Abstract
Narcolepsy with cataplexy typically occurs during adolescence and is thought to be an autoimmune disorder. Loss of hypocretin cells and a high association with HLADQB1*0602 and polymorphisms in the T-cell receptor-α (TCR) loci suggest an autoimmune disorder that may be a response to infection [1]. Environmental triggers have been suggested, including increased stress, decreased sleep, head trauma, and various other unusual triggers (eg, bee sting). However, findings may be coincidental and are likely confounded by bias recall. Increased smoking exposure in patients with narcolepsy suggests the effect is secondary to increased upper respiratory tract infections in secondary smoking [2]. More than 20 years ago, increased antistreptolysin O (ASO) and anti-DNAse B (ADB) titers were reported in a small number of patients with narcolepsy. However, a possible infectious trigger would not be detectable long after onset of narcolepsy, and if streptococcal infections were a trigger for narcolepsy onset, they would be best detected in newly identified patients with recent onset.
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