Sleep medicine · 2019
Prevalence and neurophysiological correlates of sleep disordered breathing in pediatric type 1 narcolepsy.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Filardi Marco, Demir Nurhak, Pizza Fabio, Vandi Stefano, Antelmi Elena, Noce Silvia, Bruni Oliviero, Plazzi Giuseppe
Аннотация
STUDY OBJECTIVES: To investigate the prevalence and neurophysiological correlates of obstructive sleep disordered breathing (OSA) in type 1 narcolepsy (NT1) children and adolescents.
METHODS: Thirty-eight, drug-naïve, NT1 children and adolescents and 21 age- and sex-balanced clinical controls underwent nocturnal polysomnography (PSG) and multiple sleep latency test (MSLT). According to the rules for pediatric population, an obstructive apnea-hypopnea index (Obstructive AHI) ≥ 1 (comprising obstructive and mixed events), defined comorbid OSA.
RESULTS: NT1 children showed higher prevalence of overweight/obesity and severe nocturnal sleep disruption (lower sleep efficiency, and increased N1 sleep stage percentage) coupled with higher motor activity (periodic limb movement index [PLMi] and REM atonia index) compared to clinical controls. Sleep-related respiratory variables did not differ between NT1 and clinical controls (OSA prevalence of 13.2% and 4.8%, respectively). NT1 children with OSA were younger and showed lower N2 sleep stage percentage and higher PLMi than NT1 children without comorbid OSA. Overweight/obesity was not associated with OSA in NT1.
CONCLUSIONS: Despite higher body mass index (BMI), OSA prevalence did not differ between children with NT1 and clinical controls. OSA in pediatric NT1 patients is a rare and mild comorbidity, further contributing to nocturnal sleep disruption without effects on daytime sleepiness.
METHODS: Thirty-eight, drug-naïve, NT1 children and adolescents and 21 age- and sex-balanced clinical controls underwent nocturnal polysomnography (PSG) and multiple sleep latency test (MSLT). According to the rules for pediatric population, an obstructive apnea-hypopnea index (Obstructive AHI) ≥ 1 (comprising obstructive and mixed events), defined comorbid OSA.
RESULTS: NT1 children showed higher prevalence of overweight/obesity and severe nocturnal sleep disruption (lower sleep efficiency, and increased N1 sleep stage percentage) coupled with higher motor activity (periodic limb movement index [PLMi] and REM atonia index) compared to clinical controls. Sleep-related respiratory variables did not differ between NT1 and clinical controls (OSA prevalence of 13.2% and 4.8%, respectively). NT1 children with OSA were younger and showed lower N2 sleep stage percentage and higher PLMi than NT1 children without comorbid OSA. Overweight/obesity was not associated with OSA in NT1.
CONCLUSIONS: Despite higher body mass index (BMI), OSA prevalence did not differ between children with NT1 and clinical controls. OSA in pediatric NT1 patients is a rare and mild comorbidity, further contributing to nocturnal sleep disruption without effects on daytime sleepiness.