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

Agathe Bridoux,^1,2 Stephane Moutereau,³ Ala Covali-Noroc,¹ Laurent Margarit,¹ Stephane Palfi,⁴ Jean-Paul Nguyen,⁵ Jean-Pascal Lefaucheur,^1,2 Pierre Césaro,⁶ Marie-Pia d'Ortho,⁷ Xavier Drouot<sup>1,2

1</sup>Service de Physiologie, Groupe Henri Mondor, ²Faculté de Médecine, Université Paris Est Créteil, ³Service de Biochimie, Groupe Henri Mondor, ⁴UF Neurochirurgie Fonctionnelle, Groupe Henri Mondor, Créteil, France; ⁵Service de Neurochirurgie, Hôpital Nord Laënnec, Nantes, France; ⁶Service de Neurologie, Groupe Henri Mondor, Créteil, France; ⁷Service de Physiologie, Groupe Bichat – Claude Bernard, Paris, France

Objective: 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.
Methods: 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.
Results: Our results showed a positive correlation between orexin-A levels and REM sleep without muscle atonia.
Conclusion: Our results suggest that high levels of orexin-A in Parkinson's disease may be associated with loss of REM muscle atonia.

Keywords: Parkinson, orexin-A, ventricular CSF, REM atonia