Self‐reported sleep quantity,quality and sleep hygiene in elite athletes

Sleep is essential for recovery and performance in elite athletes. While actigraphy‐based studies revealed suboptimal sleep in athletes, information on their subjective experience of sleep is scarce. Relatively unexplored is also the extent to which athletes’ sleep is adversely affected by environmental conditions and daytime behaviours, that is sleep hygiene. This study aimed to provide insight in sleep quantity, quality and its putative association with sleep hygiene. Participants were 98 elite (youth) athletes competing at the highest (inter‐)national level. Sleep quantity, quality and sleep hygiene were assessed once covering a 1‐month period by using established (sub)clinical questionnaires, and repeatedly during 7 consecutive days. Sleep quality was generally healthy, although 41% of all athletes could be classified as ‘poor sleeper’, and 12% were identified as having a sleep disorder. Daily self‐monitoring revealed sleep durations of 8:11 ± 0:45 h, but elevated wake after sleep onset of 13 ± 19 min. Sleep quality, feeling refreshed, and morning vigor were moderate at best. Regarding sleep hygiene, general measures revealed irregular sleep–wake patterns, psychological strain and activating pre‐sleep behaviours. At the daily level, blue‐light exposure and late‐evening consumption of heavy meals were frequently reported. General sleep hygiene revealed significant associations with sleep quality (0.45 < r > 0.50; P < 0.001). Results indicate that there is ample room for optimization, specifically in onset latency and in wake after sleep onset. Subtle improvements in sleep seem possible, and optimizing sleep hygiene, such as regular sleep–wake patterns and reducing psychological strain, may facilitate this sleep upgrading process.     

Sleep perception and the multiple sleep latency test in patients with primary insomnia

The purpose of this study was to examine the relationship between overnight sleep perception and the daytime multiple sleep latency test (MSLT) among individuals who were primary insomnia patients (PIPs) or good sleeper controls (GSCs). We collected overnight sleep data via polysomnography (PSG), subjective sleep data via a morning questionnaire (self‐evaluated) and MSLT data via four 20‐min naps over 8 h. Subjects included 122 PIPs and 48 GSCs. Sleep perception was calculated as subjective sleep time/objective sleep time × 100%. PIPs showed a significant difference (P < 0.001) between sleep time, as determined by PSG (387.8 ± 100 min) and self‐report (226.3 ± 160 min), but no difference was obtained for GSCs (440.6 ± 53 versus 435.4 ± 65 min). The means for sleep perception were 56.4 ± 38.8% for the PIPs and 99.3 ± 13.6% for the GSCs (P < 0.001). In the PIPs group, weak but statistically significant negative correlations (r: ?0.20 to ?0.25) were found for MSLT versus sleep perception and versus self‐ and PSG‐evaluated sleep time. Compared to PIPs with low scores on the MSLT, those with high scores had less sleep perception (%), less self‐ and PSG‐evaluated sleep time and greater sleep misperception time. GSCs did not show significant correlations between MSLT and sleep measures or differences in comparisons between individuals with high and low scores on the MSLT. These results add novel data to the literature by suggesting that 24‐h hyperarousal potentially plays a key role in the pathophysiological issues of insomnia.     

Prediction of melatonin efficacy by pretreatment dim light melatonin onset in children with idiopathic chronic sleep onset insomnia

Research has shown efficacy of melatonin treatment to advance sleep-wake rhythms in insomnia. In healthy adults, direction and magnitude of the phase shift depends on the timing of administration relative to the phase position of the circadian system. Therefore, in the present study we investigated whether in children with chronic sleep onset insomnia (SOI) efficacy of melatonin treatment in the early evening could be predicted from dim light melatonin onset (DLMO), a phase marker of the circadian system. We combined data of two previously published double blind, randomized, placebo-controlled trials in 110 participants, aged 6-12 years. Sleep was actigraphically estimated, and saliva collected, at baseline and in the third week of a 4-week treatment period with 5 mg melatonin or placebo at 18:00 or 19:00 hours. Primary outcome measures were pre- to post-treatment changes in dim light melatonin onset (DeltaDLMO), sleep onset (DeltaSO), sleep latency (DeltaSL), and total sleep duration (DeltaTSD). Melatonin advanced DLMO with +1:12 h (P < 0.001), SO with +0:42 h (P = 0.004), SL decreased with 25 min (P = 0.019), and TSD did not change significantly, as compared with placebo. In the melatonin-treated group, but not in the placebo-treated group, pretreatment DLMO was significantly related to DeltaDLMO [F(1, 29) = 7.28, P = 0.012] and DeltaSO [F(1, 25) = 7.72, P = 0.010]. The time interval between treatment administration and pretreatment DLMO (INT) was only significantly related to DeltaSO [F(1,26) = 5.40, P = 0.028]. The results suggest that in children with SOI, the efficacy of early evening melatonin to advance sleep onset and endogenous melatonin onset increases the later the pretreatment DLMO is.     

Case-control study of subjective and objective differences in sleep patterns in older adults with insomnia symptoms

Older adults have high prevalence rates of insomnia symptoms, yet it is unclear if these insomnia symptoms are associated with objective impairments in sleep. We hypothesized that insomnia complaints in older adults would be associated with objective differences in sleep compared with those without insomnia complaints. To test this hypothesis, we conducted a cross‐sectional study in which older adults with insomnia complaints (cases, n = 100) were compared with older adults without insomnia complaints (controls, n = 100) using dual‐night in‐lab nocturnal polysomnography, study questionnaires and 7 days of at‐home actigraphy and sleep diaries. Cases were noted to have reduced objective total sleep time compared with controls (25.8 ± 8.56 min, P = 0.003). This was largely due to increased wakefulness after sleep onset, and not increased sleep latency. When participants with sleep‐related breathing disorder or periodic limb movement disorder were excluded, the polysomnography total sleep time difference became even larger. Cases also had reduced slow‐wave sleep (5.10 ± 1.38 min versus 10.57 ± 2.29 min, effect size −0.29, P = 0.04). When comparing self‐reported sleep latency and sleep efficiency with objective polysomnographic findings, cases demonstrated low, but statistically significant correlations, while no such correlations were observed in controls. Cases tended to underestimate their sleep efficiency by 1.6% (±18.4%), while controls overestimated their sleep efficiency by 12.4% (±14.5%). In conclusion, we noted that older adults with insomnia complaints have significant differences in several objective sleep findings relative to controls, suggesting that insomnia complaints in older adults are associated with objective impairments in sleep.     

Internight sleep variability: its clinical significance and responsiveness to treatment in primary and comorbid insomnia

Although sleep diary and actigraphy data are usually collected daily for 1 or 2 weeks, traditional analytical approaches aggregate these data into mean values. Internight variability of sleep often accompanies insomnia. However, few studies have explored the relevance of this ‘construct’ in the context of diagnosis, clinical impact, treatment effects and/or whether having ‘variable sleep’ carries any prognostic significance. We explored these questions by conducting secondary analyses of data from a randomized clinical trial. The sample included primary (PI: n = 40) and comorbid insomnia (CMI: n = 41) sufferers receiving four biweekly sessions of cognitive–behavioural therapy (CBT) or sleep hygiene education. Using the within‐subject standard deviations of diary‐ and actigraphy‐derived measures collected for 2‐week periods [sleep onset latency (SOL), wake after sleep onset (WASO), total sleep time (TST) and sleep efficiency (SE)], we found that CMI sufferers displayed more variable self‐reported SOLs and SEs than PI sufferers. However, higher variability in diary and actigraphy‐derived measures was related to poorer sleep quality only within the PI group, as measured by the Pittsburgh Sleep Quality Index (PSQI). Within both groups, the variability of diary‐derived measures was reduced after CBT, but the variability of actigraphy‐derived measures remained unchanged. Interestingly, the variability of actigraphy measures at baseline was correlated with PSQI scores at 6‐month follow‐up. Higher SOL variability was associated with worse treatment outcomes within the PI group, whereas higher WASO variability was correlated with better treatment outcomes within the CMI group. Sleep variability differences across insomnia diagnoses, along with their distinctive correlates, suggest that mechanisms underlying the sleep disruption/complaint and treatment response in both patient groups are distinct. Further studies are warranted to support variability as a useful metric in insomnia studies.     

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.     

Subjective–objective sleep discrepancy in patients with insomnia during and after cognitive behavioural therapy: An actigraphy study

Although patients with insomnia often show a discrepancy between self‐reported and objective sleep parameters, the role of and change in this phenomenon during treatment remain unclear. The present study aimed to assess the effect of cognitive behavioural therapy for insomnia on subjective and objective sleep discrepancy of total sleep time, sleep‐onset latency and wake after sleep onset. The total sleep time discrepancy was also assessed across the entire therapy. The second aim was to examine the treatment outcome of two insomnia groups differing in sleep perception. Thirty‐six adults with insomnia (mean age = 46.7 years, SD = 13.9; 22 females) were enrolled in the final analyses. Patients underwent a 6‐week group cognitive behavioural therapy for insomnia programme. Sleep diary and actigraphy measurements were obtained during the therapy. Patients who underestimated total sleep time (n = 16; underestimating group) were compared with patients who accurately perceived or overestimated total sleep time (n = 20; accurate/overestimating group). After cognitive behavioural therapy for insomnia, a significant decrease of total sleep time and sleep‐onset latency discrepancy was observed without a change in wake after sleep onset discrepancy in the total sample. Only the underestimating group reported decreased sleep‐onset latency discrepancy after the treatment, whereas total sleep time discrepancy significantly changed in both groups. The underestimating group showed a significant decrease of total sleep time discrepancy from Week 1 to Week 2 when the sleep restriction was implemented, whereas the accurate/overestimating group showed the first significant change at Week 4. In conclusion, both groups differing in sleep perception responded similarly to cognitive behavioural therapy for insomnia, although different In conclusion, both groups differing in sleep perception responded similarly to cognitive behavioural therapy for insomnia, although different therapeutic components could play important roles in each group. components could play important roles in each group.     

Self‐administered acupressure for insomnia disorder: a pilot randomized controlled trial

Self‐administered acupressure has potential as a low‐cost alternative treatment for insomnia. To evaluate the short‐term effects of self‐administered acupressure for alleviating insomnia, a pilot randomized controlled trial was conducted. Thirty‐one subjects (mean age: 53.2 years; 77.4% female) with insomnia disorder were recruited from a community. The participants were randomized to receive two lessons on either self‐administered acupressure or sleep hygiene education. The subjects in the self‐administered acupressure group (n = 15) were taught to practise self‐administered acupressure daily for 4 weeks. The subjects in the comparison group (n = 16) were advised to follow sleep hygiene education. The primary outcome was the Insomnia Severity Index (ISI). Other measures included a sleep diary, Hospital Anxiety and Depression Scale and Short‐form Six‐Dimension. The subjects in the self‐administered acupressure group had a significantly lower ISI score than the subjects in the sleep hygiene education group at week 8 (effect size = 0.56, P = 0.03). However, this observed group difference did not reach a statistically significant level after Bonferroni correction. With regard to the secondary outcomes, moderate between‐group effect sizes were observed in sleep onset latency and wake after sleep onset based on the sleep diary, although the differences were not significant. The adherence to self‐administered acupressure practice was satisfactory, with 92.3% of the subjects who completed the lessons still practising acupressure at week 8. In conclusion, self‐administered acupressure taught in a short training course may be a feasible approach to improve insomnia. Further fully powered confirmatory trials are warranted.     

A pilot study of a novel smartphone application for the estimation of sleep onset

The aim of the study was to investigate the accuracy of Sleep On Cue: a novel iPhone application that uses behavioural responses to auditory stimuli to estimate sleep onset. Twelve young adults underwent polysomnography recording while simultaneously using Sleep On Cue. Participants completed as many sleep‐onset trials as possible within a 2‐h period following their normal bedtime. On each trial, participants were awoken by the app following behavioural sleep onset. Then, after a short break of wakefulness, commenced the next trial. There was a high degree of correspondence between polysomnography‐determined sleep onset and Sleep On Cue behavioural sleep onset, r = 0.79, P < 0.001. On average, Sleep On Cue overestimated sleep‐onset latency by 3.17 min (SD = 3.04). When polysomnography sleep onset was defined as the beginning of N2 sleep, the discrepancy was reduced considerably (M = 0.81, SD = 1.96). The discrepancy between polysomnography and Sleep On Cue varied between individuals, which was potentially due to variations in auditory stimulus intensity. Further research is required to determine whether modifications to the stimulus intensity and behavioural response could improve the accuracy of the app. Nonetheless, Sleep On Cue is a viable option for estimating sleep onset and may be used to administer Intensive Sleep Retraining or facilitate power naps in the home environment.     

Simplified sleep restriction for insomnia in general practice: a randomised controlled trial

Background

Insomnia is common in primary care. Cognitive behavioural therapy for insomnia (CBT-I) is effective but requires more time than is available in the general practice consultation. Sleep restriction is one behavioural component of CBT-I.

Aim

To assess whether simplified sleep restriction (SSR) can be effective in improving sleep in primary insomnia.

Design and setting

Randomised controlled trial of patients in urban general practice settings in Auckland, New Zealand.

Method

Adults with persistent primary insomnia and no mental health or significant comorbidity were eligible. Intervention patients received SSR instructions and sleep hygiene advice. Control patients received sleep hygiene advice alone. Primary outcomes included change in sleep quality at 6 months measured by the Pittsburgh Sleep Quality Index (PSQI), Insomnia Severity Index (ISI), and sleep efficiency (SE%). The proportion of participants reaching a predefined ‘insomnia remission’ treatment response was calculated.

Results

Ninety-seven patients were randomised and 94 (97%) completed the study. At 6-month follow-up, SSR participants had improved PSQI scores (6.2 versus 8.4, P<0.001), ISI scores (8.6 versus 11.1, P = 0.001), actigraphy-assessed SE% (difference 2.2%, P = 0.006), and reduced fatigue (difference −2.3 units, P = 0.04), compared with controls. SSR produced higher rates of treatment response (67% [28 out of 42] versus 41% [20 out of 49]); number needed to treat = 4 (95% CI = 2.0 to 19.0). Controlling for age, sex, and severity of insomnia, the adjusted odds ratio for insomnia remission was 2.7 (95% CI = 1.1 to 6.5). There were no significant differences in other outcomes or adverse effects.

Conclusion

SSR is an effective brief intervention in adults with primary insomnia and no comorbidities, suitable for use in general practice.     

Slow oscillating transcranial direct current stimulation during sleep has a sleep‐stabilizing effect in chronic insomnia: a pilot study

Recent evidence suggests that lack of slow‐wave activity may play a fundamental role in the pathogenesis of insomnia. Pharmacological approaches and brain stimulation techniques have recently offered solutions for increasing slow‐wave activity during sleep. We used slow (0.75 Hz) oscillatory transcranial direct current stimulation during stage 2 of non‐rapid eye movement sleeping insomnia patients for resonating their brain waves to the frequency of sleep slow‐wave. Six patients diagnosed with either sleep maintenance or non‐restorative sleep insomnia entered the study. After 1 night of adaptation and 1 night of baseline polysomnography, patients randomly received sham or real stimulation on the third and fourth night of the experiment. Our preliminary results show that after termination of stimulations (sham or real), slow oscillatory transcranial direct current stimulation increased the duration of stage 3 of non‐rapid eye movement sleep by 33 ± 26 min (P = 0.026), and decreased stage 1 of non‐rapid eye movement sleep duration by 22 ± 17.7 min (P = 0.028), compared with sham. Slow oscillatory transcranial direct current stimulation decreased stage 1 of non‐rapid eye movement sleep and wake time after sleep‐onset durations, together, by 55.4 ± 51 min (P = 0.045). Slow oscillatory transcranial direct current stimulation also increased sleep efficiency by 9 ± 7% (P = 0.026), and probability of transition from stage 2 to stage 3 of non‐rapid eye movement sleep by 20 ± 17.8% (P = 0.04). Meanwhile, slow oscillatory transcranial direct current stimulation decreased transitions from stage 2 of non‐rapid eye movement sleep to wake by 12 ± 6.7% (P = 0.007). Our preliminary results suggest a sleep‐stabilizing role for the intervention, which may mimic the effect of sleep slow‐wave‐enhancing drugs.     

Occupational and socioeconomic differences in actigraphically measured sleep

Occupational conditions, together with socioeconomic status, may modulate sleep. This study examined the association of occupational conditions and socioeconomic status with actigraphic measures of sleep in workers. Fifty‐five employees (40 ± 12 years) wore a wrist actigraph during sleep for seven consecutive nights. Sleep variables addressed included total sleep time, sleep efficiency, mean activity during sleep, sleep‐onset latency, and wake after sleep onset. We also measured household income, occupational class, work schedule, weekly work hours, job demand, job control, worksite social support, effort–reward imbalance, organizational justice, and workplace social capital. Multiple linear regression models were used to determine the association of occupational indicators, socioeconomic status, as well as age and gender with each sleep variable. Higher workplace social capital was associated consistently with longer total sleep time (P < 0.001), higher sleep efficiency (P < 0.05) and lower mean activity during sleep (P < 0.07). Low occupational class (P < 0.01), higher job demand (P < 0.05) and lower job control (P < 0.05) were associated with longer total sleep time. No associations were significant for sleep‐onset latency or wake after sleep onset. These preliminary results suggest that enhanced workplace social capital is closely associated with better quality and quantity of sleep.     

Sleep characteristics as predictor variables of stress systems markers in insomnia disorder

This study investigates the extent to which sleep characteristics serve as predictor variables for inflammatory, hypothalamic–pituitary–adrenal and autonomic systems markers. Twenty‐nine participants with a diagnosis of insomnia disorder based on the Diagnostic Statistical Manual of Mental Disorders, Fifth Edition (age 25.3 ± 1.6 years, insomnia duration 6.6 ± 0.8 years) and 19 healthy control sleepers (age 25.4 ± 1.4 years) underwent a 2‐week at‐home evaluation keeping a sleep diary and wearing an actigraph, followed by a visit to the Research Center to measure blood pressure, and collect blood and urine samples. The actigraphy‐ and diary‐based variables of sleep duration, sleep‐onset latency, wake after sleep onset and sleep fragmentation/number of night‐time awakenings were averaged and entered as dependent variables in regression analyses. Composite scores were calculated for the autonomic (blood pressure, norepinephrine), inflammatory (monocyte counts, interleukin‐6, C‐reactive protein) and hypothalamic–pituitary–adrenal systems (cortisol), and used as predictor variables in regression models. Compared with controls, individuals with insomnia had a shorter sleep duration (P < 0.05), and a higher hypothalamic–pituitary–adrenal and inflammatory composite score (P < 0.05). The higher inflammatory score was mainly due to higher circulating monocytes (P < 0.05), rather than differences in interleukin‐6 or C‐reactive protein. In persistent insomnia disorder, cortisol is upregulated and associated with actigraphy‐ and diary‐based wake after sleep onset, suggesting that wake after sleep onset may serve as a marker to identify individuals at increased risks for disorders associated with a hyperactive hypothalamic–pituitary–adrenal system. The absence of autonomic and pro‐inflammatory changes (interleukin‐6, C‐reactive protein), despite a substantial decrease in actigraphic sleep duration, may relate to a higher resilience to the adverse biological consequences of insomnia in this young age group.     

Am I (hyper)aroused or anxious? Clinical significance of pre‐sleep somatic arousal in young adults

Self‐reported somatic arousal remains a challenging clinical construct, particularly because only a subset of patients report symptoms such as racing heart, palpitations or increased body temperature interfering with their sleep. It is unclear whether self‐reported somatic arousal is a marker of hyperarousal or co‐morbid clinical anxiety in individuals with insomnia. Participants included 196 young adults aged 20.2 ± 1.0 years old who were predominantly females (75%). About 39% of the sample reported subthreshold insomnia, and about 8% reported clinically significant insomnia, based on their Insomnia Severity Index. Participants completed the Pre‐Sleep Arousal Scale, Beck Anxiety Inventory, Beck Depression Inventory, Arousal Predisposition Scale, and Ford Insomnia Response to Stress Test. Multivariable stepwise regression assessed which factors were independently associated with pre‐sleep cognitive (Pre‐Sleep Arousal Scale‐Cognitive) and somatic (Pre‐Sleep Arousal Scale‐Somatic) arousal. Receiver‐operating characteristic analysis assessed the predictive value to identify clinically significant anxiety (Beck Anxiety Inventory ≥ 20), insomnia (Insomnia Severity Index ≥ 15) and arousability (Arousal Predisposition Scale ≥ 32). Beck Anxiety Inventory (β = 0.42) was the best single correlate of Pre‐Sleep Arousal Scale‐Somatic, while Insomnia Severity Index (β = 0.33) was of Pre‐Sleep Arousal Scale‐Cognitive. A Pre‐Sleep Arousal Scale‐Somatic score of 12 or more identified those with clinically significant anxiety with 65% specificity and 65% sensitivity, while a cut‐off score of 14 increased its sensitivity (86%). Self‐reported pre‐sleep somatic arousal may be an index of co‐morbid clinical anxiety in individuals with insomnia. These findings aid clinicians with assessment and treatment, particularly in the absence of clinical guidelines indicating when somatically focused relaxation techniques should be included as part of multicomponent cognitive behavioural treatment of insomnia.     

Poor Sleep Has Negative Implications for Children With and Without ADHD,but in Different Ways

Background: Sleep problems are commonly reported in attention deficit hyperactivity disorder (ADHD), and are also a familiar characteristic of typical development (TD). We sought to elucidate the relationship between sleep, ADHD trait behaviors, and cognitive inattention, and how it manifests between ADHD and TD children. Participants: Eighteen children diagnosed with ADHD and 20 age-matched TD controls aged 5 to 11 years old participated in the study. Methods: Sleep profiles were assessed using Children’s Sleep Habits Questionnaire and actigraphy measures. Behavioral functioning was examined using Conners’ Parent Report Scale and attention using the computerized Conners’ Continuous Performance Task. Results: We found evidence of (a) poorer sleep quality in the ADHD group, despite no difference in actual sleep time, (b) poor sleep quality in TD children predicting increased ADHD-trait behaviors, despite no association with attention, and (c) a consistent trend for poor sleep quality predicting reduced attentional control in ADHD children, despite no association with behavior. Conclusions: Poor sleep quality affects developmental subgroups in different ways. For ADHD children, poor sleep worsens their predisposed attentional deficit, while for TD children it mimics ADHD behaviors. These findings have important implications for the debate on overdiagnosis of childhood ADHD, and the use of sleep-based interventions. Above all, they highlight the importance of promoting good sleep hygiene in all children.     

Dysfunctional beliefs and attitudes about sleep in children

The objective of the study was to determine whether associations between dysfunctional beliefs and attitudes about sleep and sleep disturbance are evident in children. Cross‐sectional data were collected from 123 children aged 8–10 years (49% boys). The participants came from ethnically diverse backgrounds from two inner‐city schools in London, UK. Children completed the Sleep Self‐Report (SSR) and the Dysfunctional Beliefs and Attitudes about Sleep (DBAS) questionnaire (which was adapted for use with children). Parents completed the Child Sleep Habits Questionnaire (CSHQ). The total DBAS score was associated with sleep disturbances defined as total SSR score (β = 0.40, P < 0.001, r² = 0.15), the SSR insomnia items (β = 0.29, P < 0.01, r² = 0.08) and the total CSHQ score (β = 0.22, P < 0.05, r² = 0.04). Some dysfunctional beliefs about sleep predicted sleep disturbance to a greater extent than others. For example, when controlling for the other DBAS subscales, the ‘control and predictability of sleep’ subscale, but not the ‘sleep requirements expectations’ subscale, predicted total SSR score and SSR insomnia items. Given this preliminary evidence that dysfunctional beliefs and attitudes about sleep appear to be associated with sleep difficulties in children, future work is needed to further developmentally adapt a version of the DBAS appropriate for use with children.     

Sleep patterns and insomnia among adolescents: a population‐based study

The aim of the current study was to examine sleep patterns and rates of insomnia in a population‐based study of adolescents aged 16–19 years. Gender differences in sleep patterns and insomnia, as well as a comparison of insomnia rates according to DSM‐IV, DSM‐V and quantitative criteria for insomnia (Behav. Res. Ther., 41 , 2003, 427), were explored. We used a large population‐based study in Hordaland county in Norway, conducted in 2012. The sample included 10 220 adolescents aged 16–18 years (54% girls). Self‐reported sleep measurements included bedtime, rise time, time in bed, sleep duration, sleep efficiency, sleep onset latency, wake after sleep onset, rate and frequency and duration of difficulties initiating and maintaining sleep and rate and frequency of tiredness and sleepiness. The adolescents reported short sleep duration on weekdays (mean 6:25 hours), resulting in a sleep deficiency of about 2 h. A majority of the adolescents (65%) reported sleep onset latency exceeding 30 min. Girls reported longer sleep onset latency and a higher rate of insomnia than boys, while boys reported later bedtimes and a larger weekday–weekend discrepancy on several sleep parameters. Insomnia prevalence rates ranged from a total prevalence of 23.8 (DSM‐IV criteria), 18.5 (DSM‐V criteria) and 13.6% (quantitative criteria for insomnia). We conclude that short sleep duration, long sleep onset latency and insomnia were prevalent in adolescents. This warrants attention as a public health concern in this age group.     

Sleep latency and duration estimates among sleep disorder patients: variability as a function of sleep disorder diagnosis, sleep history, and psychological characteristics

STUDY OBJECTIVES: Insomnia patients often report greater sleep disturbance than found via polysomnography; yet the specific patient factors related to such sleep time misperceptions are poorly understood. We sought to characterize the extent to which a diverse group of patients complaining of insomnia (n=104) misperceive overnight total sleep time and sleep latency, and to identify patient factors associated with these variations. DESIGN: Cross-sectional. SETTING: University based sleep disorders center. PATIENTS: Sleep disorder groups consisted of patients with psychophysiological insomnia (n=19), sleep state misperception (n=8), insomnia with depressive disorder (n=11), insomnia secondary to Axis I psychiatric disorder other than depression (n=21), periodic limb movement disorder (n=24), and obstructive sleep apnea (n=21). MEASUREMENT AND RESULTS: Patients completed a sleep history questionnaire and the MMPI, underwent overnight diagnostic polysomnographic assessment, and then estimated their total sleep time and sleep latency the subsequent morning. On average, patients overestimated sleep latency, but were equally likely to underestimate vs. overestimate total sleep time. Sleep time misperception was associated with longer periods of wakefulness following sleep onset, greater self-perceived sleep impairment, as well as several psychological dimensions. CONCLUSIONS: Patient factors, including sleep quality, perceptions of habitual sleep time, and current psychopathology, potentially influence sleep time estimation. Whereas psychological factors may lead to exaggeration of sleep disturbance among some patients, sleep quality itself may also influence the congruence between subjective and objective indices of sleep.     

Actigraphy‐assessed sleep during school and vacation periods: a naturalistic study of restricted and extended sleep opportunities in adolescents

School‐related sleep restriction in adolescents has been identified by studies comparing weekday and weekend sleep. This study compared weekday and vacation sleep to assess restricted and extended sleep opportunities. One‐hundred and forty‐six adolescents (47.3% male) aged 16.2 ± 1.0 years (M ± SD) from the general community wore an actigraph continuously for 4 weeks: the last week of a school term (Time‐E), the following 2‐week vacation, and the first week of the next term. Self‐reported sleep was assessed for each of the three time intervals, and chronotype was assessed using the Morningness–Eveningness Questionnaire at Time‐E. Daily actigraphy bedtime, rise‐time, time‐in‐bed, total sleep time, sleep onset latency, sleep efficiency, and % wake after sleep onset were analysed using latent growth curve modelling. The removal of school‐related sleep restriction was associated with an abrupt delay in sleep timing and increase in sleep duration. Subsequently, bedtime and rise‐time showed further linear delays throughout the vacation, while changes in time‐in‐bed were non‐significant. Sleep onset latency increased linearly, peaking in the middle of the second vacation week. Across the first vacation week, total sleep time and sleep efficiency linearly decreased, while % wake after sleep onset increased. These changes stabilized during the second vacation week. Older age and eveningness were associated with later bedtime and rise‐time, whilst females had longer time‐in‐bed, total sleep time and sleep onset latency. Compared with school days, sleep during the vacation was characterized by later timing, longer duration, lower quality and greater variability. Recovery from school‐related sleep restriction appeared to be completed within the 2 weeks of naturalistic extended sleep.     

The clinical diagnosis of the narcoleptic syndrome

Sleep–wake habits and control of postural muscle tone were investigated by self-report questionnaire in 183 subjects considered to have the narcoleptic syndrome, 62 subjects with hypersomnia and 10 with obstructive sleep apnoea. Results were compared with those in a group of 188 control subjects with normal sleep–wake habits. Excessive daytime sleepiness, determined by the Epworth Sleepiness Scale (ESS), was five times greater in the narcoleptic syndrome than in control subjects (score range 0–24, mean scores ±SD 19.6±3.0; and 4.5±3.3 respectively; P<0.001). The propensity to cataplexy, as determined by a rating scale developed to estimate the likelihood of loss of postural tone in response to sudden emotional stimuli, including laughter, was 10 times greater in narcoleptic syndrome than in control subjects (postural atonia total score range 0–600; mean±SD 334±122 and 28±45, respectively; P<0.001). Narcoleptics had more disturbances of night sleep than controls with episodes of muscle jerking, sleep walking, sleep talking and sleep terrors, as well as sleep paralysis, and higher insomnia self-rating scores. Sleep latency from bedtime to sleep-onset time was shorter in narcoleptics than controls. The hypersomniac group of 62 subjects was heterogeneous. Subsequent investigation showed that 18 subjects (29%) had idiopathic hypersomnia, four (6%) ‘incomplete’ narcolepsy without cataplexy and 10 (16%) hypersomnia accompanying a mood disorder. The mean ESS scores in this group and in subjects with obstructive sleep apnoea were comparable to those of the narcoleptic syndrome subject group. Mean postural atonia scores were similar to those of control subjects.