Pulmonology Advisor: What are believed to be the mechanisms underlying these associations?
Dr Greenstein: Current hypotheses linking sleep-disordered breathing to cognitive impairment are numerous. Mak Daulatzai, MD, MSc, PhD, penned a great review article that focuses on the effects of intermittent hypoxia.12 Take home points from this paper are that, in rat models, intermittent hypoxia increases cerebral amyloidogenesis and tau phosphorylation, which are prominent features of Alzheimer disease. In addition, hypoxia triggers neuronal and axonal degeneration in the brain.
Rosenzweig and colleagues wrote another excellent review that focuses on sleep-disordered breathing and the brain.13 In addition to the intermittent hypoxia effects, neuroinflammatory effects and ischemic preconditioning play a role in increasing the prevalence of various mood disorders.
Purported mechanisms are many and are an active area of research today.
Dr Soehner: OSA is associated with widespread brain structural changes to grey matter regions and white matter tracts supporting cognitive and emotional health, which may confer vulnerability to mood and cognitive impairments. Other mechanisms implicated in the pathogenesis of depression and cognitive impairment in OSA are intermittent hypoxia, hormonal imbalances, and systemic inflammation. Depression is also associated with increased prevalence of obesity, which may confer a risk for OSA.
Pulmonology Advisor: What are the relevant implications for clinicians in terms of screening and treatment?
Dr Greenstein: As a sleep medicine physician, I regularly advocate to my colleagues to always consider OSA as a treatable condition that may be adversely affecting their patients’ health and/or mood. Most clinicians are well aware that OSA increases the risk for heart attack, stroke, hypertension, and diabetes. The effects on the brain are less well-known but are certainly just as important.
When seeing patients with mood disorders or cognitive impairment, clinicians must consider OSA. The STOP-BANG screening questionnaire is a good starting point, but do not forget to examine your patient’s oropharynx, as crowding and retrognathia, which increase the chance that your patient has sleep-disordered breathing, may be present in thin patients.
Dr Soehner: Special attention should be paid to diagnosing OSA in pediatric patients. Given neuromaturational changes occurring through childhood and adolescence, early identification and treatment of OSA could prevent its long-term consequences for mood and cognitive function.
Among patients with severe psychiatric conditions, older age and higher body mass index predicted increased prevalence of OSA in meta-analyses.
Because excessive daytime sleepiness is a symptom common to both depression and OSA, OSA may be underdiagnosed in individuals with depression. If excessive daytime sleepiness persists following successful CPAP treatment, further screening for depression and subsequent psychiatric referral may be indicated.
Both depression and cognitive impairment may affect the patient’s ability to effectively adhere to treatment. Particular attention should be paid to troubleshooting potential barriers to adherence among patients experiencing these symptoms.
Among individuals with OSA, older age, male sex, cigarette smoking, higher body mass index, comorbid cardiometabolic conditions, higher alcohol consumption, and psychiatric medications are associated with greater vulnerability to cognitive impairment.14
Pulmonology Advisor: What are some of the most important unmet needs in this area?
Dr Greenstein: There is a huge potential to increase awareness of this complex interplay among mental health professionals. A sizeable percentage of patients suffering from various neuropsychiatric disorders have OSA and will benefit from its diagnosis and treatment. Research on the effectiveness of CPAP and other modalities of therapy to have a positive effect on these diagnoses is needed to guide us.
Dr Soehner: Many existing studies are limited by small sample sizes, the absence of statistical adjustment for comorbidities, inconsistent methodologies, and a lack of long-term follow-up. Well-powered mechanistic studies and long-term follow-up studies are still needed to clarify relationships between OSA, mood, and cognition. Standardized assessment approaches should be developed to improve the detection of mood or cognitive impairments in clinical practice.
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This article originally appeared on Pulmonology Advisor