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.

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.

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 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.

An approach to common sleep presentations in infants and toddlers.

BACKGROUND: Healthy sleep is vital for optimal child development, yet over 30% of Australian parents report having children with disrupted sleep affecting all family members. These sleep difficulties might co-exist with sleep breathing disorders, contributing to morbidity and reduced quality of life. OBJECTIVE: This article aims to provide general practitioners (GPs) with an evidence-based, biopsychosocial approach to managing common sleep problems in infants and preschool-aged children. DISCUSSION: Strategies and techniques are outlined to aid GPs in promoting healthy sleep during infancy, educating parents on typical sleep patterns and supporting families in managing problematic sleep patterns in toddlers. Emphasis is placed on a tailored approach to developing a healthy sleep environment to meet the child's needs and parental values. Valuable resources and indications for specialist consultation are included.

Optimising sleep in adolescents: The challenges.

BACKGROUND: Adolescence is a stage of significant transition as children develop into young adults. Optimal sleep is crucial during this period to ensure physical, emotional and mental wellbeing. However, it is well recognised that insufficient quality and quantity of sleep is common among adolescents worldwide. OBJECTIVE: This article aims to provide general practitioners with an overview of the key issues encountered in adolescent patients relating to sleep and summarises approaches to assessment and evidence-based management of sleep problems in this population. DISCUSSION: This review highlights the physiological changes that affect sleep during adolescence and how other factors, including unhealthy sleep behaviours, influence these. It discusses the importance of healthy sleep and the consequences of sleep disturbance in adolescents. Management strategies are outlined, focusing on the key common issues that affect sleep in the teenage years, and guidance on when to consider co-management with specialist care is provided.

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.

Assessment and management of sleep disorders in shift workers: Challenges and considerations for general practice.

BACKGROUND: Shift work is characterised by displaced sleep opportunities and associated sleep disturbance. Shift workers often report sleepiness and other wake time symptoms associated with poor sleep. However, clinical sleep disorders are also prevalent in shift workers. Although prevalence rates are similar or higher in shift workers compared with the general population, help seeking in shift workers with sleep disorders is low. OBJECTIVE: This article aims to provide general practitioners with a contemporary overview of the prevalence rates for sleep disorders in shift workers, to clarify the existing evidence relating to mental and physical health consequences of sleep disorders in shift workers and to highlight the need to consider undiagnosed sleep disorders before attributing sleep-related symptoms solely to work schedules. DISCUSSION: Symptoms of sleep loss associated with shift work overlap with symptoms experienced by individuals living with sleep disorders. Although >40% of middle-aged Australians live with a sleep disorder that requires investigation and management, symptoms in shift workers are often attributed to the work schedule and, as a result, might not be investigated for appropriate diagnosis and treatment. We argue that screening for sleep disorders in shift workers with sleep complaints should be a priority.

Sex differences in response to cognitive behavioural therapy for insomnia: A chart review of 455 patients with chronic insomnia.

BACKGROUND: Insomnia is more prevalent in females, however studies examining sex differences in response to insomnia treatment are scarce. This study assessed sex-specific differences in cognitive behavioural therapy for insomnia (CBT-I)-related changes in insomnia symptoms in a large clinical cohort. METHODS: A chart review was conducted of a clinical cohort (females n = 305, males n = 150) referred to a sleep clinic. Participants had a registered psychologist confirm diagnosis of chronic insomnia according to DSM-IV/V criteria and a Level 1 or 2 sleep study. Daily sleep diaries and questionnaires including the Insomnia Severity Index (ISI), Flinders Fatigue Scale (FFS), the Daytime Feelings and Functioning Scale (DFFS), and the Depression, Anxiety and Stress Scale-21 items (DASS), were administered at baseline, post-treatment, and three-month follow-up. Linear mixed models determined interactions between sex and timepoint on symptoms. RESULTS: Mean (SD) age was 51.7 yrs (15.7, range = 18-90 yrs), and mean BMI was 26.3 kg/m2 (4.9), neither of which differed by sex. At pre-treatment, females demonstrated higher objective total sleep time (min) [343.5 (97.6) vs 323.8 min (92.1), p = 0.044], ISI [19.7 (4.2) vs 18.6 (4.4), p = 0.033], and FFS scores [19.2 (6.0) vs 16.9 (7.2), p = 0.003]. Compared to males, females experienced a greater reduction in FFS and DFFS scores and DASS depressive symptoms (p for interaction: 0.017, 0.043, 0.016 respectively) from baseline to follow-up. The greater reduction in depressive symptoms did not persist after controlling for age, BMI, and sleep apnea severity. Subjective total sleep time similarly increased across treatment for both males [baseline: 335.7 (15.1), post: 357.9 (15.5)] and females [baseline: 318.3 (10.4), post: 354.4 (10.7)], p for interaction: 0.22. CONCLUSION: Females and males experience similar, substantial benefits from CBT-I after accounting for comorbidities, suggesting the same treatment can resolve insomnia in both sexes.

A circadian-informed lighting intervention accelerates circadian adjustment to a night work schedule in a submarine lighting environment.

STUDY OBJECTIVE: Night work has detrimental impacts on sleep and performance, primarily due to misalignment between sleep-wake schedules and underlying circadian rhythms. This study tested whether circadian-informed lighting accelerated circadian phase delay, and thus adjustment to night work, compared to blue-depleted standard lighting under simulated submariner work conditions. METHODS: Nineteen healthy sleepers (12 males; mean±SD aged 29 ±10 y) participated in two separate 8-day visits approximately one month apart to receive, in random order, circadian-informed lighting (blue-enriched and dim, blue-depleted lighting at specific times) and standard lighting (dim, blue-depleted lighting). After an adaptation night (day 1), salivary dim light melatonin onset (DLMO) assessment was undertaken from 18:00-02:00 on days 2-3. During days 3-7, participants completed simulated night work from 00:00-08:00 and a sleep period from 10:00-19:00. Post-condition DLMO assessment occurred from 21:00-13:00 on days 7-8. Ingestible capsules continuously sampled temperature to estimate daily core body temperature minimum (Tmin) time. Tmin and DLMO circadian delays were compared between conditions using mixed effects models. RESULTS: There were significant condition-by-day interactions in Tmin and DLMO delays (both p<0.001). After four simulated night shifts, circadian-informed lighting produced a mean [95%CI] 4.3 [3.3 to 5.4] h greater delay in Tmin timing and a 4.2 [3 to 5.6] h greater delay in DLMO timing compared to standard lighting. CONCLUSIONS: Circadian-informed lighting accelerates adjustment to shiftwork in a simulated submariner work environment. Circadian lighting interventions warrant consideration in any dimly lit and blue-depleted work environments where circadian adjustment is relevant to help enhance human performance, safety, and health.

Working memory performance of older adults with insomnia.

Older individuals suffering insomnia typically report declines in their cognitive performance beyond what they consider to be normal changes due to the aging process. Recent neuro-imaging studies have demonstrated frontal lobe hypo-activation among insomniac populations when compared with healthy, good sleepers. However, research is yet to confirm whether frontal lobe hypo-activation translates into objective declines when performing tasks hypothesized to draw upon this brain region. This study aimed to investigate whether older insomnia sufferers demonstrate significantly impaired performance on a challenging working memory task when compared with age-matched good sleepers. Forty-nine older individuals (mean age = 69.43 years, SD = 4.83) suffering from sleep maintenance insomnia were compared with 49 age-matched good sleepers. Cognitive performance was assessed using the Double Span Memory Task, a computer-based working memory task that requires participants to indicate the names and/or spatial locations of increasingly longer sequences of visually presented objects. After controlling for general intelligence, the individuals suffering from insomnia did not perform differently when compared with the good sleepers on either the simpler or more cognitively demanding components of the task. Older individuals with insomnia did not display an observable impairment of working memory in this study relative to good sleepers. Despite the mixed results from previous research, this study adds weight to the absence of objective impairment in insomniacs, at least while performing short-term demanding cognitive tasks.

The impact of prolonged violent video-gaming on adolescent sleep: an experimental study.

Video-gaming is an increasingly prevalent activity among children and adolescents that is known to influence several areas of emotional, cognitive and behavioural functioning. Currently there is insufficient experimental evidence about how extended video-game play may affect adolescents' sleep. The aim of this study was to investigate the short-term impact of adolescents' prolonged exposure to violent video-gaming on sleep. Seventeen male adolescents (mean age = 16 ± 1 years) with no current sleep difficulties played a novel, fast-paced, violent video-game (50 or 150 min) before their usual bedtime on two different testing nights in a sleep laboratory. Objective (polysomnography-measured sleep and heart rate) and subjective (single-night sleep diary) measures were obtained to assess the arousing effects of prolonged gaming. Compared with regular gaming, prolonged gaming produced decreases in objective sleep efficiency (by 7 ± 2%, falling below 85%) and total sleep time (by 27 ± 12 min) that was contributed by a near-moderate reduction in rapid eye movement sleep (Cohen's d = 0.48). Subjective sleep-onset latency significantly increased by 17 ± 8 min, and there was a moderate reduction in self-reported sleep quality after prolonged gaming (Cohen's d = 0.53). Heart rate did not differ significantly between video-gaming conditions during pre-sleep game-play or the sleep-onset phase. Results provide evidence that prolonged video-gaming may cause clinically significant disruption to adolescent sleep, even when sleep after video-gaming is initiated at normal bedtime. However, physiological arousal may not necessarily be the mechanism by which technology use affects sleep.