Postuma Ronald B, Gagnon Jean-François, Pelletier Amelie, Montplaisir Jacques Y
Department of Neurology, McGill University, Montreal General Hospital, Montreal, QC Canada.
Centre d'étude du sommeil et des rythmes biologiques, Hôpital du Sacré-Cœur de Montréal Montréal, 5400 Boul. Gouin Ouest, Montréal, H4J 1C5 QC Canada.
NPJ Parkinsons Dis. 2017 Mar 20;3:9. doi: 10.1038/s41531-017-0011-7. eCollection 2017.
Although some sleep disorders are markers of prodromal Parkinson's disease and dementia with Lewy bodies, it is unclear whether insomnia and somnolence can predict disease. We assessed a large cohort of patients with idiopathic rapid eye movement sleep behavior disorder and age/sex matched controls, comparing the Epworth sleepiness scale, the Insomnia Severity Index, the Pittsburgh Sleep Quality Index, and polysomnographic variables. In those with repeated scales, we assessed change over time. Finally, we assessed whether sleep abnormalities predicted defined neurodegenerative disease. The 151 patients (age = 65.9, 75% male) completed sleep scales and were included. Epworth scores were similar between patients and controls (7.0+/-4.6 vs. 7.2+/-4.7, = 0.77), and did not progress with time (change = +0.46+/-2.1, = 0.45). Epworth scores were similar between those who developed neurodegenerative disease and those remaining disease-free (6.7+/-4.4 vs. 7.1+/-4.7, = 0.70). Pittsburgh Index scores were higher in patients than controls (7.2+/-3.8 vs. 4.9+/-3.4, = 0.004), mainly driven by the sleep disturbance/medication components (reflecting rapid eye movement sleep behavior disorder symptoms/treatment). Baseline Pittsburgh scores did not predict conversion to neurodegeneration, although sleep duration increased over time in those converting to neurodegenerative disease (+0.88+/-1.32 h, = 0.014). Insomnia index scores were higher in patients than controls (10.0+/-5.5 vs. 6.35+/-4.66, < 0.001), but declined over time (-1.43+/-5.09, = 0.029) particularly in those converting to neurodegenerative disease. Finally, on polysomnogram, those with increased tonic rapid eye movement had higher risk of developing defined neurodegenerative disease (HR = 1.88, = 0.039). In summary, we found that somnolence and insomnia do not predict neurodegeneration in idiopathic rapid eye movement sleep behavior disorder. As neurodegeneration progresses through prodromal stages, patients may have increasing sleep drive and duration.
虽然一些睡眠障碍是帕金森病前驱期和路易体痴呆的标志物,但目前尚不清楚失眠和嗜睡是否能预测疾病。我们评估了一大群特发性快速眼动睡眠行为障碍患者以及年龄/性别匹配的对照组,比较了爱泼华嗜睡量表、失眠严重程度指数、匹兹堡睡眠质量指数和多导睡眠图变量。对于重复进行量表评估的患者,我们评估了随时间的变化。最后,我们评估了睡眠异常是否能预测明确的神经退行性疾病。151名患者(年龄 = 65.9岁,75%为男性)完成了睡眠量表评估并被纳入研究。患者和对照组的爱泼华评分相似(7.0±4.6 vs. 7.2±4.7,P = 0.77),且未随时间进展(变化 = +0.46±2.1,P = 0.45)。发生神经退行性疾病的患者和未患疾病的患者的爱泼华评分相似(6.7±4.4 vs. 7.1±4.7,P = 0.70)。患者的匹兹堡指数评分高于对照组(7.2±3.8 vs. 4.9±3.4,P = 0.004),主要由睡眠障碍/药物成分驱动(反映快速眼动睡眠行为障碍症状/治疗情况)。尽管向神经退行性疾病转化的患者睡眠时长随时间增加(+0.88±1.32小时,P = 0.014),但基线匹兹堡评分并不能预测向神经退行性疾病的转化。患者的失眠指数评分高于对照组(10.0±5.5 vs. 6.35±4.66,P < 0.001),但随时间下降(-1.43±5.09,P = 0.029),尤其是在向神经退行性疾病转化的患者中。最后,在多导睡眠图上,强直性快速眼动增加的患者发生明确神经退行性疾病的风险更高(风险比 = 1.88,P = 0.039)。总之,我们发现嗜睡和失眠不能预测特发性快速眼动睡眠行为障碍患者的神经退行性变。随着神经退行性变从前驱期进展,患者的睡眠驱动力和时长可能会增加。