CSF Histamine Contents in Narcolepsy, Idiopathic Hypersomnia and Obstructive Sleep Apnea Syndrome

Kanbayashi, Takashi; Kodama, Tohru; Kondo, Hideaki; Satoh, Shinsuke; Inoue, Yuichi; Chiba, Shigeru; Shimizu, Tetsuo; Nishino, Seiji

doi:10.1093/sleep/32.2.181

Cited by 159 publications

(88 citation statements)

References 34 publications

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“…To evaluate for the effects of medication on the stability of MSLT-based diagnosis, medication usage was characterized as changed or unchanged (specifically considering wake-promoting medications and selective serotonin and/ or noradrenergic reuptake inhibitors), and a Fisher exact test was performed comparing medication class changes with diagnosis change. As an exploratory analysis, demographic and clinical features were compared between those whose diagnosis changed and those whose diagnosis remained the same, using χ 2 …”

Section: Discussionmentioning

confidence: 99%

“…More cost-effective measures are needed, in addition to identification of a biomarker with diagnostic and therapeutic significance. While deficiencies in histamine have been proffered as one such biomarker, 2 these results were not replicable with more sensitive technologies. 34 Recent work suggests that somnolence in the CNS hypersomnias may derive from a gain in function in endogenous γ-aminobutyric acid (GABA) signaling mediated by a naturally occurring constituent of cerebrospinal fluid that allosterically modulates GABA A receptors.…”

Section: -32mentioning

confidence: 97%

“…1 Cataplexy is a clinical feature highly specifi c to hypocretin-defi cient narcolepsy, although is not always evident near the onset of sleepiness. The remaining CNS hypersomnias begin at a similar age, are much less likely to be associated with hypocretin defi ciency, [1][2][3][4] and lack a pathognomonic sign or symptom. 5,6 They have many features in common, including hallucinations and sleep paralysis, 1,4 unrefreshing naps, 7,8 sleep drunkenness, 1,7,8 and prolonged nocturnal sleep.…”

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confidence: 99%

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Test-Retest Reliability of the Multiple Sleep Latency Test in Narcolepsy without Cataplexy and Idiopathic Hypersomnia

Trotti

Staab²,

Rye³

2013

Journal of Clinical Sleep Medicine

179

107

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conducted within three weeks of each other.11 Inter-test intervals are generally much longer in clinical practice, and in that case the stability of MSLT features has not been established. We therefore evaluated the test-retest reliability of the MSLT in a clinic population of patients with narcolepsy without cataplexy and idiopathic hypersomnia. METHODS Patient SelectionPatients with a clinical syndrome consistent with a CNS hypersomnia (i.e., reports of problematic, excessive daytime sleepiness persisting ≥ 3 months despite adequate or supra-normal habitual sleep durations, not explained by other causes of daytime sleepiness) who had undergone 2 MSLTs were identiStudy Objectives: Differentiation of narcolepsy without cataplexy from idiopathic hypersomnia relies entirely upon the multiple sleep latency test (MSLT). However, the test-retest reliability for these central nervous system hypersomnias has never been determined. Methods: Patients with narcolepsy without cataplexy, idiopathic hypersomnia, and physiologic hypersomnia who underwent two diagnostic multiple sleep latency tests were identifi ed retrospectively. Correlations between the mean sleep latencies on the two studies were evaluated, and we probed for demographic and clinical features associated with reproducibility versus change in diagnosis. Results: Thirty-six patients (58% women, mean age 34 years) were included. Inter-test interval was 4.2 ± 3.8 years (range 2.5 months to 16.9 years). Mean sleep latencies on the fi rst and second tests were 5.5 (± 3.7 SD) and 7.3 (± 3.9) minutes, respectively, with no signifi cant correlation (r = 0.17, p = 0.31). A change in diagnosis occurred in 53% of patients, and was accounted for by a difference in the mean sleep latency (N = 15, 42%) or the number of sleep onset REM periods (N = 11, 31%). The only feature predictive of a diagnosis change was a history of hypnagogic or hypnopompic hallucinations. Conclusions S C I E N T I F I C I N V E S T I G A T I O N ST he central nervous system (CNS) hypersomnias manifest as excessive daytime sleepiness with or without prolonged nocturnal sleep in the absence of demonstrable nocturnal sleep pathology or insuffi cient sleep. They include the entities of narcolepsy with and without cataplexy and idiopathic hypersomnia. Narcolepsy with cataplexy is a chronic disease characterized by short latencies to both sleep and REM sleep on daytime nap opportunities during the multiple sleep latency test (MSLT) and is caused by immunogenetically mediated loss of hypocretin.1 Cataplexy is a clinical feature highly specifi c to hypocretin-defi cient narcolepsy, although is not always evident near the onset of sleepiness. The remaining CNS hypersomnias begin at a similar age, are much less likely to be associated with hypocretin defi ciency, 1-4 and lack a pathognomonic sign or symptom. 5,6 They have many features in common, including hallucinations and sleep paralysis, 1,4 unrefreshing naps, 7,8 sleep drunkenness, 1,7,8 and prolonged nocturnal sleep. [8][9][10] Therefore, differenti...

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Section: Discussionmentioning

confidence: 99%

Section: -32mentioning

confidence: 97%

mentioning

confidence: 99%

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Test-Retest Reliability of the Multiple Sleep Latency Test in Narcolepsy without Cataplexy and Idiopathic Hypersomnia

Trotti

Staab²,

Rye³

2013

Journal of Clinical Sleep Medicine

179

107

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“…This therapeutic approach is based on a clearly defined molecular target, the H 3 receptor, and the well established role of histaminergic neurons in qualitative and cognitive aspects of waking (Lin, 2000;Passani et al, 2004;Ligneau et al, 2007b;Anaclet et al, 2009). Moreover, a defect in the histaminergic system is the direct cause of somnolence of diverse pathological origins in animals and patients with sleep disorders (Parmentier et al, 2002;Kanbayashi et al, 2009;Nishino et al, 2009). Therefore H 3 receptor inverse agonists provide a most promising therapy for unwanted (pathological) somnolence.…”

Section: H 3 Receptors: Targets For Arousal Control and Treatment Of mentioning

confidence: 99%

Histamine H₃ Receptors and Sleep-Wake Regulation

Lin

Sergeeva²,

Haas³

2010

J Pharmacol Exp Ther

121

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The histaminergic system fulfills a major role in the maintenance of waking. Histaminergic neurons are located exclusively in the posterior hypothalamus from where they project to most areas of the central nervous system. The histamine H 3 receptors are autoreceptors damping histamine synthesis, the firing frequency of histamine neurons, and the release of histamine from axonal varicosities. It is noteworthy that this action also extends to heteroreceptors on the axons of most other neurotransmitter systems, allowing a powerful control over multiple homeostatic functions. The particular properties and locations of histamine H 3 receptors provide quite favorable attributes to make this a most promising target for pharmacological interventions of sleep and waking disorders associated with narcolepsy, Parkinson's disease, and other neuropsychiatric indications. Sleep and WakingWakefulness and consciousness depend on perturbation of intrinsic cortical activity that is achieved through ascending activating systems taking a ventral route, the ascending reticular activating system of Moruzzi and Magoun, and a dorsal route whose main station is the hypothalamus. Both pathways send direct projections to the cortex and indirect ones through the thalamus, the door to perception of sensory input. Both waking and paradoxical sleep (REM) are conscious states and need activation by subcortical structures, although in different ways.Cholinergic neurons of the brainstem and the basal forebrain discharge tonically during both wakefulness and paradoxical sleep, can directly excite cortical neurons, and facilitate the thalamo-cortical transmission by inhibiting the thalamic reticular sleep-onset generator. Brainstem and basal forebrain cholinergic neurons are excited by glutamatergic, noradrenergic, and histaminergic neurons; they are particularly important in cortical electroencephalogram arousal, but do not seem to be essential for the waking state (Szymusiak and McGinty, 1986;Lin, 2000).Monoaminergic ascending projections containing catecholamines and serotonin are involved in sleep-waking regulation and the pathophysiology of major psychiatric disorders, schizophrenia, and depression, all of which include disturbance in sleep-waking. Inhibition of catecholamine synthesis decreases waking, and psychostimulants, such as amphetamine, increase waking through accumulation of catecholamines. A lesion of the serotonergic dorsal raphe causes insomnia. These aminergic systems mediate different behavioral expressions during waking, activate immediate early genes, and facilitate locomotion, perception, and cognition (reviewed in Jones, 2005).

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“…Patients with IH may have low CSF histamine levels, 89 although this was not replicated. 36 Patients with IH may have higher total serum IgG levels than control subjects (in contrast to patients with narcolepsy with cataplexy who have lower total levels).…”

Section: Epidemiologymentioning

confidence: 98%

Central Disorders of Hypersomnolence

Khan¹,

Trotti²

2015

Chest

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The central disorders of hypersomnolence are characterized by severe daytime sleepiness, which is present despite normal quality and timing of nocturnal sleep. Recent reclassifi cation distinguishes three main subtypes: narcolepsy type 1, narcolepsy type 2, and idiopathic hypersomnia (IH), which are the focus of this review. Narcolepsy type 1 results from loss of hypothalamic hypocretin neurons, while the pathophysiology underlying narcolepsy type 2 and IH remains to be fully elucidated. Treatment of all three disorders focuses on the management of sleepiness, with additional treatment of cataplexy in those patients with narcolepsy type 1.Sleepiness can be treated with modafi nil/armodafi nil or sympathomimetic CNS stimulants, which have been shown to be benefi cial in randomized controlled trials of narcolepsy and, quite recently, IH. In those patients with narcolepsy type 1, sodium oxybate is eff ective for the treatment of both sleepiness and cataplexy. Despite these treatments, there remains a subset of hypersomnolent patients with persistent sleepiness, in whom alternate therapies are

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CSF Histamine Contents in Narcolepsy, Idiopathic Hypersomnia and Obstructive Sleep Apnea Syndrome

Cited by 159 publications

References 34 publications

Test-Retest Reliability of the Multiple Sleep Latency Test in Narcolepsy without Cataplexy and Idiopathic Hypersomnia

Test-Retest Reliability of the Multiple Sleep Latency Test in Narcolepsy without Cataplexy and Idiopathic Hypersomnia

Histamine H₃ Receptors and Sleep-Wake Regulation

Central Disorders of Hypersomnolence

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CSF Histamine Contents in Narcolepsy, Idiopathic Hypersomnia and Obstructive Sleep Apnea Syndrome

Cited by 159 publications

References 34 publications

Test-Retest Reliability of the Multiple Sleep Latency Test in Narcolepsy without Cataplexy and Idiopathic Hypersomnia

Test-Retest Reliability of the Multiple Sleep Latency Test in Narcolepsy without Cataplexy and Idiopathic Hypersomnia

Histamine H3 Receptors and Sleep-Wake Regulation

Central Disorders of Hypersomnolence

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Product

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Histamine H₃ Receptors and Sleep-Wake Regulation