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In up to 10% of cases there is a family history of the disorder. Family history is more common in narcolepsy with cataplexy. [1] There is a strong link with certain genetic variants, [27] which may make T-cells susceptible to react to the orexin-releasing neurons (autoimmunity) [30] after being stimulated by infection with H1N1 influenza. [12]
Cataplexy is the first symptom to appear in about 10% of cases of narcolepsy, [2] caused by an autoimmune destruction of hypothalamic neurons that produce the neuropeptide hypocretin (also called orexin), which regulates arousal and has a role in stabilization of the transition between wake and sleep states. [3]
It can be difficult to differentiate between cataplexy brought on by narcolepsy and true sleep paralysis, because the two phenomena are physically indistinguishable. The best way to differentiate between the two is to note when the attacks occur most often.
Primary vs. secondary (i.e. comorbid) insomnia has been reunited into a single disorder: chronic insomnia. Narcolepsy has been divided into narcolepsy type 1 and narcolepsy type 2. These two types are distinguished by the presence or absence of cataplexy and the cerebrospinal fluid hypocretin-1 level.
Autosomal dominant narcolepsy, obesity, and type 2 diabetes 347.00 G47.419 Narcolepsy without cataplexy but with hypocretin deficiency 347.01 G47.411 Narcolepsy with cataplexy but without hypocretin deficiency 347.10 G47.429 Narcolepsy secondary to another medical condition
Cataplexy, on the other hand, is an involuntary loss of muscle tone during wakefulness. The mechanism of narcolepsy is unknown, though recent findings suggest that orexin neurons in the lateral and posterior hypothalamus may play a critical role in reinforcing wakefulness. [ 7 ]
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The prevalence of narcolepsy (with cataplexy) is estimated between 1/3,300 and 1/5,000. [47] Although the true prevalence of IH is unknown, it is estimated at 1/10,000 to 1/25,000 for the long sleep form and 1/11,000 to 1/100,000 without long sleep. [ 48 ]
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