329 Discussion by competitive circulation between type A influenza strains, where dominance of type A H3N2 influenza implies relative absence of type A H1N1 in the same influenza season [173, 383, 384], hereby resulting in lower incidence rates of central disorders of hypersomnolence. Chapter 4 provides a comprehensive overview of self-reported immunological events prior to development of narcolepsy type 1, type 2 and idiopathic hypersomnia. Immunological events were frequently reported across groups, regularly within one month before hypersomnolence disorder onset. Influenza and H1N1 influenza vaccination were more common in narcolepsy type 1, and Epstein-Barr virus and other respiratory and non-respiratory infections in narcolepsy type 2 and idiopathic hypersomnia. Frequent reports of immunological events (other than those reported in narcolepsy type 1) immediately prior to the development of narcolepsy type 2 and idiopathic hypersomnia support the specificity of triggers for narcolepsy type 1, and open important new research avenues into possible underlying immunological mechanisms in narcolepsy type 2 and idiopathic hypersomnia. These studies provide important new associations between immunological events and onset of narcolepsy and idiopathic hypersomnia. Important commonalities and differences when comparing narcolepsy type 1 with narcolepsy type 2 and idiopathic hypersomnia will hereafter be presented with their implications on (possible) underlying pathophysiologies, methodological considerations that should be considered, and a future research agenda. Shedding light on the immunological triggers of narcolepsy type 1 For narcolepsy type 1 the incidence peak in 2010 was previously mainly reported in European countries with widespread Pandemrix use [56, 57]. We also identified the 2010 peak in countries where Pandemrix was not or only sporadically administered, which further substantiates the notion that besides Pandemrix vaccination, type A H1N1 influenza infection could also be a potential trigger for developing narcolepsy type 1 [57-61]. The child-specific 2013 peak in narcolepsy type 1 first surprised us (Chapter 2) but was confirmed in our follow-up study described in Chapter 3 with the addition of a similar 2013 incidence peak of narcolepsy type 1 in adults. With adult-onset narcolepsy type 1 having typically longer delays between hypersomnolence onset and diagnosis [49, 385-387], this discrepancy could be explained by the extended period of data collection and larger sample sizes that were used in our study in Chapter 3. The 2013 incidence peak further substantiates the involvement of environmental factors in hypersomnolence disorder onset, with less possible influence of media attention that was present following the 2009-2010 type 11
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