Does arousal frequency predict daytime function?

Abstract

Patients with the sleep apnoea/hypopnoea syndrome (SAHS) suffer from excessive daytime sleepiness [1,2], cognitive decrements [3,4] and decreased psychological well-being [5]. These daytime effects lead to an increased risk of vehicle accidents [6], work inefficiency [7] and poor social relationships [7]. Previous correlational studies [3,5,8,9] have looked at possible causative relationships between the nocturnal features of SAHS and daytime function. However, there is still controversy as to what extent these daytime deficits are due to sleep fragmentation, caused by brief microarousals from sleep [9], or to intermittent nocturnal hypoxaemia associated with the sleep disordered breathing [4]. Studies by GUILLEMINAULT et al. [8] and found measures of sleep disturbance and sleep fragmentation, respectively, to be the best predictors of excessive daytime sleepiness. In contrast, BEDARD et al. [4] found hypoxaemia best predicted daytime sleepiness and CHESHIRE et al. [5] found no nocturnal correlates of daytime sleepiness, but did find that hypoxaemia and sleep fragmentation significantly correlated with measures of cognitive function.These conflicting results have tended to be based on older definitions of arousal [1,4,8,9] and/or relatively small numbers of subjects [1,4,5]. It has recently been shown that brief arousals from sleep produce sleepiness [10][11][12] and impair daytime function [10]. The primary aim of the current study was to investigate the hypothesis that brief arousals from sleep cause the sleepiness and impaired daytime function found in SAHS. The secondary aim of this study was to determine whether the multiple sleep latency test (MSLT) [13] or maintenance of wakefulness test (MWT) [14] is better related to daytime function in SAHS patients. Methods SubjectsA prospective study on consecutive patients clinically referred to the sleep centre with possible SAHS was performed. All study patients had either self-reported sleepiness (defined as Epworth sleepiness scale (ESS)Š8) or two other major symptoms of SAHS [2] (table 1). Patients were aged between 18 and 75 yrs old and living within 50 miles of the sleep centre. Patients who had coexisting causes of daytime sleepiness (e.g. night or rotating shiftworkers; self-reported average sleep duration <5 h), major psychiatric and neurological disorders, and coexisting causes of hypoxaemia were excluded. Following scoring of the diagnostic polysomnography, patients with an apnoea/hypopnoea index (AHI)<5 or with evidence of coexisting sleep disorders were also excluded. One hundred and sixty-seven consecutive patients were eligible for the study and 150 One hundred and fifty patients with sleep disordered breathing were studied prospectively, comparing overnight polysomnography with daytime measures of objective sleepiness, psychological well-being and cognitive performance.Significant, but weak (r 2 <0.1), relationships were seen between several nocturnal measures (apnoea/hypopnoea index, arousals and desaturation variables) and daytime measures of ...

Long-term treatment with continuous positive airway pressure improves quality of life in obstructive sleep apnoea syndrome

“…This shows that the severity of OSAS as evaluated by conventional nocturnal measures and the extent of daytime impairment are not necessarily related, as demonstrated recently in patients with OSAS [28,31], and underlines the necessity to observe not only the physiological disturbances of OSAS but also the impact on the patients' quality of life.…”

The role of mean inspiratory effort on daytime sleepiness

“…The mean sleepiness score of UARS patients was 8.1 ¡ 3.6 (range 1-16), while the mean score of OSAS patients was 10.6 ¡ 5.2 (range [3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20]. There were 16 OSAS and three UARS patients with an ESS score w10, which was defined as the upper point of normal range of sleepiness [33].…”

“…apnoea/hypopnoea [5][6][7][8] or hypoxaemia [7][8][9]), have been postulated as the main causes of EDS. In addition, reduction in the restorative nature of sleep by arousals [10][11][12], fragmentation of sleep [13,14], a lack of slow-wave sleep [15] and a reduction in total sleep time (TST) [16], have all been suggested as possible causes of EDS.…”

Effects of Adenotonsillectomy on Parent-Reported Behavior in Children With Obstructive Sleep Apnea

“…Although counterintuitive, this is not surprising as previous studies in both adults 17 and children [18][19][20] have shown a poor relation between polysomnographic parameters and neurocognitive/ behavioral outcomes. This may be because of the complex interplay of the many polysomnographic variables and multiple other factors that affect behavior, or it may be that the effect of OSAS on behavior reflects a threshold rather than a linear dosing effect.…”