Basal electromyographic amplitude in rapid eye movement (REM) and non-rapid eye movement (NREM) sleep as a predictor of disease progression in isolated REM sleep behavior disorder.

STUDY OBJECTIVES: This study examined whether basal electromyographic (EMG) amplitude during sleep is altered in patients with isolated REM sleep behavior disorder (iRBD) and its relationship to disease progression, as well as changes across the sleep cycle.

METHODS: Baseline polysomnograms collected from 95 iRBD patients (15 converters, 80 non-converters) and matched 24 controls were analyzed. EMG amplitude was calculated from submentalis recordings across all sleep stages using 3-s mini-epochs, with REM sleep further classified as REM sleep without atonia (RWA) and non-RWA (RA) according to the presence of "any" RWA events. Kaplan-Meier analysis assessed phenoconversion risk, and EMG amplitude was compared between early and late sleep cycles within each group.

RESULTS: Group comparisons with post-hoc adjustment showed that EMG amplitude in RA and RWA was higher in non-converters than controls (adj-p < .001), while converters showed further increases of EMG amplitude in N2 and N3 (adj-p < .045). RA amplitude was higher in converters than non-converters (adj-p = .02). Increased EMG amplitude in N2, N3, and RA was associated with higher phenoconversion risk (p < .05). EMG amplitude remained stable between early and late cycles during RA in both iRBD and controls. In contrast, iRBD patients showed a significant decrease in EMG amplitude during late cycles in N2 (p < .009).

CONCLUSIONS: Elevated basal EMG amplitude during both REM and NREM sleep in iRBD patients shows potential as a prognostic marker, indicating muscle tone dysregulation beyond REM atonia loss and underscoring the need to consider broader sleep stages in iRBD evaluation. Statement of Significance This study provides compelling evidence that increased basal electromyographic amplitude during both REM and NREM sleep in isolated REM sleep behavior disorder (iRBD) patients serves as a marker of prodromal alpha-synucleinopathy. By showing that electromyographic abnormalities extend beyond discrete REM events to affect global muscle tone, our findings challenge the conventional view that iRBD pathophysiology is limited to REM-specific activity. Furthermore, the predictive value of these changes appears linked to muscle tone regulation across the sleep-wake cycle. These insights not only deepen our understanding of iRBD pathophysiology but also underscore the potential for refining diagnostic criteria.