94 Chapter 4 or even years [59, 162, 186]. Such differences in latency have previously been attributed to the multiple hit hypothesis, where genetically susceptible people must experience multiple triggers before they develop narcolepsy symptoms [4]. For some people, H1N1 vaccination could have been the trigger contributing to (but not yet) reaching the threshold for developing narcolepsy symptoms. In contrast, for others with possibly greater susceptibility (or multiple previously experienced triggers), H1N1 vaccination could have been the trigger that was strong enough to trigger the development of narcolepsy. H1N1 vaccination and infection have mainly been reported before narcolepsy development in children [56, 59, 61]. Following the multiple hit hypothesis in which potential triggers may have a cumulative effect on narcolepsy development, this suggests that H1N1 must be a relatively strong trigger. Analyses focused on this delay by monitoring individuals with hypersomnolence disorders could provide insights into the relationship between infections and/or vaccinations and the development of narcolepsy. The pathophysiologies of narcolepsy type 2 and idiopathic hypersomnia remain unknown [27]. No significant incidence increases were reported for either disorder following the 2009-2010-H1N1 pandemic. A recent report of ten individuals with idiopathic hypersomnia found all had positive Epstein– Barr virus (EBV) serology, although none reported symptomatic infection just before hypersomnia onset [187]. The current hypothesis, therefore, is that an autoimmune mechanism does not cause narcolepsy type 2 and idiopathic hypersomnia. We aimed to cross-sectionally investigate the distribution of potential immunological events in narcolepsy type 1 and 2, and idiopathic hypersomnia. Data were obtained from semi-structured interviews conducted during intake for all individuals reporting EDS and verified through external medical correspondence whenever possible. As well as the type of vaccination or infection, we identified the delay between the reported immunological events and the development of narcolepsy symptoms. Spontaneously reported non-immunological life events were also described. We hypothesized that immunological events, especially H1N1 vaccination and flu infections, would be more common in narcolepsy type 1 than in non-hypocretin-1 deficient hypersomnolence disorders.
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