Such episodes are transient, lasting seconds to minutes, and get precipitated by intense emotions. The sudden onset of muscle weakness characterizes cataplexy. In addition to excessive daytime sleepiness, patients with type 1 narcolepsy experience symptoms of disordered regulation of REM sleep (i.e., cataplexy, hypnagogic hallucinations, and sleep paralysis). It is essential to realize that patients with narcolepsy are well-rested following a brief nap or sufficient nights' sleep however, the symptoms of excessive daytime sleepiness occur within hours of awakening. The clinician should perform an investigation of behavioral (i.e., caffeine use, insufficient sleep, poor sleep hygiene, tobacco use, etc.) and alternative diagnoses (i.e., anemia, hypothyroidism, obstructive sleep apnea, etc.) of excessive daytime sleepiness. Obtaining an accurate and detailed history is imperative in the diagnosis of narcolepsy. It is worth noting that other neurological deficits are often evident in individuals who develop secondary narcolepsy, as lesions are not typically confined to the lateral hypothalamus. Although rare, lesions secondary to arteriovenous malformations, cerebrovascular accidents, inflammatory processes, and neoplasms result in the destruction of orexin-A-producing neurons. Secondary narcolepsy, on the other hand, is due to the development of lateral hypothalamic lesions. Moreover, there was an increased incidence of narcolepsy following the use of the 2009 European Pandemrix vaccination, suggesting the involvement of molecular mimicry in the development of this disorder. The onset of narcolepsy is seasonal, most often surfacing in the spring, following upper respiratory tract infections that had occurred in the preceding months. There is a near-perfect association of type 1 narcolepsy with HLA-DQB1*06:02, leading to the auto-immune hypothesis, which posits a selective, self-destruction of orexin-A producing neurons as the driving force behind the disorder. Type 1 narcolepsy (historically known as narcolepsy with cataplexy) is due to a deficiency of orexin-A, a wakefulness-promoting peptide neurotransmitter.
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