The effects of sleep deprivation on divergent thinking and attention processes

SUMMARY  Twelve male undergraduate students were deprived of sleep for one night and were tested with a series of cognitive tasks. Their performance was compared to the performance of thirteen control subjects. Two hourly tasks and three occasional tasks were administered in order to examine cognitive performance following sleep loss. In an attempt to replicate the findings of Horne (1988a), the figural form of the Torrance Tests of Creative Thinking was administered. To explore the effects of short-term sleep deprivation on attention, the following tasks were also administered: a working memory task, a trail-making task, a vowel/consonant discrimination task, and a letter recognition task. Results of the Torrance test, trail-making task and letter recognition task revealed decreases in cognitive abilities following sleep loss, although all tasks required less than 10 minutes to administer. The results of this study suggest that cognitive measures following sleep deprivation have not been adequately explored. Results support the hypothesis that sleep serves a function of cognitive restitution, particularly in the maintenance of attentional mechanisms.     

Increased cerebral response during a divided attention task following sleep deprivation

We recently reported that the brain showed greater responsiveness to some cognitive demands following total sleep deprivation (TSD). Specifically, verbal learning led to increased cerebral activation following TSD while arithmetic resulted in decreased activation. Here we report data from a divided attention task that combined verbal learning and arithmetic. Thirteen normal control subjects performed the task while undergoing functional magnetic resonance imaging (FMRI) scans after a normal night of sleep and following 35 h TSD. Behaviourally, subjects showed only modest impairments following TSD. With respect to cerebral activation, the results showed (a) increased activation in the prefrontal cortex and parietal lobes, particularly in the right hemisphere, following TSD, (b) activation in left inferior frontal gyrus correlated with increased subjective sleepiness after TSD, and (c) activation in bilateral parietal lobes correlated with the extent of intact memory performance after TSD. Many of the brain regions showing a greater response after TSD compared with normal sleep are thought to be involved in control of attention. These data imply that the divided attention task required more attentional resources (specifically, performance monitoring and sustained attention) following TSD than after normal sleep. Other neuroimaging results may relate to the verbal learning and/or arithmetic demands of the task. This is the first study to examine divided attention performance after TSD with neuroimaging and supports our previous suggestion that the brain may be more plastic during cognitive performance following TSD than previously thought.     

Dynamics of cerebral responses to sustained attention performance during one night of sleep deprivation

Total sleep deprivation (TSD) is increasingly common in modern society bringing various neurobehavioural effects. Dynamic changes of behaviour performances during TSD have been reported extensively, while the cerebral activation underlying such changes have not been elucidated clearly. This study aimed to investigate dynamic changes in cerebral responses to the fastest and slowest psychomotor vigilance task (PVT) trials during TSD. Thirty‐six healthy subjects with intermediate chronotype performed the PVT while undergoing functional magnetic resonance imaging every 2 h from 22:00 hours on the first day to 06:00 hours on the second day (i.e. 22:00, 12:00, 02:00, 04:00 and 06:00 hours; a total of five imaging sessions). Behaviourally, significant time effects were found for the PVT performance. For imaging results, significant activation alterations were found in the cognitive control network and the default mode network (DMN) for the fastest and slowest PVT trials, respectively. Time–course analysis indicated that the largest differences for behavioural results and imaging results happened in session 4 and became more prominent in session 5. Our findings provide more detailed information about the process of sustained attention activation during one night of TSD and add information regarding the effect of circadian rhythmicity and homeostatic sleep pressure on regional brain responses.     

Plasma melatonin rhythms in young and older humans during sleep, sleep deprivation, and wake

STUDY OBJECTIVES: To determine the effects of sleep and sleep deprivation on plasma melatonin concentrations in humans and whether these effects are age-dependent. DESIGN: At least 2 weeks of regular at-home, sleep/wake schedule followed by 3 baseline days in the laboratory and at least one constant routine (sleep deprivation). SETTING: General Clinical Research Center (GCRC), Brigham and Women's Hospital, Boston, MA. PARTICIPANTS: In Study 1, one group (<10 lux when awake) of 19 young men (18-30 y) plus a second group (<2 lux when awake) of 15 young men (20-28 y) and 10 young women (19-27 y); in Study 2, 90 young men (18-30 y), 18 older women (65-81 y), and 11 older men (64-75 y). All participants were in good health, as determined by medical and psychological screening. INTERVENTIONS: One to three constant routines with interspersed inversion of the sleep/wake cycle in those with multiple constant routines. MEASUREMENTS AND RESULTS: Examination of plasma melatonin concentrations and core body temperature. Study 1. There was a small, but significant effect of sleep deprivation of up to 50 hours on melatonin concentrations (increase of 9.81 +/- 3.73%, P <0.05, compared to normally timed melatonin). There was also an effect of circadian phase angle with the prior sleep episode, such that if melatonin onset occurred <8 hours after wake time, the amplitude was significantly lower (22.4% +/- 4.79%, P <0.001). Study 2. In comparing melatonin concentrations during sleep to the same hours during constant wakefulness, in young men, melatonin amplitude was 6.7% +/- 2.1% higher(P <0.001) during the sleep episode. In older men, melatonin amplitude was 37.0% +/- 12.5% lower (P <0.05) during the sleep episode and in older women, melatonin amplitude was non-significantly 10.9% +/- 8.38% lower (P = 0.13) during the sleep episode. CONCLUSIONS: Both sleep and sleep deprivation likely influence melatonin amplitude, and the effect of sleep on melatonin appears to be age dependent.     

Combination of bright light and caffeine as a countermeasure for impaired alertness and performance during extended sleep deprivation

Effects of four conditions (Dim Light-Placebo, Dim Light-Caffeine, Bright Light-Placebo and Bright Light-Caffeine) on alertness, and performance were studied during the night-time hours across 45.5 h of sleep deprivation. Caffeine (200 mg) was administered at 20.00 and 02.00 hours and bright-light exposure (>2000 lux) was from 20.00 to 08.00 hours each night. The three treatment conditions, compared to the Dim Light-Placebo condition, enhanced night-time performance. Further, the combined treatment of caffeine and all-night bright light (Bright Light-Caffeine) enhanced performance to a larger degree than either the Dim Light-Caffeine or the Bright Light-Placebo condition. Beneficial effects of the treatments on performance were largest during the early morning hours (e.g. after 02.00 hours) when performance in the Dim Light-Placebo group was at its worst. Notably, the Bright Light-Caffeine condition was able to overcome the circadian drop in performance for most tasks measured. Both caffeine conditions improved objective alertness on the Maintenance of Wakefulness Test. Taken together, the above results suggest that the combined treatment of bright light and caffeine provides an effective intervention for enhancing alertness and performance during sleep loss.     

Mood impairment is stronger in young than in older adults after sleep deprivation

Sleep deprivation commonly impairs affective regulation and causes worse mood. However, the majority of previous research concerns young adults. Because susceptibility to sleep deprivation and emotion regulation change distinctively across adult age, we tested here the hypothesis that the effect of sleep deprivation on mood is stronger in young than in older adults. In an experimental design, young (18–30 years) and older adults (60–72 years) participated in either a sleep control (young, n = 63; older, n = 47) or a total sleep deprivation condition (young, n = 61; older, n = 47). Sleepiness, mood and common symptoms of sleep deprivation were measured using established questionnaires and ratings. Sleep‐deprived participants felt more sleepy, stressed and cold, and reported lower vigour and positive affect, regardless of age. All the other outcome measures (negative affect, depression, confusion, tension, anger, fatigue, total mood disturbance, hunger, cognitive attenuation, irritability) showed a weaker response to sleep deprivation in the older group, as indicated by age*sleep deprivation interactions (ps < 0.05). The results show that older adults are emotionally less affected by sleep deprivation than young adults. This tolerance was mainly related to an attenuated increase in negative mood. This could possibly be related to the well‐known positivity effect, which suggests that older adults prioritize regulating their emotions to optimize well‐being. The results also highlight that caution is warranted when generalizing results from sleep deprivation studies across the adult lifespan.     

The effect of time on task,sleep deprivation,and time of day on simulated driving performance

Sleep deprivation and time of day have been shown to play a critical role in decreasing ability to sustain attention, such as when driving long distances. However, a gap in the literature exists regarding external factors, such as workload. One way to examine workload is via modulating time on task. This study investigated the combined effect of sleep deprivation, time of day, and time on task as a workload factor on driving performance. Twenty-one participants (18–34 years, 10 females) underwent 62 h of sleep deprivation within a controlled laboratory environment. Participants received an 8-h baseline and 9.5-h recovery sleep. Every 8 h, participants completed a Psychomotor Vigilance Task (PVT), Karolinska Sleepiness Scale (KSS), 30-min monotonous driving task and NASA-Task Load Index (TLX). Driving variables examined were lane deviation, number of crashes, speed deviation and time outside the safe zone. Workload was measured by comparing two 15-min loops of the driving track. A mixed model ANOVA revealed significant main effects of day and time of day on all driving performance measures (p < .001). There was a significant main effect of workload on lane deviation (p < .05), indicating that a longer time on task resulted in greater lane deviation. A significant main effect of day (p < .001) but not time of day for the NASA-TLX, PVT and KSS was found. Time on task has a significant further impact on driving performance and should be considered alongside sleep deprivation and time of day when implementing strategies for long-distance driving.     

Local sweating responses during recovery sleep after sleep deprivation in humans

Changes in the central control of sweating were investigated in five sleep-deprived subjects (kept awake for 40 h) during their recovery sleep under warm ambient conditions [operative temperature (T _o) was either 35 or 38° C]. Oesophageal (T _oes) and mean skin (T _sk) temperatures, chest sweat rate (m _sw,ch), and concomitant electro-encephalographic data were recorded. Throughout the night at 35 or 38° C T _o, m _sw,ch changes were measured at a constant local chest skin temperature (T _ch) of 35.5° C. The results showed that body temperatures (T _oes and T _sk) of sleep-deprived subjects were influenced by thermal and hypnogogic conditions. The m _sw,ch levels correlated positively with T _oes in the subjects studied during sleep stage 1–2 (light sleep: LS), sleep stage 3–4 (slow wave sleep: SWS) and rapid eye movement (REM) sleep. Contrary to what has been reported in normal sleep, firstly, the T _oes threshold for sweating onset differed between REM sleep and both LS and SWS, and, secondly, the slopes of the m _sw,ch versus T _oes relationships were unchanged between REM and non-REM (i.e. LS or SWS) sleep. The changes observed after sleep deprivation were hypothesized to be due to alterations in the functioning of the central nervous system controller.     

Staying vigilant during recurrent sleep restriction: dose-response effects of time-in-bed and benefits of daytime napping

Study ObjectivesWe characterized vigilance deterioration with increasing time-on-task (ToT) during recurrent sleep restriction of different extents on simulated weekdays and recovery sleep on weekends, and tested the effectiveness of afternoon napping in ameliorating ToT-related deficits.MethodsIn the Need for Sleep studies, 194 adolescents (age = 15–19 years) underwent two baseline nights of 9-h time-in-bed (TIB), followed by two cycles of weekday manipulation nights and weekend recovery nights (9-h TIB). They were allocated 9 h, 8 h, 6.5 h, or 5 h of TIB for nocturnal sleep on weekdays. Three additional groups with 5 h or 6.5 h TIB were given an afternoon nap opportunity (5 h + 1 h, 5 h + 1.5 h, and 6.5 h + 1.5 h). ToT effects were quantified by performance change from the first 2 min to the last 2 min in a 10-min Psychomotor Vigilance Task administered daily.ResultsThe 9 h and the 8 h groups showed comparable ToT effects that remained at baseline levels throughout the protocol. ToT-related deficits were greater among the 5 h and the 6.5 h groups, increased prominently in the second week of sleep restriction despite partial recuperation during the intervening recovery period and diverged between these two groups from the fifth sleep-restricted night. Daytime napping attenuated ToT effects when nocturnal sleep restriction was severe (i.e. 5-h TIB/night), and held steady at baseline levels for a milder dose of nocturnal sleep restriction when total TIB across 24 h was within the age-specific recommended sleep duration (i.e. 6.5 h + 1.5 h).ConclusionsReducing TIB beyond the recommended duration significantly increases ToT-associated vigilance impairment, particularly during recurrent periods of sleep restriction. Daytime napping is effective in ameliorating such decrement.Clinical Trial Registration{"type":"clinical-trial","attrs":{"text":"NCT02838095","term_id":"NCT02838095"}}NCT02838095, {"type":"clinical-trial","attrs":{"text":"NCT03333512","term_id":"NCT03333512"}}NCT03333512, and {"type":"clinical-trial","attrs":{"text":"NCT04044885","term_id":"NCT04044885"}}NCT04044885.     

Comparison of sustained attention assessed by auditory and visual psychomotor vigilance tasks prior to and during sleep deprivation

To date, no detailed examination of the pattern of change in reaction time performance for different sensory modalities has been conducted across the circadian cycle during sleep deprivation. Therefore, we compared sustained auditory and visual attention performance during 40 h of sleep deprivation assessing multiple metrics of auditory and visual psychomotor vigilance tasks (PVT). Forty healthy participants (14 women) aged 30.8 ± 8.6 years were studied. Subjects were scheduled for an ∼8 h sleep schedule at home prior to three–six laboratory baseline days with an 8 h sleep schedule followed by 40 h sleep deprivation. Visual and auditory PVTs were 10 min in duration, and were administered every 2 h during sleep deprivation. Data were analysed with mixed‐model anova . Sleep deprivation and circadian phase increased response time, lapses, anticipations, standard deviation of response times and time on task decrements for visual and auditory PVTs. In general, auditory vigilance was faster and less variable than visual vigilance, with larger differences between auditory and visual PVT during sleep deprivation versus baseline. Failures to respond to stimuli within 10 s were four times more likely to occur to visual versus auditory stimuli. Our findings highlight that lapses during sleep deprivation are more than just long responses due to eye closure or visual distraction. Furthermore, our findings imply that the general pattern of change in attention during sleep deprivation (e.g. circadian variation, response slowing, lapsing and anticipations, time on task decrements and state instability) is similar among sensory–motor behavioral response modalities.     

Reversal of paradoxical sleep deprivation by amygdaloid stimulation during learning

Rats were subjected to a partial, selective paradoxical sleep (PS) deprivation. Two groups were trained in a shuttle avoidance task, one receiving posttraining amygdaloid stimulations (AS). A third group received AS, but was not trained. Levels of PS in the AS trained group were higher than in the AS non-trained controls, while the reverse was true for the slow wave sleep (SWS) measure. Both AS groups had levels of PS and SWS superior to the non-AS trained rats. In a second experiment, a group of normally rested AS animals was trained in the same task with a non-AS control group. These groups did not differ in terms of learning performance. Results were believed to support the hypothesis of a close relationship between sleep and learning.     

Event-related activity and phase locking during a psychomotor vigilance task over the course of sleep deprivation

There is profound knowledge that sleep restriction increases tonic (event‐unrelated) electroencephalographic (EEG) activity. In the present study we focused on time‐locked activity by means of phasic (event‐related) EEG analysis during a psychomotor vigilance task (PVT) over the course of sleep deprivation. Twenty healthy subjects (10 male; mean age ± SD: 23.45 ± 1.97 years) underwent sleep deprivation for 24 h. Subjects had to rate their sleepiness hourly (Karolinska Sleepiness Scale) and to perform a PVT while EEG was recorded simultaneously. Tonic EEG changes in the δ (1–4 Hz), θ (4–8 Hz) and α (8–12 Hz) frequency range were investigated by power spectral analyses. Single‐trial (phase‐locking index, PLI) and event‐related potential (ERP) analyses (P1, N1) were used to examine event‐related changes in EEG activity. Subjective sleepiness, PVT reaction times and tonic EEG activity (delta and theta spectral power) significantly increased over the night. In contrast, event‐related EEG parameters decreased throughout sleep deprivation. Specifically, the ERP component P1 diminished in amplitude, and delta and theta PLI estimates decreased progressively over the night. It is suggested that event‐related EEG measures (such as the amplitude of the P1 and especially delta/theta phase‐locking) serve as a complimentary method to track the deterioration of attention and performance during sleep loss. As these measures actually reflect the impaired response to specific events rather than tonic changes during sleep deprivation they are a promising tool for future sleep research.     

Inter- and intra-individual variability in performance near the circadian nadir during sleep deprivation

The study purpose was to assess inter- and intra-individual variability in neurobehavioral function near the circadian nadir during sleep deprivation and conduct exploratory factor analyses to assess relationships among alertness and performance measures during sleep deprivation. Twenty-five healthy individuals (16 females) aged 18-25 years participated. Participants were sleep deprived for two nights under controlled laboratory conditions using a modified constant routine procedure. A comprehensive battery of neurobehavioral performance tests, subjective sleepiness (SSS), and objective alertness (MWT) were assessed. Seventeen of the 22 neurobehavioral measures were impaired by sleep deprivation (all P < 0.01). The use of multiple neurobehavioral performance measures revealed impairments for all individuals during sleep deprivation. However, sleep deprivation effects were task dependent within and between individuals. Gender contributed minimally to inter-individual variability in performance. Exploratory factor analysis reduced the 22 measures to seven independent factors. Our findings indicate that no individual was especially vulnerable or resistant to the performance impairing effects of sleep deprivation. Instead, inter- and intra-individual variability in performance during sleep deprivation was task dependent. The finding that subjective sleepiness and objective alertness were not related to any performance measure during sleep deprivation suggests that these measures may assess independent brain functions.     

Effect of driving duration and partial sleep deprivation on subsequent alertness and performance of car drivers

The effect of partial sleep deprivation and driving duration on subsequent alertness and performance in car drivers was investigated. Twenty healthy male subjects, between 25 and 55 years of age, free from any sleep disorder, took part in two simulated driving sessions carried out between 2 p.m. and 4 p.m. Before one session, subjects were sleep deprived as they were allowed to sleep only between 3 a.m. and 7 a.m. during the preceding night. Throughout the driving task, the subjects' driving performance, electroencephalogram and Karolinska Sleepiness Scale (KSS) score were recorded. The results revealed that sleep deprivation had an effect on KSS score but not on the (alpha+theta) spectral power, while driving duration had an effect on these two parameters. This effect was also influenced by sleep restriction. Time on driving task alone had a significant effect on driving performance; the sleep restriction having only an effect on one of the performances indices studied: the number of right edge-line crossings. These results are interpreted in terms of the relationship between level of alertness and performance impairment.     

Lengthening of the photoperiod influences sleep characteristics before and during total sleep deprivation in rat

The photoperiod has been evidenced to influence sleep regulation in the rat. Nevertheless, lengthening of the photoperiod beyond 30 days seems to have little effect on the 24‐hr baseline level of sleep and the response to total sleep deprivation. We studied the effects of 12:12 (habitual) and 16:8 (long) light–dark photoperiods on sleep, locomotor activity and body core temperature, before and after 24 hr of total sleep deprivation. Eight rats were submitted for 14 days to light–dark 12:12 (lights on: 08:00 hours–20:00 hours) followed by total sleep deprivation, and then for 14 days to light–dark 16:8 (light extended to 24:00 hours) followed by total sleep deprivation. Rats were simultaneously recorded for electroencephalogram, locomotor activity and body core temperature for 24 hr before and after total sleep deprivation. At baseline before total sleep deprivation, total sleep time and non‐rapid eye movement sleep per 24 hr and during extended light hours (20:00 hours–24:00 hours) were higher (13% for total sleep time) after light–dark exposure compared with habitual photoperiod, while percentage delta power in non‐rapid eye movements and rapid eye movements were unchanged. Locomotor activity and body core temperature were lower, particularly during extended light hours (20:00 hours–24:00 hours). Following total sleep deprivation, total sleep time and non‐rapid eye movements were significantly lower after long photoperiod between 20:00 hours and 24:00 hours, and between 10:00 hours and 12:00 hours, and unchanged per 24 hr. The percentage delta power in non‐rapid eye movements was lower between 08:00 hours and 11:00 hours. Total sleep deprivation decreased locomotor activity and body core temperature after habitual photoperiod exposure only. Fourteen days under long photoperiod (light–dark 16:8) increased non‐rapid eye movements sleep, and decreased sleep rebound related to total sleep deprivation (lower non‐rapid eye movements duration and delta power). This may create a model of sleep extension for the rat that has been found to favour anabolism in the brain and the periphery.     

Neural basis of alertness and cognitive performance impairments during sleepiness. I. Effects of 24 h of sleep deprivation on waking human regional brain activity

The negative effects of sleep deprivation on alertness and cognitive performance suggest decreases in brain activity and function, primarily in the thalamus, a subcortical structure involved in alertness and attention, and in the prefrontal cortex, a region subserving alertness, attention, and higher-order cognitive processes. To test this hypothesis, 17 normal subjects were scanned for quantifiable brain activity changes during 85 h of sleep deprivation using positron emission tomography (PET) and (18)Fluorine-2-deoxyglucose ((18)FDG), a marker for regional cerebral metabolic rate for glucose (CMRglu) and neuronal synaptic activity. Subjects were scanned prior to and at 24-h intervals during the sleep deprivation period, for a total of four scans per subject. During each 30 min (18)FDG uptake, subjects performed a sleep deprivation-sensitive Serial Addition/Subtraction task. Polysomnographic monitoring confirmed that subjects were awake. Twenty-four hours of sleep deprivation, reported here, resulted in a significant decrease in global CMRglu, and significant decreases in absolute regional CMRglu in several cortical and subcortical structures. No areas of the brain evidenced a significant increase in absolute regional CMRglu. Significant decreases in relative regional CMRglu, reflecting regional brain reductions greater than the global decrease, occurred predominantly in the thalamus and prefrontal and posterior parietal cortices. Alertness and cognitive performance declined in association with these brain deactivations. This study provides evidence that short-term sleep deprivation produces global decreases in brain activity, with larger reductions in activity in the distributed cortico-thalamic network mediating attention and higher-order cognitive processes, and is complementary to studies demonstrating deactivation of these cortical regions during NREM and REM sleep.     

The effects of sleep deprivation in humans: topographical electroencephalogram changes in non‐rapid eye movement (NREM) sleep versus REM sleep

Studies on homeostatic aspects of sleep regulation have been focussed upon non‐rapid eye movement (NREM) sleep, and direct comparisons with regional changes in rapid eye movement (REM) sleep are sparse. To this end, evaluation of electroencephalogram (EEG) changes in recovery sleep after extended waking is the classical approach for increasing homeostatic need. Here, we studied a large sample of 40 healthy subjects, considering a full‐scalp EEG topography during baseline (BSL) and recovery sleep following 40 h of wakefulness (REC). In NREM sleep, the statistical maps of REC versus BSL differences revealed significant fronto‐central increases of power from 0.5 to 11 Hz and decreases from 13 to 15 Hz. In REM sleep, REC versus BSL differences pointed to significant fronto‐central increases in the 0.5–7 Hz and decreases in the 8–11 Hz bands. Moreover, the 12–15 Hz band showed a fronto‐parietal increase and that at 22–24 Hz exhibited a fronto‐central decrease. Hence, the 1–7 Hz range showed significant increases in both NREM sleep and REM sleep, with similar topography. The parallel change of NREM sleep and REM sleep EEG power is related, as confirmed by a correlational analysis, indicating that the increase in frequency of 2–7 Hz possibly subtends a state‐aspecific homeostatic response. On the contrary, sleep deprivation has opposite effects on alpha and sigma activity in both states. In particular, this analysis points to the presence of state‐specific homeostatic mechanisms for NREM sleep, limited to <2 Hz frequencies. In conclusion, REM sleep and NREM sleep seem to share some homeostatic mechanisms in response to sleep deprivation, as indicated mainly by the similar direction and topography of changes in low‐frequency activity.     

Self-monitoring cognitive performance during sleep deprivation: effects of modafinil,d-amphetamine and placebo

Self-monitoring refers to the ability to assess accurately one's own performance in a specific environment. The present study investigated the effects of the stimulating drugs modafinil (300 mg) and d-amphetamine (20 mg) on the ability to self-monitor cognitive performance during 64 h of sleep deprivation (SD) and sustained mental work. Two cognitive tasks were investigated: a visual (perceptual) judgment task and a complex mental addition task. Subjects in the placebo condition displayed marked circadian and SD effects on cognitive task performance but their self-monitoring was substantively undisturbed by SD. Subjects performing under the influence of d-amphetamine likewise displayed highly proficient self-monitoring throughout the SD period. In contrast, modafinil had a disruptive effect on self-monitoring, inducing a reliable «overconfidence» effect (i.e. an overestimation of actual cognitive performance), which was particularly marked 2–4 h post-dose. Although modafinil has proven to be a safe and effective countermeasure to the effects of extensive SD on cognitive task performance, we encourage a more comprehensive understanding of the relation between its subjective and performance enhancing effects before the drug is recommended as a viable fatigue countermeasure.     

Pattern of desynchronized sleep during deprivation and recovery induced in the rat by changes in ambient temperature

The pattern of desynchronized sleep (DS) occurrence in the rat was studied during exposure to an ambient temperature (Ta) of 0 degrees C for 48 h and during a 12 h recovery period at laboratory Ta (23 degrees C) following the first and second 24 h of cold exposure. The exposure to low Ta induces a DS deprivation which is followed, during recovery, by a clear DS rebound. Both the decrease and the following increase in the amount of DS are due to changes in the frequency rather than in the duration of DS episodes. The frequency distribution of the intervals between the end of one DS episode and the beginning of the next (DS interval) has shown that two populations of DS intervals exist, i.e. short DS intervals (3 min). On the basis of this, two types of DS episodes have been identified: the 'single DS episode', which is both preceded and followed by a long DS interval, and the 'sequential DS episode', which is a DS episode occurring within a cluster or a sequence of DS episodes and is characteristically separated by short DS intervals. The occurrence of such sequential DS episodes in a 'DS cluster', allows a high amount of DS to occur without increasing the duration of the DS episode. DS clusters are repressed during cold exposure, when the DS drive is counteracted by the need to thermoregulate, and enhanced during recovery, when the DS drive is unrestrained. In contrast, the occurrence of single DS episodes is much less affected by such different experimental conditions.     

Effects of amphetamine and modafinil on the sleep/wake cycle during experimental hypersomnia induced by sleep deprivation in the cat

Modafinil is a newly discovered waking substance now being used in the treatment of hypersomnia and narcolepsy. We have shown previously in the cat that, unlike amphetamine, modafinil induces long-lasting wakefulness (W) without behavioral excitation and subsequent sleep rebound, and that its waking effect does not depend on endogenous catecholamines. To further characterize the awakening properties of modafinil and current psychostimulants in experimental models of hypersomnia, we examined the effect of oral administration of placebo, modafinil (5 mg kg-1) or amphetamine (1 mg kg-1) on the sleep/wake cycle and power spectral density (PSD) in cats after an 18-h water-tank sleep deprivation period. We found that the placebo had no effect on the dynamics of sleep recovery, while both modafinil and amphetamine induced suppression of cortical slow activity and a waking state lasting 6-8 h. After the amphetamine-induced waking period, both deep slow wave sleep (SWS2) and paradoxical sleep (PS) occurred in greater amounts than after placebo and the PSD during SWS was also increased. Thus, the cumulative time spent in W during a 48-h period was similar to that with placebo, indicating enhanced sleep rebound. In contrast, after the modafinil-induced W, the occurrence and evolution of SWS2 or PS, as well as the PSD during SWS, were similar to those seen with placebo during the same period, so that the total time spent in W in a 48-h period remained significantly higher than the control level, indicating no additional sleep rebound. These results indicate that modafinil is effective against somnolence and hypersomnia and does not produce a subsequent increase in sleep and suggest that the pharmacological profile of modafinil is different from that of amphetamine.