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

Obesity is known to predispose to obstructive sleep apnea (OSA), a condition characterized by repeated episodes of apnea or hypopnea during sleep, due to the interruption of airflow through the nose and mouth. These episodes lead to the fragmentation of sleep and to decrease in oxyhaemoglobin saturation. Patients with massive obesity, with or without daytime hypersomnolence should be systematically screened for OSA, because many of them appear to be asymptomatic and unaware of their breathing abnormalities during sleep. Polysomnography (PSG) in an attended hospital laboratory setting is the gold standard for the diagnosis of OSA. However portable recording devices can be used for screening with good sensibility and specificity, and even for diagnosis when the apnea-hypopnea index is high. However the final diagnosis can only be carried out in a sleep laboratory using PSG by highly-qualified personnel, because of the limitations of the portable recording device. There is a strong association between OSA and the risk of traffic accidents. It has been established that OSA affects quality of life. There is also increasing evidence that OSA is an independent risk factor for cardio-vascular diseases. This has been successfully demonstrated for hypertension by prospective studies. But the evidence remains weak for myocardial infarction, stroke or mortality. Treating OSA with continuous positive airway pressure (CPAP) is the treatment of choice. CPAP improves quality of life, driving simulator performance, blood pressure and sleepiness, as demonstrated by randomised placebo controlled trials. The majority of obese OSA patients are currently not being offered diagnosis testing and treatment. It's a real challenge due to the epidemic increase of obesity prevalence. Portable recording devices could be available outside the sleep laboratory in nutrition department, where morbid obesity is treated. This emphasizes the need for a real collaboration between these departments and sleep experts.
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PMID:[How do you really know if the obese patient has sleep apnea?]. 1273 28

Sleep-related breathing disorders are strongly associated with increased risk of stroke independent of known risk factors. The direction of causation favors sleep-disordered breathing leading to stroke rather than the other way around, although definitive proof of this awaits the results of prospective cohort studies. If causal, even a moderately elevated risk of stroke coupled with the high prevalence of sleep-disordered breathing could have significant public health implications. The relationship between sleep-disordered breathing and stroke risk factors is complex, and likely part of the risk for cerebrovascular events is because of higher cardiovascular risk factors in patients with increased RDI. The mechanisms underlying this increased risk of stroke are multi-factorial and include reduction in cerebral blood flow, altered cerebral autoregulation, impaired endothelial function, accelerated atherogenesis, thrombosis, and paradoxic embolism. Because of the effects of sleep-disordered breathing on vascular tone, hypertension is believed to be a major mechanism by which sleep-disordered breathing might influence risk of stroke. Because sleep-related breathing disorders are treatable patients with stroke/TIA should undergo investigation, with a thorough sleep history interview, physical examination, and polysomnography. Treatment of sleep apnea has been shown to improve quality of life, lower blood pressure, improve sleep quality, improve neurocognitive functioning, and decrease symptoms of excessive daytime sleepiness [98]. Further treatment trials are needed to determine whether treatment improves outcome after stroke and whether treatment may serve as secondary prophylaxis and modify the risk of recurrent stroke or death.
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PMID:Sleep-disordered breathing and stroke. 1280 Jul 80

Intrathecal baclofen (ITB) therapy is a widely recognized management technique for severe, disabling spasticity in individuals with cerebral palsy and spinal and brain injuries. Its utility in the stroke population has only been recognized recently. Unlike the aforementioned patient populations, many stroke survivors are ambulatory and are able to maintain a certain degree of functional independence through compensatory use of the uninvolved limbs. Clinicians often fail to recognize the potential enhancement in the function of these individuals if they gain better control of their spastic limbs. Other spasticity treatments, such as oral medications and neurolytic procedures, offer the advantage of being nonsurgical; however, not every stroke patient will respond well to them. Some patients may not tolerate the systemic side effects of oral medications, such as drowsiness and sedation. In patients with severe multilimb spasticity, phenol and even high doses of botulinum toxin may not adequately control spasticity. ITB therapy offers the advantage of effectively decreasing severe, diffuse spasticity without causing untoward effects on arousal and cognition. This article will review the efficacy of ITB therapy in treating spasticity and enhancing function in stroke survivors.
Top Stroke Rehabil 2001
PMID:Intrathecal baclofen therapy for stroke-related spasticity. 1452 50

Obstructive sleep apnea is an increasingly well-recognized disease characterized by periodic collapse of the upper airway during sleep. This leads to either complete or partial obstruction of the airway, resulting in apneas, hypopneas, or both. This disorder causes daytime somnolence, neurocognitive defects, and depression. It affects almost every system in the body, resulting in an increased incidence of hypertension, cardiovascular disease, stroke, pulmonary hypertension, cardiac arrhythmias, and altered immune function. It also increases the risk of having an accident, presumably as a result of associated somnolence. The gold standard for the diagnosis of sleep apnea is an overnight polysomnogram. Split-night studies are becoming increasingly common and allow for quicker implementation of therapy at a reduced cost. Treatment options for sleep apnea include weight loss, positional therapy, oral devices, continuous positive airway pressure (CPAP), and upper airway surgery. CPAP is the most efficacious and widely used therapy. Its complications include nasal congestion or dryness, mask discomfort, and claustrophobia. Heated humidifiers, newer types of masks, and nasal steroids have improved tolerance of this therapy. Bilevel positive-pressure therapy can be considered for patients who find it difficult to exhale against the consistently increased pressure of CPAP. The disease requires aggressive treatment to improve quality of life and prevent its complications.
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PMID:Obstructive sleep apnea. 1456 40

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

Obstructive sleep apnea is common and considered to be a risk factor for hypertension, stroke and coronary disease. Accordingly, the presence of sleep apnea is probably a predictor of premature death. Continuous positive airway pressure is an effective treatment of obstructive sleep apnea. It has been demonstrated that such treatment improves daytime sleepiness and quality-of-life. To determine mortality in obstructive sleep apnea patients treated with nasal continuous positive airway pressure, we followed 296 patients given continuous positive airway pressure for 11 years 6 months. At the end of the study 26 of the 296 patients had died, mainly from cardiovascular disease. Mortality was 7% (95% confidence interval: 3%-9%) at 5 years. Three independent factors of death identified by forward stepwise selection were included in a Cox analysis. These factors were 1) smoking as a categorical covariate (>30 pack-years), 2) age and 3) forced expiratory volume in 1 s. When the 52 patients with an associated chronic obstructive pulmonary disease (forced expiratory volume in 1 s/vital capacity<0.65) with obstructive sleep apnea were excluded form analysis, mortality of the 244 remailing patients was 2% at 5 years, a rate observed in the general population. Subsequently, it appears that nasal continuous positive airway pressure corrects for the risk of premature death suspected in obstructive sleep apnea patients. Mortality in obstructive sleep apnea patients treated with continuous positive airway pressure is near to that of the general population, particularly when patients with an associated chronic respiratory disease are excluded.
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PMID:[Mortality in treated sleep apnea syndrome]. 1464 8

To determine if oral/systemic delivery of baclofen can effectively decrease spastic hypertonia due to acquired brain injury (traumatic brain injury, stroke, anoxia, or encephalopathy). Tertiary care outpatient rehabilitation center directly attached to a university hospital. Patients were a convenience sample recruited consecutively who had been referred for treatment of their spastic hypertonia to our spasticity clinic over a 5-year period. The spastic hypertonia was due to an acquired brain injury by either traumatic brain injury (TBI), stroke, or anoxic brain injury. All patients were more than 6 months postinjury or illness. Retrospective review of patients before and after initiation of treatment with oral baclofen, per standardized clinical data sheets. Thirty-five patients (22 TBI patients) were started on oral baclofen and were reevaluated between 1 to 3 months after initiation of treatment. Data for motor tone (Ashworth scores), spasm scores (Penn spasm frequency score), and deep tendon reflex scores were collected on the affected upper extremity (UE) and lower extremity (LE) side(s). Normal extremities were not assessed. Differences over time were assessed via descriptive statistics and Wilcoxon signed-rank. After 1 to 3 months of treatment when subjects had reached their maximal tolerated dosage, the average LE Ashworth score in the affected lower extremities (LEs) decreased from 3.5 to 3.2 (P =.0003), the reflex score decreased from 2.5 to 2.2 (P =.0274), and there was no statistical difference in the spasm score (P >.05). When the 22 TBI patients are analyzed separately, the average LE Ashworth score decreased from 3.5 to 3.2 (P =.0044) and the reflex score decreased from 2.7 to 2.0 (P =.0003). There was no statistically significant change in UE tone, spasm frequency, or reflexes after 1 to 3 months of treatment (P >.05). The average dosage at follow-up was 57 mg/day of baclofen (range 15-120 mg/day). There was a 17% incidence of somnolence that limited the maximum daily dosage of the medication. The oral delivery of baclofen is capable of reducing LE spastic hypertonia resulting from acquired brain injury. The lack of effect upon the upper extremities may be due to receptor specificity issues. GABA-B receptors may be less involved in the modulation of UE spastic hypertonia.
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PMID:Orally delivered baclofen to control spastic hypertonia in acquired brain injury. 1524 21

Obstructive sleep apnea syndrome (OSAS) is characterized by repeated oropharyngeal occlusions occurring during sleep. The prevalence of moderate OSAS (with an apnea-hypopnea index = or >15/h) is 9% and 4% in male and female, respectively. It is associated with an abnormally high frequency of cardiovascular disease (hypertension, stroke, coronary heart disease) and excessive daytime sleepiness responsible for an increased frequency of work and road accidents. Because the treatment of OSAS provides many benefits to patients and society, it is very important to obtain an early diagnosis. The diagnosis of OSAS is based on the combination of characteristic clinical features plus compatible findings on instrumental tests in which multiple physiologic signals are monitored simultaneously during a night of sleep. A full night polysomnography, conducted by a technologist in a sleep laboratory, is the gold standard for the diagnosis of suspected OSAS, but the capacity for performing polysomnography is limited. On the basis of the high incidence and prevalence of OSAS, of the limited number of sleep laboratories, long waiting times and high costs recommendations have been formulated for the use of unattended portable systems in the assessment of OSAS. The main clinical aspects of of OSAS, the diagnostic approach with full night polysomnography and unattended portable systems, the differential diagnosis and some examples of cardiorespiratory portable monitoring are presented in this paper.
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PMID:Diagnosis of sleep apnea. 1528 50

Obstructive sleep apnea (OSA) is a common medical condition that occurs in approximately 5% to 15% of the population. The pathophysiology of OSA is characterized by repetitive occlusions of the posterior pharynx during sleep that obstruct the airway, followed by oxyhemoglobin desaturation, persistent inspiratory efforts against the occluded airway, and termination by arousal from sleep. Obstructive sleep apnea is associated with daytime sleepiness and fatigue, likely due to fragmented sleep from recurrent arousals. Substantial evidence shows that patients with OSA have an increased incidence of hypertension compared with individuals without OSA and that OSA is a risk factor for the development of hypertension. Recent studies show that OSA may be implicated in stroke and transient ischemic attacks. Obstructive sleep apnea appears to be associated with coronary heart disease, heart failure, and cardiac arrhythmias. Pulmonary hypertension may be associated with OSA, especially in patients with preexisting pulmonary disease. Although the exact cause that links OSA with cardiovascular disease is unknown, there is evidence that OSA is associated with a group of proinflammatory and prothrombotic factors that have been identified to be important in the development of atherosclerosis. Obstructive sleep apnea is associated with increased daytime and nocturnal sympathetic activity. Autonomic abnormalities seen in patients with OSA include increased resting heart rate, decreased R-R interval variability, and increased blood pressure variability. Both atherosclerosis and OSA are associated with endothelial dysfunction, increased C-reactive protein, interleukin 6, fibrinogen, and plasminogen activator inhibitor, and reduced fibrinolytic activity. Obstructive sleep apnea has been associated with enhanced platelet activity and aggregation. Leukocyte adhesion and accumulation on endothelial cells are common in both OSA and atherosclerosis. Clinicians should be aware that OSA may be a risk factor for the development of cardiovascular disease.
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PMID:Obstructive sleep apnea and cardiovascular disease. 1530 32

Obstructive sleep apnea (OSA) occurs commonly in the U.S. population and is seen in both obese as well as non-obese individuals. OSA is a disease characterized by periodic upper airway collapse during sleep, which then results in either apnea, hypopnea, or both. The disorder leads to a variety of medical complications. Neuropsychiatric complications include daytime somnolence, cognitive dysfunction, and depression. Increased incidence of motor vehicle accidents has been documented in these patients and probably reflects disordered reflex mechanisms or excessive somnolence. More importantly, vascular disorders such as hypertension, stroke, congestive cardiac failure, arrhythmias, and atherosclerosis occur frequently in these patients. The lungs may be affected by pulmonary hypertension and worsening of asthma. Recent data from several laboratories demonstrate that obstructive sleep apnea is characterized by an inflammatory response. Cytokines are elaborated during the hypoxemic episodes leading to inflammatory responses as marked clinically by elevated C-reactive protein (CRP). As elevated CRP levels are considered markers of the acute phase response and characterize progression of vascular injury in coronary artery disease, it is likely that obstructive sleep apnea could lead to worsening of vasculopathy. Moreover, as inflammatory mechanisms regulate bronchial asthma, it is also likely that cytokines and superoxide radicals generated during hypoxemic episodes could exacerbate reactive airway disease. Patients with Cough, Obstructive sleep apnea, Rhinosinusitis, and Esophageal reflux clustered together can be categorized by the acronym, "CORE", syndrome. The purpose of this manuscript is to review the inflammatory responses that occur in patients with obstructive sleep apnea and relate them to the occurrence of cardiopulmonary disease.
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PMID:Obstructive sleep apnea, inflammation, and cardiopulmonary disease. 1535 23


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