The ability to self‐monitor cognitive performance during 60 h total sleep deprivation and following 2 nights recovery sleep

We aimed to investigate whether self‐monitoring of performance is altered during 60 h of total sleep deprivation, following 2 nights of recovery sleep, and by task difficulty and/or subjective sleepiness. Forty adults (22 females, aged 19–39 years) underwent a 5‐day protocol, with a well‐rested day, 66 h total sleep deprivation (last test session at 60 h), and 2 nights of 8 h recovery sleep. An arithmetic task (MATH) with three difficulty levels assessed working memory. The Psychomotor Vigilance Task assessed sustained attention. Arithmetic accuracy and Psychomotor Vigilance Task median reaction time measured objective performance. Subjective performance was measured with self‐reported accuracy and speed. Objective–subjective differences assessed self‐monitoring ability. The performance on both tasks declined during total sleep deprivation and improved following recovery. During total sleep deprivation, participants accurately self‐monitored performance on the Psychomotor Vigilance Task; however, they overestimated cognitive deficits on MATH, self‐reporting performance as worse than actually observed. Following recovery, participants overestimated the extent of performance improvement on the Psychomotor Vigilance Task. Task difficulty influenced self‐monitoring ability, with greater overestimation of performance deficits during total sleep deprivation as difficulty increased. Subjective sleepiness predicted subjective performance ratings at several time points, only for the Psychomotor Vigilance Task. The ability to self‐monitor performance was impaired during total sleep deprivation for working memory and after recovery sleep for the Psychomotor Vigilance Task, but was otherwise accurate. The development of self‐monitoring strategies, assessing both subjective perceptions of performance and subjective sleepiness, within operational contexts may help reduce the consequences of sleep‐related impairments.     

Improved vigilance after sodium oxybate treatment in narcolepsy: a comparison between in‐field and in‐laboratory measurements

This two‐centre observational study of vigilance measurements assessed the feasibility of vigilance measurements on multiple days using the Sustained Attention to Response Task and the Psychomotor Vigilance Test with portable task equipment, and subsequently assessed the effect of sodium oxybate treatment on vigilance in patients with narcolepsy. Twenty‐six patients with narcolepsy and 15 healthy controls were included. The study comprised two in‐laboratory days for the Maintenance of Wakefulness Test and the Oxford Sleep Resistance test, followed by 7‐day portable vigilance battery measurements. This procedure was repeated for patients with narcolepsy after at least 3 months of stable treatment with sodium oxybate. Patients with narcolepsy had a higher Sustained Attention to Response Task error count, lower Psychomotor Vigilance Test reciprocal reaction time, higher Oxford Sleep Resistance test omission error count adjusted for test duration (Oxford Sleep Resistance test_OMIS/MIN), and lower Oxford Sleep Resistance test and Maintenance of Wakefulness Test sleep latency compared with controls (all P < 0.01). Treatment with sodium oxybate was associated with a longer Maintenance of Wakefulness Test sleep latency (P < 0.01), lower Oxford Sleep Resistance test_OMIS/MIN (P = 0.01) and a lower Sustained Attention to Response Task error count (P = 0.01) in patients with narcolepsy, but not with absolute changes in Oxford Sleep Resistance test sleep latency or Psychomotor Vigilance Test reciprocal reaction time. It was concluded that portable measurements of sustained attention as well as in‐laboratory Oxford Sleep Resistance test and Maintenance of Wakefulness Test measurements revealed worse performance for narcoleptic patients compared with controls, and that sodium oxybate was associated with an improvement of sustained attention and a better resistance to sleep.     

Scheduled napping as a countermeasure to sleepiness in air traffic controllers

The aims of this study were to measure sleep during a planned nap on the night shift; and to use objective measures of performance and alertness to compare the effects of the nap opportunity versus staying awake. Twenty-eight air traffic controllers (mean age 36 years, nine women) completed four night shifts (two with early starts and two with late starts). Each type of night shift (early/late start) included a 40-min planned nap opportunity on one occasion and no nap on the other. Polysomnographic data were used to measure sleep and waking alertness [spectral power in the electroencephalogram (EEG) during the last hour of the night shift and the occurrence of slow rolling eye movements (SEMs) subsequent to the nap]. Psychomotor performance task [Psychomotor Vigilance Task (PVT)] was completed at the beginning and end of the shift, and after the nap (or an equivalent time if no nap was taken). Nap sleep latencies were relatively long (mean = 19 min) and total sleep time short (mean = 18 min), with minimal slow wave sleep (SWS, mean = 0%), and no rapid eye movement sleep. Nap sleep resulted in improved PVT performance (mean and slowest 10% of reaction time events), decreased spectral power in the EEG and reduced the likelihood of SEMs. The occurrence of SWS in the nap decreased spectral power in the EEG. This study indicates that although sleep taken at work is likely to be short and of poor quality it still results in an improvement in objective measures of alertness and performance.     

In‐flight sleep,pilot fatigue and Psychomotor Vigilance Task performance on ultra‐long range versus long range flights

This study evaluated whether pilot fatigue was greater on ultra‐long range (ULR) trips (flights >16 h on 10% of trips in a 90‐day period) than on long range (LR) trips. The within‐subjects design controlled for crew complement, pattern of in‐flight breaks, flight direction and departure time. Thirty male Captains (mean age = 54.5 years) and 40 male First officers (mean age = 48.0 years) were monitored on commercial passenger flights (Boeing 777 aircraft). Sleep was monitored (actigraphy, duty/sleep diaries) from 3 days before the first study trip to 3 days after the second study trip. Karolinska Sleepiness Scale, Samn–Perelli fatigue ratings and a 5‐min Psychomotor Vigilance Task were completed before, during and after every flight. Total sleep in the 24 h before outbound flights and before inbound flights after 2‐day layovers was comparable for ULR and LR flights. All pilots slept on all flights. For each additional hour of flight time, they obtained an estimated additional 12.3 min of sleep. Estimated mean total sleep was longer on ULR flights (3 h 53 min) than LR flights (3 h 15 min; P(F) = 0.0004). Sleepiness ratings were lower and mean reaction speed was faster at the end of ULR flights. Findings suggest that additional in‐flight sleep mitigated fatigue effectively on longer flights. Further research is needed to clarify the contributions to fatigue of in‐flight sleep versus time awake at top of descent. The study design was limited to eastward outbound flights with two Captains and two First Officers. Caution must be exercised when extrapolating to different operations.     

An experimental study of adolescent sleep restriction during a simulated school week: changes in phase,sleep staging,performance and sleepiness

This laboratory study investigated the impact of restricted sleep during a simulated school week on circadian phase, sleep stages and daytime functioning. Changes were examined across and within days and during a simulated weekend recovery. Participants were 12 healthy secondary school students (six male) aged 15–17 years [mean = 16.1 years, standard deviation (SD) = 0.9]. After 2 nights with 10 h (21:30–07:30 hours), time in bed was restricted to 5 h for 5 nights (02:30–07:30 hours), then returned to 10 h time in bed for 2 nights (21:30–07:30 hours). Saliva was collected in dim light on the first and last sleep restriction nights to measure melatonin onset phase. Sleep was recorded polysomnographically, and the Psychomotor Vigilance Task (PVT) and Karolinska Sleepiness Scale were undertaken 3‐hourly while awake. Average phase delay measured by melatonin was 3 h (SD = 50 min). Compared to baseline, sleep during the restriction period contained a smaller percentage of Stages 1 and 2 and rapid eye movement (REM) and a greater percentage of Stage 4. PVT lapses increased significantly during sleep restriction and did not return to baseline levels during recovery. Subjective sleepiness showed a similar pattern during restriction, but returned to baseline levels during recovery. Results suggest that sustained attention in adolescents is affected negatively by sleep restriction, particularly in the early morning, and that a weekend of recovery sleep is insufficient to restore performance. The discrepancy between sleepiness ratings and performance may indicate a lack of perception of this residual impairment.     

Tiagabine is associated with sustained attention during sleep restriction: evidence for the value of slow-wave sleep enhancement?

STUDY OBJECTIVES: To evaluate the impact of enhanced slow-wave sleep (SWS) on behavioral, psychological, and physiologic changes resulting from sleep restriction DESIGN: A double-blind, parallel-group, placebo-controlled design was used to compare tiagabine, 8 mg, (a SWS-enhancing drug) to placebo during 4 nights of sleep restriction (time in bed = 5 hours per night). Behavioral, psychological, and physiologic measures of the impact of sleep restriction were compared between groups at baseline, during sleep restriction, and following recovery sleep. SETTING: Two sleep research laboratories. PARTICIPANTS: Thirty-eight healthy adults; 9 men and 10 women (mean age: 26.0 +/- 6.1 years) in the placebo group and 8 men and 11 women (mean age: 26.7 +/- 8.1 years) in the tiagabine 8 mg group INTERVENTIONS: Both experimental groups underwent 4 nights of sleep restriction. Each group received either tiagabine 8 mg or placebo on all sleep-restriction nights, and both groups received placebo on baseline and recovery nights. MEASUREMENTS AND RESULTS: Polysomnography documented a SWS-enhancing effect of tiagabine. The placebo group displayed the predicted deficits due to sleep restriction on the Psychomotor Vigilance Task and the Multiple Sleep Latency Test. Compared with placebo, the tiagabine group did not demonstrate impairment in sustained attention on the Psychomotor Vigilance Test, performed better on the Wisconsin Card Sorting Task, reported more restorative sleep, and had less of an increase in afternoon-evening salivary free cortisol. Multiple Sleep Latency Test, ratings of sleepiness, recovery sleep, and other measures did not differ between groups. CONCLUSIONS: To our knowledge these findings are the first to be consistent with the hypothesis that pharmacologic SWS enhancement reduces selective aspects of the behavioral, psychological, and physiologic impact of sleep restriction.     

Perception of experimental pain is reduced after provoked waking from rapid eye movement sleep

Patients with chronic pain often complain of pain when they wake at night, but the accuracy of their perception of the pain after waking at night is unknown. While cognitive functions are reduced for a short time after waking from sleep, a situation known as sleep inertia, it is unclear how sleep inertia may affect the perception of pain. We investigated the effects of sleep inertia on the perception of experimentally induced pain. Fourteen male volunteers were exposed to a randomized thermal heat stimulus of 43.1 °C ‘hot’ and 46.5 °C ‘hurting’ during provoked waking from Stage 2 sleep, slow wave sleep and rapid eye movement (REM) sleep. Subjects rated their pain on awakening on a Visual Analogue Scale at 30 s after awakening and each minute thereafter for 5 min. We found no change in pain perception over the 5‐min period irrespective of temperature used or sleep stage. However, perceived pain when awoken abruptly from REM sleep was significantly lower than the awake score for both the hot (P = 0.0069) and hurting (P = 0.0025) temperatures. Pain perception when woken from Stage 2 sleep or slow wave sleep was not significantly different from perception when awake. Our findings indicate that sleep inertia reduces pain perception when awoken abruptly from REM. This suggests that patients who wake up in pain either perceive accurately the pain they are experiencing, or at worst underestimate the level of pain if woken from REM sleep.     

Emotional working memory during sustained wakefulness

In the present study we investigated whether one night of sleep deprivation can affect working memory (WM) performance with emotional stimuli. Twenty‐five subjects were tested after one night of sleep deprivation and after one night of undisturbed sleep at home. As a second aim of the study, to evaluate the cumulative effects of sleep loss and of time‐of‐day changes on emotional WM ability, the subjects were tested every 4 h, from 22:00 to 10:00 hours, in four testing sessions during the sleep deprivation period (deprivation sessions: D1, D2, D3 and D4). Subjects performed the following test battery: Psychomotor Vigilance Task, 0‐back task, 2‐back task and an ‘emotional 2‐back task’ with neutral, positive and negative emotional pictures selected from the International Affective Picture System. Results showed lower accuracy in the emotional WM task when the participants were sleep‐deprived relative to when they had slept, suggesting the crucial role of sleep for preserving WM ability. In addition, the accuracy for the negative pictures remains stable during the sessions performed from 22:00 to 06:00 hours (D1, D2 and D3), while it drops at the D4 session, when the participants had accumulated the longest sleep debt. It is suggested that, during sleep loss, attentional and WM mechanisms may be sustained by the higher arousing characteristics of the emotional (negative) stimuli.     

Effects of artificial dawn on sleep inertia,skin temperature,and the awakening cortisol response

The effect of artificial dawn during the last 30 min of sleep on subsequent dissipation of sleep inertia was investigated, including possible involvement of cortisol and thermoregulatory processes. Sixteen healthy subjects who reported difficulty with waking up participated in random order in a control and an artificial dawn night. Sleep inertia severity was measured by subjective ratings of sleepiness and activation, and by performance on an addition and a reaction time task measured at 1, 15, 30, 45, 60, and 90 min after waking up at habitual wake up time at workdays. At all intervals, saliva samples were collected for cortisol analysis. Sleep electroencephalogram was recorded during the 30 min prior to waking up; core body temperature and skin temperatures were recorded continuously until 90 min after waking up. Subjective sleepiness was significantly decreased and subjective activation increased after waking up in the artificial dawn condition as compared with control, in which lights were turned on at waking up. These effects can be explained by effects of artificial dawn on skin temperature and amount of wakefulness during the 30 min prior to the alarm. Artificial dawn accelerated the decline in skin temperature and in the distal‐to‐proximal skin temperature gradient after getting up. No significant effects of artificial dawn on performance, core body temperature, and cortisol were found. These results suggest that the physiology underlying the positive effects of artificial dawn on the dissipation of sleep inertia involves light sleep and an accelerated skin temperature decline after awakening.     

Sleep extension versus nap or coffee,within the context of ‘sleep debt’

Though extended night‐time sleep mostly reduces the ‘afternoon dip’, little is known about evening benefits to alertness, or about comparisons with an afternoon nap or caffeine. Twenty healthy carefully screened adults, normal waking alertness levels, underwent four counterbalanced conditions: usual night sleep; night sleep extended<90 min (usual bed‐time); up to 20 min afternoon nap; and 150 mg afternoon caffeine (versus decaffeinated coffee). Sleepiness was measured by afternoon and evening multiple sleep latency test (MSLTs), longer psychomotor vigilance test (PVT) sessions and a subjective sleepiness scale. Sleep was extended by average of 74 min, and all participants could nap 15–20 min. Sleep extension had little effect on PVT determined modest levels of morning sleepiness. Afternoon and evening MSLTs showed all active treatments significantly reduced the ‘dip’, with nap most effective until mid‐evening; next effective was caffeine, then extension. Late evening sleepiness and subsequent sleep did not differ between conditions. Arguably, participants may have experienced some ‘sleep debt’, given they extended sleep and reflected some sleepiness within settings sensitive to sleepiness. Nevertheless, extended sleep seemed largely superfluous and inefficient in reducing modest levels of sleepiness when compared with a timely nap, and even caffeine. Sleep, such as food and fluid intakes, can be taken to excess of real biological needs, and for many healthy adults, there is a level of modest daytime sleepiness, only unmasked by very sensitive laboratory measures. It may reflect a requirement for more sleep or simply be within the bounds of normal acceptability.     

Effect of 64 hours of sleep deprivation upon sleep in geriatric normals and insomniacs

Fifty-eight geriatric normal and chronic insomniac sleepers were screened with sleep recordings to define groups of 12 Normal (Sleep Efficiency greater than 85%) and Insomniac (Sleep Efficiency less than 80%) sleepers. All subjects then had 4 baseline sleep nights, 64 hours of total sleep loss, and 4 recovery nights. Insomniacs, had lower sleep efficiencies and less REM than Normals during baseline. Sleep efficiency was high (97%) in both groups on the first recovery night but decreased toward baseline values in both groups between the second (Normal) and fourth (Insomniac) recovery night. The groups had relatively little slow wave sleep, but had a significant increase on the first recovery night. Five Normals and one Insomniac had REM latency of less than 15 min on their first recovery night. This REM latency was found to be significantly correlated with the amount of slow wave sleep on baseline. Decreased REM latency in initial recovery sleep was interpreted as evidence of decreased pressure for slow wave sleep in aging.     

Acute exposure to evening blue‐enriched light impacts on human sleep

Light in the short wavelength range (blue light: 446–483 nm) elicits direct effects on human melatonin secretion, alertness and cognitive performance via non‐image‐forming photoreceptors. However, the impact of blue‐enriched polychromatic light on human sleep architecture and sleep electroencephalographic activity remains fairly unknown. In this study we investigated sleep structure and sleep electroencephalographic characteristics of 30 healthy young participants (16 men, 14 women; age range 20–31 years) following 2 h of evening light exposure to polychromatic light at 6500 K, 2500 K and 3000 K. Sleep structure across the first three non‐rapid eye movement non‐rapid eye movement – rapid eye movement sleep cycles did not differ significantly with respect to the light conditions. All‐night non‐rapid eye movement sleep electroencephalographic power density indicated that exposure to light at 6500 K resulted in a tendency for less frontal non‐rapid eye movement electroencephalographic power density, compared to light at 2500 K and 3000 K. The dynamics of non‐rapid eye movement electroencephalographic slow wave activity (2.0–4.0 Hz), a functional index of homeostatic sleep pressure, were such that slow wave activity was reduced significantly during the first sleep cycle after light at 6500 K compared to light at 2500 K and 3000 K, particularly in the frontal derivation. Our data suggest that exposure to blue‐enriched polychromatic light at relatively low room light levels impacts upon homeostatic sleep regulation, as indexed by reduction in frontal slow wave activity during the first non‐rapid eye movement episode.     

The Effects of a Chronic Limitation of Sleep Length

Fifteen male subjects (Ss) were studied once each week while on a sleep regime of 5 1/2 hrs of sleep a night for 60 days. The electroencephalogram and electro-oculogram were recorded in the laboratory once each week. Performance was measured each week using the Wilkinson Vigilance Task, the Wilkinson Addition Test, and a word memory test, and grip strength was measured using a hand dynomometer. The Zung Depression Scale and the Gough Adjective Check List were used to measure mood. The Ss completed a sleep log on a daily basis. The effect on sleep of the restricted regime was to initially increase the absolute amount of stage 4 sleep. But by the 5th week of the study the stage 4 amount decreased to near baseline levels. The initial effect on REM sleep was to sharply reduce this type of sleep when compared with baseline values. During the course of the experiment there was a REM deprivation of some 25% of baseline values and 30 min in absolute amount. During the course of the experiment the latency to the onset of the first stage 4 and the latency to the first REM period were reduced. Only the Wilkinson Vigilance Task showed a decline in performance associated with continued restricted sleep. The sleep logs revealed that initially the Ss experienced difficulty in arousing from sleep in the morning and felt drowsy during the day, but these effects did not continue throughout the experiment. The mood scales showed no changes associated with continuing to sleep 5 1/5 hrs a night. These findings suggest that a chronic loss of sleep as much as 2 1/2 hours a night is not likely to result in major behavioral consequences.     

Sleep slow oscillations favour local cortical plasticity underlying the consolidation of reinforced procedural learning in human sleep

We investigated changes of slow‐wave activity and sleep slow oscillations in the night following procedural learning boosted by reinforcement learning, and how these changes correlate with behavioural output. In the Task session, participants had to reach a visual target adapting cursor's movements to compensate an angular deviation introduced experimentally, while in the Control session no deviation was applied. The task was repeated at 13:00 hours, 17:00 hours and 23:00 hours before sleep, and at 08:00 hours after sleep. The deviation angle was set at 15° (13:00 hours and 17:00 hours) and increased to 45° (reinforcement) at 23:00 hours and 08:00 hours. Both for Task and Control nights, high‐density electroencephalogram sleep recordings were carried out (23:30?19:30 hours). The Task night as compared with the Control night showed increases of: (a) slow‐wave activity (absolute power) over the whole scalp; (b) slow‐wave activity (relative power) in left centro‐parietal areas; (c) sleep slow oscillations rate in sensorimotor and premotor areas; (d) amplitude of pre‐down and up states in premotor regions, left sensorimotor and right parietal regions; (e) sigma crowning the up state in right parietal regions. After Task night, we found an improvement of task performance showing correlations with sleep slow oscillations rate in right premotor, sensorimotor and parietal regions. These findings suggest a key role of sleep slow oscillations in procedural memories consolidation. The diverse components of sleep slow oscillations selectively reflect the network activations related to the reinforced learning of a procedural visuomotor task. Indeed, areas specifically involved in the task stand out as those with a significant association between sleep slow oscillations rate and overnight improvement in task performance.     

Laboratory and field studies of naps and caffeine as practical countermeasures for sleep-wake problems associated with night work

STUDY OBJECTIVES: To evaluate the effects of napping, caffeine, and napping plus caffeine on performance and alertness in both laboratory and field settings. DESIGN: (1) Laboratory Study: parallel-groups design with random assignment to 1 of 4 experimental conditions. (2) Field Study: crossover design. SETTING: Sleep laboratory and field settings. PARTICIPANTS: (1) Laboratory Study: 68 healthy individuals; (2) Field Study: 53 shiftworkers who worked nights or rotating shifts. INTERVENTIONS: (1) Laboratory Study: an evening nap opportunity before the first 2 of 4 consecutive simulated night shifts plus placebo taken all 4 nights, caffeine taken nightly, the combination of the nap and caffeine conditions, or placebo. (2) Field Study: an evening nap on the first 2 of 4 consecutive night shifts plus caffeine taken nightly versus placebo taken nightly without naps. MEASUREMENTS AND RESULTS: (1) Laboratory Study: Napping, caffeine, and their combination all improved alertness and performance as measured by Maintenance of Wakefulness Test and Psychomotor Vigilance Task, but the combination of napping and caffeine was best in improving alertness. (2) Field Study: Napping plus caffeine improved performance as measured by Psychomotor Vigilance Test and decreased subjective sleepiness in individuals working the night shift. CONCLUSIONS: Napping plus caffeine helps improve performance and alertness of night-shift workers.     

Exercise and sleep in community‐dwelling older adults: evidence for a reciprocal relationship

Exercise behaviour and sleep are both important health indicators that demonstrate significant decreases with age, and remain modifiable well into later life. The current investigation examined both the chronic and acute relationships between exercise behaviour and self‐reported sleep in older adults through a secondary analysis of a clinical trial of a lifestyle intervention. Seventy‐nine community‐dwelling, initially sedentary, older adults (mean age = 63.58 years, SD = 8.66 years) completed daily home‐based assessments of exercise behaviour and sleep using daily diary methodology. Assessments were collected weekly and continued for 18 consecutive weeks. Multilevel models revealed a small positive chronic (between‐person mean‐level) association between exercise and wake time after sleep onset, and a small positive acute (within‐person, day‐to‐day) association between exercise and general sleep quality rating. The within‐person exercise and general sleep quality rating relationship was found to be reciprocal (i.e. sleep quality also predicted subsequent exercise behaviour). As such, it appears exercise and sleep are dynamically related in older adults. Efforts to intervene on either sleep or exercise in late‐life would be wise to take the other into account. Light exposure, temperature regulation and mood may be potential mechanisms of action through which exercise can impact sleep in older adults.     

Pupillary instability as an accurate,objective marker of alertness failure and performance impairment

Pupillary instability reflects alterations in autonomic nervous system activity and has been shown to reflect change in alertness. However, the extent to which it can predict subsequent performance impairment and alertness failure is not clear. Eighteen healthy young adults (group age = 21.44 ± 3.24 years, 10 men) underwent 40 hr of continuous wakefulness, completing an 11‐min Pupillographic Sleepiness Test (PST), the Karolinska Sleepiness Scale and a 10‐min Psychomotor Vigilance Task (PVT) every 2 hr. Waking electroencephalography was recorded continuously and scored for microsleeps and slow eye movements (SEMs) during PVTs. Pupillary instability was sensitive to time awake, significantly increasing after 18 hr of wakefulness. The time course of impairment was almost identical to PVT lapses, microsleeps and SEMs. Receiver operating characteristic curve analysis demonstrated reasonable sensitivity and specificity of pupillary instability in correctly classifying PVT lapses, microsleeps and SEMs above individual baseline thresholds (all AUC values >0.78, p < 0.0001). Preliminary cut‐off scores ranging from 10 to 11.5 mm/min for varying impairment thresholds are proposed for young adults. If reproducible in field settings, the PST may be a strong candidate as a fitness for duty/fitness to drive tool for detecting drowsiness‐related impairment.     

An approach to understanding sleep and depressed mood in adolescents: person‐centred sleep classification

Depressive mood in youth has been associated with distinct sleep dimensions, such as timing, duration and quality. To identify discrete sleep phenotypes, we applied person‐centred analysis (latent class mixture models) based on self‐reported sleep patterns and quality, and examined associations between phenotypes and mood in high‐school seniors. Students (n = 1451; mean age = 18.4 ± 0.3 years; 648 M) completed a survey near the end of high‐school. Indicators used for classification included school night bed‐ and rise‐times, differences between non‐school night and school night bed‐ and rise‐times, sleep‐onset latency, number of awakenings, naps, and sleep quality and disturbance. Mood was measured using the total score on the Center for Epidemiologic Studies‐Depression Scale. One‐way anova tested differences between phenotype for mood. Fit indexes were split between 3‐, 4‐ and 5‐phenotype solutions. For all solutions, between phenotype differences were shown for all indicators: bedtime showed the largest difference; thus, classes were labelled from earliest to latest bedtime as ‘A’ (n = 751), ‘B’ (n = 428) and ‘C’ (n = 272) in the 3‐class solution. Class B showed the lowest sleep disturbances and remained stable, whereas classes C and A each split in the 4‐ and 5‐class solutions, respectively. Associations with mood were consistent, albeit small, with class B showing the lowest scores. Person‐centred analysis identified sleep phenotypes that differed in mood, such that those with the fewest depressive symptoms had moderate sleep timing, shorter sleep‐onset latencies and fewer arousals. Sleep characteristics in these groups may add to our understanding of how sleep and depressed mood associate in teens.     

Impact of sleep inertia on visual selective attention for rare targets and the influence of chronotype

Sleep inertia is affected by circadian phase, with worse performance upon awakening from sleep during the biological night than biological day. Visual search/selective visual attention performance is known to be sensitive to sleep inertia and circadian phase. Individual differences exist in the circadian timing of habitual wake time, which may contribute to individual differences in sleep inertia. Because later chronotypes awaken at an earlier circadian phase, we hypothesized that later chronotypes would have worse visual search performance during sleep inertia than earlier chronotypes if awakened at habitual wake time. We analysed performance from 18 healthy participants [five females (22.1 ± 3.7 years; mean ± SD)] at ~1, 10, 20, 30, 40 and 60 min following electroencephalogram‐verified awakening from an 8 h in‐laboratory sleep opportunity. Cognitive throughput and reaction times of correct responses were impaired by sleep inertia and took ~10–30 min to improve after awakening. Regardless whether chronotype was defined by dim light melatonin onset or mid‐sleep clock hour on free days, derived from the Munich ChronoType Questionnaire, the duration of sleep inertia for cognitive throughput and reaction times was longer for later chronotypes (n = 7) compared with earlier chronotypes (n = 7). Specifically, performance for earlier chronotypes showed significant improvement within ~10–20 min after awakening, whereas performance for later chronotypes took ~30 min or longer to show significant improvement (P < 0.05). Findings have implications for decision making immediately upon awakening from sleep, and are consistent with circadian theory suggesting that sleep inertia contributes to longer‐lasting impairments in morning performance in later chronotypes.     

Subjective–objective sleep discrepancy among older adults: associations with insomnia diagnosis and insomnia treatment

Discrepancy between subjective and objective measures of sleep is associated with insomnia and increasing age. Cognitive behavioural therapy for insomnia improves sleep quality and decreases subjective–objective sleep discrepancy. This study describes differences between older adults with insomnia and controls in sleep discrepancy, and tests the hypothesis that reduced sleep discrepancy following cognitive behavioural therapy for insomnia correlates with the magnitude of symptom improvement reported by older adults with insomnia. Participants were 63 adults >60 years of age with insomnia, and 51 controls. At baseline, participants completed sleep diaries for 7 days while wearing wrist actigraphs. After receiving cognitive behavioural therapy for insomnia, insomnia patients repeated this sleep assessment. Sleep discrepancy variables were calculated by subtracting actigraphic sleep onset latency and wake after sleep onset from respective self‐reported estimates, pre‐ and post‐treatment. Mean level and night‐to‐night variability in sleep discrepancy were investigated. Baseline sleep discrepancies were compared between groups. Pre–post‐treatment changes in Insomnia Severity Index score and sleep discrepancy variables were investigated within older adults with insomnia. Sleep discrepancy was significantly greater and more variable across nights in older adults with insomnia than controls, P ≤ 0.001 for all. Treatment with cognitive behavioural therapy for insomnia was associated with significant reduction in the Insomnia Severity Index score that correlated with changes in mean level and night‐to‐night variability in wake after sleep onset discrepancy, P < 0.001 for all. Study of sleep discrepancy patterns may guide more targeted treatments for late‐life insomnia.