Division of Neurosurgery, Department of Clinical Neuroscience, Faculty of Medicine, University of Calgary, Foothills Medical Centre, Calgary, AB, T2N 2T9, Canada.
Exp Brain Res. 2010 Sep;206(1):1-13. doi: 10.1007/s00221-010-2312-5. Epub 2010 Jun 10.
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.
多系统萎缩(MSA)是一种进行性神经退行性疾病,其特征为帕金森症(MSA-P)、小脑和自主神经功能障碍。在帕金森病(PD)中,运动皮质 mu 和 beta 频带振荡的调制受损可能与运动徐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,这些振荡在自愿运动前 1-2 秒出现事件相关去同步(ERD),而未接受治疗的患者仅持续约 0.5 秒。在三名 MSA-P 患者服用常规多巴胺能药物时,从硬膜下条带电极记录运动皮质节律。在准备线索后,患者根据外部线索进行腕部伸展运动,以响应 GO 线索。此外,还在相同线索下进行想象中的腕部伸展运动和自我节奏的腕部伸展运动时进行记录。在特定于个体的频带中检查 ERD 和事件相关同步。所有患者在外部线索和自我节奏条件下,在特定于个体的 40 Hz 以下的频带中均显示出与运动相关的 ERD。在自我提示运动之前,一名患者的准备 ERD 潜伏期为 900 毫秒,而另外两名患者的潜伏期则在运动开始时或之后。在外源性任务中,两名患者观察到持续时间较短(<1.3 秒)的与准备线索相关的 ERD,而该 ERD 未持续到运动开始。在两名患者中,想象运动导致与 GO 线索相关的 ERD,其幅度较小。这些结果表明,接受左旋多巴治疗的 MSA 患者运动皮质振荡的调制与未接受治疗的 PD 患者相似。这些发现表明,MSA 患者的皮质激活减少,可能与基底节发生的病理生理变化有关,并且与这些患者通常从多巴胺能治疗中获得的不良临床反应相关。