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Light therapy is used to treat sleep and circadian rhythm disorders, yet there are limited studies on whether light therapy impacts electroencephalographic (EEG) activity during sleep. Therefore, we aimed to provide an overview of research studies that examined the effects of light therapy on sleep macro- and micro-architecture in populations with sleep and circadian rhythm disorders. We searched for randomized controlled trials that used light therapy and included EEG sleep measures using MEDLINE, PubMed, CINAHL, PsycINFO and Cochrane Central Register of Controlled Trials databases. Five articles met the inclusion criteria of patients with either insomnia or delayed sleep–wake phase disorder (DSWPD). These trials reported sleep macro-architecture outcomes using EEG or polysomnography. Three insomnia trials showed no effect of the timing or intensity of light therapy on total sleep time, wake after sleep onset, sleep efficiency and sleep stage duration compared to controls. Only one insomnia trial reported significantly higher sleep efficiency after evening light therapy (>4000 lx between 21:00–23:00 h) compared with afternoon light therapy (>4000 lx between 15:00–17:00 h). In the only DSWPD trial, six multiple sleep latency tests were conducted across the day (09:00 and 19:00 h) and bright light (2500 lx) significantly lengthened sleep latency in the morning (09:00 and 11:00 h) compared to control light (300 lx). None of the five trials reported any sleep micro-architecture measures. Overall, there was limited research about the effect of light therapy on EEG sleep measures, and studies were confined to patients with insomnia and DSWPD only. More research is needed to better understand whether lighting interventions in clinical populations affect sleep macro- and micro-architecture and objective sleep timing and quality.

Introduction While digital health interventions (DHIs) can potentially address the unmet needs for sleep health services, little is known about their implementation in practice. The current study aimed to explore primary care health providers’ attitudes and beliefs towards DHIs for sleep and implementation into practice. Methods A cross-sectional online survey was administered to Australian primary care health professionals: general practitioners (GPs), community nurses, and community pharmacists. Semi-structured interviews were conducted within a sub-sample of participants exploring their experiences with DHIs and perceived barriers/facilitators for embedding DHIs into primary care. Semi-structured interviews were thematically analysed using the framework approach to contextualise survey findings. Results Ninety-six surveys were returned (GPs = 36, nurses = 30, and pharmacists = 30) and 45 interviews conducted (GPs = 17, nurses = 14, and pharmacists = 14). From the survey, GPs were more likely to endorse familiarity ( p = 0.009) and use ( p

Abstract Methods for predicting circadian phase have been developed for healthy individuals. It is unknown whether these methods generalize to clinical populations, such as delayed sleep–wake phase disorder (DSWPD), where circadian timing is associated with functional outcomes. This study evaluated two methods for predicting dim light melatonin onset (DLMO) in 154 DSWPD patients using ~ 7 days of sleep–wake and light data: a dynamic model and a statistical model. The dynamic model has been validated in healthy individuals under both laboratory and field conditions. The statistical model was developed for this dataset and used a multiple linear regression of light exposure during phase delay/advance portions of the phase response curve, as well as sleep timing and demographic variables. Both models performed comparably well in predicting DLMO. The dynamic model predicted DLMO with root mean square error of 68 min, with predictions accurate to within ± 1 h in 58% of participants and ± 2 h in 95%. The statistical model predicted DLMO with root mean square error of 57 min, with predictions accurate to within ± 1 h in 75% of participants and ± 2 h in 96%. We conclude that circadian phase prediction from light data is a viable technique for improving screening, diagnosis, and treatment of DSWPD.

Insomnia is a highly prevalent sleep disorder with strong bidirectional associations with depressive symptoms. The circadian preference for eveningness has been shown to be associated with depressive symptoms in insomnia and other mental health conditions. However, there is a lack of studies in insomnia investigating whether objective measures, such as dim light melatonin onset (DLMO) or polysomnographic (PSG) sleep, are associated with depressive symptoms. Therefore, we investigated the associations between subjective measures (questionnaires assessing anxiety, sleep quality and circadian preference, and sleep diary) and depressive symptoms and whether the addition of objective measures (DLMO, PSG parameters) would strengthen the associations with depressive symptoms. In 115 insomnia disorder patients we found that anxiety was strongly associated with depressive symptoms in a model including circadian preference, dysfunctional beliefs of sleep, and self-reported previous depressive symptoms (R2 = 0.496, p < 0.001). The addition of sleep diary measures did not strengthen the model. We also found that the addition of objective measures (DLMO, PSG parameters) did not improve the subjective associations with depressive symptoms. Our data suggest that objective circadian markers are less important in the prediction of depressive symptoms in insomnia compared to subjective measures.

Introduction Insomnia is a highly prevalent and costly condition that is associated with increased health risks and healthcare utilisation. Anecdotally, cannabis use is frequently reported by consumers to promote sleep. However, there is limited research on the effects of cannabis on sleep and daytime function in people with insomnia disorder using objective measures. This proof-of-concept study will evaluate the effects of a single dose of an oral cannabis-based medicine on sleep and daytime function in participants with chronic insomnia disorder.Methods and analysis A randomised, crossover, placebo-controlled, single-dose study design will be used to test the safety and efficacy of an oral oil solution (‘ETC120’) containing 10 mg Δ9-tetrahydrocannabinol (THC) and 200 mg cannabidiol (CBD) in 20 participants diagnosed with chronic insomnia disorder. Participants aged 35–60 years will be recruited over an 18-month period commencing August 2019. Each participant will receive both the active drug and matched placebo, in a counterbalanced order, during two overnight study assessment visits, with at least a 1-week washout period between each visit. The primary outcomes are total sleep time and wake after sleep onset assessed via polysomnography. In addition, 256-channel high-density electroencephalography and source modelling using structural brain MRI will be used to comprehensively examine brain activation during sleep and wake periods on ETC120 versus placebo. Next-day cognitive function, alertness and simulated driving performance will also be investigated.Ethics and dissemination Ethics approval was received from Bellberry Human Research Ethics Committee (2018-04-284). The findings will be disseminated in a peer-reviewed open-access journal and at academic conferences.Trial registration number ANZCTRN12619000714189.

Abstract In this retrospective cohort study, we describe acceptability, tolerability and potential efficacy of cognitive behavioural therapy (CBT) in Insomnia Disorder subtypes, derived from polysomnography (PSG): insomnia with normal-sleep duration (I-NSD) and insomnia with short-sleep duration (I-SSD). All research volunteers were offered access to digital CBT, single component sleep restriction therapy and face-to-face group CBT. Follow-up occurred at three months post-treatment using the insomnia severity index (ISI). 96 participants (61 females, mean age of 41 years) were grouped into either normal-sleep (n = 53) or short-sleep (n = 43). CBT was acceptable to 63% of participants (normal-sleep = 31, short-sleep = 29), with 28 completing therapy (tolerability: normal-sleep = 11, short-sleep = 17). For potential efficacy, 39 (normal-sleep = 20, short-sleep = 19) out of 96 participants (41%) completed a follow-up ISI assessment. In this reduced sample, mean (SD) ISI scores decreased across both groups (normal-sleep: 18.0 (4.0) to 10.7 (4.6); short-sleep: 16.5 (5.5) to 11.0 (6.3); both P

Effective treatment of obstructive sleep apnoea (OSA) is primarily determined by adherence to the selected intervention. The most common treatment pathways are mechanical devices such as continuous positive airway pressure (CPAP) or a mandibular advancement device, often combined with weight loss therapy. Weight reduction is usually an adjunct therapy but may be used as a secondary treatment in mild-to-moderate OSA when mechanical treatments cannot be tolerated. To enhance the uptake and adherence to treatment, clinicians may assess patient's personality profiles and psychological readiness. There is a paucity of evidence related to these aspects of patient care and this article outlines the current research in relation to patient presentation, treatment uptake and barriers, and methods to enhance treatment adherence. This article disseminates personality traits observed in patients with OSA and identifies vulnerable groups who may require additional support to increase treatment adherence. It summarises the current evidence for treatment barriers in patients with OSA. Low self-efficacy in relation to CPAP and weight loss adherence will be explored as well as the potential to predict treatment responders and enhance therapeutic uptake and adherence. Extending personality traits into research and clinical practice could potentially result in more successful CPAP therapy and weight loss treatment outcomes.

Abstract Background and aims The prevalence of chronic benzodiazepine use in primary care settings remains high despite clear evidence of adverse health outcomes resulting from long‐term use and the availability of effective alternative behavioural therapies. Eliciting factors influencing past or current usage experience of benzodiazepine users and their future behavioural intention regarding discontinuation or alternative behavioural therapy adoption could be useful in developing informed strategies facilitating successful benzodiazepine withdrawal in long‐term users. The aim of this study was to identify patient factors influencing their current long‐term benzodiazepine use, past withdrawal attempt, and future intention to trial safer alternative behavioural therapies. Additionally, the study also aimed to explore patients' preference for information sources on behavioural therapies. Methods Point of purchase surveys were conducted with patients obtaining benzodiazepines from selected pharmacies across New South Wales (NSW), Australia. Survey items included the Beliefs about Medicines Questionnaire (BMQ‐specific), questions about patient's sociodemographic characteristics, as well as their views about long‐term benzodiazepine use and behavioural therapies. Results Seventy‐five patients were recruited from 12 pharmacies across New South Wales (NSW). The surveys were conducted from November 2016 to July 2017. The mean (±SD) age of the participants was 54.3 (±16.7) with a range of 23 to 86 years, and 67% of the participants had been using the benzodiazepine for at least 1 year. Lower‐education levels, stronger beliefs about the necessity of use, and lower concerns about ongoing benzodiazepine use were significantly associated with prolonged use. Sixty‐four percent of the participants were not interested in behavioural therapies, and there was a significant relationship between the participants' future preference for behavioural therapies and their concerns about the potential adverse effects of benzodiazepines. A majority of the participants rated general practitioners (GPs) as their first choice and pharmacists as the second choice for discussing behavioural therapies. Conclusions Specific individual sociodemographic characteristics of benzodiazepine users and their medication‐related beliefs influence their current benzodiazepine usage and future intention to trial behavioural therapies as an alternative to their benzodiazepines. Based on the reported preferences of benzodiazepine users in this study, developing and evaluating GP‐pharmacist collaborative services to improve the uptake of behavioural therapies as an alternative to benzodiazepines can be recommended.

Background: Insomnia disorder is a highly prevalent health condition, affecting ~10–15% of the adult population worldwide. A central feature of insomnia is hyperarousal characterized as persistent and increased somatic, cognitive and cortical stimulation. Hyperarousal leads to a state of conditioned arousal that disrupts both sleep and daytime function. Research studies have shown increases in body temperature, heart rate, electroencephalographic activity, catecholamines, and oxygen consumption as a measure of metabolic rate. These findings provide evidence of increased physiological activation in insomnia however results are not consistent. The aim of the systematic review was to determine if metabolic rate in patients with insomnia is increased in keeping with the hyperarousal hypothesis.Methods: We searched Pubmed, Web of Science, CINAHL, PsycINFO, EMBASE, and Scopus databases for observational and interventional studies that have measured metabolic rate in insomnia. Study characteristics were extracted and summarized and a risk of bias was performed for each of the studies.Results: Two reviewers screened 963 abstracts with 35 articles of interest for full-text review. Four articles evaluating 75 participants were included in this systematic review. Two studies showed increased oxygen consumption across 24 h in insomnia patients compared with good-sleeping controls. One study which measured oxygen consumption at only a single timepoint showed no difference between insomnia patients and good-sleeping controls. A further study evaluating the effect of lorazepam on oxygen consumption in patients with chronic insomnia showed that lorazepam reduced metabolic rate during the night time only.Conclusions: These findings show that metabolic rate appears to be increased across 24 h in line with the hyperarousal model of insomnia. However, these increases in metabolic rate in insomnia were minor compared to good-sleeping controls and the clinical significance is unclear. Larger, methodologically robust studies are required to confirm these findings and the effect of any increase in metabolic rate on sleep-wake disturbances or pathophysiology.

BackgroundDelayed 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).MethodsThis 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.FindingsBetween 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.ConclusionsIn 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 registrationThis trial was registered with the Australian New Zealand Clinical Trials Registry, ACTRN12612000425897.

Objective/BackgroundAlthough polysomnography (PSG) is the gold-standard measure for assessing disease severity in obstructive sleep apnea (OSA), it has limited value in identifying individuals experiencing significant neurobehavioural dysfunction. This study used a brief and novel computerised test battery to examine neurobehavioural function in adults with and without OSA.Patients/Methods204 patients with untreated OSA [age 49.3 (12.5) years; body mass index, [BMI] 33.6 (8.0) kg/m2; Epworth sleepiness scale 12 (4.9)/24; apnea hypopnea index 33.6 (25.8)/h] and 50 non-OSA participants [age 39.2 (14.0) years; BMI 25.8 (4.2) kg/m2, ESS 3.6 (2.3)/24]. All participants completed a computerised neurobehavioural battery during the daytime in the sleep clinic. The OSA group subsequently underwent an overnight PSG. The 30 min test battery assessed cognitive domains of visual spatial scanning and selective attention (Letter Cancellation Test), executive function (Stroop task) and working memory (2- and 3-Back tasks), and a validated sustained attention task (psychomotor vigilance task, PVT). Group differences in performance were compared. Associations between disease severity and performance were examined in the OSA group.ResultsAfter controlling for age, gender and education, OSA patients demonstrated impaired performance on the Stroop-Text, 2 and 3-Back tasks, and the PVT compared with the non-OSA group. OSA patients had worse performance on the LCT with fewer average hits albeit with better accuracy. Some OSA polysomnographic disease severity measures were weakly correlated with performance.ConclusionsThis brief test battery may provide a sensitive, standardised method of assessing daytime dysfunction in OSA.

OBJECTIVES:The aim of this preliminary study was to evaluate if Sleep Restriction Therapy for insomnia is associated with modifications to physiological arousal, indexed through overnight measures of plasma cortisol concentrations and core body temperature. METHODS:In a pre-to-post open label study design, eleven patients with chronic and severe Psychophysiological Insomnia underwent 5 weeks of Sleep Restriction Therapy. RESULTS:Eight (73%) patients out of 11 consented completed therapy and showed a decrease in insomnia severity pre-to-post treatment (mean (SD): 18.1 (2.8) versus 8.4 (4.8); p = .001). Six patients were analyzed with pre-to-post overnight measures of temperature and cortisol. Contrary to our hypothesis, significantly higher levels of plasma cortisol concentrations were found during the early morning at post-treatment compared to baseline (p < .01), while no change was observed in the pre-sleep phase or early part of the night. Core body temperature during sleep was however reduced significantly (overall mean [95% CI]: 36.54 (°C) [36.3, 36.8] versus 36.45 [36.2, 36.7]; p < .05). CONCLUSIONS:Sleep Restriction Therapy therefore was associated with increased early morning cortisol concentrations and decreased core body temperature, supporting the premise of physiological changes in functioning after effective therapy. Future work should evaluate change in physiological variables associated with clinical treatment response. TRIAL REGISTRATION:Australian New Zealand Clinical Trials Registry ANZCTR 12612000049875.

Although portable instruments have been used in the assessment of sleep disturbance for patients with low back pain (LBP), the accuracy of the instruments in detecting sleep/wake episodes for this population is unknown. This study investigated the criterion validity of two portable instruments (Armband and Actiwatch) for assessing sleep disturbance in patients with LBP. 50 patients with LBP performed simultaneous overnight sleep recordings in a university sleep laboratory. All 50 participants were assessed by Polysomnography (PSG) and the Armband and a subgroup of 33 participants wore an Actiwatch. Criterion validity was determined by calculating epoch-by-epoch agreement, sensitivity, specificity and prevalence and bias- adjusted kappa (PABAK) for sleep versus wake between each instrument and PSG. The relationship between PSG and the two instruments was assessed using intraclass correlation coefficients (ICC 2, 1). The study participants showed symptoms of sub-threshold insomnia (mean ISI = 13.2, 95% CI = 6.36) and poor sleep quality (mean PSQI = 9.20, 95% CI = 4.27). Observed agreement with PSG was 85% and 88% for the Armband and Actiwatch. Sensitivity was 0.90 for both instruments and specificity was 0.54 and 0.67 and PABAK of 0.69 and 0.77 for the Armband and Actiwatch respectively. The ICC (95%CI) was 0.76 (0.61 to 0.86) and 0.80 (0.46 to 0.92) for total sleep time, 0.52 (0.29 to 0.70) and 0.55 (0.14 to 0.77) for sleep efficiency, 0.64 (0.45 to 0.78) and 0.52 (0.23 to 0.73) for wake after sleep onset and 0.13 (-0.15 to 0.39) and 0.33 (-0.05 to 0.63) for sleep onset latency, for the Armband and Actiwatch, respectively. The findings showed that both instruments have varied criterion validity across the sleep parameters from excellent validity for measures of total sleep time, good validity for measures of sleep efficiency and wake after onset to poor validity for sleep onset latency.

IntroductionElectronic devices in the bedroom are broadly linked with poor sleep in adolescents. This study investigated whether there is a dose-response relationship between use of electronic devices (computers, cellphones, televisions and radios) in bed prior to sleep and adolescent sleep patterns.MethodsAdolescents aged 11-17 yrs (n = 1,184; 67.6% female) completed an Australia-wide internet survey that examined sleep patterns, sleepiness, sleep disorders, the presence of electronic devices in the bedroom and frequency of use in bed at night.ResultsOver 70% of adolescents reported 2 or more electronic devices in their bedroom at night. Use of devices in bed a few nights per week or more was 46.8% cellphone, 38.5% computer, 23.2% TV, and 15.8% radio. Device use had dose-dependent associations with later sleep onset on weekdays (highest-dose computer adjOR = 3.75: 99% CI = 2.17-6.46; cellphone 2.29: 1.22-4.30) and weekends (computer 3.68: 2.14-6.32; cellphone 3.24: 1.70-6.19; TV 2.32: 1.30-4.14), and later waking on weekdays (computer 2.08: 1.25-3.44; TV 2.31: 1.33-4.02) and weekends (computer 1.99: 1.21-3.26; cellphone 2.33: 1.33-4.08; TV 2.04: 1.18-3.55). Only 'almost every night' computer use (: 2.43: 1.45-4.08) was associated with short weekday sleep duration, and only 'almost every night' cellphone use (2.23: 1.26-3.94) was associated with wake lag (waking later on weekends).ConclusionsUse of computers, cell-phones and televisions at higher doses was associated with delayed sleep/wake schedules and wake lag, potentially impairing health and educational outcomes.