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

Insomnia is a disorder of initiation and maintenance of sleep that results in daytime somnolence. The differential diagnosis of the various forms of insomnia is based primarily on the history, including information from the sleeping partner. The possibility of underlying depression or sleep apnea must be given consideration in every patient with insomnia, because inappropriate therapy may be dangerous in these instances. In general, the benzodiazepines have supplanted the traditional hypnotics in the treatment of insomnia.
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PMID:Diagnosis and treatment of insomnia. 288 77

Sleep onset during the multiple sleep latency test was scored by three criteria for 21 patients with narcolepsy and 21 patients with obstructive sleep apnea: a single epoch of stage 1, three consecutive epochs of stage 1, and a single epoch of stage 2 or REM. Mean sleep latency for both groups was predictably shortest using a single epoch of stage 1 and longest using a single epoch of stage 2 or REM. All estimates of sleep latency were highly correlated. It was concluded that a single epoch of any stage of sleep is an appropriate measure of sleep latency for patients with narcolepsy, although a modified scoring system should be developed for patients with sleep apnea. The obstructive apneic episodes prevented or delayed sleep onset on 4.8% to 33.3% of trials depending on the specific criteria used to determine sleep latency. Such apnea-related interruptions to sleep should be taken into account when assessing daytime somnolence in patients with sleep apnea.
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PMID:Determination of sleep latency in polysomnographic evaluations of daytime somnolence in patients with sleep apnea and patients with narcolepsy. 292 26

Napoleon would sleep very little. He frequently woke up during night and worked. Brief sleeping time in day repaired his fatigue. He had also a short and thick neck. In the last fourth of his life he progressively suffered from obesity, daily involuntary sleepiness and his intellectual capabilities undoubtedly decreased. Our experience of 48 cases of sleep apnea syndrome diagnosed by mean of polysomnography allow no to think that Napoleon suffered from this disease. Historical consequences of this pathology is discussed.
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PMID:[Did Napoleon suffer from sleep apnea syndrome?]. 304 29

A 37-year-old man with a 19-year history of progressive autosomal-dominant olivopontocerebellar degeneration developed excessive daytime sleepiness and paroxysmal episodes that clinically resembled an ictal or postictal state. Polysomnography showed sleep apnea. Long-term therapy with trazodone resulted in resolution of the paroxysmal episodes, disappearance of daytime sleepiness, and gradual improvement of sleep architecture over several months.
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PMID:Sleep apnea in olivopontocerebellar degeneration: treatment with trazodone. 316 75

Behavioral control of abnormal breathing in sleep was studied to determine if an intervention procedure could reduce apnea duration and also SaO2 (blood oxygen) desaturation levels. Sleep apnea patients (n = 11) were instructed while awake that tones would be presented in sleep whenever an apnea event occurred. They were told to breathe deeply to the tones and were given practice in doing so. Intervention and nonintervention hours alternated across 2 nights following 2 baseline nights. As expected, during the intervention hours, the duration but not the frequency of apneic events was reduced. The procedure also resulted in higher SaO2 levels during the intervention hours. Daytime sleepiness was not greater following intervention but sleep staging effects were observed. The results are sufficiently promising to warrant additional research.
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PMID:Behavioral control of abnormal breathing in sleep. 325 50

Recent reports that nearly all patients with narcolepsy have the HLA-DR2 phenotype suggest that autoimmunity may underly the etiology or pathogenesis of this disorder. Of 11 narcoleptic patients in the present study, 9 were HLA-DR2, confirming the strong association with this class II antigen but indicating that this is not an obligatory phenotype. In contrast only 3/10 patients with sleep apnea were HLA-DR2, suggesting that this form of excessive somnolence has a different etiopathogenesis. Significant levels of rheumatoid factor, antinuclear antibodies or autoantibodies to native DNA, denatured DNA, histones, Sjogren's syndrome B antigen, or Smith antigen were undetectable in sera from narcoleptic patients. Antibodies to rodent brain, primate brain stem, and neurocytotoxic antibodies were also not found. These results along with the absence of laboratory signs and clinical features of a systemic inflammatory process indicate that if narcolepsy is an autoimmune disease, the underlying lesion or pathologic condition may be confined to the central nervous system.
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PMID:HLA-DR2 association with excessive somnolence in narcolepsy does not generalize to sleep apnea and is not accompanied by systemic autoimmune abnormalities. 326 67

Snoring usually is trivial and unimportant, but it can turn into a social or medical problem. Obesity, hypertension and heart disease are more frequent among snorers than among nonsnorers, and especially snorers with hypersomnia during the day are at risk. Hypersomnia in association with snoring usually signifies obstructive sleep apnea. Increased resistance in the upper airways, together with negative inspiratory pharyngeal pressure and muscular hypotonia during deep non-REM and REM sleep, lead to collapse of the pharynx, hypoxia and hypercapnia. Only after arousal from sleep does muscle tone return, pharyngeal obstruction reopen and airflow resume. Since this process can occur 300 or 400 times a night, repetitive alveolar hypoventilation leads to pulmonary-arterial hypertension and cor pulmonale, and the repetitive sympathetic activations can cause systemic hypertension or serious cardiac arrhythmias. The countless arousals deprive the sufferer of deep non-REM and REM sleep and their consequence is sleep fragmentation. The symptoms are excessive daytime sleepiness, intellectual deterioration and personality and behavioral changes. Oronasomaxillofacial, endocrine and neuromuscular anomalies and diseases predispose to sleep apnea, and alcohol or CNS-depressant drugs can favour its occurrence. Diagnosis is made by nighttime oxymetry, and if this is abnormal, by polysomnography. After polysomnography it is possible to distinguish between obstructive and nonobstructive sleep apnea, and the decisions for an adequate treatment can be made.
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PMID:[Dangerous snoring. Sleep-apnea syndrome]. 331 92

Sleep apnoea syndromes are a frequent disease, with an incidence of more than 1% in the adult population, a strong male predominance, and a maximal frequency between 40 and 60 years. Their clinical manifestations are dominated by snoring and daytime sleepiness, at times associated with morning headaches, intellectual deficiency, sexual impotence. Obesity, hypertension and polycythemia are not uncommon. These patients are at risk for accidents due to sleepiness, sudden death due to sleep apnoea-related cardiac arrhythmias, ischemic attacks related to hypertension and polycythemia and right heart failure secondary to pulmonary hypertension and alveolar hypoventilation. The most frequent form of sleep apnoea syndromes include obstructive and mixed apnoeas. Their mechanism involves both anatomic factors (upper airway narrowing) and functional factors (defective activation of upper airways dilatory muscles) which lead to upper airway occlusion upon inspiration during sleep. Two therapeutic strategies are possible: a surgical one, uvulopalatopharyngoplasty, the efficacy of which is inconstant and unpredictable and nasal continuous positive airway pressure, which is constantly efficacious but constraining. Central sleep apnoea syndromes are rare, less clearly defined and more difficult to treat.
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PMID:[Sleep apnea syndromes in adults]. 332 Dec 51

Although the initial sleep disorders classifications provided a framework for categorizing diagnoses, these early instruments had a number of limitations. Among their shortcomings were a lack of specific diagnostic criteria, limited clinical validation, and an overreliance on sleep laboratory findings. As a result, many of the diagnoses were not only poorly substantiated, but they lacked clinical relevance. Also, because of a fusing of diagnoses, a causal relationship was implied that may have been nonexistent and could misdirect the treatment focus. The ICD-10 represents a clinically based diagnostic classification. Furthermore, this classification system includes diagnostic criteria and encourages multiple diagnoses for a more complete description of the patient's clinical presentation. In addition, the ICD-10 allows for differentiation of psychogenic, developmental, and organic factors. Finally, it can be fully applied in the office setting, which allows physicians to maximize their interviewing and assessment skills to complete the diagnoses and subsequent treatment plans. Thus, this classification system strongly reinforces the doctor-patient relationship. It also facilitates consideration of the entire scope of the patient's problems in a truly biopsychosocial perspective. The prevalence of insomnia ranges across studies from 20 to 30% of the adult population. Before adulthood, its prevalence is below 2%. About 5% of adults complain of excessive daytime sleepiness. Among the conditions of excessive daytime sleepiness, narcolepsy has a prevalence of 0.1% and sleep apnea not more than 1% in the general adult population. Nightmares have a prevalence of about 5% in adulthood and 20% in childhood. Sleepwalking and night terrors have a prevalence of less than 1% in adulthood and 15 and 5%, respectively, in childhood.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nosology and prevalence of sleep disorders. 333 58

Besides sleep apnea, the main disorders of excessive daytime sleepiness include narcolepsy and hypersomnia. Narcolepsy is characterized by periods of irresistible sleepiness and sleep attacks of brief duration and, most often, by one or more of the auxiliary symptoms: cataplexy, sleep paralysis, and hypnogogic hallucinations. Generally, sleepiness and sleep attacks in hypersomnia are of longer duration and are more resistible than in narcolepsy; also, the auxiliary symptoms are absent. There are three types of hypersomnia: idiopathic, secondary, and periodic. Nocturnal sleep is typically disrupted in narcolepsy, whereas in idiopathic hypersomnia it is prolonged and in secondary hypersomnia it is variable. The exact causes of narcolepsy and idiopathic hypersomnia are unknown; however, there is evidence for genetic predisposition for either disorder. In secondary hypersomnia causative factors include: neurologic, such as head injuries, cerebrovascular insufficiency, and brain tumors; general medical, such as metabolic disorders, various intoxications, and conditions leading to brain hypoxia; and psychiatric, most notably depression. Although the cause of periodic hypersomnia is unclear, most research supports the notion of underlying organic disease. Often, the evaluation of patients with excessive daytime sleepiness can be completed in the office setting, based on the sleep history and a thorough neurologic, general medical, and psychiatric assessment. Whenever indicated, ancillary laboratory studies, such as computed tomography and magnetic resonance scans, should be performed. Sleep laboratory recordings generally are not necessary unless there is suspicion of sleep apnea or narcolepsy in the absence of auxiliary symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Disorders of excessive sleepiness: narcolepsy and hypersomnia. 333 60


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