![]() 1,2 Episodes of cataplexy start abruptly, are often bilateral, and generally last for 2 hours) is strongly discouraged. Cataplexy is a brief and sudden loss of muscle tone with retained consciousness that is precipitated by strong emotion, often laughter. Signs of REM sleep dissociation, most specifically cataplexy, are also part of the symptom profile. 2Ĭlinicians treating a patient with excessive daytime sleepiness should determine and measure the patient’s sleepiness, review nocturnal sleep and daily activities, assess comorbid conditions, review medications that affect sleep, and evaluate any other contributing primary sleep disorders that may cause excessive daytime sleepiness. 1,2 These patients generally fall asleep for only seconds to minutes and awaken from these brief naps feeling refreshed. It occurs most often in sedentary or monotonous situations and can range from abrupt sleep attacks with no prodromal symptoms to unintended lapses into sleep. The primary symptom of narcolepsy is excessive daytime sleepiness-ie, the inability to stay awake and alert during major waking episodes of the day. The combination of excessive daytime sleepiness, cataplexy, sleep-related hallucinations, and sleep paralysis collectively form the symptom tetrad for narcolepsy. 1 Lastly, the HLA association may also implicate autoimmunity in the pathogenesis of narcolepsy. 2 Seasonal and infectious factors have been proposed as potential environmental triggers. 1,2 However, twin studies show fairly low concordance rates among monozygotic twins, suggesting an environmental influence as well. The risk of developing narcolepsy is 10 to 40 times higher in first-degree relatives of affected patients. Familial association also points to the influence of genetics. The human leukocyte antigen (HLA) subtype DQB1*0602 is strongly associated with narcolepsy with cataplexy and low hypocretin levels. 1,2 In addition, genetics play a role in the pathogenesis of narcolepsy. Deficiency in hypocretin, a neurotransmitter that is produced in the lateral hypothalamus and is involved in maintaining wakefulness and preventing rapid eye movement (REM)sleep, underlies narcolepsy especially in the presence of cataplexy. The pathophysiological basis for narcolepsy is complex and may involve a variety of factors. This article provides an overview of the clinical features of narcolepsy, as well as strategies for managing and treating the condition. 4,5 In particular, narcolepsy is associated with driving difficulties and an increased risk of motor vehicle accidents. ![]() 3,5 If left untreated, the disorder can have negative effects on social, educational, and occupational functioning. 2 Narcolepsy has been linked to significant patient and societal burden, such as increased healthcare system utilization and costs and decreased employment rates and occupational productivity. ![]() ![]() In recent years, the medical community has developed a greater understanding of the clinical features and pathophysiological basis for narcolepsy, but the disorder remains underrecognized and underdiagnosed. 1,4 This diagnostic delay may be due to variations in symptom onset and presentation. 4 Although symptoms typically present in adolescence or early adulthood (with peaks at ages 15 and 35), diagnosis is commonly delayed about 10 years, particularly in women. 1 Approximately 1 in every 2000 to 3000 people is affected by narcolepsy, 2,3 and the disorder occurs nearly equally in men and women. It is categorized as a central disorder of hypersomnolence, with a primary complaint of daytime sleepiness not caused by disturbed nocturnal sleep or misaligned circadian rhythms. ![]() Narcolepsy is a chronic neurological sleep disorder in which the brain’s natural sleep-wake cycle is disrupted. This article provides an overview of the clinical manifestations, diagnosis, and treatment options for this condition. ABSTRACT: Narcolepsy is a chronic neurological sleep disorder that is characterized by excessive sleepiness and can have negative effects on daytime activities and quality of life. ![]()
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