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The pathophysiology of residual sleepiness in treated obstructive sleep apnoea (OSA) remains poorly understood. Animal models suggest that it may involve neuronal damage due to intermittent hypoxia and sleep fragmentation. In a cohort of 122 continuous positive airway pressure (CPAP) treated OSA patients referred for maintenance of wakefulness test, we explored the determinants of (objective) alertness and those of (subjective) sleepiness assessed by Epworth Sleepiness Scale.We found that in logistic models, residual hypoxic burden was significatively associated with objective impaired alertness (OR=1.005, 95% CI 1.002 to 1.008), p=0.003), whereas arousal index >25/h was significatively associated with subjective residual sleepiness (OR=1.23, 95% CI 1.05to 1.43, p=0.02). This suggests that hypoxia and sleep fragmentation may be involved in different dimensions of residual hypersomnolence in treated OSA.
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Tankéré et al. (2025) studied this question.
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