12/26/2023 0 Comments Cataplexy medication![]() ![]() This was linked to two pandemic 2009-10 H1N1 influenza vaccines. A sudden increase in narcolepsy in children was seen in Finland and other European countries in 2010.Possible triggers include head trauma, infection and change in sleep habits.Most cases are sporadic but a familial form occurs in a small proportion of narcolepsy patients.Narcolepsy is associated with a specific HLA allele, DQB1*0602.Possibly, immunological mechanisms may lead to loss of hypocretin. Narcolepsy may be caused by the loss of a relatively few neurons that are responsible for producing the neuropeptide hypocretin in the CNS. This is derived from the hypothalamus and is thought to be involved in sleep/wake cycles, food intake and pleasure-seeking behaviour. The peptide hypocretin (orexin) may be involved.The precise cause of narcolepsy is unknown both environmental and genetic factors may play a part: First-degree relatives are at increased risk of narcolepsy compared with the general population.It is possible that incidence statistics would increase if diagnostic features were recognised at an earlier age. One study found that narcolepsy with cataplexy was often linked to complex movement disorders. Less than 5% of narcolepsy with cataplexy occurs in children.A smaller number of narcolepsy cases presents at around 35 years. Age of onset is typically around adolescence.P atients with narcolepsy without cataplexy are thought to represent only 36% of all narcolepsy patients. The prevalence of narcolepsy type 1 is between 25 and 100 per 100,000 people.Importantly, management also needs to involve sleep hygiene advice, safety measures whenever applicable and guidance with regard to the social sequelae of cataplexy.Ĭataplexy Drop attacks Narcolepsy Pseudocataplexy Sodium oxybate Syncope. Symptomatic treatment is possible with antidepressants and sodium oxybate. Over time, these severe symptoms evolve to the milder adult phenotype, and this pattern is crucial to recognize when assessing the outcome of uncontrolled case series with potential treatments such as immunomodulation. Cataplexy shows remarkable differences in childhood compared to adults, with profound facial hypotonia and complex active motor phenomena. ![]() Currently, the diagnosis of cataplexy is made almost solely on clinical grounds, based on history taking and (home) videos. Childhood narcolepsy, with its profound facial hypotonia, can be confused with neuromuscular disorders, and the active motor phenomenona resemble those found in childhood movement disorders such as Sydenham's chorea. They can be differentiated from cataplexy using thorough history taking, supplemented with (home)video recordings whenever possible. Cataplexy mimics include syncope, epilepsy, hyperekplexia, drop attacks and pseudocataplexy. Next to narcolepsy, cataplexy can sometimes be caused by other diseases, such as Niemann-Pick type C, Prader Willi Syndrome, or lesions in the hypothalamic or pontomedullary region. Moreover, childhood cataplexy differs from the presentation in adults, with a prominent facial involvement, already evident without clear emotional triggers ('cataplectic facies') and 'active' motor phenomena especially of the tongue and perioral muscles. The expression of cataplexy varies widely, from partial episodes affecting only the neck muscles to generalized attacks leading to falls. Although cataplexy is rare, its recognition is important as in most cases, it leads to a diagnosis of narcolepsy, a disorder that still takes a median of 9 years to be diagnosed. This review describes the diagnosis and management of cataplexy: attacks of bilateral loss of muscle tone, triggered by emotions and with preserved consciousness.
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