Abstract
The physiological impact of severe levels of obstructive sleep apnoea and the benefits of treatment are well documented. Yet more of the population suffer sleep apnoea of moderate severity. However, we still have substantial gaps in our understanding on the physiological impact and treatment of people with sleep apnoea of moderate severity. Our study addressed whether moderate obstructive sleep apnoea (OSA) had an impact on cerebral blood flow, cognition, or microsleeps. It also explored the effect of 6–7 months of auto-titrating positive airway pressure (APAP) therapy on physiological measurements and quality-of-life in persons with moderate OSA.
Twenty-four patients aged 32–79 years (median age 59, 10 female), who had previously presented to the Christchurch Hospital Sleep Unit and subsequently diagnosed with sleep apnoea of moderate severity consented to our study. Following a Level II polysomnography to confirm their suitability to participate, thirteen of these participants, aged 43–79 years (median age 59, 4 female), were placed on APAP therapy, with instructions to use it for at least 4 hr per night for 70% or more of the nights. The remaining 11 participants aged 32–79 years (median age 62, 6 female), were placed in an untreated cohort. Placement in the treated cohort was dependent on order of presentation with those first recruited offered a place in the treated cohort. A third group of seven healthy controls aged 42–73 years (median age 62, 4 female) with an apnoea, hypopnea index (AHI) < 5 were recruited from a database of normal volunteers. The absence of sleep apnoea’s was confirmed by polysomnography in all seven participants. All three groups underwent an MRI ASL scan of cerebral perfusion, completed cognitive tests covering five cognitive domains – attention, executive functioning, memory, speed of processing, and visuospatial – and undertook a 30-minute task in which they were required to continuously track a constantly moving target for the purpose of detecting microsleeps. This behavioural data, along with video recordings of eye movement and closure, were visually rated to identify microsleeps. Finally, the Epworth sleepiness scale (ESS), Pittsburgh sleep quality index (PSQI), and Short-form 36 Health survey questionnaire (SF-36) were completed. All measurements were repeated after the intervention period of 6–7 months during which time the treated cohort received APAP therapy.
Global cerebral perfusion did not differ at baseline between participants with sleep apnoea of moderate severity and healthy controls (mean 49.26 ml/100g/min vs 48.73 respectively, p = .899, d = 0.06). Furthermore, global cerebral perfusion rates at follow-up for the treated cohort, were not significantly different to baseline (mean 51.64 vs 48.56, p = .150, d =0.42). Although a comparison of regional perfusion, as shown in the multi-sliced images, between the treated cohort, the untreated cohort, and the control group show a positive effect of change in the treated cohort over the other two, particularly in the right cerebral cortex/cingulate gyrus region and the right angular/supramarginal gyri, no statistically significant distinct regions of improved cerebral perfusion were identified.
The normalized and standardized composite cognitive score also did not differ at baseline between moderate OSA and healthy controls (median 0.26 vs 0.73, p = .166, d = -0.62). Repeat testing of cognition at the completion of 6–7 months of APAP therapy found no evidence of a difference between baseline and follow-up on total cognition (mean = 0.22 vs 0.36, p = .560, d = -0.17. However, despite memory showing a significant improvement (p = .001) there was a clear test-retest effect in all three groups.
Microsleep was also tested at baseline. Participants with moderate OSA (0–126 microsleeps, median 0) and healthy controls (0–2 microsleeps, median 0) displayed a similar propensity to microsleeps (p = .253, d = 2.1). No difference in microsleeps were observed between participants compliant with APAP treatment compared to their baseline result (median 0, range 0–5, vs. median 0, range 0–13, p = .344). Several markers of day-time sleepiness and quality of live improved in our treatment cohort: Epworth Sleepiness Scale (median 8 down from 11, p = .003, d =1.96), PSQI (mean 15.69 up from 14.23, p = .046, d = 0.94) and Minnesota Short Form 36 (mean 76.31 up from 66.09, p = .035, d = 0.93).
This research was unable to demonstrate any change in cerebral perfusion, cognition, or microsleeps following 6-7 months of APAP treatment. However, improvements in daytime sleepiness, sleep quality and quality of life are consistent with the observation that most participants who used APAP in this study wished to continue its use past its conclusion. This indicates a clinical benefit in treating moderate OSA not otherwise supported.