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Excessive daytime sleepiness (EDS), cataplexy, and/or other dissociated REM sleep symptoms such hypnagogic hallucinations and sleep paralysis are characteristics of narcolepsy. Antidepressants are being used to treat cataplexy and EDS in narcolepsy patients. These medications have an amphetamine-like effect on the central nervous system (CNS). Other kinds of medications are also used, including gamma-hydroxybutyrate (GHB), a short-acting sedative for EDS/fragmented nighttime sleep, and modafinil, a non-amphetamine wake-promoting drug for EDS. Based on the identification of narcolepsy genes in animals, the primary pathophysiology of human narcolepsy has recently been clarified. The genes responsible for the pathogenesis of canine narcolepsy (hypocretin/orexin ligand and its receptor) have been discovered using both forward (positional cloning) and reverse (mouse gene knockout) genetics. Novel hypothalamic neuropeptides called hypocretins and orexins have a role in a number of hypothalamic processes, including neuroendocrine and energy balance. Although hypocretin-related gene mutations are uncommon in humans, hypocretin-ligand deficiency is a common cause of narcolepsy-cataplexy. The clinical, pathophysiological, and pharmacological facets of narcolepsy are covered in this review.
Premkumar et al. (2024) studied this question.