Abstract
Background
Obstructive sleep apnoea (OSA) is as common if not more common in people with multiple sclerosis (MS) versus the general population. However, in contrast to the typical OSA risk factors in the general population, MS is far more common in women versus men, many of whom are not obese. Thus, while some people with MS likely get OSA via the same mechanisms as the general population (i.e., anatomical compromise), others may develop OSA due to specific MS-related consequences (e.g., CNS lesions that effect respiratory or upper airway neuromuscular control- i.e. via non-anatomical mechanisms). Accordingly, we investigated if the key OSA endotypes that contribute to OSA differ in people with MS in those with versus without OSA.
Methods
Nine people with MS with moderate-severe OSA (AHI=41±22events/h) and seven people with MS without moderate-severe OSA (AHI=9±3events/h) completed in-home level 2 sleep studies (n=11 Boston, n=5 Sydney). OSA endotypes were estimated using validated algorithms from the staged sleep study airflow signals and compared between those with versus without moderate-severe OSA.
Results
Respiratory control instability (loop gain) was significantly higher in people with OSA versus without (0.62±0.2 vs. 0.45±1, p=0.04). Upper airway collapsibility was also higher in OSA participants (Vpassive at the lowest decile= 53±13 vs. 74±6 %eupnea, p<0.01). Other OSA endotypes were not systematically different between groups.
Discussion
These findings suggest that while some people with MS likely get OSA via primary anatomically driven mechanisms, in others, OSA may be largely driven via non-anatomical mechanisms, potentially related to MS-specific disease consequences.