J Clin Sleep Med JCSM Off Publ Am Acad Sleep Med. Test-retest reliability of the multiple sleep latency test in narcolepsy without cataplexy and idiopathic hypersomnia. ICSD-2: International Classification of Sleep Disorders, 2nd ed. Challenges in diagnosing narcolepsy without cataplexy: a consensus statement. 2014 16:433.īaumann CR, Mignot E, Lammers GJ, Overeem S, Arnulf I, Rye D, et al. The hypocretin system and psychiatric disorders. A putative link between childhood narcolepsy and obesity. Rapid eye movement sleep behavior disorder and rapid eye movement sleep without atonia in narcolepsy. Restless legs syndrome is frequent in narcolepsy with cataplexy patients. Plazzi G, Ferri R, Antelmi E, Bayard S, Franceschini C, Cosentino FII, et al. Periodic leg movements during sleep and wakefulness in narcolepsy. 2013 9:955–65.ĭauvilliers Y, Pennestri M-H, Petit D, Dang-Vu T, Lavigne G, Montplaisir J. Roth T, Dauvilliers Y, Mignot E, Montplaisir J, Paul J, Swick T, et al. Narcolepsy as an autoimmune disease: the role of H1N1 infection and vaccination. Partinen M, Kornum BR, Plazzi G, Jennum P, Julkunen I, Vaarala O. Reduced number of hypocretin neurons in human narcolepsy. A mutation in a case of early onset narcolepsy and a generalized absence of hypocretin peptides in human narcoleptic brains. Peyron C, Faraco J, Rogers W, Ripley B, Overeem S, Charnay Y, et al. Age at onset of narcolepsy in two large populations of patients in France and Quebec. 2002 58:1826–33.ĭauvilliers Y, Montplaisir J, Molinari N, Carlander B, Ondze B, Besset A, et al. Prevalence of narcolepsy symptomatology and diagnosis in the European general population. Ohayon MM, Priest RG, Zulley J, Smirne S, Paiva T. ICSD-3: International Classification of Sleep Disorders, 3rd ed. In the near future, the efficacy of new wake-promoting drugs, anticataplectic agents, hypocretin replacement therapy and immunotherapy at the early stages of the disease should also be evaluated.ĪASM: American Academy of Sleep Medicine. Associated symptoms and comorbid conditions, such as hypnagogic/hypnopompic hallucinations, sleep paralysis, disturbed nighttime sleep, unpleasant dreams, REM- and non REM-related parasomnias, depressive symptoms, overweight/obesity, and obstructive sleep apnea, should also be taken into account and managed, if required. Importantly, clinically relevant subjective and objective measures of daytime sleepiness are required to monitor the treatment efficacy and to provide guidance on whether the treatment goals are met. Other psychostimulants can also be used, such as methylphenidate, pitolisant and rarely amphetamines, as third-line therapy. In recent years, narcolepsy treatment has changed with the widespread use of modafinil/armodafinil for daytime sleepiness, antidepressants (selective serotonin and dual serotonin and noradrenalin reuptake inhibitors) for cataplexy, and sodium oxybate for both symptoms. Treatment options may vary from a single drug that targets several symptoms, or multiple medications that each treats a specific symptom. Despite major advances in our understanding of narcolepsy mechanisms, its current management is only symptomatic. On the other hand, in narcolepsy type 2, cerebrospinal fluid hypocretin-1 levels are normal and cataplexy absent. Narcolepsy type 1 is characterized by excessive daytime sleepiness and cataplexy and is associated with hypocretin-1 deficiency. Narcolepsy type 1 and narcolepsy type 2 are central disorders of hypersomnolence.
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