scholarly journals P019 Obstructive sleep apnoea endotypes in people with multiple sclerosis

2021 ◽  
Vol 2 (Supplement_1) ◽  
pp. A27-A28
Author(s):  
S Carter ◽  
H Hensen ◽  
A Krishnan ◽  
A Chiang ◽  
J Carberry ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Obstructive Sleep Apnoea ◽  
Group Analysis ◽  
Respiratory Control ◽  
Upper Airway ◽  
Sleep Apnoea ◽  
Loop Gain ◽  
Male Predominance ◽  
Arousal Threshold ◽  
Obstructive Sleep

Abstract Purpose Obstructive sleep apnoea (OSA) is common in people with multiple sclerosis (MS) despite a lack of typical risk factors for OSA in people with MS such as obesity and male predominance. Therefore, underlying factors other than sex and obesity may be particularly important in the pathogenesis of OSA in people with MS. Thus, the primary aim of this study was to determine the relative contributions of OSA endotypes in people with MS and compare this to matched controls with OSA only. Methods Eleven people with MS and OSA (MS-OSA group) (apnoea-hypopnoea index [AHI]>5events/h) and eleven controls matched for OSA severity, age and sex without MS (OSA group) were studied. Participants underwent a detailed overnight polysomnography with an epiglottic pressure catheter and genioglossus intramuscular electrodes to allow for quantification of pathophysiological contributors to OSA. This included the respiratory arousal threshold, genioglossus muscle responsiveness, respiratory loop gain and upper airway collapsibility. Results Measures of the four primary OSA endotypes were not different between the MS-OSA and OSA groups (e.g. NREM respiratory arousal threshold -27±15 vs. -23±8 cmH2O respectively, p=0.24). Within group analysis indicated higher loop gain in non-obese MS-OSA participants compared to obese MS-OSA participants (0.53±0.11 vs. 0.37±0.11, p=0.04). Conclusions Overall, OSA endotypes are similar between MS-OSA participants and matched OSA controls. However, within the MS-OSA group, non-obese participants have higher loop gain (unstable respiratory control) compared to obese participants. Thus, unstable respiratory control may play an important role in OSA pathogenesis in many people with MS.

scholarly journals Role of common hypnotics on the phenotypic causes of obstructive sleep apnoea: paradoxical effects of zolpidem

2017 ◽  
Vol 50 (6) ◽  
pp. 1701344 ◽  
Author(s):  
Jayne C. Carberry ◽  
Lauren P. Fisher ◽  
Ronald R. Grunstein ◽  
Simon C. Gandevia ◽  
David K. McKenzie ◽  
...  
Keyword(s):  
Obstructive Sleep Apnoea ◽  
Muscle Activity ◽  
Upper Airway ◽  
Sleep Apnoea ◽  
Double Blind ◽  
Genioglossus Muscle ◽  
Airway Narrowing ◽  
Arousal Threshold ◽  
Obstructive Sleep ◽  
Airway Collapsibility

Hypnotics are contraindicated in obstructive sleep apnoea (OSA) because of concerns of pharyngeal muscle relaxation and delayed arousal worsening hypoxaemia. However, human data are lacking. This study aimed to determine the effects of three common hypnotics on the respiratory arousal threshold, genioglossus muscle responsiveness and upper airway collapsibility during sleep.21 individuals with and without OSA (18–65 years) completed 84 detailed sleep studies after receiving temazepam (10 mg), zolpidem (10 mg), zopiclone (7.5 mg) and placebo on four occasions in a randomised, double-blind, placebo-controlled, crossover trial (ACTRN12612001004853).The arousal threshold increased with zolpidem and zopicloneversusplacebo (mean±sd−18.3±10 and −19.1±9versus−14.6±7 cmH2O; p=0.02 and p<0.001) but not with temazepam (−16.8±9 cmH2O; p=0.17). Genioglossus muscle activity during stable non-REM sleep and responsiveness during airway narrowing was not different with temazepam and zopicloneversusplacebo but, paradoxically, zolpidem increased median muscle responsiveness three-fold during airway narrowing (median −0.15 (interquartile range −1.01 to −0.04)versus−0.05 (−0.29 to −0.03)% maximum EMG per cmH2O epiglottic pressure; p=0.03). The upper airway critical closing pressure did not change with any of the hypnotics.These doses of common hypnotics have differential effects on the respiratory arousal threshold but do not reduce upper airway muscle activity or alter airway collapsibility during sleep. Rather, muscle activity increases during airway narrowing with zolpidem.

scholarly journals Exposure to mild intermittent hypoxia increases loop gain and the arousal threshold in participants with obstructive sleep apnoea

2019 ◽  
Vol 597 (14) ◽  
pp. 3697-3711 ◽  
Author(s):  
Raichel M. Alex ◽  
Gino S. Panza ◽  
Huzaifa Hakim ◽  
M. Safwan Badr ◽  
Bradley A. Edwards ◽  
...  
Keyword(s):  
Obstructive Sleep Apnoea ◽  
Intermittent Hypoxia ◽  
Sleep Apnoea ◽  
Loop Gain ◽  
Arousal Threshold ◽  
Obstructive Sleep

Morphine alters respiratory control but not other key obstructive sleep apnoea phenotypes: a randomised trial

2020 ◽  
Vol 55 (6) ◽  
pp. 1901344
Author(s):  
Rodrigo T. Martins ◽  
Jayne C. Carberry ◽  
David Wang ◽  
Luke Rowsell ◽  
Ronald R. Grunstein ◽  
...  
Keyword(s):  
Upper Airway ◽  
Sleep Apnoea ◽  
Loop Gain ◽  
Ventilatory Control ◽  
Pharyngeal Muscle ◽  
Arousal Threshold ◽  
Ventilatory Responses ◽  
Obstructive Sleep ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility

Accidental opioid-related deaths are increasing. These often occur during sleep. Opioids such as morphine may worsen obstructive sleep apnoea (OSA). Thus, people with OSA may be at greater risk of harm from morphine. Possible mechanisms include respiratory depression and reductions in drive to the pharyngeal muscles to increase upper airway collapsibility. However, the effects of morphine on the four key phenotypic causes of OSA (upper airway collapsibility (pharyngeal critical closure pressure; Pcrit), pharyngeal muscle responsiveness, respiratory arousal threshold and ventilatory control (loop gain) during sleep) are unknown.21 males with OSA (apnoea–hypopnoea index range 7–67 events·h−1) were studied on two nights (1-week washout) according to a double-blind, randomised, cross-over design (ACTRN12613000858796). Participants received 40 mg of MS-Contin on one visit and placebo on the other. Brief reductions in continuous positive airway pressure (CPAP) from the therapeutic level were delivered to induce airflow limitation during non-rapid eye movement (REM) sleep to quantify the four phenotypic traits. Carbon dioxide was delivered via nasal mask on therapeutic CPAP to quantify hypercapnic ventilatory responses during non-REM sleep.Compared to placebo, 40 mg of morphine did not change Pcrit (−0.1±2.4 versus −0.4±2.2 cmH2O, p=0.58), genioglossus muscle responsiveness (−2.2 (−0.87 to −5.4) versus −1.2 (−0.3 to −3.5) μV·cmH2O−1, p=0.22) or arousal threshold (−16.7±6.8 versus −15.4±6.0 cmH2O, p=0.41), but did reduce loop gain (−10.1±2.6 versus −4.4±2.1, p=0.04) and hypercapnic ventilatory responses (7.3±1.2 versus 6.1±1.5 L·min−1, p=0.006).Concordant with recent clinical findings, 40 mg of MS-Contin does not systematically impair airway collapsibility, pharyngeal muscle responsiveness or the arousal threshold in moderately severe OSA patients. However, consistent with blunted chemosensitivity, ventilatory control is altered.

scholarly journals O023 Impact of weight loss of OSA pathophysiology

2021 ◽  
Vol 2 (Supplement_1) ◽  
pp. A10-A11
Author(s):  
A Wong ◽  
S Landry ◽  
K Yang ◽  
S Joosten ◽  
L Thomson ◽  
...  
Keyword(s):  
Weight Loss ◽  
Upper Airway ◽  
Sleep Apnoea ◽  
Loop Gain ◽  
Arousal Threshold ◽  
Post Surgery ◽  
Obstructive Sleep ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility ◽  
The Impact

Abstract Introduction Obesity is a major risk factor for developing obstructive sleep apnoea (OSA), however, the underlying mechanisms are not fully understood. We aimed to assess the impact of weight loss on all OSA endotypes (i.e. upper airway collapsibility, muscle compensation, respiratory arousal threshold, and loop gain). Methods We analysed data from 40 OSA patients (collated from 3 centres) who underwent bariatric surgery. Demographics and clinical polysomnograms (PSG) were performed at baseline and at between 6–18 months post-surgery. OSA endotypes were measured during sleep using non-invasive endotyping methods (derived from clinical PSG). Results Participants lost 28±14 kg and had a post-surgery reduction in the AHI of 19.6 (Interquartile range[IQR] -9.8 to -35.4) events/hr [from baseline 39.9 (24.3 to 65.6) events/hr to 17.0 (9.9 to 33.3) events/hr]. Following surgical weight loss, there was significant improvement in collapsibility (∆6.2 [IQR -1.4 to 13]%Veupnoea, p&lt;0.0001), as well as significant reduction in loop gain and arousal threshold (∆-0.06 [-0.17 to 0.009], p&lt;0.001 and ∆-13.7 [-24.8 to -1.8]%Veupnoea, p&lt;0.001 respectively). There was no significant change in muscle compensation. Conclusion Our findings suggest that weight loss improves upper airway collapsibility and reduces loop gain and the arousal threshold, providing novel insights about the mechanisms by which obesity causes OSA. Further analysis is underway to determine whether knowledge of the baseline OSA endotypes (in isolation and/or in combination) can predict which individuals will have a response to weight loss alone.

Volume-pressure properties of the upper airway in normal subjects and patients with obstructive sleep apnoea

Respirology ◽  
1999 ◽  
Vol 4 (1) ◽  
pp. 69-75 ◽  
Author(s):  
Denan Wu ◽  
Wataru Hida ◽  
Yoshihiro Kikuchi ◽  
Shinichi Okabe ◽  
Hajime Kurosawa ◽  
...  
Keyword(s):  
Obstructive Sleep Apnoea ◽  
Upper Airway ◽  
Normal Subjects ◽  
Sleep Apnoea ◽  
Obstructive Sleep

scholarly journals Acetazolamide improves loop gain but not the other physiological traits causing obstructive sleep apnoea

2012 ◽  
Vol 590 (5) ◽  
pp. 1199-1211 ◽  
Author(s):  
Bradley A. Edwards ◽  
Scott A. Sands ◽  
Danny J. Eckert ◽  
David P. White ◽  
James P. Butler ◽  
...  
Keyword(s):  
Obstructive Sleep Apnoea ◽  
Sleep Apnoea ◽  
The Other ◽  
Physiological Traits ◽  
Loop Gain ◽  
Obstructive Sleep

scholarly journals O013 The pathogenesis of obstructive sleep apnea in individuals with comorbid insomnia and obstructive sleep apnoea (COMISA)

2021 ◽  
Vol 2 (Supplement_1) ◽  
pp. A6-A7
Author(s):  
E Brooker ◽  
L Thomson ◽  
S Landry ◽  
B Edwards ◽  
S Drummond
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Upper Airway ◽  
Severity Index ◽  
Loop Gain ◽  
Comorbid Insomnia ◽  
Arousal Threshold ◽  
Obstructive Sleep ◽  
High Loop ◽  
Insomnia Severity

Abstract Obstructive sleep apnea (OSA) and Insomnia are prevalent sleep disorders which are highly comorbid. This frequent co-occurrence suggests a shared etiology may exist. OSA is caused by the interaction of four pathophysiological traits: a highly collapsible upper airway, elevated loop gain, a low arousal threshold, and poor muscle compensation. No study has ascertained whether these traits are influenced by insomnia. We aimed to quantify the four traits which contribute to OSA in individuals diagnosed with comorbid insomnia and OSA (COMISA). We non-invasively determined these traits in 52 COMISA patients (Age: 56±14 years) with mild-to-severe OSA (AHI=21.2±10.63 events/h) using polysomnography. Our results indicated that 83% of COMISA patients had a low arousal threshold and only 2% of patients exhibited a highly collapsible airway using previously defined thresholds. Multiple linear regression revealed the arousal threshold (b=0.24, 95%CI[0.11, 0.37], β=0.47, p&lt;0.001) and loop gain (b=23.6, 95%CI[7.02, 40.18], β=0.33, p&lt;0.01) were the strongest predictors of OSA severity in our sample. There was no significant relationship between the arousal threshold and insomnia severity measured by the insomnia severity index (ISI). Further work is being performed to compare these findings with a matched sample of OSA only participants. Our preliminary findings demonstrate OSA in COMISA is characterized by a mildly collapsible airway/low arousal threshold phenotype and is largely driven by non-anatomical factors including a low arousal threshold and high loop gain. OSA treatments which are effective in patients with mild anatomical compromise and raise the arousal threshold may provide therapeutic benefit in COMISA patients.

Sign in / Sign up

Export Citation Format

Share Document