Obstructive Sleep Apnea Alters Sleep Stage Transition Dynamics

Abstract

IntroductionEnhanced characterization of sleep architecture, compared with routine polysomnographic metrics such as stage percentages and sleep efficiency, may improve the predictive phenotyping of fragmented sleep. One approach involves using stage transition analysis to characterize sleep continuity.Methods and Principal FindingsWe analyzed hypnograms from Sleep Heart Health Study (SHHS) participants using the following stage designations: wake after sleep onset (WASO), non-rapid eye movement (NREM) sleep, and REM sleep. We show that individual patient hypnograms contain insufficient number of bouts to adequately describe the transition kinetics, necessitating pooling of data. We compared a control group of individuals free of medications, obstructive sleep apnea (OSA), medical co-morbidities, or sleepiness (n = 374) with mild (n = 496) or severe OSA (n = 338). WASO, REM sleep, and NREM sleep bout durations exhibited multi-exponential temporal dynamics. The presence of OSA accelerated the “decay” rate of NREM and REM sleep bouts, resulting in instability manifesting as shorter bouts and increased number of stage transitions. For WASO bouts, previously attributed to a power law process, a multi-exponential decay described the data well. Simulations demonstrated that a multi-exponential process can mimic a power law distribution.Conclusion and SignificanceOSA alters sleep architecture dynamics by decreasing the temporal stability of NREM and REM sleep bouts. Multi-exponential fitting is superior to routine mono-exponential fitting, and may thus provide improved predictive metrics of sleep continuity. However, because a single night of sleep contains insufficient transitions to characterize these dynamics, extended monitoring of sleep, probably at home, would be necessary for individualized clinical application.

Sleep Fragmentation Does Not Explain Misperception of Latency or Total Sleep Time

“…For example, survival analysis and similar approaches focusing on sleep stage transition dynamics have been shown to capture fragmentation related to OSA more effectively than standard metrics. [14][15][16] Although the basis for sleep misperception remains uncertain, understanding this phenomenon is important for epidemiological assessments of sleep duration as well as clinical assessment of patient with insomnia. Recent data emphasizes the importance of perception, as the first group to perform objective PSG testing in a large longitudinal cohort clearly demonstrated that health risks such as hypertension, diabetes, and mortality, previously attributed to insomnia symptoms or selfreported short sleep durations, may in fact be mainly attributed to the subset of patients with the combination of insomnia symptoms and objective short TST on PSG.…”

“…We note that characterizing sleep architecture through stage percentage is an insensitive method for capturing sleep fragmentation. 16,21 Therefore, we also investigated bout duration for each sleep stage across these groups. This approach allowed us to assess whether more sensitive measures could support the hypothesis that fragmentation drives misperception.…”

“…For example, prior work in characterizing sleep architecture in sleep apnea patients indicates that stage percentages are an insensitive measure of sleep fragmentation, whereas sleep bout duration analytics showed better sensitivity. [14][15][16] We previously investigated PSG features such as sleep stage percentage or sleep efficiency as possible correlations between misperception of TST and architecture of sleep; however, none of these served as predictors. 7 In this study, we tested the hypothesis that TST misperception was related to sleep fragmentation via analysis of CDF plots.…”

Adipose tissue in obesity and obstructive sleep apnoea

“…OSA is characterised by recurring episodes of upper airway obstruction during sleep [21], intermittent hypoxia [22], sleep fragmentation [23], excessive daytime sleepiness [21] and increased cardiovascular risk [24]. Upper airway collapse during sleep can be prevented by the application of nasal continuous positive airway pressure (CPAP), which is the treatment of choice for moderateto-severe OSA in adults.…”

Association of Naso-Oro-Pharyngeal Structures with the Sleep Architecture in Suspected Obstructive Sleep Apnea

“…Another study suggested that sleep efficiency, sleep latency, and N1 did not differ between control group, mild apnea and severe apnea. On the other hand, N2 and REM latency increased with the severity of AHI with the decrease in N3 and REM [14]. Other literature suggests that at least in children sleep architecture do not differ with the position dependent AHI [15].…”