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PubMed1998

Effects of paradoxical sleep deprivation on thermoregulation in the rat.

Rats were subjected to chronic paradoxical sleep deprivation (PSD) by the disk-over-water method to determine if they would develop the sustained increase in core (hypothalamic) temperature (T(hy)); elevated temperature setpoint (Tset); and the attenuation of the normal decline in core temperature during the transition from wake to sleep observed in rats subjected to total sleep deprivation (TSD). PSD rats did not show a significant elevation in T(hy). PSD rats and their yoked controls (PSC) were provided with a continuously available operant by which they could increase ambient temperature (Tamb). Change in Tset was assessed by evaluating operant behavior as a function of hypothalamic and intraperitoneal temperature (T(ip)). Unlike TSD rats, PSD and PSC rats maintained near-baseline Tamb at all T(hy) and T(ip) values throughout the deprivation, indicating no change in Tset. As deprivation progressed, PSD rats displayed an attenuation of the normal fall of T(hy) and T(ip) during the transition from wake to sleep. PSC rats did not. During the final quarter of survival time, T(ip) in PSD rats actually rose above waking values during the transition to NREM. These results indicate that PS loss may alter thermoregulation during sleep. It would appear that selective PSD is sufficient to attenuate the normal decline in T(hy) and T(ip) during NREM sleep, whereas NREM loss is required for elevations in T(hy) and Tset.

Animals↗
PubMed1984

Effects of 72 hour sleep deprivation on urinary cortisol and indices of metabolism.

Cortisol, urea, glucose, electrolytes, and other compounds were measured in five consecutive 24 h urine collections during a 72 h sleep deprivation study in six young men. Urine was collected during a 24 h predeprivation day, 3 days of sleep deprivation, and a recovery day. Whereas urinary cortisol decreased only slightly, marked changes in other urinary constituents were observed. During sleep deprivation, urinary urea rose markedly, glucose decreased, and urinary electrolytes decreased. These data indicate that sleep deprivation under ad lib food and water conditions can cause disturbances in normal metabolism.

Adolescent↗
PubMed1999

Effects of 50mg amisulpride on EEG, psychomotor and cognitive functions in healthy sleep-deprived subjects.

Amisulpride, a substituted benzamide, binds selectively to the dopamine D2- and D3-receptors. It has higher affinity for limbic compared to striatal dopamine receptors in vivo. At low doses, amisulpride facilitates dopamine transmission via a selective blockade of presynaptic D2- and D3-receptors. Amisulpride is an active antipsychotic compound effective at low doses for negative symptoms and at high doses for positive symptoms of schizophrenia. The CNS profile of multiple doses of a low dosage regimen of amisulpride (50 mg once daily for 4 days) was assessed in a randomised, double-blind, 3-way crossover, placebo-controlled study carried out in 12 young sleep-deprived (for 36 h) subjects, using EEG and various measures of psychomotor and cognitive functions. Caffeine slow release (600 mg) was used as a positive reference. Multiple doses of 50 mg amisulpride once daily were devoid of any detrimental effects on EEG and psychomotor performance and cognitive function after total sleep deprivation. In addition, 50mg amisulpride partially antagonized the deleterious effects of sleep deprivation on EEG and subjective sedation as shown by trends, and a significant increase in EEG relative beta power and a decrease in subjective sedation. These effects were more pronounced at the end of sleep deprivation, suggesting possible alerting effects of amisulpride at this dose level. Caffeine significantly antagonized the detrimental effects of sleep deprivation on vigilance (increase in EEG beta waves, speed of reaction, sustained attention and reduction in subjective sedation). In conclusion, the present results demonstrate that 50 mg amisulpride is devoid of detrimental effects on EEG, psychomotor and cognitive performance after sleep deprivation, a situation well-known to amplify such effects if they exist. Moreover, some data suggest possible alerting effects of this low dosage regimen of amisulpride.

Adult↗
PubMed2002

Effects of sleep deprivation on gamma-amino-butyric acid and glutamate contents in rat brain.

OBJECTIVE: To investigate the effects of sleep deprivation on the contents of gamma-amino-butyric acid (GABA) and glutamate (GLU) in rat brain. METHODS: Thirty rats were assigned into sleep-deprivation (SD, n=10) group (subjected to treatment on small platforms 6.5 cm of diameter), tank control (TC, n=10) group (treated on large platforms 14 cm of diameter) and control group kept in cages (CC, n=10). Rats in SD group were deprived of rapid eye movement sleep for 96 h by "flower pot" technique. High-performance liquid chromatography was used to determine the GABA and GLU contents in the 3 brain regions of the rats: the frontal cortex, hypothalamus and brain stem. RESULTS: The rats in SD group showed an increase in the contents of GABA and lowered ratio of GLU/GABA in all the 3 brain regions (P<0.01) compared with the rats in CC group; GLU contents were also increased in the brain stem and hypothalamus of the rats in SD group (P<0.05). No significant changes were found in TC group. CONCLUSION: Rapid eye movement sleep deprivation induces significant changes in the contents and proportion of amino-acid neurotransmitter in rat brain.

Animals↗
PubMed1982

[Sleep deprivation as activating procedure in EEG of patients with and without epileptic seizures. I. Generalized paroxysmal discharges ].

The EEGs of 459 patients with and 442 patients without epileptic seizures showed generalized spike wave (s/w) paroxysms in 126 cases and generalized slow wave paroxysms in 63 cases before and/or after sleep deprivation. In patients with epileptic seizures s/w paroxysms appeared in 23%, whereas in patients without epileptic seizures. S/w paroxysms were present in only 5%. The difference is statistically highly significant. The frequency of generalized slow wave paroxysms showed with 6% and 8% respectively no statistical significance. In 91% of patients with s/w paroxysms the latter appeared already in the waking phases of the EEG following sleep deprivation. All s/w paroxysms which appeared in the sleep EEG were demonstrable already in stage I according to Rechtschaffen and Kales. The rate of activation of s/w paroxysms following sleep deprivation was 42% in patients with epileptic seizures, that of slow wave paroxysms was 38%. Although the number of patients with s/w paroxysms increases by approximately 100% following sleep deprivation they comprise still only 9.6% of all 459 patients with epileptic seizures. Combined with EEGs which show slow wave paroxysms or focal disturbances the incidence increases to 17%. Sleep deprivation as an activating procedure therefore provides a significant contribution to the confirmation of the diagnosis of epilepsy as well as control of therapy of epileptic patients whose routine EEG does not show typical pathological signs.

Electroencephalography↗
PubMed1992

Effects of sleep deprivation on fos-like immunoreactivity in the rat brain.

The molecular mechanisms involved in sleep regulation and function are largely unknown, and our understanding of the localization of such mechanisms within specific brain structures is still incomplete. In this work, we explored the consequences of sleep deprivation by the immunocytochemical mapping of the induction of the protein product of the immediate early gene c-fos in the brain of sleep-deprived rats. The expression of Fos protein is an indicator of neuronal activity. In addition, since immediate early genes can function as "third messengers" and regulate the transcription of a number of target genes, their induction could be directly relevant to the homeostasis and functions of sleep. The present results show that, as a result of 24 hours of manual sleep deprivation, Fos-like immunoreactive cells are found in specific brain areas. These areas include the medial preoptic area of the hypothalamus, the nucleus accumbens, the lateral septum, several regions of the dorsal pontine tegmentum (central gray, dorsal raphe, locus coeruleus, pedunculopontine and laterodorsal tegmental nuclei, parabrachial nuclei) and an area medial to the parabigeminal nucleus at the ponto-mesencephalic junction. Some of these areas had already been implicated in slow-wave sleep and desynchronized sleep regulation.

Animals↗
PubMed1983

The incentive effect and sleep deprivation.

In order to examine the effect of a small amount of sleep following 3 3/4 days (90 h) of wakefulness, 10 infantry soldiers took part in a laboratory-based experiment. At the end of the vigil, a 2-h sleep was preceded and followed by a cognitive test session consisting of encoding and decoding. In order to simulate a realistic situation, subjects were not told the scheduled length of their vigil until a few hours before their 2-h sleep. Following the test-sleep-test period, 27 h were allowed for sleep and rest. Results indicated that after 3 nights without sleep, performance was, on the average, 55% of the control values. During the test session before the 2-h sleep, performance improved by 30%, to 85% of control values, indicating the considerable effect that incentive can have on even severely sleep-deprived subjects. The reserve mental capacity demonstrable during sleep deprivation indicates the caution that is needed if the effects of "undiluted" sleep loss are sought; it also emphasises once again the lack of knowledge concerning the function of sleep.

Adult↗
PubMed2004

Total sleep deprivation increases the costs of shifting between simple cognitive tasks.

In two experiments we studied the effects of one night of total sleep deprivation on task-shift costs. In different conditions shifts were between types of judgment (extradimensional shifts) and between stimulus-response mappings (intradimensional shifts). In addition, with an alternating-runs procedure we used short and long response-to-stimulus intervals and also external precues to vary the opportunities for advance configuration of task sets. Under all conditions sleep deprivation increased shift costs derived from the 20% slowest reaction times, which were insensitive to the opportunities for advance configuration. Shift costs derived from the 20% fastest reaction times were increased only for extradimensional shifts. As indicated by congruency effects, the increase of shift costs after a night without sleep cannot be attributed to increased interference between competing task sets. The findings suggest that total sleep deprivation increases task-set instability and thus lapsing, in particular in conditions with long stimulus-to-response intervals and in shift trials. In addition total sleep deprivation seems to increase the duration of an exogenously controlled process involved in extradimensional shifts.

Adult↗
PubMed1982

Sleep deprivation procedure produces stomach lesions in rats.

Sprague-Dawley male rats were deprived of food for 40 hr and subjected to sleep deprivation by the "flower pot" or handling intervention procedures during the final 24 hr. Five of six rats in the flower pot group exhibited stomach erosions. Only one rat in the handling group, and no rats in a food deprived control group showed such erosions. The flower pot group also had higher levels of corticosterone than the food deprived control group. These findings argue for more serious consideration of the effects of the stress of procedures for sleep deprivation.

Animals↗
PubMed2000

Cortisol circadian rhythms during the menstrual cycle and with sleep deprivation in premenstrual dysphoric disorder and normal control subjects.

BACKGROUND: In this study we extended previous work by examining whether disturbances in the circadian rhythms of cortisol during the menstrual cycle distinguish patients with premenstrual dysphoric disorder (PMDD) from normal control (NC) subjects. In addition, we tested the differential response to the effects of early and late partial sleep deprivation on cortisol rhythms. METHODS: In 15 PMDD and 15 NC subjects we measured cortisol levels every 30 min from 6:00 PM to 9:00 AM during midfollicular (MF) and late luteal (LL) menstrual cycle phases and also during a randomized crossover trial of early (sleep 3:00 AM-7:00 AM) versus late (sleep 9:00 PM-1:00 AM) partial sleep deprivation administered in two subsequent and separate luteal phases. RESULTS: In follicular versus luteal menstrual cycle phases we observed altered timing but not quantitative measures of cortisol secretion in PMDD subjects, compared with NC subjects: in the LL versus MF phase the cortisol acrophase was a mean of 1 hour earlier in NC subjects, but not in PMDD subjects. The effect of sleep deprivation on cortisol timing measures also differed for PMDD versus NC subjects: during late partial sleep deprivation (when subjects' sleep was earlier), the cortisol acrophase was almost 2 hours earlier in PMDD subjects. CONCLUSIONS: Timing rather than quantitative measures of cortisol secretion differentiated PMDD subjects from NC subjects both during the menstrual cycle and in response to early versus late sleep deprivation interventions.

Adult↗
PubMed2004

Modafinil vs. caffeine: effects on fatigue during sleep deprivation.

INTRODUCTION: The extent to which modafinil and caffeine reverse fatigue effects (defined as performance decrements with time on task) during total sleep deprivation was investigated. METHODS: There were 50 healthy young adults who remained awake for 54.5 h (06:30 day 1 to 13:00 day 3). A 10-min vigilance test was administered bi-hourly from 08:00 day 1 until 22:00 day 2. At 23:55 day 2 (after 41.5 h awake), double-blind administration of one of five drug doses (placebo; modafinil 100, 200, or 400 mg; or caffeine 600 mg; n = 10 per group) was followed by hourly testing from 00:00 through 12:00 day 3. Response speed (reciprocal of reaction time) across the 10-min task (by 1-min block) was analyzed prior to and after drug administration. RESULTS: A fatigue effect (response speed degradation across the 10-min task) was exacerbated by sleep deprivation and circadian rhythmicity. Prior to the drug, this effect was maximal between 08:00 and 12:00 day 3 (24-28 h sleep deprivation). Modafinil 400 mg attenuated fatigue in a manner comparable to that seen with caffeine 600 mg; these effects were especially salient during the circadian nadir of performance (06:00 through 10:00); modafinil 200 mg also reversed fatigue, but for a shorter duration (3 min) than modafinil 400 mg (8 min) or caffeine 600 mg (6 min). DISCUSSION AND CONCLUSIONS: Time-on-task effects contributed to the performance degradation seen during sleep deprivation; effects which were reversed by caffeine and, at appropriate doses, by modafinil. Because the duration of efficacy for reversing time-on-task effects was shorter at lower drug dosages, the latter must be considered when determining the appropriate dose to use during sustained operations.

Adolescent↗
PubMed2004

Effect of sleep deprivation on shuttle run score in middle-aged amateur athletes. Influence of initial score.

AIM: The aim of the present study was to investigate the effect of sleep deprivation on shuttle run score (corresponding to an estimated VO2 peak) in middle-aged amateur athletes. METHODS: Twenty-two athletes, training 9.2 hours a week (+/-4), performed a Leger and Gadoury shuttle test daily in a 4-day series that included a pre-test in day 0, 28 hours without sleep before test 1 (and 10 another hours after the test and before bedtime for a sleep deprivation of 38 hours), and then 10 hours of sleep before each of days 2 and 3. RESULTS: Shuttle run score showed no significant difference over the 4 days; however, the change in shuttle run score on day 2 was significantly correlated with the initial score. CONCLUSIONS: This result suggests that effect of sleep deprivation on shuttle run score is dependent on initial score and may encourage high level aerobic athletes to avoid sleep deprivation 2 days before a competition.

Adult↗
PubMed1992

Selected problems of analysis and interpretation of the effects of sleep deprivation on temperature and performance rhythms.

One of the major methodological-analytic problems encountered by researchers in sleep deprivation involves the examination and analysis of the relationship between sleep loss and rhythmic influences on performance. The comparison of performance rhythms with physiological rhythms, e.g., body temperature, generated under the same conditions of sleep deprivation, has become an important means of testing for an endogenous source of the rhythmicity in the data and for clarifying the nature of the proposed oscillator system. Should the data sets be correlated before or after their separation into monotonic and rhythmic parts? Correlating the raw data without separating them into their components can yield negative results, while, in reality, some of the major underlying rhythms may be highly related. The example used in this chapter showed strong cross correlations of the circadian components of temperature and two performance tasks. Sleep deprivation is thus seen to interact with performance rhythms. This interaction is only revealed after the data are analyzed and broken into their component parts. This procedure leads to the conclusion that certain performance rhythms and temperature may share the same generating oscillators.

Body Temperature↗
PubMed1994

Effect of chronic REM sleep deprivation on pituitary, hypothalamus and hippocampus PGE2 and PGD2 biosynthesis in the mouse.

Given the often reported relationships between sleep-wake regulation and the cerebral prostaglandins (PGs), the effect of chronic rapid eye movement (REM) sleep deprivation on brain PGE2 and PGD2 biosynthesis in mouse was evaluated, since they are known to have opposite actions as respectively wake- and sleep-inducing substances. Mice were subjected to 5 and 10 days of REM sleep deprivation by the flower pot technique. After sacrifice, PGE2 and PGD2 were determined in the pituitary, hypothalamus and hippocampus. Except in the pituitary where no changes were shown, the PGE2/PGD2 ratio was significantly enhanced after 5 and 10 days of REM sleep loss, when compared to control. These results showed an alteration of cerebral PGE2 and PGD2 biosynthesis, resulting in a shift from PGD2 toward PGE2. These results were not consistent with a role of PGD2 as a sleep-promoting substance as, if that was the case, it would be increased during the REM sleep deprivation. But they do not rule out its involvement as a facilitating substance.

Animals↗
PubMed1998

Relationships between thyroid hormone and antidepressant responses to total sleep deprivation in mood disorder patients.

BACKGROUND: Acute transient antidepressant effects of sleep deprivation are consistently observed in 50% of depressed patients, but the mechanisms of these, at times, dramatic improvements in mood have not been adequately elucidated. Some, but not all, studies suggest a relationship to increased thyroid-stimulating hormone (TSH) secretion. METHODS: TSH and other thyroid indices were measured at 8:00 AM after a baseline night's sleep and at 8:00 AM following a night of total sleep deprivation (S.D.) in 34 medication-free, affective disorder patients assessed with Hamilton, Beck, and Bunney-Hamburg depression ratings as well as two hourly self-ratings on a visual analog scale. RESULTS: Compared with baseline, S.D. induced highly significant increases in TSH, levothyroxine, free levothyroxine, and triiodothyronine. The 12 S.D. responders tended to have greater TSH increases than the 15 nonresponders (p < .10). The change in Beck depression ratings significantly correlated with the change in TSH (r = -.40, p = .0496, n = 24). CONCLUSIONS: These data are consistent with several other reports of a significant relationship between degree of antidepressant response to S.D. and increases in TSH measured at 8:00 AM near their usual nadir. Acute removal of the sleep-related break on the hypothalamic-pituitary-thyroid axis remains a promising candidate for the mechanism of sleep deprivation-induced improvement in mood in depressed patients.

Adult↗
PubMed2003

Caffeine effects on marksmanship during high-stress military training with 72 hour sleep deprivation.

PURPOSE: Navy SEALs (sea, air, land) are elite special warfare units that conduct unconventional warfare primarily in marine environments. Marksmanship accuracy and sighting time were quantified with 62 male trainees during Navy SEAL Hell Week, which involves the combined stress of sleep loss, operational combat scenarios, and cold-wet environmental conditions. Caffeine was administered to minimize deficits due to sleep deprivation. METHODS: Volunteers dry-fired a disabled rifle equipped with a laser-based marksmanship simulator system to measure shooting speed and accuracy. The target was a 2.3-cm diameter circle at a distance of 5 m, simulating a 46 cm target at a distance of 50 m. Marksmanship was assessed prior to training, and at 73 and 80 h into Hell Week. Volunteers were randomly assigned to 1 of 4 treatments: 100, 200, or 300 mg of caffeine or a placebo. Dosing occurred 72 h after training commenced. RESULTS: The combined effects of almost 73 h of total sleep deprivation and operational and environmental stress degraded all marksmanship accuracy measures (p < 0.05) as shown by the 37.5% increase in percent of targets missed, 38% increase in distance from center of mass of the target, and the 235% increase in shot group tightness. Sighting time increased by 53% or 3.1 s after 73 h of sleep deprivation (p < 0.05). Sighting time was significantly faster in sleep deprived individuals after taking 200 or 300 mg of caffeine compared with placebo or 100 mg of caffeine. No differences in accuracy measures between caffeine treatment groups were evident at any test period. CONCLUSION: During periods of sleep deprivation combined with other stressors, the use of 200 or 300 mg of caffeine enabled SEAL trainees to sight the target and pull the trigger faster without compromising shooting accuracy.

Adult↗
PubMed1996

The impact of sleep deprivation on erotic erections.

OBJECTIVE AND METHODS: The audiovisual stimulation penogram seems to be an appropriate screening test for erectile failure. However, falsely abnormal findings in psychogenically impotent patients with severe excitement inhibition can be found. Since disinhibitory effects may occur after sleep deprivation, we evaluated RigiScan results during audiovisual stimulation before and after sleep deprivation in 36 psychogenically impotent men. RESULTS: In our patients, sleep deprivation induced an increase in penile tumescence and rigidity before intracavernous injection of prostaglandin E1 as well as after the injection. CONCLUSION: Our data suggest that sleep deprivation combined with vascular testing and visual stimulation might lead to more precise diagnosis in male impotence.

Adult↗
PubMed1995

Effect of total sleep deprivation on reaction time and waking EEG activity in man.

Nine paid volunteers were sleep deprived over a period of 40 hours. Every 2 hours during total sleep deprivation (TSD) and after recovery sleep, oral temperature (OT), reaction time (RT) in a vigilance task and electroencephalogram (EEG) with eyes open and closed (C3, C4, T3 and T4) were recorded. Ten artifact-free samples from each condition were Fourier transformed. Absolute power was calculated for six bands. Analyses of variance with deprivation and time of day as factors showed the following significant results: 1) TSD induced an increase in RT, of theta power in all derivations, of beta power in both centrals and a decrease of alpha power with eyes closed; OT was not affected. 2) All bands showed a peak of power at 1800 hours, 2 hours in advance of the OT acrophase at 2000 hours. All variables recovered baseline values after 1 night of sleep. Significant linear correlations of hours of wakefulness with EEG and RT, and of EEG power with OT and RT, were observed. The present findings show a linear increase in EEG power and RT with TSD, and a diurnal oscillation of EEG power, which is independent of TSD.

Adult↗