0799 Precipitation of Dream Enactment Behavior in the setting of β -Blocker therapy. (25th May 2022)

• Record Type: Journal Article
• Authors: Patel, Jay; Moshtagh-Sisan, Mahtab; Sarrami, Kayvon; Avidan, Alon
• Is Part Of: Sleep. Volume 45(2022)Supplement 1
• Page Start: A346
• Page End: A347
• Publication Date: 2022-05-25
• Subjects: Sleep -- Physiological aspects -- Periodicals; Sleep disorders -- Periodicals; Sommeil -- Aspect physiologique -- Périodiques; Sommeil, Troubles du -- Périodiques; Sleep disorders; Sleep -- Physiological aspects; Sleep -- physiological aspects; Sleep Wake Disorders; Psychophysiology; Electronic journals; Periodicals; 616.8498
• DOI: 10.1093/sleep/zsac079.795
• Languages: English
• ISSNs: 0161-8105

Abstract

Abstract: Introduction: REM sleep behavior disorder (RBD) is defined by dream enactment behavior (DEB) and REM sleep without muscle atonia (RWA). It is proposed that in both isolated and secondary RBD, the loss of REM sleep atonia is related to a failure of spinal motoneuron inhibition in the rostral pons. RBD is most commonly isolated, although it has been attributed to serotonergic antidepressant medication. This is the first report of metoprolol succinate (MS) provoking DEB in patients with RWA which helps shed more light on the mechanism of DEB in RBD. Report of Cases: A 51-year-old male with a new diagnosis of atrial fibrillation (AF) was referred for evaluation of snoring and hypersomnolence. Polysomnography (PSG) revealed obstructive sleep apnea and RWA. DEB was not observed. Compliance with PAP therapy improved his symptoms. Persistent AF required the use of Metoprolol Succinate (MS), which precipitated aggressive DEB. Discontinuation of MS resulted in clinical resolution of DEB. Conclusion: The data sheds more light on the potential role of β- blockers, in general, and MS, in particular, in precipitating DEB in susceptible individuals with RWA. While MS is an uncommon cause of visual hallucinations, the data here indicates that it might increase susceptibility to DEB in those who are at risk (RWA). Potential mechanisms include the following: β-blockers bind to serotonin receptors and precipitate DEB in the setting of RWA. β-blockers may also precipitate DEB by suppressing melatonin release via specific inhibition of central beta-adrenoreceptors culminating in sleep instability and DEB as a consequence. This case illustrates a clinically important role of the β-blocker MS, in precipitating DEB, and the need to avoid these agents in the setting of injurious parasomnias. We recommend that clinicians keep a vigilant eye for the exacerbation of DEB in people with RBD who are prescribed β-blockers. Support (If Any):