Slowing of electroencephalogram in rapid eye movement sleep behavior disorder

• Published in: Annals of neurology Vol. 53; no. 6; pp. 774 - 780
• Main Authors: Livia Fantini, Maria, Gagnon, Jean-François, Petit, Dominique, Rompré, Sylvie, Décary, Anne, Carrier, Julie, Montplaisir, Jacques
• Format: Journal Article
• Language: English
• Published: Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.06.2003; Willey-Liss
• Subjects: Aged; Biological and medical sciences; Brain - physiopathology; Cognition - physiology; Electroencephalography; Female; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy; Humans; Male; Medical sciences; Nervous system (semeiology, syndromes); Neurology; Polysomnography; REM Sleep Behavior Disorder - diagnosis; REM Sleep Behavior Disorder - physiopathology; Wakefulness - physiology; Human; Electrodiagnosis; Nervous system diseases; Sleep disorder; Electroencephalography; Neurological disorder; Rapid eye movement sleep; Behavioral disorder
• ISSN: 0364-5134; 1531-8249
• DOI: 10.1002/ana.10547

Rapid eye movement (REM) sleep behavior disorder (RBD) is characterized by a loss of atonia and an increase in phasic muscle activity during REM sleep, leading to complex nocturnal motor behaviors. Brainstem structures responsible for the pathogenesis of RBD are also implicated in cortical activation. To verify the hypothesis that electroencephalogram (EEG) activation will be impaired in RBD, we performed quantitative analyses of waking and REM sleep EEG in 15 idiopathic RBD patients and 15 age‐ and gender‐matched healthy subjects. During wakefulness, RBD patients showed a considerably higher θ power in frontal, temporal, and occipital regions with a lower β power in the occipital region. The dominant occipital frequency was significantly lower in RBD. During REM sleep, β power in the occipital region was lower in RBD. This study shows for the first time an impaired cortical activation during both wakefulness and REM sleep in idiopathic RBD, despite an absence of changes on sleep architecture compared with controls. EEG slowing in these patients may represent an early sign of central nervous system dysfunction, perhaps paralleled by subclinical cognitive deficits. The topographical distribution of EEG slowing and possible pathophysiological mechanisms are discussed in light of the known association between RBD and neurodegenerative disorders. Ann Neurol 2003;53:774–780