0686 Sleep Stage Dynamics in Patients with Sleep Bruxism

Abstract

Introduction Sleep bruxism (SB) is classified as a sleep-related movement disorder and represented by repetitive and recurrent episodes of rhythmic masticatory muscle activity (RMMA). It has been reported that cortical arousal and sleep stage shift are associated with the occurrence of RMMA while sleep structure in SB patients has been known to be within normal range. We hypothesized that sleep stage transition dynamics are different in SB patients compared to those in healthy controls, and the occurrence of RMMA is associated with aspects of sleep stage dynamics in SB patients. Methods Fifteen healthy controls and 15 patients with severe SB underwent overnight PSG after an adaptation PSG. Sleep variables and survival curves of continuous runs of each sleep stage (N1, N2, N3 and REM) were compared between control and SB groups. For SB patients, stage transition dynamics were analyzed for 3 epochs before and after the epoch with RMMA and the probability of the stage (N2, N3 and REM) fragmentation by transition to wake or N1 was calculated for each epoch. Survival curves of continuous runs of each sleep stage, which were terminated with or without RMMA, were also compared. Results There were no significant differences in sleep variables between groups except for shorter sleep latency, shorter REM latency and longer total N1 duration in SB than in controls. REM sleep and N2 were significantly less continuous in SB than in controls. For N2, N3 and REM, stage fragmentation probability was significantly increased for the epoch with RMMA compared to the baseline epoch. Meanwhile, the occurrence of RMMA neither affected the continuity of N2 nor REM, rather the occurrence of RMMA followed more continuous N3 runs. Conclusion Sleep stage dynamics differed between SB and healthy controls. RMMA does not result in sleep disruption but is more likely associated with dissipation of sleep pressure. Less continuity of REM sleep in SB may provide insights into the underlying pathophysiological mechanism of SB, possibly related to REM sleep processes such as cortical desynchronized states or brainstem activation.