It consists of stimulant drugs (mostly dopaminergic) to suppress daytime sleepiness and sleep attacks, antidepressants (mostly noradrenergic) for cataplexy and other REM-associated symptoms, occasionally hypnotics for disturbed night-time sleep and γ-hydroxybutyrate (GHB) for all three symptoms. Narcolepsy with cataplexy is the most severe example of sleepiness in human beings. Most studies suggest that the loss of hypocretin-containing neurons in NC might be attributable to an autoimmune process. Recent studies have shown that there is a marked decrease in hypocretin-1 levels in the cerebrospinal fluid (CSF) of patients with narcolepsy and a decrease in the number of hypocretin neurons in post-mortem brain tissues of narcolepsy subjects. The age at onset ranges from early childhood to 50–60 years of age with a bimodal distribution, including a large peak around 15 years and a smaller peak at approximately 36 years of age. Cataplexy is a partial or complete loss of muscle tone triggered by strong emotions. The main symptom is excessive daytime sleepiness, but patients can also develop abnormal rapid eye movement (REM) sleep manifestations including cataplexy, sleep paralysis and hypnagogic hallucinations. Narcolepsy with cataplexy (NC) is a rare sleep disorder. ▪ Describe treatments for NC likely to be available in the future as based on the review ▪ Describe current treatments for NC as based on the review ▪ Describe the clinical characteristics of narcolepsy with cataplexy (NC) as based on the review Upon completion of this activity, participants should be able to: Potential development of new wake-promoting drugs, anticataplectic medications, slow-wave sleep-enhancing treatments, hypocretin-replacement therapy and immunotherapy at early stages of the disease needs to be evaluated in the near future. The treatment of narcolepsy has evolved over the past few years with the widespread use of modafinil for daytime sleepiness, antidepressants for cataplexy and γ-hydroxybutyrate (sodium oxybate) for both symptoms. The cause of neural loss could be autoimmune since most patients have the human leukocyte antigen DQB1*0602 allele that predisposes individuals to NC. Pathophysiological studies have shown that NC is caused by the early loss of neurons in the hypothalamus that produce hypocretin/orexin, a wakefulness-associated neurotransmitter present in cerebrospinal fluid. In this article, we will describe the main symptoms and the current and future treatments of NC. Narcolepsy with cataplexy (NC) is a disabling orphan sleep disorder characterized by excessive daytime sleepiness, cataplexy and other dissociated manifestations of rapid eye movement sleep (hypnagogic hallucinations and sleep paralysis), as well as frequent movement and awakening during night-time sleep.
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