CSF hypocretin-1 levels in narcolepsy, Kleine-Levin syndrome, and other hypersomnias and neurological conditions.

Détails

ID Serval
serval:BIB_62E7CE2D2DF3
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
CSF hypocretin-1 levels in narcolepsy, Kleine-Levin syndrome, and other hypersomnias and neurological conditions.
Périodique
Journal of Neurology, Neurosurgery, and Psychiatry
Auteur⸱e⸱s
Dauvilliers Y., Baumann C.R., Carlander B., Bischof M., Blatter T., Lecendreux M., Maly F., Besset A., Touchon J., Billiard M., Tafti M., Bassetti C.L.
ISSN
0022-3050[print], 0022-3050[linking]
Statut éditorial
Publié
Date de publication
12/2003
Volume
74
Numéro
12
Pages
1667-1673
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: ppublish
Résumé
OBJECTIVE: To determine the role of CSF hypocretin-1 in narcolepsy with and without cataplexy, Kleine-Levin syndrome (KLS), idiopathic and other hypersomnias, and several neurological conditions. PATIENTS: 26 narcoleptic patients with cataplexy, 9 narcoleptic patients without cataplexy, 2 patients with abnormal REM-sleep-associated hypersomnia, 7 patients with idiopathic hypersomnia, 2 patients with post-traumatic hypersomnia, 4 patients with KLS, and 88 patients with other neurological disorders. RESULTS: 23 patients with narcolepsy-cataplexy had low CSF hypocretin-1 levels, while one patient had a normal hypocretin level (HLA-DQB1*0602 negative) and the other two had intermediate levels (familial forms). One narcoleptic patient without cataplexy had a low hypocretin level. One patient affected with post-traumatic hypersomnia had intermediate hypocretin levels. The KLS patients had normal hypocretin levels while asymptomatic, but one KLS patient (also affected with Prader-Willi syndrome) showed a twofold decrease in hypocretin levels during a symptomatic episode. Among the patients without hypersomnia, two patients with normal pressure hydrocephalus and one with unclear central vertigo had intermediate levels. CONCLUSION: Low CSF hypocretin-1 is highly specific (99.1%) and sensitive (88.5%) for narcolepsy with cataplexy. Hypocretin ligand deficiency appears not to be the major cause for other hypersomnias, with a possible continuum in the pathophysiology of narcolepsy without cataplexy and idiopathic hypersomnia. However, partial hypocretin lesions without low CSF hypocretin-1 consequences cannot be definitely excluded in those disorders. The existence of normal hypocretin levels in narcoleptic patients and intermediate levels in other rare aetiologies needs further investigation, especially for KLS, to establish the functional significance of hypocretin neurotransmission alterations.
Mots-clé
Adolescent, Adult, Carrier Proteins/cerebrospinal fluid, Disorders of Excessive Somnolence/cerebrospinal fluid, Disorders of Excessive Somnolence/genetics, Feeding Behavior/physiology, Female, Humans, Intracellular Signaling Peptides and Proteins, Male, Middle Aged, Nervous System Diseases/cerebrospinal fluid, Nervous System Diseases/genetics, Neuropeptides/cerebrospinal fluid, Phenotype, REM Sleep Parasomnias/cerebrospinal fluid, REM Sleep Parasomnias/genetics
Pubmed
Web of science
Open Access
Oui
Création de la notice
24/01/2008 15:55
Dernière modification de la notice
20/08/2019 14:19
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