Ventricular orexin-A (hypocretin-1) levels correlate with rapid-eye-movement sleep without atonia in Parkinson's disease.
Identifieur interne : 000B95 ( Main/Exploration ); précédent : 000B94; suivant : 000B96Ventricular orexin-A (hypocretin-1) levels correlate with rapid-eye-movement sleep without atonia in Parkinson's disease.
Auteurs : Agathe Bridoux [France] ; Stephane Moutereau ; Ala Covali-Noroc ; Laurent Margarit ; Stephane Palfi ; Jean-Paul Nguyen ; Jean-Pascal Lefaucheur ; Pierre Césaro ; Marie-Pia D'Ortho ; Xavier DrouotSource :
- Nature and science of sleep ; 2013.
Abstract
Patients with Parkinson's disease frequently complain of sleep disturbances and loss of muscle atonia during rapid-eye-movement (REM) sleep is not rare. The orexin-A (hypocretin-1) hypothalamic system plays a central role in controlling REM sleep. Loss of orexin neurons results in narcolepsy-cataplexy, a condition characterized by diurnal sleepiness and REM sleep without atonia. Alterations in the orexin-A system have been also documented in Parkinson's disease, but whether these alterations have clinical consequences remains unknown.
DOI: 10.2147/NSS.S41245
PubMed: 23847436
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en">Patients with Parkinson's disease frequently complain of sleep disturbances and loss of muscle atonia during rapid-eye-movement (REM) sleep is not rare. The orexin-A (hypocretin-1) hypothalamic system plays a central role in controlling REM sleep. Loss of orexin neurons results in narcolepsy-cataplexy, a condition characterized by diurnal sleepiness and REM sleep without atonia. Alterations in the orexin-A system have been also documented in Parkinson's disease, but whether these alterations have clinical consequences remains unknown.</div>
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