Event-related desynchronization of motor cortical oscillations in patients with multiple system atrophy
Event-related desynchronization of motor cortical oscillations in patients with multiple system atrophy
复制标题
多系统萎缩患者运动皮质振荡的事件相关去同步化
DOI：
10.1007/s00221-010-2312-5
复制
发表时间：
2010
影响因子：
2
通讯作者：
J. Dostrovsky
中科院分区：
文献类型：
--
作者：
R. Levy;A. Lozano;A. Lang;J. Dostrovsky
多系统萎缩（MSA）是一种进行性神经退行性疾病，其特征是帕金森综合征（MSA-P）、小脑和自主神经功能障碍。在帕金森氏病（PD）中，运动皮质μ和β范围振荡的调制受损可能与运动迟缓的病理生理学有关。在正常受试者和接受左旋多巴治疗的PD患者中，这些振荡的事件相关去极化（ERD）发生在自主运动之前1-2秒，而在未经治疗的患者中仅持续约0.5秒。运动皮质节律记录从硬膜下带状电极在三名患者的MSA-P，而他们的常规多巴胺能药物。在一个准备好的提示之后，患者进行外部提示的手腕伸展运动以进行提示。此外，录音期间获得想象的手腕伸展运动相同的线索，并在自定步调的手腕伸展。ERD和事件相关的同步进行了检查，在特定主题的频带。所有患者在外部提示和自我起搏条件下，均在低于~40 Hz的受试者特定频带中显示出运动相关ERD。1例患者自我提示运动前的预备ERD潜伏期为900 ms，另2例患者运动开始时或运动开始后的潜伏期为900 ms。在外部线索任务中，在两名患者中观察到短暂持续（<1.3 s）的准备好的线索相关ERD，该ERD不持续到运动开始。想象的运动导致围棋线索相关的ERD的幅度较小，在相同的两名患者。这些结果表明，调制的运动皮质振荡的MSA患者与左旋多巴治疗是类似的，发生在未经治疗的PD患者。研究结果表明，MSA患者的皮质激活减少，可能与基底神经节发生的病理生理变化有关，并与这些患者通常使用多巴胺能治疗获得的不良临床反应相关。
Multiple system atrophy (MSA) is a progressive neurodegenerative disease characterized by parkinsonism (MSA-P), cerebellar and autonomic deficits. In Parkinson’s disease (PD), an impaired modulation of motor cortical mu and beta range oscillations may be related to the pathophysiology of bradykinesia. Event-related desynchronization (ERD) of these oscillations occur for 1–2 s preceding a voluntary movement in normal subjects and patients with PD treated with levodopa while only lasting around 0.5 s in untreated patients. Motor cortical rhythms were recorded from subdural strip electrodes in three patients with MSA-P while taking their regular dopaminergic medications. Following a ready cue, patients performed an externally cued wrist extension movement to a go cue. In addition, recordings were obtained during imagined wrist extension movements to the same cues and during self-paced wrist extensions. ERD and event-related synchronization were examined in subject-specific frequency bands. All patients showed movement-related ERD in subject-specific frequency bands below ~40 Hz in both externally cued and self-paced conditions. Preparatory ERD latency preceding self-cued movement was 900 ms in one patient and at or after movement onset in the other two patients. In the externally cued task, a short lasting (<1.3 s) ready cue-related ERD that was not sustained to movement onset was observed in two patients. Imagined movements resulted in go cue-related ERD with a smaller magnitude in the same two patients. These results indicate that the modulation of motor cortical oscillations in patients with MSA that are treated with levodopa is similar to that occurring in untreated patients with PD. The findings suggest that cortical activation in patients with MSA is diminished, may be related to pathophysiological changes occurring in the basal ganglia and correlates with the poor clinical response that these patients typically obtain with dopaminergic therapy.