0947 Clinical Characteristics of Childhood Narcolepsy Following the H1n1 Pandemics: Preliminary Data From the Pediatric Working Group of the Sleep Research Network

Simakajornboon, Narong; Melendres, Cecilia; Sheldon, Stephen H.; Super, Elizabeth; Naqvi, Kamal; Brockbank, Justin; Beckerman, Robert C.; Amin, Raouf S.; Lew, Jenny; Malow, Beth A.; Marcus, Carole L.; Mason, Andrew L.; Chervin, Ronald D.; Kheirandish‐Gozal, Leila; Mignot, Emmanuel

doi:10.1093/sleepj/zsx050.946

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“…A follow‐up study from the same group showed a return of the narcolepsy incidence to the pre‐pandemic level in 2011 and 2012, supporting the role of actual H1N1 infection in the development of narcolepsy 46 . In the United States, the preliminary data from the Pediatric Working Group of the Sleep Research Network has revealed a seasonal pattern of narcolepsy onset in cases after 2009 H1N1 pandemic and recent cases had higher rates of streptococcal and influenza infection 14,47 …”

Section: Pathogenesismentioning

confidence: 87%

“…46 In the United States, the preliminary data from the Pediatric Working Group of the Sleep Research Network has revealed a seasonal pattern of narcolepsy onset in cases after 2009 H1N1 pandemic and recent cases had higher rates of streptococcal and influenza infection. 14,47 Several studies have indicated that autoimmune processes may underlie the pathogenesis of loss of hypocretin neurons in patients with narcolepsy. Three main autoimmune-mediated mechanisms have been proposed as the mechanisms underlying the loss of hypocretin neurons including autoimmunity, superantigenmediated T cell activation, and non-T cell-mediated MHC II activation.…”

Section: Pathogenesismentioning

confidence: 99%

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Narcolepsy in Children: Sleep disorders in children, A rapidly evolving field seeking consensus

Dye

Simakajornboon

2021

Pediatric Pulmonology

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Narcolepsy is a life‐long sleep disorder with two distinct subtypes, narcolepsy type I and narcolepsy type II. It is now well recognized that the loss of hypocretin neurons underlies the pathogenesis of narcolepsy type I, however, the pathogenesis of narcolepsy type II is currently unknown. Both genetic and environmental factors play an important role in the pathogenesis of narcolepsy. There is increasing evidence that autoimmune processes may play a critical role in the loss of hypocretin neurons. Infections especially streptococcus and influenza have been proposed as a potential trigger for the autoimmune‐mediated mechanism. Several recent studies have shown increased cases of pediatric narcolepsy following the 2009 H1N1 pandemic. The increased cases in Europe seem to be related to a specific type of H1N1 influenza vaccination (Pandemrix), while the increased cases in China are related to influenza infection. Children with narcolepsy can have an unusual presentation at disease onset including complex motor movements which may lead to delayed diagnosis. All classic narcolepsy tetrads are present in only a small proportion of children. The diagnosis of narcolepsy is confirmed by either obtaining cerebrospinal fluid hypocretin or overnight sleep study with the multiple sleep latency test (MSLT). There are limitations of using MSLT in young children such that a negative MSLT test cannot exclude narcolepsy. HLA markers have limited utility in narcolepsy, but it may be useful in young children with clinical suspicion of narcolepsy. For management, both pharmacologic and non‐pharmacologic treatments are important in the management of narcolepsy. Pharmacotherapy is primarily aimed to address excessive daytime sleepiness and REM‐related symptoms such as cataplexy. In addition to pharmacotherapy, routine screening of behavioral and psychosocial issues is warranted to identify patients who would benefit from bio‐behavior intervention.

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Section: Pathogenesismentioning

confidence: 87%