2018
DOI: 10.1093/sleep/zsy063.1128
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1129 Central Sleep Apnea after Hypoglossal Nerve Stimulation

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Cited by 3 publications
(5 citation statements)
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“…In addition, there is an overall reduced sensitivity of brain chemoreceptors to CO 2 due to long-term exposure to nocturnal hypercapnia with sleep apnea. 20,[28][29][30] After UAS device activation, the resolution of sleep-related obstruction and restoration of normal lower nocturnal values of PCO 2 , coupled with decreased receptor chemosensitivity, may result in a blunted inspiratory drive. These events may eventually disappear with continuous OSA treatment and progressive adaptation of chemoreceptors to the new levels of nocturnal PCO 2 .…”
Section: Discussionmentioning
confidence: 99%
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“…In addition, there is an overall reduced sensitivity of brain chemoreceptors to CO 2 due to long-term exposure to nocturnal hypercapnia with sleep apnea. 20,[28][29][30] After UAS device activation, the resolution of sleep-related obstruction and restoration of normal lower nocturnal values of PCO 2 , coupled with decreased receptor chemosensitivity, may result in a blunted inspiratory drive. These events may eventually disappear with continuous OSA treatment and progressive adaptation of chemoreceptors to the new levels of nocturnal PCO 2 .…”
Section: Discussionmentioning
confidence: 99%
“…To date, there is only 1 case of treatment-emergent CSA after UAS reported in the literature. Chan et al 20 found that after implantation, their patient had a significant number of central apneas (respiratory event index [REI] 45 events/h, 25 central apneas) during in-laboratory device titration; however, the central apneas resolved after the patient's device configuration was changed to (---) 0.6 to 1.6 V to optimize stimulation of the tongue base during awake endoscopy (AHI 2.08 events/h). In our cohort, we found an overall low prevalence of possible treatment-emergent CSA (3.3%, n = 5).…”
Section: Discussionmentioning
confidence: 99%
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