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黑质纹状体多巴胺能神经元退行性变在 REM 睡眠行为障碍发病机制中的意义。

The implication of nigrostriatal dopaminergic degeneration in the pathogenesis of REM sleep behavior disorder.

机构信息

Department of Nuclear Medicine, Seoul National University Bundang Hospital, Bundang-gu, Seongnam, Korea.

出版信息

Eur J Neurol. 2010 Mar;17(3):487-92. doi: 10.1111/j.1468-1331.2009.02854.x. Epub 2009 Nov 24.

DOI:10.1111/j.1468-1331.2009.02854.x
PMID:19968708
Abstract

BACKGROUND AND PURPOSE

The pathogenesis of rapid eye movement (REM) sleep behavior disorder (RBD) is not clear despite its frequent association with Parkinson's disease (PD). We investigated whether the nigrostriatal dopaminergic system is involved in the development of idiopathic RBD.

METHODS

Fourteen patients with RBD, 14 patients with PD and 12 normal controls were included in the study. The diagnosis of RBD was confirmed on polysomnography. All the participants performed single-photon emission computed tomography imaging 3 h after injection of [(123)I]FP-CIT. During REM sleep of the RBD patients, each 30-s epoch was rated as 'tonic' when there was at least 50% of tonically maintained chin electromyography (EMG) activity in the epoch. Phasic EMG activities were calculated as the percentage of 3-s mini-epoch containing phasic EMG events (leg and chin, separately).

RESULTS

The RBD patients showed a trend of lower binding in the striatum than the normal controls (P = 0.07), and the significance was revealed in the putamen (P = 0.02). However, in 11 individual cases of the 14 RBD patients, the dopamine transporter (DAT) densities in the putamen still remained within the normal range. In the RBD patients, there was no correlation between EMG activities and DAT densities.

CONCLUSIONS

Nigrostriatal dopaminergic degeneration could be a part of the pathogenesis of RBD, but not essential for the development of RBD. The lack of correlation between RBD severity and DAT densities suggests that another pathogenic process not related to nigrostriatal dopaminergic transmission may be implicated in RBD.

摘要

背景与目的

尽管快速眼动(REM)睡眠行为障碍(RBD)常与帕金森病(PD)相关,但其发病机制仍不清楚。我们研究了黑质纹状体多巴胺能系统是否参与了特发性 RBD 的发生。

方法

本研究纳入了 14 例 RBD 患者、14 例 PD 患者和 12 名正常对照者。RBD 的诊断通过多导睡眠图确认。所有参与者在注射 [(123)I]FP-CIT 后 3 小时进行单光子发射计算机断层扫描成像。在 RBD 患者的 REM 睡眠期间,当每个 30 秒的时相中至少有 50%的持续颏肌肌电图(EMG)活动时,该时相被评为“强直”。将 EMG 活动分为 3 秒的微时相,计算其中包含的相位 EMG 事件(分别为腿部和颏部)的百分比。

结果

与正常对照组相比,RBD 患者的纹状体结合呈下降趋势(P = 0.07),且在壳核中差异具有统计学意义(P = 0.02)。然而,在 14 例 RBD 患者中的 11 例中,壳核中的多巴胺转运体(DAT)密度仍在正常范围内。在 RBD 患者中,EMG 活动与 DAT 密度之间无相关性。

结论

黑质纹状体多巴胺能退变可能是 RBD 发病机制的一部分,但不是 RBD 发生的必要条件。RBD 严重程度与 DAT 密度之间缺乏相关性表明,另一种与黑质纹状体多巴胺传递无关的致病过程可能与 RBD 有关。

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