Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sleep apnea and associated daytime sleepiness and fatigue are common manifestations of mainly obese middle-aged men. The onset of sleep apnea peaks in middle age, and its morbid and mortal sequelae include complications from accidents and cardiovascular events. The pathophysiology of sleep apnea remains obscure. The purpose of this study was to test three separate, albeit closely related, hypotheses. 1) Does sleep apnea contribute to the previously reported changes of plasma cytokine (tumor necrosis factor-alpha and interleukin-6) and leptin levels independently of obesity? 2) Among obese patients, is it generalized or visceral obesity that predisposes to sleep apnea? 3) Is apnea a factor independent from obesity in the development of insulin resistance? Obese middle-aged men with sleep apnea were first compared with nonapneic age- and body mass index (BMI)-matched obese and age-matched lean men. All subjects were monitored in the sleep laboratory for 4 consecutive nights. We obtained simultaneous indexes of sleep, sleep stages, and sleep apnea, including apnea/hypopnea index and percent minimum oxygen saturation. The sleep apneic men had higher plasma concentrations of the adipose tissue-derived hormone, leptin, and of the inflammatory, fatigue-causing, and insulin resistance-producing cytokines tumor necrosis factor-alpha and interleukin-6 than nonapneic obese men, who had intermediate values, or lean men, who had the lowest values. Because these findings suggested that sleep apneics might have a higher degree of insulin resistance than the BMI-matched controls, we studied groups of sleep-apneic obese and age- and BMI-matched nonapneic controls in whom we obtained computed tomographic scan measures of total, sc, and visceral abdominal fat, and additional biochemical indexes of insulin resistance, including fasting plasma glucose and insulin. The sleep apnea patients had a significantly greater amount of visceral fat compared to obese controls (<0.05) and indexes of sleep disordered breathing were positively correlated with visceral fat, but not with BMI or total or sc fat. Furthermore, the biochemical data confirmed a higher degree of insulin resistance in the group of apneics than in BMI-matched nonapneic controls. We conclude that there is a strong independent association among sleep apnea, visceral obesity, insulin resistance and hypercytokinemia, which may contribute to the pathological manifestations and somatic sequelae of this condition.
 ...
PMID:Sleep apnea and daytime sleepiness and fatigue: relation to visceral obesity, insulin resistance, and hypercytokinemia. 1072 86

Sleep-related breathing disorders, ranging from habitual snoring to the increased upper airway resistance syndrome to sleep apnea, are now recognized as major health problems. The majority of patients have excessive daytime sleepiness and tiredness. Neuropsychological dysfunction results in poor work performance, memory impairment, and even depression. Until recently, the coexistence of cardiovascular and cerebrovascular diseases with sleep-related breathing disorders was thought to be the result of shared risk factors, such as age, sex, and obesity. However, in the past 5 years several epidemiologic studies have demonstrated that sleep-related breathing disorders are an independent risk factor for hypertension, probably resulting from a combination of intermittent hypoxia and hypercapnia, arousals, increased sympathetic tone, and altered baroreflex control during sleep. Sleep apnea may lead to the development of cardiomyopathy and pulmonary hypertension. Early recognition and treatment of sleep-related breathing disorders may improve cardiovascular function.
 ...
PMID:Sleep-related breathing disorders and cardiovascular disease. 1075 96

There is evidence that daytime tiredness is caused by apnea/hypopnea with oxygen desaturation and/or by sleep fragmentation due to arousals. The aim of this study was to investigate objective and subjective sleep and awakening quality and daytime vigilance--objectified by midmorning mapping of vigilance-controlled EEG (V-EEG)--in sleep apnea patients (N: 18), as compared with age- and sex-matched normal controls (N: 18) as well as to correlate nocturnal respiratory distress and arousals to daytime brain function. Statistical analyses demonstrated a deterioration in subjective and objective sleep and awakening quality in apnea patients. Midmorning V-EEG mapping in apnea patients exhibited less total power, more delta and theta, less alpha and beta activity, as well as a slower dominant frequency and centroid of the total activity compared to controls, which suggests a vigilance decrement. The Spearman rank correlation between 6 polysomnographically registered respiratory variables and 36 diurnal quantitative EEG measures demonstrated the following: the higher the apnea, apnea-hypopnea, snoring and desaturation indices and the lower the minimum and average low oxygen saturation, the more pronounced was diurnal tiredness. Eleven arousal measures based on ASDA criteria showed the following significant correlations: the higher the nocturnal arousal index and the more arousals due to hypopneas, the greater was daytime tiredness. On the other hand, the greater the average frequency change during arousals and the more spontaneous arousals, the better was daytime vigilance. Our findings show that, in contrast to the lengthy Multiple Sleep Latency (MSLT) and Maintenance of Wakefulness (MWT) tests which evaluate sleep pressure under resting conditions conducive to sleep, V-EEG mapping provides a brief objective measure of a sleep apnea patient's daytime tiredness under conditions of wakefulness more appropriate to reflect the patient's everyday life.
 ...
PMID:[Daytime tiredness correlated with nocturnal respiratory and arousal variables in patients with sleep apnea: polysomnographic and EEG mapping studies]. 1081 4

The multiple chemical sensitivities syndrome (MCS) and other chronic syndromes causing fatigue, headache and other protean CNS symptoms without observable signs, are proposed to result from hypoxia/hypercapnia (H/H) due to disturbed breathing. The concept is explained in terms of sleep apnea (SA), although H/H could result from causes other than SA. Reasons for considering this etiologic linkage are as follows: 1. MCS symptoms resemble those of SA. 2. The only physical signs associated with MCS (upper airway inflammation and obstruction) can aggravate SA. 3. The only neuropsychiatric finding common among MCS symptomatics, reduced verbal recall, is associated with SA. 4. Many MCS symptomatics attribute onset of their condition to a pesticide or solvent exposure. Solvent neurotoxicity may cause cacosmia, a symptom of MCS and SA. 5. Improved upper airway patency, a first-line therapy in SA, may improve symptoms in some MCS-like conditions. Implications for diagnosis and treatment of MCS are discussed.
 ...
PMID:Chemical sensitivity and fatigue syndromes from hypoxia/hypercapnia. 1085 79

Hypersomnia (excessive sleepiness) refers to an increased sleep propensity with a subjective craving for sleep, involuntary naps and "sleep attacks" during the day and/or prolonged nighttime sleep with sleep drunkeness. Excessive sleepiness should be separated from fatigue and lack of energy associated with a variety of medical and psychiatric diseases. Hypersomnia is reported by 2-5% of the adult population and can lead to poor work, accidents and neuropsychiatric disturbances. Sleep apnea syndrome (SAS), narcolepsy, chronic sleep deprivation (insufficiency), and restless legs/periodic limb movements in sleep syndrome (RLS/PLMS) represent the most common causes of hypersomnia. The diagnosis of these conditions can often be suspected on clinical grounds. However, an overnight polysomnography and a multiple sleep latency test are often additionally required for definite diagnosis. Treatment options include nasal CPAP for SAS, stimulants for narcolepsy, sleep prolongation for sleep insufficiency, and dopaminergic agents for RLS/PLMS.
 ...
PMID:[Hypersomnia--etiology, clinic, diagnosis and therapy of excessive sleepiness]. 1095 47

An obese 23-year-old man with sleep-disordered breathing and primary pulmonary hypertension (PPH) had been administered oral beraprost sodium, anticoagulant warfarin, and home oxygen therapy, at another hospital as treatment for the PPH, but he had not experienced any symptomatic improvement. The patient had a body mass index of 32.4kg/m2, and complained of fatigue, shortness of breath on exertion, excessive daytime sleepiness, and snoring. Arterial blood gas analysis showed a PaO2 and a PaCO2 of 70.9 and 31.2mmHg, respectively. A polysomnographic study revealed central sleep apnea with an apnea-hypopnea index (AHI) of 29.7episodes/h. The patient showed improvement of daytime sleepiness after starting nocturnal nasal bilevel positive airway pressure (BiPAP) therapy for the central sleep apnea, but his pulmonary hypertension, measured in the daytime, worsened. The patient died suddenly while walking to the bathroom in the morning 1 month after initiation of BiPAP therapy. It is necessary to consider the possibility of sudden death when nasal BiPAP therapy is given to a PPH patient with central sleep apnea.
 ...
PMID:Primary pulmonary hypertension with central sleep apnea: sudden death after bilevel positive airway pressure therapy. 1098 61

Excessive daytime sleepiness (EDS) is a frequent symptom of patients with obstructive sleep apnoea (OSA). EDS is a high-risk factor for accidents at work and on the road. Thirty untreated patients with different levels of severity of OSA were studied concerning night sleep and EDS. The criterion for severity was the respiratory disturbance index (RDI): 15 patients were classified as 'moderately' apnoeic (RDI < 40), 15 as 'severely' apnoeic (RDI > 40). Following night-time polysomnography, objective and subjective aspects of EDS were studied. To assess objective EDS the Maintenance of Wakefulness Test (MWT) and a computer-based vigilance performance test were used. Subjective EDS was determined using the Stanford Sleepiness Scale (SSS), the Epworth Sleepiness Scale (ESS) and the Visual Analogue Scales for Performance (VAS-P) and Tiredness (VAS-T). Well-being was assessed using the Scale of Well-Being by von Zerssen (Bf-S/Bf-S'). Severe apnoea patients spent more time in stage 1 and less in slow-wave sleep. MWT latencies tended to be shorter in the severe apnoea group. Vigilance testing revealed no group differences. Patients with moderate apnoea described themselves as more impaired in all subjective scales, but only SSS scores reached statistical significance. Our results suggest that there is no simple correlation between polysomnographic and respiratory sleep variables at night on the one hand, and the extent of EDS on the other hand. Furthermore, subjective and objective evaluation of EDS does not yield the same results. New approaches which allow a more detailed analysis of night sleep and daytime function are required to identify high-risked patients.
 ...
PMID:Excessive daytime sleepiness in patients suffering from different levels of obstructive sleep apnoea syndrome. 1101 70

SIDS is almost invariably sleep-related. Viable syndrome aetiology must be compatible with its many epidemiologically diverse risk factors, each of which directly or indirectly associates with the creation of psychological and/or physiological infant stress, and the subsequent disruption of normal, contented sleep. During essential deep 'rebound' recovery sleep, arousal ability and upper airway muscle tone decrease further to that in normal sleep, with subsequent upper airway obstruction. When stress impact causes sufficient sleep disruption and physiological fatigue, a failure to arouse and so restore sufficient tone to overcome such obstruction results in sudden, unexpected death. SIDS has therefore many causes which share a final lethal mechanical pathway. Evidence is presented for obstructive apnoea during sleep as being the primary syndrome death mode, for sleep disruption, reduced arousal ability, and infant stress in SIDS, and for risk factor association with the creation of this stress. Specific infant vulnerability in the first 6 months of life to stress predominantly related to total dependency on a carer for gratification of need, and to obstructive sleep apnoea due to normal anatomical, physical, and respiratory immaturity, including rapid physiological fatigue, and peaks in sleep and thermal stress vulnerability, are discussed. Further reasons for the limited age period of SIDS, and for reduced neonatal risk, are given. Prone sleeping risk can relate to positional airway obstruction during normal sleep without prior infant stress. Much of SIDS aetiology appears to concern factors related to socio-economic deprivation and subsequent sub-optimal infant care.
 ...
PMID:Infant stress and sleep deprivation as an aetiological basis for the sudden infant death syndrome. 1117 74

To assess the available evidence for a causal role of driver sleepiness in car crashes or car crash injury, and to quantify the effect, a systematic review of the international literature was conducted. The review included all studies with a fatigue-related exposure measure, a crash or crash injury outcome measure and a comparison group, regardless of publication status, language or date of the study. Eighteen cross-sectional studies and one case-control study fulfilled the inclusion criteria. The fatigue-related exposures investigated in these studies were sleep disorders (n = 14), shift work (n = 2), sleep deprivation/fragmentation (n = 1), and excessive daytime sleepiness (n = 2). Only one study used an injury outcome measure. Studies were limited in their ability to establish a causal relationship by their design, by biases, and in many cases, by small sample sizes. The better quality cross-sectional studies were suggestive of a positive relationship between fatigue and crash risk, but could not provide reliable estimates of the strength of the association. The case-control study provided moderately strong evidence for an association between sleep apnoea and risk of driver injury, with an adjusted odds ratio of 7.2 (95% confidence interval 2.4-21.8). We conclude that the direct epidemiological evidence for a causal role of fatigue in car crashes is weak, but suggestive of an effect. To estimate the burden of injury due to fatigue-related crashes in the population, information is required from well-designed observational epidemiological studies about the prevalence of fatigue in the car driving population and the size of the risk this confers.
 ...
PMID:The role of driver sleepiness in car crashes: a systematic review of epidemiological studies. 1118 20

1. The effects of diabetes on the electrical and contractile function of skeletal muscle are variable, depending on muscle fibre type distribution. The muscles of the upper airway have a characteristic fibre distribution that differs from previously studied muscles, but the effects of diabetes on upper airway muscle function are unknown. Normally, contraction of upper airway muscles, such as the sternohyoids, dilates and/or stabilizes the upper airway, thereby preventing its collapse. Diabetes is associated with obstructive sleep apnoea in which there is collapse of the upper airway due to failure of the upper airway musculature to maintain airway patency. Therefore, the purpose of the present study was to determine the effects of diabetes on the electrical and contractile characteristics of upper airway muscle. 2. Rats were treated with vehicle (sodium citrate buffer; pH 4.5) or with streptozotocin to induce diabetes, confirmed by the presence of hyperglycaemia, and the contractile and electrical properties of the sternohyoid were compared in these two groups. Isometric contractile properties and membrane potentials were determined in isolated sternohyoid muscles in physiological saline solution at 25 degrees C. 3. Streptozotocin had no effect on sternohyoid muscle fatigue, the tension-frequency relationship or membrane potentials, but did increase contraction time, half-relaxation time, twitch tension and tetanic tension. 4. Streptozotocin-induced diabetes has no effect on sternohyoid muscle fatigue or the tension-frequency relationship, but does reduce contractile kinetics and increases force generation. These effects are not due to changes in resting membrane potential. These data are evidence that the association of sleep apnoea and diabetes is not due to effects on upper airway muscle contractile properties.
 ...
PMID:Contractile and electrical properties of sternohyoid muscle in streptozotocin diabetic rats. 1120 73


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>