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Results for “SLEEP DEPRIVATION”

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PubMed1992

Effect of sleep deprivation on brain metabolism of depressed patients.

OBJECTIVE: Sleep deprivation is a rapid, nonpharmacologic antidepressant intervention that is effective for a subset of depressed patients. The objective of this study was to identify which brain structures' activity differentiates responders from nonresponders and to study how metabolism in these brain regions changes with mood. METHOD: Regional cerebral glucose metabolism was assessed by positron emission tomography (PET) with [18F]deoxyglucose (FDG) before and after total sleep deprivation in 15 unmedicated awake patients with unipolar major depression and 15 normal control subjects, who did the continuous performance test during FDG uptake. RESULTS: After sleep deprivation, four patients showed a 40% or more improvement on the Hamilton Rating Scale for Depression. Before sleep deprivation the depressed responders had a significantly higher cingulate cortex metabolic rate than the depressed nonresponders, and this normalized after sleep deprivation. The normal control subjects and nonresponding depressed patients showed no change in cingulate metabolic rate after sleep deprivation. CONCLUSIONS: Overactivation of the limbic system as assessed by PET scans may characterize a subset of depressed patients. Normalization of activity with sleep deprivation is associated with a decrease in depression.

Adult↗

PubMed1998

Decrease in muscarinic M2 receptors from synaptosomes in the pons and hippocampus after REM sleep deprivation in rats.

The effects of both REM sleep deprivation and its recovery on pontine and hippocampus muscarinic M2 receptors were investigated in synaptosomes using [3H]-AF-DX 384 as a ligand. Animals were divided into three groups: REM sleep deprivation group (small platforms 6.5 cm of diameter); stress group (large platforms 14 cm of diameter) and cage control group. In a second experiment REM sleep-deprived animals were allowed 48 h of recovery. REM sleep-deprived rats showed a reduction in M2 receptors compared with both intact and stress groups. Changes in M2 receptors were also observed after 48 h of recovery from REM sleep deprivation only in hippocampus. The enhancement of acetylcholine release during both REM sleep deprivation and recovery could explain the present findings.

Animals↗

PubMed1999

Transcriptional activity in the brain during sleep deprivation.

Molecular biological techniques combined with experimental sleep deprivation have revealed alterations in gene transcriptional activity of several proteins which may mediate the effects of prolonged wakefulness in the brain. During sleep deprivation gene transcription is altered in neuronal systems known to participate in the regulation of vigilance and sleep, ie the norardenergic and cholinergic systems, and several neuropeptides and cytokines. The study of immediate early genes during sleep deprivation has revealed increased transcriptional activity in those brain areas that are active during wakefulness. Systemic search for alterated levels of messenger RNA in sleep-deprived brain has revealed signal transduction proteins and metabolic enzymes which may mediate changes in neuronal function during prolonged wakefulness. The purpose of this article is to give a short overview of those genes whose transcription is affected by sleep deprivation according to the current literature, and to characterize the possible role of these genes in sleep regulation.

Animals↗

PubMed2003

Total sleep deprivation elevates blood pressure through arterial baroreflex resetting: a study with microneurographic technique.

STUDY OBJECTIVES: Sleep deprivation has a profound effect on cardiovascular regulation through the autonomic nervous system. This study examined the effect of 24-hour total sleep deprivation on muscle sympathetic nerve activity (MSNA), which is a direct measurement of the postganglionic sympathetic efferent innervating the vascular bed in the skeletal muscle and other circulatory structures. DESIGN: The study was performed on 6 young healthy men. The factors exerting influence on MSNA, such as aging, obesity, body posture, activity, intensity of illumination, and food and beverage consumption were strictly controlled. Burst rate and burst incidence were used as parameters of MSNA. The burst rate, burst incidence, heart rate, and systolic and diastolic blood pressure were measured after total sleep deprivation and control sleep. To perform a linear regression analysis of arterial baroreflex (ABR), the incidence of MSNA bursts corresponding to a given diastolic blood pressure (%MSNA) was examined. MEASUREMENT AND RESULTS: The diastolic blood pressure was significantly higher after total sleep deprivation than after control sleep (66.5 +/- 1.7 vs 57.4 +/- 3.3 mm Hg). The burst rate (9.6 +/- 1.8 vs 13.3 +/- 2.7 bursts/min) and burst incidence (21.6 +/- 4.5 vs 30.3 +/- 8.9 bursts/100 heart beats) of MSNA were significantly lower after total sleep deprivation than after control sleep (P < .05). Analysis of the ABR disclosed a significant linear regressive relation between %MSNA and diastolic blood pressure in every subject after both total sleep deprivation and control sleep. This result implies that the ABR regulates the occurrence of MSNA bursts under different diastolic blood pressure conditions. The threshold (X-axis intercept) of the blood pressure regression line (ie, an indicator of the ABR set point) shifted by 12 +/- 4.3 mm Hg toward a higher blood pressure level after total sleep deprivation (P < .05). The ABR sensitivity, or the slope of the regression line, tended to be less steep after total sleep deprivation than after control sleep, although it was not statistically significant (P = .09). CONCLUSIONS: The diastolic blood pressure increased and both burst rate and burst incidence of MSNA decreased after total sleep deprivation. The results show that resetting of the ABR toward a higher blood pressure level occurred after total sleep deprivation. This ABR resetting probably brings about an increase in arterial blood pressure after total sleep deprivation.

Adult↗

PubMed2004

Does sleep or sleep deprivation increase epileptiform discharges in pediatric electroencephalograms?

OBJECTIVE: Sleep deprivation before obtaining an electroencephalogram (EEG) is believed both to increase the likelihood of sleep during an EEG and to increase the detection of interictal epileptiform discharges. However, depriving a child of sleep poses a burden on both the parent and the child. The objective of this study was to compare the effects of sleep, standard sleep deprivation, partial sleep deprivation, and no sleep deprivation on the odds of an epileptiform abnormality in outpatient pediatric EEGs. METHODS: Data were collected from all pediatric EEGs performed at a busy, university-based neurologic practice during two 2-month periods. During the first period, all EEGs were performed as ordered, either standard sleep-deprived (SSD) or non-sleep-deprived (NSD). During the second 2 months, SSD EEGs were performed per routine. However, non-SSD families were instructed to keep their children awake 2 hours later the night before the EEG. Those who complied were classified as partially sleep-deprived (PSD). Patient characteristics across protocols were compared with chi(2) and analysis of variance tests as appropriate. The odds of epileptiform and abnormal findings associated with sleep, NSD, PSD, and SSD EEGs were calculated using logistic regression. RESULTS: Of 820 eligible EEGs, sleep occurred in 22% of NSD, 44% of PSD, and 57% of SSD EEGs. The sample size of this study allowed for an 85% power, with alpha of.05, to detect an absolute increased EEG yield of 10%. Neither the presence of sleep (odds ratio [OR]: 0.99; 95% confidence interval [CI]: 0.69-1.42) nor the use of PSD (OR: 0.90; 95% CI: 0.50-1.62) or SSD (OR: 0.96; 95% CI: 0.63-1.47) protocols increased the odds of epileptiform EEGs. CONCLUSIONS: Sleep deprivation should not be used routinely to increase the yield of pediatric EEGs.

Adolescent↗

PubMed1993

A clinical trial of sleep deprivation in combination with antidepressant medication.

The literature suggests that sleep deprivation can potentiate the effect of antidepressant medication in depressed patients. However, the clinical efficacy of sleep deprivation has not been demonstrated definitively, in part because it is difficult to design an adequate control condition. We conducted a trial of sleep deprivation in 26 depressed patients who remained symptomatic despite 3 months of treatment with antidepressant medication. Since the literature indicates that early sleep deprivation (ESD), carried out in the first half of the night, is a less effective antidepressant than late sleep deprivation (LSD), carried out in the second half of the night, we designed a study that attempted to use ESD as a control condition for LSD. Patients were randomly assigned to ESD or LSD, received a total of 4 nights of sleep deprivation over 2 weeks, and were followed in clinic for the 3 subsequent weeks. ESD proved to be as effective an antidepressant as LSD, with the overall sample showing a mild, but statistically significant, response. There was a significant correlation between patients' acute response at the time of the first course of sleep deprivation treatments and their improvement over the course of the study. There were significant changes in plasma levels of thyroid stimulating hormone, free triiodothyronine, prolactin, and cortisol measured at 8 a.m. before and after sleep deprivation, and in the followup period, but there were no significant correlations between changes in hormonal levels and either acute or chronic response to sleep deprivation.

Adult↗

PubMed2005

Neurocognitive consequences of sleep deprivation.

Deficits in daytime performance due to sleep loss are experienced universally and associated with a significant social, financial, and human cost. Microsleeps, sleep attacks, and lapses in cognition increase with sleep loss as a function of state instability. Sleep deprivation studies repeatedly show a variable (negative) impact on mood, cognitive performance, and motor function due to an increasing sleep propensity and destabilization of the wake state. Specific neurocognitive domains including executive attention, working memory, and divergent higher cognitive functions are particularly vulnerable to sleep loss. In humans, functional metabolic and neurophysiological studies demonstrate that neural systems involved in executive function (i.e., prefrontal cortex) are more susceptible to sleep deprivation in some individuals than others. Recent chronic partial sleep deprivation experiments, which more closely replicate sleep loss in society, demonstrate that profound neurocognitive deficits accumulate over time in the face of subjective adaptation to the sensation of sleepiness. Sleep deprivation associated with disease-related sleep fragmentation (i.e., sleep apnea and restless legs syndrome) also results in neurocognitive performance decrements similar to those seen in sleep restriction studies. Performance deficits associated with sleep disorders are often viewed as a simple function of disease severity; however, recent experiments suggest that individual vulnerability to sleep loss may play a more critical role than previously thought.

Cognition Disorders↗

PubMed1996

Alterations in synaptosomal calcium concentrations after rapid eye movement sleep deprivation in rats.

Rapid eye movement sleep deprivation alters behavioral and physiological, as well as cellular functioning and responsiveness. Since intracellular calcium concentration plays an important role in regulating cellular functions, it was hypothesized that such deprivation might induce changes in intracellular calcium concentration. Therefore, in this study, rats were deprived of rapid eye movement sleep by the flower-pot technique, and total, bound and free calcium concentrations were estimated in synaptosomal preparations from the cerebrum, cerebellum, brainstem, midbrain, pons and medulla. Rapid eye movement sleep deprivation was continued for two or four days and suitable control experiments were conducted to rule out the effects of non-specific factors. Total calcium concentration increased in the brainstem but showed a decrease in the cerebellum and cerebrum. After four days deprivation, the free calcium concentration always decreased; however, the bound calcium concentration decreased in the cerebrum and cerebellum but increased in the brainstem. After two days' deprivation, the medulla was the only region where the bound calcium increased while the free form decreased; only the free form decreased in the pons, while the midbrain was never affected. The results suggest that there was a net efflux of calcium in the cerebellum and cerebrum, but a net influx in the brainstem. The findings support our hypothesis and help to explain earlier observations. Since it is known that calcium plays an important role in cellular functioning, these changes in calcium concentration may be the underlying mechanism for rapid eye movement sleep deprivation-induced cellular expressions and behavior of neurons.

Animals↗

PubMed2001

Serum thyrotropin concentrations and bioactivity during sleep deprivation in depression.

BACKGROUND: One night of sleep deprivation induces a brief remission in about half of depressed patients. Subclinical hypothyroidism may be associated with depression, and changes in hypothalamic-pituitary-thyroid function may affect the mood response to sleep deprivation. We wished to define precisely the status of the hypothalamic-pituitary-thyroid axis of depressed patients during sleep deprivation and the possible relationship of hypothalamic-pituitary-thyroid function to the mood response. METHODS: We studied 18 patients with major depressive disorder and 10 normal volunteers. We assessed mood before and after sleep. We measured serum thyrotropin every 15 minutes during the night of sleep deprivation, thyrotropin bioactivity, the thyrotropin response to protirelin the next afternoon, and other indexes of hypothalamic-pituitary-thyroid function. To determine if the changes were limited to the hypothalamic-pituitary-thyroid axis, we measured serum cortisol, which also has a circadian secretory pattern. RESULTS: Nocturnal serum thyrotropin concentrations were consistently higher in responders, entirely because of elevated levels in the women reponders. Responders had exaggerated responses to protirelin the next afternoon. The bioactivity of thyrotropin in nonresponders was significantly greater than in responders (F(1,8. 99) = 7.52; P =.02). Other thyroid indexes and serum cortisol concentrations were similar among groups. CONCLUSIONS: Depressed patients have mild compensated thyroid resistance to thyrotropin action, not subclinical autoimmune primary hypothyroidism. Sleep deprivation responders compensate by secreting more thyrotropin with normal bioactivity; nonresponders compensate by secreting thyrotropin with increased bioactivity.

Adult↗

PubMed1994

Lithium sustains the acute antidepressant effects of sleep deprivation: preliminary findings from a controlled study.

Early morning sleep deprivation (patient awake from 0200 to 2200 hours) produces a same-day antidepressant effect in approximately one-half of patients with major depression. Unfortunately, these antidepressant effects are short-lived and patients usually relapse to baseline depression levels within 48 hours. Recent work suggests, however, that the use of lithium with early morning sleep deprivation sustains this rapid antidepressant effect and makes it clinically useful. In a 30-day study, we compared the abilities of four different treatments (lithium plus early morning sleep deprivation, lithium plus a control sleep deprivation procedure, and desipramine with either of the two sleep manipulations) to induce a rapid (next-day) and sustained antidepressant response in 16 depressed patients. Lithium plus early morning sleep deprivation produced a quicker response than lithium with the control sleep deprivation, and the response was sustained for at least 30 days. In this design, however, lithium/early morning sleep deprivation was no faster than either of the two desipramine/sleep deprivation conditions in inducing remission. These results support the results of previous studies and suggest further investigation of this novel sleep/pharmacologic intervention is warranted.

Adult↗

PubMed2005

Decreased brain activation during a working memory task at rested baseline is associated with vulnerability to sleep deprivation.

STUDY OBJECTIVE: To examine whether differences in patterns of brain activation under baseline conditions relate to the differences in sleep-deprivation vulnerability. DESIGN: Using blood oxygenation level dependent (BOLD) functional magnetic resonance imaging, we scanned 33 healthy young men while they performed the Sternberg working memory task following a normal night of sleep and again following 30 hours of sleep deprivation. From this initial group, based on their Sternberg working memory task performance, we found 10 subjects resilient to sleep deprivation (sleep deprivation-resilient group) and then selected 10 age- and education-matched subjects vulnerable to sleep deprivation (sleep deprivation-vulnerable group). SETTING: Inpatient General Clinical Research Center and outpatient functional magnetic resonance imaging center. PATIENTS OR PARTICIPANTS: Data from 10 young men (mean age 27.8 +/- 1.7 years) in the sleep deprivation-resilient group and 10 young men (mean age 28.2 +/- 1.9 years) in the sleep deprivation-vulnerable group were included in the final analyses. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: We compared functional magnetic resonance imaging BOLD signal at rested baseline and sleep deprivation states in the 2 groups. As hypothesized, following sleep deprivation, both groups showed significant decreases in global brain activation compared to their rested group baseline. At rested baseline and in the sleep-deprivation state, the sleep deprivation-resilient group had significantly more brain activation than did the sleep deprivation-vulnerable group. There were also differences in functional circuits within and between groups in response to sleep deprivation. CONCLUSIONS: These preliminary data suggest that patterns of brain activation during the Sternberg working memory task at the rested baseline and the sleep-deprivation state, differ across individuals as a function of their sleep-deprivation vulnerability.

Adolescent↗

PubMed1984

Effects of sleep deprivation on thermoregulation during exercise.

Five fit men completed a practice, control, and sleep deprivation exercise test. Two nights of normal sleep preceded the control test, and 33 h of wakefulness preceded the sleep deprivation test. These tests consisted of 20 min of rest followed by 40 min of cycle-ergometer exercise (50% of peak O2 uptake, VO2) in a temperate (ambient temperature, 28 degrees C; relative humidity, 30%)-environment. Esophageal temperature (Tes), local sweat rate (mds), and chest thermal conductance (kch) were continuously measured. During exercise a 0.7 and 0.5 degrees C rise in Tes was found for the sleep deprivation and control tests, respectively. This increase in Tes values from rest to the end of exercise was greater (P = 0.08) for the sleep deprivation than control test. Total body sweat rate, calculated from Potter balance measurements, was 27% less (P less than 0.01) for the sleep deprivation than the control test. Both mds and kch values were lower (P less than 0.05) during the final 20 min of exercise for the sleep deprivation than control test. Final exercise mds values were 19% lower (P less than 0.05) for the sleep deprivation than control test. An asynchronous rather than a normal synchronous mds pattern was frequently observed during the sleep deprivation test. During the sleep deprivation test, the mds sensitivity (delta mds X delta Tes-1) was 38% lower (P less than 0.01) and kch sensitivity (delta kch X delta Tes-1) was 42% lower (P less than 0.05) than during the control test. These data indicate that sleep deprivation decreases evaporative and dry heat loss during moderate-intensity exercise.

Adolescent↗

PubMed2006

Effects of 3-nitropropionic acid administration on memory and hippocampal lipid peroxidation in sleep-deprived mice.

Numerous studies have described memory deficits following sleep deprivation. There is also evidence that the absence of sleep increases brain oxidative stress. The present study investigates the effects of a pro-oxidant agent--3-nitropropionic acid (3-NP)--on hippocampal oxidative stress and passive avoidance performance of sleep-deprived mice. Mice were repeatedly treated i.p. with saline or 5 or 15 mg/kg 3-NP and sleep-deprived for 24 h by the multiple platform method--groups of 4-5 animals placed in water tanks, containing 12 platforms (3 cm in diameter) surrounded by water up to 1 cm beneath the surface or kept in their home cage (control groups). The results showed that: (1) neither a 24 h sleep deprivation period nor 3-NP repeated treatment alone were able to induce memory deficits and increased hippocampal lipid peroxidation; (2) this same protocol of sleep deprivation, combined with 15 mg/kg 3-NP repeated treatment, induced memory deficits and an increase in hippocampal lipid peroxidation. The results support the involvement of hippocampal oxidative stress in the memory deficits induced by sleep deprivation and the hypothesis that normal sleep would prevent oxidative stress.

Animals↗

PubMed2003

Cocaine-induced genital reflexes during paradoxical sleep deprivation and recovery.

Paradoxical sleep deprivation (PSD) for 96 h together with cocaine administration elicits genital reflexes (penile erection [PE] and ejaculation [EJ]) in rats. Our objective was to examine genital reflexes after periods of 24, 48, 72, 96, 120, and 144 h of PSD and during a 4-day recovery period in acute cocaine-administered rats. After 24 h of PSD followed by cocaine administration, animals started to display PE and EJ, peaking in the 96th h of PSD, whereas PE and EJ were absent in control animals. The effects of more than 96 h of PSD decrease genital reflexes as observed after 120 and 144 h. Genital reflexes were present in the recovery periods but diminished gradually during the period evaluated. Even short periods of PSD probably cause supersensitivity of dopamine (DA) receptors and exacerbate the effects of cocaine on dopaminergic pathways to induce frequent PE and EJ.

Animals↗

PubMed2004

Sleep deprivation increases the activation of nuclear factor kappa B in lateral hypothalamic cells.

Sleep deprivation increases sleep propensity in rats and mice as well as the production of several sleep-regulatory substances. Nuclear factor kappa B (NF-kappa B) is a transcription factor implicated in the activation of many of these sleep-promoting substances. A unique population of neurons immunoreactive for the p65 subunit of NF-kappa B was previously localized within the caudal dorsolateral hypothalamus of rats. Therefore, we evaluated the effect of sleep deprivation on NF-kappa Bp65-immunoreactivity (IR) in cells of this region in rats as well as its nuclear translocation in a kappa B-lacZ transgenic mouse line. In rats after 6 h of sleep deprivation beginning at light onset, the number of neurons with NF-kappa Bp65-IR increased significantly in the caudal lateral hypothalamus, specifically the magnocellular lateral hypothalamus adjacent to the subthalamus. Sleep deprivation also significantly increased the number of cells expressing NF-kappa B-dependent beta-galactosidase in the magnocellular lateral hypothalamus, zona incerta dorsal, as well as the adjacent subthalamus in the transgenic mice. These results suggest that NF-kappa B expressing cells within the lateral hypothalamus may be important in the maintenance of the sleep-wake cycle.

Active Transport, Cell Nucleus↗

PubMed2003

The cumulative cost of additional wakefulness: dose-response effects on neurobehavioral functions and sleep physiology from chronic sleep restriction and total sleep deprivation.

OBJECTIVES: To inform the debate over whether human sleep can be chronically reduced without consequences, we conducted a dose-response chronic sleep restriction experiment in which waking neurobehavioral and sleep physiological functions were monitored and compared to those for total sleep deprivation. DESIGN: The chronic sleep restriction experiment involved randomization to one of three sleep doses (4 h, 6 h, or 8 h time in bed per night), which were maintained for 14 consecutive days. The total sleep deprivation experiment involved 3 nights without sleep (0 h time in bed). Each study also involved 3 baseline (pre-deprivation) days and 3 recovery days. SETTING: Both experiments were conducted under standardized laboratory conditions with continuous behavioral, physiological and medical monitoring. PARTICIPANTS: A total of n = 48 healthy adults (ages 21-38) participated in the experiments. INTERVENTIONS: Noctumal sleep periods were restricted to 8 h, 6 h or 4 h per day for 14 days, or to 0 h for 3 days. All other sleep was prohibited. RESULTS: Chronic restriction of sleep periods to 4 h or 6 h per night over 14 consecutive days resulted in significant cumulative, dose-dependent deficits in cognitive performance on all tasks. Subjective sleepiness ratings showed an acute response to sleep restriction but only small further increases on subsequent days, and did not significantly differentiate the 6 h and 4 h conditions. Polysomnographic variables and delta power in the non-REM sleep EEG-a putative marker of sleep homeostasis--displayed an acute response to sleep restriction with negligible further changes across the 14 restricted nights. Comparison of chronic sleep restriction to total sleep deprivation showed that the latter resulted in disproportionately large waking neurobehavioral and sleep delta power responses relative to how much sleep was lost. A statistical model revealed that, regardless of the mode of sleep deprivation, lapses in behavioral alertness were near-linearly related to the cumulative duration of wakefulness in excess of 15.84 h (s.e. 0.73 h). CONCLUSIONS: Since chronic restriction of sleep to 6 h or less per night produced cognitive performance deficits equivalent to up to 2 nights of total sleep deprivation, it appears that even relatively moderate sleep restriction can seriously impair waking neurobehavioral functions in healthy adults. Sleepiness ratings suggest that subjects were largely unaware of these increasing cognitive deficits, which may explain why the impact of chronic sleep restriction on waking cognitive functions is often assumed to be benign. Physiological sleep responses to chronic restriction did not mirror waking neurobehavioral responses, but cumulative wakefulness in excess of a 15.84 h predicted performance lapses across all four experimental conditions. This suggests that sleep debt is perhaps best understood as resulting in additional wakefulness that has a neurobiological "cost" which accumulates over time.

Adult↗

PubMed2003

Oculomotor impairment during chronic partial sleep deprivation.

OBJECTIVE: The effects of chronic partial sleep (sleep deprivation) and extended sleep (sleep augmentation) followed by recovery sleep on oculomotor function were evaluated in normal subjects to explore the usefulness of oculomotor assessment for alertness monitoring in fitness-for-duty testing. METHODS: Sixty-six commercial drivers (24-62 years, 50m/16f) participated in a 15 day study composed of 3 training days with 8h time in bed per night, 7 experimental days with subjects randomly assigned to either 3, 5, 7, or 9h time in bed, and 3 recovery nights with 8h time in bed. Data from 57 subjects were used. Saccadic velocity (SV), initial pupil diameter (IPD), latency to pupil constriction (CL), and amplitude of pupil constriction (CA) were assessed and correlated with the sleep latency test (SLT), the Stanford sleepiness scale (SSS), and simulated driving performance. RESULTS: Regression analyses showed that SV slowed significantly in the 3 and 5h groups, IPD decreased significantly in the 9h group, and CL increased significantly in the 3h group. SLT and SSS significantly correlated with SV, IPD, CL, and driving accidents for the 3h group, and with CL for the 5h group. Analyses also showed a significant negative correlation between decreasing SV and increasing driving accidents in the 3h group and a significant negative correlation between IPD and driving accidents for the 7h group. CONCLUSIONS: The results demonstrate a sensitivity primarily of SV to sleepiness, and a correlation of SV and IPD to impaired simulated driving performance, providing evidence for the potential utility of oculomotor indicators in the detection of excessive sleepiness and deterioration of complex motor performance with chronic partial sleep restriction. SIGNIFICANCE: This paper shows a relationship between sleep deprivation and oculomotor measures, and suggests a potential utility for oculometrics in assessing operational performance readiness under sleep restricted conditions.

Accidents, Traffic↗

PubMed1999

Effects of modafinil and amphetamine on sleep-wake cycle after sleep deprivation in cats.

AIM: The effects of modafinil and amphetamine on sleep-wake cycle and cortical power spectrum were assessed in the cats before and after sleep deprivation. METHODS: The sleep deprivation in the cats was used with the water tank technique. Cats were administrated with modafinil (5 mg.kg-1 p.o.) or amphetamine (1 mg.kg-1) before and after sleep deprivation. RESULTS: The waking effect of 8-10 h induced by modafinil before and after sleep deprivation was similar and was not followed by an increase in sleep rebound. On the contrary, the arousal effect about 8 h evoked by amphetamine after sleep deprivation was less lasting than that of 10-12 h observed in normal conditions and followed by an amplified rebound in both deep slow wave sleep and paradoxical sleep. CONCLUSION: These results suggest the efficiency of modafinil against somnolence and hypersomnia without increasing subsequent sleep.

Amphetamine↗