Sleep-wake state discrepancy does not impair the efficacy of cognitive behavioural therapy for insomnia: Findings from a large clinic sample.

The current study determined the extent to which sleep-wake state discrepancy impairs the efficacy of cognitive behavioural therapy for insomnia in a real-world clinical sample. Sleep-wake state discrepancy occurs when there is an inconsistency between a person's subjective and objective sleep, and is a common phenomenon amongst patients with insomnia. Limited information is available on the effectiveness of cognitive behavioural therapy for insomnia in treating patients who experience significant sleep-wake state discrepancy in "real-world" samples. In the present study, all patients with insomnia received cognitive behavioural therapy for insomnia through an outpatient insomnia program (N = 386; mean age = 51.96 years, SD = 15.62; 65.97% [N = 254] female). Prior to treatment, participants completed a polysomnography sleep study and sleep diary, which was used to calculate sleep-wake state discrepancy. At pre-treatment, post-treatment and 3-month follow-up, participants completed the Insomnia Severity Index and other questionnaires, and 1 week of sleep diaries from which sleep-onset latency, wake after sleep onset and other sleep variables were calculated. There were no differences in self-reported sleep-onset latency, wake after sleep onset or Insomnia Severity Index scores at post-treatment or 3-month follow-up between quintiles of sleep-wake state discrepancy. These results indicate that sleep-wake state discrepancy at pre-treatment does not predict treatment response to cognitive behavioural therapy for insomnia. Future research could examine multi-night assessments of sleep-wake state discrepancy to determine whether variations in discrepancy may relate to pre-treatment insomnia severity and cognitive behavioural therapy for insomnia outcomes.

Circadian aspects in the aetiology and pathophysiology of insomnia.

Because the endogenous circadian pacemaker is a very strong determinant of alertness/sleep propensity across the 24 h period, its mistiming may contribute to symptoms of insomnia (e.g., difficulties initiating sleep and maintaining sleep) and to the development of insomnia disorder. Despite the separation of insomnia and circadian rhythm disorders in diagnostic nosology implying independent pathophysiology, there is considerable evidence of co-morbidity and interaction between them. Sleep onset insomnia is associated with later timed circadian rhythms and can be treated with morning bright light to shift rhythms to an earlier timing. It is also possible that the causal link may go in both directions and that having a delayed circadian rhythm can result in enough experiences of delayed sleep onset to lead to some conditioned insomnia or insomnia disorder further exacerbating a delayed circadian rhythm. Early morning awakening insomnia is associated with an advanced circadian phase (early timing) and can be treated with evening bright light resulting in a delay of rhythms and an improved ability to sleep later in the morning and to obtain more sleep. There is some evidence suggesting that sleep maintenance insomnia is associated with a blunted amplitude of circadian rhythm that may be treated with increased regularity of sleep and light exposure timing. However, this is an insomnia phenotype that requires considerably more circadian research as well as further insomnia clinical research with the other insomnia phenotypes incorporating circadian timing measures and treatments.

The efficacy of intensive sleep retraining for insomnia: A systematic review and research agenda.

Intensive sleep retraining (ISR) is a brief behavioural treatment for sleep onset insomnia, administered in just a single overnight treatment session. This systematic review evaluates existing trials about the efficacy of intensive sleep retraining for treating insomnia, to inform whether there is enough evidence to recommend its use for clinical practice. A systematic literature search was conducted across three databases, yielding 108 results. Of these studies, three were deemed suitable for inclusion in this review. The included studies consistently reported significant reductions in insomnia symptoms following intensive sleep retraining, particularly decreases in sleep diary-derived sleep latency and increases in total sleep time. Based on these inconclusive but promising findings, a research agenda is proffered to test intensive sleep retraining as a treatment for insomnia. Large randomised controlled trials are needed to elucidate the potential benefits of intensive sleep retraining for different populations with insomnia, as are mechanistic trials to test which components underlie its seemingly therapeutic effects. Since more practical modalities of intensive sleep retraining administration have been developed, such trials are more feasible to conduct now than ever before.

The Good Sleeper Scale-15 items: a questionnaire for the standardised assessment of good sleepers.

Research with 'good sleepers' is ubiquitous, yet there are no standardised criteria to identify a 'good sleeper'. The present study aimed to create and validate a questionnaire for identifying good sleepers for use in research studies known as the Good Sleeper Scale-15 items (GSS-15). Data were derived from a population-based survey of Australian adults (n = 2,044). A total of 23 items were chosen for possible inclusion. An exploratory factor analysis (EFA) was conducted on ~10% of the survey dataset (n = 191) for factor identification and item reduction. A confirmatory factor analysis (CFA) was conducted on the remaining data (n = 1,853) to test model fit. Receiver operating characteristic curves and correlations were conducted to derive cut-off scores and test associations with sleep, daytime functioning, health, and quality-of-life. The EFA identified six factors: 'Sleep Difficulties', 'Timing', 'Duration', 'Regularity', 'Adequacy', and 'Perceived Sleep Problem'. The CFA showed that model fit was high and comparable to other sleep instruments, χ2 (63) = 378.22, p < 0.001, root mean square error of approximation = 0.05, with acceptable internal consistency (α = 0.76). Strong correlations were consistently found between GSS-15 global scores and outcomes, including 'a good night's sleep' (r = 0.7), 'feeling un-refreshed' (r = -0.59), and 'experienced sleepiness' (r = -0.51), p < 0.001. Cut-off scores were derived to categorise individuals likely to be a good sleeper (GSS-15 score ≥40) and those very likely to be a good sleeper (GSS-15 score ≥45). The GSS-15 is a freely available, robust questionnaire that will assist in identifying good sleepers for the purpose of sleep research. Future work will test relationships with other sleep measures in community and clinical samples.

Co-morbid insomnia and sleep apnea (COMISA): recent research and future directions.

PURPOSE OF REVIEW: Insomnia and obstructive sleep apnea have previously been viewed as completely independent conditions. However, there is now increasing recognition that insomnia and sleep apnea frequently co-occur. Co-morbid insomnia and sleep apnea (COMISA) is a highly prevalent condition that is associated with impairment of sleep, daytime function, mental health and physical health outcomes, and mortality risk. This review aims to provide an update on COMISA prevalence, consequences, treatment approaches, and future research directions. RECENT FINDINGS: People with COMISA experience worse sleep, mental health, physical health, quality of life and longevity compared to people with neither condition, and often compared to those with insomnia alone and sleep apnea alone. Emerging evidence suggests that cognitive behavioral therapy for insomnia is an effective treatment in the presence of treated and untreated sleep apnea, that may also improve manifestations and subsequent management of sleep apnea. Future research is required to understand the etiology of COMISA, and to develop and implement tailored treatment approaches. SUMMARY: It is important for sleep and respiratory technicians, researchers and clinicians to be aware of the high co-morbidity rates, consequences, and treatment requirements of patients with co-morbid insomnia and sleep apnea.

Comorbid insomnia and sleep apnoea is associated with all-cause mortality.

BACKGROUND: Increased mortality has been reported in people with insomnia and in those with obstructive sleep apnoea (OSA). However, these conditions commonly co-occur and the combined effect of comorbid insomnia and sleep apnoea (COMISA) on mortality risk is unknown. This study used Sleep Heart Health Study (SHHS) data to assess associations between COMISA and all-cause mortality risk. METHODS: Insomnia was defined as difficulties falling asleep, maintaining sleep and/or early morning awakenings from sleep ≥16 times per month, and daytime impairments. OSA was defined as an apnoea-hypopnoea index ≥15 events·h-1. COMISA was defined if both conditions were present. Multivariable adjusted Cox proportional hazards models were used to determine the association between COMISA and all-cause mortality (n=1210) over 15 years of follow-up. RESULTS: 5236 participants were included. 2708 (52%) did not have insomnia/OSA (reference group), 170 (3%) had insomnia-alone, 2221 (42%) had OSA-alone and 137 (3%) had COMISA. COMISA participants had a higher prevalence of hypertension (OR 2.00, 95% CI 1.39-2.90) and cardiovascular disease (CVD) (OR 1.70, 95% CI 1.11-2.61) compared with the reference group. Insomnia-alone and OSA-alone were associated with higher risk of hypertension but not CVD compared with the reference group. Compared with the reference group, COMISA was associated with a 47% (hazard ratio 1.47, 95% CI 1.06-2.07) increased risk of mortality. The association between COMISA and mortality was consistent across multiple definitions of OSA and insomnia. CONCLUSIONS: COMISA was associated with higher rates of hypertension and CVD at baseline, and an increased risk of all-cause mortality compared with no insomnia/OSA.

The association of co-morbid insomnia and sleep apnea with prevalent cardiovascular disease and incident cardiovascular events.

Insomnia and obstructive sleep apnea commonly co-occur (co-morbid insomnia and sleep apnea), and their co-occurrence has been associated with worse cardiometabolic and mental health. However, it remains unknown if people with co-morbid insomnia and sleep apnea are at a heightened risk of incident cardiovascular events. This study used longitudinal data from the Sleep Heart Health Study (N = 5803) to investigate potential associations between co-morbid insomnia and sleep apnea and cardiovascular disease prevalence at baseline and cardiovascular event incidence over ~11 years follow-up. Insomnia was defined as self-reported difficulties initiating and/or maintaining sleep AND daytime impairment. Obstructive sleep apnea was defined as an apnea-hypopnea index ≥ 15 events per hr sleep. Co-morbid insomnia and sleep apnea was defined if both conditions were present. Data from 4160 participants were used for this analysis. The prevalence of no insomnia/obstructive sleep apnea, insomnia only, obstructive sleep apnea only and co-morbid insomnia and sleep apnea was 53.2%, 3.1%, 39.9% and 1.9%, respectively. Co-morbid insomnia and sleep apnea was associated with a 75% (odd ratios [95% confidence interval]; 1.75 [1.14, 2.67]) increase in likelihood of having cardiovascular disease at baseline after adjusting for pre-specified confounders. In the unadjusted model, co-morbid insomnia and sleep apnea was associated with a twofold increase (hazard ratio, 95% confidence interval: 2.00 [1.33, 2.99]) in risk of cardiovascular event incidence. However, after adjusting for pre-specified covariates, co-morbid insomnia and sleep apnea was not significantly associated with incident cardiovascular events (hazard ratio 1.38 [0.92, 2.07]). Comparable findings were obtained when an alternative definition of insomnia (difficulties initiating and/or maintaining sleep without daytime impairment) was used.

EEG power spectral responses to wind farm compared with road traffic noise during sleep: A laboratory study.

Wind turbine noise is dominated by low frequencies for which effects on sleep relative to more common environmental noise sources such as road traffic noise remain unknown. This study examined the effect of wind turbine noise compared with road traffic noise on sleep using quantitative electroencephalogram power spectral analysis. Twenty-three participants were exposed to 3-min samples of wind turbine noise and road traffic noise at three sound pressure levels (33, 38 and 43 dBA) in randomised order during established sleep. Acute (0-30 s) and more sustained (30-180 s) effects of noise presentations during N2 and N3 sleep were examined using spectral analysis of changes in electroencephalogram power frequency ranges across time in 5-s intervals. Both noise types produced time- and sound pressure level-dependent increases in electroencephalogram power, but with significant noise type by sound pressure level interactions in beta, alpha, theta and delta frequency bands (all p < 0.05). Wind turbine noise showed significantly lower delta, theta and beta activity immediately following noise onset compared with road traffic noise (all p < 0.05). However, alpha activity was higher for wind turbine noise played at lower sound pressure levels (33 dBA [p = 0.001] and 38 dBA [p = 0.003]) compared with traffic noise during N2 sleep. These findings support that spectral analyses show subtle effects of noise on sleep and that electroencephalogram changes following wind turbine noise and road traffic noise onset differ depending on sound pressure levels; however, these effects were mostly transient and had little impact on conventionally scored sleep. Further studies are needed to establish if electroencephalogram changes associated with modest environmental noise exposures have significant impacts on sleep quality and next-day functioning.

Correspondence between physiological and behavioural responses to vibratory stimuli during the sleep onset period: A quantitative electroencephalography analysis.

Behavioural responses to auditory stimuli cease in late N1 or early N2 sleep. Yet, responsiveness to minimal intensity tactile stimuli and the correspondence with sleep microstructure during the sleep onset period is unknown. The aim of the present study was to investigate sleep microstructure using quantitative electroencephalography analysis when participants behaviourally responded to minimal intensity vibratory stimuli compared to when participants did not respond to stimuli during the sleep onset period. Eighteen participants wore a device that emitted vibratory stimuli to which individuals responded by tapping their index finger. A fast Fourier transform using multitaper-based estimation was applied to electroencephalography signals in 5-s epochs. Participants exhibited increases in higher frequencies 5 s before and immediately after the stimulus presentation when they responded to the stimulus compared to when they did not respond during all sleep stages. They also had greater delta power after stimulus onset when they did not respond to stimuli presented in N1 and N2 sleep compared to when they did respond. Participants responded to a significantly greater proportion of stimuli in wake than in N1 sleep (p < .001, d = 2.38), which was also significantly greater than the proportion of responses in N2 sleep (p < .001, d = 1.12). Participants showed wake-like sleep microstructure when they responded to vibratory stimuli and sleep-like microstructure when they did not respond during all sleep stages. The present study adds to the body of evidence characterising N1 sleep as a transitional period between sleep and wake containing rapid fluctuations between these two states.

A systematic review and meta-analysis of wind turbine noise effects on sleep using validated objective and subjective sleep assessments.

Little is known about the potential impacts of wind turbine noise (WTN) on sleep. Previous research is limited to cross-sectional studies reporting anecdotal impacts on sleep using inconsistent sleep metrics. This meta-analysis sought to comprehensively review studies evaluating the impact of WTN using widely accepted and validated objective and subjective sleep assessments. Search terms included: "wind farm noise", "wind turbine noise", "wind turbine sound", "wind turbine noise exposure" AND "sleep". Only original articles published in English published after the year 2000 and reporting sleep outcomes in the presence of WTN using polysomnography, actigraphy or psychometrically validated sleep questionnaires were included. Uniform outcomes of the retrieved studies were meta-analysed to examine WTN effects on objective and subjective sleep outcomes. Nine studies were eligible for review and five studies were meta-analysed. Meta-analyses (Hedges' g; 95% confidence interval [CI]) revealed no significant differences in objective sleep onset latency (0.03, 95%  CI -0.34 to 0.41), total sleep time (-0.05, 95%  CI -0.77 to 0.67), sleep efficiency (-0.25, 95%  CI -0.71 to 0.22) or wake after sleep onset (1.25, 95%  CI -2.00 to 4.50) in the presence versus absence of WTN (all p > .05). Subjective sleep estimates were not meta-analysed because measurement outcomes were not sufficiently uniform for comparisons between studies. This systematic review and meta-analysis suggests that WTN does not significantly impact key indicators of objective sleep. Cautious interpretation remains warranted given variable measurement methodologies, WTN interventions, limited sample sizes, and cross-sectional study designs, where cause-and-effect relationships are uncertain. Well-controlled experimental studies using ecologically valid WTN, objective and psychometrically validated sleep assessments are needed to provide conclusive evidence regarding WTN impacts on sleep.

Co-occurring depression and insomnia in Australian primary care: recent scientific evidence.

Depression and insomnia commonly co-occur, resulting in greater morbidity for patients, and difficult diagnostic and treatment decisions for clinicians. When patients report symptoms of both depression and insomnia, it is common for medical practitioners to conceptualise the insomnia as a secondary symptom of depression. This implies that there is little purpose in treating insomnia directly, and that management of depression will improve both the depression and insomnia symptoms. In this review, we present an overview of research investigating the comorbidity and treatment approaches for patients presenting with depression and insomnia in primary care. Evidence shows that clinicians should avoid routinely conceptualising insomnia as a secondary symptom of depression. This is because insomnia symptoms: (i) often occur before mood decline and are independently associated with increased risk of future depression; (ii) commonly remain unchanged following depression treatment; and (iii) predict relapse of depression after treatment for depression only. Furthermore, compared with control, cognitive behaviour therapy for insomnia improves symptoms of both depression and insomnia. It is critical that primary care clinicians dedicate specific diagnostic and treatment attention to the management of both depression (eg, psychotherapy, antidepressants) and insomnia (eg, cognitive behaviour therapy for insomnia administered by trained therapists or psychologists through a mental health treatment plan referral, by online programs, or by a general practitioner or nurse) when they co-occur. These treatments may be offered concurrently or sequentially (eg, insomnia treatment followed by depression treatment, or vice versa), depending on presenting symptoms, history, lifestyle factors and other comorbidities.

Primary care management of chronic insomnia: a qualitative analysis of the attitudes and experiences of Australian general practitioners.

BACKGROUND: Chronic insomnia is a highly prevalent disorder, with ten to thirty percent of Australian adults reporting chronic difficulties falling asleep and/or staying asleep such that it causes significant daytime impairment. Current Australian general practice guidelines recommend cognitive behavioural therapy for insomnia (CBTi) as first line treatment for insomnia, however research suggests that most general practice consultations for insomnia result in a prescription for hypnotic or sedative medicines. Although the first point of contact for patients experiencing symptoms of insomnia is often general practice, little is known about the current role, experiences and capacity of Australian general practitioners to manage insomnia. This study aimed to address that gap by exploring the attitudes and opinions of general practitioners regarding insomnia management, to inform the development and implementation of new models of best practice insomnia care within general practice. METHODS: A descriptive, pragmatic qualitative study. Purposive sampling was used to recruit practising Australian general practitioners, varying in age, years of experience and geographic location. Semi-structured interviews were conducted, and data analysed using thematic analysis.  RESULTS: Twenty-eight general practitioners participated in the study. Three major themes were identified: 1) Responsibility for insomnia care; 2) Complexities in managing insomnia; and 3) Navigating treatment pathways. Whilst general practitioners readily accepted responsibility for the management of insomnia, provision of care was often demanding and difficult within the funding and time constraints of general practice. Patients presenting with comorbid mental health conditions and insomnia, and decision-making regarding long-term use of benzodiazepines presented challenges for general practitioners. Whilst general practitioners confidently provided sleep hygiene education to patients, their knowledge and experience of CBTi, and access and understanding of specialised referral pathways for insomnia was limited.  CONCLUSIONS: General practitioners report that whilst assessing and managing insomnia can be demanding, it is an integral part of general practice. Insomnia presents complexities for general practitioners. Greater clarity about funding options, targeted education about effective insomnia treatments, and referral pathways to specialist services, such as benzodiazepine withdrawal support and psychologists, would benefit insomnia management within general practice.

A PERIOD3 variable number tandem repeat polymorphism modulates melatonin treatment response in delayed sleep-wake phase disorder.

We examined whether a polymorphism of the PERIOD3 gene (PER3; rs57875989) modulated the sleep-promoting effects of melatonin in Delayed Sleep-Wake Phase Disorder (DSWPD). One hundred and four individuals (53 males; 29.4 ±10.0 years) with DSWPD and a delayed dim light melatonin onset (DLMO) collected buccal swabs for genotyping (PER34/4 n = 43; PER3 5 allele [heterozygous and homozygous] n = 60). Participants were randomised to placebo or 0.5 mg melatonin taken 1 hour before desired bedtime (or ~1.45 hours before DLMO), with sleep attempted at desired bedtime (4 weeks; 5-7 nights/week). We assessed sleep (diary and actigraphy), Pittsburgh Sleep Quality Index (PSQI), Insomnia Severity Index (ISI), Patient-Reported Outcomes Measurement Information System (PROMIS: Sleep Disturbance, Sleep-Related Impairment), Sheehan Disability Scale (SDS) and Patient- and Clinician-Global Improvement (PGI-C, CGI-C). Melatonin treatment response on actigraphic sleep onset time did not differ between genotypes. For PER34/4 carriers, self-reported sleep onset time was advanced by a larger amount and sleep onset latency (SOL) was shorter in melatonin-treated patients compared to those receiving placebo (P = .008), while actigraphic sleep efficiency in the first third of the sleep episode (SE T1) did not differ. For PER3 5 carriers, actigraphic SOL and SE T1 showed a larger improvement with melatonin (P < .001). Melatonin improved ISI (P = .005), PROMIS sleep disturbance (P < .001) and sleep-related impairment (P = .017), SDS (P = .019), PGI-C (P = .028) and CGI-C (P = .016) in PER34/4 individuals only. Melatonin did not advance circadian phase. Overall, PER34/4 DSWPD patients have a greater response to melatonin treatment. PER3 genotyping may therefore improve DSWPD patient outcomes.

Increased sensitivity of the circadian system to light in delayed sleep-wake phase disorder.

KEY POINTS: This is the first study to demonstrate an altered circadian phase shifting response in a circadian rhythm sleep disorder. Patients with delayed sleep-wake phase disorder (DSWPD) demonstrate greater sensitivity of the circadian system to the phase-delaying effects of light. Increased circadian sensitivity to light is associated with later circadian timing within both control and DSWPD groups. DSWPD patients had a greater sustained pupil response after light exposure. Treatments for DSWPD should consider sensitivity of the circadian system to light as a potential underlying vulnerability, making patients susceptible to relapse. ABSTRACT: Patients with delayed sleep-wake phase disorder (DSWPD) exhibit delayed sleep-wake behaviour relative to desired bedtime, often leading to chronic sleep restriction and daytime dysfunction. The majority of DSWPD patients also display delayed circadian timing in the melatonin rhythm. Hypersensitivity of the circadian system to phase-delaying light is a plausible physiological basis for DSWPD vulnerability. We compared the phase shifting response to a 6.5 h light exposure (∼150 lux) between male patients with diagnosed DSWPD (n = 10; aged 20.8 ± 2.3 years) and male healthy controls (n = 11; aged 22.4 ± 3.3 years). Salivary dim light melatonin onset (DLMO) was measured under controlled conditions in dim light (<3 lux) before and after light exposure. Correcting for the circadian time of the light exposure, DSWPD patients exhibited 31.5% greater phase delay shifts than healthy controls. In both groups, a later initial melatonin phase was associated with a greater magnitude phase shift, indicating that increased circadian sensitivity to light may be a factor that contributes to delayed phase, even in non-clinical groups. DSWPD patients also had reduced pupil size following the light exposure, and showed a trend towards increased melatonin suppression during light exposure. These findings indicate that, for patients with DSWPD, assessment of light sensitivity may be an important factor that can inform behavioural therapy, including minimization of exposure to phase-delaying night-time light.

Efficacy of melatonin with behavioural sleep-wake scheduling for delayed sleep-wake phase disorder: A double-blind, randomised clinical trial.

BACKGROUND: Delayed Sleep-Wake Phase Disorder (DSWPD) is characterised by sleep initiation insomnia when attempting sleep at conventional times and difficulty waking at the required time for daytime commitments. Although there are published therapeutic guidelines for the administration of melatonin for DSWPD, to our knowledge, randomised controlled trials are lacking. This trial tested the efficacy of 0.5 mg melatonin, combined with behavioural sleep-wake scheduling, for improving sleep initiation in clinically diagnosed DSWPD patients with a delayed endogenous melatonin rhythm relative to patient-desired (or -required) bedtime (DBT). METHODS: This randomised, placebo-controlled, double-blind clinical trial was conducted in an Australian outpatient DSWPD population. Following 1-wk baseline, clinically diagnosed DSWPD patients with delayed melatonin rhythm relative to DBT (salivary dim light melatonin onset [DLMO] after or within 30 min before DBT) were randomised to 4-wk treatment with 0.5 mg fast-release melatonin or placebo 1 h before DBT for at least 5 consecutive nights per week. All patients received behavioural sleep-wake scheduling, consisting of bedtime scheduled at DBT. The primary outcome was actigraphic sleep onset time. Secondary outcomes were sleep efficiency in the first third of time in bed (SE T1) on treatment nights, subjective sleep-related daytime impairment (Patient Reported Outcomes Measurement Information System [PROMIS]), PROMIS sleep disturbance, measures of daytime sleepiness, clinician-rated change in illness severity, and DLMO time. FINDINGS: Between September 13, 2012 and September 1, 2014, 307 participants were registered; 116 were randomised to treatment (intention-to-treat n = 116; n = 62 males; mean age, 29.0 y). Relative to baseline and compared to placebo, sleep onset occurred 34 min earlier (95% confidence interval [CI] -60 to -8) in the melatonin group. SE T1 increased; PROMIS sleep-related impairment, PROMIS sleep disturbance, insomnia severity, and functional disability decreased; and a greater proportion of patients showed more than minimal clinician-rated improvement following melatonin treatment (52.8%) compared to placebo (24.0%) (P < 0.05). The groups did not differ in the number of nights treatment was taken per protocol. Post-treatment DLMO assessed in a subset of patients (n = 43) was not significantly different between groups. Adverse events included light-headedness, daytime sleepiness, and decreased libido, although rates were similar between treatment groups. The clinical benefits or safety of melatonin with long-term treatment were not assessed, and it remains unknown whether the same treatment regime would benefit patients experiencing DSWPD sleep symptomology without a delay in the endogenous melatonin rhythm. CONCLUSIONS: In this study, melatonin treatment 1 h prior to DBT combined with behavioural sleep-wake scheduling was efficacious for improving objective and subjective measures of sleep disturbances and sleep-related impairments in DSWPD patients with delayed circadian phase relative to DBT. Improvements were achieved largely through the sleep-promoting effects of melatonin, combined with behavioural sleep-wake scheduling. TRIAL REGISTRATION: This trial was registered with the Australian New Zealand Clinical Trials Registry, ACTRN12612000425897.

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.

The effects of anticipating a high-stress task on sleep and performance during simulated on-call work.

On-call work is used to manage around the clock working requirements in a variety of industries. Often, tasks that must be performed while on-call are highly important, difficult and/or stressful by nature and, as such, may impact the level of anxiety that is experienced by on-call workers. Heightened anxiety is associated with poor sleep, which affects next-day cognitive performance. Twenty-four male participants (20-35 years old) spent an adaptation, a control and two counterbalanced on-call nights in a time-isolated sleep laboratory. On one of the on-call nights they were told that they would be required to do a speech upon waking (high-stress condition), whereas on the other night they were instructed that they would be required to read to themselves (low-stress condition). Pre-bed anxiety was measured by the State Trait Anxiety Inventory form x-1, and polysomnography and quantitative electroencephalogram analyses were used to investigate sleep. Performance was assessed across each day using the 10-min psychomotor vigilance task (09:30 hours, 12:00 hours, 14:30 hours, 17:00 hours). The results indicated that participants experienced no significant changes in pre-bed anxiety or sleep between conditions. However, performance on the psychomotor vigilance task was best in the high-stress condition, possibly as a result of heightened physiological arousal caused by performing the stressful task that morning. This suggests that performing a high-stress task may be protective of cognitive performance to some degree when sleep is not disrupted.

Co-morbid OSA and insomnia increases depression prevalence and severity in men.

BACKGROUND AND OBJECTIVE: Obstructive sleep apnoea (OSA) and insomnia coexist in clinical populations but prevalence in the community and risk factors remain largely unknown. We examined the prevalence and profile of previously undiagnosed co-morbid OSA and insomnia symptoms (COMISA) in community-dwelling men. METHODS: Men (n = 700, aged 58.5 ± 11.0 (mean ± SD) years) without a prior diagnosis of OSA completed full at-home unattended polysomnography, the Pittsburgh Sleep Quality Index and 36-item short form (SF-36) survey (2007-2012). Insomnia symptoms included difficulty initiating/maintaining sleep in the presence of daytime fatigue (DIMS-F). Depressive symptoms were assessed using the Beck Depression Inventory-1A, Centre for Epidemiological Studies Depression Scale and Patient Health Questionnaire-9 (PHQ-9) (2007-2010). Univariate (χ2 and analysis of variance (ANOVA)) and multiple linear regressions were used to compare data from four groups of individuals: neither disorder; previously undiagnosed OSA (apnoea-hypopnoea index ≥ 10) or DIMS-F alone; and COMISA. RESULTS: COMISA prevalence was 6.7%. Depression prevalence (COMISA, 42.6%; DIMS-F, 21.6%; OSA, 8.4%, χ2 = 71.6, P < 0.00) and symptom scale scores (e.g. PHQ-9 mean ± SD: 16.1 ± 5.5 c.f. DIMS-F: 14.0 ± 4.9, P < 0.01 and OSA: 11.4 ± 3.0, P = 0.01) were highest in men with COMISA. In COMISA, respiratory and arousal indices were similar to those observed in OSA whilst reductions in subjective sleep and day dysfunction scores were similar to DIMS-F. After adjustment, predicted mean depression scores were all higher in DIMS-F and COMISA using linear regression (e.g. PHQ-9 ß (95% CI): DIMS-F: 2.3 (1.2, 3.5); COMISA: 4.1 (3.0, 5.1)). CONCLUSION: Men with COMISA have a greater prevalence, and severity, of depression than men with only one disorder.

The relationship between a night's sleep and subsequent daytime functioning in older poor and good sleepers.

Those suffering insomnia symptoms generally report daytime impairments. However, research has not assessed whether this relationship holds on a nightly basis, despite the strongly held belief that a night of poor sleep impairs mood and functioning the following day. The objective of this study was to test this relationship in a group of older poor sleepers with insomnia symptoms compared with good sleepers. This study utilized a within-subjects design to investigate day-to-day subjective daytime functioning and its relation to the previous night's sleep. Seventeen older individuals (mean age: 67.5 years) were identified with a retrospective questionnaire and 2 weeks of sleep-wake diary to have poor sleep consistent with insomnia. Seventeen good sleepers (mean age: 67.8 years) were selected using the same measures. Participants reported their beliefs about sleep and daytime functioning on the Dysfunctional Beliefs and Attitudes about Sleep Scale (DBAS-16). One week later they commenced a 14-day period of sleep-wake diaries and concurrent responses to a modified Daytime Insomnia Symptom Scale (DISS). Results showed significant night-to-day covariation between sleep efficiency and daytime functioning for individuals with poor sleep (r = 0.34), but not for good sleepers (r = 0.08). Those poor sleepers who held this covariation belief most strongly were those who subsequently showed this night-to-day relationship the most strongly (r = 0.56). This was not true for good sleepers. For those suffering insomnia, these findings demonstrate their belief that a poor sleep is followed by an impaired daytime, consistent with their experience.

Delayed melatonin circadian timing, lower melatonin output, and sleep disruptions in myopic, or short-sighted, children.

STUDY OBJECTIVES: This study investigated the differences in melatonin circadian timing and output, sleep characteristics, and cognitive function in myopic and non-myopic (or emmetropic) children, aged 8-15 years. METHODS: Twenty-six myopes (refractive error [mean ±â€…standard error mean] -2.06 ±â€…0.23 diopters) and 19 emmetropes (-0.06 ±â€…0.04 diopters), aged 11.74 ±â€…2.31 years were recruited. Circadian timing was assessed using salivary dim-light melatonin onset (DLMO), collected half-hourly for 7 hours, beginning 5 hours before and finishing 2 hours after individual average sleep onset in a sleep laboratory. Nocturnal melatonin output was assessed via aMT6s levels from urine voids collected from 05:30 pm to 8:00 am the following morning. Actigraphy-derived objective sleep timing were acquired for a week prior to the sleep laboratory visit. Cognitive assessments of sustained attention (using psychomotor vigilance task [PVT]) and working memory (using digit spans) were performed on the night of sleep laboratory. RESULTS: Myopic children (9:07 pm ±â€…14 minutes) exhibited a DLMO phase-delay of 1 hour 8 minutes compared to emmetropes (7:59 pm ±â€…13 minutes), p = 0.002. aMT6s melatonin levels were significantly lower among myopes (18.70 ±â€…2.38) than emmetropes (32.35 ±â€…6.93, p = 0.001). Myopes also exhibited significantly delayed sleep onset, delayed wake-up time, poor and reduced sleep, and more evening-type diurnal preference than emmetropes (all p < 0.05). Finally, myopes showed a slower reaction time in the PVT (p < 0.05), but not digit span tasks at night. CONCLUSIONS: These findings suggest a potential association between circadian rhythm dysfunction and myopia in children.