Abstract
Sleepiness does not affect the prevalence and subtype of mild cognitive impairment, and discriminative ability of cognitive screening tests in detecting mild cognitive impairment http://ow.ly/se9u30mMtYc
From the author:
How sleepiness can inform clinicians about the presence of cognitive deficits and the risk of further cognitive decline in older adults is an intriguing question. The comments made by P. Steiropoulos and co-workers in their correspondence led us to perform supplementary analyses using the Epworth Sleepiness Scale in our cohort [1]. We first explored whether the presence of self-reported sleepiness modified the prevalence of mild cognitive impairment (MCI) in subjects with obstructive sleep apnoea (OSA) (mild, moderate and severe OSA were combined) and controls. In the OSA group, MCI tended to be less prevalent in subjects reporting sleepiness (Epworth Sleepiness Scale score of 10 and higher) compared to those reporting no sleepiness. More specifically, MCI was found in 31.7% of sleepy subjects and in 45.6% of nonsleepy OSA participants (χ2(1)=2.05; p=0.15). In the control group, sleepiness was not associated with a higher prevalence of MCI (37.5% had MCI in nonsleepy controls compared to 33.3% with MCI in sleepy control subjects; χ2(1)=0.03; p=0.86). When the association between sleepiness and MCI subtypes was explored (i.e. amnestic versus non-amnestic and single cognitive domain affected versus multiple cognitive domains affected), no group differences were found between OSA subjects with and without sleepiness (figure 1). Our exploratory results suggest that self-reported daytime sleepiness is not associated with increased neurocognitive impairments in our cohort of OSA and control participants.
We then explored whether the presence of self-reported sleepiness modified the discriminatory abilities of the Montreal Cognitive Assessment (MoCA) and the Mini-Mental State Examination (MMSE) in our OSA and control subjects. In the sleepy OSA group, the MoCA showed an area under the curve (AUC) of 0.82 (95% CI 0.69–0.95) with an optimal cut-off value of 27, while the MMSE had an AUC of 0.67 (95% CI 0.50–0.85) and an optimal cut-off of 29. Similar results were observed in the OSA group without sleepiness: the MoCA showed an AUC of 0.84 (95% CI 0.75–0.93; optimal cut-off of 27) whereas the MMSE had an AUC of 0.71 (95% CI 0.58–0.83; optimal cut-off of 29). We were not able to perform the receiver operating characteristic curve analyses in the control group, because sleepiness was present in only six participants, with only two presenting a MCI. However, our exploratory analyses suggest that sleepiness in OSA participants does not affect the discriminative abilities of both cognitive screening tests in detecting MCI.
In conclusion, in our cohort of OSA and control participants, sleepiness was not associated with increased prevalence of MCI and/or its different subtypes. Sleepiness was also not associated with changes in MoCA and MMSE discriminatory abilities. Previous studies have shown that OSA with significant sleepiness could lead to reduced performance in cognitive tests measuring attention and memory [2]. Our OSA subjects are probably different from subjects included in some previous studies, as 40.4% of them had cognitive impairment severe enough to warrant a diagnosis of MCI. Cognitive impairment in our cohort may have caused difficulties in accurately assessing sleepiness using the Epworth Sleepiness Scale. In fact, we recently found that OSA participants with MCI report less subjective cognitive complaints compared to those without MCI, possibly because they had early impairment of metacognitive processes, including lower self-criticism and judgment [3]. Further studies should therefore use a combination of subjective and objective measures of sleepiness to understand its impact on cognitive functioning in older adults with OSA. How sleepiness could represent a marker of a more impacted brain in the context of OSA in ageing remains unclear. This question is relevant, since sleepiness is not only one of the first daytime consequences reported by OSA patients, but also a well-known behavioural symptom of early dementia [4].
Footnotes
Conflict of interest: K. Gagnon has nothing to disclose.
Conflict of interest: N. Gosselin reports grants from Canadian Institutes of Health Research (government agency grant) and Fonds de Recherche en Santé du Québec (government agency grant and salary award), during the conduct of the study.
Support statement: This work was supported by the Government of Canada, Canadian Institutes of Health Research (MOP123294). Funding information for this article has been deposited with the Crossref Funder Registry.
- Received November 6, 2018.
- Accepted November 8, 2018.
- Copyright ©ERS 2019