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

Obstructive sleep apnea syndrome is a complex disorder that has been associated with a variety of abnormalities of the upper airway, including tonsil and adenoid hypertrophy, nasal obstruction, retrognathia, and macroglossia. The cause of the airway obstruction in acromegaly is believed to be related to osseous and soft-tissue changes surrounding the upper airway, which lead to narrowing and subsequent collapse during sleep. We describe the results of treatment in seven patients with both sleep apnea and acromegaly. Four patients were treated by transsphenoidal hypophysectomy alone with a resolution of sleep apnea syndrome. One underwent hypophysectomy followed by postoperative radiation therapy, which reduced his apnea. Three patients underwent unsuccessful uvulopalatopharyngoplasty. Successful treatment of the primary disorder, in this case acromegaly, resulted in improved breathing during sleep in five patients. This series would suggest that acromegalic patients with sleep apnea should be treated for their pituitary tumor to reduce growth hormone before consideration of surgery to enlarge or bypass the upper airway.
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PMID:Obstructive sleep apnea syndrome and acromegaly. 802 37

The present study was designed to determine the effect of sleep on reflex pharyngeal dilator muscle activation by stimuli of negative airway pressure in human subjects. Intra-oral bipolar surface electrodes were used to record genioglossus electromyogram (EMG) responses to 500 ms duration pressure stimuli of 0 and -25 cmH2O applied, via a face-mask, in four normal subjects. Stimuli were applied during early inspiration in wakefulness and in periods of non-rapid-eye-movement (non-REM) sleep, defined by electroencephalographic (EEG) criteria. The rectified and integrated EMG responses to repeated interventions were bin averaged for the 0 and -25 cmH2O stimuli applied in wakefulness and sleep. Response latency was defined as the time when the EMG activity significantly increased above prestimulus levels. Response magnitude was quantified as the in ratio of the EMG activity for an 80 ms post-stimulus period to an 80 ms prestimulus period; data from after the subject's voluntary reaction time for tongue protrusion (range, 150-230 ms) were not analysed. Application of the -25 cmH2O stimuli caused genioglossus muscle activation in wakefulness and sleep, but in all subjects response magnitude was reduced in sleep (mean decrease, 61%; range, 52-82%; P = 0.011, Student's paired t test). In addition, response latency was increased in sleep in each subject (mean latency awake, 38 ms; range, 30-50 ms; mean latency asleep, 75 ms; range, 40-110 ms; P = 0.072, Student's paired t test). Application of the -25 cmH2O stimuli caused arousal from sleep on 90% occasions, but in all cases the reflex genioglossus muscle responses (maximum latency, 110 ms) always proceeded any sign of EEG arousal (mean time to arousal, 643 ms; range, 424-760 ms). These results show that non-REM sleep attenuates reflex genioglossus muscle activation by stimuli of negative airway pressure. Attenuation of this reflex by sleep may impair the ability of the upper airway to defend itself from suction collapse by negative pressures generated during inspiration; this may have implications for the pathogenesis of obstructive sleep apnoea.
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PMID:The effect of sleep on reflex genioglossus muscle activation by stimuli of negative airway pressure in humans. 804 29

Sleep deprivation can induce or worsen nocturnal respiratory disturbances. In patients with sleep apnea hypopnea, sleep abnormalities consist of repetitive episodes of arousals and awakenings that lead to sleep fragmentation. Because the propensity for upper airway collapse is increased in these patients, we wondered if sleep fragmentation could increase upper airway collapsibility and contribute to the pathogenesis of this disease. In eight normal subjects, upper airway collapsibility was assessed during sleep by progressively decreasing the pressure in a nasal mask while recording airflow, mask, and esophageal pressures. The critical pressure was determined by the relationship between breath-by-breath values of maximal inspiratory airflow of each flow-limited inspiratory cycle and the corresponding mask pressure. Critical pressure was measured twice in each subject: after one night of total sleep deprivation and after one night of sleep fragmentation using auditory stimuli. The two measures were done in random order 1 wk apart. A polysomnographic recording was obtained the night after each measurement of critical pressure. Sleep architecture was identical after sleep deprivation and fragmentation. Sleep-related breathing abnormalities were more frequent after sleep fragmentation than after sleep deprivation. Critical pressure was -17.1 +/- 6.8 cm H2O (mean +/- SEM) after sleep deprivation, and -12.3 +/- 6.3 cm H2O after sleep fragmentation (p < 0.05), corresponding to an earlier closing of the upper airway. We conclude that sleep fragmentation leads to a higher upper airway collapsibility than does sleep deprivation.
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PMID:Effects of sleep deprivation and sleep fragmentation on upper airway collapsibility in normal subjects. 804 33

The management of simple snoring in adults is reviewed. Snoring is associated with oscillations of the soft palate and adjacent structures, as a consequence of a critically reduced pharyngeal cross-sectional area under conditions of sleep-induced flow limitation. Anatomical and physiological factors resulting in upper airway collapse and snoring are reviewed. The conservative treatment of snoring encompasses weight loss, alcohol and sedatives avoidance, as well as smoking cessation. Nasal obstruction should be relieved, either medically or surgically. If these measures fail, polysomnography should be performed. Patients with obstructive sleep apnoea should be offered nasal continuous positive airway pressure therapy. Uvulopalatopharyngoplasty can be proposed to nonapnoeic snorers, with a good chance of success, as far as reported snoring is concerned. Unfortunately, this has not been confirmed by objective recordings, and long-term results have not been adequately studied.
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PMID:Management of simple snoring in adults. 812 96

The high prevalence of obstructive sleep apnea (OSA) has only recently been appreciated, in part because the symptoms and signs of chronic sleep disruption are often overlooked in spite of their debilitating consequences. They typically develop insidiously during a period of years. We now know that the lives of millions of people each year are significantly impaired by the sequelae of OSA. Many of these patients go unrecognized, with tremendous medical and economic consequences for individual patients and for society. Evidence indicates that chronic, heavy snoring may be associated with increased long-term cardiovascular and neurophysiologic morbidity. Therefore considerable interest lies in the study of the epidemiology and the natural history of these related disorders. The fundamental problem in OSA is the periodic collapse of the pharyngeal airway during sleep. The pathophysiology of this phenomenon is reviewed in some detail. During apneas caused by obstruction, airflow is impeded by the collapsed pharynx in spite of continued effort to breathe. This causes progressive asphyxia, which increasingly stimulates breathing efforts against the collapsed airway, typically until the person is awakened. Hypopneas predominate in some patients and are caused by partial pharyngeal collapse. The clinical sequelae of OSA relate to the cumulative effects of exposure to periodic asphyxia and to sleep fragmentation caused by apneas and hypopneas. Some patients with frequent, brief apneas and hypopneas and normal underlying cardiopulmonary function may have considerable sleep disruption without much exposure to nocturnal hypoxia. Patients with sleep apnea often have excessive daytime sleepiness. As the disorder progresses, sleepiness becomes increasingly irresistible and dangerous, and patients develop cognitive dysfunction, inability to concentrate, memory and judgment impairment, irritability, and depression. These problems may lead to family and social problems and job loss. Cardiac and vascular morbidity in OSA may include systemic hypertension, cardiac arrhythmias, pulmonary hypertension, cor pulmonale, left ventricular dysfunction, stroke, and sudden death. The challenge for the clinician is to routinely consider the diagnosis and to incorporate several basic questions in the historical review of systems regarding daytime or inappropriate sleepiness. The diagnosis of OSA is made with polysomnography, and the decision to treat is based on an overall assessment of the severity of sleep-disordered breathing, sleep fragmentation, and associated clinical sequelae. The therapeutic options for the management of OSA are reviewed. Recognition and appropriate treatment of OSA and related disorders will often significantly enhance the patient's quality of life, overall health, productivity, and safety on the highways.
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PMID:Obstructive sleep apnea. 814 53

Patients with obstructive sleep apnoea syndrome frequently present distinct changes in the craniofacial skeleton that result in a structural narrowing of the pharynx and promote pharyngeal collapse during sleep. The evaluation of the clinical data of patients with and without craniofacial dysmorphia reveals that mean age, mean Broca index and the number of additional diseases is decreased in patients with craniofacial dysmorphia. Young patients or patients with normal weight and OSAS usually present such skeletal changes. The number of sleep-related breathing disorders and the extent of nocturnal desaturation are also decreased in the group of patients with dysmorphia. The structure of sleep is similarly disturbed in both groups. In most cases patients with severe obstructive sleep apnoea have normal cephalometric data.
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PMID:[Obstructive sleep apnea syndrome caused by craniofacial abnormalities]. 815 3

We report on an 83 yr old man with hypersomnia and central sleep apnoea (CSA). He had several possible causes for CSA, including a central nervous system lesion, hypocapnia and anatomical narrowing of the airway at the hypopharyngeal level. We postulate that reduced central respiratory drive occurring in conjunction with upper airway narrowing may have led to central apnoeas. These in turn could have facilitated a complete passive hypopharyngeal collapse at the end of each apnoea, as visualized by somnofluoroscopy. The CSA could also have been favoured by respiratory instability due to chronic hypocapnia.
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PMID:Central sleep apnoea syndrome with upper airway collapse. 849 10

Hunter's syndrome is one of a group of heritable metabolic disorders caused by decreased activity of one or more of the lysosomal enzymes responsible for mucopolysaccharide catabolism, resulting in excessive deposition of mucopolysaccharides in skeletal and soft tissues. Pulmonary conditions, such as airway obstruction, sleep apnea syndrome, atalectasis, recurrent pneumonia and difficult endotracheal intubation are known to be associated with these rare disorders and have been reported. We report the findings at laryngotracheobronchoscopy of a patient with Hunter's syndrome with airway symptoms and, supported by analysis of previously reported cases of airway problems associated with the syndrome, suggest that tracheobronchomalacia with classifiable major airway collapse (MAC) may be the pathological correlate for this clinical picture. The endoscopic technique and characteristic findings of tracheobronchomalacia/MAC are discussed, as well as the natural history and pathophysiology of this condition, which is characterized by weakness of the tracheal wall due to softening of the supporting cartilage and hypotonia of the myoelastic elements with reduction in the tracheal lumen.
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PMID:Tracheobronchomalacia in Hunter's syndrome. 850 49

Obstructive sleep apnea is a breathing disorder characterized by repeated collapse of the upper airway during sleep, with cessation of breathing. Four percent of middle-aged men and 2 percent of middle-aged women meet minimal criteria for the sleep apnea syndrome. Risk factors include loud, chronic snoring, obesity (especially nuchal), hypertension, excessive daytime sleepiness, and an increased tendency for automobile and work-related accidents. Cardiovascular comorbidity and complications include systemic hypertension, arrhythmias and possibly myocardial ischemia and myocardial infarction in patients with coronary artery disease. Diagnosis is confirmed by a sleep study; currently, polysomnography is the optimum test. Treatment options range from behavioral therapy alone for mild cases to a combination of behavioral approaches and continuous positive airway pressure and/or surgery for moderate and severe cases. Continuous positive airway pressure is the most effective noninvasive treatment. Primary care physicians play a key role in the identification, management and follow-up of patients with sleep apnea.
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PMID:Sleep apnea: is your patient at risk? National Heart, Lung, and Blood Institute Working Group on Sleep Apnea. 854 58

The imaging techniques of the upper airway (UA) now permit a description of the characteristics of pharyngeal collapse during the course of obstructive apnoea. The start is oropharyngeal with active movements anterior and posterior of the soft palate and a falling back of the tongue. The extension occurs almost systematically towards the hypopharynx. A displacement of the hyoid bone and of the cervical spine is noted synchronously with thoracoabdominal movements. These imaging techniques of UA show the occurrence of passive pharyngeal collapse during certain types of central apnoea. In snorers and in apnoeics, there is a reduction of the calibre of the pharynx. However, these abnormalities are not specific and do not enable the diagnosis to be confirmed nor an estimate of the severity of the sleep apnoea syndrome. Cephalometry and computed tomography of the pharynx should be carried out particularly when a uvulopalatopharyngoplasty (UPPP) is envisaged. For practical purposes, the existence on cephalometry of retrognathism with an MP-H > 24 mm and a PAS distance of < 5 mm is associated with a poor result for UPPP. The same thing applies when macroglossia or a reduction of the surface of the hypopharynx is found on computed tomography.
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PMID:[Upper airways and sleep apnea syndrome]. 856 75


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