Parkinsonism with excessive daytime sleepiness - A narcolepsy-like disorder?
Parkinsonism with excessive daytime sleepiness - A narcolepsy-like disorder?
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DOI：
10.1007/s00415-005-0614-5
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发表时间：
2005-02-01
影响因子：
6
通讯作者：
Bassetti, CL
中科院分区：
文献类型：
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作者：
Baumann, C;Ferini-Strambi, L;Bassetti, CL
背景帕金森病患者在多项睡眠潜伏期试验（MPEST）中表现为白天过度嗜睡（EDS）、幻觉、REM睡眠行为障碍（RBD）、平均睡眠潜伏期短和睡眠发作REM期（SOREMP）。在这些患者中，已经提出了嗜睡样睡眠-觉醒障碍的病理生理学。患者和方法我们研究了14例帕金森综合征和EDS的连续患者。标准研究包括评估帕金森综合征的持续时间和严重程度（Hoehn & Yahr评分）、埃普沃思嗜睡评分（ESS）、"REM症状"史（RBD/幻觉/睡眠麻痹/昏厥样发作）、多导睡眠图（PSG）、MREM和测量脑脊液（CSF）下丘脑泌素-1（食欲素A）水平。结果男12例，女2例，年龄54~82岁，平均69岁。平均持续时间和Hoehn & Yahr评分分别为6.3年和2.2。诊断包括特发性帕金森病（IPD，n = 10），弥漫性路易体痴呆（n = 3）和多系统萎缩（n = 1）。所有患者的ESS ≥ 10（平均12;范围10 - 18）。除2例患者外，所有患者均报告了"REM症状"（幻觉：n = 9; RBD：n = 9）。没有患者报告出现晕厥样症状或睡眠瘫痪。PSG检查发现睡眠呼吸暂停（呼吸暂停低通气指数> 10/h，n = 7）、睡眠期肢体周期性运动（PLMS指数> 10/h，n = 6）和RBD（n = 5）特征，MRI检查发现10例患者平均睡眠潜伏期<5 min，2例患者出现SOREMP。与对照组（n = 20，平均497 pg/ml;范围350 - 603）相比，8名患者的CSF下丘脑分泌素-1水平正常，2名患者的水平较低（分别为221和307 pg/ml）。结论发作性睡病和帕金森综合征合并EDS的病理生理学中存在"最终共同通路"的假说不成立。睡眠呼吸暂停和PLMS可能在帕金森病患者EDS的发病机制中起着被低估的作用。
Background Parkinsonian patients with excessive daytime sleepiness (EDS), hallucinations, REM sleep behavior disorder (RBD), short mean sleep latencies, and sleep-onset REM periods (SOREMP) on multiple sleep latency tests (MSLT) have been reported. In these patients a narcolepsy-like pathophysiology of sleep-wake disturbances has been suggested. Patients and methods We studied 14 consecutive patients with Parkinsonism and EDS. Standard studies included assessment of duration and severity of Parkinsonism (Hoehn & Yahr score), Epworth sleepiness score (ESS), history of "REM-symptoms" (RBD/hallucinations/sleep paralysis/ cataplexy-like episodes), polysomnography (PSG), MSLT, and measurement of cerebrospinal fluid (CSF) levels of hypocretin-1 ( orexin A). Results There were 12 men and 2 women ( mean age 69 years; range 54 - 82). The mean duration and the Hoehn&Yahr score were 6.3 years and 2.2, respectively. Diagnoses included idiopathic Parkinson's disease (IPD, n= 10), dementia with diffuse Lewy bodies ( n= 3), and multisystem atrophy ( n= 1). The ESS was = 10 in all patients ( mean 12; range 10 - 18). "REM-symptoms" were reported by all but two patients ( hallucinations: n= 9; RBD: n= 9). None of the patients reported cataplexy-like symptoms or sleep paralysis. On PSG sleep apnea ( apnea hypopnea index > 10/h, n= 7), periodic limb movements during sleep (PLMS-index > 10/h, n= 6), and features of RBD ( n= 5) were found. On MSLT mean sleep latency was < 5 minutes in 10 patients, and SOREMP were found in two patients. When compared with controls ( n= 20, mean 497 pg/ml; range 350 - 603), CSF hypocretin-1 levels were normal in 8 patients and low in 2 patients ( 221 and 307 pg/ml, respectively). Conclusion These findings do not support the hypothesis of a "final common pathway" in the pathophysiology of narcolepsy and Parkinsonism with EDS. Sleep apnea and PLMS may play a so-far underestimated role in the pathogenesis of EDS in Parkinsonian patients.