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Journal of sleep research, 2011-03, Vol.20 (1pt1), p.45-49
2011
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Autor(en) / Beteiligte
Titel
Relationship between clinical characteristics of narcolepsy and CSF orexin‐A levels
Ist Teil von
  • Journal of sleep research, 2011-03, Vol.20 (1pt1), p.45-49
Ort / Verlag
Oxford, UK: Blackwell Publishing Ltd
Erscheinungsjahr
2011
Quelle
Wiley Online Library Journals Frontfile Complete
Beschreibungen/Notizen
  • Summary Although an abnormally low cerebrospinal fluid (CSF)‐orexin level is well known to be a specific finding in narcoleptic patients, the relationships between the severity of the core symptoms of narcolepsy [i.e. daytime sleepiness and increased rapid eye movement (REM) propensity], as well as levels of obesity, and CSF‐orexin levels have not been well elucidated. The aim of this study was to examine the relationship between these characteristic symptoms of narcolepsy and CSF‐orexin level. Fifty‐three patients with narcolepsy with cataplexy (NA/CA) and 17 without cataplexy (NA w/o CA) were enrolled. Sleep latency and sleep onset REM latency were measured using the multiple sleep latency test (MSLT). Multiple linear regression analysis was used to determine factors associated with both mean sleep latency and mean sleep onset REM latency on MSLT, with %body mass index (BMI), gender, onset age, length of excessive daytime sleepiness (EDS) morbidity, diagnostic subgroup and CSF‐orexin levels being used as independent variables. The NA/CA group included a significantly higher number of patients with undetectable CSF‐orexin levels and shorter sleep onset and rapid eye movement (SOREM) latency, as well as a higher %BMI, versus NA w/o CA. Multiple linear regression analysis revealed that sleep latency was associated significantly with CSF‐orexin levels and gender. With regard to sleep onset REM latency and %BMI, only CSF‐orexin levels appeared to be a significantly associated factor. In narcoleptic patients, the severity of both excessive daytime sleepiness and increased REM propensity, as well as the level of obesity, could be associated with CSF‐orexin deficiency, rather than with subcategories of the disorder.

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