Narcolepsy and Idiopathic Hypersomnolence

Choo, Kah Lin; Guilleminault, Christian

doi:10.1016/s0272-5231(05)70440-8

Cited by 13 publications

(5 citation statements)

References 45 publications

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“…Med. 2006;166:1739-1743 N A R C O L E P S Y I S A D I Sabling sleep disorder that affects approximately 1 in 2000 individuals in the general US population 1 and in Europe 2 and is characterized by excessive daytime sleepiness, cataplexy, hypnagogic hallucinations, and sleep paralysis. 3 Since the discovery of the extremely close association of narcolepsy and the human leukocyte antigen (HLA)-DR2, 4,5 it has been suggested that the immune system might play a pathogenic role because it is known that HLA haplotypes are linked to a number of autoimmune diseases.…”

Section: Discussionmentioning

confidence: 99%

Plasma Levels of Tumor Necrosis Factor α and Soluble Tumor Necrosis Factor Receptors in Patients With Narcolepsy

et al. 2006

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Section: Discussionmentioning

confidence: 99%

Plasma Levels of Tumor Necrosis Factor α and Soluble Tumor Necrosis Factor Receptors in Patients With Narcolepsy

et al. 2006

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“…Low levels of orexin or its receptors are associated with narcolepsy – a serious neurological disease that is characterized by inability to produce stabilized periods of either sleep or wakefulness, resulting in awakenings during night and sleep periods, including intrusion of REM sleep (with atonia) into wakefulness. The dramatic muscle atonia periods during wakefulness are often triggered by positive emotions (Choo & Guilleminault ).…”

Section: Problems With Sleepmentioning

confidence: 99%

Sleep, its regulation and possible mechanisms of sleep disturbances

2013

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The state of sleep consists of different phases that proceed in successive, tightly regulated order through the night forming a physiological program, which for each individual is different but stabile from one night to another. Failure to accomplish this program results in feeling of unrefreshing sleep and tiredness in the morning. The program core is constructed by genetic factors but regulated by circadian rhythm and duration and intensity of day time brain activity. Many environmental factors modulate sleep, including stress, health status and ingestion of vigilance-affecting nutrients or medicines (e.g. caffeine). Acute sleep loss results in compromised cognitive performance, memory deficits, depressive mood and involuntary sleep episodes during the day. Moreover, prolonged sleep curtailment has many adverse health effects, as evidenced by both epidemiological and experimental studies. These effects include increased risk for depression, type II diabetes, obesity and cardiovascular diseases. In addition to voluntary restriction of sleep, shift work, irregular working hours, jet lag and stress are important factors that induce curtailed or bad quality sleep and/or insomnia. This review covers the current theories on the function of normal sleep and describes current knowledge on the physiologic effects of sleep loss. It provides insights into the basic mechanisms of the regulation of wakefulness and sleep creating a theoretical background for understanding different disturbances of sleep.

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“…Narcolepsy is characterized by two principal symptoms, excessive daytime sleepiness and cataplexy, and three supplementary symptoms, hypnagogic or hypnopompic hallucinations, sleep paralysis, and fragmented nocturnal sleep. 74 Cataplexy and hallucinations are considered symptoms of the intrusion of REM sleep signs into wakefulness.…”

Section: New Perspectives: Orexin and The Control Of Sleep And Wakefumentioning

confidence: 99%

Neurophysiological Mechanisms of Sleep and Wakefulness: A Question of Balance

Sinton

McCarley

2004

Semin Neurol

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Following a summary of the stages of sleep and wakefulness as monitored with the electroencephalogram and electromyogram, important aspects of the neurophysiology and neuroanatomy of the circuits of vigilance state control are reviewed. A homeostatic drive for sleep and a circadian influence work in concert to determine sleepiness. These processes influence sleep-promoting and central arousing neuronal systems, the former dependent on a group of neurons in the hypothalamic ventrolateral preoptic area and the latter governed by neurons in the pons and basal forebrain. The interactive neuronal circuit that is formed by these cell groups ensures the balance between sleep and wakefulness and the rapid transition to and from sleep. As sleep deepens, the switch to rapid eye movement (REM) sleep occurs. This transition can also be viewed as a balance between one group of pontine neurons that discharge only during REM sleep and another group that cease to discharge during REM sleep. This article concludes with future perspectives based on the recent discovery of the orexin cell group. Orexinergic neurons may be critical both for promoting wakefulness at certain times in the daily cycle and for controlling the switch into REM sleep.

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Narcolepsy and Idiopathic Hypersomnolence

Cited by 13 publications

References 45 publications

Plasma Levels of Tumor Necrosis Factor α and Soluble Tumor Necrosis Factor Receptors in Patients With Narcolepsy

Plasma Levels of Tumor Necrosis Factor α and Soluble Tumor Necrosis Factor Receptors in Patients With Narcolepsy

Sleep, its regulation and possible mechanisms of sleep disturbances

Neurophysiological Mechanisms of Sleep and Wakefulness: A Question of Balance

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