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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sleep-disordered breathing seems to play a role in pathogenesis of stroke: for example, it was showed that snoring is a risk factor for stroke. Sleep disorders and sleep-disordered breathing increase the risk for stroke, probably by influencing systemic and cerebral blood circulation, causing hypoxaemia during night. This theory is supported by the fact of higher prevalence of stroke in the morning. During REM sleep there is a higher requirement for oxygen; as most sleep apnoeas occur during REM, it is possible that there is a relative hypoxaemia during this sleep stage. Stroke, including hemispheric stroke, can cause or aggravate the pre-existing sleep-disordered breathing. There are contradictory data in the literature regarding the influence of stroke on sleep architecture. Sleep disorders are associated with poorer stroke outcome, so their detection and treatment can be important in secondary stroke prophylaxis and will improve the patient's functioning and quality of life.
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PMID:[Sleep disorders as a risk factors for stroke]. 1187 95

Although the incidence of strokes is not maximal during sleeping hours, several lines of evidence make it probable that sleep in combination with breathing disorders like snoring and obstructive apneas are risk factors for ischemic strokes: the natural history of snoring and obstructive sleep apnea shows a higher incidence of strokes than in undisturbed sleep, the prevalence of snoring and sleep apneas in stroke patients is by far higher than in non-stroke patients; odds-ratios of stroke are higher in snorers and apneic patients than in normals, although the correction for confounders seems never perfect. The analysis of potential pathomechanisms linking sleep disordered breathing to strokes is another approach to the main topic: snoring and sleep apnea induce hypertension and arrhythmia, the carotid intima-media-thickness is increased, carotid atheromas are more common among apneics than among normals, the flow in the A. cerebri media is as well altered as the reaction to angiotensine II, noradrensine, isoproterenol and bradykinin. Homocysteine is increased, plasminogen activator inhibitor type 1 is inhibited and platelets are activated leading to an increased risk of thrombosis. There are no studies showing the effectiveness of treatment with nasal continuous positive airway pressure (nCPAP) on the rehabilitation of apneic stroke patients, but the outcome of non-apneic stroke patients is better than that of apneic stroke patients.
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PMID:Sleep and stroke. 1192 38

Obstructive sleep apnoea is a disease of increasing importance because of its neurocognitive and cardiovascular sequelae. Abnormalities in the anatomy of the pharynx, the physiology of the upper airway muscle dilator, and the stability of ventilatory control are important causes of repetitive pharyngeal collapse during sleep. Obstructive sleep apnoea can be diagnosed on the basis of characteristic history (snoring, daytime sleepiness) and physical examination (increased neck circumference), but overnight polysomnography is needed to confirm presence of the disorder. Repetitive pharyngeal collapse causes recurrent arousals from sleep, leading to sleepiness and increased risk of motor vehicle and occupational accidents. The surges in hypoxaemia, hypercapnia, and catecholamine associated with this disorder have now been implicated in development of hypertension, but the association between obstructive sleep apnoea and myocardial infarction, stroke, and congestive heart failure is not proven. Continuous positive airway pressure, the treatment of choice for obstructive sleep apnoea, reduces sleepiness and improves hypertension.
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PMID:Obstructive sleep apnoea. 1250 19

Four basic control mechanisms of breathing (brainstem respiratory centre, peripheral and central chemoreceptors, intero- and exteroceptive reflexes and suprapontine influences), as well as their sleep-related disorders are analysed. A decrease in central chemoreceptor sensitivity to CO2 and an increase in upper airway resistance during sleep result in hypoventilation and mild hypoxaemia already in physiological conditions. Compensatory increase in ventilatory effort with synchronous inhibition of pharyngeal dilators during sleep reduces the upper airway lumen manifesting with snoring, upper airway resistance syndrome, and OSA. The resulting hypoxaemia may cause marked cardiovascular, neuro-psychic, endocrine-metabolic and behavioural disorders. The augmented ventilatory effort and hypoxaemia evoke reflex dilation of airways and arousal from sleep, stimulating the sympatho-adrenal system, which provokes autoresuscitation by gasping preventing fatal asphyxia. Failure of this autoresuscitation mechanism seems to cause SIDS. Elimination of voluntary breathing by sleep either in Ondine's curse induced by lesions of respiratory centre, or in congenital central hypoventilation syndrome caused by insufficient central chemoreceptors result in respiratory failure and death. Nocturnal attacks of bronchial and cardiac asthma, lung oedema and other consequences of pulmonary congestion are also discussed. The pathomechanism of extreme daytime sleepiness, chronic fatigue, and disorders of memory, cognitive and other brain functions, are also analysed. Severe cardiovascular consequences of SAS may manifest acutely as angina pectoris, myocardial infarction. dysrhythmias, transient ischaemic attacks and even stroke or sudden cardiac death. OSAS may result also in development of hypertension, central obesity, diabetes mellitus, erectile dysfunction, depression, and various behavioural disorders.
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PMID:[Regulation of respiration and its sleep-related disorders]. 1244 39

Previous reports have shown an association between snoring and stroke but it is not clear whether this reflects confounding factors nor whether the association is attributable to obstructive sleep apnoea (OSA). We performed a case-control study of 181 patients admitted to hospital with first-ever stroke and community control subjects matched individually for age, sex and general practitioner. Subjects were interviewed with a structured questionnaire to identify snoring, daytime sleepiness and stroke risk factors. The association between snoring alone and stroke was not statistically significant: odds ratio (95% CI) 1.44 (0.88, 2.41). Daytime sleepiness was, however, significantly associated with stroke: odds ratio 3.07 (1.65, 6.08). Multiple logistic regression showed that hypertension, current smoking, taking alcohol regularly (negatively) and a higher Epworth sleepiness score were independently associated with stroke. The results suggest that the previously reported association between 'simple' snoring and stroke might have been due to poor controlling for confounding variables. Our study suggests an association with greater sleepiness prestroke, the cause of which is unclear, although OSA is a possible candidate.
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PMID:Snoring, daytime sleepiness and stroke: a case-control study of first-ever stroke. 1463 43

Undiagnosed obstructive sleep apnea (OSA) can contribute to hypertension, cardiovascular disease, stroke, and detract from overall quality of life. Dentists can play an important role in detecting, making recommendations for, and treating OSA with oral appliances (OAs). A survey of 18 questions of knowledge and opinion of, educational background for, and clinical experience with OSA and OAs was mailed to 500 general practice dentists in Indiana, United States. Two hundred survey returns produced 192 valid responses. Responders reported strong positive opinions toward OSA and OAs. However, 58% of dentists could not identify common signs and symptoms of OSA, and 55% of dentists did not know the mechanism for mandibular advance devices. Only 39% of dentists could identify snoring, mild OSA, and intolerance to continuous positive airway pressure as possible indications for OA treatment. Respondents reported a general lack of education about both OSA and OAs. Only 31 (16%) were taught about this issue in dental school; 77 (40%) knew little or nothing about OA treatment for OSA patients; 57 (30%) learned from postgraduate training. Cooperation and referrals between dentists and physicians were rated as "poor." Of the responders, 54% never consulted with physicians for a suspected OSA patient in their practice; 75% of dentists reported they have never been referred patients by physicians; and 80% of dentists never or less than five times prescribed OAs to OSA patients. Results suggest a need for increased education and training regarding OSA and OAs in dental school, as well as increased cooperation between dentists and physicians for better patient care.
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PMID:Knowledge, opinions, and clinical experience of general practice dentists toward obstructive sleep apnea and oral appliances. 1521 92

Obstructive sleep apnea hypopnea syndrome (OSAHS) is characterized by repetitive upper airway obstruction during sleep and it is commonly seen in the adult population, 4% in the men, 2% in the women. The most common nocturnal symptom is snoring while the most common daytime symptom is excessive daytime sleepiness. The gold standard in the diagnosis is polysomnography. Nasal continuous positive airway pressure is the most efficient therapy in the treatment and prevention of the disease. The OSAHS may cause cardiovascular complications in long-term, including systemic hypertension, pulmonary hypertension, congestive heart failure, arrhythmias, stroke and myocardial infarction. All these complications increase the morbidity and mortality of OSAHS. In this paper, effects of OSAHS on cardiovascular system were reviewed.
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PMID:[The effects of obstructive sleep apnea hypopnea syndrome on cardiovascular system]. 1575 2

Complete or partial collapse of the upper airway during sleep has different effects on the human body ranging from noisy breathing (snoring) to significant cardiovascular sequelae as seen in obstructive sleep apnea (OSA). Snoring is very common in the adult population and has been associated with morbidity in epidemiological studies. A variety of treatments may be used for primary snoring (snoring without symptoms) but none are universally successful. The upper airway resistance syndrome is thought to occur when incomplete obstruction of the upper airway results in frequent disruptions in sleep. Whether it is a true "syndrome" or just one end of the continuum of OSA is unclear. Obstructive sleep apnea causes not only sleep disruption but oxygen desaturation. It has been associated with numerous cardiovascular sequelae, including hypertension (systemic and pulmonary), arrhythmias, and stroke. Nasal continuous positive airway pressure (CPAP) is the current treatment of choice, with lesser alternatives including oral appliances, surgery, and weight loss. Further study on outcomes is required to determine how aggressively to treat these syndromes.
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PMID:Obstructive sleep apnea syndromes. 1605 14

The aim of the study was to evaluate the prevalence, the covariates and determinants of respiratory pauses during sleep in a sample of French middle-aged males. Study subjects were 850 active males, aged 22-66 years; 88.4% of them answered the question on breathing pauses during sleep from a structured, validated sleep questionnaire. Forty-one (=5.4%) subjects reported breathing pauses at least once a week; these "positive responders" were older, heavier and had larger neck- and waist girths as compared to subjects with negative answers. Loud habitual snoring, various sleep disturbances, excessive daytime sleepiness, a doctor diagnosis of sleep apnoea, history of stroke and hypertension were significantly more frequent among subjects with breathing pauses during sleep. The prevalence found in this survey was close to that reported from the UK (5.2%). However, by logistic regression, we identified novel determinants of breathing pauses i.e. habitual snoring, loud snoring, and excessive sleepiness, factors well known in clinical setting, but never previously reported in epidemiologic studies.
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PMID:Witnessed breathing pauses during sleep: a study in middle-aged French males. 1614 Feb 28

Sleep-disordered breathing is very common and is associated with an increased risk of cardiovascular disease, cardiac arrhythmia and stroke. There are two types of sleep apnea: obstructive and central. The objective of this review is to provide a broad perspective of the pathophysiological and clinical aspects of the two types of apnea and to discuss their cardiovascular adverse effects. The diagnosis of sleep apnea syndrome is based on polysomnography, and severity is measured with an apnea-hypopnea index that counts the total number of apneas per hour of sleep. Recent large epidemiologic studies have shown that sleep apnea affects about 16% of men and 5% of women between 30 and 65 years of age. Obstructive sleep apnea is characterized by abnormal collapse of the pharyngeal airway during sleep, snoring, vigorous inspiratory efforts causing frequent arousal, and excessive daytime drowsiness. Central sleep apnea with Cheyne-Stokes respiration is a form of periodic breathing with frequent periods of hyperventilation, and carries a poor prognosis in patients with heart failure. Obstructive apnea can also have substantial health consequences. Although the exact mechanism linking sleep apnea with cardiovascular disease is unknown, there is evidence that obstructive apnea is associated with a group of proinflammatory and prothrombic factors that are also important in the development of atherosclerosis. Nocturnal and daytime sympathetic activity is elevated after sleep apnea. Autonomic abnormalities include an increased resting heart rate, decreased cardiac rhythm activity, and increased blood pressure variability. Obstructive apnea is associated with endothelial dysfunction, increased C-reactive protein and cytokine expression, elevated fibrinogen levels and decreased fibrinolytic activity. Enhanced platelet activity and aggregation, leukocyte adhesion and accumulation of endothelial cells are common in both obstructive apnea and atherosclerosis. Surges in sympathetic activity, blood pressure, ventricular wall tension and afterload adversely affect ventricular function. Many studies have shown that patients with obstructive apnea have an increased incidence of daytime hypertension, and this syndrome is recognized as an independent risk factor for hypertension. Obstructive apnea is associated with myocardial ischemia (silent or symptomatic), acute coronary events, stroke and transient ischemic attacks, cardiac arrhythmia, pulmonary hypertension and heart failure. Central sleep apnea is frequent in severe heart failure. Most heart failure patients with pulmonary congestion chronically hyperventilate because of stimulation of vagal irritant receptors and central and peripheral chemosensitivity. When PaCO2 falls below the threshold required to stimulate breathing, the central drive to respiratory muscles and air inflow ceases and central apnea ensues. Apnea, hypoxia, CO2 retention and arousals provoke elevated sympathetic activity, increased afterload and elevated left ventricular transmural pressure, and promote the progression of heart failure. Tentative relationships have been identified between central apnea and markers of inflammation, oxidative stress and endothelial dysfunction. Recent mid-terms trials showed that nocturnal use of positive airway pressure in patients with the two types of apnea alleviates symptoms, reduces sympathetic activity, improves ventricular function and quality of life, and reduces daytime drowsiness. More studies are needed to understand the mechanisms underlying the relationship between sleep apnea and cardiovascular disease, but clinicians should be aware of this link and should attempt to identify patients with these syndromes.
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PMID:[Sleep apnea syndromes and cardiovascular disease]. 1614 10


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