112 Chapter 4 responsible for the infections reported in this study often remain unknown. Symptoms caused by influenza infection for instance substantially overlap with respiratory syncytial virus (RSV), and influenza infection could also manifest with non-respiratory symptoms [204]. We therefore decided to report clinical diagnoses instead of underlying pathogens. EBV infections were the exception as they were generally verified using serology. Future studies should aim to use polymerase chain reaction (PCR) instead of serology for EBV detection as it identifies explicitly ongoing EBV infections [205]. The retrospective nature and self-reports of infection and vaccination history are limitations of this study resulting in possible recall bias. It is often difficult to recall precise timing of the EDS onset for people with a central disorder of hypersomnolence, especially in absence of cataplexy. People are also likely to remember events occurring close to life-changing events (such as hypersomnolence disorder onset). The symptom onset and infection and vaccination histories were generally documented during the semi-structured intake interview, and medical history was also checked through available correspondence with other healthcare providers such as the general practitioner. We hereby included as detailed information as possible in our analyses to limit the possible effects of recall bias. By including all people with a central disorder of hypersomnolence who visited our clinic between 2010 and 2020 we have also taken out possible selection bias effects despite being a specialized sleep-wake clinic. Our analyses included people with an ICSD-3 complaint and a clinical diagnosis. In Appendix B, we repeated the analyses excluding those with a clinical diagnosis and found highly comparable results. Conclusions Our results have identified various immunological events related to narcolepsy type 1 onset, including H1N1 influenza vaccinations, flu, and other respiratory and non-respiratory infections. A different distribution of immunological events with relatively more EBV, other respiratory and non-respiratory infections was seen in narcolepsy type 2 and idiopathic hypersomnia. Infections and influenza vaccinations were often reported within days to weeks of hypersomnolence symptom onset, making a causal relationship plausible. Our study opens a new research path into possible immunological pathophysiology underlying non-hypocretin-1 deficient central hypersomnolence diagnoses, including EBV and other respiratory infections.
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