Institut du Cerveau et de Moelle épinière, Centre de Neuroimagerie de Recherche, Paris, France.
Brain. 2013 Jul;136(Pt 7):2120-9. doi: 10.1093/brain/awt152.
In Parkinson's disease, rapid eye movement sleep behaviour disorder is an early non-dopaminergic syndrome with nocturnal violence and increased muscle tone during rapid eye movement sleep that can precede Parkinsonism by several years. The neuronal origin of rapid eye movement sleep behaviour disorder in Parkinson's disease is not precisely known; however, the locus subcoeruleus in the brainstem has been implicated as this structure blocks muscle tone during normal rapid eye movement sleep in animal models and can be damaged in Parkinson's disease. Here, we studied the integrity of the locus coeruleus/subcoeruleus complex in patients with Parkinson's disease using combined neuromelanin-sensitive, structural and diffusion magnetic resonance imaging approaches. We compared 24 patients with Parkinson's disease and rapid eye movement sleep behaviour disorder, 12 patients without rapid eye movement sleep behaviour disorder and 19 age- and gender-matched healthy volunteers. All subjects underwent clinical examination and characterization of rapid eye movement sleep using video-polysomnography and multimodal imaging at 3 T. Using neuromelanin-sensitive imaging, reduced signal intensity was evident in the locus coeruleus/subcoeruleus area in patients with Parkinson's disease that was more marked in patients with than those without rapid eye movement sleep behaviour disorder. Reduced signal intensity correlated with the percentage of abnormally increased muscle tone during rapid eye movement sleep. The results confirmed that this complex is affected in Parkinson's disease and showed a gradual relationship between damage to this structure, presumably the locus subcoeruleus, and abnormal muscle tone during rapid eye movement sleep, which is the cardinal marker of rapid eye movement sleep behaviour disorder. In longitudinal studies, the technique may also provide early markers of non-dopaminergic Parkinson's disease pathology to predict the occurrence of Parkinson's disease.
在帕金森病中，快速眼动睡眠行为障碍是一种早期的非多巴胺能综合征，伴有夜间暴力和快速眼动睡眠期间肌肉张力增加，可在帕金森病出现前数年出现。帕金森病中快速眼动睡眠行为障碍的神经元起源尚不清楚；然而，脑桥中的蓝斑下核已被认为是该结构在动物模型中阻止正常快速眼动睡眠期间的肌肉张力，并可能在帕金森病中受损。在这里，我们使用结合神经黑色素敏感、结构和弥散磁共振成像方法研究了帕金森病患者蓝斑/蓝斑下核复合体的完整性。我们比较了 24 例帕金森病和快速眼动睡眠行为障碍患者、12 例无快速眼动睡眠行为障碍患者和 19 名年龄和性别匹配的健康志愿者。所有受试者均接受了临床检查和视频多导睡眠图及多模态成像 3T 下快速眼动睡眠的特征描述。使用神经黑色素敏感成像，帕金森病患者的蓝斑/蓝斑下核区域的信号强度明显降低，且有快速眼动睡眠行为障碍的患者比无快速眼动睡眠行为障碍的患者更为明显。信号强度降低与快速眼动睡眠期间异常增加的肌肉张力百分比相关。结果证实该复合体在帕金森病中受到影响，并显示出该结构（推测为蓝斑下核）损伤与快速眼动睡眠期间异常肌肉张力之间的渐进关系，而快速眼动睡眠行为障碍正是其主要标志物。在纵向研究中，该技术还可能提供非多巴胺能帕金森病病理的早期标志物，以预测帕金森病的发生。
