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This chapter discusses the neurochemistry of excessive daytime sleepiness (EDS) with various etiologies. It presents a brief discussion of basic sleep physiology and narcolepsy symptoms to explain the specific neurochemistry of hypersomnia. The significant roles hypocretin deficiency and postnatal cell death of hypocretin neurons as the major pathophysiological process underlying narcolepsy with cataplexy emerged from a decade of investigation, employing both animal and human models. The chapter talks about idiopathic hypersomnia and hypocretin non-deficient primary hypersomnia. It explains how hypocretin ligand deficiency may cause narcolepsy phenotype. Narcolepsy symptoms can also occur during the course of other neurological conditions, and discovery of hypocretin ligand deficiency in idiopathic narcolepsy has led to new insights into the pathophysiology of symptomatic narcolepsy and EDS. The metabolic data may support the hypothesis of a primary deficient arousal system in patients with idiopathic hypersomnia.