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Reduced upper airway muscle activity during sleep is a key contributor to obstructive sleep apnea pathogenesis. Hypoglossal nerve stimulation activates upper airway dilator muscles, including the genioglossus, and has the potential to reduce obstructive sleep apnea severity. The objective of this study was to examine the safety, feasibility and efficacy of a novel hypoglossal nerve stimulation system (HGNS; Apnex Medical, St Paul, MN, USA) in treating obstructive sleep apnea at 12 months following implantation. Thirty-one subjects (35% female, age 52.4 ± 9.4 years) with moderate to severe obstructive sleep apnea and unable to tolerate positive airway pressure underwent surgical implantation and activation of the hypoglossal nerve stimulation system in a prospective single-arm interventional trial. Primary outcomes were changes in obstructive sleep apnea severity (apnea-hypopnea index, from in-laboratory polysomnogram) and sleep-related quality of life [Functional Outcomes of Sleep Questionnaire (FOSQ)]. Hypoglossal nerve stimulation was used on 86 ± 16% of nights for 5.4 ± 1.4 h per night. There was a significant improvement (P < 0.001) from baseline to 12 months in apnea-hypopnea index (45.4 ± 17.5 to 25.3 ± 20.6 events h(-1) ) and Functional Outcomes of Sleep Questionnaire score (14.2 ± 2.0 to 17.0 ± 2.4), as well as other polysomnogram and symptom measures. Outcomes were stable compared with 6 months following implantation. Three serious device-related adverse events occurred: an infection requiring device removal; and two stimulation lead cuff dislodgements requiring replacement. There were no significant adverse events with onset later than 6 months following implantation. Hypoglossal nerve stimulation demonstrated favourable safety, feasibility and efficacy.

This study examined the nature and characteristics of sleep‐disordered breathing, including obstructive sleep apnea and central sleep apnea, in patients with post‐stroke dysphagia, to determine the demographic, anthropometric and clinical variables that were associated with sleep‐disordered breathing. Thirty‐nine patients diagnosed with acute stroke (28 males and 11 females with a mean age of 72.3 ± 10.0 years) underwent overnight polysomnography (within 3.9 ± 1.6 days after admission). Sleep‐disordered breathing was described by the apnea–hypopnea index and its obstructive and central components by the obstructive apnea–hypopnea index and central apnea–hypopnea index, respectively. Severity of dysphagia was assessed using the Mann Assessment of Swallowing Ability score. Severity of stroke and functional dependence were assessed by the National Institute of Health Stroke Scale and the modified Barthel index, respectively. Most of the cohort (87%) had moderate‐to‐severe dysphagia (Mann Assessment of Swallowing Ability of 143.2 ± 19.9). Sleep‐disordered breathing (apnea‐hypopnea index ≥ 5 events/hr) was present in 38 participants (97%) with a mean apnea–hypopnea index of 37.5 ± 24.4 events/hr. Sleep‐disordered breathing was predominantly obstructive in nature, with a mean obstructive apnea–hypopnea index and central apnea–hypopnea index of 19.6 ± 15.7 and 11.4 ± 17.6 events/hr, respectively. Multivariate linear regression analyses showed that the apnea–hypopnea index was associated with sex (p =.0001), body mass index (p =.029) and the modified Barthel index (p =.006); the obstructive apnea–hypopnea index was associated with the Mann Assessment of Swallowing Ability (p =.006), sex (p =.004) and body mass index (p =.015) and had a nonlinear relationship with the modified Barthel index (p =.019); and the central apnea–hypopnea index was associated with sex (p =.027) and the modified Barthel index (p =.019). The present study showed that dysphagia severity was associated with obstructive sleep apnea severity and this association was independent of sex, modified Barthel index and body mass index. However, stroke‐induced dysphagia was not associated with central sleep apnea or overall sleep‐disordered breathing. [ABSTRACT FROM AUTHOR]

Restless legs syndrome has been associated with serum iron deficiency in clinical studies. However, studies investigating this relationship have had inconsistent results and there are no studies in young adults. Therefore, we investigated the relationship between serum measures of iron stores and restless legs syndrome in young adults in the community. Participants in the Western Australian Pregnancy Cohort (Raine) Study answered questions on restless legs syndrome (n = 1,100, 54% female) at age 22 years, and provided serum measures of iron stores (ferritin and transferrin saturation) at ages 17 and 22 years. Restless legs syndrome was diagnosed when four International RLS Study Group criteria were met (urge to move, dysaesthesia, relief by movement, worsening during evening/night) and these symptoms occurred ≥5 times per month. Logistic regression was used to assess associations between serum iron stores and restless legs syndrome, adjusting for potential confounders. The prevalence of restless legs syndrome at age 22 years was 3.0% (n = 33, 70% female). Among those who provided restless legs syndrome and iron data at age 22 years (n = 865), the median (interquartile range) ferritin was not different between the restless legs syndrome (55 [29.5–103.5] µg L−1) and the non‐restless legs syndrome group (65.0 [35.0–103.3] µg L−1, p = 0.2), nor were there differences in iron deficiency prevalence (p = 0.36). There was no association between restless legs syndrome (22 years) and iron stores (17, 22 years) before or after adjustment for potential confounders. There was no association between restless legs syndrome at 22 years and iron stores at 17 or 22 years in this cohort. Serum iron stores may not be a useful indicator of restless legs syndrome risk in young adults in the community. [ABSTRACT FROM AUTHOR]