Narcolepsy

Narcolepsy be a chronic neurological disorder wey dey impair de ability to regulate sleep–wake cycles, den specifically dey impact REM (rapid eye movement) sleep. De symptoms of narcolepsy dey include excessive daytime sleepiness (EDS), sleep-related hallucinations, sleep paralysis, disturbed nocturnal sleep (DNS), den cataplexy. People plus narcolepsy typically get poor quality of sleep.

Der be two recognized forms of narcolepsy: type 1 den type 2.American Academy of Sleep Medicine. International Classification of Sleep Disorders, 3rd ed.; American Academy of Sleep Medicine: Darien, CT, USA, 2014. Narcolepsy type 1 (NT1) fi be clinically characterized by symptoms of EDS den cataplexy, den/anaa go get cerebrospinal fluid (CSF) orexin levels of less dan 110 pg/ml. Cataplexy be transient episodes of aberrant muscle tone, chaw typically dey loss of muscle tone, wey be associated plus strong emotion.Moscovitch, A.; Partinen, M.; Guilleminault, C. The positive diagnosis of narcolepsy and narcolepsy's borderland. Neurology 1993, 43, 55–60. Insyd pediatric-onset narcolepsy, active motor phenomena no be uncommon.Postiglione, E.; Antelmi, E.; Pizza, F.; Lecendreux, M.; Dauvilliers, Y.; Plazzi, G. The clinical spectrum of childhood narcolepsy. Sleep Med. Rev. 2018, 38, 70–85 Cataplexy fi be mistaken for syncope, tics, anaa seizures. Narcolepsy type 2 (NT2) no get features of cataplexy, den CSF orexin levels be normal. Sleep-related hallucinations, both hypnagogic (going to sleep) den hypnopompic (on awakening), be vivid hallucinations wey fi be auditory, visual, anaa tactile wey fi occur independent of anaa insyd combination plus an inability to move (sleep paralysis).

Narcolepsy be a clinical syndrome of hypothalamic disorder, buh de exact cause of narcolepsy be unknown, plus potentially chaw causes. A leading consideration for de cause of narcolepsy type 1 be say e be an autoimmune disorder. Proposed pathophysiology as an autoimmune disease dey suggest antigen presentation by DQ0602 to specific CD4+ T cells wey dey result in CD8+ T-cell activation den consequent injury to orexin producing neurons.Ollila, H.M., Sharon, E., Lin, L., Sinnott-Armstrong, N., Ambati, A., Yogeshwar, S.M., Hillary, R.P., Jolanki, O., Faraco, J., Einen, M. and Luo, G., 2023. Narcolepsy risk loci outline role of T cell autoimmunity and infectious triggers in narcolepsy. Nature communications, 14(1), p.2709. Dem dey suggest familial trends of narcolepsy to be higher dan previously appreciated. Familial risk of narcolepsy among first-degree relatives be high. Na dem report relative risk for narcolepsy insyd a first-degree relative to be 361.8.Wing, Y.K., Chen, L., Lam, S.P., Li, A.M., Tang, N.L., Ng, M.H., Cheng, S.H., Ho, C.K., Mok, V., Leung, H.W. and Lau, A., 2011. Familial aggregation of narcolepsy. Sleep medicine, 12(10), pp.947-951. However, der be a spectrum of symptoms dem find insyd dis study, from asymptomatic abnormal sleep test findings to significantly symptomatic.Wing, Y.K., Chen, L., Lam, S.P., Li, A.M., Tang, N.L., Ng, M.H., Cheng, S.H., Ho, C.K., Mok, V., Leung, H.W. and Lau, A., 2011. Familial aggregation of narcolepsy. Sleep medicine, 12(10), pp.947-951.

De autoimmune process be thought to be triggered insyd genetically susceptible individuals by an immune-provoking experience, such as an infection plus H1N1 influenza. Secondary narcolepsy fi occur as a consequence of anoda neurological disorder. Dem fi see secondary narcolepsy insyd sam individuals plus traumatic brain injury, tumors, Prader–Willi syndrome anaa oda diseases wey dey affect de parts of de brain wey dey regulate wakefulness anaa REM sleep. Diagnosis typically dey base on de symptoms den sleep studies, after excluding alternative causes of EDS. EDS sanso fi be caused by oda sleep disorders such as insufficient sleep syndrome, sleep apnea, major depressive disorder, anemia, heart failure, den drinking alcohol.

While der be no cure, behavioral strategies, lifestyle changes, social support, den medications fi help. Lifestyle den behavioral strategies fi include identifying den avoiding anaa desensitizing emotional triggers for cataplexy, dietary strategies wey fi reduce sleep-inducing chows den drinks, scheduled anaa strategic naps, den maintaining a regular sleep-wake schedule. Social support, social networks, den social integration be resourcesGottlieb, B.H. and Bergen, A.E., 2010. Social support concepts and measures. Journal of psychosomatic research, 69(5), pp.511-520. wey fi lie insyd de communities wey relate to living plus narcolepsy. Medications dem use to treat narcolepsy primarily target EDS den/anaa cataplexy. Dese medications dey include alerting agents (e.g., modafinil, armodafinil, pitolisant, solriamfetol), oxybate medications (e.g., twice nightly sodium oxybate, twice nightly mixed oxybate salts, den once nightly extended-release sodium oxybate), den oda stimulants (e.g., methylphenidate, amphetamine). Der sanso be de use of antidepressants such as tricyclic antidepressants, selective serotonin reuptake inhibitors (SSRIs), den serotonin–norepinephrine reuptake inhibitors (SNRIs) for de treatment of cataplexy.

Estimates of frequency dey range from 0.2 to 600 per 100,000 people insyd chaw countries. De condition often dey begin insyd kiddie time, plus males den females be affected equally. Untreated narcolepsy dey increase de risk of motor vehicle collisions den falls.

 References 

 External links 


 European Sleep Research Society (ESRS)


Category:Ailments of unknown cause
Category:Amphetamine
Category:Rare diseases
Category:Sleep disorders
Category:Hypersomnolence disorders
Category:Translated from MDWiki