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Query: UMLS:C0037315 (sleep apnea)
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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

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

Growth hormone (GH) and prolactin (PR) secretion were evaluated in 28 patients who had sleep apnea or narcolepsy but no other primary neurologic or endocrine disorders. Eighty-one percent of subjects with impaired alertness failed to demonstrate serum GH concentrations in excess of 5 ng per milliliter following oral administration of L-DOPA, 500 mg. Diminished GH responses to sleep and intravenous arginine were observed in 57 percent and 44 percent, respectively, of patients tested. Sleep-related PRL release was less than normal in women with narcolepsy, with or without sleep apnea. All patients had at least one abnormality in GH or PRL secretion.
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PMID:Disordered growth hormone and prolactin secretion in primary disorders of sleep. 57 7

The association of sleep apnea with daytime hypersomnolence without obesity, and its potentially lethal cardiopulmonary sequelae, make it crucial that this condition be distinguished from narcolepsy. A patient with retrognathia who had been diagnosed as a narcoleptic for 15 years had the primary complaint of excessive daytime sleepiness. Sleep laboratory evaluation showed severe hypoxemia and a mean of 366 upper airway obstructions per night. The patient was treated with a tracheotomy; this resulted in relief of the sleep-related upper airway obstructions, hypoxemia, and hypersomnolence.
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PMID:Retrognathia and sleep apnea. A life-threatening condition masquerading as narcolepsy. 57 59

A patient with hypersomnolence, micrognathia, and respiratory insufficiency had been treated eight years for narcolepsy. Sleep apnea because of upper airway obstruction was found, and a tracheostomy was performed. Following this the hypersomnolence and respiratory insufficiency resolved. This case emphasizes the importance of carefully evaluating the condition of patients complaining of hypersomnolence to detect those with intermittent upper airway obstruction occurring during sleep.
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PMID:Hypersomnolence and intermittent upper airway obstruction. Occurrence caused by micrognathia. 57 27

Primary sleep disorders include narcolepsy, the Pickwickian syndrome, sleep apnea in infants and other rare conditions. Secondary sleep disorders occur in depression, alcoholism, endocrinopathies, heart failure and pregnancy. Medical symptomatology often increases during rapid-eye-movement (REM) sleep, when physiologic activity is high. Insomnia, the most common sleep disorder, requires careful work-up, attempts at environmental manipulation and judicious short-term pharmacotherapy. Pharmacologic manipulation of sleep is beset with complications. A basic understanding of properties and side effects of the sleep-inducing drugs is needed in order to select the optimal agent.
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PMID:Sleep disorders and insomnia. 62 43

Narcolepsy may affect as many as 200,000 Americans. The illness involves a neurologic defect in the regulation of sleep and wakefulness. The chief symptoms are sleepiness, inappropriate sleep episodes, and cataplexy. A characteristic history of cataplexy establishes the diagnosis. Narcoleptic patients also frequently complain of hypnagogic hallucinations, sleep paralysis, blackouts (or automatic behavior), and disturbed nocturnal sleep. Narcolepsy usually develops in adolescence and is a life-long illness. Symptoms may also appear in young children who may be misdiagnosed as hyperactive or psychotic. No completely satisfactory treatment is available at the present time. The current treatments of choice are methylphenidate (for sleepiness and sleep episodes) and imipramine (for cataplexy). Medication dosages must be adjusted for individual patients. A careful history of the illness can rule out hypothyroidism, hypoglycemia, and epilepsy. Sleep apnea is a serious complication of narcolepsy and may be life threatening.
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PMID:Narcolepsy. Diagnosis and treatment. 105 17

Very few epidemiological surveys have specifically studied relationships between sleep disturbances and psychiatric diseases. In this review, we preferred to use the classification proposed in 1979 by the Association of Sleep Disorders Centers. It includes four main categories: insomnias, excessive sleepiness, troubles of the wake/sleep schedule and parasomnias. Evaluating psychiatric disorders among general populations is easier owing to DSM III and DSM III-R criteria, but there are not equivalent criteria in evaluating sleep disorders. It is almost impossible to realize polysomnographic recordings in large samples, therefore sleep disorders are to be detected by questionnaires. It has been shown that there is a good correlation between self-reports and polysomnographic recordings among clinical and general samples. The prevalence of insomnia, defined as difficulties of initiating and maintaining sleep, is estimated between 9 and 31%. It is higher among women, elderly people, separated and divorced subjects, and low educational levels' groups. It has to be noticed that polysomnographic records of some subjective insomniacs are not different from those of good sleepers, sleep latency excepted. These subjective (and not objective) insomniacs have high scores in anxiety scale, depression scale, or psychologic distress. Insomnia is more frequently noted amongst subjects with psychiatric diagnoses, especially major depressive disorders and anxiety disorders. Depressive disorders are present in 21-40% of insomniacs versus 0-1% of non-insomniacs, and anxiety disorders in 13-24% of insomniacs versus 3-10% of non-insomniacs. In depressive disorders, sleep alterations are frequently noted: they are difficulties of initiating and maintaining sleep, decreasing proportion of slow-wave sleep, decreasing time of REM (rapid eye movement) sleep and REM sleep latency, and increasing density of REM sleep. Of these modifications, the last two ones seem to be specific for depression. The relationships between sleep, aging and depression are more complex than previously noted. For example, differences between depressed and non-depressed subjects depend on the age of the population. The prevalence of hypersomnia is lower than the insomnia's. It varies between 2 and 4%. It is more frequently noted among young people, and never married subjects. Two specific aetiologies must be looked for: sleep apnea syndrome and narcolepsy. These diagnoses are respectively found in 45% and 24% of hypersomniacs examined in American Sleep Centers. Hypersomnias are objectived by the Multiple Sleep Latency Test, which measures the physiologic sleep tendency.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Sleep disorders in psychiatric diseases. Epidemiological aspects]. 129 83

The multiple sleep latency test (MSLT) has proved to be a useful diagnostical tool for patients complaining of excessive daytime sleepiness (EDS). The intention of the present study was to investigate the structure of MSLT naps and in particular sleep spindle and k-complex density in three different groups of EDS patients. MSLT was performed at 8 a.m., 10 a.m. 12 a.m., 2. p.m. and 4 p.m.. Each recording lasted 20 minutes and was not stopped even if sleep occurred before 20 min. Sleep was scored visually. Spindle and k-complex density was determined per minute of S2 sleep. Statistical analysis used ANOVA. Each of the three groups consisted of 15 patients. Diagnosis of narcolepsy, sleep apnea, of EDS due to a psychiatric disorder has been confirmed subsequently. There were 5 female and 10 male narcoleptics (mean age: 43.9 +/- 10.9 years), 2 female and 13 male obstructive sleep apnea patients (mean age: 53.9 +/- 10.9 years) and 7 female and 8 male patients complaining of EDS, in whom a psychiatric disorder was diagnosed (mean age: 38.8 +/- 13.8 years). Narcoleptics sent more than half of the recording time of 100 min asleep (52.9%). Apnea patients slept 41.3% and psychogenic EDS patients 22.7%. The proportion of sleep stages 1 and 2 in narcoleptics (S2/S1 = 1:1) was clearly different from the other two (apnea patients: S2/S1 = 4:1; psychogenic EDS patients: S2/S1 = 3:1). 18.5% of the naps contained stage REM and during the afternoon naps 0.9% of S3 in the narcoleptics. Neither REM nor S3 was observed in the others.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Quality of day time sleep in the multiple sleep latency tests in patients with narcolepsy, obstructive sleep apnea and psychogenic hypersomnia]. 148 26


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