Program

Executive Summary：
Dr. Naoko Tachibana is Director of Center for Sleep-related disorders in Kansai Electric Power Hospital and Chief Director of Division of Sleep Medicine, Kansai Electric Power Medical Research Institute in Osaka. She has dual specialties in psychiatry and neurology. After clinical training in Stanford Sleep Clinic and Sleep HealthCenters affiliated to Brigham and Women's Hospital, she obtained a status of International Sleep Specialist and RPSGT. Her main interest is sleep related movement and behavior disorders as research, but during recent fifteen years her activity has involved sleep medicine education for the young medics who just have started their career, and sleep technologists, aiming at developing efficient and feasible sleep lab system in Japanese general hospital settings. To pursue this purpose, she also acts as Guest Professor in Department of Medical Technology, Osaka University of Division of Health Sciences. She is an ex-president of Integrated Sleep Medicine Society Japan (ISMSJ) and a member of many national and international medical societies and boards. She also runs a local non-profit organization called Osaka Sleep Health Network

Lecture Abstract：
When Schenck and colleagues discovered REM sleep behavior disorder (RBD) for the first time, it was classified as REM sleep related parasomnia, and sleep researchers were excited as RBD appeared to be human equivalence to Jouvet’s experimental cats behaving in the dream. Isolated (idiopathic) RBD (iRBD), however, is now recognized as harbinger of synucleinopathies. PSG-confirmed iRBD alone has been revealed to a strongest biomarker for expecting future phenoconversion to Parkinson’s disease (PD). It should be noted that not all the RBD seem to occur before the onset of PD, and according to a large timeline cohort study, RBD was more likely to develop in dementia with Lewy bodies (DLB) than in PD. In order to confirm a diagnosis of RBD, polysomnography (PSG) with video-monitoring is essential and it contains huge data. Most of the previous studies dealing with RBD utilized PSG only as a diagnostic tool, and few studies focused on longitudinal change/progression of PSG data. It seems that greater REM sleep without atonia (RSWA) and earlier EEG slowing mark higher conversion risk. In this lecture, I will talk about putative pathophysiological hypotheses about two types of temporal patterns of onset (iRBD → PD/DLB vs. PD/DLB → RBD) from the viewpoint of PSG/EEG, and put emphasis on the importance of raw data of these investigations.