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• W3003258182 abstract "Free AccessCommentaryImpaired central control of sleep depth propensity as a common mechanism for excessive overnight wake time: implications for sleep apnea, insomnia and beyond Danny J. Eckert, PhD, Alexander Sweetman, PhD Danny J. Eckert, PhD *Address correspondence to: Danny J. Eckert, PhD, Adelaide Institute for Sleep Health, Flinders University, 5 Laffer Drive, Bedford Park, South Australia, Australia 5042; Tel: +61 8 7421 9780; Email: E-mail Address: [email protected] Search for more papers by this author , Alexander Sweetman, PhD Search for more papers by this author Published Online:March 15, 2020https://doi.org/10.5664/jcsm.8268Cited by:5SectionsAbstractPDF ShareShare onFacebookTwitterLinkedInRedditEmail ToolsAdd to favoritesDownload CitationsTrack Citations AboutABSTRACTCitation:Eckert DJ, Sweetman A. Impaired central control of sleep depth propensity as a common mechanism for excessive overnight wake time: implications for sleep apnea, insomnia and beyond. J Clin Sleep Med. 2020;16(3):341–343.INTRODUCTIONA wealth of cardiorespiratory and neurophysiological data are collected during standard overnight polysomnography. However, most of this detailed information–which is time consuming and costly to collect and analyze using conventional approaches–is ignored. For example, in obstructive sleep apnea (OSA), clinical decisions rely heavily on a single frequency metric, the apnea-hypopnea index (AHI). However, the AHI is a poor predictor of treatment response and disease consequences.1–3 Polysomnography is not recommended as part of the diagnostic process for insomnia except when sleep-disordered breathing or periodic limb movement disorder (PLMD) is also suspected.4 However, given the 30% to 50% comorbidity of insomnia and OSA5,6 and high co-occurrence of insomnia and PLMD,7 this is often the majority of patients. Like the shortcomings of the AHI, standard polysomnography metrics of sleep continuity/fragmentation such as sleep efficiency and the arousal index are also poor predictors of symptoms and disease consequences.8–10 Thus, development of more precise and informative clinical and research tools from polysomnography data are a priority for the field of sleep medicine. Accordingly, new metrics have recently been investigated. For example, the area under the curve of the O2 trace or “hypoxic burden,” has superior predictive performance of cardiovascular mortality than the AHI.11In accordance with these objectives, in this issue of the Journal of Clinical Sleep Medicine, Younes and Giannouli used the recently developed innovative odds-ratio-product (ORP) technique12,13 to investigate the mechanistic origin of excessive overnight wakefulness in healthy controls and people referred for polysomnography with and without OSA, PLMD and insomnia symptoms.14 Briefly, the ORP provides moment-to-moment quantification (in 3-second intervals) of sleep depth using Fourier transform signal processing techniques from standard EEG recordings. An ORP of 2.5 indicates complete alertness/wakefulness whereas 0 indicates deep sleep/zero likelihood of arousal. Younes and Giannouli found that regardless of comorbid OSA or PLMD, those with excessive overnight wake time, defined as objective sleep efficiency < 80%, had higher ORP values. In addition, ORP was higher in those with insomnia symptoms, which were very common in the clinical referral cohort (> 65%). Similarly, sleep depth was much lighter within the 9s following arousal (higher ORP-9) in people with insomnia symptoms and excessive overnight wake time. This indicates a slower transition of sleep depth following arousal and greater susceptibility to subsequent arousal/awakening events in these individuals.As appropriately acknowledged by the authors, the retrospective approach had several potential limitations such as differences between groups in age, BMI, absence of validated insomnia questionnaires and different study types (ie, home versus in-laboratory and full versus split night). These potential confounders will require further investigation in future studies. Nonetheless, the current novel findings are interesting and intriguing for several reasons. Indeed, they provide novel insight into the pathophysiology of common sleep disorders, new knowledge on the interaction between key comorbidities, have potential implications for therapy and generate important questions in which to pursue in future research studies.For example, the notion that an individual’s sleep depth propensity following arousal (ORP-9) is an important determinant of excessive overnight wake time and not influenced by sleep disorders characterized by repetitive arousals, challenges the concept that excessive wake time is a direct consequence of OSA or PLMD. Rather, as highlighted in the paper via several preliminary/emerging lines of evidence,14 this suggests that this centrally mediated phenomenon is a fixed trait. This provides insight into pathophysiology and raises questions for therapy. For instance, the propensity to wake up too easily to airway narrowing in OSA (low respiratory arousal threshold) contributes to OSA pathophysiology for at least one-third of patients with OSA.15,16 If the ORP-9 is a key contributor to the respiratory arousal threshold and is minimally modifiable, this may limit the therapeutic efficacy of strategies directed toward this trait. Indeed, recent work to increase the arousal threshold to reduce OSA severity in people with low arousal thresholds with various hypnotics has yielded no or modest improvements.17–19 Thus, it would be of interest to determine the effects of various sleep promotion aids on the ORP-9.Alternatively, cognitive and behavioral therapy for insomnia (CBT-I) is the first-line treatment for insomnia20 and is beneficial in patients with comorbid insomnia and OSA.21 Given the association between ORP-9, nocturnal wakefulness and insomnia highlighted in the Younes and Giannouli paper, it will be important to investigate the interplay between ORP-9, objective wakefulness, and OSA during CBT-I in patients with comorbid insomnia and OSA to further elucidate these potential mechanisms.The high comorbidity of insomnia and OSA may be reflective of reciprocal bidirectional relationships between the two disorders (Figure 1).5,6 The current findings not only provide quantifiable evidence for the hyper-arousal hypothesis for insomnia which to date, has been largely theoretical/indirect, but also indicate an additional potential link between insomnia and OSA. Indeed, the current findings are consistent with central impairment in sleep depth regulation which may be a common pathogenic mechanism for insomnia and OSA. Thus, ORP investigations in people with comorbid insomnia and OSA, including during intervention trials, may provide additional important insights into the mechanisms by which the two disorders interact (Figure 1).22Figure 1: Potential mechanisms and manifestations by which insomnia and OSA interact.The hyper-arousal model of insomnia indicates that conditioned cognitive (anxiety, stress, ruminations, selective-attention, etc.) and physiological (increased heart rate, core body temperature, etc.) arousal may contribute to difficulties initiating and maintaining sleep. Alternatively, a low arousal threshold may contribute to the pathophysiology of OSA in many patients, manifesting in increased nocturnal arousals, sleep fragmentation, and an insomnia complaint. The ORP may reflect an underlying hyper-arousal mechanism which reduces sleep depth and increases susceptibility to arousal, thereby de-stabilizing sleep and promoting greater periods of extended wake time.Download FigureTo conclude, the current paper by Younes and Giannouli sheds new light on a potential cause of excessive overnight wake time and paves the way for multiple new lines of investigation. While these novel data represent a major step forward and the ORP-9 explains a substantial proportion of the variance in excessive overnight wake time, more than half of the variance remains unexplained. Thus, incorporation of ORP techniques in conjunction with other emerging metrics of sleep fragmentation in future studies are likely to be informative. Finally, while recent findings indicate that sleep depth as measured by the ORP is not an important mediator of blood pressure in people with OSA,23 the current work highlights the impact that new metrics such as the ORP derived from standard polysomnography variables can have to help address the key pathophysiological and treatment questions facing the field.DISCLOSURE STATEMENTBoth authors have seen and approved the manuscript. Dr. Eckert is funded by a National Health and Medical Research Council (NHMRC) of Australia Senior Research Fellowship (1116942). Dr. Sweetman is funded by the Cooperative Research Centre for Alertness, Safety and Productivity, a consortium between the Australian Government, Academia and Industry. Dr. Eckert holds a Collaborative Research Centre (CRC) Consortium Grant between the Australian Government, Academia and Industry (Industry partner: Oventus Medical), has research grants from Apnimed and Bayer and serves on the Advisory Board for Apnimed and as a consultant for Bayer outside of the current work. Dr. Sweetman reports no conflicts of interest.REFERENCES1. Punjabi NM. Counterpoint: is the apnea-hypopnea index the best way to quantify the severity of sleep-disordered breathing? No. Chest. 2016;149(1):16–19. https://doi.org/10.1378/chest.14-2261 CrossrefGoogle Scholar2. Edwards BA, Wellman A, Owens RL. PSGs: more than just the AHI. J Clin Sleep Med. 2013;9(6):527–528. https://doi.org/10.5664/jcsm.2738 LinkGoogle Scholar3. Heinzer R, Eckert D. Treatment for obstructive sleep apnoea and cardiovascular diseases: are we aiming at the wrong target? Lancet Respir Med. 2019 Dec 12. [Epub ahead of print]. https://doi.org/10.1016/S2213-2600(19)30351-0 Google Scholar4. 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Does arousal frequency predict daytime function? Eur Respir J. 1998;12(6):1264–1270. https://doi.org/10.1183/09031936.98.12061264 CrossrefGoogle Scholar9. Vakulin A, Catcheside PG, Baulk SD, et al.. Individual variability and predictors of driving simulator impairment in patients with obstructive sleep apnea. J Clin Sleep Med. 2014;10(6):647–655. https://doi.org/10.5664/jcsm.3792 LinkGoogle Scholar10. Vakulin A, D’Rozario A, Kim JW, et al.. Quantitative sleep EEG and polysomnographic predictors of driving simulator performance in obstructive sleep apnea. Clin Neurophysiol. 2016;127(2):1428–1435. https://doi.org/10.1016/j.clinph.2015.09.004 CrossrefGoogle Scholar11. Azarbarzin A, Sands SA, Stone KL, et al.. The hypoxic burden of sleep apnoea predicts cardiovascular disease-related mortality: the Osteoporotic Fractures in Men Study and the Sleep Heart Health Study. Eur Heart J. 2019;40(14):1149–1157. https://doi.org/10.1093/eurheartj/ehy624 CrossrefGoogle Scholar12. 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Arousal from sleep: implications for obstructive sleep apnea pathogenesis and treatment. J Appl Physiol. 2014;116(3):302–313. https://doi.org/10.1152/japplphysiol.00649.2013 CrossrefGoogle Scholar17. Carter SG, Carberry JC, Cho G, et al.. Effect of 1 month of zopiclone on obstructive sleep apnoea severity and symptoms: a randomised controlled trial. Eur Respir J. 2018;52(1):1800149. https://doi.org/10.1183/13993003.00149-2018 CrossrefGoogle Scholar18. Eckert DJ, Malhotra A, Wellman A, White DP. Trazodone increases the respiratory arousal threshold in patients with obstructive sleep apnea and a low arousal threshold. Sleep. 2014;37(4):811–819. https://doi.org/10.5665/sleep.3596 CrossrefGoogle Scholar19. Eckert DJ, Owens RL, Kehlmann GB, et al.. Eszopiclone increases the respiratory arousal threshold and lowers the apnoea/hypopnoea index in obstructive sleep apnoea patients with a low arousal threshold. Clin Sci (Lond). 2011;120(12):505–514. https://doi.org/10.1042/CS20100588 CrossrefGoogle Scholar20. Qaseem A, Kansagara D, Forciea MA, Cooke M, Denberg TDClinical Guidelines Committee of the American College of Physicians. Management of chronic insomnia disorder in adults: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2016;165(2):125–133. https://doi.org/10.7326/M15-2175 CrossrefGoogle Scholar21. Sweetman A, Lack L, Bastien C. Co-morbid insomnia and sleep apnea (COMISA): prevalence, consequences, methodological considerations, and recent randomized controlled trials. Brain Sci. 2019;9(12):371. https://doi.org/10.3390/brainsci9120371 CrossrefGoogle Scholar22. Sériès F. Can improving sleep influence sleep-disordered breathing? Drugs. 2009;69(Suppl 2):77–91. https://doi.org/10.2165/11532000-000000000-00000 CrossrefGoogle Scholar23. Kim JS, Azarbarzin A, Wang R, et al.. Association of novel measures of sleep disturbances with blood pressure: the Multi-Ethnic Study of Atherosclerosis. Thorax. 2020;75(1):57–63. https://doi.org/10.1136/thoraxjnl-2019-213533 CrossrefGoogle Scholar Previous article Next article FiguresReferencesRelatedDetailsCited by Prevalence and associations of co-morbid insomnia and sleep apnoea in an Australian population-based sampleSweetman A, Melaku Y, Lack L, Reynolds A, Gill T, Adams R and Appleton S Sleep Medicine, 10.1016/j.sleep.2021.03.023, , Online publication date: 1-Mar-2021. Bi-directional relationships between co-morbid insomnia and sleep apnea (COMISA)Sweetman A, Lack L, McEvoy R, Smith S, Eckert D, Osman A, Carberry J, Wallace D, Nguyen D and Catcheside P Sleep Medicine Reviews, 10.1016/j.smrv.2021.101519, , (101519), Online publication date: 1-Jun-2021. Effects Of Hypnotics On Obstructive Sleep Apnea Endotypes And Severity: Novel Insights Into Pathophysiology And TreatmentCarter S and Eckert D Sleep Medicine Reviews, 10.1016/j.smrv.2021.101492, , (101492), Online publication date: 1-Apr-2021. Cognitive behavioural therapy for insomnia reduces sleep apnoea severity: a randomised controlled trialSweetman A, Lack L, McEvoy R, Antic N, Smith S, Chai-Coetzer C, Douglas J, O'Grady A, Dunn N, Robinson J, Paul D, Eckert D and Catcheside P ERJ Open Research, 10.1183/23120541.00161-2020, Vol. 6, No. 2, (00161-2020), Online publication date: 1-Apr-2020. Randomized controlled trial of an integrated approach to treating insomnia and improving the use of positive airway pressure therapy in veterans with comorbid insomnia disorder and obstructive sleep apneaAlessi C, Fung C, Dzierzewski J, Fiorentino L, Stepnowsky C, Rodriguez Tapia J, Song Y, Zeidler M, Josephson K, Mitchell M, Jouldjian S and Martin J Sleep, 10.1093/sleep/zsaa235, Volume 16 • Issue 3 • March 15, 2020ISSN (print): 1550-9389ISSN (online): 1550-9397Frequency: Monthly Metrics History Submitted for publicationJanuary 8, 2020Submitted in final revised formJanuary 9, 2020Accepted for publicationJanuary 9, 2020Published onlineMarch 15, 2020 Information© 2020 American Academy of Sleep Medicine" @default.
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