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PubMed1985

The effect of sleep deprivation on activity of the genioglossus muscle.

Sleep deprivation appears to increase the severity of obstructive sleep apnea, and inadequate activation of the genioglossus muscle may play an important role in the pathogenesis of obstructive sleep apnea. Therefore, we investigated the effect of sleep deprivation on genioglossal electromyographic (EMG) activity. Eleven men were studied during room air breathing and CO2 rebreathing before sleep deprivation (control), after 1 night of sleep deprivation, and the day after sleep recovery. We measured inspired minute ventilation, tidal volume, respiratory frequency, and peak integrated inspiratory genioglossal EMG activity. After sleep deprivation, no significant changes in inspiratory minute ventilation or tidal volume occurred during room air breathing or CO2 rebreathing, but the breathing frequency during CO2 rebreathing increased significantly after sleep deprivation. Genioglossal EMG activity was diminished during CO2 rebreathing after sleep deprivation, but this was significant only in subjects 30 yr of age and older. The fall in EMG activity was independent of changes in tidal volume. All variables returned towards control levels after sleep recovery. We conclude that sleep deprivation selectively decreases genioglossal EMG activity during CO2 rebreathing in awake older subjects. This influence of sleep deprivation may play a role in the pathogenesis or severity of obstructive sleep apnea.

Adult↗

PubMed1981

Maintenance of therapeutic effects of total sleep deprivation by limitation of subsequent sleep. A pilot study.

In a previous study it was shown that in endogenous depression repeated sleep deprivation (SD) during clomipramine treatment resulted in rapid improvement after each SD. However, except after the first night, relapses were observed after all sleep nights following SD (the "recovery nights"). The present pilot study had a therapeutic aim, namely to prevent these relapses. We were interested in whether limitation of sleep during the recovery nights might prevent these relapses and whether different amounts of sleep would have different effects on the course of mood after recovery sleep. Ten endogenously depressed patients were treated with clomipramine and with three SD's. Five patients slept for approximately 2 h, and the other five for about 5 h during the second and third recovery nights. On average, no relapse was shown by these patients and, in fact, there was some additional improvement after these nights, in contrast to the findings in the previous study, where patients were allowed unlimited sleep.

Clinical Trials as Topic↗

PubMed2000

Voluntary oculomotor performance upon awakening after total sleep deprivation.

The potential impact of sleep inertia on measures of voluntary oculomotor control have been surprisingly neglected. The present study examined the effects of 40 hours of sleep deprivation on saccadic (SAC) and smooth pursuit (SP) performance, attentional/visual search performance (Letter Cancellation Task, LCT) and subjective sleepiness (Sleepiness Visual Analog Scale, SVAS) recorded immediately after awakening. Standard polysomnography of nine normal subjects was recorded for 3 nights (1 adaptation, AD; 1 baseline, BSL; 1 recovery, REC); BSL and REC were separated by a period of 40 h of continuous wakefulness, during which subjects were tested every two hours. Within 30 s of each morning awakening, a test battery (SAC, SP, LCT, SVAS) was administered to subjects in bed. For data analysis, mean performance obtained during the day preceding the sleep deprivation night was considered as "Diurnal Baseline" and compared to performance upon awakening from nocturnal sleep. As a consequence of sleep deprivation, SWS percentage was doubled during REC. Saccade latency increased and velocity decreased significantly upon awakening from REC as compared to the other three conditions (Diurnal baseline, AD awakening, BSL awakening); accuracy was unaffected. As regards SP, phase did not show any impairment upon awakening, while velocity gain upon awakening from REC was significantly lower as compared to the other conditions. Finally, number of hits on LCT upon awakening from REC was significantly lower and subjective sleepiness higher as compared to Diurnal Baseline. It is concluded that 40 h of sleep deprivation significantly impaired performance to SAC and SP tasks recorded upon awakening from recovery sleep. This performance worsening is limited to the measures of speed, while both SAC accuracy and SP phase do not show a significant decrease upon awakening. Since saccadic velocity has recently been found to negatively correlate with simulator vehicle crash rates, it is suggested that the adverse effects of sleep deprivation on sleep inertia magnitude should be avoided by any personnel who may have to perform critical tasks involving high oculomotor control immediately after awakening.

Adult↗

PubMed1996

Modulation of IL-1 beta gene expression in the rat CNS during sleep deprivation.

We hypothesize that sleep homeostasis involves, at least in part, the immune system modulator interleukin-1 beta (IL-1 beta). Using the reverse transcription-polymerase chain reaction, IL-1 beta mRNA levels in the rat CNS were evaluated after a period of sleep deprivation. In addition, IL-1 beta gene expression was analyzed before the projected onset of activity and rest phase in free-running animals. No changes in IL-1 beta mRNA were observed in the circadian cycle, but 24 h of sleep deprivation resulted in a 2-fold increase in the level of IL-1 beta mRNA in the hypothalamus and in the brain stem compared with controls (p < 0.0002 and (p < 0.0001 respectively). The alteration in IL-1 beta mRNA levels following sleep deprivation supports the hypothesis that modulation of IL-1 beta gene expression is involved in the sleep homeostatic process.

Animals↗

PubMed2001

Hormonal responses to exercise after partial sleep deprivation and after a hypnotic drug-induced sleep.

The aim of this study was to determine the hormonal responses, which are dependent on the sleep wake cycle, to strenuous physical exercise. Exercise was performed after different nocturnal regimens: (i) a baseline night preceded by a habituation night; (ii) two nights of partial sleep deprivation caused by a delayed bedtime or by an early awakening; and (iii) two nights of sleep after administration of either a hypnotic compound (10 mg zolpidem) or a placebo. Eight well-trained male endurance athletes with a maximal oxygen uptake of 63.5 +/- 3.8 ml x kg(-1) x min(-1) (mean value +/- s(x)) were selected on the basis of their sleeping habits and their physical training. Polygraphic recordings of EEG showed that both nights with partial sleep loss led to a decrease (P< 0.01) in stage 2 and rapid eye movement sleep. A delayed bedtime also led to a decrease (P < 0.05) in stage 1 sleep. Zolpidem had no effect on the different stages of sleep. During the afternoon after an experimental night, exercise was performed on a cycle ergometer. After a 10-min warm-up, the participants performed 30 min steady-state cycling at 75% VO(2-max) followed by a progressively increased workload until exhaustion. The recovery period lasted 30 min. Plasma growth hormone, prolactin, cortisol, catecholamine and lactate concentrations were measured at rest, during exercise and after recovery. The concentration of plasma growth hormone and catecholamine were not affected by partial sleep deprivation, whereas that of plasma prolactin was higher (P < 0.05) during the trial after an early awakening. Plasma cortisol was lower (P < 0.05) during recovery after both sleep deprivation conditions. Blood lactate was higher (P < 0.05) during submaximal exercise performed after both a delayed bedtime and an early awakening. Zolpidem-induced sleep did not affect the hormonal and metabolic responses to subsequent exercise. Our results demonstrate only minor alterations in the hormonal responses to exercise after partial sleep deprivation.

Adult↗

PubMed2006

Effects of sleep deprivation on lateral visual attention.

Sleep loss temporarily impairs vigilance and sustained attention. Because these cognitive abilities are believed to be mediated predominantly by the right cerebral hemisphere, this article hypothesized that continuous sleep deprivation results in a greater frequency of inattention errors within the left versus right visual fields. Twenty-one participants were assessed several times each day during a 40-h period of sustained wakefulness and following a night of recovery sleep. At each assessment, participants engaged in a continuous serial addition task while simultaneously monitoring a 150 degrees visual field for brief intermittent flashes of light. Overall, omission errors were most common in the leftmost peripheral field for all sessions, and did not show any evidence of a shift in laterality as a function of sleep deprivation. Relative to rested baseline and postrecovery conditions, sleep deprivation resulted in a global increase in omission errors across all visual locations and a general decline in serial addition performance. These findings argue against the hypothesis that sleep deprivation produces lateralized deficits in attention and suggest instead that deficits in visual attention produced by sleep deprivation are global and bilateral in nature.

Adult↗

PubMed1975

Circadian rhythms of catecholamine excretion, shooting range performance and self-ratings of fatigue during sleep deprivation.

Circadian rhythms in urinary catecholamine excretion, performance and self-ratings were studied in two experiments with a total of 29 subjects who were deprived of sleep for 72 hr. Adrenaline excretion and fatigue ratings showed the most consistent circadian variations; noradrenaline and performance rhythms were more irregular. The average crest phase for adrenaline excretion was around 1400 hr, for noradrenaline about 0800 hr, for performance 1700 hr and for fatigue 0500 hr. Twenty-four hour levels of performance and 'subjective arousal' decreased over the three days of sleep deprivation, while adrenaline excretion levels increased.

Adult↗

PubMed1984

The thyroid function in young men during prolonged exercise and the effect of energy and sleep deprivation.

Thyroid function has been investigated in 24 young military cadets participating in a 5 d ranger training course with heavy physical exercise, calorie deficiency and deprivation of sleep. The cadets were divided into three groups, each differing in the amount of sleep and food consumption. The serum levels of thyroid hormones (T4, FT4, T3, rT3) and TBG showed a biphasic pattern during the course. Initially there was an increased secretion concomitant with an increased deiodination of T4 to T3 and rT3 mainly due to physical exercise. When the activities lasted for several days without sufficient food supply the thyroid secretion decreased simultaneously with an alteration of the peripheral conversion of T4 to rT3 instead of T3. A significant correlation was found between the changes in total and free thyroxine (r = 0.9) and between the increase in rT3 and decrease in T3 (r = 0.6). TSH decreased during the first day of activities and remained low throughout the course. The TSH response to TRH stimulation was greatly reduced during the course due to physical exercise and calorie deficiency. The present investigation demonstrates that the thyroid function is strongly affected by prolonged physical exercise and a negative energy balance, whereas sleep deprivation does not have any significant influence. The results indicate that the alteration observed is not regulated just by the hypothalamo-pituitary-thyroid-axis alone.

Adult↗

PubMed1978

The diagnostic value of the short sleep EEG and other provocative methods following sleep deprivation.

One hundred and eighty-five EEGs recorded after deprivation of sleep for 24 h were evaluated. Valuable diagnostic information was found in 59% of the EEG recordings; 24% of the EEGs contained seizure activity. The duration of the stages of sleep and the frequency of seizure activity, paroxysmal sharp wave groups and localizing findings were analyzed. The sleep stages A to C (based on the Loomis scale) were reached for about equal duration by an EEG recording of 30--40 min; sleep stage D was reached only shortly and stage E was not observed. Pathological EEG findings appeared for the most part in the sleep stages A and B. Localized findings were pronounced in stage C. No significant differences pertaining to the occurrence and form of EEG patterns were found between patient groups with primary generalized seizures, psychomotor seizures or those with unclarified disturbances of consciousness. The combination of the short sleep EEG following 24 h of sleep deprivation with subsequent use of the additional provocative methods of hyperventilation, photostimulation and hydration, yielded, in all, new information in 50% of the patients. Each of these additional methods contributed nearly equally to this information.

Adult↗

PubMed1988

Serial partial sleep deprivation in depression--clinical effects and dexamethasone suppression test results.

Thirty depressed patients were deprived of sleep during the second half of the night after they were characterized according to their Research Diagnostic Criteria diagnosis, severity of depression, current medication and dexamethasone suppression test status. After applying partial sleep deprivation (PSD) treatment three times within 1 week, we observed in 17 patients an improvement of their initial depressive symptomatology of 50% or more. No pretreatment variable except the degree of improvement after the first PSD was predictive for therapeutic effects of the entire PSD series. Beneficial effects of PSDs were not specific for the endogenous type of depression. A trend was found indicating that concurrent psychotropic drug treatment enhances the beneficial effect of serial PSDs.

Adult↗

PubMed1992

Circadian rhythm in plasma noradrenaline of healthy sleep-deprived subjects.

Under normal sleep-wake conditions, noradrenaline (NA) secretions in supine subjects exhibit a weak circadian variation with a peak that occurs around noon; the sleep span is characterized by reduced NA secretion. Some investigators have reported that the circadian NA rhythm is completely obliterated during sleep deprivation. In our laboratory, plasma NA was assayed every hour for 24 h in nine healthy men 20-23 years of age. All men were deprived of sleep and were required to eat and walk around every hour to prevent sleep. However, subjects remained supine for 20 min before blood samples were collected to eliminate the effect of activity. Persistence of a slight decrease in the night concentration in several subjects, despite sleep deprivation, suggests that NA secretion may be influenced by a biological clock whose activity becomes visible when the influence of posture is removed.

Adult↗

PubMed2006

Extracellular adenosine in the human brain during sleep and sleep deprivation: an in vivo microdialysis study.

STUDY OBJECTIVES: To examine the pattern of extracellular adenosine in the human brain during sleep deprivation, sleep, and normal wake. DESIGN: Following recovery from implantation of clinical depth electrodes, epilepsy patients remained awake for 40 continuous hours, followed by a recovery sleep episode. SETTING: Neurology ward at UCLA Medical Center. PATIENTS OR PARTICIPANTS: Seven male epilepsy patients undergoing depth electrode localization of pharmacologically refractory seizures. INTERVENTIONS: All subjects were implanted with depth electrodes, a subset of which were customized to contain microdialysis probes. Microdialysis samples were collected during normal sleep, sleep deprivation, and recovery sleep from human amygdalae (n = 8), hippocampus (n = 1), and cortex (n = 1). MEASUREMENTS AND RESULTS: In none of the probes did we observe an increase in extracellular adenosine during the sleep deprivation. There was a significant, though very small, diurnal oscillation (2.5%) in 5 of the 8 amygdalae. There was no effect of epileptogenicity on the pattern of extracellular adenosine. CONCLUSIONS: Our observations, along with those in animal studies, indicate that the role of extracellular adenosine in regulating sleep pressure is not a global brain phenomenon but is likely limited to specific basal forebrain areas. Thus, if energy homeostasis is a function of sleep, an increased rate of adenosine release into the extracellular milieu of the amygdala, cortex, or hippocampus is unlikely to be a marker of such a process.

Adenosine↗

PubMed2000

Effects of sleep deprivation on neural circulatory control.

Effects of sleep deprivation on neural cardiovascular control may have important clinical implications. We tested the hypothesis that sleep deprivation increases heart rate, blood pressure, and sympathetic activity and potentiates their responses to stressful stimuli. We studied 8 healthy subjects (aged 40+/-5 years, 6 men and 2 women). Blood pressure, heart rate, forearm vascular resistance, and muscle sympathetic nerve activity were measured at rest and during 4 stressors (sustained handgrip, maximal forearm ischemia, mental stress, and cold pressor test). Measurements were obtained twice, once after normal sleep and once after a night of sleep deprivation. All measurements were obtained in a blinded, randomized manner. In comparison with normal sleep, sleep deprivation resulted in an increase in blood pressure (normal sleep versus sleep deprivation=82+/-8 versus 86+/-7 mm Hg, mean+/-SEM, P=0.012) and a decrease in muscle sympathetic nerve activity (normal sleep versus sleep deprivation=28+/-6 versus 22+/-6 bursts/min, P=0.017). Heart rate, forearm vascular resistance, and plasma catecholamines were not significantly changed by sleep deprivation, nor did sleep deprivation affect autonomic and hemodynamic responses to stressful stimuli. Sleep deprivation results in increased resting blood pressure, decreased muscle sympathetic nerve activity, and no change in heart rate. Thus, the pressor response to sleep deprivation is not mediated by muscle sympathetic vasoconstriction or tachycardia.

Adult↗

PubMed2003

Clinical effects of sleep fragmentation versus sleep deprivation.

Common symptoms associated with sleep fragmentation and sleep deprivation include increased objective sleepiness (as measured by the Multiple Sleep Latency Test); decreased psychomotor performance on a number of tasks including tasks involving short term memory, reaction time, or vigilance; and degraded mood. Differences in degree of sleepiness are more related to the degree of sleep loss or fragmentation rather than to the type of sleep disturbance. Both sleep fragmentation and sleep deprivation can exacerbate sleep pathology by increasing the length and pathophysiology of sleep apnea. The incidence of both fragmenting sleep disorders and chronic partial sleep deprivation is very high in our society, and clinicians must be able to recognize and treat Insufficient Sleep Syndrome even when present with other sleep disorders.

Forced Expiratory Volume↗

PubMed2005

Modafinil as an adjunctive treatment to sleep deprivation in depression.

Sleep deprivation (SD) is a rapid-acting treatment for depression, but its clinical efficacy is hampered by high relapse rates after recovery sleep, and its effectiveness is reduced by the demanding effort needed for the patient to stay awake. To our knowledge, this is the first reported case of a successful treatment of depression with the combination of SD and the wakefulness-promoting agent modafinil. We suggest that modafinil may reinforce the action of SD, possibly by preventing daytime naps and microsleep, and may sustain the antidepressant effect of SD, possibly by stabilizing the resynchronization between the circadian clock and the sleep-wake cycle.

Aged↗

PubMed1997

Activities of monoamine oxidase (MAO) A and B in discrete regions of rat brain after rapid eye movement (REM) sleep deprivation.

Rapid eye movement (REM) sleep deprivation increases monoaminergic (noradrenergic and serotonergic) turnover and their metabolites in whole brain of rats. This increase in metabolites may indicate increased activity of the enzymes responsible for the inactivation of monoamines. To test this hypothesis, we assayed the activity of monoamineoxidases (MAOs) A and B in hippocampus, hypothalamus, brainstem and its divisions pons and medulla oblongata in rats deprived of REM sleep for 96 h. REM sleep deprivation was carried out by the flower-pot technique. A control group remained in their home cages. MAO A was assayed by using [14C]-5-hydroxytryptamine as the substrate (50 microM final concentration) and MAO B by using [14C]-beta-phenylethylamine (2 microM final concentration). The enzymes were assayed in the mitochondrial fraction.The results obtained showed that a significant decrease in the activity of MAO A was obtained in the brainstem and an increase in medulla oblongata and no statistical differences in the activity of MAO B in brainstem, pons and medulla oblongata and MAO A in pons; there were also no differences in the activities of both MAO A and B in hippocampus and hypothalamus. Although our results confirmed previous data regarding changes in MAO A activity in brainstem and medulla oblongata, they did not confirm our hypothesis that the increase in monamine turnover and metabolites in the brain would be the result of increased MAO activity.

Animals↗

PubMed1990

Sleep and sleep deprived EEG in partial and generalized epilepsy.

Sleep and sleep deprivation are often used for EEG activation in epilepsy. We compared postprandial naps and day-long sleep deprived EEGs in 36 patients with generalized seizures, 57 complex partial seizure patients, and 7 individuals with mixed seizure disorders. Ten of 36 generalized seizure patients had normal sleep and sleep deprived EEGs, while both were normal in 16 of 57 partial seizure patients. Both were abnormal in 18 of 36 generalized and 22 of 57 partial epileptics. Seven generalized seizure patients had epileptiform discharges or seizures during afternoon naps but normal sleep deprived EEGs. No partial seizure patients had normal sleep deprived EEGs and abnormal nap, but 29 of 57 had abnormalities or seizures only with sleep deprivation. All 7 mixed seizure patients had abnormal sleep and sleep deprived studies, and 6 had seizures, 4 on both studies. Natural sleep may facilitate the appearance of generalized seizures or epilepti-form discharges, while sleep deprivation may accentuate the yield of EEG abnormality in partial epilepsy. Either is likely to be abnormal in patients with mixed seizures and encephalopathy. Natural sleep and sleep deprived EEGs are an appropriate combination in the evaluation of refractory seizures.

Adolescent↗

PubMed1998

Microsleep during partial sleep deprivation in depression.

BACKGROUND: Sleep deprivation (SD) exerts a beneficial effect on mood and sleep in about 60% of depressed patients usually followed by a relapse into depression after the recovery night. Short phases of sleepiness, especially naps in the early morning, may be responsible for this phenomenon. METHODS: To evaluate the effect of short, even ultrashort phases of sleep-microsleep (MS) during partial sleep deprivation (PSD) on mood, cognitive psychomotor performance (CPP), and sleep, an electroencephalograph (EEG) was continuously recorded over 60 hours in 12 patients with major depression. Subjective mood was assessed by a visual analogue scale and CPP by a letter cancellation test. RESULTS: The results illustrate that in depressed patients during PSD the amount of MS is increased, predominantly in the early morning, which was subjectively unrecognized and not observed by nursing staff. Patients with a low cumulative amount of MS during PSD improved significantly in mood, CPP, and sleep pattern compared to the patients with a high amount of MS who showed only slight changes. CONCLUSION: Therefore, accumulated MS may influence the SD-induced positive effects in depressed patients.

Adult↗