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Results for “SLEEP DEPRIVATION”

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PubMed2002

Complexity and non-linear description of diurnal cortisol and growth hormone secretory patterns before and after sleep deprivation.

OBJECTIVE: The circadian secretory profiles of cortisol and growth hormone (hGH) in normal subjects are interrelated. Slight alterations in cortisol secretion are paralleled by similar ones of hGH secretion. Under physiological conditions an inhibitory effect of glucocorticoids on hGH secretion is more potent than a stimulatory one, while in normal young subjects the nychtohemeral cortisol and hGH levels are lower and higher, respectively, post 24 hours total sleep-deprivation, compared to baseline values. The aim of the present work was to further assess the qualitative characteristics of the 24-hour secretory patterns of these two hormones before and after 24 hours total sleep deprivation, by studying their non-linear profiles using fractal analysis. METHODS: Cortisol and hGH were measured in 24-hour samples drawn from 10 healthy men (mean age SD: 24 +/- 1 yr, mean BMI SD: 25 +/- 1 kg/m2) before and after 24 hours total sleep deprivation. Twenty-four hour blood sampling was performed serially every 30 min the day before and the day after total sleep deprivation. The 24-hour hormone profiles were analyzed by Fourier spectrum, in order to verify periodicities; the corresponding attractors were drawn and their respective fractal dimensions were calculated using the box counting method. RESULTS: Diurnal cortisol levels before sleep deprivation gave rise to a fractal attractor with a D0 fractal dimension of 2.65 +/- 0.03, which decreased, post-sleep deprivation, to D0: 2.18 +/- 0.04. Growth hormone before sleep deprivation gave rise to a fractal attractor with a D0 dimension of 1.96 +/- 0.60, which increased to 2.24 +/- 0.60 post-sleep deprivation. These post-sleep deprivation changes of the fractal dimensions of cortisol and hGH, suggest that sleep deprivation leads to a more regular secretory profile of cortisol, while it tends to render hGH secretory profile less regular. Additionally, these changes of the fractal dimensions parallell the previously described quantitative overall changes of these hormones. CONCLUSIONS: The post-sleep deprivation decrease of cortisol fluctuation might reflect the mechanism by which sleep deprivation temporarily improves mood in melancholic depression, a condition associated with hyperactivity of the hypothalamic-pituitary-adrenal axis.

Adult↗

PubMed2004

Anxiogenic effect of sleep deprivation in the elevated plus-maze test in mice.

RATIONALE: Several clinical studies demonstrate that the absence of periods of sleep is closely related to occurrence of anxiety symptoms. However, the basis of these interactions is poorly understood. Studies performed with animal models of sleep deprivation and anxiety would be helpful in the understanding of the mechanisms underlying this relationship, but some animal studies have not corroborated clinical data, reporting anxiolytic effects of sleep deprivation. OBJECTIVES: The aim of the present study was to verify the effects of different protocols of sleep deprivation in mice tested in the elevated plus-maze and to assess the effect of chlordiazepoxide and clonidine. METHODS: Three-month-old male mice were sleep-deprived for 24 or 72 h using the methods of single or multiple platforms in water tanks. Mice kept in their home cages were used as controls. Plus-maze behavior was observed immediately after the deprivation period. RESULTS: Mice that were sleep-deprived for 72 h spent a lower percent time in the open arms of the apparatus than control animals. This sleep deprivation-induced anxiety-like behavior was unaffected by treatment with chlordiazepoxide (5.0 and 7.5 mg/kg IP), but reversed by an administration of 5 or 10 microg/kg IP clonidine. CONCLUSION: The results indicate that under specific methodological conditions sleep deprivation causes an increase in anxiety-like behavior in mice exposed to the elevated plus-maze.

Animals↗

PubMed1999

[Therapeutic sleep deprivation and phototherapy].

Since ancient times the influence of chronobiological factors on the pathogenesis, course, and treatment of depression has been well known. Amongst antidepressive treatment strategies two are based on chronobiological knowledge: therapeutic sleep deprivation, which exerts a rapid and dramatic, albeit usually short-lasting, improvement of mood in the majority of patients with major depressive disorder, and light therapy with full-spectrum bright light. About sixty percent of all depressed patients improve after a single night of total or partial sleep deprivation. It has been shown that a combination of pharmacotherapy with antidepressants and sleep deprivation is superior to pharmacotherapy alone. Moreover, sleep deprivation has proved to hasten the onset of action of antidepressant medication and repeated sleep deprivation can also be an efficient treatment strategy in drug refractory depression. Light therapy with bright artificial light is especially beneficial in patients with a fall/winter pattern of depressive symptomatology that has been termed seasonal affective disorder. Similar to sleep deprivation, bright light therapy is characterized by a fast onset of antidepressant action and by the exertion of additive properties to antidepressive medication. Bright light therapy, beginning in the morning after partial sleep deprivation, is able to prevent the depressive relapse after the next night of sleep in sleep deprivation responders.

Antidepressive Agents↗

PubMed2003

Increased turnover of Na-K ATPase molecules in rat brain after rapid eye movement sleep deprivation.

It has been shown that rapid eye movement (REM) sleep deprivation increases Na-K ATPase activity. Based on kinetic study, it was proposed that increased activity was due to enhanced turnover of enzyme molecules. To test this, anti-alpha1 Na-K ATPase monoclonal antibody (mAb 9A7) was used to label Na-K ATPase molecules. These labeled enzymes were quantified on neuronal membrane by two methods: histochemically on neurons in tissue sections from different brain areas, and by Western blot analysis in control and REM sleep-deprived rat brains. The specific enzyme activity was also estimated and found to be increased, as in previous studies. The results confirmed our hypothesis that after REM sleep deprivation, increased Na-K ATPase activity was at least partly due to increased turnover of Na-K ATPase molecules in the rat brain.

Animals↗

PubMed1983

[Effect of delta-sleep-inducing peptide and its analogs on the encephalogram of normal rabbits during sleep deprivation and on learning processes in the rat].

The delta-sleep-inducing peptide and its 10 analogues increased the total amount of slow oscillations in the rabbit EEG and shifted the spectrum towards the long-wave area. When comparing the EEGs of intact and sleep--deprived rats, the effect of delta-peptide was stronger in the latter animals. The learning of rats in U-shaped labyrinth before and after sleep deprivation suggested that delta-peptide improved the learning in sleep-deprived animals. Experiments with negative influences showed that the delta-peptide could be a protective anti-stress factor.

Animals↗

PubMed1989

Effects of sleep deprivation on cognitive ability and skills of pediatrics residents.

The stress and long working hours of medical residency have become the basis for controversy over whether current training structures and processes adversely affect residents' skills and well-being and the quality of patient care. The authors measured cognitive and skills performances of 45 sleep-deprived pediatrics residents by using questions like those on the pediatrics board certification examination and using patient-care tasks that required coordination and dexterity. The residents were randomly divided into two groups--one stayed awake for 24 hours, the other for 34 hours--and were tested on cognitive and skills performances before and after sleep deprivation. Sleep deprivation did not have a significant effect on cognitive performance. Of the three skills tested, the residents overall needed more time to perform umbilical artery catheterization, but the group deprived of sleep for 34 hours performed vein cannulation more quickly than the group deprived for 24 hours. Implications for these findings are discussed in the context of the ongoing controversy over the structure and process of medical education.

Animals↗

PubMed2003

Effect of sleep deprivation on saccades and eyelid blinking.

In this study the effect of sleep deprivation on specific components of eye and eyelid movement was investigated in a group of young and healthy subjects. The duration of sleep deprivation was 20 h. Each subject had to execute different saccade tasks: reflexive saccades, voluntary prosaccades and antisaccades. Saccade latency, number of saccade errors and blink rate during the saccade tasks were evaluated as predictors of performance decrements resulting from sleep deprivation. The present study showed no significant deterioration of latency and number of errors in the different saccade tasks. However, the blink rate was significantly higher after a night without sleep than before. It is concluded that the blink rate appears to be a promising psychophysical measurement and a more sensitive parameter than saccade performance to evaluate the effects of 20 h of sleep deprivation. These results encourage further research on this topic.

Adult↗

PubMedDate not supplied

[Characteristics of the functioning of the human hypophyseal-gonadal system during 1-time sleep deprivation].

The authors studied indices of the activity of the hypophyseogonadal system under the conditions of single sleep deprivation of 24-36 h duration and in the period of recovery. Eleven healthy men aged 21 to 26 were recruited in the study. Two series of investigations were performed: I--the examinees were studied before, after 24 h sleep deprivation and after the first recovery night; II--the scheme of investigation was identical but it included electroauriculopuncture 5-6 h after the start of sleep deprivation. The 24 h sleep deprivation was accompanied by an increase in ACTH and LH secretion, a decrease in the levels of STH, prolactin, total androgens and progesterone in the examinees' blood. On the whole, electroauriculopuncture optimized the activity of the hypophyseogonadal system expressed in lesser changes in the secretion of the above hormones in response to sleep deprivation.

Adaptation, Physiological↗

PubMed2006

Effects of sleep deprivation on cortical excitability in patients affected by juvenile myoclonic epilepsy: a combined transcranial magnetic stimulation and EEG study.

OBJECTIVE: To investigate the effect of sleep deprivation on corticospinal excitability in patients affected by juvenile myoclonic epilepsy (JME) using different transcranial magnetic stimulation (TMS) parameters. METHODS: Ten patients with JME and 10 normal subjects underwent partial sleep deprivation. Motor threshold (MT), motor evoked potential amplitude (MEP), and silent period (SP) were recorded from the thenar eminence (TE) muscles. Short latency intracortical inhibition (SICI) and short latency intracortical facilitation (SICF) were studied using paired magnetic stimulation. TMS was performed before and after sleep deprivation; EEG and TMS were performed simultaneously. RESULTS: In patients with JME, sleep deprivation induced a significant decrease in SICI and an increase in SICF, which was associated with increased paroxysmal activity. A significant decrease in the MT was observed. No significant changes in any TMS parameters were noted in normal subjects after sleep deprivation. The F wave was unchanged by sleep deprivation in both control subjects and in patients with JME. CONCLUSIONS: In patients with JME, sleep deprivation produces increases in corticospinal excitability in motor areas as measured by different TMS parameters.

Adolescent↗

PubMed2005

Effect of sleep deprivation on righting reflex in the rat is partially reversed by administration of adenosine A1 and A2 receptor antagonists.

BACKGROUND: Similarities between naturally occurring sleep and general anesthesia suggest that the two states may interact physiologically. The authors have previously demonstrated that sleep deprivation potentiates anesthetic-induced loss of righting reflex (LORR) in rats. One possible mediator for this effect is adenosine, which accumulates in the brains of sleep-deprived animals and reduces anesthetic requirements. The authors tested in rats the hypothesis that potentiating effects of sleep deprivation on LORR can be altered by adenosine A1 and A2a receptor antagonists. METHODS: Five experiments were conducted. In each, rats underwent four trials, consisting of a 24-h period of either sleep deprivation or ad libitum activity followed by administration of a fixed dose of an adenosine antagonist or vehicle. Rats were then given isoflurane, and the time to LORR and recovery were measured. Each experiment tested a specific dose of an A1 receptor antagonist (8-cyclopentyltheophylline given via microinjection into the basal forebrain), an A2a receptor antagonist (ZM241385 via intraperitoneal administration), or both. In each experiment, all rats received all combinations of activity and drug/vehicle, separated by 5-7 days. RESULTS: In rested rats, neither antagonist altered the time to LORR. In sleep-deprived rats, both ZM241385 and 8-cyclopentyltheophylline prolonged the time to LORR and shortened recovery in a dose-dependent manner. Prolongation also occurred when subtherapeutic doses of both agents were coadministered. CONCLUSION: Both antagonists partially reversed the effect of sleep deprivation on anesthetic action. This result implies that deprivation-induced changes in adenosine receptor activity can alter LORR. Neither antagonist completely reversed this effect, suggesting possible non-adenosine-mediated effects of sleep deprivation.

Adenosine A1 Receptor Antagonists↗

PubMed2002

A comparison of sleep deprivation and narcolepsy in terms of complex cognitive performance and subjective sleepiness.

OBJECTIVES: (i) To expose 'normal sleepers' to a 32-h sleep deprivation protocol and evaluate the impact of this deprivation on a complex performance task i.e. the paced auditory serial addition test (PASAT). (ii) To compare these sleep deprivation performance findings with historical data on the impact of sleepiness secondary to narcolepsy on PASAT performance measures. (iii) To investigate the recuperative effects of a brief nap period on both sleepiness and PASAT performance for the sleep-deprived subjects. (iv) To compare these post-nap effects with historical data relating to the impact of napping on both sleepiness and PASAT performance for subjects with narcolepsy. BACKGROUND: Previous research has demonstrated that sleepiness induced by sleep deprivation in normal sleepers may lead to cognitive impairment across a range of performance tasks. Sleepiness secondary to narcolepsy has also been noted to impair cognitive function especially for complex processing tasks. Direct comparison of the effects of sleepiness on performance between non-pathological and pathological sleepiness states is confounded, however, by methodological differences in research design especially in relation to levels of induced sleepiness and performance task selection. The purpose of the current study was to undertake a sleep deprivation study that achieved a methodological match with published data evaluating the impact of sleepiness on cognitive performance for subjects with narcolepsy. This methodological matching allowed for a more precise comparison of the impact of sleepiness on performance between non-pathological and pathological sleepiness groups. RESULTS: Normal sleepers required a 32-h deprivation protocol to develop a subjective level of sleepiness that equated with that identified by subjects with narcolepsy. This induced sleepiness in normal sleepers did not result in any significant decrement in complex performance, a finding that was in contrast to the performance decrement previously found in subjects with narcolepsy with equivalent subjective sleepiness ratings. A 20-min nap produced more improvement in both arousal and cognitive processing performance for the subjects with narcolepsy than for the current sleep-deprivation cohort. CONCLUSION: This study identified significant differences in the impact of sleepiness on complex performance between non-pathological sleep-deprived subjects and subjects with narcolepsy. This paper explores these differences in relation to the potential for both quantitative and qualitative differences that exist in the nature of sleepiness between non-pathological and pathological sleepiness states.

Journal Article↗

PubMed1983

Effects of sleep deprivation on signal detection measures of vigilance: implications for sleep function.

In an attempt to tease out the extent to which the performance decline during sleep deprivation might be due to a fall in the inherent capacity (d') of a subject, the parameters of the theory of signal detection were applied to auditory vigilance data obtained five times per 24 h during 60 h of continuous wakefulness. Eight subjects were exposed to both control and deprivation conditions in a balanced design. Oral temperature and self-assessed alert-drowsy reports were taken at three hourly intervals. The value of d' exhibited a significant stepwise decline during deprivation, falling sharply within the usual sleep period and levelling out during the daytime. Both temperature and self-assessment data exhibited clear circadian rhythms overlying the declines due to deprivation. The changes in d' were seen to be consistent with a brain "restitutive" role for sleep function.

Adult↗

PubMed1999

The acceptability of sleep-deprived electroencephalograms.

The aim of this study was to ascertain the acceptability of sleep-deprived EEGs to parents and their young child. Fifty unselected children having a sleep-deprived EEG were recruited. Data were collected from a sleep diary, a parent questionnaire and the request form of the EEG. Data collected covered developmental, learning and behavioural problems and the acceptability of the sleep-deprived EEG. There were 29 males (58%) in the study group. The average age was 8.6 years (range 2-17 years). Fifty percent of parents found it difficult to keep their child awake at night and 30% of parents found it difficult to wake their child in the morning. Fifty-four percent of parents reported their child had difficult behaviour on the day of the EEG. None had seizures provoked by sleep deprivation.

Adolescent↗

PubMed1992

Sleep deprivation and impaired cognition. Possible role of brain catecholamines.

To assess the role of brain catecholamines in cognitive decline associated with sleep deprivation, 40 healthy male volunteers were randomized to conditions of total sleep deprivation or 40.5 h of rest. Within each sleep condition, subjects were further randomized to treatment with a 2-day regimen of placebo or alpha-methyl-para-tyrosine (AMPT), a catecholamine synthesis inhibitor. Cognitive performance was measured repeatedly over time using a computerized performance assessment battery. Treatment with AMPT or treatment with sleep deprivation increased sleepiness without producing marked or consistent deterioration in performance. By contrast, subjects who received both treatments reported greater sleepiness than those receiving either treatment alone, and developed severe cognitive impairment on a variety of tasks. These findings, along with previous evidence that catecholamine-enhancing drugs improve performance in sleep-deprived individuals, support the view that decline in cognitive performance during sleep deprivation may be mediated by brain catecholamines.

Adult↗

PubMed1982

[The value of EEG after sleep deprivation for the diagnosis of epileptic seizures, epilepsy and other cerebral disorders].

114 electroencephalographic and 49 clinical criteria of 1010 patients, including 64 healthy volunteers, were evaluated by means of a computer. In 549 patients with epileptic seizures spike wave (sw) paroxysms were seen in 13.3%. Following a 24-hour period of sleep deprivation sw paroxysms were present in 24.2% cases which represents an increase of 82.0%. The number of cases with focal discharges increased in this group from 21.3% initially to 27.5% after sleep deprivation, representing an increase of only 29.1%. The percentage increase in sw paroxysms and focal discharges following sleep deprivation was approximately as marked also in patients without epileptic seizures, so that sleep deprivation was found to be equally useful in patients with non-epileptic cerebral disorders. The rate of activation is higher in children and juveniles than in adults. Similarly, it is higher in patients with awaking epilepsy than in patients with sleep epilepsy. The influence of sleep deprivation and that of sleep, respectively, upon the provocation of EEG changes was not sharply differentiated. By counting sw paroxysms in the EEG before sleep deprivation, in the waking EEG following sleep deprivation, as well as in the subsequent sleeping EEG further evidence was obtained, however, supporting the suggestion that special significance may be attributed to sleep deprivation as a provocation method. If the activation of sw paroxysms and focal changes is related to sleep and sleep stages it can be shown that their frequency decreases from stage 1 to stage 4. In particular, the short fluctuations in vigilance, the waking reactions frequently occurring under routine laboratory conditions and the transitions between sleep stages were seen to assume trigger functions.

Adolescent↗

PubMed2002

Paradoxical sleep deprivation increases plasma endothelin levels.

The endothelins (ET-1, 2 and 3) constitute a family of 21 amino acid peptides with potent biological activities. ET-1 is one of the most potent endogenous vasoconstrictors so far identified and its increased concentration in plasma appears to be closely related to the pathogenesis of arterial hypertension as well as to obstructive sleep apnea (OSA). OSA patients exhibit repetitive episodes of apnea and hypopnea that result in hypoxia and consecutive arousals. These patients are chronically sleep deprived, which may aggravate the hypertensive features, since literature data show that sleep deprivation results in hypertension both in humans and in animals. Based on the reported relationship between ET-1, hypertension and sleep deprivation consequences, the purpose of the present study was to determine plasma ET concentrations in paradoxical sleep-deprived animals. Male Wistar rats, 3 to 4 months old (N = 10 per group), were deprived of sleep for 24 and 96 h by the platform technique and plasma ET-(1/2) was measured by radioimmunoassay. Analysis of plasma revealed that 96 h of sleep deprivation induced a significant increase in ET-(1/2) release (6.58 fmol/ml) compared to control (5.07 fmol/ml). These data show that sleep deprivation altered plasma ET-(1/2) concentrations, suggesting that such an increase may participate in the genesis of arterial hypertension and cardiorespiratory changes observed after sleep deprivation.

Analysis of Variance↗

PubMed2006

Sex differences in sleep: the response to sleep deprivation and restraint stress in mice.

STUDY OBJECTIVES: Numerous clinical studies and sleep surveys have shown pronounced sex differences in the occurrence of insomnia and other sleep pathologies. It has been suggested that sex differences in sleep, while subtle under baseline conditions, may increase in magnitude under biological or environmental challenges. However, controlled and experimental studies on sleep under challenged conditions rarely include female subjects. In this context, we examined sex differences in sleep in the mouse, not only under baseline conditions, but also after sleep deprivation and restraint stress. DESIGN: Adult male and female C57BL/6J mice were implanted with electrodes to record sleep-wake architecture and sleep electroencephalogram under baseline conditions and after 6 hours of sleep deprivation or 1 hour of restraint stress at the beginning of the daily light phase. RESULTS: Although baseline sleep patterns slightly differed between the sexes, the homeostatic recovery response to sleep deprivation was similar. In contrast, the changes in sleep after restraint stress were markedly different between male and female mice, with males displaying a stronger initial suppression of sleep and a stronger rebound of rapid-eye-movement sleep later in the recovery phase. CONCLUSIONS: In mice, the fundamental homeostatic properties of sleep regulation may not differ between the sexes, but the way sleep is affected and disrupted by environmental influences may be sex dependent. The latter may reflect sex differences in stress sensitivity.

Animals↗

PubMed1987

Sleep deprivation and cardiorespiratory function. Influence of intermittent submaximal exercise.

The effects of 64 h of sleep deprivation upon cardiorespiratory function was studied in 11 young men (VO2max = 55.5 ml kg-1 min-1, STPD). Six subjects engaged in normal sedentary activities, while the others walked on a treadmill at 28% VO2max for one hour in every three; eight weeks later, sleep deprivation was repeated with a crossover of subjects. Immediate post-deprivation measurement of VO2max showed a small but statistically significant decrease (-3.8 ml min-1 kg-1, STPD), with no difference between exercise and control trials. The final decrement in aerobic power was not due to a loss of motivation, as 88% (21 of 24) of post-deprivation tests still showed a plateau of VO2max; in addition, terminal heart rates (198 vs 195 beats min-1), respiratory exchange ratios (1.14 vs 1.15) and blood lactate levels (12.1 vs 11.8 mmol l-1) were not significantly different after sleep deprivation. The decrease in VO2max was associated with a lower VEmax (127 vs 142 l min-1, BTPS) and a substantial haemodilution (13%). Physiological responses to sub-maximal exercise showed persistence of the normal diurnal rhythm in heart rate and oxygen consumption, with no added effects due to sleep deprivation. However, ratings of perceived exertion (Borg scale) increased significantly throughout sleep deprivation. The findings are consistent with a mild respiratory acidosis, secondary to reduced cortical arousal and/or a progressive depletion of tissue glycogen stores which are not altered appreciably by moderate physical activity.

Adult↗