337 Discussion peaks and similar associations with preceding type A H1N1 influenza season severity and self-reported respiratory infections provide first clues of a comparable immunological aetiology of narcolepsy type 2 and idiopathic hypersomnia without long sleep time compared to narcolepsy type 1. The wide variety of immunological events that were identified suggests somewhat nonspecific vulnerability of the hypocretinergic system to environmental triggers, leading to narcolepsy type 1, and possibly also narcolepsy type 2 and idiopathic hypersomnia without long sleep time. It is important to note that the absence of hypocretin deficiency in the cerebrospinal fluid of individuals with narcolepsy type 2 and idiopathic hypersomnia without long sleep time should not directly be mistaken for a well-functioning hypocretin system. Animal studies have suggested that considerable loss of hypocretin neurons is necessary before this is measurable within the cerebrospinal fluid and in case of partial depletion, the remaining neurons otherwise try to compensate (possibly in combination with upregulation of histamine) [437, 438]. Whether subtler human hypocretin reductions could possibly result in excessive daytime sleepiness (in absence of cataplexy) which remains untraceable in the cerebrospinal fluid has not yet been studied and should be considered (Figure 1). Whether other neuronal cell populations involved in sleep-wake regulation are the target of a possible immunological reaction in the context of narcolepsy type 2 and idiopathic hypersomnia, requires similar investigation. 11
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