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Respiratory muscle weakness is a major cause of morbidity and mortality in patients with neuromuscular diseases (NMDs). Respiratory involvement in NMDs can manifest broadly, ranging from milder insufficiency that may affect only sleep initially to severe insufficiency that can be life threatening. Patients with neuromuscular diseases exhibit very often sleep-disordered breathing, which is frequently overlooked until symptoms become more severe leading to irreversible respiratory failure necessitating noninvasive ventilation (NIV) or even tracheostomy. Close monitoring of respiratory function and sleep evaluation is currently the standard of care. Early recognition of sleep disturbances and initiation of NIV can improve the quality of life and prolong survival. This review discusses the respiratory impairment during sleep in patients with NMDs, the diagnostic tools available for early recognition of sleep-disordered breathing and the therapeutic options available for overall respiratory management of patients with NMDs.

Background. Obstructive Sleep Apnea Syndrome (OSAS) is associated with inflammation, but obesity may be a confounding factor. Thus, the aim of this study was to explore differences in serum levels of inflammation markers between obese individuals with or without OSAS.Methods. Healthy individuals (n=61) from an outpatient obesity clinic were examined by polysomnography and blood analysis, for measurement of TNF-α, IL-6, CRP, and fibrinogen levels. According to Apnea-Hypopnea Index (AHI), participants were divided into two BMI-matched groups: controls (AHI n=23) and OSAS patients (AHI ≥ 15/h,n=38).Results. OSAS patients had significantly higher TNF-αlevels (P<.001) while no other difference in the examined inflammation markers was recorded between groups. Overall, TNF-αlevels were correlated with neck circumference (P<.001), AHI (P=.002), and Oxygen Desaturation Index (P=.002).Conclusions. Obese OSAS patients have elevated TNF-αlevels compared to BMI-matched controls, suggesting a role of OSAS in promoting inflammation, possibly mediated by TNF-a.