Narcolepsy is a rare disorder of sleep regulation characterized by symptoms of excessive daytime sleepiness (EDS) and/or cataplexy. Narcolepsy is categorized as either type I (with cataplexy) or type II (without cataplexy). Prevalence is 20–50 per 100 000 population and incidence is approximately 1 per 100 000 person-years (PY) in the United States and European countries.
The leading etiopathogenesis hypothesis for type 1 narcolepsy (NT1) is the multiple-hit theory: the cooccurrence of genetic predisposition, environmental factors, and triggering events leading to immune-mediated destruction of hypocretin-producing neurons. This phenomenon is associated with increased T-cell reactivity to hypocretin [9–12]. Hypocretin (also known as Orexin) serves a stabiliser type function for both sleep and wakefulness.
Influenza A(H1N1) pdm09 infection has been proposed as a major environmental trigger for the autoimmune process leading to narcolepsy [10]. Studies from Beijing, China found a 3-fold increase in narcolepsy onset following the 2009 H1N1 pandemic, and this increase returned to baseline following the pandemic. Wang et al recently published a study in the Journal of Sleep, they looked at the change to epidemiology of narcolepsy from the H1N1 pandemic.
Wang et al found that compared to the pre-pandemic period, the incidence of narcolepsy was 4.17- and 1.42-fold higher during and postpandemic, respectively. The incidence among children aged 5–9 years increased more substantially than other age groups during the pandemic period. They concluded that this study suggests the role of the A(H1N1) pdm09 virus in trigging narcolepsy. However they did concede that future research is needed to confirm these changes and investigate mechanisms linking the influenza virus to narcolepsy.
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