Journal of Neurology and Neuroscience

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Commentry - (2023) Volume 0, Issue 0

Causes of Obstructive Sleep Apnea and Associated Comorbidities Involved in Cognitive Impairment of Patients

Lawrence McCloskey*
Department of Behavioral Health, Wellspan Health System, York, Pennsylvania, USA
*Correspondence: Lawrence McCloskey, Department of Behavioral Health, Wellspan Health System, York, Pennsylvania, USA, Email:

Received: 29-May-2023, Manuscript No. IPJNN-23-13786; Editor assigned: 31-May-2023, Pre QC No. IPJNN-23-13786 (PQ); Reviewed: 14-Jun-2023, QC No. IPJNN-23-13786; Revised: 21-Jun-2023, Manuscript No. IPJNN-23-13786 (R); Published: 29-Jun-2023, DOI: 10.4172/2171-6625.23.S6.004


As anyone with an interest in this subject knows, the obstructive Sleep Apnea Syndrome (OSA) is a very common condition in middle-aged and older adults which is commonly associated with serious outcomes like reduced quality of life and increased all-cause mortality. Despite some dissent, there has emerged a rough consensus after decades of research that OSA is also associated with mild cognitive impairments across a range of domains. Although different reviewers have stressed different ones, my own conclusion after perusal of this vast literature is that Attention/Working Memory (A/WM), Executive Function (EF), Episodic Memory (EM) and Speed of Information Processing (SIP) may be most vulnerable, as they are in depression and many other illnesses that are often comorbid with OSA, including obesity, coronary atherosclerosis, Hypertension (HTN) and Diabetes Mellitus (DM), in accord with what Gaquoine in called “Frontal-Subcortical Ischemia” [1-3]. Therefore, some authorities have suspected that such comorbidities may account for these impairments instead of OSA itself. Moreover, the inconsistent correlations, summing to nil in several meta-analyses, between the severity of OSA and impairment in cognition further undercuts causality [1]. Commented here on the very scant literature which addresses this important question directly.

Borges, et al. asserted truly in that EF is “a multifaceted construct” whose impairment might not “be shown when following the widely held practice” which holds widely across other cognitive domains in this literature, of measuring it by only one or a couple of tests [4]. Matched by age, gender, education, intelligence and body-mass index, 22 treatment-naïve OSA patients and 22 controls, all without obesity, psychopathology, HTN or DM, did not differ on tests of attention, working memory, planning, updating, set-shifting, and dual-tasking, inhibition, flexibility, and verbal fluency. Acknowledging their “limited sample size,” the authors concluded that “no clinically significant executive effects are found in moderate and severe (OSA) patients who are otherwise healthy”.

Seemingly unaware that they were partially replicating the study above, Gnoni, et al. in early “undertook a proof of the concept to define the cognitive pattern in a (rare) group of male, middle-aged patients with untreated OSA who present without comorbidities” of any kind [5]. Compared to 7 “healthy peopleeducation- matched” controls, 11 patients with severe OSA performed often substantially worse on tests of “executive functioning, visuospatial short-term memory vigilance and psychomotor control” which were “largely in keeping with previous studies of OSA patients with associated multiple comorbidities”. They also reported,” for the first time, diminished social cognition”. Revealing a threshold effect, patients with mild OSA “performed better than those with severe OSA on most of those same tasks and rarely worse than controls”.

Unaware in turn of the contemporaneous study above, I sought also in early 2023 to approach causality from a different direction by controlling comorbidities through multiple regressions [1]. After partialing the presence or absence of HTN and DM among 39 patients with mild to severe OSA, the Apnea- Hypopnea Index (AHI; the most common measure of severity) but not the Nadir Of Oxygen Saturation (NOS; the most common measure of deoxygenation) predicted demographically corrected, composite scores of several tests apiece which tapped A/WM, EF and EM, accounting for 10-13 percent of the variance. I interpreted this dose-response relationship as evidence that OSA may cause mild deficits in these three cognitive domains beyond those attributable to at least two of its most frequent comorbidities.

These three germane studies (all that I could find) suffer by tiny samples (as must be expected in proofs of concept), so all stand in dire need of replication. Two of them sought the advantage of a theoretical test of OSA’s unique cognitive effects by recruiting more or less “pure” patients at the cost of generalizability beyond the sliver of OSA patients without contributory comorbidities [4,5]. This strategy prevented the discovery of effects which might arise only in synergy with comorbidities, however, and they contradicted each other sharply besides. The third sought generalizability by accepting “all comers” at the risk of the pitfalls of statistical control (like overfitting), while covarying only two of OAS’s most frequent comorbidities.

The next step to follow the latter (my own) strategy would be:

• To recruit a large, diverse sample to yield power enough to control via multiple regression for more comorbidities (preferably coded as continuous variables, like blood-pressure readings, rather than simply present or absent);

• To control for demographic confounds while conserving precious degrees of freedom by administering cognitive tests with demographically-corrected norms; and

• To form composite measures of several tests in each cognitive domain to cancel error and to map “multifaceted constructs” like EF. More investigators also might consider polysomnographic variables other than the traditional AHI and NOS, including markers of sleep fragmentation (like the arousal index) and sleep microstructure (like sleep spindles). Yet their relation to mentation has been inconsistent, too [6,7].


The particular cognitive impairments in OSA do seem to support the oft-repeated hypothesis of frontal-subcortical ischemia, inasmuch as they do occur as well in patients with documented dysfunction in those areas. Their pathophysiology in OSA remains highly speculative, however, and their geography unconfirmed. In a meta-review of morphometric and functionalconnectivity studies, for example, Yeung concluded that “no brain region…was consistently reported across the metaanalyses as significantly atrophied”. I wonder therefore whether the cognitive tests which are taken to be the most “frontal” or executive are merely the most sensitive to diffuse or variegated cerebral dysfunction because they tap into broad networks.



Conflict of Interest



Citation: McCloskey L (2023) Causes of Obstructive Sleep Apnea and Associated Comorbidities Involved in Cognitive Impairment of Patients. J Neurol Neurosci Vol.14 No.S6:004