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A, Smith BJ. Psychological therapies for the treatment of anxiety disorders in chronic obstructive pulmonary disease.

Oral appliances should be considered in patients with mild or moderate disease or those unable to tolerate CPAP. New, minimally invasive surgical techniques are currently being developed to achieve better patient outcomes and reduce surgical morbidity. Successful long-term management of OSA requires careful patient education, enlistment of the family's support and the adoption of selfmanagement and patient goal setting principles.

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Background Studies report that up to 80% of individuals with chronic obstructive pulmonary disease (COPD) may struggle with symptoms of depression. However, this major comorbidity in COPD is rarely managed effectively. A number of recent studies indicate that left untreated, COPD-related depression is associated with worse quality of life, worse compliance with COPD treatment plan, increased exacerbations, hospital admissions, and healthcare costs when compared to individuals with COPD without depression. Regrettably, COPD practice guidelines do not provide conclusive treatment recommendations for the use of antidepressants in patients with COPD, and base their guidelines on findings from trials in the general population. This may be problematic, as there is an elevated risk of respiratory issues associated with antidepressant treatment and COPD. Evaluating effectiveness and safety of pharmacological interventions specifically for patients with COPD and depression was therefore paramount. Objectives To assess the effectiveness and safety of pharmacological interventions for the treatment of depression in patients with COPD. Search methods The last search was performed on 26 November 2018. We initially searched the following databases via the Specialised Trials Registers of the Cochrane Airways and Common Mental Disorders Groups (

Obstructive sleep apnoea (OSA) is a respiratory condition occurring during sleep characterised by repeated collapse of the upper airway. Patients with OSA show altered brain structure and function that may manifest as impaired neuroplasticity. We assessed this hypothesis in 13 patients with moderate-to-severe OSA and 11 healthy control subjects. Transcranial magnetic stimulation was used to induce and measure neuroplastic changes in the motor cortex by assessing changes in motor-evoked potentials (MEPs) in a hand muscle. Baseline measurements of cortical excitability included active (AMT) and resting motor thresholds (RMT), and the maximal stimulator output producing a 1-mV MEP. Intracortical inhibition (ICI) was investigated with short-and long-interval ICI paradigms (SICI and LICI, respectively), and neuroplastic changes were induced using continuous theta burst stimulation (cTBS). At baseline, differences were found between groups for RMT (9.5% maximal stimulator output higher in OSA) and 1-mV MEPs (10.3% maximal stimulator output higher in OSA), but not AMT. No differences were found between groups for SICI or LICI. The response to cTBS was different between groups, with control subjects showing an expected reduction in MEP amplitude after cTBS, whereas the MEPs in patients with OSA did not change. The lack of response to cTBS suggests impaired long-term depression-like neuroplasticity in patients with OSA, which may be a consequence of sleep fragmentation or chronic blood gas disturbance in sleep. This reduced neuroplastic capacity may have implications for the learning, retention or consolidation of motor skills in patients with OSA.