![]() ![]() Cataplexy occasionally occurs in conjunction with other neurological conditions, such as Nieman-Pick Type C disease, but the pathophysiological links in these neurological conditions with the hypocretin abnormalities are presently not well established. Occurrence of cataplexy is tightly associated with impairment of hypocretin/orexin neurotransmission, and it rarely occurs as an isolated symptom. Although EDS is not specific for narcolepsy and is seen in other primary and secondary EDS disorders (such as sleep apnea syndrome), cataplexy is generally regarded as pathognomonic. Quality of life studies suggest that the impact of narcolepsy is equivalent to that of Parkinson's disease. Symptoms most often begin between adolescence and young adulthood, however it may also occur earlier in childhood or not until the third or fourth decade of life. Narcolepsy usually occurs in association with cataplexy and other symptoms, which commonly include hypnagogic or hypnopompic hallucinations, sleep paralysis, automatic behavior, and disrupted nocturnal sleep. 3.2 HLA, immune system, and etiology of narcolepsy.3.1 Deficiency in hypocretin (orexin) transmission in narcolepsy.2.3 Histocompatibility Human Leukocyte Antigen (HLA) testing.2.2 Cerebrospinal fluid (CSF) hypocretin-1 assessment. ![]() 2.1 Polysomnography, nocturnal and daytime sleep studies.1.3 Hypnagogic or hypnopompic hallucinations.1.1 Sleepiness or excessive daytime sleepiness (EDS). ![]()
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