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      Obstructive sleep apnea co-morbidity in patients with fibromyalgia: a single-center retrospective analysis and literature review

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          Abstract

          Background: Fibromyalgia (FM) is a chronic medical condition characterized by widespread pain, sleep disturbance, and cognitive dysfunction. Sleep disorders are thought to play a prominent role in the etiology and symptomatic management of FM, specifically obstructive sleep apnea (OSA). In order to provide collaborative care, we need a better understanding of any overlapping presentation of FM and OSA. We conducted a site-wide review of patients from 2012–2016 to identify FM patients diagnosed with OSA.

          Methods: Charts were reviewed in patients aged 18 and above from 2012–2016 using ICD codes from a clinical data repository. Intersection of patients with a diagnosis of FM and OSA in clinics of psychiatry, sleep, rheumatology, and other outpatient clinics was compared. Polysomnography order patterns for FM patients were investigated.

          Results: Co-morbidity was highest in the sleep clinic (85.8%) compared to psychiatry (42.0%), rheumatology (18.7%), and other outpatient clinics (3.6%) ( p<0.001). In the rheumatology and other outpatient clinics, 93.5% and 96% of patients respectively, had no polysomnography ordered. Pairwise comparison of co-morbidity in clinics: sleep vs psychiatry, sleep vs rheumatology, sleep vs other clinics, psychiatry vs rheumatology, psychiatry vs other clinics, and rheumatology vs other clinics were statistically significant after applying a Sidak adjustment to the p-values (all p<0.001).

          Conclusion: Our analysis suggests that there could be a correlation between FM and OSA, and referral to sleep studies is recommended in the management of patients with FM. The varying prevalence of FM patients with co-morbid OSA in sleep clinics when compared to other outpatient clinics suggests a discrepancy in the identification of FM patients with OSA. When properly screened, OSA co-morbidity has the potential to be higher in other outpatient clinics.

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          Most cited references31

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          The association of sleep and pain: an update and a path forward.

          Ample evidence suggests that sleep and pain are related. However, many questions remain about the direction of causality in their association, as well as mechanisms that may account for their association. The prevailing view has generally been that they are reciprocally related. The present review critically examines the recent prospective and experimental literature (2005-present) in an attempt to update the field on emergent themes pertaining to the directionality and mechanisms of the association of sleep and pain. A key trend emerging from population-based longitudinal studies is that sleep impairments reliably predict new incidents and exacerbations of chronic pain. Microlongitudinal studies employing deep subjective and objective assessments of pain and sleep support the notion that sleep impairments are a stronger, more reliable predictor of pain than pain is of sleep impairments. Recent experimental studies suggest that sleep disturbance may impair key processes that contribute to the development and maintenance of chronic pain, including endogenous pain inhibition and joint pain. Several biopsychosocial targets for future mechanistic research on sleep and pain are discussed, including dopamine and opioid systems, positive and negative affect, and sociodemographic factors.
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            Brain mechanisms of pain affect and pain modulation.

            Recent animal studies reveal ascending nociceptive and descending modulatory pathways that may contribute to the affective-motivational aspects of pain and play a critical role in the modulation of pain. In humans, a reliable pattern of cerebral activity occurs during the subjective experience of pain. Activity within the anterior cingulate cortex and possibly in other classical limbic structures, appears to be closely related to the subjective experience of pain unpleasantness and may reflect the regulation of endogenous mechanisms of pain modulation.
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              Sleep loss and REM sleep loss are hyperalgesic.

              Disturbed sleep is observed in association with acute and chronic pain, and some data suggest that disturbed and shortened sleep enhances pain. We report the first data showing, in healthy, pain-free, individuals, that modest reductions of sleep time and specific loss of rapid eye movement (REM) sleep produces hyperalgesia the following morning. Two repeated-measures design protocols were conducted: (1) a sleep-loss protocol with 8 hours time-in-bed, 4 hours time-in-bed, and 0 hours time-in-bed conditions and (2) a REM sleep-loss protocol with 8 hours time-in-bed, 2 hours time-in-bed, REM deprivation, and non-REM yoked-control conditions. The studies were conducted in an academic hospital sleep laboratory. Healthy pain-free normal sleepers, 7 in the sleep-loss protocol and 6 in the REM sleep-loss protocol, participated. Finger-withdrawal latency to a radiant heat stimulus tested at 10:30 AM and 2:30 PM and the Multiple Sleep Latency Test conducted at 10:00 AM, noon, 2:00 PM, and 4:00 PM were measured. Finger-withdrawal latency was shortened by 25% after 4 hours of time in bed the previous night relative to 8 hours of time in bed (p < .05), and REM sleep deprivation relative to a non-REM yoked-control sleep-interruption condition shortened finger-withdrawal latency by 32% (p < .02). These studies showed that the loss of 4 hours of sleep and specific REM sleep loss are hyperalgesic the following day. These findings imply that pharmacologic treatments and clinical conditions that reduce sleep and REM sleep time may increase pain.
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                Author and article information

                Journal
                Open Access Rheumatol
                Open Access Rheumatol
                OARRR
                rheu
                Open Access Rheumatology : Research and Reviews
                Dove
                1179-156X
                29 April 2019
                2019
                : 11
                : 103-109
                Affiliations
                [1 ]Department of Psychiatry, Loyola University Medical Center , Maywood, IL 60153, USA
                [2 ]Loyola Stritch School of Medicine , Maywood, IL 60153, USA
                [3 ]Biostatistics Core, Clinical Research Office, Loyola University Medical Center , Maywood, IL 60153, USA
                [4 ]Informatics and Systems Development, Loyola University Medical Center , Maywood, IL 60153, USA
                Author notes
                Correspondence: Edwin S MereshDepartment of Psychiatry, Loyola University Medical Center , 2160 S. First Ave, Bldg 105, Rm 1940, Maywood, IL60153, USATel +1 708 216 3274Email Emeresh@ 123456lumc.edu
                Article
                196576
                10.2147/OARRR.S196576
                6500898
                31118843
                95c75c3b-c3d6-4a28-bc1c-67a6a36d427a
                © 2019 Meresh et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                : 01 December 2018
                : 22 February 2019
                Page count
                Figures: 1, Tables: 2, References: 36, Pages: 7
                Categories
                Original Research

                fibromyalgia,obstructive sleep apnea,co-morbidity,sleep,rheumatology,psychiatry

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