain an appropriate road position and a posted speed and more drivers getting involved in an accident. Secondly, the results indicate that caffeine - more specifically slow-release caffeine - can serve as a valuable countermeasure to these performance decrements, in the absence of any important side-effects, especially when its application is of an acute nature and when there is no opportunity to take a nap.

Adult↗

PubMedDate not supplied

Sleep deprivation in the rat by the disk-over-water method.

Chronic sleep deprivation may be required to reveal the most serious physiological consequences of sleep loss, but it usually requires strong stimulation which can obscure the interpretation of effects. The disk-over-water method permits chronic sleep deprivation of rats with gentle physical stimulation that can be equally applied to yoked control rats. A series of studies with this method has revealed little or no pathology in the control rats. The deprived rats show a reliable syndrome that includes temperature changes (which vary with the sleep stages that are lost); heat seeking behavior; increased food intake; weight loss; increased metabolic rate; increased plasma norepinephrine; decreased plasma thyroxine; an increased triiodothyronine-thyroxine ratio; and an increase of an enzyme which mediates thermogenesis by brown adipose tissue. The temperature changes are attributable to excessive heat loss and an elevated thermoregulatory setpoint, both of which increase thermoregulatory load, and the other changes are interpretable as responses to this increased load. This pattern indicates that sleep serves a thermoregulatory function in the rat. The sleep deprived rats also show stereotypic ulcerative and hyperkeratotic lesions localized to the tail and plantar surfaces of the paws, and they die within a matter of weeks; the mediation of these changes is unresolved.

Animals↗

PubMed1978

Sleep deprivation and circadian rhythm in depression.

The effect of total sleep deprivation for one night on the depressive state (measured using the depression rating scale of Bojanovsky and Chloupkova) and the patients' actual state of well being (measured using the self-rating scale of von Zerssen) is investigated in a group of 40 randomly selected inpatient depressives (29 endogenous depressives, 11 neurotic depressives) over a period of 36 h. The endogenous depressives exhibited a statistically significant change. The total index of the depression scale improved by 22.6%, recorded as a 'daily mean difference'. The individual symptoms of depressive mood, lack of interest, inhibition and inappetence were significantly improved. The feature of vital disorders and its common appearance with diurnal variations correlates positively with the degree of sleep deprivation effect. The symptomatology of the neurotic depressive patients also showed a significant improvement but the relatively small group of particularly severe neurotic depressives who also exhibited vital disorders is not representative. In a group of cases, sleep deprivation caused reversion in the depressive symptomatology not only during the night of deprivation but influenced the diurnal rhythm of the depressive symptomatology on the following day, in a therapeutically favourable direction. The results are compared with those of other studies. The methodological problems are discussed and methodological improvements for further investigation are proposed.

Adjustment Disorders↗

PubMed2003

Dopamine receptor D2 and D3 gene variants are not associated with the antidepressant effect of total sleep deprivation in bipolar depression.

Total sleep deprivation (TSD) is an effective treatment for mood disorders that is thought to act through an enhancement in several neurotransmitter pathways including dopaminergic transmission. Genetic factors are likely to play a major role in determining individual differences in TSD response. The aim of this study is to investigate the influence of dopamine receptor D3 (DRD3) and dopamine receptor D2 (DRD2) variants on TSD antidepressant efficacy in bipolar disorder. One hundred twenty-four depressed inpatients affected by bipolar disorder (DSM-IV) were treated with TSD and were genotyped for DRD3 first exon Gly/Ser variants and DRD2 codon 311 Ser/Cys variants using polymerase chain reaction techniques. DRD3 and DRD2 variants were not associated with TSD outcome. Consideration of possible stratification effects such as gender, age at onset and duration of illness did not reveal any association either. The tested gene variants are not a main factor influencing TSD outcome in bipolar disorder.

Adult↗

PubMed2000

Effects of sleep deprivation on daytime sleepiness in primary insomnia.

STUDY OBJECTIVES: This study investigated changes in MSLT scores and recovery sleep following total sleep deprivation in subjects with insomnia as compared to normal sleepers. DESIGN: Matched-groups design. SETTING: A sleep disorders center in a large medical center. PARTICIPANTS: Ten individuals with psychophysiological insomnia and ten age- and sex-matched normal sleepers served as subjects. INTERVENTIONS: Subjects underwent total sleep deprivation after baseline polysomnography and MSLT. A post-deprivation MSLT was obtained, as well as polysomnography on the recovery night and an MSLT after the recovery night. MEASUREMENTS AND RESULTS: Both groups showed significant decreases in MSLT scores following total sleep deprivation, as compared to baseline. Both groups had significantly shorter scores on a nighttime MSLT compared to a daytime MSLT. The insomnia group also showed a significant increase in total sleep time on the recovery night compared to baseline. CONCLUSIONS: The MSLT is sensitive to changes in sleepiness associated with total sleep deprivation in individuals with primary insomnia.

Adult↗

PubMed1989

Observed behavior as a predictor of the response to sleep deprivation in depressed patients.

Total sleep deprivation (TSD) in depressive patients is known to produce sudden changes in mood, but the factors involved in these mood changes are poorly understood. In this study the role of psychomotor activation was investigated by examining the relationships between baseline measures of activation and subsequent clinical response to TSD. Two methods were used to assess the degree of activation: global judgment (clinical ratings) and direct observation and registration of behavior (ethological methods). Behavioral and global assessments took place 1 day before TSD during a medication-free psychiatric interview. The amount of looking displayed during the interview was negatively correlated with the subsequent clinical response to TSD, while body- and object-touching hand movements showed a positive correlation. During switches from speaking turn and at the start of the patients' speaking turn, responders to TSD showed more hand movements than nonresponders. No relation was found between clinical ratings of the degree of psychomotor activation and the TSD response. Our data suggest that the clinical response to TSD may be predicted and therefore possibly mediated by dimensions of activation. For the detection of these dimensions, behavioral observation appears to be more suitable than global clinical judgment.

Adult↗

PubMed2004

Sleep deprivation does not affect operative results in cardiac surgery.

BACKGROUND: There has been an increasing trend towards the mandatory reduction in work hours for physicians because of the fear that sleep-deprived (SD) surgeons are more prone to make mistakes. We hypothesized that sleep deprivation would not be associated with increased morbidity or mortality in cardiac operations. METHODS: A retrospective review was done of all cases performed by all attending cardiac surgeons from January 1994 to April 2003. Complication rates of cases performed by SD surgeons were compared with cases done when the surgeons were not sleep-deprived (NSD). A surgeon was deemed sleep deprived if he or she performed a case the previous evening that started between 10:00 pm and 5:00 am, or ended between the hours of 11:00 pm and 7:30 am. RESULTS: A total of 6,751 cases were recorded in the Society of Thoracic Surgeons database over the 9-year period examined. Of these, 339 cases (5%) were performed by SD surgeons, and 6,412 (95%) cases were performed by NSD surgeons. Mortality rates for coronary artery bypass operations showed no significant differences (1.7% [SD = 4/223] vs 3.1% [NSD = 133/4206)] p = 0.34). Operative (p = 0.47), pulmonary (p = 0.60), renal (p = 0.93), neurologic (p = 0.11), and infectious (p = 0.87) complications of all cases also failed to show any statistically significant differences in any group. Perfusion times, cross-clamp times, and the use of blood products were also similar between groups. CONCLUSIONS: Sleep deprivation does not affect operative morbidity or mortality in cardiac surgical operations. These data do not support a need for work hour restrictions on surgeons.

Adult↗

PubMed1984

Exercise in a cold environment after sleep deprivation.

Seven subjects exercised to thermal comfort in a cold environment (O degrees C, 2.5 m X s-1) after normal sleep (control) and following a 50-h period of sleep deprivation. Resting core temperature (rectal) taken before the subject entered the cold environment was significantly lower (-0.5 degrees C, P less than 0.05) following the 50-h period of wakefulness. However, rectal temperature was not different after 15 min of exercise during the two exposures, suggesting that the subjects stored heat more rapidly during the first 15 min of exercise after sleep deprivation. No significant differences in self-chosen exercise intensity, significant differences in self-chosen exercise intensity, heart rate, metabolic rate, or exercise time were evident between the control and sleep deprived exposures. Fifty hours of sleep deprivation failed to alter the core temperature response during exercise in severe cold stress, and subjects chose identical work rates to minimize fatigue and cold sensation. The results suggest that the 50-h sleep deprivation period was not a true physiological stress during exercise in a cold environment. (Supported by Contract #DAMD 17-81-C1023.)

Adult↗

PubMed1990

The effects of total sleep deprivation and subsequent treatment with clomipramine on depressive symptoms and sleep electroencephalography in patients with a major depressive disorder.

In the present study patients with a major depressive disorder were first subjected to total sleep deprivation (TSD) and then treated with clomipramine. Sleep electroencephalography (EEG) was registered prior to and after TSD, during the 2 initial nights of antidepressive treatment and after 19 days. A negative correlation between response to TSD and clomipramine was found. TSD did not differentially influence the sleep EEG (responders vs nonresponders): responders tended, however, to show a more classical depressive sleep pattern prior to TSD. Clomipramine profoundly suppressed rapid eye movement (REM) sleep; the amount of initial REM sleep reduction, however, did not correlate significantly with therapy response after 3 weeks of treatment.

Adolescent↗

PubMed1993

Mania following sleep deprivation.

A first episode of mania is described in a previously healthy man who was partially sleep deprived for four nights. The sleep deprivation preceded the psychosis. During the psychotic episode he believed that he was the Messiah. This case is discussed in the light of reports exploring the relationship between psychosis and sleep deprivation.

Adult↗

PubMed2006

'One night' sleep deprivation stimulates hippocampal neurogenesis.

Neurogenesis in the adult hippocampus can be up- or downregulated in response to a variety of physiological and pathological conditions. Among these, dysregulation of hippocampal neurogenesis has been recently implicated in the pathogenesis of depression. In addition, in animal models of depression, a variety of antidepressant treatments reverse that condition by increasing neurogenesis. As one night sleep deprivation is known to improve mood in depressed patients for at least 1 day, we investigated whether a comparable treatment may affect hippocampal neurogenesis in adult rats. Accordingly, rats were sleep-deprived by gentle handling for 12 h during their physiological period of rest, and were injected with bromodeoxyuridine 4 h and 2 h before the end of sleep deprivation. They were then perfused immediately thereafter, or after 15 days and 30 days. We found that 12 h sleep deprivation significantly increased cell proliferation and the total number of surviving cells in the hippocampal dentate gyrus soon after sleep deprivation, as well as 15 days and 30 days later, in comparison to control rats allowed to sleep. No changes were instead found in the subventricular zone of the lateral ventricles, indicating that 12 h sleep deprivation selectively triggers neurogenic signals to the hippocampus. The present data include acute sleep deprivation among the conditions which upregulate hippocampal neurogenesis and raise the possibility that such response could be implicated in the beneficial effects elicited in depressed patients by one night sleep deprivation. Thus, the findings could contribute to the understanding of the intriguing relationship between depression and neurogenesis in the adult brain.

Animals↗

PubMed1994

Local sweating responses during recovery sleep after sleep deprivation in humans.

Changes in the central control of sweating were investigated in five sleep-deprived subjects (kept awake for 40 h) during their recovery sleep under warm ambient conditions [operative temperature (T(o)) was either 35 or 38 degrees C]. Oesophageal (T(oes)) and mean skin (Tsk) temperatures, chest sweat rate (msw,ch), and concomitant electro-encephalographic data were recorded. Throughout the night at 35 or 38 degrees C T(o), msw,ch changes were measured at a constant local chest skin temperature (Tch) of 35.5 degrees C. The results showed that body temperatures (T(oes) and Tsk) of sleep-deprived subjects were influenced by thermal and hypnogogic conditions. The msw,ch levels correlated positively with T(oes) in the subjects studied during sleep stage 1-2 (light sleep: LS), sleep stage 3-4 (slow wave sleep: SWS) and rapid eye movement (REM) sleep. Contrary to what has been reported in normal sleep, firstly, the T(oes) threshold for sweating onset differed between REM sleep and both LS and SWS, and, secondly, the slopes of the msw,ch versus T(oes) relationships were unchanged between REM and non-REM (i.e. LS or SWS) sleep. The changes observed after sleep deprivation were hypothesized to be due to alterations in the functioning of the central nervous system controller.

Adult↗

PubMed1994

Decreased muscarinic receptor binding in rat brain after paradoxical sleep deprivation: an autoradiographic study.

Previous work demonstrated that paradoxical sleep deprivation (PSD) leads to a decrease in yawning behavior elicited by cholinergic agonists, suggesting that a downregulation of cholinergic muscarinic receptors may occur after PSD. More recent work using intracerebral injections of muscarinic agonists has suggested a critical role for M2 receptors in paradoxical sleep. In this study [3H]AF-DX 384 was used to investigate the effects of PSD on M2-type cholinergic receptors throughout the brain using quantitative autoradiography. After 96 h of paradoxical sleep deprivation, [3H]AF-DX 384 binding was generally reduced throughout the brain, and significantly so in the olfactory tubercle (-20%), n. accumbens (-23%), frontal caudate-putamen (-16%), islands of Callejas (-20%), piriform cortex (-24%), lateral (-26%) and medial (-24%) septum, anteromedial (-19%), ventrolateral (-22%), and lateral geniculate (-15%) nuclei of thalamus, deep layers of the superior colliculus (-15%), entorhinal cortex (-12%) and subiculum (-23%). [3H]AF-DX 384 binding was reduced in pontine structures, but not to a higher degree than in other brain areas. The observed downregulation of M2-type muscarinic receptors after PSD may be causally related to the previously reported decrease in cholinergically induced behaviors after PSD.

Animals↗

PubMed1989

Changes in 24-hour urinary excretion of MHPG after four continuous nights of REM sleep deprivation in human volunteers.

Eight healthy volunteers were deprived of rapid eye movement (REM) sleep for 4 consecutive nights. Twenty-four-hour urine samples were collected to determine levels of 3-methoxy-4-hydroxyphenylglycol (MHPG) during basal, REM sleep deprivation, and REM recovery conditions. A control experiment was carried out in four subjects who were awakened in non-REM sleep for 4 consecutive nights. Subjects deprived of REM sleep showed significant MHPG increases on night 4 of sleep deprivation. MHPG levels in the control condition decreased, but not significantly. When MHPG levels in both experimental and control conditions were compared in the same four subjects, a significant difference was observed, indicating an effect of the control condition. Increased MHPG levels were related to REM sleep reduction and to the time and number of awakenings. Our findings seem to support an inverse homeostatic relationship between norepinephrine metabolism and REM sleep.

Adult↗