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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Daytime complaints like fatigue, sleepiness and cognitive dysfunction in neuromuscular disease can be due to nocturnal hypercapnia and hypoxemia. Daytime respiratory diagnostics does not reflect sleep disordered breathing. Nocturnal pulse oxymetry and capnography were performed in 11 patients (15-75 years old) with different slowly progressive neuromuscular diseases. Only four patients complained of dyspnea. Pulmonary function was abnormal in three patients. Blood gas samples showed a hypoxemia in three patients. Pulse oxymetry results were pathological in six patients. Nine patients presented abnormal capnographies. According to these results either nocturnal oxygen application was initiated or ventilatory parameters were modified. Daytime symptoms and muscular strength improved markedly. Capnography and pulse oxymetry should be performed during the course of neuromuscular disease to detect respiratory insufficiency. Capnography seems to be a more sensitive indicator for respiratory impairment especially when artificial ventilation has been initiated.
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PMID:Respiratory monitoring in neuromuscular disease - capnography as an additional tool? 1151 50

The authors have investigated whether treatment of sleep apnoea with nasal continuous positive airway pressure (nCPAP) improves depressive symptoms, personal activities of daily living (ADL), cognitive functioning and delirium in patients that have suffered a stroke. Sixty-three patients consecutively admitted to a stroke rehabilitation unit 2-4 weeks after a stroke, with an apnoea/hypopnoea index > or =15, were randomized to either nCPAP treatment (n=33) or a control group (n=30). Four patients dropped out after randomization. Both groups were assessed at baseline and after 7 and 28 nights using the Montgomery-Asberg Depression Rating Scale (MADRS), Barthel-ADL index, and the Mini-Mental State Examination (MMSE) scale. Compared to the control group, depressive symptoms (MADRS total score) improved in patients randomized to nCPAP treatment (p=0.004). No significant treatment effect was found with regard to delirium, MMSE or Barthel-ADL index. Delirium and low cognitive level (MMSE score) explained poor compliance with nCPAP. Depressive symptoms are reduced through nasal continuous positive airway pressure treatment in patients with severe stroke and sleep apnoea. Compliance with nasal continuous positive airway pressure treatment is a problem in stroke patients, especially when delirium and severe cognitive impairment occur.
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PMID:Nasal continuous positive airway pressure in stroke patients with sleep apnoea: a randomized treatment study. 1210 81

Sleep apnoea syndrome (SAS) is a known risk factor for vascular diseases and stroke. Structural brain damage, manifesting as an overt neurological deficit or more subtly as cognitive dysfunction, is a frequent symptom in SAS. The presence of a biochemical marker of cerebral injury would be of great benefit in SAS to screen for even small brain damage and to monitor efficiacy of therapy. Therefore, in 10 patients with mild SAS (age 50.8+/-9.9 yrs, respiratory disturbance index (RDI) 18+/-3.6, lowest arterial oxygen saturation (min Sa,O2) 80.5+/-4.06%) and nine patients with severe SAS (age 50.3+/-11.5 yrs, RDI 75.4+/-21.7, min Sa,O2 56.56+/-14.58%), serum concentrations of neuron-specific enolase (NSE), S-100beta protein, and beta-trace were measured just before and after sleep using commercially available assays. Only serum levels in the normal range could be found, independent of when the blood was taken or the degree of SAS. Structural cerebral injury caused by sleep apnoea syndrome in patients without neurological symptoms or previous cerebrovascular events may be too small to produce a measurable increase in S-100beta, neuron-specific enolase and beta-trace serum concentrations or subclinical cerebral damage may be outside the lower detection limits of the analytical methods which were used. There is a need for biochemical markers and more sensitive methods for detecting small cerebral injury in sleep apnoea syndrome.
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PMID:Biochemical markers of cerebrovascular injury in sleep apnoea syndrome. 1216 64

Epidemiologic literature suggests that persons with clinically diagnosed sleep apnoea frequently have impaired cognitive function, but whether milder degrees of sleep-disordered breathing (SDB) are associated with cognitive dysfunction in the general population is largely unknown. Approximately 1700 subjects free of clinically diagnosed SDB underwent at-home polysomnography (PSG) as part of the Sleep Heart Health Study (SHHS) and completed three cognitive function tests within 1-2 years of their PSG: the Delayed Word Recall Test (DWR), the WAIS-R Digit Symbol Subtest (DSS), and the Word Fluency test (WF). A respiratory disturbance index (RDI) was calculated as the number of apnoeas and hypopnoeas per hour of sleep. After adjustment for age, education, occupation, field centre, diabetes, hypertension, body-mass index, use of CNS medications, and alcohol drinking status, there was no consistent association between the RDI and any of the three cognitive function measures. There was no evidence of a dose-response relation between the RDI and cognitive function scores and the adjusted mean scores by quartiles of RDI never differed from one another by more than 5% for any of the tests. In this sample of free-living individuals with mostly mild to moderate levels of SDB, the degree of SDB appeared to be unrelated to three measures of cognitive performance.
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PMID:Measures of cognitive function in persons with varying degrees of sleep-disordered breathing: the Sleep Heart Health Study. 1222 Mar 23

Sleep related breathing disorders (especially sleep apnea syndrome--SAS) limit the patient through deteriorated nocturnal sleep, insufficient wakefulness, daytime inefficiency and tiredness including a cognitive impairment, through higher rate of road accidents, higher co morbidity, through impaired quality of life and higher mortality. The society pays for the SAS patient higher medical costs and other expenses related to the accidents, co morbidity and lower professional productivity.
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PMID:[Socioeconomic aspects of sleep-related breathing disorders]. 1244 38

Patients with Parkinson's disease (PD) and parkinsonian syndromes (eg, dementia with Lewy bodies, multisystem atrophy, and Shy-Drager syndrome) suffer from daytime sleepiness. Sleepiness in PD is common (10% to 50% of patients) and very real, often approaching levels observed in the prototypical disorder of sudden-onset sleep, viz, and narcolepsy with cataplexy. Physicians need to be vigilant in assessing parkinsonian patients for sleepiness, because treatment can dramatically enhance quality of life and prevent the significant morbidity and mortality that attends daytime sleepiness. Men with advanced disease, cognitive impairment, drug-induced psychosis, and orthostatic hypotension are most at risk for developing pathologic sleepiness. Because primary sleep disorders can coexist with Parkinsonism (eg, sleep apnea, insufficient or interrupted sleep), these potential causes should be carefully assessed with polysomnography and treated appropriately. Dopaminomimetics may exacerbate sleepiness in a small subset of patients. The primary pathologies involved in Parkinsonism appear to be the greatest contributors to the development of daytime sleepiness. Sleepiness in Parkinsonism, especially a narcolepsy-like phenotype, may necessitate treatment with wake-promoting agents, such as bupropion, modafinil, or traditional psychostimulants.
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PMID:Sleepiness and Unintended Sleep in Parkinson's Disease. 1267 Apr 12

Vascular dementia is the second most common type of dementia. The subcortical ischaemic form (SIVD) frequently causes cognitive impairment and dementia in elderly people. SIVD results from small-vessel disease, which produces either arteriolar occlusion and lacunes or widespread incomplete infarction of white matter due to critical stenosis of medullary arterioles and hypoperfusion (Binswanger's disease). Symptoms include motor and cognitive dysexecutive slowing, forgetfulness, dysarthria, mood changes, urinary symptoms, and short-stepped gait. These manifestations probably result from ischaemic interruption of parallel circuits from the prefrontal cortex to the basal ganglia and corresponding thalamocortical connections. Brain imaging (computed tomography and magnetic resonance imaging) is essential for correct diagnosis. The main risk factors are advanced age, hypertension, diabetes, smoking, hyperhomocysteinaemia, hyperfibrinogenaemia, and other conditions that can cause brain hypoperfusion such as obstructive sleep apnoea, congestive heart failure, cardiac arrhythmias, and orthostatic hypotension. Cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL)and some forms of cerebral amyloid angiopathy have a genetic basis. Treatment is symptomatic and prevention requires control of treatable risk factors.
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PMID:Subcortical ischaemic vascular dementia. 1284 65

The obstructive sleep apnoea syndrome (OSAS) is caused by upper airway collapse during sleep. These episodes are associated with recurrent oxyhaemoglobin desaturations and arousals which lead to disruption of the sleep pattern and cognitive deterioration. Factors such as age, male sex, menopause, tobacco and alcohol consumption and anatomic abnormalities are demonstrated risk factors for OSAS development. Obesity, specially of abdominal type, is also a very strong predictor of OSAS, increasing the risk of apnoea by ten times. OSAS prevalence may reach 80% and 50% en males and females with morbid obesity respectively. OSAS induces sympathoexcitation, insulin resistance, renin-angiotensin system activation, oxidative stress, endothelial dysfunction, hypercoagulability and reduction of fibrinolysis leading to hypertension and increased cardiovascular risk. The best diagnostic procedure is polysomnography. Obesity treatment is followed by a dramatic improvement in OSAS. Weight loss of 10% results in reductions of apnoea index by 26%. Application of a positive pressure system is a very effective treatment for OSAS which reduces the apnoea index and improves cardiovascular risk and cognitive impairment.
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PMID:[The obstructive sleep apnoea syndrome in obesity: a conspirator in the shadow]. 1538 14

Sleep-disordered breathing in children has been associated with cognitive impairment. The purpose of this study was to examine the impact of tonsillectomy and adenoidectomy (T&A) on sleep, respiration and cognitive function in children of pre-school age with obstructive sleep apnoea (OSA) from a low-income community population. Altogether, 19 children attending state-funded pre-school programmes underwent overnight polysomnography and cognitive assessment before and following surgical treatment for OSA; 19 matched controls were also assessed. Following T&A, OSA subjects' delta sleep increased, rapid eye movement sleep decreased, and respiratory and arousal indices improved. There were no significant differences in OSA subjects' post-operative sleep or respiratory measures compared to controls. Prior to T&A, cognitive scores were significantly lower in OSA subjects versus controls; following T&A, OSA subjects' scores improved compared to pre-operative scores and did not differ from those of matched controls. Following tonsillectomy and adenoidectomy, at-risk pre-schoolers recruited directly from the community showed normalised sleep and respiratory patterns and improved cognitive scores. These findings, in this uniquely vulnerable population, which is unlikely to seek evaluation and treatment for obstructive sleep apnoea, underscore the potential value of outreach screening programmes for sleep-disordered breathing, particularly among low-income groups of pre-school age.
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PMID:Cognition, sleep and respiration in at-risk children treated for obstructive sleep apnoea. 1568 82

Ischemic or hemorrhagic cerebrovascular disease (CVD) produces injury of brain regions important for executive function, behavior, and memory leading to decline in cognitive functions and vascular dementia (VaD). Cardiovascular disease may cause VaD from hypoperfusion of susceptible brain areas. CVD may worsen degenerative dementias such as Alzheimer disease (AD). Currently, the global diagnostic category for cognitive impairment of vascular origin is vascular cognitive disorder (VCD). VCD ranges from vascular cognitive impairment (VCI) to VaD. The term VCI is limited to cases of cognitive impairment of vascular etiology, without dementia; VCI is equivalent to vascular mild cognitive impairment (MCI). Risk factors for VaD include age, hypertension, diabetes, smoking, cardiovascular disease (coronary heart disease, congestive heart failure, peripheral vascular disease), atrial fibrillation, left ventricular hypertrophy, hyperhomocysteinemia, orthostatic hypotension, cardiac arrhythmias, hyperfibrinogenemia, sleep apnea, infection, and high C-reactive protein. Research on biomarkers revealed increased CSF-NFL levels in VaD, whereas CSF-tau was normal. CSF-TNF-alpha, VEGF, and TGF-beta were increased in both AD and VaD. VaD shows low CSF acetylcholinesterase levels. This condition responds to acetylcholinesterase inhibitors, confirming the central role of cholinergic deficit in its pathogenesis. Evidence strongly suggests that control of vascular risk factors, in particular hypertension, could prevent VaD.
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PMID:Vascular dementia. Advances in nosology, diagnosis, treatment and prevention. 1587 77


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