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    • br Conclusion Key contributions of this study are the sugges

    2018-11-15


    Conclusion Key contributions of this study are the suggestion that one week of antibiotic treatment is insufficient to effect important changes in the gut ecosystem in most CFS participants, that reducing the levels of gram-positive gut microbiota is associated with some improvement in objective sleep parameters and self-reported vigor in CFS patients, and that high levels of Lactobacilli may be detrimental to mood. In sum, this pilot study provides preliminary evidence that changes to microbiota in a clinical population (CFS) may alter sleep. However, changes to the antibiotic regime, adding a placebo control group, using a larger sample size and measuring sleep polysomnographically are needed to clarify and extend these findings.
    Conflict of interest
    Acknowledgements This study was supported by Bioscreen (Aust) Pty Ltd. MJ was supported by a National Health and Medical Research Council of Australia Early Career Fellowship (APP#1036292) and a postdoctoral fellowship from Victoria University. The authors wish to thank Amy Wallis for her assistance with the interpretation of the study findings.
    Introduction Severity of obstructive sleep dna staining (OSA) has been defined by the quantity of apnea and hypopnea events (i.e. the apnea/hypopnea index, or AHI) occurring per hour of recorded sleep. Early detection of these events was accomplished via the use of oronasal thermistors. However, this technique cannot assess for respiratory effort; which has been identified to cause frequent arousals from sleep due to intrathoracic pressure swings that occur with little or no detectable change in thermistor signals [1–3]. Encephalography (EEG) arousals occurring in the absence of apneas and hypopneas with evidence of increased intrathoracic pressure swings can be included with AHI to an index known as the respiratory disturbance index (RDI). Elevation of RDI without significant increase in AHI is suggestive of upper airway flow limitation and clinically can be diagnosed as upper airway resistance syndrome (UARS). The International Classification of Sleep Disorders has placed UARS in the diagnostic category of OSA disorders [4]; however UARS may be more challenging to diagnosis. Diagnosis requires evidence of intrathoracic pressure changes culminating in arousals, defined as a respiratory effort related arousal (RERA), versus significant quantifiable reductions in air flow seen in OSA [5]. While there is strong evidence highlighting the cardiovascular risk of OSA [6,7], epinephrine has been proposed that other forms of sleep disordered breathing (SDB) such as UARS can be correlated with excessive-daytime-sleepiness – EDS [8–10], long-term cardiovascular complications [11,12] and significant costs to society [13–15]. The finding of RERAs has increased the sensitivity of diagnosing SDB, especially in individuals with a high clinical suspicion without polysomnogram (PSG) data supporting a clear diagnosis of OSA. The reference measurement for respiratory effort and intrathoracic pressure is esophageal pressure monitoring [16]. Chervin et al. showed a decreased esophageal pressure nadir and less sleep time with esophageal pressure more negative than 10cm of water after adenotonsillectomy in children, suggestive of improved upper airway resistance after this procedure [17]. In clinical practice, the usage of respiratory inductance plethysmography (RIP) is accepted for measurement of respiratory effort in place of esophageal pressure monitoring by measuring thoraco-abdominal excursion during breathing versus direct measurement of intrathoracic pressure [18]. The principle of diagnosing SDB beyond quantitative airflow reductions remains important for recognition of the full spectrum pathology. Inspiratory flow limitation (IFL) can be observed as flattening of the flow tracing on PSG. Physiologically, IFL indicates absence of an increase in flow despite an elevation in negative intrathoracic pressure indicating increasing effort [19]. Condos described this phenomenon during his study when titrating continuous positive airway pressure (CPAP) to where the inspiratory flow was rounded rather than plateaued. The flattening of the inspiratory flow is related to resistance of the airway which can occur even with application of positive airway pressure [20]. The presence of inspiratory flow limitation is vital to the understanding of UARS and subsequently as a diagnostic tool for this population.