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BackgroundEvaluation and interpretation of the literature on obstructive sleep apnea (OSA) allows for consolidation and determination of the key factors important for clinical management of the adult OSA patient. Toward this goal, an international collaborative of multidisciplinary experts in sleep apnea evaluation and treatment have produced the International Consensus statement on Obstructive Sleep Apnea (ICS:OSA).MethodsUsing previously defined methodology, focal topics in OSA were assigned as literature review (LR), evidence-based review (EBR), or evidence-based review with recommendations (EBR-R) formats. Each topic incorporated the available and relevant evidence which was summarized and graded on study quality. Each topic and section underwent iterative review and the ICS:OSA was created and reviewed by all authors for consensus.ResultsThe ICS:OSA addresses OSA syndrome definitions, pathophysiology, epidemiology, risk factors for disease, screening methods, diagnostic testing types, multiple treatment modalities, and effects of OSA treatment on multiple OSA-associated comorbidities. Specific focus on outcomes with positive airway pressure (PAP) and surgical treatments were evaluated.ConclusionThis review of the literature consolidates the available knowledge and identifies the limitations of the current evidence on OSA. This effort aims to create a resource for OSA evidence-based practice and identify future research needs. Knowledge gaps and research opportunities include improving the metrics of OSA disease, determining the optimal OSA screening paradigms, developing strategies for PAP adherence and longitudinal care, enhancing selection of PAP alternatives and surgery, understanding health risk outcomes, and translating evidence into individualized approaches to therapy.

Summary Laboratory polysomnography provides gold‐standard measures of sleep physiology, but multi‐night investigations are resource intensive. We assessed the night‐to‐night stability via reproducibility metrics for sleep macrostructure and electroencephalography oscillations in a group of cognitively normal adults attending two consecutive polysomnographies. Electroencephalographies were analysed using an automatic algorithm for detection of slow‐wave activity, spindle and K‐complex densities. Average differences between nights for sleep macrostructure, electroencephalography oscillations and sleep apnea severity were assessed, and test–retest reliability was determined using two‐way intraclass correlations. Agreement was calculated using the smallest real differences between nights for all measures. Night 2 polysomnographies showed significantly greater time in bed, total sleep time (6.3 hr versus 6.8 hr, p < 0.001) and percentage of rapid eye movement sleep (17.5 versus 19.7, p < 0.001). Intraclass correlations were low for total sleep time, percentage of rapid eye movement sleep and sleep efficiency, moderate for percentage of slow‐wave sleep and percentage of non‐rapid eye movement 2 sleep, good for slow‐wave activity and K‐complex densities, and excellent for spindles and apnea–hypopnea index with hypopneas defined according to 4% oxygen desaturation criteria only. The smallest real difference values were proportionally high for most sleep macrostructure measures, indicating moderate agreement, and proportionally lower for most electroencephalography microstructure variables. Slow waves, K‐complexes, spindles and apnea severity indices are highly reproducible across two consecutive nights of polysomnography. In contrast, sleep macrostructure measures all demonstrated poor reproducibility as indicated by low intraclass correlation values and moderate agreement. Although there were average differences in percentage of rapid eye movement sleep and total sleep time, these were numerically small and perhaps functionally or clinically less significant. One night of in‐laboratory polysomnography is enough to provide stable, reproducible estimates of an individual's sleep concerning measures of slow‐wave activity, spindles, K‐complex densities and apnea severity. [ABSTRACT FROM AUTHOR]

Introduction: Obstructive sleep apnea (OSA) is associated with Alzheimer's disease (AD) biomarkers in cognitively normal (CN) and mild cognitive impaired (MCI) participants. However, independent and combined effects of OSA, amyloid beta (Aβ) and tau‐accumulation on AD time‐dependent progression risk is unclear. Methods: Study participants grouped by biomarker profile, as described by the A/T/N scheme, where "A" refers to aggregated Aβ, "T" aggregated tau, and "N" to neurodegeneration, included 258 CN (OSA‐positive [OSA+] [A+TN+ n = 10, A+/TN− n = 6, A−/TN+ n = 10, A−/TN− n = 6 and OSA‐negative [OSA‐] [A+TN+ n = 84, A+/TN− n = 11, A−/TN+ n = 96, A−/TN− n = 36]) and 785 MCI (OSA+ [A+TN+ n = 35, A+/TN− n = 15, A−/TN+ n = 25, A−/TN− n = 16] and OSA− [A+TN+ n = 388, A+/TN− n = 28, A−/TN+ n = 164, A−/TN− n = 114]) older‐adults from the Alzheimer's Disease Neuroimaging Initiative cohort. Cox proportional hazards regression models estimated the relative hazard of progression from CN‐to‐MCI and MCI‐to‐AD, among baseline OSA CN and MCI patients, respectively. Multi‐level logistic mixed‐effects models with random intercept and slope investigated the synergistic associations of self‐reported OSA, Aβ, and tau burden with prospective cognitive decline. Results: Independent of TN‐status (CN and MCI), OSA+/Aβ+ participants were approximately two to four times more likely to progress to MCI/AD (P <.001) and progressed 6 to 18 months earlier (P <.001), compared to other participants combined (ie, OSA+/Aβ−, OSA−/Aβ+, and OSA−/Aβ−). Notably, OSA+/Aβ− versus OSA−/Aβ− (CN and MCI) and OSA+/TN− versus OSA−/TN− (CN) participants showed no difference in the risk and time‐to‐MCI/AD progression. Mixed effects models demonstrated OSA synergism with Aβ (CN and MCI [β = 1.13, 95% confidence interval (CI), 0.74 to 1.52, and β = 1.18, 95%CI, 0.82 to 1.54]) respectively, and with tau (MCI [β = 1.31, 95% CI, 0.87 to 1.47]), P <.001 for all. Discussion: OSA acts in synergism with Aβ and with tau, and all three acting together result in synergistic neurodegenerative mechanisms especially as Aβ and tau accumulation becomes increasingly abnormal, thus leading to shorter progression time to MCI/AD in CN and MCI‐OSA patients, respectively. [ABSTRACT FROM AUTHOR]

Background: Melatonin may reduce REM-sleep behavior disorder (RBD) symptoms in Parkinson's disease (PD), though robust clinical trials are lacking.Objective: To assess the efficacy of prolonged-release (PR) melatonin for RBD in PD.Methods: Randomized, double-blind, placebo-controlled, parallel-group trial with an 8-week intervention and 4-week observation pre- and postintervention (ACTRN12613000648729). Thirty PD patients with rapid eye movement sleep behavior disorder were randomized to 4 mg of prolonged-release melatonin (Circadin) or matched placebo, ingested orally once-daily before bedtime. Primary outcome was the aggregate of rapid eye movement sleep behavior disorder incidents averaged over weeks 5 to 8 of treatment captured by a weekly diary. Data were included in a mixed-model analysis of variance (n = 15 per group).Results: No differences between groups at the primary endpoint (3.4 events/week melatonin vs. 3.6 placebo; difference, 0.2; 95% confidence interval = -3.2 to 3.6; P = 0.92). Adverse events included mild headaches, fatigue, and morning sleepiness (n = 4 melatonin; n = 5 placebo).Conclusion: Prolonged-release melatonin 4 mg did not reduce rapid eye movement sleep behavior disorder in PD. © 2019 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society. [ABSTRACT FROM AUTHOR]

Study Objectives: We have previously estimated that the prevalence of obstructive sleep apnea (OSA) among World Trade Center rescue and recovery workers is 75% and identified that having symptoms of chronic rhinosinusitis (CRS) is an independent risk factor for OSA in this population. Nasal inflammation and/or elevated awake nasal resistance that carried over into sleep could explain this association. To understand the mechanism(s) for the elevated risk of OSA observed in World Trade Center responders with CRS symptoms we examined if elevated awake supine nasal resistance was associated with OSA, CRS and/or nasal inflammatory biomarkers., Methods: A total of 601 individuals (83% male, average age 53 years, body mass index = 29.9 ± 5.5 kg/m 2 ) enrolled in the World Trade Center Health Program and without significant snoring prior to September 11, 2001 underwent 2 nights of home sleep apnea testing, measurements of anterior rhinomanometry in the supine position, and nasal lavage., Results: Awake supine nasal resistance was not associated with OSA; 74.8% and 74.4% of the participants with low and high nasal resistance respectively, had OSA. Patients with CRS had elevated nasal inflammatory markers (interleukin 6, interleukin 8, eosinophilic cationic protein, and neutrophil) but did not have high nasal resistance. Nasal inflammatory markers were not correlated with nasal resistance., Conclusions: As awake nasal resistance did not explain the relationship of CRS to OSA in this large and well characterized dataset, our findings suggest that either "sleep" nasal resistance or other factors such as increased supraglottic inflammation, perhaps through impairing upper airway reflex mechanisms, or systemic inflammation are involved in the pathophysiology of OSA in the World Trade Center population., Citation: Ayappa I, Laumbach R, Black K, et al. Nasal resistance and inflammation: mechanisms for obstructive sleep apnea from chronic rhinosinusitis. J Clin Sleep Med . 2024;20(10):1627-1636., (© 2024 American Academy of Sleep Medicine.)

People with schizophrenia (SZ) display substantial neurocognitive deficits that have been implicated as major contributors to poor daily functioning and disability. Previous reports have identified a number of predictors of poor neurocognition in SZ including demographics, symptoms, and treatment adherence, as well as body mass index, aerobic fitness, and exercise activity. However, the putative impact of sleep has received relatively limited consideration, despite sleep disturbances, which are pervasive in this population, resulting in symptoms that are strikingly similar to the neurocognitive deficits commonly observed in SZ. Here we argue for the consideration of the impact of sleep on neurocognition in people with SZ and propose recommendations for future research to elucidate the links between sleep parameters, neurocognition and daily functioning., Competing Interests: CONFLICTS OF INTEREST The authors declare that they have no conflicts of interest.

Introduction: Obstructive sleep apnea (OSA) is associated with Alzheimer's disease (AD) biomarkers in cognitively normal (CN) and mild cognitive impaired (MCI) participants. However, independent and combined effects of OSA, amyloid beta (Aβ) and tau-accumulation on AD time-dependent progression risk is unclear., Methods: Study participants grouped by biomarker profile, as described by the A/T/N scheme, where "A" refers to aggregated Aβ, "T" aggregated tau, and "N" to neurodegeneration, included 258 CN (OSA-positive [OSA+] [A+TN+ n = 10, A+/TN- n = 6, A-/TN+ n = 10, A-/TN- n = 6 and OSA-negative [OSA-] [A+TN+ n = 84, A+/TN- n = 11, A-/TN+ n = 96, A-/TN- n = 36]) and 785 MCI (OSA+ [A+TN+ n = 35, A+/TN- n = 15, A-/TN+ n = 25, A-/TN- n = 16] and OSA- [A+TN+ n = 388, A+/TN- n = 28, A-/TN+ n = 164, A-/TN- n = 114]) older-adults from the Alzheimer's Disease Neuroimaging Initiative cohort. Cox proportional hazards regression models estimated the relative hazard of progression from CN-to-MCI and MCI-to-AD, among baseline OSA CN and MCI patients, respectively. Multi-level logistic mixed-effects models with random intercept and slope investigated the synergistic associations of self-reported OSA, Aβ, and tau burden with prospective cognitive decline., Results: Independent of TN-status (CN and MCI), OSA+/Aβ+ participants were approximately two to four times more likely to progress to MCI/AD (P < .001) and progressed 6 to 18 months earlier (P < .001), compared to other participants combined (ie, OSA+/Aβ-, OSA-/Aβ+, and OSA-/Aβ-). Notably, OSA+/Aβ- versus OSA-/Aβ- (CN and MCI) and OSA+/TN- versus OSA-/TN- (CN) participants showed no difference in the risk and time-to-MCI/AD progression. Mixed effects models demonstrated OSA synergism with Aβ (CN and MCI [β = 1.13, 95% confidence interval (CI), 0.74 to 1.52, and β = 1.18, 95%CI, 0.82 to 1.54]) respectively, and with tau (MCI [β = 1.31, 95% CI, 0.87 to 1.47]), P < .001 for all., Discussion: OSA acts in synergism with Aβ and with tau, and all three acting together result in synergistic neurodegenerative mechanisms especially as Aβ and tau accumulation becomes increasingly abnormal, thus leading to shorter progression time to MCI/AD in CN and MCI-OSA patients, respectively., (© 2020 the Alzheimer's Association.)