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

Sudden infant death syndrome (SIDS) is diagnosed by the absence of lethal autopsy findings, or in a resuscitatable, "near miss" form with cyanosis, apnea, and bradycardia. The event is unexpected, although a minor respiratory infection is common, and occurs during sleep, between 1 and 6 months of age. There is growing evidence that the victims have had previous hypoxic episodes. Although suffocation is no longer considered a tenable explanation, other forms of airway obstruction are still postulated by many; the evidence, however, favors hypoxia as the common feature. A lethal arrhythmia had been proposed by several groups, based on inappropriate reflex activity, "pathology" of the conduction system, and the long QT syndrome, but the evidence is against arrhythmia as the primary event in most cases of SIDS. Based on the reversible "near miss," apnea is likely as the primary event in SIDS. Several reflexes have the ability to produce apnea, in addition to the relatively common sleep apnea; the crucial aspect, rather, appears to be thefailure of the immature infant to resume respiration. The possibility exists that the infant, who did not have to breather for 9 months of fetal life, literally is not alarmed and aroused by the persistance of apnea. In human and animal studies, respiratory infections and sleep deprivation have been proved to increase the likelihood and duration of sleep apnea. If primary apnea continues for long (45 seconds or more), a dangerous positive feedback develops into hypoxic apnea. Hhis will persist until circulatory failure occurs, or until gasping occurs. The gasp is a highly effective mechanism at birth, but will occur too late for autoresuscitation after the anerobic capacity of fetal life dimineshes; we believe this capacity lasts for approximately 1 month, accounting for the hiatus of crib death, sparing the first month. The "near-miss" infant, after resuscitation, should be monitored at home, if practical, until 6 months of age. A simple cardiac monitor for bradycardia has definite advantage over an apnea monitor alone.
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PMID:Sudden infant death syndrome (crib death). 1 76

Periodic sleep apnea, a chronic sleep deprivation state, in which marked changes in the arterial PO2 and PCO2 tensions have been recorded, is a relatively new syndrome not previously reported in pregnancy. It is characterized by episodes of apnea, prevalently obstructive, during sleep. The majority of patients with this syndrome have snored heavily for years, suggesting a causal relationship between snoring and periodic sleep apnea. The effects of prolonged snoring on alveolar ventilation and systemic pressure(s) suggest that this snoring has physiopathological implications on maternal cardio-respiratory reserve and indirectly upon the fetus, especially as there are recordable changes in fetal heart rate and also a change in the acid-base status of the fetus. The possibility that this syndrome may have an adverse effect upon the fetus is stressed.
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PMID:Fetal response to periodic sleep apnea: a new syndrome in obstetrics. 4 1

In this part of the chapter we have used new terminology and developed a new system for classification of sleep disorders in children. We suggest that excessive daytime sleepiness should be investigated by clinicians before troubles at school necessitate referral. The narcolepsy-hypersomnia syndrome generally has not been recognized in the pediatric age group. Symptoms of excessive fear of falling asleep need to be viewed in this context. Sleep apnea-hypersomnia has received insufficient attention in the American literature. It is a syndrome that affects both adults and children with potentially disastrous cardiovascular and pulmonary complications. The relationship of the sleep apnea-hypersomnia syndrome to the sudded infant death syndrome remains speculative, although preliminary results from our longitudinal study have indicated a possible link. Both the narcolepsy-hypersomnia and the sleep apnea-hypersomnia syndromes are reviewed in detail. In contrast, we review briefly the NREM dyssomnias, including night terrors, sleepwalking, sleep talking and enuresis. All are well known to clinicians dealing with children, and we have related them to findings emanating from the sleep laboratory. We suggest that they are physiologically rather than psychogenically based and frequently represent immaturities of the central nervous system. Finally, the insomnias of childhood are presented. We emphasize that they are rare, and after ruling out organic conditions and drug-dependency syndromes, cultural styles or family stresses generally account for the majority of complaints.
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PMID:The pathophysiology of sleep disorders in pediatrics. Part II. Sleep disorders in children. 5 11

A sleep apnea syndrome has been diagnosed in eight children (age range 5-14). Before undertaking therapeutic trials, sleep and respiration were extensively studied. Sleep and respiration were again analyzed 3 months after tonsillectomy and adenoidectomy (6 cases) or tracheostomy with insertion of valve (2 cases). Sleep induced apneic apisodes in these children who had normal respiration during wakefulness. Three types of apnea (central, upper airway, and mixed) were recorded in each case. The minimum number of apneas recorded during a single night was 75; the maximum was 816. Polygraphic monitoring demonstrated greatly disturbed sleep. Sleep changes were quantitative as well as qualitative. REM sleep percent was decreased, but stages 3 and 4 NREM sleep were also impaired. A relationship between stages 3-4 NREM sleep and respiration was noted: stages 3-4 sleep disappeared when apneic episodes were numerous; no apnea was recorded during stage 4 sleep. Follow-up nocturnal recordings of two tracheostomized children with valve open, then closed, confirmed this "stage 4/no apnea" relationship. Apneas were also noted to induce marked sinus arrhythmia during sleep.
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PMID:[Sleep and respiration in the syndrome "apnea during sleep" in the child]. 6 Feb 23

The authors studied the direct and integrated EMG activities of the cricothyroid (CT) and chin muscles in 7 patients with the sleep apnea syndrome. They noted: (1) A tonic activity with phasic inspiratory reinforcements in the CT during wakefulness. (2) A decrease in the tonic activity without any modification of the phasic inspiratory reinforcement during sleep. (3) A decrease or even disappearance of the phasic activity during sleep-induced hypopneas. (4) A complete cessation of both the tonic and the phasic activities of the CT during obstruction apneas: resumption of respiration is marked by the reappearance first of the phasic inspiratory activity and secondly of the tonic one. (5) In some patients similar activities are recorded in the chin muscles during wakefulness, sleep and sleep apnea. These results favor possible obstruction of the upper airway at the laryngeal level: the conjunction of inhibition of the inspiratory activity of the laryngeal muscles with the subsequent closing of the glottis and inspiratory depressure could produce an obstruction.
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PMID:EMG activity of cricothyroid and chin muscles during wakefulness and sleeping in the sleep apnea syndrome. 8 45

Information which has emerged thus far relates to the overall transmitter mechanisms of sleep. The data, while conflicting, point to the involvement of many neuroregulators at numerous integrative levels of the process. However the long term question still remain: what triggers and maintain sleep, what stops sleep, what occurs to the body and brain during sleep--in essence, why sleep? These questions are now problems for behavioral neurochemists, whereas in a previous era, they were problems for philosophers. Unfortunately, our answers to date, while in another idiom, have hardly been more complete or satisfying. To answer these questions, it will be necessary to understand, in detail, the manner in which neurobiochemical processes relate to the functional physiology of sleep. Although existing studies have given invaluable insight into the neurochemical anatomy of sleep, we have only recently acquired the technical and biochemical expertise necessary to investigate sleep as it occurs normally. Future research must focus on the dynamic changes associated with the regulatory mechanisms of neurotransmitters. Many questions can be asked. With sleep transitions, what changes occur in transmitter content, synthesis, or release? Are there changes in metabolic pathways, reflecting a shift from intra- to interneuronal metabolism? What changes occur in pre- and postsynaptic neurotransmitter receptors to affect sensitivity? What constraints do genetic (245) and environmental (246) factors impose upon these mechanisms? Knowledge of such parameters will allow us to construct more complete models of the neuroregulatory basis of sleep and waking. However, as we acquire this knowledge, we must avoid the temptation of assuming causation when the evidence merely shows correlation. Neuroregulation are involved in the control of number different behaviors; and, at present, we have few, if any, methods of establishing causative links between a specific neuroregulator and a specific behavioral state. Yet, even without an understanding of what "causes" sleep, we may be able to develop pharmacological agents which permits discrete alteration of sleep mechanisms in a more physiological and specific manner. This potential for manipulation of sleep is of obvious importance in illnesses such as insomnia, narcolepsy, and sleep apnea (247, 248). In addition, it may be valuable in the treatment of such conditions as psychosis and depression, where sleep disturbances are an important component of the illness. For example, delirium tremens might be best understood as a psychotic episode which is the result of an aspect of sleep emerging into wakefulness. The range and breadth of both the basic questions and the potential application of sleep research portend an exciting future for this field.
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PMID:Neuroregulators and sleep mechanisms. 16 54

A series of 235 consecutive patients refferred to the Stanford University Sleep Disorders Clinic with the complaint of excessive daytime sleepiness (EDS) were investigated extensively. A satisfactory final diagnosis involving a consistent syndrome or pathogenic process was made in all but 7 patients. In the course of this work a variety of tests, including prolonged polygraphic monitoring of multiple variables and CSF measurements before and after probenecid ingestion, were utilized. Different syndromes were confirmed (harmonious hypersomnia, subwakefulness syndrome); the definitions of others were clarified and extended (narcolepsy, drug dependency, periodic hypersomnia associated with menstruation, upper airway sleep apnea in children). Two new entities were tentatively identified (narcolepsy with sleep apnea, the neutral state syndrome). Narcolepsy and upper airway sleep apnea accounted for the majority of the cases (199). A strategic schema utilizing specific categories and frequency of occurrence in the case series is presented to improve the diagnosis of the complaint of excessive daytime sleepiness by the practicing physician. This case series was analysed in order to develop tentatively a meaningful nosology.
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PMID:235 cases of excessive daytime sleepiness. Diagnosis and tentative classification. 18 92

The sleep state characteristics of infant sleep apnea were studied in 36 twins examined by polygraphy at 40, 44, and 52 weeks after conception. The definition of sleep apnea is dependent upon the length of apnea, sleep state, and post-conceptional age. None of the infants had apnea longer than 20 seconds and apnea of 10 seconds or longer was uncommon. The attack rates for apneas 2 to 4.9 seconds long were highest in REM and lowest in qliet sleep. The attack rates for apneas 5 to 9.9 seconds long were equal in REM and indeterminate and lowest in quiet sleep. The percentage of infants with apnea of 10 seconds or longer at 40 weeks was highest in REM (27%) and indeterminate sleep (42%) and lowest in quiet sleep (12%). At 52 weeks, apnea 10 seconds or longer during REM decreased to 0%. The effect of maturation on apnea varies with sleep state. Over the period from 40 to 52 weeks, quiet sleep apnea was unchanged and indeterminate sleep apnea decreased only between 40 and 44 weeks. Although REM apnea 2 to 4.9 seconds long was unchanged, REM apnea 5 to 9.9 seconds long decreased between 40 and 44 weeks, and REM apnea of 10 seconds or longer decreased from 27% at 40 weeks to 0% at 52 weeks. This suggests that semi-independent apnea turn-on and turn-off mechanism operate during REM sleep. A correlation between brief apneas and the longer apneas was seen only during REM sleep. For all sleep states, there was no correlation between the levels of apnea of 5 seconds or longer at 40, 44, and 52 weeks.
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PMID:The sleep state characteristics of apnea during infancy. 18 81

This report is based on a study of 53 infants, 28 of whom had clinically observed prolonged apnea (greater than or equal to 20 seconds) during sleep whereas the remaining did not. In addition to the clinical observations, each infant was studied in a sleep laboratory during a complete nap, and a continuous recording was made of respiratory activity and rapid eye movements. Measurements were made of all apneic pauses (greater than or equal to 2 seconds) observed in the laboratory and the two groups of infants were compared in terms of the frequency and average duration of apneic pauses, the longest apneic pause, the amount of periodic apnea, and the relative amount of apnea. The infants with prolonged sleep apnea had, during a single nap, more frequent and longer apneic pauses and more periodic apnea. This supports the hypothesis that respiratory instability during sleep and prolonged apnea have a common etiology. By employing a multiple linear regression model and including all laboratory apnea measures in a single analysis, a composite laboratory score was developed to differentiate members of the two groups. It would thus appear that the study of infants during a single nap could assist in the identification of infants at risk for prolonged sleep apnea and provide an indirect method for determining the influence of a number of variables on the occurrence of prolonged sleep apnea. Pediatrics, 59:962-970, 1977, SLEEP, APNEA, RESPIRATORY INSTABILITY.
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PMID:Prolonged sleep apnea and respiratory instability: a discriminative study. 19 14

Eleven patients with upper airway apnoea during sleep (one with SHY-Drager syndrome) were monitored polygraphically for wakefulness, sleep, and cardiovascular variables. Systemic hypertension and most of the severe arrhythmias recorded during sleep were secondary to repetitive obstructive apnonea and were mediated through the autonomic nervous system. Sleep related elevations of pulmonary arterial pressure were not influenced by atropine or impaired autonomic functions. Upper airway sleep apnoea is sleep related; the type of sleep (REM or NREM) is critical in the appearance of abnormalities. The distinction between two patient subgroups (total sleep dependent and NREM sleep dependent) has haemodynamic, and possibly long-term, implications. Sleep apnoea syndrome should be looked for in pateints with the Shy-Drager syndrome.
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PMID:Sleep apnoea syndrome: states of sleep and autonomic dysfunction. 19 9


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