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      Update in respiratory sleep disorders: Epilogue to a modern review series : Series Editorial-Epilogue

      1 , 2 , 3 , 4 , 5

      Respirology

      Wiley

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          Most cited references 23

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          Adult obstructive sleep apnoea.

          Obstructive sleep apnoea is an increasingly common disorder of repeated upper airway collapse during sleep, leading to oxygen desaturation and disrupted sleep. Features include snoring, witnessed apnoeas, and sleepiness. Pathogenesis varies; predisposing factors include small upper airway lumen, unstable respiratory control, low arousal threshold, small lung volume, and dysfunctional upper airway dilator muscles. Risk factors include obesity, male sex, age, menopause, fluid retention, adenotonsillar hypertrophy, and smoking. Obstructive sleep apnoea causes sleepiness, road traffic accidents, and probably systemic hypertension. It has also been linked to myocardial infarction, congestive heart failure, stroke, and diabetes mellitus though not definitively. Continuous positive airway pressure is the treatment of choice, with adherence of 60-70%. Bi-level positive airway pressure or adaptive servo-ventilation can be used for patients who are intolerant to continuous positive airway pressure. Other treatments include dental devices, surgery, and weight loss.
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            Is Open Access

            Reliability of Sleep Measures from Four Personal Health Monitoring Devices Compared to Research-Based Actigraphy and Polysomnography

            Polysomnography (PSG) is the “gold standard” for monitoring sleep. Alternatives to PSG are of interest for clinical, research, and personal use. Wrist-worn actigraph devices have been utilized in research settings for measures of sleep for over two decades. Whether sleep measures from commercially available devices are similarly valid is unknown. We sought to determine the validity of five wearable devices: Basis Health Tracker, Misfit Shine, Fitbit Flex, Withings Pulse O2, and a research-based actigraph, Actiwatch Spectrum. We used Wilcoxon Signed Rank tests to assess differences between devices relative to PSG and correlational analysis to assess the strength of the relationship. Data loss was greatest for Fitbit and Misfit. For all devices, we found no difference and strong correlation of total sleep time with PSG. Sleep efficiency differed from PSG for Withings, Misfit, Fitbit, and Basis, while Actiwatch mean values did not differ from that of PSG. Only mean values of sleep efficiency (time asleep/time in bed) from Actiwatch correlated with PSG, yet this correlation was weak. Light sleep time differed from PSG (nREM1 + nREM2) for all devices. Measures of Deep sleep time did not differ from PSG (SWS + REM) for Basis. These results reveal the current strengths and limitations in sleep estimates produced by personal health monitoring devices and point to a need for future development.
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              Quantifying the ventilatory control contribution to sleep apnoea using polysomnography.

              Elevated loop gain, consequent to hypersensitive ventilatory control, is a primary nonanatomical cause of obstructive sleep apnoea (OSA) but it is not possible to quantify this in the clinic. Here we provide a novel method to estimate loop gain in OSA patients using routine clinical polysomnography alone. We use the concept that spontaneous ventilatory fluctuations due to apnoeas/hypopnoeas (disturbance) result in opposing changes in ventilatory drive (response) as determined by loop gain (response/disturbance). Fitting a simple ventilatory control model (including chemical and arousal contributions to ventilatory drive) to the ventilatory pattern of OSA reveals the underlying loop gain. Following mathematical-model validation, we critically tested our method in patients with OSA by comparison with a standard (continuous positive airway pressure (CPAP) drop method), and by assessing its ability to detect the known reduction in loop gain with oxygen and acetazolamide. Our method quantified loop gain from baseline polysomnography (correlation versus CPAP-estimated loop gain: n=28; r=0.63, p<0.001), detected the known reduction in loop gain with oxygen (n=11; mean±sem change in loop gain (ΔLG) -0.23±0.08, p=0.02) and acetazolamide (n=11; ΔLG -0.20±0.06, p=0.005), and predicted the OSA response to loop gain-lowering therapy. We validated a means to quantify the ventilatory control contribution to OSA pathogenesis using clinical polysomnography, enabling identification of likely responders to therapies targeting ventilatory control.
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                Author and article information

                Journal
                Respirology
                Respirology
                Wiley
                13237799
                January 2018
                January 2018
                November 06 2017
                : 23
                : 1
                : 16-17
                Affiliations
                [1 ]Division of Pulmonary, Critical Care and Sleep Medicine; University of California San Diego; La Jolla California USA
                [2 ]National Heart and Lung Institute; Imperial College London; London UK
                [3 ]Academic Unit of Sleep and Breathing; Royal Brompton Hospital; London UK
                [4 ]West Australian Sleep Disorders Research Institute; Sir Charles Gairdner Hospital; Nedlands Western Australia Australia
                [5 ]Centre for Sleep Science, School of Anatomy, Physiology and Human Biology; University of Western Australia; Perth Western Australia Australia
                Article
                10.1111/resp.13211
                © 2017

                http://doi.wiley.com/10.1002/tdm_license_1.1

                http://onlinelibrary.wiley.com/termsAndConditions#vor

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