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How treatable is narcolepsy with current pharmacotherapy and what does the future hold?

Narcolepsy is a lifelong sleep disorder characterized by excessive daytime sleepiness (EDS), cataplexy, sleep paralysis, hypnagogic/hypnopompic hallucinations and disturbed nocturnal sleep. It is a rare condition, with an estimated prevalence of 0.02–0.05% in the general population [1]. Disease onset occurs before the age of 18 in more than 50% of the patients, with long diagnostic delays, especially in children [2]. Narcolepsy can be comorbid with additional sleep disorders (obstructive sleep apnea, restless legs syndrome and REM behavior disorder), neuropsychiatric, metabolic and cardiovascular diseases [1]. The International Classification of Sleep Disorders (ICSD-3) recognizes two different phenotypes. In narcolepsy type 1 (NT1), EDS is associated with cataplexy and/or reduced levels of hypocretin in the cerebrospinal fluid (CSF). Narcolepsy type 2 (NT2) presents similar EDS and abnormal REM sleep manifestations on polysomnography (PSG), while cataplexy is absent and hypocretin levels in the CSF are normal or slightly reduced [1,3]. NT1 is presumed to have an autoimmune basis that induces loss of hypothalamic orexin neurons in genetically predisposed individuals [1,4,5]. NT2 may be caused by less extensive injury to those neurons, but data are quite limited, and its pathogenesis remains largely unclear [1].