95 Potential Immunological Triggers for Central Disorders of Hypersomnolence Material and methods Data collection All people who attended the tertiary sleep-wake clinic Sleep-Wake Centre SEIN Heemstede with a central disorder of hypersomnolence diagnosis between January 2010 and January 2020 were included in this observational study. Infection/influenza vaccination history was integrated into our semi-structured clinical interview since the 2009-2010-H1N1 pandemic in people who newly visited the clinic complaining of EDS. The infection and vaccination history were documented during this intake interview. Complete medical records were reviewed, and detailed data were extracted on infections, influenza vaccinations, symptoms (EDS presence and date of onset, cataplexy presence and onset), sleep test results (MSLT mean sleep latency and sleep-onset rapid eye movement period [SOREMP] count, and polysomnography SOREMP presence), objective biomarkers (CSF hypocretin-1 levels, and HLA-DQB1*0602 positivity) and Epworth sleepiness scale (ESS) scores. Correspondence from other healthcare providers (often the general practitioner) was generally available and in a substantial portion of subjects the infection/vaccination history was verified with the included medical history. The extracted infection/influenza vaccination history included the infection/ influenza vaccination type and its timing. Our analysis incorporated all infections and influenza vaccinations that occurred prior to the onset of the hypersomnolence disorder, without considering possible subjective beliefs on causality. Only people with a known infection and influenza vaccination history were included and our statistical analyses specifically focused on immunological events before the onset of the hypersomnolence disorder. Infections were identified through clinical diagnosis and/or laboratory testing. If there was no formal diagnosis of the infection, then the symptoms experienced were extracted. Subjects were excluded from further analyses if the onset dates of EDS and cataplexy (in the case of narcolepsy type 1) were unknown. We separately described other (non-infectious) life events reported before the onset of the central disorder of hypersomnolence and immunological events reported before the substantial worsening (disease progression) of the symptoms of the hypersomnolence disorder. Disease progression was defined as an immunological event followed by a physician-verified increase in EDS or cataplexy (in frequency or intensity) or the development of EDS or cataplexy as a new hypersomnolence disorder symptom. Subjects were not routinely asked for non-infectious life events before onset or events prior to worsening of their central disorder of hypersomnolence. The non-infectious events and events 4
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