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

The observation that the narcotic antagonist naloxone could inhibit analgesia produced by electrical stimulation of the brain indicated the involvement of an endogenous chemical in the relief of pain. Multiple endogenous opioid peptides have been identified that have similar pharmacological properties to known narcotic analgesics. The biosynthesis, release, and degradation of opioid peptides have been studied in order to better understand how the manipulation of endogenous opioid systems can be used to produce or augment analgesia. The results of our studies reveal that various conditions and manipulations, such as electrical brain stimulation, acupuncture, stress, and the administration of opioid analgesics, can cause the release of endogenous opioid peptides and possibly endogenous nonpeptide substances. It has also been discovered that nonopioid peptides, such as cholecystokinin, calcitonin, and angiotensin II, can alter the action of opioid analgesics by antagonizing or potentiating their effects. An understanding of the role of endogenous peptides in endogenous opioid mechanisms is necessary for the development of new ways to treat pain and such other disorders as sleep apnea in children (sudden infant death syndrome), head injury, and opioid addiction that involve the activation or alteration of endogenous opioid systems.
Ann Emerg Med 1986 Sep
PMID:The role of endogenous peptides in the action of opioid analgesics. 352 91

Continuous positive airway pressure via the nasal route (nasal CPAP) is effective in reducing the frequency of occlusive and mixed patterns of sleep apnea. Little is known about long-term patient compliance with this therapeutic modality, however. In order to evaluate this, questionnaires were mailed to 24 sleep apnea patients who had received a nasal CPAP system for nightly use. Patients were requested not to sign the questionnaire. At the time of mailing, the patients had possessed their nasal CPAP equipment for 10.3 +/- 8 months (mean +/- SD). Twenty patients (83 percent) responded to the questionnaire. Sixteen responders used nasal CPAP during all nightly sleep time, and two used it for all but one and 2.5 hours of nightly sleep time, respectively. One individual used it on alternate nights, and one patient did not use it all. Thus, 17 of 20 (85 percent) responders were compliant. Including information about the four nonresponders, obtained by means other than questionnaire, 18 of 24 (75 percent) patients were compliant with therapy. All but two patients were obese at the time sleep apnea was diagnosed. Only 50 percent of questionnaire responders reported weight loss after receiving nasal CPAP, and these individuals were frequent nasal CPAP users. The most common complaints were mask discomfort (14 responders) and nasal dryness and congestion (13 responders). We conclude that long-term home nasal CPAP is a viable therapy that is conscientiously applied and well-tolerated by most sleep apnea patients.
Chest 1986 Sep
PMID:Patient compliance with nasal CPAP therapy for sleep apnea. 352 83

Men who snore heavily have an increased incidence of hypertension, angina, stroke, and neuropsychologic dysfunction, which may be due to nocturnal oxygen desaturation. Nocturnal oxygen therapy might be beneficial to such individuals by improving oxygenation and relieving tissue hypoxia. Twenty-eight asymptomatic heavy snoring men were recruited for polysomnographic monitoring during sleep. During the first half-night, air was breathed through a nasal cannula, and during the latter half-night, 2 L/min oxygen was administered. Breathing air, 20 subjects demonstrated sleep apneas, hypopneas and nocturnal oxygen desaturation. Eighteen subjects had more than ten apneas plus hypopneas per hour. Thirteen subjects reached low oxygen saturation below 80 percent and eight below 70 percent. Only 13 of the 20 subjects showed improvement with oxygen therapy. Apneas alone were not decreased in frequency and were lengthened with oxygen therapy. Episodes of oxygen desaturation were improved by oxygen therapy and consequently, rates of hypopnea were decreased. Severe sleep apnea, hypopnea and oxygen desaturation are common in asymptomatic male snorers, and oxygen therapy is not always beneficial.
Chest 1987 Sep
PMID:Snoring, nocturnal hypoxemia, and the effect of oxygen inhalation. 362 20

A patient operated upon for a midline cerebellar hemangioblastoma developed failure of automatic respiration during sleep, together with central sleep apnea syndrome, approximately two years after receiving radiation therapy to the brain. Clinical and CT scan findings were compatible with a diagnosis of radiation necrosis as the cause of his abnormal respiratory control.
Chest 1987 Sep
PMID:Radiation necrosis causing failure of automatic ventilation during sleep with central sleep apnea. 362 38

A review of the sleep of 31 patients 45 years old or older undergoing nocturnal penile tumescence studies showed that 19 had a previously undiagnosed sleep disorder. Of the patients 9 had periodic leg movements in sleep, 9 had sleep apnea and 1 had both disorders. In 10 of these patients the sleep disorders affected nocturnal penile tumescence by disrupting sleep and causing brief periods of detumescence, movement artifacts and delays in the tumescing phase of nocturnal penile tumescence. These disruptions resulted in an apparently abnormal nocturnal penile tumescence that appeared as if the patient had difficulty in achieving or maintaining an erection. The nocturnal penile tumescence disruptions may have reflected only a disruption of the necessary conditions for normal nocturnal penile tumescence to occur, namely adequate sleep and rapid eye movement sleep. The results strongly suggest that failure to measure concurrent sleep parameters and screen for occult sleep disorders could result in the incorrect diagnosis of abnormal nocturnal penile tumescence.
J Urol 1986 Sep
PMID:Problems in the interpretation of nocturnal penile tumescence studies: disruption of sleep by occult sleep disorders. 373 35

The bronchoconstriction of asthma displays a circadian rhythm with exacerbations often occurring in the early morning hours. Gas exchange abnormalities during sleep in patients with severe asthma have been documented; however, the influence of sleep on gas exchange in the asthmatic with few or no daytime or nocturnal symptoms is poorly understood. To determine if abnormalities in oxygenation might occur during sleep, we studied 12 stable adult asthmatic patients with reversible airflow obstruction during sleep on three consecutive nights, with night 1 being for acclimatization. On test nights 2 and 3, the subjects received, in random double-blind fashion, either inhaled fenoterol or its placebo. Spirometry was performed before and after bronchodilator treatment and on the next morning. The mean FEV1 was 63 percent predicted before treatment. There was significant (p less than 0.05) improvement in FEV1 on fenoterol night after treatment which was also present the next morning. Mean prefenoterol FEV1 was 2.04 +/- .15 (SEM) and increased to 2.61 +/- .17 after the bronchodilator. The mean morning FEV1 was 2.27 +/- .20. Mean preplacebo FEV1 was 2.07 +/- .12 and did not change significantly with placebo bronchodilator. Sleep analysis demonstrated no significant differences in total sleep time or duration of oxyhemoglobin desaturation between nights. The incidence of sleep disordered breathing was very low (0.14 apneas/hour). The frequency of apneas and hypopneas did not change significantly with treatment. Two of the 12 subjects experienced an asthma attack on placebo night which did not recur following active bronchodilator administration. We conclude that stable asthmatic patients with few nocturnal complaints have a low frequency of disordered breathing and desaturation events during sleep.
Chest 1986 Sep
PMID:Breathing during sleep in stable asthmatic subjects. Influence of inhaled bronchodilators. 374 44

Parafunctional activity (toothgrinding, toothclenching and bruxism) is a common problem which may lead to masticatory muscle and temporomandibular joint pain, and may result from sleep arousal or disturbances. Sleep apnea is another common sleep disorder which results in disrupted sleep architecture and frequent arousals. Because sleep apnea leads to sleep arousals, and because sleep arousals are thought to result in increased parafunctional activity, we undertook the present study to determine the relationship between sleep apnea and parafunctional activity. We were also interested in assessing the effects of sleep posture on sleep disordered breathing and parafunctional activity. We prospectively studied 24 patients who were referred to the clinical sleep apnea laboratory for study. They underwent standard nocturnal polysomnographic examination; in addition, masticatory activity was measured with a masseter electromyogram. Patients slept in the supine and lateral decubitus positions. Nocturnal clenching was slightly higher in patients with sleep apnea than those without (12.2 vs 7.6 clenches/hr, p = 0.18), and there was a correlation between the clench index (CI) and apnea plus hypopnea index (A + HI) by linear regression (r = 0.49, p less than 0.05). There were significant falls in both the A + HI (64.4 +/- 28.8 vs 36.5 +/- 36.7, p = 0.02) and CI (12.5 +/- 12.1 vs 7.0 +/- 8.6, p = 0.04) in the lateral decubitus vs supine sleeping positions. We conclude that there is an association between obstructive sleep apnea and parafunctional activity, that sleep position affects the incidence of both sleep disordered breathing and parafunctional activity, and that analysis of apneas and hypopneas in both supine and lateral decubitus sleeping positions may be helpful.
Chest 1986 Sep
PMID:Effect of sleep position on sleep apnea and parafunctional activity. 374 57

As awareness and understanding of obstructive sleep apnea has increased so has the number of treatments for this disorder. Options include surgical procedures: tracheostomy, palatopharyngoplasty (PPP), and mandibular advancement. Other treatments are medication, nasal CPAP, Tongue Retaining Device, and a position alarm. With these numerous choices available, it is important that reliable indicators be developed to guide treatment choice. And although PPP surgery is a one-time intervention with possibility of permanent correction, reports of percentages of successful treatment have varied widely from 85% to 0%. This has led us to investigate predictors of successful treatment. Twenty-two patients treated with PPP following their diagnosis by standard clinical polysomnography were restudied an average of 8 weeks later. When 11 successful cases were compared to 11 unsuccessful cases, successes were found to be initially more severely apneic (mean AI = 90.55 versus 49.45). Palatopharyngoplasty appears to be most appropriate for the sleep apnea patient whose apnea index is 70 or above and less effective for milder cases.
Laryngoscope 1986 Sep
PMID:Severity of sleep apnea as a predictor of successful treatment by palatopharyngoplasty. 374 95

In 1982 facilities for investigation of patients with sleep disorders were established at Auckland Hospital on a trial basis. Twenty patients with the obstructive sleep apnoea syndrome had been investigated and treated by the end of 1983. All were advised to avoid alcohol and sedatives and the obese patients were encouraged to lose weight. In the more severely affected patients either nasal continuous positive airway pressure or tracheostomy was used. The method of diagnosis and treatment are discussed.
N Z Med J 1985 Sep 11
PMID:Obstructive sleep apnoea in Auckland: diagnosis and treatment. 386 52

Sleep apnea syndrome is estimated to affect as many as 2 to 3 percent of the adult male population. Excessive snoring and daytime sleepiness are but a few of the many clues to diagnosis. The hypoxemia occurring as a result of apnea may lead to pulmonary hypertension. Depressed respiratory center neural output or upper airway occlusion during sleep may cause the apnea. There are a number of treatment options available.
Am Fam Physician 1985 Sep
PMID:Sleep apnea syndrome. 389 92


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