Association between the atherogenic index of plasma and left ventricular hypertrophy in patients with obstructive sleep apnea: a retrospective cross-sectional study.

BACKGROUND: The atherogenic index of plasma (AIP) is a simple and reliable marker of insulin resistance and is closely associated with various cardiovascular diseases (CVDs). However, the relationships between AIP and left ventricular (LV) geometric indicators have not been adequately assessed. This study was carried out to investigate the association between AIP and LV geometric abnormalities in obstructive sleep apnea (OSA) patients. METHODS: This retrospective cross-sectional study included a total of 618 OSA patients (57.3 ± 12.4 years, 73.1% males, BMI 28.1 ± 4.2 kg/m2) who underwent echocardiography. Patients with OSA were diagnosed with clinical symptoms and an apnea-hypopnea index ≥ 5.0. LV hypertrophy (LVH) was defined as left ventricular mass index (LVMIh2.7) ≥ 50.0 g/m2.7 for men and 47.0 g/m2.7 for women. AIP was calculated as log10 (TG/HDL-C). RESULTS: Compared with the non-LVH group, AIP was significantly higher in the LVH group (0.19 ± 0.29 vs 0.24 ± 0.28, P = 0.024) and the concentric LVH group (0.18 ± 0.29, 0.19 ± 0.30, 0.20 ± 0.26 and 0.29 ± 0.29 in the control, concentric remodeling, eccentric hypertrophy and concentric hypertrophy groups, respectively, P = 0.021). Meanwhile, in the group of patients with the highest AIP tertile, the levels of LVMIh2.7 (42.8 ± 10.5, 43.2 ± 9.3 and 46.1 ± 12.1 in the T1, T2 and T3 groups, respectively, P = 0.003), and the prevalence of LVH (25.2%, 24.0% and 34.6% in the T1, T2 and T3 groups, respectively, P = 0.032) and concentric LVH (10.7%, 9.8% and 20.2% in the T1, T2 and T3 groups, respectively, P = 0.053) were higher compared with those in the other groups. Positive correlations between AIP and LV geometric indicators including the LVMIh2.7, LVMIBSA, LV mass (LVM), diastolic left ventricular inner diameter (LVIDd), diastolic left ventricular posterior wall thickness (PWTd) and diastolic interventricular septal thickness (IVSTd), were revealed according to correlation analysis (P < 0.05). Furthermore, AIP was independently associated with LVMIh2.7 according to multivariate linear regression model (ß = 0.125, P = 0.001). Notably, AIP remained independently associated with an elevated risk of LVH [odds ratio (OR) = 1.317 per 1 standard deviation (SD) increment, 95% confidence interval (CI): 1.058 - 1.639, P = 0.014) and concentric LVH (OR = 1.545 per 1 SD increment, 95% CI: 1.173 - 2.035, P = 0.002) after fully adjusting for all confounding risk factors by multivariate logistic regression analyses. CONCLUSIONS: AIP was independently associated with an increased risk of LVH and concentric LVH in OSA patients. Therefore, AIP, as a practical and cost-effective test, might be useful in monitoring hypertrophic remodeling of the heart and improving CVDs risk stratification in clinical management of OSA.

Sleep health primary care clinical resource.

BACKGROUND: Obstructive sleep apnoea (OSA) and insomnia are the two most common sleep disorders and are frequent reasons for presentation in Australian general practice. OBJECTIVE: This article describes the development, content and suggested uses of the online sleep health primary care clinical resource, which provides general practitioners and other primary healthcare professionals with evidence-based information on the aetiology, assessment, management, referral and ongoing care for OSA and chronic insomnia. DISCUSSION: The Royal Australian College of General Practitioners-accepted clinical resource for the management of OSA and chronic insomnia in primary care was developed by the Australian National Centre for Sleep Health Services Research. The resource is designed to be used during consultations (eg following the steps in assessment and management and the use of online questionnaires for the assessment of OSA [Epworth Sleepiness Scale/OSA50/STOP-Bang] and insomnia [Sleep Condition Indicator/and Insomnia Severity Index]) and as an education/training tool (eg evidence on the role of continuous positive airway pressure/mandibular advancement splints for management of OSA and brief behavioural therapy for insomnia/cognitive behavioural therapy for insomnia for the management of insomnia).

Diagnosis of obstructive sleep apnoea in primary care.

BACKGROUND: Obstructive sleep apnoea (OSA) is a highly prevalent condition associated with significant adverse health consequences affecting multiple organ systems. As the first point of contact for most patients with OSA, general practitioners (GPs) have an important role in the diagnosis of this common sleep disorder. OBJECTIVE: The aim of this paper is to improve awareness of common risk factors for and clinical presentation of OSA in primary care to improve patient health outcomes. We seek to understand how screening tools, such as the OSA50 questionnaire and the Epworth Sleepiness Scale, can help GPs identify patients who are at high risk for OSA with significant daytime sleepiness. DISCUSSION: Patients at high risk of symptomatic moderate-severe OSA should proceed to further investigation with sleep study testing. Referral to a sleep physician should be considered for patients with complex presentations or other suspected sleep disorders, commercial drivers, and those who fail to comply with or respond to initial OSA treatments.

Management of obstructive sleep apnoea in primary care.

BACKGROUND: Obstructive sleep apnoea (OSA) is common in the community and is increasing in prevalence. Primary care plays a pivotal role in the diagnosis and management of OSA. OBJECTIVE: This article focuses on the management options for a patient with an established diagnosis of OSA and provides a guide for driving licensing requirements. Indications for continuous positive airway pressure (CPAP) are discussed and tips provided to consider when conducting a review appointment, including trouble shooting. DISCUSSION: There are several treatment options available for patients with an established diagnosis of OSA. Selecting the optimal therapy involves aligning the symptoms and severity of OSA with the presence of comorbidities. CPAP is a highly effective therapy for symptomatic adults with moderate-to-severe OSA and for some symptomatic patients with mild OSA. Early trouble shooting of side effects and using supportive interventions increases the probability of long-term adherence, which is key to symptomatic improvement.

Comorbid Insomnia and Sleep Apnea: COMISA.

The term "comorbid insomnia and sleep apnea" (COMISA) has been used to categorize the co-occurrence of the most prevalent and impacting sleep disorders. Meanwhile, both insomnia and sleep apnea have been shown to be associated with increased stress levels and cardiometabolic risk, a major cause of mortality. The better knowledge about such convergence would be critical for better understanding pathophysiological pathways and mechanisms. This article provides an overview of epidemiologic aspects, clinical findings, and mechanisms subsiding COMISA. Odontostomatological approach with mandibular advancement devices are discussed as an effective therapeutic approach in these patients.

Association of MRI Indexes of the Perivascular Space Network and Cognitive Impairment in Patients with Obstructive Sleep Apnea.

Background The role of perivascular space (PVS) dysfunction in obstructive sleep apnea (OSA) requires further study. Purpose To compare MRI indexes of PVS across patients with differing severities of OSA and relate them with disease characteristics and treatment. Materials and Methods This single-center prospective study included healthy controls (HCs) and patients with complaints of snoring who underwent MRI and cognitive evaluation between June 2021 and December 2022. Participants with complaints of snoring were classified into four groups (snoring, mild OSA, moderate OSA, and severe OSA). PVS networks were assessed at MRI using PVS volume fraction, extracellular free water (FW), and diffusion tensor imaging analysis along the PVS (DTI-ALPS). One-way analysis of variance and Pearson correlation were used for analysis. Alterations in PVS indexes and cognitive performance after treatment were assessed in 15 participants with moderate OSA. Results A total of 105 participants (mean age, 33.4 years ± 8.9 [SD]; 80 males) and 50 HCs (mean age, 37.0 years ± 8.6; 33 males) were included. Higher mean PVS volume fraction was observed in participants with severe OSA (n = 23) than in patients with mild OSA (n = 36) (0.11 vs 0.10; P = .03). Participants with severe OSA exhibited higher mean FW index (0.11) than both HCs (0.10; P < .001) and patients with mild OSA (0.10; P = .003). All patient groups had lower DTI-ALPS than HCs (range, 1.5-1.9 vs 2.1; all P < .001). DTI-ALPS correlated with cognitive performance on the Stroop Color and Word Test (r range, -0.23 to -0.24; P value range, .003-.005). After treatment, PVS indexes changed (P value range, <.001 to .01) and cognitive performance improved (P value range, <.001 to .03). Conclusion Differences in PVS indexes were observed among participants with differing severities of OSA and HCs. Indexes correlated with measures of cognitive function, and changes in indexes and improvement in cognitive performance were observed after treatment in participants with moderate OSA. © RSNA, 2024 Supplemental material is available for this article. See also the editorial by Port in this issue.

[Adaptive servo-ventilation in patients with heart failure and sleep apnea: Insights from the ADVENT-HF trial].

Heart failure is strongly associated with obstructive and central sleep apnea. The landmark 2015 SERVE-HF trial showed that using adaptive servo-ventilation (ASV) for central sleep apnea (CSA) management was associated with an increased risk of all-cause and cardiovascular mortality among heart failure patients with reduced ejection fractions. Based on the result, the American Academy of Sleep Medicine and the European Society of Cardiology have recommended against the use of ASV for the treatment of CSA in patients with heart failure with an ejection fraction≤45%. Recently, the results from the ADVENT-HF trial have been formally published, indicating that ASV does not increase adverse outcomes and can improve patients' quality of life. Here, we go over these findings in detail.

Association of obstructive sleep apnea with risk of lung cancer: a nationwide cohort study in Korea.

Current knowledge regarding the relationship between obstructive sleep apnea (OSA) and the risk of lung cancer is limited. This study aimed to evaluate associations between OSA and the incidence of lung cancer based on the Korean National Health Information Database. The study outcome was the incidence of newly diagnosed lung cancer, and a Cox proportional hazards model was used for analysis. A total of 181,070 adult patients newly diagnosed with OSA between 2011 and 2018 were matched with those without OSA by up to 1:5 propensity score matching based on age and sex. During follow-up over (mean ± standard deviation) 9.1 ± 2.0 years, 2614 incident cases of lung cancer were identified. The incidence rate was 39.51 per 100,000 person-years in the OSA group, and 24.93 per 100,000 person-years in the control group. After adjusting for income and the presence of comorbidities, the association remained significant (hazard ratio [HR] 1.95, 95% confidence interval [CI] 1.74-2.18, p-value < 0.001). The adjusted HR for incident lung cancer was 2.14 (95% CI 1.69-2.70) in female patients with OSA, and 1.90 (95% CI 1.67-2.16) in male patients with OSA. The risk of incident lung cancer increased with age, with a HR of 2.99 (95% CI 2.46-3.64) in those aged ≥ 65 years. This nationwide study showed an independent association between OSA and an increased risk of lung cancer in the Korean population.

Relationship between obstructive sleep apnoea syndrome and gastrointestinal diseases: a systematic review and Meta-analysis.

Studies exploring the association between obstructive sleep apnoea syndrome (OSA) and gastrointestinal diseases (GID) are important for enhancing clinical outcomes. This study aimed to systematically assess the association between these two diseases. Adhering to PRISMA guidelines, a comprehensive literature search was conducted across databases including PubMed, Web of Science, Willey Library, Cochrane Library and Scopus. This search focused on English literature published up to January 2024. Literature screening, quality assessment (using the NOS scale) and data extraction were performed by two independent researchers. Statistical analyses were performed using the meta-package of the R.4.2.2 software. An initial screening of 2178 papers was conducted and 11 studies were included. Meta-analysis results showed a significant association between OSA and GID (p < 0.01). Subgroup analyses further indicated a stronger association between OSA and GID in Asian populations compared to Europe and the United States. In addition, both benign and malignant GID were significantly associated with OSA, with a pronounced association for malignant GID than for benign GID. The results of publication bias analysis revealed no significant bias (Begg's test p = 0.45, Egger's test p = 0.60). This study uncovers a notable association between OSA and GID, especially in Asian populations, suggesting that clinicians should consider the potential connection between these two diseases during diagnosis and treatment. However, due to the heterogeneity and limitations of the study, these conclusions need to be further validated through more comprehensive research.

Exosomes regulate SIRT3-related autophagy by delivering miR-421 to regulate macrophage polarization and participate in OSA-related NAFLD.

PURPOSE: To analyze the role of and mechanism underlying obstructive sleep apnea (OSA)-derived exosomes in inducing non-alcoholic fatty liver (NAFLD). METHODS: The role of OSA-derived exosomes was analyzed in inducing hepatocyte fat accumulation in mice models both in vivo and in vitro. RESULTS: OSA-derived exosomes caused fat accumulation and macrophage activation in the liver tissue. These exosomes promoted fat accumulation; steatosis was more noticeable in the presence of macrophages. Macrophages could internalize OSA-derived exosomes, which promoted macrophage polarization to the M1 type. Moreover, it inhibited sirtuin-3 (SIRT3)/AMP-activated protein kinase (AMPK) and autophagy and promoted the activation of nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasomes. The use of 3-methyladenine (3-MA) to inhibit autophagy blocked NLRP3 inflammasome activation and inhibited the M1 polarization of macrophages. miR-421 targeting inhibited SIRT3 protein expression in the macrophages. miR-421 was significantly increased in OSA-derived exosomes. Additionally, miR-421 levels were increased in OSA + NAFLD mice- and patient-derived exosomes. In the liver tissues of OSA and OSA + NAFLD mice, miR-421 displayed similar co-localization with the macrophages. Intermittent hypoxia-induced hepatocytes deliver miR-421 to the macrophages via exosomes to inhibit SIRT3, thereby participating in macrophage M1 polarization. After OSA and NAFLD modeling in miR-421-/- mice, liver steatosis and M1 polarization were significantly reduced. Additionally, in the case of miR-421 knockout, the inhibitory effects of OSA-derived exosomes on SIRT3 and autophagy were significantly alleviated. Furthermore, their effects on liver steatosis and macrophage M1 polarization were significantly reduced. CONCLUSIONS: OSA promotes the delivery of miR-421 from the hepatocytes to macrophages. Additionally, it promotes M1 polarization by regulating the SIRT3/AMPK-autophagy pathway, thereby causing NAFLD.

SENP1 regulates intermittent hypoxia-induced microglia mediated inflammation and cognitive dysfunction via wnt/ß-catenin pathway.

Obstructive sleep apnea syndrome (OSAS), characterized by repeated narrow or collapse of the upper airway during sleep, resulting in periodic reductions or cessations in ventilation, consequent hypoxia, hypercapnia, increased sympathetic activity and sleep fragmentation, places a serious burden on society and health care. Intermittent hypoxia (IH), which cause central nervous system (CNS) inflammation, and ultimately lead to neuropathy, is thought to be a crucial contributor to cognitive impairment in OSAS. Wnt signaling pathway exerts an important role in the regulation of CNS disorders. Particularly, it may be involved in the regulation of neuroinflammation and cognitive dysfunction. However, its underlying mechanism remains poorly understood. Accumulating evidence demonstrated that Wnt signaling pathway may inhibited in a variety of neurological disorders. Recently studies revealed that SUMOylation was participated in the regulation of neuroinflammation. Members of Wnt/ß-catenin pathway may be targets of SUMOylation. In vitro and in vivo molecular biology experiments explored the regulatory mechanism of SUMOylation on Wnt/ß-catenin in IH-induced neuroinflammation and neuronal injury, which demonstrated that IH induced the SUMOylation of ß-catenin, microglia mediated inflammation and neuronal damage. Moreover, SENP1 regulated the de-SUMOylation of ß-catenin, triggered Wnt/ß-catenin pathway, and alleviated neuroinflammation and neuronal injury, thus improving IH-related mice cognitive dysfunction.

Contribution of Obstructive Sleep Apnea to Asthmatic Airway Inflammation and Impact of Its Treatment on the Course of Asthma.

Asthma and obstructive sleep apnea (OSA) are very common respiratory disorders in the general population. Beyond their high prevalence, shared risk factors, and genetic linkages, bidirectional relationships between asthma and OSA exist, each disorder affecting the other's presence and severity. The author reviews here some of the salient links between constituents of the alternative overlap syndrome, that is, OSA comorbid with asthma, with an emphasis on the effects of OSA or its treatment on inflammation in asthma. In the directional relationship from OSA toward asthma, beyond direct influences, multiple factors and comorbidities seem to contribute.

Mechanical Interactions Between the Upper Airway and the Lungs that Affect the Propensity to Obstructive Sleep Apnea in Health and Chronic Lung Disease.

Obstructive sleep apnea (OSA) is a common disorder characterized by repetitive narrowing and collapse of the upper airways during sleep. It is caused by multiple anatomic and nonanatomic factors but end-expiratory lung volume (EELV) is an important factor as increased EELV can stabilize the upper airway via caudal traction forces. EELV is impacted by changes in sleep stages, body position, weight, and chronic lung diseases, and this article reviews the mechanical interactions between the lungs and upper airway that affect the propensity to OSA. In doing so, it highlights the need for additional research in this area.

Obstructive Sleep Apnea Effects on Chronic Airway Disease Exacerbations-Missed Opportunities for Improving Outcomes in Chronic Obstructive Pulmonary Disease and Asthma.

In patients with chronic obstructive pulmonary disease (COPD) and asthma, exacerbations determine the natural history of both diseases. Patients with both respiratory diseases who suffer from obstructive sleep apnea (OSA) as a comorbidity (overlap syndromes) have a higher risk of exacerbations and hospitalization. In cases of OSA/COPD and OSA/asthma, continuous positive airway pressure treatment is indicated. Adequate adherence to therapy appears to reduce exacerbations and their severity, especially in OSA/COPD overlap. However, there is a lack of randomized trials that definitively demonstrate this evidence.

The Role of Obstructive Sleep Apnea in Hypercapnic Respiratory Failure Identified in Critical Care, Inpatient, and Outpatient Settings.

An emerging body of literature describes the prevalence and consequences of hypercapnic respiratory failure. While device qualifications, documentation practices, and previously performed clinical studies often encourage conceptualizing patients as having a single "cause" of hypercapnia, many patients encountered in practice have several contributing conditions. Physiologic and epidemiologic data suggest that sleep-disordered breathing-particularly obstructive sleep apnea (OSA)-often contributes to the development of hypercapnia. In this review, the authors summarize the frequency of contributing conditions to hypercapnic respiratory failure among patients identified in critical care, emergency, and inpatient settings with an aim toward understanding the contribution of OSA to the development of hypercapnia.

Changes in plasma concentrations of novel vascular and inflammatory biomarkers in obstructive sleep apnea patients pre- and post-stroke.

BACKGROUND: Obstructive sleep apnea (OSA) is increasingly recognized as a common condition in the general population and causes significant OSA-associated morbidities including cardiovascular and cerebrovascular events such as cerebral small vessel disease (CSVD) and stroke. METHODS: In this study, using sensitive ELISA immunoassays, we measured subset of endothelial/vascular and inflammatory biomarkers as well as neurofilament light chain (NfL), a sensitive marker for neuroaxonal injury, using plasma from OSA patients post-stroke (Acute Cerebral Infarction (ACI), N = 26) to determine their usefulness as potential prognostic markers in disease progression. RESULTS: Our results showed significantly increased plasma TNFα and NfL concentrations and decreased concentrations of platelet derived growth factor (PDGF-AA) in post-stroke OSA patients with more severe white matter hyperintensities (WMHs). And after separating the patients based on sex, compared to females, male post-stroke OSA patients with severe WMHs have increased circulating levels of inflammatory chemokine CXCL10 and cytokine Interleukin-10 (IL-10) and significantly decreased levels of Angiopoietin-1 (Ang-1) an important protein responsible for endothelial/vascular integrity functions. Importantly, in a subset of newly diagnosed OSA patients (without prior history of stroke), significantly increased plasma CXCL10 levels and decreased plasma Ang-1 levels were also readily observed when compared to healthy controls, indicating possible altered endothelial integrity and ongoing vascular inflammation in these newly diagnosed OSA patients. CONCLUSIONS: In summary, our study has identified a novel set of plasma biomarkers including PDGF-AA, CXCL10 and Ang-1 for their potential prognostic value for disease outcomes pre- and post-stroke in OSA patients and use as surrogate markers to measure efficacy of treatment modalities.

Mitochondrial dysfunction is associated with cognitive impairment in adults with OSA without dementia.

STUDY OBJECTIVES: Increased reactive oxygen species associated with loss of mitochondrial function affect synaptic activity, which is an important mechanism underlying cognitive decline. This study assesses the role of mitochondrial proteins in neuron-derived exosomes (NDEs) on cognitive impairment in patients with obstructive sleep apnea (OSA) without dementia. METHODS: Analyses were conducted in 268 study participants with complete polysomnography data, cognitive tests, and important clinical data available. NDEs were isolated immunochemically for enzyme-linked immunosorbent assay quantification of mitochondrial proteins, i.e., humanin and mitochondrial open reading frame of the 12S rRNA-c (MOTS-c), and synaptic protein, i.e., neurogranin (NRGN). A mediation analysis of the relationship between sleep parameters and cognition was performed using humanin, MOTS-c, and NRGN values as a mediating factor. Twenty-two patients with moderate to severe OSA who received CPAP therapy were followed up, and humanin, MOTS-c and NRGN levels were reassessed after 1 year of treatment. RESULTS: All participants were divided into the OSA + MCI group (n = 91), OSA-MCI group (n = 89), MCI group (MCI without OSA) (n = 38) and control group (normal cognitive state without OSA) (n = 50). The mean CD63-normalized NDE levels of humanin, MOTS-c, and NRGN in the OSA + MCI group were higher than those in the OSA-MCI and control groups. The NDE levels of humanin, MOTS-c, and NRGN in the MCI group were lower than those in controls. The odds of cognitive impairment in patients with OSA were higher with higher NDE levels of humanin, MOTS-c, and NRGN (odds ratio (OR): 2.100, 95 % confidence interval (CI): 1.646-2.679, P < 0.001; OR: 5.453, 95 % CI: 3.112-9.556, P < 0.001; OR: 3.115, 95 % CI: 2.163-4.484, P < 0.001). The impaired cognitive performance was associated with higher NDE levels of humanin (ß: 0.505, SE: 0.048, P < 0.001), MOTS-c (ß: 0.580, SE: 0.001, P < 0.001), and NRGN (ß: 0.585, SE: 0.553, P < 0.001). The relationship between sleep parameters (mean SaO2 and T90) and MoCA scores was mediated by the NDE levels of humanin, MOTS-c, and NRGN with the proportion of mediation varying from 35.33 % to 149.07 %. Receiver operating characteristic curve revealed an area under the curve of 0.905 for humanin, 0.873 for MOTS-c, and 0.934 for NRGN to predict MCI in OSA patients without dementia. Increased humanin, MOTS-c, and NRGN levels significantly decreased after CPAP treatment. CONCLUSIONS: Mitochondrial dysfunction is implicated in cognitive impairment in OSA patients without dementia, and mainly mediates the association between intermittent hypoxia and cognitive impairment in adults with OSA without dementia. Mitochondrial dysfunction can be partially reversible by CPAP treatment. Mitochondrial proteins can be used as markers of cognitive impairment in patients with OSA.

Resting-state fMRI network efficiency as a mediator in the relationship between the glymphatic system and cognitive function in obstructive sleep apnea hypopnea syndrome: Insights from a DTI-ALPS investigation.

INTRODUCTION: Obstructive sleep apnea hypopnea syndrome (OSAHS) is associated with cognitive impairment and physiological complications, necessitating further understanding of its mechanisms. This study investigates the relationship between glymphatic system function, brain network efficiency, and cognitive impairment in OSAHS patients using diffusion tensor image analysis along the perivascular space (DTI-ALPS) and resting-state fMRI. MATERIALS AND METHODS: This study included 31 OSAHS patients and 34 age- and gender-matched healthy controls (HC). All participants underwent GE 3.0T magnetic resonance imaging (MRI) with diffusion tensor image (DTI) and resting-state fMRI scans. The DTI-ALPS index and brain functional networks were assessed. Differences between groups and correlations with clinical characteristics were analyzed. Additionally, the mediating role of brain network efficiency was explored. Finally, receiver operating characteristics (ROC) analysis assessed diagnostic performance. RESULTS: OSAHS patients had significantly lower ALPS-index (1.268 vs. 1.431, p < 0.0001) and moderate negative correlation with Apnea Hypopnea Index (AHI) (r = -0.389, p = 0.031), as well as moderate positive correlation with Montreal Cognitive Assessment (MoCA) (r = 0.525, p = 0.002). Moreover, global efficiency (Eg) of the brain network was positively correlated with the ALPS-index and MoCA scores in OSAHS patients (r = 0.405, p = 0.024; r = 0.56, p = 0.001, respectively). Furthermore, mediation analysis showed that global efficiency partially mediated the impact of glymphatic system dysfunction on cognitive impairment in OSAHS patients (indirect effect = 4.58, mediation effect = 26.9 %). The AUROC for identifying OSAHS and HC was 0.80 (95 % CI 0.69 to 0.91) using an ALPS-index cut-off of 1.35. CONCLUSIONS: OSAHS patients exhibit decreased ALPS-index, indicating impaired glymphatic system function. Dysfunction of the glymphatic system can affect cognitive function in OSAHS by disrupting brain functional network, suggesting a potential underlying pathological mechanism. Additionally, preliminary findings suggest that the ALPS-index may offer promise as a potential indicator for OSAHS.

[Cervicogenic dysphagia: a case report]. / Tservikogennaya disfagiya: sluchai iz praktiki.

The article presents a case of pharyngeal dysphagia and obstructive sleep apnea syndrome caused by degenerative-dystrophic changes in the cervical spine with the formation of large cervical osteophytes at the C3-C6 level. Osteophytes caused deformation of the posterior wall of the hypopharynx and narrowing of its lumen by 20-25% from the level of the arytenoid cartilages to the upper parts of the epiglottis. CT scan also showed the intervertebral disc heights lost, as well as osteophytes at the posterolateral margins of the vertebral bodies (disc osteophyte complex). Osteosclerosis in combination with facet arthrosis caused spinal and foraminal stenosis.