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Automated telemedicine interventions could potentially improve adherence to continuous positive airway pressure (CPAP) therapy. Examining the effects of telemedicine-delivered obstructive sleep apnea (OSA) education and CPAP telemonitoring with automated patient feedback messaging on CPAP adherence. This four-arm, randomized, factorial design clinical trial enrolled 1,455 patients (51.0% women; age, 49.1 ± 12.5 yr [mean ± SD]) referred for suspected OSA. Nine hundred and fifty-six underwent home sleep apnea testing, and 556 were prescribed CPAP. Two telemedicine interventions were implemented: 1) web-based OSA education (Tel-Ed) and 2) CPAP telemonitoring with automated patient feedback (Tel-TM). Patients were randomized to 1) usual care, 2) Tel-Ed added, 3) Tel-TM added, or 4) Tel-Ed and Tel-TM added (Tel-both). The primary endpoint was 90-day CPAP usage. Secondary endpoints included attendance to OSA evaluation, and change in Epworth Sleepiness Scale score. CPAP average daily use at 90 days was 3.8 ± 2.5, 4.0 ± 2.4, 4.4 ± 2.2, and 4.8 ± 2.3 hours in usual care, Tel-Ed, Tel-TM, and Tel-both groups. Usage was significantly higher in the Tel-TM and Tel-both groups versus usual care (P = 0.0002 for both) but not for Tel-Ed (P = 0.10). Medicare adherence rates were 53.5, 61.0, 65.6, and 73.2% in usual care, Tel-Ed, Tel-TM, and Tel-both groups (Tel-both vs. usual care, P = 0.001; Tel-TM vs. usual care, P = 0.003; Tel-Ed vs. usual care, P = 0.07), respectively. Telemedicine education improved clinic attendance compared with no telemedicine education (show rate, 68.5 vs. 62.7%; P = 0.02). The use of CPAP telemonitoring with automated feedback messaging improved 90-day adherence in patients with OSA. Telemedicine-based education did not significantly improve CPAP adherence but did increase clinic attendance for OSA evaluation. Clinical trial registered with www.clinicaltrials.gov (NCT02279901).

Study Objective: Sleep hygiene recommendations are widely disseminated despite the fact that few systematic studies have investigated the empirical bases of sleep hygiene in the home environment. For example, studies have yet to investigate the relative effects of a given dose of caffeine administered at different times of day on subsequent sleep. Methods: This study compared the potential sleep disruptive effects of a fixed dose of caffeine (400 mg) administered at 0, 3, and 6 hours prior to habitual bedtime relative to a placebo on self-reported sleep in the home. Sleep disturbance was also monitored objectively using a validated portable sleep monitor. Results: Results demonstrated a moderate dose of caffeine at bedtime, 3 hours prior to bedtime, or 6 hours prior to bedtime each have significant effects on sleep disturbance relative to placebo (p < 0.05 for all). Conclusion: The magnitude of reduction in total sleep time suggests that caffeine taken 6 hours before bedtime has important disruptive effects on sleep and provides empirical support for sleep hygiene recommendations to refrain from substantial caffeine use for a minimum of 6 hours prior to bedtime. Citation: Drake C; Roehrs T; Shambroom J; Roth T. Caffeine effects on sleep taken 0, 3, or 6 hours before going to bed. J Clin Sleep Med 2013;9(11):1195–1200.

Abstract Rationale Home respiratory polygraphy may be a simpler alternative to in-laboratory polysomnography for the management of more symptomatic patients with obstructive sleep apnea, but its effectiveness has not been evaluated across a broad clinical spectrum. Objectives To compare the long-term effectiveness (6 mo) of home respiratory polygraphy and polysomnography management protocols in patients with intermediate-to-high sleep apnea suspicion (most patients requiring a sleep study). Methods A multicentric, noninferiority, randomized controlled trial with two open parallel arms and a cost-effectiveness analysis was performed in 12 tertiary hospitals in Spain. Sequentially screened patients with sleep apnea suspicion were randomized to respiratory polygraphy or polysomnography protocols. Moreover, both arms received standardized therapeutic decision-making, continuous positive airway pressure (CPAP) treatment or a healthy habit assessment, auto-CPAP titration (for CPAP indication), health-related quality-of-life questionnaires, 24-hour blood pressure monitoring, and polysomnography at the end of follow-up. The main outcome was the Epworth Sleepiness Scale measurement. The noninferiority criterion was −2 points on the Epworth scale. Measurements and Main Results In total, 430 patients were randomized. The respiratory polygraphy protocol was noninferior to the polysomnography protocol based on the Epworth scale. Quality of life, blood pressure, and polysomnography were similar between protocols. Respiratory polygraphy was the most cost-effective protocol, with a lower per-patient cost of 416.7€. Conclusions Home respiratory polygraphy management is similarly effective to polysomnography, with a substantially lower cost. Therefore, polysomnography is not necessary for most patients with suspected sleep apnea. This finding could change established clinical practice, with a clear economic benefit. Clinical trial registered with www.clinicaltrials.gov (NCT 01752556).

Exercise can improve sleep by reducing sleep latency and increasing slow-wave sleep (SWS). Some studies, however, report adverse effects of exercise on sleep architecture, possibly due to a wide variety of experimental conditions used. We examined the effect of exercise on quality of sleep using standardized exercise parameters and novel analytical methods. In a cross-over intervention study we examined the effect of 60 min of vigorous exercise at 60% V ˙ O 2 max on the metabolic state, assessed by core body temperature and indirect calorimetry, and on sleep quality during subsequent sleep, assessed by self-reported quality of sleep and polysomnography. In a novel approach, envelope analysis was performed to assess SWS stability. Exercise increased energy expenditure throughout the following sleep phase. The subjective assessment of sleep quality was not improved by exercise. Polysomnography revealed a shorter rapid eye movement latency and reduced time spent in SWS. Detailed analysis of the sleep electro-encephalogram showed significantly increased delta power in SWS (N3) together with increased SWS stability in early sleep phases, based on delta wave envelope analysis. Although vigorous exercise does not lead to a subjective improvement in sleep quality, sleep function is improved on the basis of its effect on objective EEG parameters.

Background The screening of digital footprint for clinical purposes relies on the capacity of wearable technologies to collect data and extract relevant information’s for patient management. Artificial intelligence (AI) techniques allow processing of real-time observational information and continuously learning from data to build understanding. We designed a system able to get clinical sense from digital footprints based on the smartphone’s native sensors and advanced machine learning and signal processing techniques in order to identify suicide risk. Method/design The Smartcrisis study is a cross-national comparative study. The study goal is to determine the relationship between suicide risk and changes in sleep quality and disturbed appetite. Outpatients from the Hospital Fundación Jiménez Díaz Psychiatry Department (Madrid, Spain) and the University Hospital of Nimes (France) will be proposed to participate to the study. Two smartphone applications and a wearable armband will be used to capture the data. In the intervention group, a smartphone application (MEmind) will allow for the ecological momentary assessment (EMA) data capture related with sleep, appetite and suicide ideations. Discussion Some concerns regarding data security might be raised. Our system complies with the highest level of security regarding patients’ data. Several important ethical considerations related to EMA method must also be considered. EMA methods entails a non-negligible time commitment on behalf of the participants. EMA rely on daily, or sometimes more frequent, Smartphone notifications. Furthermore, recording participants’ daily experiences in a continuous manner is an integral part of EMA. This approach may be significantly more than asking a participant to complete a retrospective questionnaire but also more accurate in terms of symptoms monitoring. Overall, we believe that Smartcrises could participate to a paradigm shift from the traditional identification of risks factors to personalized prevention strategies tailored to characteristics for each patient. Trial registration number NCT03720730. Retrospectively registered.

Study Objectives: To evaluate the validity of an ambulatory electroencephalographic (EEG) monitor for the estimation of sleep continuity and architecture in healthy adults. Methods: Healthy, good sleeping participants (n = 14) were fit with both an ambulatory EEG monitor (Sleep Profiler) and a full polysomnography (PSG) montage. EEG recordings were gathered from both devices on the same night, during which sleep was permitted uninterrupted for eight hours. The study was set in an inpatient clinical research suite. PSG and Sleep Profiler records were scored by a neurologist board certified in sleep medicine, blinded to record identification. Agreement between the scored PSG record, the physician-scored Sleep Profiler record, and the Sleep Profiler record scored by an automatic algorithm was evaluated for each sleep stage, with the PSG record serving as the reference. Results: Results indicated strong percent agreement across stages. Kappa was strongest for Stage N3 and REM. Specificity was high for all stages; sensitivity was low for Wake and Stage N1, and high for Stage N2, Stage N3, and REM. Agreement indices improved for the manually scored Sleep Profiler record relative to the autoscore record. Conclusions: Overall, the Sleep Profiler yields an EEG record with comparable sleep architecture estimates to PSG. Future studies should evaluate agreement between devices with a clinical sample that has greater periods of wake in order to better understand utility of this device for estimating sleep continuity indices, such as sleep onset latency and wake after sleep onset. Citation: Finan PH, Richards JM, Gamaldo CE, Han D, Leoutsakos JM, Salas R, Irwin MR, Smith MT. Validation of a wireless, self-application, ambulatory electroencephalographic sleep monitoring device in healthy volunteers. J Clin Sleep Med 2016;12(11):1443–1451.

(1) Background: Home sleep apnea testing, known as polysomnography type 3 (PSG3), underestimates respiratory events in comparison with in-laboratory polysomnography type 1 (PSG1). Without head electrodes for scoring sleep and arousal, in a home environment, patients feel unfettered and move their bodies more naturally. Adopting a natural position may decrease obstructive sleep apnea (OSA) severity in PSG3, independently of missing hypopneas associated with arousals. (2) Methods: Patients with suspected OSA performed PSG1 and PSG3 in a randomized sequence. We performed an additional analysis, called reduced polysomnography, in which we blindly reassessed all PSG1 tests to remove electroencephalographic electrodes, electrooculogram, and surface electromyography data to estimate the impact of not scoring sleep and arousal-based hypopneas on the test results. A difference of 15 or more in the apnea–hypopnea index (AHI) between tests was deemed clinically relevant. We compared the group of patients with and without clinically relevant differences between lab and home tests (3) Results: As expected, by not scoring sleep, there was a decrease in OSA severity in the lab test, similar to the home test results. The group of patients with clinically relevant differences between lab and home tests presented more severe OSA in the lab compared to the other group (mean AHI, 42.5 vs. 20.2 events/h, p = 0.002), and this difference disappeared in the home test. There was no difference between groups in the shift of OSA severity by abolishing sleep scoring in the lab. However, by comparing lab and home tests, there were greater variations in supine AHI and time spent in the supine position in the group with a clinically relevant difference, either with or without scoring sleep, showing an impact of the site of the test on body position during sleep. These variations presented as a marked increase or decrease in supine outcomes according to the site of the test, with no particular trend. (4) Conclusions: In-lab polysomnography may artificially increase OSA severity in a subset of patients by inducing marked changes in body position compared to home tests. The location of the sleep test seems to interfere with the evaluation of patients with more severe OSA.

Study Objectives: Onera Health has developed the first wireless, patch-based, type-II polysomnography (PSG) system, the Onera Sleep Test System, to allow studies to be performed unattended at the patient’s home or in any bed at a medical facility. The goal of this multicenter study was to validate data collected from the patch-based PSG to a traditional PSG for sleep staging and apnea-hypopnea index. Methods: Simultaneous traditional PSG and patch-based PSG study data were obtained in a sleep laboratory from 206 participants with a suspected sleep disorder recruited from 7 clinical sites. Blinded, randomized scoring of the traditional PSG and patch-based PSG recordings was completed according to The AASM Manual for the Scoring of Sleep and Associated Events: Rules, Terminology and Technical Specifications (Version 2.6) criteria by 3 independent scorers. Results: Concordance correlation coefficients were high between the patch-based device and traditional PSG across essential sleep and respiratory variables—total sleep time (.87); wake (.84); non-rapid eye movement (REM) (.80); non-REM sleep stage 1 (N1) (.72); non-REM sleep stage 2 (N2) (.71); non-REM sleep stage 3 (N3) (.64); REM (.80); and apnea-hypopnea index (AHI) (.94). There was substantial agreement between epoch sleep staging scored on the patch-based device and traditional PSG (average Cohen’s kappa of 0.62 ± 0.13 across all scorers). Conclusions: The patch-based type-II PSG had a similar performance on sleep staging and respiratory variables when compared to traditional PSG, thus making it possible to use the patch-based PSG for a routine PSG study. These results open the possibility of performing unattended PSG studies efficiently and accurately outside the sleep laboratory improving access to high quality sleep assessments for patients with sleep disorders. Clinical Trial Registration: Registry: ClinicalTrials.gov; Name: Validation Study of a Patch-based PSG System; URL: https://clinicaltrials.gov/study/NCT05310708 ; Identifier: NCT05310708. Citation: Viniol C, Galetke W, Woehrle H, et al. Clinical validation of a wireless patch-based polysomnography system. J Clin Sleep Med . 2025;21(5):813–823.

Objective: A recent double-blind randomized placebo-controlled study demonstrated 3-month efficacy and safety of a novel pediatric-appropriate prolonged-release melatonin (PedPRM) for insomnia in children and adolescents with autism spectrum disorder (ASD) and neurogenetic disorders (NGD) with/without attention-deficit/hyperactivity disorder comorbidity. Long-term efficacy and safety of PedPRM treatment was studied. Methods: A prospective, open-label efficacy and safety follow-up of nightly 2, 5, or 10 mg PedPRM in subjects who completed the 13-week double-blind trial (51 PedPRM; 44 placebo). Measures included caregiver-reported Sleep and Nap Diary, Composite Sleep Disturbance Index (CSDI), caregiver's Pittsburgh Sleep Quality Index (PSQI), Epworth Sleepiness Scale, and quality of life (WHO-5 Well-Being Index). Results: Ninety-five subjects (74.7% males; mean [standard deviation] age, 9 [4.24]; range, 2–17.5 years) received PedPRM (2/5 mg) according to the double-blind phase dose, for 39 weeks with optional dose adjustment (2, 5, or 10 mg/day) after the first 13 weeks. After 52 weeks of continuous treatment (PedPRM-randomized group) subjects slept (mean [SE]) 62.08 (21.5) minutes longer (p = 0.007); fell asleep 48.6 (10.2) minutes faster (p < 0.001); had 89.1 (25.5) minutes longer uninterrupted sleep episodes (p = 0.001); 0.41 (0.12) less nightly awakenings (>50% decrease; p = 0.001); and better sleep quality (p < 0.001) compared with baseline. The placebo-randomized group also improved with PedPRM. Altogether, by the end of 39-week follow-up, regardless of randomization assignment, 55/72 (76%) of completers achieved overall improvement of ≥1 hour in total sleep time (TST), sleep latency or both, over baseline, with no evidence of decreased efficacy. In parallel, CSDI child sleep disturbance and caregivers' satisfaction of their child's sleep patterns (p < 0.001 for both), PSQI global (p < 0.001), and WHO-5 (p = 0.001) improved in statistically significant and clinically relevant manner (n = 72) compared with baseline. PedPRM was generally safe; most frequent treatment-related adverse events were fatigue (5.3%) and mood swings (3.2% of patients). Conclusion: PedPRM, an easily swallowed formulation shown to be efficacious versus placebo, is an efficacious and safe option for long-term treatment (up to 52 weeks reported here) of children with ASD and NGD who suffer from insomnia and subsequently improves caregivers' quality of life.

The antidepressant efficacy and safety of seltorexant monotherapy in major depressive disorder (MDD) was investigated in a placebo-controlled, placebo lead-in, randomized, double-blind, phase 1b study. Participants were randomized to receive seltorexant (20 mg or 40 mg) or placebo. The treatment effect was assessed by changes in the Hamilton Rating Scale for Depression-17 item (HDRS 17 ) from treatment-period baseline to week 5 in lead-in placebo non-responders (“enriched” intent-to-treat analysis set). As a secondary outcome, the effect of seltorexant on HDRS 17 was assessed in patients with and without subjective insomnia. Seltorexant’s effects on polysomnography, serum cortisol, and cortisol waking response were also measured. In total, 128 participants were enrolled, including 86 in the enriched sample (lead-in placebo non-responders). The mean changes from baseline (SD) in HDRS 17 score at week 5 differed significantly across arms: −7.0 (5.04) for seltorexant 20 mg, −5.5 (4.34) for seltorexant 40 mg, and −4.4 (3.67) for placebo (p = 0.0456), which was attributable to the difference between the 20 mg and placebo arms (p = 0.0049). Improvement in depression severity at week 5 for seltorexant 20 mg was greater in patients with higher baseline insomnia severity (nominal p = 0.0059). The treatment benefit in the 20 mg arm remained significant when HDRS scores were adjusted by removing the sleep items (nominal p = 0.0289). The mean HDRS 17 change versus placebo was numerically larger in the 20 mg than the 40 mg arm, consistent with data from a previous study in which seltorexant was administered adjunctively to conventional antidepressants. In secondary analyses, the waking cortisol response decreased in the 20 mg arm but not the 40 mg or placebo arms, and while total sleep increased more in the 40 mg arm, this arm also showed reduced REM onset latency and increased stage N1 sleep, which were not evident in the 20 mg arm. These biomarker data suggest mechanistic hypotheses that may account for the apparent curvilinear dose-response relationship of seltorexant. Trial Registration: ClinicalTrials.gov, NCT03374475.