![]() Further understanding of the neurobiology of cataplexy and how it relates to hypocretin deficiency should improve our understanding of the brain’s emotional processing and provide insights into REM sleep and its control. Pitolisant is a new agent for treating the excessive daytime sleepiness of narcolepsy that also helps cataplexy control by increasing histamine concentrations in the hypothalamus. Sodium oxybate is probably the most effective drug for severe cataplexy, taken before overnight sleep and once through the night its precise mechanism of action remains obscure. For starters, individuals with Niemann-Pick type C disease (NPC) may experience cataplexy along with cognitive impairment and dementia. Antidepressant drug therapy at relatively low doses is the traditional treatment these most likely work through inhibiting REM sleep, predominantly by increasing brain monoamine concentrations. While cataplexy is often associated with narcolepsy, the Sleep Foundation points out that 30 of cataplexy episodes are related to other disorders. ![]() Cataplexy can be the most disabling symptom of the narcolepsy syndrome, severely limiting normal activities of daily living. A defining and enigmatic aspect is that certain emotional stimuli usually trigger the episodes. The semiology of cataplexy differs between adults and children. The occurrence of sleep happens at any time, even though the person is engaged in any act, for example. Cataplexy reflects the dysregulation of rapid-eye-movement (REM) sleep, such that REM-sleep atonia intrudes inappropriately into wakefulness as brief episodes of either focal or total paralysis of voluntary muscle. People with narcolepsy enter REM sleep quickly. Remarkably and almost invariably, the clinical phenomenon of cataplexy results from the loss of around 40 000 hypocretin-containing neurones in the lateral hypothalamus in the context of narcolepsy type 1.
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