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

The Pickwickian Syndrome stimulated new pathophysiological concepts in regard to control of ventilation. With the advent of sleep laboratories, the peculiar sleep apnea occurring in some of these patients has been explained on the basis of intermittent upper airway obstruction. Two patients with different manifestations of the Pickwickian Syndrome are presented. The suggestion is made that these two subsyndromes should have unique designations. The Auchincloss Syndrome is manifested by right heart failure and respiratory acidosis in obese patients who are alert and have no major abnormality of breathing pattern. The fundamental cause of this abnormality is the increased work of breathing caused by the obesity. The cost of breathing is so high that the ventilatory regulation is compromised and respiratory acidosis results. The Gastaut Syndrome is characterized principally by hypersomnia and sleep apnea. The fundamental defect is upper airway obstruction during sleep, resulting in increased work of breathing, which together with the increased work caused by obesity leads to respiratory acidosis and right ventricular failure. Hypersomnia, rather than heart failure or respiratory acidosis, is the major manifestation of this syndrome, and is the result of sleep loss.
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PMID:Pickwickian syndrome, 20 years later. 117 87

An awakening has taken place over the last 25 years to the science of sleep disorders. Foremost amongst these, both in the medical world and the public eye, has been Sleep Apnoea Syndrome (SAS). The prevalence is thought to be the order of 1-2%. Males are eight times more commonly affected than females, although after the menopause the gap narrows considerably. Sleep apnoea occurs in children, usually in relation to large tonsils and adenoids, but in adult life patients usually present between the age of 40 and 60 and the prevalence increases with age. Numerous apnoeas or hypopnoeas during the night's sleep result in disordered sleep architecture and unrefreshing sleep. This is usually accompanied by night-long snoring which may lead to marital discord and even complaints from neighbours. Symptoms on waking may be a headache and a feeling of not being refreshed by sleep. Sleepiness during the day can interfere with work and social activities and may produce risks to the patient and others if it occurs while operating dangerous machinery or driving. Over a longer time scale SAS results in intellectual and memory deterioration, a higher incidence of ischaemic heart disease, hypertension, polycythemia and pulmonary hypertension. Right heart failure is particularly likely if there is chronic airflow obstruction contributing to a low arterial oxygen level. Asystolic periods and tachyarrhythmias may occur during apnoeic periods. The increased mortality of SAS relates to coronary and cerebrovascular disease and arrhythmias. Sudden death occurs with greater frequency in patients with SAS, mainly at night.
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PMID:Sleep apnoea: causes, consequences and treatment. 141 52

Treacher Collins Syndrome is a rare bilateral congenital deformity occurring in 1 in 10,000 births. It is also known, in the European literature, as Franceschetti Syndrome, and is additionally known as mandibulofacial dysostosis. It is a syndrome with a very wide spectrum of manifestations characterized by distortions of the orbit secondary to hypoplasia of the maxilla, mandible, and, most markedly, of the zygoma. Soft tissue deformities include lower lid colobomas, laxity and dystopia of the lateral canthus, microtia, and a paucity of the muscular aponeurosis of the midface. The syndrome is frequently accompanied by significant hearing loss, early failure to thrive, chronic respiratory insufficiency, and sleep apnea. Intelligence is usually within normal limits although learning disabilities are common in early life. These major anatomical and physiological abnormalities, as well as the psychological and social stigma associated with severe facial deformity, make this syndrome one of the most challenging reconstructive problems presented to the craniofacial surgeon.
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PMID:Treacher Collins syndrome: present concepts of the disorder and their surgical correction. 277

Based on results on central chemosensitivity in cats, paired stimuli were applied for therapy to infants with central respiratory insufficiency of various degrees. An unspecific respiratory stimulus, e.g. light for 1 s, was followed by a jet of either O2 or 2% CO2 in O2 for 1.5 s. The unspecific and the chemical stimuli were interspaced by 0.5 s. The combined stimulation was repeated every 10 s. The program was triggered by using threshold values of transcutaneous pO2. In infants with intratrachial tubes or tracheostoma we used the end tidal pCO2 for triggering the stimulation. The method could prevent hypoxemia during sleep in non-ventilated subjects with sleep apnea syndromes or in infants with severe hypoxemia during sleep after being rescued from Sudden Infant Death Syndrome (SIDS). In patients with Ondine's Curse Syndrome (OCS) with its CO2 insensitivity, paired stimuli were used in order to condition the chemical function of the respiratory system. Polysomnograms from 310 clinically healthy infants including healthy siblings of SIDS victims revealed instability of arterial pO2 and low CO2 sensitivity during sleep within the second month and the fourth to ninth month of life, respectively. These data challenge the described method as a potential preventive or therapeutic measure to defeat SIDS and sleep apnea syndromes in conjunction with disturbed chemical regulation of respiration.
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PMID:Transcutaneous monitoring as trigger for therapy of hypoxemia during sleep. 367 92

Maternal cigarette smoking has a high correlation with sudden Infant Death Syndrome, a condition in which cardiorespiratory failure occurs during an hypoxic episode, as in sleep apnea. Pregnant rats were given nicotine infusions of 2 or 6 mg/kg/day throughout gestation, regimens that produce plasma nicotine levels spanning the range in smokers. The day after birth, animals in the high dose group displayed excessive mortality during hypoxic challenge. These animals were found to be deficient in an essential response component, namely adrenomedullary catecholamine release that is required to maintain neonatal cardiac rhythm during hypoxia; the defect was in adrenal cell function rather than in altered innervation or nicotinic receptor desensitization. We also examined brainstem and forebrain noradrenergic mechanisms that are involved in neonatal respiratory control. The nicotine group showed suppressed spontaneous neuronal activity, but were hyperresponsive to hypoxia. As these projections are inhibitory for respiration, the nicotine-induced sensitization would be expected to contribute to respiratory arrest during hypoxia. Prenatal nicotine exposure may thus provide a useful animal model with which to study the physiological mechanisms that underlie Sudden Infant Death Syndrome, while at the same time providing a biological explanation for the association of the syndrome with smoking.
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PMID:Loss of neonatal hypoxia tolerance after prenatal nicotine exposure: implications for sudden infant death syndrome. 755 77

Oesophageal pressure (Pes) and oronasal flow are necessary to describe upper airway obstruction in patients with obstructive sleep apnoea syndrome (OSAS), but Pes interferes with sleep. We developed a device applying an oscillating flow (20 Hz) through a nasal mask. An additional flow (2.6 l/min) is needed to reduce dead space and humidity. 24 patients (age 55.8 +/- 8.3 years, BMI 28.6 +/- 3.9, RDI 38.6 +/- 19.4, Raw 0.27 +/- 0.07 kPa/s/l) underwent polygraphy (oronasal flow, thoracic and abdominal effort, oxygen saturation, microphone, heart rate). Pes and oscillatory impedance (OI) were measured simultaneously. During snoring, hypopnoeas and apnoeas we compared Pes, OI and effort values for the detection of number and period of airway obstruction. The average Pes during habitual snoring was -3.2 +/- 0.8, during hypopnoeas -3.9 +/- 1.1 and during apnoeas -4.4 +/- 1.6 kPa. We found no significant difference in respect of the number and period of obstruction in patients with apnoeas, whereas in patients with incomplete obstruction (hypopnoea) Pes and OI were found to be more sensitive in detecting obstruction than effort (period: 27.0 +/- 9.1 sec (Pes), 29.0 +/- 4.8 sec (OI) vs. 20.0 +/- 6.8 sec (effort); number: 34.0 +/- 9.1 (Pes), 35.0 +/- 8.5 (OI) vs. 23.0 +/- 9.5 (effort). There is a significant correlation between Pes and OI (r = 0.89). OI is shown to be equally sensitive in identifying Upper Airway Resistance Syndrome as compared to Pes. This method is more convenient than conventional measurements such as Pes and it could be an alternative.
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PMID:[Comparative study of thoracic and abdominal effort, respiratory oscillatory impedance (ROI) and intrathoracic pressure in sleep apnea syndrome]. 934 Jun 34

In order to study both the prevalence of Primary Sleep Disorders (PSD) and sleepiness, and their association to the Chronic Fatigue Syndrome (CFS), 46 unselected outpatients (34 women, mean age 36.5) were examined clinically and underwent two nights of all-night polysomnography and multiple sleep latency tests (MSLT). Forty-six percent presented with a Sleep Apnea/Hypopnea Syndrome Index (AHI>=5), 5% with a Periodic Limb Movements syndrome. No subject received a diagnosis of Narcolepsy or Idiopathic Hypersomnia. Thirty percent showed the presence of objective sleepiness as measured by MSLT<10 minutes. Objective and subjective measures of sleepiness were not associated with CFS, nor with the double diagnosis of CFS and a PSD. The presence of PSD or sleepiness was not associated with any of the clinical scales that were used to measure anxiety, depression, somatisation, physical or mental fatigue, or functional status impairment. Fifty-four percent of CFS patients had no PSD, and 69% no sleepiness. These patients could not be distinguished clinically from patients having a PSD or from those with sleepiness. Therefore, it is unlikely that CFS is simply a somatic expression of any PSD observed in our sample or of sleepiness per se.
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PMID:How significant are primary sleep disorders and sleepiness in the chronic fatigue syndrome? 1138 99

Obstructive sleep apnoea (OSA) is a very prevalent disorder particularly amongst middle-aged, obese men, although its existence in women as well as in lean individuals is increasingly recognized. Despite the early recognition of the strong association between OSA and obesity, and OSA and cardiovascular problems, sleep apnoea has been treated as a 'local abnormality' of the respiratory track rather than as a 'systemic illness'. In 1997, we first reported that the pro-inflammatory cytokines interleukin (IL)-6 and tumour necrosis factor-alpha (TNF alpha) were elevated in patients with disorders of excessive daytime sleepiness (EDS) and proposed that these cytokines were mediators of daytime sleepiness. Also, we reported a positive correlation between IL-6 or TNF alpha plasma levels and the body mass index (BMI). In subsequent studies, we showed that IL-6, TNF alpha, leptin and insulin levels were elevated in sleep apnoea independently of obesity and that visceral fat, was the primary parameter linked with sleep apnoea. The association of OSA with insulin resistance and diabetes type 2 has been confirmed since then in several epidemiological and clinical studies. Furthermore, our findings that women with polycystic ovary syndrome (PCOS, a condition associated with hyperandrogenism and insulin resistance) were much more likely than controls to have sleep disordered breathing (SDB) and daytime sleepiness support the pathogenetic role of insulin resistance in OSA. Other findings that support the view that sleep apnoea and sleepiness may be manifestations of a serious metabolic disorder, namely the Metabolic or Visceral Obesity Syndrome, include: obesity without sleep apnoea is associated with daytime sleepiness; PCOS and diabetes type 2 are independently associated with EDS after controlling for SDB, obesity and age; and increased prevalence of sleep apnoea in postmenopausal women, with hormonal replacement therapy associated with a significantly reduced risk for OSA. In conclusion, accumulating evidence provides support to our model of the bi-directional, feedforward, pernicious association between sleep apnoea, sleepiness, inflammation and insulin resistance, all promoting atherosclerosis and cardiovascular disease.
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PMID:Metabolic disturbances in obesity versus sleep apnoea: the importance of visceral obesity and insulin resistance. 1282 41

Patients with COPD who are hypoxaemic during wakefulness become more hypoxaemic during sleep. The most severe episodes of nocturnal desaturation generally occur during REM sleep. There is a strong relationship between nocturnal O2 saturation and the level of daytime PaO2: the more pronounced daytime hypoxaemia, the more severe nocturnal hypoxaemia. The worsening of hypoxaemia is due to a variable combination of alveolar hypoventilation and ventilation-perfusion mismatching, alveolar hypoventilation being the predominant mechanism, at least during REM sleep. The consequences of sleep-related hypoxaemia include peaks of pulmonary hypertension due to hypoxic pulmonary vasoconstriction, generally observed in patients with marked daytime hypoxaemia. Cardiac arrhythmias have been described but their clinical relevance has not been established. The prevalence of obstructive sleep apnoea syndrome (OSAS) is not greater in chronic obstructive pulmonary disease (COPD) patients than in the general population, but this association (Overlap Syndrome) is not rare since COPD and OSAS are both frequent diseases. Overlap patients are at a higher risk of developing respiratory insufficiency than are pure OSAS patients. Polysomnography is only indicated in COPD patients who are suspected of having OSAS. The treatment of nocturnal hypoxaemia is conventional O2 therapy (> or = 16/24 h) in COPD patients with marked daytime hypoxaemia (PaO2 < 55-60 mmHg) and conventional O2 therapy plus nocturnal non-invasive ventilation in some patients with marked hypercapnia. At present data are not sufficient for justifying the use of isolated nocturnal oxygen therapy in COPD patients with nocturnal desaturation but with mild daytime hypoxaemia (PaO2 > 60 mmHg).
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PMID:Sleep and chronic obstructive pulmonary disease. 1523 53

Several drugs have been described as possible treatments for Sleep Apnea/Hypopnea Syndrome (SAHS) but the data available does not support their use. In an animal model of central apnea the use of mirtazapine produced a significant reduction of apneas. We present a male patient, 82 years old, with excessive daytime sleepiness and loud snoring during at least 10 years. An overnight polysomnography (PSG) revealed an apnea/hypopnea index of 54.9 events per hour of sleep with a minimum pulse oximetric saturation (SaO(2)) of 78% and an arousal index of 40.4 per hour. A nasal CPAP titration in the second half of the night showed suppression of apneas with a CPAP level of 8 cmH(2)O. The patient refused to use the CPAP device and began with 15 mg of mirtazapine at bedtime. A second PSG performed after 3 months of mirtazapine showed a significant reduction in the apnea/hypopnea index (9.3 events per hour of sleep; 81% minimal oxygen saturation (SaO(2))). Clinically, the patient and his wife reported a clear reduction of excessive daytime sleepiness and an improvement in self-reported functioning and well-being without any important side effects. This successful case appears to be the first report with mirtazapine in human SAHS and supports the need for an appropriate clinical trial with this drug.
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PMID:Effectiveness of mirtazapine in the treatment of sleep apnea/hypopnea syndrome (SAHS). 1534 98


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