Khalil, Melissa

Abstract Introduction Patients presenting with daytime somnolence need to be evaluated for common etiologies including sleep-related breathing disorders, shift work disorder, insufficient sleep, insomnia and disorders of hypersomnolence. Sleep disordered breathing (SDB) is one of the most common causes of daytime sleepiness. We postulate that treatment of SDB may actually worsen symptoms, if associated with poor sleep due to positive airway pressure (PAP) therapy. Methods N/A Results A 49-year-old female presented to our clinic with increased daytime somnolence. She was diagnosed with obstructive sleep apnea (OSA) at an outside center 3 years ago and was started on auto PAP therapy with pressure settings at 6-10 cmH2O. She had 100% usage, 95th percentile pressure of 9 cm H2O, and a residual Apnea Hypopnea Index (AHI) of 1.1. The patient reported excessive daytime sleepiness, with an Epworth Sleepiness Scale of 16, requiring a daily 3-hour nap. Further sleep history revealed that she had multiple nocturnal awakenings due to discomfort with PAP therapy, including mask related issues causing sleep disruption. Several mask adjustments did not result in any sleep improvement. We decided to re-evaluate her with an in-lab polysomnography. Diagnostic data revealed an overall AHI of 1.6, supine AHI of 12.0, and lateral AHI of 1.5. Mean oxygen saturation was 94.6% with a nadir of 89.0%. The patient was advised to discontinue PAP therapy, and to sleep on her sides, which led to improvement in her sleep quality and daytime sleepiness. Conclusion Positional OSA, defined by greater than 50% increase in AHI in supine position compared to non-supine position, with or without AHI less than 5 in non-supine position, is seen in up to 50-60% of patients with OSA. In addition, intolerance to CPAP has been noted in 29-83% of patients. We need to be clinically aware of the potential effect of PAP devices, or oral appliances, on sleep disruption among intolerant patients. Among this group, conservative therapies like positional therapy or weight loss may be more effective for symptom management, especially for mild SDB. Support (if any)

Abstract Introduction Restless legs syndrome (RLS) is a common disorder of unpleasant sensations during inactivity, an urge to move the legs, and hyperarousal. The pathophysiology is incompletely understood. Treatments are not always successful or carry side effects. Methods (Case Report) Results A 45-year-old woman presented with over a decade of RLS and sleep-onset insomnia. The diagnosis was based on the International RLS Study Group criteria. The severity was assessed by the nightly occurrence and Insomnia Severity Index (ISI) of 25. Interfering neurologic or sleep disorders, medications, and abnormal blood work were ruled out. Different dopamine agonists resulted in augmentation. Caffeine was stopped. Polysomnography revealed periodic limb movement with sleep fragmentation. Gabapentin was partially effective and poorly tolerated at high doses, but continued at 600 mg. While using Dextromethorphan (DXM) for an upper respiratory infection, the patient found dramatic improvement of her RLS symptoms. Independently, she discontinued Gabapentin, and continued DXM 30 mg for 6 months, with consistent improvement. ISI decreased to 10. Ultimately, considering its expense, DXM was tapered, and Tramadol initiated. The pathophysiology of RLS is partially understood. Studies showed abnormalities in iron regulation, low adenosine tone, enhanced glutamatergic activity, inflammation, and a genetic predisposition, as contributing factors. Alpha-2-delta calcium channel ligands inhibit the presynaptic glutamate release. Central nervous system iron deficiency may increase glutamatergic tone. Ketamine, an N-methyl-D-aspartate (NMDA) receptor antagonist, inhibits the activation of NMDA receptor by glutamate and decreases glutamate presynaptic release. Ketamine was reported to effectively treat RLS. DXM, another NMDA receptor antagonist, has not been reported to treat RLS in the literature. Additionally, an association between inflammation and RLS was described, and limited data showed anti-inflammatory effect of DXM. Conclusion Patients with RLS suffer from their symptoms’ burden. Approved medications could carry side effects, or augmentation. We report a case of severe RLS with dramatic and sustained improvement with DXM. Support (if any)

Abstract Introduction Sleep-related symptoms have been associated with adverse health outcomes, including increased mortality risk. Studies that analyzed the correlation between sleep and mortality focused on the single effect of self-reported sleep duration or relied on nonstructured questionnaires about sleep. In order to evaluate the detrimental effects of sleep disorders, studies should be based on well-structured and validated questionnaires that inquire about different components of sleep, including sleep quality. In addition, taking into consideration the fluctuations in sleep duration over the study period is essential. We aimed to assess the association between sleep quality and all-cause mortality in community-dwelling adults living in rural Ecuador. Methods Individuals aged ≥40 years enrolled in the prospective population-based Three Villages Study cohort were included. Sleep quality was assessed by means of the Pittsburgh Sleep Quality Index (PSQI). Study participants were evaluated at baseline and at every annual door-to-door survey until they remained enrolled in the study. Mixed models Poisson regression for repeated PSQI determinations and multivariate Cox-proportional hazards models were fitted to estimate mortality risk according to sleep quality. Results Analysis included 1494 individuals (mean age: 56.6 ± 12.5 years; 56% women) followed for a median of 6.3 ± 3.3 years. At baseline, 978 (65%) individuals had good sleep quality and 516 (35%) had poor sleep quality. The effects of PSQI scores changing over time on mortality was confounded by the impact of the SARS-CoV-2 pandemic on both. One hundred ninety-five individuals (13%) died during the follow-up, resulting in a crude mortality rate of 1.58 per 100 person years (95% C.I.: 1.27-1.88) for individuals with good sleep quality, and 3.18 (95% C.I.: 2.53-3.82) for those with poor sleep quality at baseline. A multivariate Cox-proportional hazards model showed that individuals with poor sleep quality at baseline were 1.38 times (95% C.I.: 1.02-1.85) more likely to die compared to those with good sleep quality; in this model, increased age, poor physical activity, and high fasting glucose remained significant. Conclusion Poor sleep quality is associated with increase mortality risk among middle-aged and older adults. Support (if any)