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

Wakefulness, NREM sleep, and REM sleep are accompanied by specific changes in breathing control, which arise from the interaction of automatic (metabolic, involuntary) and behavioural (voluntary and involuntary control systems. Considering the complexity in the neuroanatomy and neurophysiology of breathing control, it is not surprising that neurologic disorders are frequently accompanied by sleep disordered breathing. An introduction on pathophysiology, clinical features, diagnosis, and treatment of sleep disordered breathing in such diseases as stroke, epilepsy, dementia, spinal cord disease, polyneuropathies, and myopathies is presented.
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PMID:Sleep disordered breathing in neurologic disorders. 1204 98

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

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

Obstructive sleep apnea can be diagnosed in approximately 60% of stroke survivors in the postacute period and has been found to be associated with increased mortality and a worse functional outcome at 3 and 12 mo after discharge. In this study, 38 patients undergoing rehabilitation after stroke underwent sleep studies by using the AutoSet Portable II Plus device; obstructive sleep apnea was found in 18 of the patients, and five consecutively diagnosed patients were treated on the ward with nasal continuous positive airway pressure. The research has shown that it is feasible to routinely implement a diagnostic and therapeutic approach to sleep apnea on the rehabilitation ward, which is hoped to have a positive influence on mortality, functional outcome, and secondary prevention.
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PMID:Diagnosis and treatment of obstructive sleep apnea in a stroke rehabilitation unit: a feasibility study. 1217 72

Sleep apnea (SA) syndromes of different etiologies are known to induce complications including cardiovascular diseases and stroke. However, the exact mechanisms involved in cerebral ischemia remain obscure. We measured the cerebral blood flow velocities (CBFV) by means of transcranial Doppler sonography in an 81-year-old patient who presented with an acute ischemic stroke caused by an intracranial middle cerebral artery (MCA) stenosis in the presence of SA syndrome. During apnea episodes simultaneous recordings revealed reduced intra-arterial oxygen but increased carbon dioxide saturation. This resulted in an increased CBFV (220 to 320 cm/s) and suggested intermittent hemodynamic relevance of a structurally only moderate MCA stenosis. Intracranial artery stenosis can become hemodynamically significant due to episodic hypercapnia in patients with SA. This may cause ischemic infarction in the periphery of the related cerebral vascular territories.
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PMID:Acceleration of cerebral blood flow velocity in a patient with sleep apnea and intracranial arterial stenosis. 1224 90

Sleep-disordered breathing (obstructive and central sleep apnea) is common in persons who have had a cerebrovascular accident (CVA). This article describes both sleep-disordered breathing and CVAs and reviews the related risk factors that link them together. In addition, the article discusses sleep-disordered breathing after CVA. The article concludes by presenting the clinical implications of this topic for nurses.
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PMID:Sleep-disordered breathing and stroke. 1235 90

Sleep disordered breathing (SDB) frequently comes to medical attention for the first time when patients are hospitalized for diagnosis and treatment of an associated condition (eg, poorly controlled hypertension, myocardial infarction, congestive heart failure, stroke, or problems related to management of diabetes mellitus). Diagnosis of SDB is generally performed in a specialized facility, which is often inconvenient and expensive for the hospitalized patient. Expectant perioperative management of patients with sleep apnea is critical, particularly if they are previously undiagnosed. An ideal diagnostic strategy for these patients has not been defined. Continuous positive airway pressure (CPAP) is the mainstay of treatment of patients with sleep apnea. Unfortunately, it is often difficult for very ill patients to tolerate CPAP, unless it is administered with a high level of expertise.
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PMID:Management of the hospitalized patient with sleep disordered breathing. 1239 59

Patients with sleep disordered breathing (SDB) are at increased risk for cardiovascular disease including hypertension, angina, myocardial infarction, and stroke. Neurohumoral and hemodynamic responses to untreated sleep apnea are likely mechanisms that produce functional and structural changes within the cardiovascular system. Obesity, higher blood pressure, and advancing age, which are common characteristics of patients with SDB, contribute to the overall risk for cardiovascular disease. Recent studies indicate that OSA is associated with or aggravates other risk markers for cardiovascular disease. These factors include leptin, C-reactive protein, homocysteine, and insulin resistance syndrome. Elevations in C-reactive protein and glucose intolerance may be correlated with the severity of SDB. The impact of alleviating SDB on these cardiovascular risk factors has not been fully elucidated. Regardless, assessment of overall cardiovascular risk in patients with sleep apnea is warranted to identify those individuals that are high-risk who require immediate attention and intervention or in those that should be treated more aggressively.
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PMID:Sleep disordered breathing and risk factors for cardiovascular disease. 1239 60

The evolution of subjective sleep and sleep electroencephalogram (EEG) after hemispheric stroke have been rarely studied and the relationship of sleep variables to stroke outcome is essentially unknown. We studied 27 patients with first hemispheric ischaemic stroke and no sleep apnoea in the acute (1-8 days), subacute (9-35 days), and chronic phase (5-24 months) after stroke. Clinical assessment included estimated sleep time per 24 h (EST) and Epworth sleepiness score (ESS) before stroke, as well as EST, ESS and clinical outcome after stroke. Sleep EEG data from stroke patients were compared with data from 11 hospitalized controls and published norms. Changes in EST (>2 h, 38% of patients) and ESS (>3 points, 26%) were frequent but correlated poorly with sleep EEG changes. In the chronic phase no significant differences in sleep EEG between controls and patients were found. High sleep efficiency and low wakefulness after sleep onset in the acute phase were associated with a good long-term outcome. These two sleep EEG variables improved significantly from the acute to the subacute and chronic phase. In conclusion, hemispheric strokes can cause insomnia, hypersomnia or changes in sleep needs but only rarely persisting sleep EEG abnormalities. High sleep EEG continuity in the acute phase of stroke heralds a good clinical outcome.
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PMID:Evolution of sleep and sleep EEG after hemispheric stroke. 1246 1

The role of patent foramen ovale (PFO) in cryptogenic stroke is still debated, but from recent follow-up studies it seems that the amount of right-to-left shunt (RLS) and the association with atrial septal aneurysm (ASA) are major determinants of stroke recurrence. PFO and RLS through the atrial chambers have been recently studied in a number of conditions not or marginally related to cerebrovascular disease. Historically the first studies addressed the presence of RLS in scuba divers as a possible abnormality related to decompression sickness (DS) of unknown aetiology. Despite initial debate there is now robust evidence to claim that patency of foramen ovale increases the risk of developing DS by two and half to four times. Patients with PFO-related DS tend to have early occurrence of symptoms after surfacing and a clinical presentation that indicates brain or upper cervical spinal cord involvement. Recent reports suggest that divers with hemodynamically significant RLS may have an increased risk of developing clinically asymptomatic multiple brain lesions. PFO has been found in patients suffering from migraine with aura with approximately the same frequency as that encountered in cryptogenic stroke patients. This finding has prompted speculations on the possible role of RLS in increasing the stroke risk in migraineurs and in the pathophysiology of the aura. Recent reports showing that migraine with aura is dramatically improved after transcatheter closure of PFO suggest that migraine with aura may indeed be triggered by humoral factors that reach the brain by escaping the pulmonary filter. A RLS is involved in a rare condition known as platypnea-orthodeoxia and perhaps underlies an increased risk of cerebral complications after major orthopedic surgery. Valsalva-like activities often precede the occurrence of attacks of transient global amnesia (TGA) and abnormalities consistent with hypoperfusion of deep limbic structures have been reported during a typical TGA episode. This had raised the hypothesis that TGA may be triggered by paradoxical embolism of platelets aggregates in the posterior circulation, but the search for an increased frequency of PFO in TGA patients has yielded conflicting results. Conditions that determine an increase in pulmonary pressure may facilitate the opening of the virtual interatrial valve and thus promoting shunting of blood to the left heart chambers which in turn might contribute to further desaturation of arterial blood. It is therefore not surprising that RLS has been found in 70% of patients with chronic obstructive pulmonary disease and increased pulmonary pressure and in the same proportion of patients with obstructive sleep apnoea, a condition that ultimately may result in pulmonary hypertension. In conclusion, from the evidence gathered so far the picture is emerging of an important role of PFO in a number of non-stroke conditions, either as causative factor or as associated condition predisposing to complications. The availability of simple diagnostic techniques such as transcranial Doppler (TCD) to assess RLS will undoubtedly contribute a great deal of knowledge on the relevance in medicine of this hitherto neglected condition.
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PMID:Clinical impact of patent foramen ovale diagnosis with transcranial Doppler. 1247 Aug 46


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