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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The authors studied the occurrence of depression in 100 randomly selected patients with narcolepsy and in 30 patients with hypersomnia. In the isolated form of idiopathic narcolepsy (without signs of cataplexy, sleep paralysis or hypnagogic hallucinations) depression occurred 28.6 per cent of cases. In idiopathic narcolepsy with cataplexy or other symptoms of sleep dissociation, depression was found in 17.2 per cent of cases. In idiopathic hypersomnia the occurrence of depression was 26.1 per cent. In the majority of cases the endogenous form of depression was observed. In the symptomatic form of narcolepsy and hypersomnia the occurence of depression has not been noted in any case. In most cases a parallel clincial course has been observed between the manifestation of depression and narcolepsy or hypersomnia. During a remission of the depressive state the hypersomniac symptoms decreased or disappeared totally. The authors furter discuss the possible pathophysiological mechanisms of the above mentioned symptoms. They are of the opinion that an important role is played by the secretion and metabolism of the cerebral monamines.
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PMID:Depresssion in narcolepsy and hypersommia. 16 33

Previous investigations have indicated that one of the most consistent EEG sleep findings in depressive patients has been a shortened REM latency. On the basis of these studies, we have concluded that with the exception of drug withdrawal states (such as CNS depressant or amphetamine withdrawal and narcolepsy) shortened REM latency points to a strong affective component in the patient's illness. Short REM latency has also been observed in patients suffering from schizo-affective illness as well as in certain schizophrenic patients who require tricyclic antidepressants in their management. Furthermore, this psychobiologic marker is a persistent, rather than a transient phenomenon, and can be observed over a period of several weeks unless a patient's condition becomes more favorable through clinical intervention. This present report indicates that short REM latency is found in virtually all primary depressive illness and is absent in secondary depression. Thus, REM latency appears to be a dependable, measurable marker for diagnosing primary depression, and we argue that the phenomenon is independent of age, drug effect and changes in other sleep parameters. It is expected that EEG sleep and motor measurements can yield further significant data and improve differential diagnosis in psychiatry, in much the same way that laboratory data support other medical specialities.
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PMID:REM latency: a psychobiologic marker for primary depressive disease. 18 39

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

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

Neurochemical analyses were performed on brains obtained at post mortem from 3 patients with narcolepsy. The salient findings were an increase in noradrenergic and serotonergic neuronal activity, a decrease in dopaminergic neuronal activity, and, in 2 of the 3 brains, a decrease in the number of alpha-1-noradrenergic receptors in the frontal cortex and amygdala. A pathophysiological model for narcolepsy is developed on the basis of these findings. The neurobiology of narcolepsy is compared with that of depression. The role of MHC--class II gene products in the genesis of narcolepsy is discussed. Some treatment implications follow.
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PMID:A perspective on narcolepsy. 133 29

Primary insomnia, major depression, and narcolepsy are usually considered to be separate disorders, distinguished by different polysomnographic profiles. But do polysomnographic data provide adequate evidence to segregate the three disorders, or might they display fundamentally the same sleep disturbance, differing only in degree? To test the viability of these two alternate hypotheses, the authors performed a meta-analysis of controlled polysomnographic studies of these disorders. A summary measure of degree of sleep disturbance was constructed from five variables: wakefulness after sleep onset, percentage of stage 1 sleep, percentage of stage 3 + 4 sleep, rapid eye movement (REM) latency, and REM density. The results of available studies for each variable were combined using a weighted average of effect sizes. An overall "sleep disturbance index" was then calculated by combining the estimates for the five above listed variables. On both the individual measures and especially on the summary index, insomnia, depression, and narcolepsy were arrayed on a simple continuum of progressively more severe sleep disturbance--congruent with the clinical observation that these disorders display progressively more disturbed sleep. These findings suggest that sleep can be disturbed in only a limited number of ways: in evaluating sleep architecture, it may not be possible to elaborate much beyond a single axis of good-to-bad sleep. Thus, polysomnographic measures may not provide adequate evidence to classify insomnia, depression, and narcolepsy as separate entities.
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PMID:Good sleep, bad sleep: a meta-analysis of polysomnographic measures in insomnia, depression, and narcolepsy. 146 88

Children and adolescents doing poorly in school or at home or both are often labelled as suffering from attention deficit hyperactivity disorder (ADHD). Frequently the referred child is not examined systematically for the presence of other disorders. This paper presents the diagnostic criteria and management of disorders that may be wrongly identified as ADHD or may coexist with ADHD, thus complicating identification and treatment. The disorders discussed are depression, mania, primary disorder of vigilance, narcolepsy, developmental specific learning disorders, conduct disorders, and acquired neurologic deficits.
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PMID:Attention deficit hyperactivity disorder: the differential diagnosis. 200 14

Bright white light (500lx) for 4 h/day was applied to seven narcoleptic patients (age 47-65 years, mean 55 years). The effects of the light on the disturbed sleep-wake cycle in narcoleptics were investigated by the measurement of the following parameters: (1) excessive daytime sleepiness and sustained attention (multiple sleep latency test); (2) rest-activity cycles; (3) self-ratings (mood, anxiety, tiredness); (4) urinary cycles of 6-OH melatonin sulphate and cortisol; (5) sleep EEG. Treatment with bright light showed neither objective nor subjective changes in the clinical symptoms of narcolepsy. While similar "dosage" light applications can phase shift human circadian rhythms and improve depression and hypersomnia in winter depression, it is not an appropriate treatment for narcolepsy.
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PMID:Bright white light does not improve narcoleptic symptoms. 275 54

Based on self-rating questionnaire evaluation of symptoms of major affective disorder, 67% of patients who presented to a major sleep disorders center reported an episode of depression within the previous 5 years, and 26% described themselves as depressed at presentation. Furthermore, patients with sleep apnea, narcolepsy, or sleep-related periodic leg movements all averaged high rates of self-reported depressive symptomatology, which suggests that sleep disorders should be considered in the differential diagnosis of affective disorders, and vice versa. Change scores on the Profile of Mood States were obtained for four subgroups of patients who were undergoing conventional treatment. Significant improvement in scores was observed in obstructive sleep apneics treated surgically and in patients with sleep-related periodic leg movements placed on clonazepam, but not in narcoleptics placed on a stimulant or in insomniacs with chronic use of sedative-hypnotic drugs who were withdrawn from sleep medications. Differential improvement in POMS scores after treatment for different sleep disorders could mean that the relationship to mood disturbance differs for different sleep disorders.
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PMID:Self-reported depressive symptomatology, mood ratings, and treatment outcome in sleep disorders patients. 292 84


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