On the ability to self-monitor cognitive performance during sleep deprivation: a calibration study

SUMMARY  The antagonistic effects of extensive sleep deprivation (SD) on human cognitive performance are well documented. However, one aspect of human performance that has not been investigated with respect to its susceptibility to SD is the 'metacognitive' ability to self-monitor overt performance. In the present study, 16 male subjects participated in an experiment requiring sustained cognitive work during a three day period. One of the cognitive tasks required the mental addition of rapidly presented numbers. On each trial, subjects reported the sum and then provided a subjective confidence rating to indicate the degree of certainty in their response. As expected, performance on the sequential addition task deteriorated with increasing fatigue and returned to baseline following a recovery sleep. However, calibration analyses, which quantify a number of properties of the relationship between subjective and overt performance, revealed that the correlation between confidence and performance (calibration), the ability to differentiate correct from incorrect judgments (resolution), and validity of subjective 'certainty', were all unaffected by SD. Hence, in the absence of external feedback from the environment, people have access to fairly reliable internal feedback about their performance during periods of sustained and vigilant cognitive activity.     

Recovery sleep and performance following sleep deprivation with dextroamphetamine

Twelve subjects were studied to determine the after-effects of using three 10-mg doses of dextroamphetamine to sustain alertness during sleep deprivation. Sleep architecture during recovery sleep was evaluated by comparing post-deprivation sleep beginning 15 h after the last dextroamphetamine dose to post-deprivation sleep after placebo. Performance and mood recovery were assessed by comparing volunteers who received dextroamphetamine first (during sleep deprivation) to those who received placebo first. Stages 1 and 2 sleep, movement time, REM latency, and sleep latency increased on the night after sleep deprivation with dextroamphetamine vs. placebo. Stage 4 was unaffected. Comparisons to baseline revealed more stage 1 during baseline than during either post-deprivation sleep period and more stage 2 during baseline than during sleep following placebo. Stage 4 sleep was lower during baseline than it was after either dose, and REM sleep was lower during baseline and after dextroamphetamine than after placebo. Sleep onset was slowest on the baseline night. Next-day performance and mood were not different as a function of whether subjects received dextroamphetamine or placebo during deprivation. These data suggest dextroamphetamine alters post-deprivation sleep architecture when used to sustain alertness during acute sleep loss, but next-day performance and subjective mood ratings are not substantially affected. A recovery sleep period of only 8 h appears to be adequate to regain baseline performance levels after short-term sleep deprivation.     

Sharp and sleepy: evidence for dissociation between sleep pressure and nocturnal performance

While sleep restriction decreases performance, not all individuals are equal with regard to sensitivity to sleep loss. We tested the hypothesis that performance could be independent of sleep pressure as defined by EEG alpha-theta power. Twenty healthy subjects (10 vulnerable and 10 resistant) underwent sleep deprivation for 25 h. Subjects had to rate their sleepiness (Karolinska Sleepiness Scale) and to perform a 10-min psychomotor vigilance task (PVT) every 2 h (20:00-08:00 hours). Sleep pressure was measured by EEG power spectral analysis (alpha-theta band 6.0-9.0 Hz). Initial performance, EEG spectral power and KSS score were equal in both groups (ANOVA, NS). The performance of vulnerable subjects significantly increased during the night (rANOVA, P < 0.01), whereas resistant subjects globally sustained their performance. Homeostatic pressure and subjective sleepiness significantly increased during the night (rANOVA, P < 0.01) identically in both categories (rANOVA, NS). Resistant subjects sustained their reaction time independently of the increase in homeostatic pressure. The phenotypic determinants of vulnerability to extended wakefulness remain unknown.     

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.     

Slow-wave sleep deprivation and waking function

SUMMARY  Slow-wave sleep (SWS) has been theorized to be an intense form of nonREM sleep, but selective deprivation of SWS or Stage 4 sleep has not been shown to cause greater decrements in alertness or performance, compared to deprivation or disruption of the other stages of sleep. The present experiment examined the effects of marked SWS deprivation (SD) for two nights, a control sleep disruption (CD) condition in which minutes of SWS were preserved, and a no sleep disruption (ND) condition. Daytime sleepiness was assessed with the multiple sleep latency test (MSLT) and performance was evaluated with the simulated assembly line task (SALT), neither of which was used in previous studies of SWS or Stage 4 sleep deprivation. In agreement with prior studies, two nights of SD did not cause greater daytime sleepiness than did CD, although sleepiness in both conditions was increased compared to the ND condition. In addition, neither SD nor CD caused declines in performance or mood. However, post hoc analysis suggests an interaction between SWS and sleep duration, such that sufficient SWS may tend to prevent adverse effects of mild sleep loss on waking function.     

Relationships between affect, vigilance, and sleepiness following sleep deprivation

This pilot study examined the relationships between the effects of sleep deprivation on subjective and objective measures of sleepiness and affect, and psychomotor vigilance performance. Following an adaptation night in the laboratory, healthy young adults were randomly assigned to either a night of total sleep deprivation (SD group; n = 15) or to a night of normal sleep (non-SD group; n = 14) under controlled laboratory conditions. The following day, subjective reports of mood and sleepiness, objective sleepiness (Multiple Sleep Latency Test and spontaneous oscillations in pupil diameter, PUI), affective reactivity/regulation (pupil dilation responses to emotional pictures), and psychomotor vigilance performance (PVT) were measured. Sleep deprivation had a significant impact on all three domains (affect, sleepiness, and vigilance), with significant group differences for eight of the nine outcome measures. Exploratory factor analyses performed across the entire sample and within the SD group alone revealed that the outcomes clustered on three orthogonal dimensions reflecting the method of measurement: physiological measures of sleepiness and affective reactivity/regulation, subjective measures of sleepiness and mood, and vigilance performance. Sleepiness and affective responses to sleep deprivation were associated (although separately for objective and subjective measures). PVT performance was also independent of the sleepiness and affect outcomes. These findings suggest that objective and subjective measures represent distinct entities that should not be assumed to be equivalent. By including affective outcomes in experimental sleep deprivation research, the impact of sleep loss on affective function and their relationship to other neurobehavioral domains can be assessed.     

Patterns of performance degradation and restoration during sleep restriction and subsequent recovery: a sleep dose-response study

Daytime performance changes were examined during chronic sleep restriction or augmentation and following subsequent recovery sleep. Sixty-six normal volunteers spent either 3 (n = 18), 5 (n= 16), 7 (n = 16), or 9 h (n = 16) daily time in bed (TIB) for 7 days (restriction/augmentation) followed by 3 days with 8 h daily TIB (recovery). In the 3-h group, speed (mean and fastest 10% of responses) on the psychomotor vigilance task (PVT) declined, and PVT lapses (reaction times greater than 500 ms) increased steadily across the 7 days of sleep restriction. In the 7- and 5-h groups speed initially declined, then appeared to stabilize at a reduced level; lapses were increased only in the 5-h group. In the 9-h group, speed and lapses remained at baseline levels. During recovery, PVT speed in the 7- and 5-h groups (and lapses in the 5-h group) remained at the stable, but reduced levels seen during the last days of the experimental phase, with no evidence of recovery. Speed and lapses in the 3-h group recovered rapidly following the first night of recovery sleep; however, recovery was incomplete with speed and lapses stabilizing at a level comparable with the 7- and 5-h groups. Performance in the 9-h group remained at baseline levels during the recovery phase. These results suggest that the brain adapts to chronic sleep restriction. In mild to moderate sleep restriction this adaptation is sufficient to stabilize performance, although at a reduced level. These adaptive changes are hypothesized to restrict brain operational capacity and to persist for several days after normal sleep duration is restored, delaying recovery.     

Age, performance and sleep deprivation

Young subjects are frequently involved in sleep-related accidents. They could be more affected than older drivers by sleep loss and therefore worsen their driving skills quicker, or have a different perception of their level of impairment. To test these hypotheses we studied variations of reaction time (RT), a fundamental prerequisite for safe performing, as measured by lapses, i.e. responses > or = 500 ms and self-assessment of performance and sleepiness after a night awake and after a night asleep in a balanced crossover design in young versus older healthy subjects. Ten young (20-25 years old) and 10 older volunteers (52-63 years old) were tested with and without 24 h of sleep deprivation. Without sleep deprivation, RTs were slower in older subjects than in the younger ones. However, after sleep deprivation, the RTs of young subjects increased while that of the older subjects remained almost unaffected. Sleepiness and self-perception of performance were equally affected in both age groups showing different perception of performance in the age groups. Our findings are discussed in terms of vulnerability to sleep-related accidents.     

Age and individual variability in performance during sleep restriction

The effect of sleep loss on reaction time (RT) performance varies as a function of age, with RTs of older subjects typically showing less decrement (relative to rested baseline) than those of younger subjects. In the current paper, we examined the nature of this relationship in a 7-day sleep restriction study. The number of repeated measures made it possible to model both intra-individual trajectories over days and individual differences in these trajectories. Results revealed (a) consistent individual differences in RT patterns over time after controlling for experimental design effects; (b) less cumulative RT decline among older individuals regardless of the degree of sleep restriction; and (c) consistent individual variability in performance patterns even after accounting for the effects of age.     

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.     

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.     

Changes in direct current potentials during sleep deprivation

Previous research reported changes in steady-state brain electrical activity during sleep. However, due to the quasi-linear nature of the Direct Current (DC) changes, artifact contamination was a potential confound. The present study was performed to further explore DC potentials and to help establish its validity. Twenty-five male university students (13 control and 12 sleep-deprived; mean age 19 y (range 17–27 y) served as subjects. During wakefulness, subjects were tested every hour while standard EEG activity recordings were made, as well as DC measurement. Split plot analyses of variance (ANOVAs) revealed that changes in DC activity levels differed between the two groups. The control subjects showed the same pattern of decreasing DC observed previously with a return to baseline levels during waking hours. The sleep-deprived subjects showed a smaller decrease in DC level through the night, followed by a rise in DC level that continued until the end of the 24 h study. It was concluded that DC measurement reflects changes in brain state associated with fatigue that are not attributable to artifactual processes.     

Effects of adaptogens on granulocytopoiesis during paradoxical sleep deprivation

We studied the effects of extracts from Siberian ginseng, Rhodiola rosea, bergenia, and ginseng (G115) and pantohematogen on granulocytopoiesis after paradoxical sleep deprivation. The effects of adaptogens on the blood system were most pronounced during hyperplasia of granulocytopoiesis. Natural preparations were divided into groups depending on their activity. Extracts of Siberian ginseng and Rhodiola rosea did not modulate granulocytopoiesis. Ginseng G115 extract suppressed granulocytopoiesis. Bergenia extract and pantohematogen produced ambiguous effects on the granulocytic hemopoietic stem.     

EEG spectral power and cognitive performance during sleep inertia: the effect of normal sleep duration and partial sleep deprivation

Sleep inertia (SI) is a transient period occurring immediately after awakening, usually characterized by performance decrement. When sleep is sufficient, SI is moderate, and produces few or no deficit. When it is associated with prior sleep deprivation, SI shows dose-dependent negative effects on cognitive performance, especially when subjects have been awaken in slow wave sleep (SWS). In the present study, spectral analysis was applied during the last 10 min before and the first 10 min after awakening, and during 1 h after awakening while subjects performed the Stroop test. Seventeen subjects were divided into a Control group who slept 8 h, and a Sleep Deprived group who slept only 2 h. The results show that performance was normal in the Control group, whereas reaction time was increased during the first half hour and error level during the second half hour in the Sleep Deprived group. Spectral analysis applied on the waking EEG during the whole test session showed that alpha activity was increased in both groups, but theta power only in the Sleep Deprived group. There was a high positive correlation in sleep deprived subjects between delta power during the last 10 min of sleep and subsequent performance decrement in speed and accuracy. Comparison of individual records showed a high positive correlation between spectral power before and after awakening in the Control group (generally in the sense of an increased frequency band), but no correlation was found in the Sleep Deprived group who exhibited a rather disorganized pattern. We discuss these results in terms of incoherence in the EEG continuity during sleep offset after prior sleep loss, which could partly account for the performance decrement observed during SI in sleep deprived subjects.     

The pendulum technique for paradoxical sleep deprivation in rats

A new technique for paradoxical sleep (PS) deprivation in rats is presented. Animals are prevented from entering into PS by allowing them to sleep for only brief periods of time. This is accomplished by an apparatus which moves the animals' cages backwards and forwards like a pendulum. At the extremes of the motion postural imbalance is produced in the animals forcing them to walk downwards to the other side of their cages. A minimal amount of PS and a moderate amount of slow wave sleep (SWS) were detected during a deprivation period of 72 hrs. Following the deprivation treatment the recovery of sleep was monitored for 3 hrs; at the beginning of the light period for one group and at the beginning of the dark period for a second group. The sleep-waking patterns of two baseline groups were established at the time when the recovery sleep was examined in the deprivation groups. The deprivation treatment resulted in a significant increase in the amount of PS and a significant decrease in the amount of SWS. The extent of PS increase was similar in both deprivation groups, in spite of a large difference in the amount of SWS. The decrease of SWS mainly occurred during recovery sleep in the light. It was observed that sleep in the dark differs from sleep in the light in behavioural aspects.     

Slow-wave sleep during a brief nap is related to reduced cognitive deficits during sleep deprivation

Sleeping for a short period (i.e. napping) may help mitigate impairments in cognitive processing caused by sleep deprivation, but there is limited research on effects of brief naps in particular. Here, we tested the effect of a brief nap opportunity (30- or 60-min) during a period of sleep deprivation on two cognitive processes with broad scope, placekeeping and vigilant attention. In the evening, participants (N = 280) completed a placekeeping task (UNRAVEL) and a vigilant attention task (Psychomotor Vigilance Task [PVT]) and were randomly assigned to either stay awake overnight or sleep at home. Sleep-deprived participants were randomly assigned to receive either no nap opportunity, a 30-min opportunity, or a 60-min opportunity. Participants who napped were set up with polysomnography. The next morning, sleep participants returned, and all participants completed UNRAVEL and the PVT. Sleep deprivation impaired performance on both tasks, but nap opportunity did not reduce the impairment, suggesting that naps longer than those tested may be necessary to cause group differences. However, in participants who napped, more time spent in slow-wave sleep (SWS) was associated with reduced performance deficits on both tasks, effects we interpret in terms of the role of SWS in alleviating sleep pressure and facilitating memory consolidation.     

Unihemispheric sleep deprivation in bottlenose dolphins

SUMMARY  Unihemispheric and bihemispheric sleep deprivation were performed in bottlenose dolphins. One brain hemisphere was capable of being deprived of delta (0.5-3.0 Hz) sleep in the former condition. Here, an increase in sleep pressure was observed during sleep deprivation in the deprived hemisphere. In the recovery sleep, following unihemispheric sleep deprivation, there was a rebound of delta sleep only in the deprived hemisphere. Following bihemispheric sleep deprivation the animals exhibited an increase in delta sleep in both hemispheres.     

Nocturnal sustained attention during sleep deprivation can be predicted by specific periods of subjective daytime alertness in normal young humans

In our 24-h society, nocturnal sleep-related accidents are common. Because all individuals are not equal in their responses to sleep loss, it is very important to identify predictors of vulnerability to sleep deprivation in normal subjects. We investigated the performance of a cognitive test of sustained attention, electroencephalogram theta/alpha power, subjective sleepiness, and two circadian markers (core temperature and melatonin) in 18 healthy men (nine morning types and nine evening types, 21.4 +/- 1.9 years) during a 36-h sleep deprivation in a constant routine protocol. Sleep need (self-reported) and baseline sleep structure were also investigated. Nighttime performance impairment was defined as the difference between the mean nocturnal number of lapses (00:00-07:30 [corrected] hours) and the mean diurnal number of lapses (07:30-20:30 hours) expressed as a percentage. Feeling fully alert in the morning just after awakening and/or sleepy in early afternoon were the only two factors (Multiple R > 0.80, > 60% of explained variance) which better predicted the decrease in performances of nocturnal operational tasks requiring sustained attention.     

Gene expression in the rat brain during sleep deprivation and recovery sleep: an Affymetrix GeneChip study

Previous studies have demonstrated that macromolecular synthesis in the brain is modulated in association with the occurrence of sleep and wakefulness. Similarly, the spectral composition of electroencephalographic activity that occurs during sleep is dependent on the duration of prior wakefulness. Since this homeostatic relationship between wake and sleep is highly conserved across mammalian species, genes that are truly involved in the electroencephalographic response to sleep deprivation might be expected to be conserved across mammalian species. Therefore, in the rat cerebral cortex, we have studied the effects of sleep deprivation on the expression of immediate early gene and heat shock protein mRNAs previously shown to be upregulated in the mouse brain in sleep deprivation and in recovery sleep after sleep deprivation. We find that the molecular response to sleep deprivation and recovery sleep in the brain is highly conserved between these two mammalian species, at least in terms of expression of immediate early gene and heat shock protein family members. Using Affymetrix Neurobiology U34 GeneChips , we also screened the rat cerebral cortex, basal forebrain, and hypothalamus for other genes whose expression may be modulated by sleep deprivation or recovery sleep. We find that the response of the basal forebrain to sleep deprivation is more similar to that of the cerebral cortex than to the hypothalamus. Together, these results suggest that sleep-dependent changes in gene expression in the cerebral cortex are similar across rodent species and therefore may underlie sleep history-dependent changes in sleep electroencephalographic activity.