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PubMedDate not supplied

Effect of epilepsy and sleep deprivation on the rate of benign epileptiform transients of sleep.

Seventy-eight individuals with EEG records containing benign epileptiform transients of sleep (BETS) were identified among 7,400 records reviewed in our laboratory in a 6-year period. The records contained no other abnormality in 51 patients (65%). Genuine epileptiform discharges were found in the records of 19 patients; 14 had a history of epilepsy. Thirty-five patients (45%) had a proven history of epilepsy with antiepileptic drug (AED) therapy. In the records of these patients, the mean number of BETS per unit of time was significantly higher (11.88 +/- 2) than in the record of the rest of the laboratory population with BETS (6.89 +/- 0.9) (p less than 0.02). Among five conventional surface montages, ipsilateral ear referential montage (IERM) showed a significantly higher number of BETS per unit of time than did any other surface montage used in the study. Thirty-nine records (50%) were performed after sleep deprivation (SD). When only IERM was considered, SD records showed a significantly higher number of BETS per unit of time (7.36 +/- 1.1) than did non-SD records (3.89 +/- 0.69) (p less than 0.01). Our findings support the general consensus that individual BETS may be normal variants, but a high occurrence of BETS in the record should raise suspicion of underlying epilepsy.

Adolescent↗

PubMed1984

Epileptic seizures in alcoholism and diagnostic value of EEG after sleep deprivation.

Alcoholism and epileptic seizures frequently coincide. Two groups can be distinguished clinically and by EEG. In one group (group I), seizures occur only during a period of alcohol withdrawal or partial withdrawal and can only be explained because of alcoholism in the history of the patient. In the other group (group II), seizures occur spontaneously, as well as during alcohol withdrawal, and epileptogenic factors (residual brain damage, former epileptic seizures, and a family history of seizures) probably play an important role in the manifestation of the seizures. Paroxysms or focal abnormalities are rarely seen in group I; in group II, EEG abnormalities are seen approximately as frequently as in other epileptic conditions. Both groups were examined to determine the extent of their EEG abnormalities after 24 h of sleep deprivation. Before and after sleep deprivation, only 4% of 52 chronic alcoholic patients without epileptogenic risk factors had EEG foci. Of the 52, 2% before sleep deprivation and 8% after sleep deprivation had generalized paroxysms. Of 128 chronic alcoholic patients with additional epileptogenic factors, 19% before sleep deprivation and 24% after sleep deprivation had EEG foci, and 17% before and 28% after sleep deprivation had generalized paroxysms. The pathogenesis of epileptic seizures in both groups and the therapeutic consequences are discussed.

Adult↗

PubMed1981

Effects of sleep deprivation on depressed patients of different nosological groups.

In a study of 80 patients who received 164 treatments with sleep deprivation, the following questions were addressed: Do depressive patients of different subgroups respond differently to sleep deprivation? what complications arise? does the same patient react in the same way to multiple treatments? are there differences between responders and nonresponders? Results indicate that: (1) Endogenous depressions (unipolar, bipolar, and involutional) and psychotic depressions in schizophrenic patients improve significantly the day after sleep deprivation. However, on the second day, after a night's recovery sleep, a significant improvement occurs in neurotic depressives, whereas the endogenous and psychotic depressions worsen again. (2) Schizophrenic patients with a postpsychotic depression respond as well to sleep deprivation as patients with bipolar depression. (3) Complications arise very rarely in sleep deprivation therapy. (4) Patients in all the diagnostic categories studied can respond very differently to multiple treatments with sleep deprivation. (5) Responders and nonresponders do not differ in age, sex, or psychopathological state before sleep deprivation, and psychotropic drugs have no apparent effect on the therapeutic response.

Adult↗

PubMed2004

Sleep deprivation, energy expenditure and cardiorespiratory function.

Participants in the sport of adventure racing often choose to go without sleep for a period of greater than 24 h while partaking in prolonged submaximal exercise. This study examined the effect of 30 h of sleep deprivation and intermittent physical exercise, on the cardiorespiratory markers of submaximal exercise in six subjects. Six subjects with the following physical characteristics participated in the study (mean +/- SD): age 22 +/- 0.3 years, height 180 +/- 5 cm, body mass: 77 +/- 5 kg, VO2peak 44 +/- 5 ml. kg (-1). min (-1). Three subjects engaged in normal sedentary activities while three others cycled on a cycle ergometer at 50 % VO2peak for 20 min out of every two hours during thirty hours of sleep deprivation. One week later sleep deprivation was repeated with a cross over of subjects. Every four hours, subjects completed assessments of cardiorespiratory function during 50 % VO2peak cycling. A 3 x 8 repeated measures ANOVA revealed a significantly lower heart rate with sleep deprivation (p < 0.05), but no other significant effects (p > 0.05) on respiratory gas exchange variables. Neither sleep deprivation, nor a combination of sleep deprivation and five hours of moderate intensity cycling, appear to be limiting factors to the physiological capacity to perform submaximal exercise.

Adult↗

PubMed1996

Age-dependent suppression of nocturnal growth hormone levels during sleep deprivation.

Although the major daily peak in plasma growth hormone (GH) level normally occurs during the early part of nocturnal sleep, it is known that in about one quarter of young healthy men, peaks in circulating human GH occur before sleep onset. Possible factors associated with these nocturnal peaks were investigated in the absence of sleep, including subjectively defined sleepiness, electroencephalographically defined drowsiness and short lapses into sleep, measures of cortisol and temperature. Healthy men between the ages of 20 and 34 years were studied in a between-subjects design, 16 assigned to a sleep deprivation group, and 16 age matched and assigned to a group permitted to sleep. The average GH peak level in the sleeping subjects was 19.9 micrograms/l (+/- 8.4 SD). In the sleep-deprivation group there was a wide range of nocturnal GH patterns, from no detectable rise to normal nocturnal levels (average peak of 10.5 +/- 10.0 micrograms/l). Within the narrow age range sampled, age, body mass index, temperature and cortisol failed to predict nocturnal GH peak in the sleeping group, but regression analysis found age to be a significant negative predictor of nocturnal GH peak level in sleep-deprived subjects. All sleep-deprived subjects who had peak GH levels over 7 micrograms/l were 24 years of age or less. Subjective sleepiness and electroencephalographically defined drowsiness failed to predict either the peak level of GH during sleep deprivation or the cumulative amount measured across the night. These results suggest that the well-known suppressive effect of sleep deprivation on GH secretion is an age-dependent phenomenon which evolves during early adulthood.

Adult↗

PubMed2002

Short-term homeostasis of REM sleep assessed in an intermittent REM sleep deprivation protocol in the rat.

An intermittent rapid eye movement (REM) sleep deprivation protocol was applied to determine whether an increase in REM sleep propensity occurs throughout an interval without REM sleep comparable with the spontaneous sleep cycle of the rat. Seven chronically implanted rats under a 12 : 12 light-dark schedule were subjected to an intermittent REM sleep deprivation protocol that started at hour 6 after lights-on and lasted for 3 h. It consisted of six instances of a 10-min REM sleep permission window alternating with a 20-min REM sleep deprivation window. REM sleep increased throughout the protocol, so that total REM sleep in the two REM sleep permission windows of the third hour became comparable with that expected in the corresponding baseline hour. Attempted REM sleep transitions were already increased in the second deprivation window. Attempted transitions to REM sleep were more frequent in the second than in the first half of any 20-min deprivation window. From one deprivation window to the next, transitions to REM sleep changed in correspondence to the amount of REM sleep in the permission window in-between. Our results suggest that: (i) REM sleep pressure increases throughout a time segment similar in duration to a spontaneous interval without REM sleep; (ii) it diminishes during REM sleep occurrence; and (iii) that drop is proportional to the intervening amount of REM sleep. These results are consistent with a homeostatic REM sleep regulatory mechanism that operates in the time scale of spontaneous sleep cycle.

Activity Cycles↗

PubMedDate not supplied

Sleep deprivation and resident performance.

Cognitive and complex motor performance may be impaired by extended sleep deprivation, but objective data concerning the effects in residents of the sleep deprivation engendered by usual hospital on-call schedules are scant and conflicting. We studied three cohorts of surgical residents (N = 26) who were on call every other night. Each resident kept a sleep diary, gave a self-assessment of motivation and fatigue, and underwent a battery of psychometric tests each morning for 18 or 19 days. The psychometric tests measured cognition, discernment, visual and auditory vigilance, and rapid eye-hand coordination. Sleep deprivation was defined as the lack of four hours of continuous sleep during the preceding 24 hours, and it occurred during 89% of the on-call nights. Daily testing in a repeated-measures design allowed each participant to serve as his or her own control. Sleep deprivation did not affect overall cognitive or motor performance. Further analysis of the correlation between sleep parameters (total sleep and longest uninterrupted sleep interval) and performance on each component of the psychometric test battery identified changes in performance on some tests but only trivial effects due to sleep. The assumption that sleep deprivation associated with usual on-call schedules impairs cognitive and motor performance of residents such that clinical care of patients may be compromised is not supported by our observations.

Adult↗

PubMed2004

Uncoupling proteins and sleep deprivation.

In both humans and animals sleep deprivation (SD) produces an increase in food intake and in energy expenditure (EE). The increase in EE is a core element of the SD syndrome and, in rats, is negatively correlated with survival rate. However, the mechanisms involved are not understood. A large component of resting EE is accounted for by the mitochondrial proton leak, which is mediated by uncoupling proteins (UCPs). We measured UCP2, UCP3, and UCP5 mRNA levels in rats during the spontaneous sleep/waking cycle and after short (8 hours) and long (7 days) SD. During spontaneous sleep and waking there was no change in the level of mitochondrial uncoupling as measured by UCPs expression, either in the brain or in peripheral tissues. During SD, by contrast, UCP3 expression in skeletal muscle was elevated, but the increase was similar, compared to sleep, after both short-term and long-term SD. UCP2 expression, on the other hand, was strongly increased in the liver and skeletal muscle of long-term sleep deprived animals and much less so, or not at all, in yoked controls or in rats that lost only 8 hours of sleep. Since the skeletal muscle is the largest tissue in the body, an elevated muscular expression of UCP2 is likely to affect the overall resting EE and may thus contribute to its increase after SD.

Animals↗

PubMed2006

Sleep deprivation and hormone therapy in postmenopausal women.

BACKGROUND AND PURPOSE: Sleep complaints increase after menopause, but literature on the effect of postmenopausal hormone therapy (HT) on sleep is controversial. The purpose of this study was to determine the effect of ageing and HT on sleep quality, assessed using polysomnography, and on the accuracy of the subjective estimation of sleep quality in women before and after sleep deprivation. PATIENTS AND METHODS: Twenty postmenopausal women (aged 58-72 years) were recruited: 10 HT-users and 10 non-HT-users. Eleven young women (aged 20-26 years) served as controls. Polysomnography and subjective sleep quality were measured on four consecutive nights: adaptation, baseline, 40-h sleep deprivation and recovery. RESULTS: Although the postmenopausal women slept worse than the controls at baseline, and in particular during the recovery night, their recovery response to sleep deprivation was well preserved. At baseline, HT-users had a shorter latency to rapid eye movement (REM) (P=0.043), with fewer awakenings from slow wave sleep (SWS) (P=0.029) but more from REM (P=0.033) than non-HT-users. During recovery, the HT-users had more stage 2 sleep (P=0.048) and less slow wave activity (SWA) in the first non-rapid eye movement (NREM) sleep episode (P=0.021) than the non-HT-users. The poor correlation between subjective and objective sleep quality at baseline became significant during recovery. CONCLUSIONS: Although sleep in postmenopausal women was worse than in young controls, the recovery response following sleep deprivation was relatively well preserved. HT offered no significant advantage to sleep at baseline and slightly weakened the recovery response to prolonged wakefulness.

Adult↗

PubMed2006

Cellular consequences of sleep deprivation in the brain.

Several recent studies have used transcriptomics approaches to characterize the molecular correlates of sleep, waking, and sleep deprivation. This analysis may help in understanding the benefits that sleep brings to the brain at the cellular level. The studies are still limited in number and focus on a few brain regions, but some consistent findings are emerging. Sleep, spontaneous wakefulness, short-term, and long-term sleep deprivation are each associated with the upregulation of hundreds of genes in the cerebral cortex and other brain areas. In fruit flies as well as in mammals, three categories of genes are consistently upregulated during waking and short-term sleep deprivation relative to sleep. They include genes involved in energy metabolism, synaptic potentiation, and the response to cellular stress. In the rat cerebral cortex, transcriptional changes associated with prolonged sleep loss differ significantly from those observed during short-term sleep deprivation. However, it is too early to draw firm conclusions relative to the molecular consequences of sleep deprivation, and more extensive studies using DNA and protein arrays are needed in different species and in different brain regions.

Brain↗

PubMed2005

Cytomorphometric changes in rat brain neurons after rapid eye movement sleep deprivation.

Rapid eye movement sleep plays a vital role in the survival of animals. Its deprivation causes alterations in brain functions and behaviors including activities of important enzymes, neurotransmitter levels, impairment of neural excitability and memory consolidation. However, there was a lack of knowledge regarding the effects of rapid eye movement sleep deprivation on neuronal morphology that may get affected much earlier than any permanent damage to the neurons. In the present study, some of these issues have been addressed by studying the effects of rapid eye movement sleep deprivation on various morphological parameters viz. neuronal perimeter, area and shape of neurons located in brain areas known to regulate rapid eye movement sleep and as a control in other brain areas which do not regulate rapid eye movement sleep. The results showed that rapid eye movement sleep deprivation differentially affected neurons depending on their physiological correlates of rapid eye movement sleep and neurotransmitter content. The effects could be reversed if the animals were allowed to recover from rapid eye movement sleep loss or by applying alpha1-adrenergic antagonist, prazosin. The findings in rats support reported data and help explaining previous observations.

Adrenergic alpha-1 Receptor Antagonists↗

PubMed2001

Rapid eye movement sleep deprivation induces an increase in acetylcholinesterase activity in discrete rat brain regions.

Some upper brainstem cholinergic neurons (pedunculopontine and laterodorsal tegmental nuclei) are involved in the generation of rapid eye movement (REM) sleep and project rostrally to the thalamus and caudally to the medulla oblongata. A previous report showed that 96 h of REM sleep deprivation in rats induced an increase in the activity of brainstem acetylcholinesterase (Achase), the enzyme which inactivates acetylcholine (Ach) in the synaptic cleft. There was no change in the enzyme's activity in the whole brain and cerebrum. The components of the cholinergic synaptic endings (for example, Achase) are not uniformly distributed throughout the discrete regions of the brain. In order to detect possible regional changes we measured Achase activity in several discrete rat brain regions (medulla oblongata, pons, thalamus, striatum, hippocampus and cerebral cortex) after 96 h of REM sleep deprivation. Naive adult male Wistar rats were deprived of REM sleep using the flower-pot technique, while control rats were left in their home cages. Total, membrane-bound and soluble Achase activities (nmol of thiocholine formed min(-1) mg protein(-1)) were assayed photometrically. The results (mean +/- SD) obtained showed a statistically significant (Student t-test) increase in total Achase activity in the pons (control: 147.8 +/- 12.8, REM sleep-deprived: 169.3 +/- 17.4, N = 6 for both groups, P<0.025) and thalamus (control: 167.4 +/- 29.0, REM sleep-deprived: 191.9 +/- 15.4, N = 6 for both groups, P<0.05). Increases in membrane-bound Achase activity in the pons (control: 171.0 +/- 14.7, REM sleep-deprived: 189.5 +/- 19.5, N = 6 for both groups, P<0.05) and soluble enzyme activity in the medulla oblongata (control: 147.6 +/- 16.3, REM sleep-deprived: 163.8 +/- 8.3, N = 6 for both groups, P<0.05) were also observed. There were no statistically significant differences in the enzyme's activity in the other brain regions assayed. The present findings show that the increase in Achase activity induced by REM sleep deprivation was specific to the pons, a brain region where cholinergic neurons involved in REM generation are located, and also to brain regions which receive cholinergic input from the pons (the thalamus and medulla oblongata). During REM sleep extracellular levels of Ach are higher in the pons, medulla oblongata and thalamus. The increase in Achase activity in these brain areas after REM sleep deprivation suggests a higher rate of Ach turnover.

Acetylcholinesterase↗

PubMed2004

Sleep deprivation and hemispheric asymmetry for facial recognition reaction time and accuracy.

We investigated the processing of emotional stimuli during a non-sleep-deprived state and following sleep deprivation in 36 right-handed men. Using the visual half-field technique, cartoon line drawings of emotional facial expressions were flashed on a computer screen for 250 msec. The participants were instructed to remember the content of the picture seen and to recognize it among nine alternatives shown immediately after the display of a single picture. Compared to the nondeprived condition, response latencies increased and accuracy decreased in sleep deprivation. Moreover, response latencies indicated that the performance of the right hemisphere deteriorated more following sleep deprivation than did the performance of the left hemisphere. The results also showed that hemispheric preference (for response latencies and response accuracy) tended to favour the left hemisphere when the participants were tested during sleep deprivation.

Adult↗

PubMed1987

Sleep deprivation as a probe in the elderly.

Decreased slow-wave sleep (SWS) and sleep continuity are major effects of healthy aging and of associated psychopathological states. Using sleep deprivation, we studied the extent to which age- and psychopathology-related sleep "decay" is reversible in aged normal, depressed, and demented subjects. Depression or probable Alzheimer's dementia compromised the augmentation of sleep continuity and SWS seen in healthy elderly following sleep deprivation. Rapid eye movement (REM) latency decreased during recovery sleep in the controls but increased in both patient groups. Compared with demented patients, depressed elderly had greater severity of sleep continuity disturbance both before and after sleep deprivation, a more protracted course of recovery sleep, and increased slow-wave density in the second non-REM (NREM) sleep period (during recovery). The REM sleep time was diminished in dementia compared with depression both at baseline and during recovery sleep. These differential effects of age, health, and neuropsychiatric disease on recovery from sleep loss are relevant to recovery or reversal theories of sleep and have implications for daytime well-being in the elderly.

Aged↗

PubMed1999

Short-term total sleep deprivations does not selectively impair higher cortical functioning.

Previous research has shown that total sleep deprivation produces impairment in sustained attention and vigilance especially if the deprivation period is greater than 48 hours. However little is known about the effects of sleep deprivation on performance of tasks considered to be measures of higher cortical functioning such as tests of cognitive flexibility and the capacity to shift from one response set to another. One current hypothesis is that sleep deprivation of a shorter duration (34-36 hours) adversely affects higher cortical function while effects on attention and vigilance tasks are relatively mild. Performance on an intelligence test, a test of sustained attention and tests designed to measure higher cortical function were compared in a group of 29 subjects who underwent 34-36 hours of continuous sleep deprivation and 32 normal sleeping control subjects. No significant group performance differences in the hypothesized direction were noted on any measure. One night of total sleep deprivation does not appear to impair performance on tasks that are designed to assess higher cortical functioning.

Adult↗

PubMed2005

Partial sleep deprivation therapy combined with sertraline induces more rapid improvements in quality of life items in major depressive disorder.

BACKGROUND: Total or partial sleep deprivation was showed to have rapid antidepressive effects in depression. Sleep deprivation therapy in major depression constitutes insufficient antidepressive treatment response and depressive symptoms reoccur after one night of recovery. Combination of antidepressant medication with sleep deprivation therapy is generally indicated. These combination therapies were found more favorable overall therapeutic effect than antidepressive monotherapy. METHODS: In this study, we examined the Quality of Life changes with the antidepressive therapy using partial sleep deprivation plus sertraline and sertraline monotherapy in patients with major depressive disorder. Thirteen patients received six partial sleep deprivation therapies in addition to sertraline, that sleep schedule in deprivation nights started at 11:00-12:00 p.m. to 03:00 a.m. and 11 patients treated with sertraline monotherapy as a control group. Quality of Life was evaluated with the WHOQOL-100, depression and the accompanying anxiety were also assessed at baseline and at the end of the 4th week. RESULTS: Patients treated with combination therapy improved significantly and more rapidly. Rapid improvement in quality of life in major depressive disorder was showed in patients treated with combination of late partial sleep deprivation and sertraline. LIMITATIONS: Small sample size, the lack of placebo group and short duration of the study are the main limitations. CONCLUSIONS: In clinical practice, QOL improvement can be accelerated using combination of partial sleep deprivation with the sertraline therapy.

Adult↗

PubMed2004

Effects of sleep deprivation on spontaneous arousals in humans.

STUDY OBJECTIVES: The hierarchical definition of arousals from sleep includes a range of physiologic responses including microarousals, delta and K-complex bursts, and variations in autonomic system. Whether patterns in slow-wave electroencephalographic activity and autonomic activation are primary forms of arousal response can be addressed by studying effects of total sleep deprivation. We therefore examined changes in arousal density during recovery sleep in healthy subjects. DESIGN: Participants spent 6 consecutive 24-hour periods in the laboratory. Nights 1 and 2 were baseline nights followed by 64-hour total sleep deprivation, then 2 consecutive recovery nights. SETTING: Sleep-deprivation protocol was conducted under laboratory conditions with continuous behavioral and electrophysiologic monitoring. PARTICIPANTS: Twelve drug-free men aged 27.4 +/- 7.9 years were studied. None reported sleepiness or altered sleep-wake cycle, and none had neurologic, psychiatric or sleep disorders. INTERVENTION: N/A. MEASUREMENTS AND RESULTS: Arousals were classified into 4 levels: microarousals, phases of transitory activation, and delta and K-complex bursts. Sleep deprivation induced changes in the density of considered arousals except phases of transitory activation, with a distinct pattern among the different types. The greatest change was found for microarousals, which showed a significant decrease in the first recovery night (P = .01), with return to baseline thereafter. A fall in K-complex and delta-burst density was noted in the first recovery night, not, however, reaching statistical significance. The phases of transitory activation rate were virtually unaffected throughout the experimental nights. CONCLUSIONS: We conclude that homeostatic sleep processes exert an inhibitory effect on arousal response from sleep with a significant effect only on the microarousal density. Decreased delta and K-complex burst rates, though not significant, support the hypothesis that they may be activating processes, probably modulated by factors independent from those implicated in cortical arousal.

Adult↗

PubMed2006

Random number generation during sleep deprivation: effects of caffeine on response maintenance and stereotypy.

Neurophysiological and functional imaging studies have demonstrated that frontal regions of the brain are particularly responsive to homeostatic sleep pressure. Previous neuropsychological studies indicate that sleep deprivation causes impairments in prefrontal cortical function. Random number generation (RNG) is thought to provide a sensitive index of executive functions that rely on the prefrontal cortex. The present study tested the hypothesis that sleep deprivation would impair RNG and that caffeine would mitigate this impairment. Healthy young men (n = 21) participated in two 40-h sleep deprivations 1 week apart. During each sleep deprivation period subjects received either caffeine or placebo according to a randomized, double-blind cross-over design, and they completed an oral RNG task at 3-h intervals. Comparison of test sessions at analogous times of day revealed that sleep deprivation was associated with significant drops in the number of responses, a threefold increase in the percentage of rule violations, 59% greater response redundancy and a 20% increase in stereotypy of adjacent response pairs. Sleep deprivation did not consistently alter counting tendency. Caffeine ameliorated the decrease in the number of responses but did not mitigate other deficits in RNG that arose during sleep deprivation. These findings are consistent with prior reports of diminished vigilance and increased perseveration during extended wakefulness. They support the conclusion that caffeine preserves simple aspects of cognitive performance during sleep deprivation, whereas caffeine may not prevent detrimental effects of sleep deprivation on some complex cognitive functions.

Adult↗