Ventricular orexin-A (hypocretin-1) levels correlate with rapid-eye-movement sleep without atonia in Parkinson's disease

• Published in: Nature and science of sleep Vol. 5; no. default; pp. 87 - 91
• Main Authors: Bridoux, Agathe, Moutereau, Stephane, Covali-Noroc, Ala, Margarit, Laurent, Palfi, Stephane, Nguyen, Jean-Paul, Lefaucheur, Jean-Pascal, Césaro, Pierre, d'Ortho, Marie-Pia, Drouot, Xavier
• Format: Journal Article
• Language: English
• Published: New Zealand Dove Medical Press Limited 01-01-2013; Taylor & Francis Ltd; Dove Medical Press
• Subjects: Medical research; Medicine, Experimental; Narcolepsy; Parkinson's disease; Rapid Communication; REM sleep; Sleep; Sleep disorders; orexin-A; REM atonia; ventricular CSF; Parkinson
• ISSN: 1179-1608; 1179-1608
• DOI: 10.2147/NSS.S41245

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.
Here, we measured orexin-A levels in ventricular cerebrospinal fluid from eight patients with Parkinson's disease (four males and four females) who underwent ventriculography during deep brain-stimulation surgery and performed full-night polysomnography before surgery.
Our results showed a positive correlation between orexin-A levels and REM sleep without muscle atonia.
Our results suggest that high levels of orexin-A in Parkinson's disease may be associated with loss of REM muscle atonia.