Active clinical trials for "Sleep Apnea Syndromes"

With the advent of electricity, light at night has become a ubiquitous part of our society. The main purpose of this study is to determine whether sleeping with dim light (40 lux), the brightness of a night light) in your bedroom for 5 consecutive nights will result in increased markers of inflammation in the blood compared to sleeping in darkness during the night in patients with obstructive sleep apnea (OSA). A secondary aim is to examine the effects on insulin sensitivity, other blood proteins, and RNA molecules as a result of sleeping with dim light. RNA molecules are substances in blood that dictate what type of proteins the body should make.

Obstructive sleep apnea (OSA) is a medical problem whose importance is increasing in recognition and awareness. The National Commission on Sleep Disorders estimates that 15 million Americans have OSA, many of whom remain undiagnosed (24). OSA is associated with the development of hypertension and other cardiovascular diseases (1,2). Patients with OSA, like those with congestive heart failure, hypertension, hypercholesterolemia and diabetes, exhibit impaired EDV (25-32). OSA is also associated with impairments in endothelium-dependent cerebral blood flow responses, which may be a risk factor for stroke (33). Impaired EDV is a result of reduced production or inadequate action of nitric oxide. Since EDV worsens with disease progression and improves with disease treatment, it serves as a prognostic marker of vascular function (34-37). In OSA, hypoxia and neurohumoral disturbances increase generation of reactive oxygen species (ROS) that neutralize nitric oxide and impair endothelium-dependent responses (9,10,38). One source of ROS in endothelial cells is the enzyme xanthine oxidase (38). XO is an enzyme present in the vascular endothelium that significantly contributes to generation of ROS in congestive heart failure, hypercholesterolemia and diabetes (13-17). Inhibition of XO improves endothelium-dependent resistance vessel responses in these populations (13-17), but it is unknown if XO significantly contributes to oxidative stress and endothelial dysfunction in OSA. The central hypothesis of this application is that inhibition of XO with allopurinol will reduce oxidative stress and generation of ROS, thereby improving nitric oxide bioavailability and EDV in OSA. Our hypothesis has been formulated on the basis that patients with OSA experience repeated hypoxemia that increases activity of XO and other enzymes, thus increasing the generation of ROS that negatively impact EDV. Hypoxia is detrimental to vascular homeostasis since it increases generation of ROS through direct mechanisms and via activation of XO.

The purpose of this study is to identify the mechanism(s) by which OSA exacerbates the age-linked decline in systemic testosterone concentrations by conducting a randomized order sham-controlled crossover study that dynamically evaluates the entire hypothalamic-pituitary testicular axis across a wide age range.

This study is to determine whether sleep disorders contribute to impaired quality of life and mobility in patients with Bronchiolitis Obliterans syndrome and whether non invasive positive airways pressure ventilation can improve sleep, quality of life and mobility in this patient group.

This study will evaluate the effect of treatment of obstructive sleep apnea on insulin sensitivity in pregnant women. Women in their third trimester of pregnancy will be randomized to receive treatment or no treatment for one month.

In obstructive sleep apnea (OSA), the upper airway recurrently closes during sleep. The mechanisms that lead to airway closure are not completely understood. Some studies have shown that there is progressive narrowing of the pharyngeal airway across breaths during expiration (Progressive Expiratory Narrowing, PEN) preceding an obstructive apnea. The investigators will assess the viscoelastic properties of the pharyngeal airway and its role in PEN.

Obstructive sleep apnea (OSA) has traditionally been attributed only to a collapsible upper airway. However, it is increasingly recognized that multiple additional non-anatomical mechanisms contribute to the disease. Higher rates of OSA in patients with post-traumatic stress disorder (PTSD) than in those without PTSD have been reported however the mechanism behind this increased prevalence has not been investigated. Our hypothesis is that patients with PTSD have a predisposition to OSA due to a lower respiratory arousal threshold (wake up too easily) than patients without PTSD. The goal of this project will be to study and compare the ArTH in patients with PTSD and those without. In addition, we plan to see whether medications can be used to increase the arousal threshold and treat OSA in patients with PTSD.

In obstructive sleep apnea (OSA), the upper airway recurrently closes during sleep. The mechanisms that lead to airway closure are not completely understood. Models to study mechanisms of airway collapse have been proposed. However, these models have not been tested in the human upper airway. Gas density and viscosity are different gas properties that influence upper airway collapse and are variables of different models. In this study, subjects will breathe gas mixtures of different densities and viscosities for brief periods of time in order to test those models.

The official definition of depression or major depressive disorder, is a psychological disorder which is characterised by a persistent low mood or loss of interest in previously pleasurable activities, for over two weeks. It is one of the leading causes of disability world-wide and is one of the most common mental health disorders, affecting 5-10% of the world population at any one time. However, a major problem with this condition is the over-use of antidepressants. The number of anti-depressant prescriptions has doubled in the last decade and cost the NHS £780,000 per day in 2015. Many of the symptoms of obstructive sleep apnoea syndrome (OSAS) are similar to symptoms of depression, such as fatigue, low mood, difficulty concentrating and un-refreshing sleep. This means that patients could be misdiagnosed with depression and begin on courses of antidepressants which don't improve their symptoms. A very high association between OSAS and depression has been consistently recorded in research studies. Similarly, the primary treatment for OSAS, continuous positive airway pressure (CPAP) has been shown to significantly improve depressive symptoms in these patients. However, when studying the effects CPAP therapy has on patients with OSAS, one of the main factors which can cause differences is in antidepressant use. A lot of studies have excluded those who are on them, while quite a lot failed to note the antidepressant use. Therefore, this study aims to focus on those patients who are on antidepressant therapy but not gaining remission in their symptoms. These patients may be classed as anti-depressant treatment resistant.

The study is designed to investigate the natural course of Primary snoring in 1-2 years or more and the different effect of drug and surgical treatment applied in children with obstructive sleep apnea (OSAS) by comparing the polysomnography(PSG) and sleep questionaires in 6 months after treatment.