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Clinical features and diagnosis of narcolepsy in adults

Thomas E Scammell, MD
Section Editor
Ruth Benca, MD, PhD
Deputy Editor
April F Eichler, MD, MPH


Narcolepsy is a clinical syndrome of daytime sleepiness with cataplexy, hypnagogic hallucinations, and sleep paralysis. It is one of the most common causes of disabling daytime sleepiness after obstructive sleep apnea [1,2]. Other diagnoses may be worth considering, and a general approach to the patient with chronic sleepiness is presented elsewhere. (See "Approach to the patient with excessive daytime sleepiness".)

The epidemiology, clinical features, etiology, and diagnosis of narcolepsy are reviewed here. Narcolepsy in children and the treatment of narcolepsy in adults are reviewed separately. (See "Narcolepsy in children" and "Treatment of narcolepsy in adults".)


Narcolepsy type 1 (narcolepsy with cataplexy) is estimated to have a prevalence of 25 to 50 per 100,000 people and an incidence of 0.74 per 100,000 person-years [3-5]. It is equally common in men and women [6-8]. Narcolepsy typically begins in the teens and early twenties, but occasionally occurs as early as five years of age or after 40 years of age. The prevalence of narcolepsy type 2 (narcolepsy without cataplexy) is uncertain because it is not as well studied; however, it has been estimated to be 20 to 34 per 100,000 people [8,9].


Loss of orexin (hypocretin) signaling, genetic factors, and rare brain lesions can cause narcolepsy.

Orexin/hypocretin — Narcolepsy results from the loss of the neuropeptides, orexin-A and orexin-B (also known as hypocretin-1 and hypocretin-2). These neurotransmitters are products of the prepro-orexin gene and are made by neurons in the lateral hypothalamus [10,11]. Orexin-A and -B have excitatory effects when they bind the ox1 and ox2 receptors on postsynaptic neurons.

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Literature review current through: Nov 2017. | This topic last updated: Mar 20, 2017.
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