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The purpose of this guideline is to optimize evaluation and management of patients with obesity hypoventilation syndrome (OHS). A multidisciplinary panel identified and prioritized five clinical questions. The panel performed systematic reviews of available studies (up to July 2018) and followed the Grading of Recommendations, Assessment, Development, and Evaluation evidence-to-decision framework to develop recommendations. All panel members discussed and approved the recommendations. After considering the overall very low quality of the evidence, the panel made five conditional recommendations. We suggest that: ) clinicians use a serum bicarbonate level <27 mmol/L to exclude the diagnosis of OHS in obese patients with sleep-disordered breathing when suspicion for OHS is not very high (<20%) but to measure arterial blood gases in patients strongly suspected of having OHS, ) stable ambulatory patients with OHS receive positive airway pressure (PAP), ) continuous positive airway pressure (CPAP) rather than noninvasive ventilation be offered as the first-line treatment to stable ambulatory patients with OHS and coexistent severe obstructive sleep apnea, ) patients hospitalized with respiratory failure and suspected of having OHS be discharged with noninvasive ventilation until they undergo outpatient diagnostic procedures and PAP titration in the sleep laboratory (ideally within 2-3 mo), and ) patients with OHS use weight-loss interventions that produce sustained weight loss of 25% to 30% of body weight to achieve resolution of OHS (which is more likely to be obtained with bariatric surgery). Clinicians may use these recommendations, on the basis of the best available evidence, to guide management and improve outcomes among patients with OHS.

Overweight/obesity is a common, reversible risk factor for obstructive sleep apnea severity (OSA). The purpose of this guideline is to provide evidence-based recommendations for the management of overweight/obesity in patients with OSA. The Grading of Recommendations, Assessment, Development and Evaluation approach was used to evaluate the literature. Clinical recommendations were formulated by a panel of pulmonary, sleep medicine, weight management, and behavioral science specialists. Behavioral, pharmacological, and surgical treatments promote weight loss and can reduce OSA severity, reverse common comorbidities, and improve quality of life, although published studies have methodological limitations. After considering the quality of evidence, feasibility, and acceptability of these interventions, the panel made a strong recommendation that patients with OSA who are overweight or obese be treated with comprehensive lifestyle intervention consisting of 1) a reduced-calorie diet, 2) exercise or increased physical activity, and 3) behavioral guidance. Conditional recommendations were made regarding reduced-calorie diet and exercise/increased physical activity as separate management tools. Pharmacological therapy and bariatric surgery are appropriate for selected patients who require further assistance with weight loss. Weight-loss interventions, especially comprehensive lifestyle interventions, are associated with improvements in OSA severity, cardiometabolic comorbidities, and quality of life. The American Thoracic Society recommends that clinicians regularly assess weight and incorporate weight management strategies that are tailored to individual patient preferences into the routine treatment of adult patients with OSA who are overweight or obese.

Electronic 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. Adolescents 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. Over 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). Use 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.

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). 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. 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. 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. This trial was registered with the Australian New Zealand Clinical Trials Registry, ACTRN12612000425897.

Insomnia disorder (ID) is a heterogeneous disorder with proposed subtypes based on objective sleep duration. We speculated that insomnia subtyping with additional power spectral analysis and measurement of response to acute sleep restriction may be informative in overall assessment of ID. To explore alternative classifications of ID subtypes, insomnia patients (n = 99) underwent two consecutive overnight sleep studies: (i) habitual sleep opportunity (polysomnography, PSG) and, (ii) two hours less sleep opportunity (electroencephalography, EEG), with the first night compared to healthy controls (n = 25). ID subtypes were derived from data-driven classification of PSG, EEG spectral power and interhemispheric EEG asymmetry index. Three insomnia subtypes with different sleep duration and NREM spectral power were identified. One subtype (n = 26) had shorter sleep duration and lower NREM delta power than healthy controls (short-sleep delta-deficient; SSDD), the second subtype (n = 51) had normal sleep duration but lower NREM delta power than healthy controls (normal-sleep delta-deficient; NSDD) and a third subtype showed (n = 22) no difference in sleep duration or delta power from healthy controls (normal neurophysiological sleep; NNS). Acute sleep restriction improved multiple objective sleep measures across all insomnia subtypes including increased delta power in SSDD and NSDD, and improvements in subjective sleep quality for SSDD ( p  = 0.03), with a trend observed for NSDD ( p  = 0.057). These exploratory results suggest evidence of novel neurophysiological insomnia subtypes that may inform sleep state misperception in ID and with further research, may provide pathways for personalised care.

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 < 0.01). Those with normal-sleep were more likely to respond (≥6-point ISI reduction) to CBT compared to short-sleep (70%, n = 14/20 vs. 37%, n = 7/19 respectively, P = 0.038). In this cohort, 60 (63%) of participants attempted CBT and of those 28 (47%) completed therapy. Results may be comparable to clinical participants with implications for the successful translation of CBT for insomnia.

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.

Background The high and increasing demand for obstructive sleep apnea (OSA) care has exceeded the capacity of specialist sleep services prompting consideration of whether general practitioners could have an enhanced role in service delivery. However, little is known about the current involvement, experiences and attitudes of Australian general practitioners towards OSA. The purpose of this study was to provide an in-depth analysis of Australian general practitioners’ experiences and opinions regarding their care of patients with OSA to inform the design and implementation of new general practice models of care. Methods Purposive sampling was used to recruit participants with maximum variation in age, experience and location. Semi-structured interviews were conducted and were analysed using Thematic Analysis. Results Three major themes were identified: (1) General practitioners are important in recognising symptoms of OSA and facilitating a diagnosis by others; (2) Inequities in access to the assessment and management of OSA; and (3) General practitioners currently have a limited role in the management of OSA. Conclusions When consulting with patients with symptoms of OSA, general practitioners see their primary responsibility as providing a referral for diagnosis by others. General practitioners working with patients in areas of greater need, such as rural/remote areas and those of socio-economic disadvantage, demonstrated interest in being more involved in OSA management. Inequities in access to assessment and management are potential drivers for change in future models of care for OSA in general practice.

Abstract Study Objectives Cardiovascular autonomic dysfunction, as measured by short-term diurnal heart rate variability (HRV), has been reported in older adults with mild cognitive impairment (MCI). However, it is unclear whether this impairment also exists during sleep in this group. We, therefore, compared overnight HRV during sleep in older adults with MCI and those with subjective cognitive impairment (SCI). Methods Older adults (n = 210) underwent overnight polysomnography. Eligible participants were characterized as multi-domain MCI or SCI. The multi-domain MCI group was comprised of amnestic and non-amnestic subtypes. Power spectral analysis of HRV was conducted on the overnight electrocardiogram during non-rapid eye movement (NREM), rapid eye movement (REM), N1, N2, N3 sleep stages, and wake periods. High-frequency HRV (HF-HRV) was employed as the primary measure to estimate parasympathetic function. Results The MCI group showed reduced HF-HRV during NREM sleep (p = 0.018), but not during wake or REM sleep (p > 0.05) compared to the SCI group. Participants with aMCI compared to SCI had the most pronounced reduction in HF-HRV across all NREM sleep stages—N1, N2, and N3, but not during wake or REM sleep. The naMCI sub-group did not show any significant differences in HF-HRV during any sleep stage compared to SCI. Conclusions Our study showed that amnestic MCI participants had greater reductions in HF-HRV during NREM sleep, relative to those with SCI, suggesting potential vulnerability to sleep-related parasympathetic dysfunction. HF-HRV, especially during NREM sleep, may be an early biomarker for dementia detection.

ObjectiveInsomnia is the most prevalent sleep disorder, with few effective pharmacotherapies. Anecdotal reports and recent preclinical research suggest that cannabinol (CBN), a constituent of Cannabis sativa derived from delta-9-tetrahydrocannabinol, could be an effective treatment. Despite this, the isolated effects of CBN on sleep have yet to be systematically studied in humans.MethodsThe present protocol paper describes a randomised, double-blind, placebo-controlled, single-dose, three-arm, cross-over, proof-of-concept study which investigates the effects of CBN on sleep and next-day function in 20 participants with clinician-diagnosed insomnia disorder and an Insomnia Severity Index Score ≥15. Participants receive a single fixed oral liquid dose of 30 mg CBN, 300 mg CBN and matched placebo, in random order on three treatment nights; each separated by a 2-week wash-out period. Participants undergo overnight sleep assessment using in-laboratory polysomnography and next-day neurobehavioural function tests. The primary outcome is wake after sleep onset minutes. Secondary outcomes include changes to traditional sleep staging, sleep-onset latency and absolute spectral power during non-rapid eye movement (NREM) sleep. Tertiary outcomes include changes to sleep spindles during NREM sleep, arousal indices, absolute spectral power during REM sleep and subjective sleep quality. Safety-related and exploratory outcomes include changes to next-day simulated driving performance, subjective mood and drug effects, postural sway, alertness and reaction time, overnight memory consolidation, pre and post-sleep subjective and objective sleepiness; and plasma, urinary, and salivary cannabinoid concentrations. The study will provide novel preliminary data on CBN efficacy and safety in insomnia disorder, which will inform larger clinical trials.Ethics and disseminationHuman Research Ethics Committee approval has been granted by Bellberry (2021-08-907). Study findings will be disseminated in a peer-reviewed journal and at academic conferences.Trial registration numberNCT05344170.