The study findings are indicative of noteworthy disparities in cognitive function, depression, and anxiety-associated emotional challenges between the No or Mild OSA and the Moderate to Severe OSA groups. This discernment posits a deleterious impact of OSA on both cognitive function and emotional states, with this influence exhibiting escalated prominence in proportion to OSA severity (AUC = 0.785, 0.737). Substantiation through multiple logistic regression and correlation analyses serves to underscore that age, AHI, nocturnal oxygen saturation levels, and anxiety primarily intertwine with cognitive impairment. Concurrently, depression and anxiety align most prominently with AHI. Furthermore, it is worth noting that the existence of anxiety within the context of OSA stands as an autonomous factor contributing to the manifestation of cognitive impairment.
Cognitive function entails the intricate process through which the human brain acquires external stimuli, processes them, and internalises them as mental activities, facilitating the assimilation and application of knowledge. It encompasses diverse facets such as memory, executive function, linguistic expression, spatial perception, numerical acumen, as well as comprehension and discernment[17]. The meticulous analysis of clinical data in this investigation has underscored that OSA predominantly impacts cognitive domains associated with spatial perception, executive function, language, abstraction, delayed recall, orientation, the capacity to suppress cognitive interference, short-term memory, and attention. Similar studies, such as the one conducted by Andrew E Beaudin et al.[18], involving 1084 participants subjected to PSG, MoCA, Rey Auditory Verbal Learning Test (RAVLT), and WAIS-IV Digit-Symbol Coding (DSC) to evaluate information processing speed, have demonstrated significantly diminished memory and information processing speed in OSA-afflicted individuals compared to those unaffected (p < 0.05). In the study conducted by Alexa J Watach[19], it was discerned that adolescents grappling with both obesity and OSA displayed notably diminished executive function in comparison to the control group (p < 0.003). A staggering 45% of patients manifested compromised executive function, with a substantial 30% encountering clinically notable impairment. In the study orchestrated by Li Qi et al.[20], involving 203 participants, attention and short-term memory assessments encompassing the Trail Making Test (TMT), digit span Test (DST), and Complex Figure Test (CFT) were administered. Outcomes demonstrated markedly reduced overall cognitive function in severe OSA patients, particularly in the realm of attention, in contrast to the non-OSA cohort (p < 0.05), thereby congruent with the present study's discoveries. Nevertheless, in Yaouhi's study[21], centred on a cohort of moderate to severe OSA patients, evaluations focusing on alertness, vigilance, divided attention, working memory, and episodic memory disclosed only mild memory and motor impairments, with no discernible cognitive deficits in other domains. Although the extent of cognitive debilitation precipitated by OSA remains a subject of contention, a preponderance of research substantiates the culmination that has been reached. Our study augments this body of knowledge by furnishing additional clinical substantiation to support this prevailing consensus.
Depression and anxiety are frequently encountered emotional challenges. Our experimental outcomes markedly indicate a considerably heightened incidence of depression and anxiety among patients afflicted with moderate to severe OSA, when compared to the control group[22, 23]. This concurs harmoniously with prior meta-analyses, reinforcing the robustness of our findings. The corpus of our research furnishes pivotal clinical validation for this phenomenon. Our meticulous data scrutiny, encompassing correlation analysis and multiple logistic regression, has unveiled a direct, linear correlation between the frequency of apneas or hypopneas during nocturnal hours, quantified as Apnea-Hypopnea Index (AHI), and the severity of depression and anxiety. In succinct terms, a patient's proclivity for frequent occurrences of these respiratory events during sleep correlates with the intensity of depression and anxiety experienced. AHI emerges as an independent risk factor underpinning the manifestation of depression and anxiety. The intricate mechanics underlying the emotional ramifications of OSA remain shrouded in uncertainty, yet multiple plausible theories have been posited. Primarily, OSA patients are often beleaguered by daytime fatigue and sleep disturbances engendered by the erratic nocturnal hypoxia and sleep architecture disruptions, significantly impinging on diurnal activities[24]. Notably, Jackson, M. L.'s research revealed that a considerable 22.7% of 109 untreated OSA patients exhibited clinical depression, with 24.8% resorting to antidepressants[25]. Significantly lower sleep quality and diminished quality of life were correlated with clinical depression. In a separate study, Carneiro-Barrera, A.'s findings accentuated the substantial enhancements achievable through weight loss and lifestyle interventions in mitigating OSA-induced daily functional impairment and psychological manifestations[26]. Secondly, OSA patients routinely manifest neurochemical imbalances[27]. Research conducted by Vgontzas, A. N. spotlighted markedly higher plasma concentrations of inflammatory and fatigue-inducing cytokines[29], such as tumour necrosis factor-α and interleukin-6, among obese male OSA patients compared to their non-OSA obese counterparts. These cytokines have been acknowledged as contributory factors to daytime sleepiness. The application of etanercept, a drug neutralising tumour necrosis factor-α and inflammatory cytokines[29], in experimental settings on OSA-afflicted obese males led to a significant attenuation of daytime sleepiness. This intervention reaffirmed the profound interrelation between cytokine elevation and OSA[30]. Lastly, the nexus between chronic diseases and depression is firmly established[31]. OSA patients are often confronted with an array of chronic complications, encompassing obesity, hypertension, cardiovascular afflictions, and diabetes. Emotional struggles, typified by depression and anxiety, might transpire as secondary ramifications in the wake of these chronic maladies.
Furthermore, our study tentatively ascertained that the coexistence of anxiety and OSA serves as an autonomous catalyst for cognitive impairment, signifying that the amalgamation of anxiety with OSA might potentially exacerbate cognitive decline. Nevertheless, the dearth of pertinent mechanistic investigations and corresponding clinical trials underscores the necessity for further probing and exploration.
Continuous Positive Airway Pressure (CPAP) stands as a potent therapeutic modality for OSA management. Its principal mechanism revolves around augmenting positive pressure within the pharyngeal cavity to counterbalance the negative pressure incurred during inhalation, thus averting airway collapse. The extant body of research, fortified by meticulous meta-analyses, postulates that CPAP intervention not only ameliorates daytime sleepiness and emotional perturbations within OSA patients, but also exerts a discernible impact on enhancing cognitive function[32]. Assorted clinical studies have corroborated the salutary effects of CPAP treatment[33–35], spotlighting marked enhancements in attention, working memory, and executive function post-treatment. Concurrently, symptoms of depression and anxiety are markedly mitigated. Recent investigations have proffered the notion that certain pharmacological agents hold the potential to alleviate clinical manifestations of OSA. Murillo-Rodríguez, E., for instance, validated the efficacy of modafinil in significantly ameliorating daytime hypersomnia resulting from OSA, concomitantly abating symptoms of depression and cognitive decline[36].
It is imperative to acknowledge certain limitations inherent in our study. Primarily, the relatively modest sample size warrants consideration for future research, with a recommendation to expand the sample pool to substantiate the intricate interplay between OSA, cognitive function, and emotional dynamics. Additionally, the absence of a post-treatment follow-up for individuals grappling with moderate to severe OSA imparts a sense of incompleteness to our investigation, warranting further comprehensive exploration in subsequent studies.