Abstract
The authors hypothesized that if locomotor drive increases along with rapid eye movement (REM) sleep without atonia in idiopathic REM sleep behavior disorder (RBD), then RBD patients would have greater corticomuscular coherence (CMC) values during REM sleep than at other sleep stages and than in healthy control subjects during REM sleep. To explore this hypothesis, we analyzed beta frequency range CMC between sensorimotor cortex electroencephalography (EEG) and chin/limb muscle EMG in idiopathic RBD patients. Eleven drug naive idiopathic RBD patients and 11 age-matched healthy control subjects were included in the present study. All participants completed subjective sleep questionnaires and underwent polysomnography for one night. The CMC value between EEGs recorded at central electrodes and EMGs acquired at leg and chin muscles were computed and compared by repeated measures analysis of variance (ANOVA). Sleep stages and muscle (i.e., chin vs. leg) served as within-subject factors, and group served as the between-subject factor. Repeated measures ANOVA revealed no significant main effect of group (F1,20 = 0.571, p = 0.458) or muscle (F1,20 = 1.283, p = 0.271). However, sleep stage was found to have a significant main effect (F2.067,41.332 = 20.912, p < 0.001). The interaction between group and sleep stage was significant (F2.067,41.332 = 3.438, p = 0.040). RBD patients had a significantly higher CMC value than controls during REM sleep (0.047 ± 0.00 vs. 0.052 ± 0.00, respectively, p = 0.007). This study reveals increased CMC during REM sleep in patients with RBD, which indicates increased cortical locomotor drive. Furthermore, this study supports the hypothesis that sufficient locomotor drive plays a role in the pathophysiology of RBD in addition to REM sleep without atonia.
Highlights
Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia characterized by dream enactment and lack of normal atonia during REM sleep (Ju et al, 2011)
Rapid eye movement sleep behavior disorder is characterized by vigorous dream enactment behavior (DEB) and abnormally increased phasic and/or tonic EMG activity during REM sleep (Iranzo et al, 2009b)
Because REM sleep without atonia (RSWA) is insufficient to cause DEB, a core symptom of REM sleep behavior disorder (RBD), increased locomotor drive and/or RSWA has been suggested to be responsible for the clinical expression of human RBD (Boeve et al, 2007)
Summary
Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia characterized by dream enactment and lack of normal atonia during REM sleep (Ju et al, 2011). It has been proposed that the sublaterodorsal or analogous nucleus projects directly to spinal interneurons, causing active inhibition of muscle activity during REM sleep (Frenette, 2010). The structure in man analogous to the subcoeruleus region in cat and the sublaterodorsal nucleus in rat has been proposed as the nucleus crucial to the pathophysiology of RBD (Boeve et al, 2007; Luppi et al, 2010). Degeneration, or pharmacological manipulations of the sublaterodorsal magnocellular reticular formation are sufficient to cause REM sleep without atonia (RSWA), but insufficient to cause dream enactment behavior (DEB; Mahowald and Schenck, 2009). Sufficient locomotor drive is necessary in the setting of RSWA to result in clinical
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