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

THREE CLASSES OF CENTRAL SRBD ARE DISTINGUISHED: 1. Central sleep apnea (CSA), 2. Cheyne-Stokes Respiration as a subgroup of CSA and 3. central hypoventilation syndromes. Reduced or completely absent central respiratory drive without upper airway obstruction is the common feature of central SRBD. Hypoventilation syndromes most often occur secondary in patients with neuromuscular, pulmonary or sceletal diseases or in patients with massive obesity. In patients with hypoventilation during sleep nocturnal and exertional dyspnea and headaches are frequently reported symptoms. Excessive daytime sleepiness is the key symptom in patients with central sleep apnea syndrome. Cheyne-Stokes Respiration is frequent in heart failure patients but in many cases does not cause symptoms specific for the breathing disorder. If there are symptoms or if ambulatory recording of breathing during sleep suggests a sleep related breathing disorder, polysomnography is then performed to definitively rule out or confirm the diagnosis and to initiate treatment, if needed. The indication for treatment in asymptomatic patients with central sleep apnea and Cheyne-Stokes Respiration may be difficult, as there are very little data concerning the long-term benefit in these patients. Symptomatic patients and those with severe central sleep apnea should be treated. Oxygen and CPAP may be effective in 20-30% of patients each. If these treatment options are ineffective, non-invasive pressure support ventilaiton can be used. In patients suffering from hypoventilation syndromes the treatment of choice is non-invasive pressure support ventilaiton combined with supplemental oxygen, if required.
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PMID:Central sleep related breathing disorders - diagnostic and therapeutic features. 2207 76

Central sleep apnoea (CSA) is a disorder characterised by repetitive episodes of decreased ventilation due to complete or partial reduction in the central neural outflow to the respiratory muscles. Hyperventilation plays a prime role in the pathogenesis of CSA. Chronic heart failure and dwelling at high altitude are classical conditions in which CSA is induced by hyperventilation. Hyperventilation syndrome (HVS) is a prevalent behavioural condition in which minute ventilation exceeds metabolic demands, resulting in haemodynamic and chemical changes that produce characteristic dysphoric symptoms. HVS is frequently caused by anxiety disorders and panic attacks. Until now, medical literature has focussed primarily on daytime symptoms of behavioural hyperventilation. It is currently unknown how this condition may affect sleep. Three cases are reported in which behavioural hyperventilation was associated with occurrence of significant central sleep apnoea, which was not present during normal tidal breathing in steady sleep. Therefore, behavioural hyperventilation should be added to the list of known clinical conditions associated with CSA.
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PMID:Behavioural hyperventilation as a novel clinical condition associated with central sleep apnoea: a report of three cases. 2312 77

Central sleep apnea is not uncommon in children with neurologic disorders. The mechanisms include increased ventilatory chemosensitivity to carbon dioxide level. Conventional treatments include oxygen, noninvasive ventilation, and in patients with heart failure, improving cardiac output. Here, we present a case of a 9-year-old male with Angelman syndrome, epilepsy, insomnia, and central sleep apnea. The patient was initially evaluated for nighttime awakenings and pauses in breathing. Sustained-release melatonin was used to improve his nighttime awakenings. A polysomnography confirmed central sleep apnea. We saw a reduction in arousals and improvement in insomnia with sustained-release melatonin. On a repeat study, central sleep apnea was improved. We hypothesize that sustained-release melatonin, by improving sleep continuity and reducing arousals, might improve central sleep apnea. Studies are needed to test the hypothesis.
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PMID:Central sleep apnea: does stabilizing sleep improve it? 2322 Jul 92

Central sleep apnea is common in patients with advanced heart failure. Apneic episodes are associated with hypoxemia, hypercapnia, and neurohumoral activation resulting in a rise in pulmonary vascular resistance. This case report describes a patient with a left ventricular assist device implanted for severe heart failure in whom unrecognized central sleep apnea resulted in under-filling of the left ventricle and a reduction in left ventricular assist device inflow.
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PMID:Central sleep apnea interfering with adequate left ventricular filling in a patient with left ventricular assist device. 2337 70

Obstructive sleep apnea results from structural compromise of the upper airway and decreased muscle tone during sleep. Central sleep apnea is usually due to instability of the feedback mechanism of the body that controls respiration. While positional changes commonly affect the severity of obstructive sleep apnea, the effect of positional changes on the severity of central sleep apnea is less well known.
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PMID:A case of positional central sleep apnea. 2349 39

Sleep-disordered breathing (SDB) causes hypoxemia, negative intrathoracic pressure, and frequent arousal, contributing to increased cardiovascular disease mortality and morbidity. Obstructive sleep apnea syndrome (OSAS) is linked to hypertension, ischemic heart disease, and cardiac arrhythmias. Successful continuous positive airway pressure (CPAP) treatment has a beneficial effect on hypertension and improves the survival rate of patients with cardiovascular disease. Thus, long-term compliance with CPAP treatment may result in substantial blood pressure reduction in patients with resistant hypertension suffering from OSAS. Central sleep apnea and Cheyne-Stokes respiration occur in 30-50% of patients with heart failure (HF). Intermittent hypoxemia, nocturnal surges in sympathetic activity, and increased left ventricular preload and afterload due to negative intrathoracic pressure all lead to impaired cardiac function and poor life prognosis. SDB-related HF has been considered the potential therapeutic target. CPAP, nocturnal O2 therapy, and adaptive servoventilation minimize the effects of sleep apnea, thereby improving cardiac function, prognosis, and quality of life. Early diagnosis and treatment of SDB will yield better therapeutic outcomes for hypertension and HF.
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PMID:Therapeutic strategies for sleep apnea in hypertension and heart failure. 2350 23

Neurophysiologically, central apnea is due to a temporary failure in the pontomedullary pacemaker generating breathing rhythm. As a polysomnographic finding, central apneas occur in many pathophysiological conditions. Depending on the cause or mechanism, central apneas may not be clinically significant, for example, those that occur normally at sleep onset. In contrast, central apneas occur in a number of disorders and result in pathophysiological consequences. Central apneas occur commonly in high-altitude sojourn, disrupt sleep, and cause desaturation. Central sleep apnea also occurs in number of disorders across all age groups and both genders. Common causes of central sleep apnea in adults are congestive heart failure and chronic use of opioids to treat pain. Under such circumstances, diagnosis and treatment of central sleep apnea may improve quality of life, morbidity, and perhaps mortality. The mechanisms of central sleep apnea have been best studied in congestive heart failure and hypoxic conditions when there is increased CO2 sensitivity below eupnea resulting in lowering eupneic PCO2 below apneic threshold causing cessation of breathing until the PCO2 rises above the apneic threshold when breathing resumes. In many other disorders, the mechanism of central sleep apnea (CSA) remains to be investigated.
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PMID:Central sleep apnea. 2372 Feb 83

Central sleep apnea is a breathing disorder that manifests as repetitive cessation of the breath during the sleep. The occurrence of breathing disorders after cervical laminectomy has been exceptionally described as a complication after cervical decompressive laminectomy for cervical stenotic myelopathy. In 1994, Naim-ur-Rahman reported the first case of postoperative central sleep apnea following C3-C6 laminectomy, occurring right after surgery and associated with spyncterial incontinence, that spontaneously recovered three weeks after onset. Recently we described a rare complication of cervical laminectomy for cervical stenotic myelopathy: the onset was delayed from surgery (nearly two weeks later) and cervical stenotic myelopathy was not associated to any other neurological sign of spinal cord damage as demonstrated by the neurophysiological assessment. Possible familiar predisposition can be matter of discussion. No definite interpretation of pathophysiological mechanisms can ultimately explain the occurrence of delayed and isolated central sleep apnea after laminectomy for the treatment of cervical stenotic myelopathy. Such a reversible and benign complication remain unpredictable in the best surgical hands.
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PMID:Transient breathing disorders after posterior cervical surgery for degenerative diseases: pathophysiological interpretation. 2482 50

In acute stroke, OSA has been found to impair rehabilitation and increase mortality but the effect of central apnea is more unclear. The aim of the present study was to evaluate the feasibility of using limited ambulatory recording system (sleep mattress to evaluate nocturnal breathing and EOG-electrodes for sleep staging) in sleep disordered breathing (SDB) diagnostics in mild acute cerebral ischemia patients and to discover the prevalence of various SDB-patterns among these patients. 42 patients with mild ischemic stroke or transient ischemic attack were studied. OSA was found in 22 patients (52.4%). Central apnea was found in two patients (4.8%) and sustained partial obstruction in only one patient (2.4%). Sleep staging with EOG-electrodes only yielded a similar outcome as scoring with standard rules. OSA was found to be common even after mild stroke. Its early diagnosis and treatment would be favourable in order to improve recovery and reduce mortality. Our results suggest that OSA can be assessed by a limited recording setting with EOG-electrodes, sleep mattress, and pulse oximetry.
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PMID:Screening sleep disordered breathing in stroke unit. 2499 37

Central sleep apnoea (CSA) is characterised by recurrent apnoeas during sleep with no associated respiratory effort. It mostly results from withdrawal of the wakefulness drive in sleep leaving ventilation under metabolic control. A detailed physiological understanding of the control of breathing in wakefulness and sleep is essential to the understanding of CSA. It encompasses a diverse group of conditions with differing aetiologies and pathophysiology. Likewise treatment varies according to underlying aetiology. Some of the conditions such as idiopathic (primary) CSA (ICSA) are relatively rare and benign. On the other hand Cheyne-Stokes breathing (CSB) pattern is quite common in patients with heart failure and might be a prognostic indicator of poor outcome. Unfortunately modern medical management of heart failure does not seem to have significantly reduced the prevalence of CSA in this group. Since the adoption of positive airway pressure (PAP) as a common treatment modality of obstructive sleep apnoea (OSA), complex CSA has been increasingly observed either as treatment emergent or persistent CSA. Depending on the particular condition, various treatment strategies have been tried in the past two decades which have included hypnotic therapy, respiratory stimulants, judicious administration of carbon dioxide, oxygen therapy, PAP and bi-level ventilatory support with a backup rate. In the past decade adaptive servo ventilation (ASV) has been introduced with much promise. Various studies have shown its superiority over other treatment modalities. Ongoing long term studies will hopefully shed more light on its impact on cardiovascular morbidity and mortality. Other rare forms are still poorly understood and treatments remain suboptimal.
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PMID:Central sleep apnoea-a clinical review. 2610 51


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