Stuart J McCarter1, Erik K St Louis2, David J Sandness1, Ethan J Duwell1, Paul C Timm1, Bradley F Boeve3, Michael H Silber3. 1. Mayo Center for Sleep Medicine, Mayo Clinic and Foundation, Rochester, MN, USA. 2. Mayo Center for Sleep Medicine, Mayo Clinic and Foundation, Rochester, MN, USA; Department of Medicine, Mayo Clinic and Foundation, Rochester, MN, USA; Department of Neurology, Mayo Clinic and Foundation, Rochester, MN, USA. Electronic address: stlouis.erik@mayo.edu. 3. Mayo Center for Sleep Medicine, Mayo Clinic and Foundation, Rochester, MN, USA; Department of Neurology, Mayo Clinic and Foundation, Rochester, MN, USA.
Abstract
OBJECTIVES: We aimed to determine whether visual and automated rapid eye movement (REM) sleep without atonia (RSWA) methods could accurately diagnose patients with idiopathic REM sleep behavior disorder (iRBD) and comorbid obstructive sleep apnea (OSA). METHODS: In iRBD patients (n = 15) and matched controls (n = 30) with and without OSA, we visually analyzed RSWA phasic burst durations, phasic, tonic, and "any" muscle activity by 3-s mini-epochs, phasic activity by 30-s (AASM rules) epochs, and automated REM atonia index (RAI). Group RSWA metrics were analyzed with regression models. Receiver operating characteristic (ROC) curves were used to determine the best diagnostic cutoff thresholds for REM sleep behavior disorder (RBD). Both split-night and full-night polysomnographic studies were analyzed. RESULTS: All mean RSWA phasic burst durations and muscle activities were higher in iRBD patients than in controls (p <0.01). Muscle activity (phasic, "any") cutoffs for 3-s mini-epoch scorings were as follows: submentalis (SM) (15.8%, 19.5%), anterior tibialis (AT) (29.7%, 29.7%), and combined SM/AT (39.5%, 39.5%). The tonic muscle activity cutoff was 0.70% and RAI (SM) cutoff 0.86. The phasic muscle burst duration cutoffs were 0.66 s for SM and 0.71 s for AT. Combining phasic burst durations with RSWA muscle activity improved the sensitivity and specificity of iRBD diagnosis. CONCLUSIONS: This study provides evidence for quantitative RSWA diagnostic thresholds applicable in iRBD patients with OSA. Our findings in this study were very similar to those seen in patients with Parkinson's disease-REM sleep behavior disorder (PD-RBD), consistent with a common mechanism and presumed underlying etiology of synucleinopathy in both groups.
OBJECTIVES: We aimed to determine whether visual and automated rapid eye movement (REM) sleep without atonia (RSWA) methods could accurately diagnose patients with idiopathic REM sleep behavior disorder (iRBD) and comorbid obstructive sleep apnea (OSA). METHODS: In iRBD patients (n = 15) and matched controls (n = 30) with and without OSA, we visually analyzed RSWA phasic burst durations, phasic, tonic, and "any" muscle activity by 3-s mini-epochs, phasic activity by 30-s (AASM rules) epochs, and automated REM atonia index (RAI). Group RSWA metrics were analyzed with regression models. Receiver operating characteristic (ROC) curves were used to determine the best diagnostic cutoff thresholds for REM sleep behavior disorder (RBD). Both split-night and full-night polysomnographic studies were analyzed. RESULTS: All mean RSWA phasic burst durations and muscle activities were higher in iRBD patients than in controls (p <0.01). Muscle activity (phasic, "any") cutoffs for 3-s mini-epoch scorings were as follows: submentalis (SM) (15.8%, 19.5%), anterior tibialis (AT) (29.7%, 29.7%), and combined SM/AT (39.5%, 39.5%). The tonic muscle activity cutoff was 0.70% and RAI (SM) cutoff 0.86. The phasic muscle burst duration cutoffs were 0.66 s for SM and 0.71 s for AT. Combining phasic burst durations with RSWA muscle activity improved the sensitivity and specificity of iRBD diagnosis. CONCLUSIONS: This study provides evidence for quantitative RSWA diagnostic thresholds applicable in iRBD patients with OSA. Our findings in this study were very similar to those seen in patients with Parkinson's disease-REM sleep behavior disorder (PD-RBD), consistent with a common mechanism and presumed underlying etiology of synucleinopathy in both groups.
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