Sobell Department of Motor Neuroscience & Movement Disorders, UCL, Institute of Neurology, The National Hospital for Neurology & Neurosurgery, Queen Square, London, United Kingdom.
Department of Neurology, University of Ljubljana, Slovenia.
Mov Disord. 2015 Jul;30(8):1098-106. doi: 10.1002/mds.26167. Epub 2015 Mar 5.
A number of neurophysiological abnormalities have been described in patients with Parkinson's disease, but very few longitudinal studies of how these change with disease progression have been reported. We describe measures of motor cortex inhibition and plasticity at 6 and 12 mo in 12 patients that we previously reported at initial diagnosis. Given the well-known interindividual variation in these measures, we were particularly concerned with the within-subject changes over time.
Patients were assessed clinically, and transcranial magnetic stimulation (TMS) was used to measure motor cortical excitability, inhibition (short interval intracortical inhibition, cortical silent period), and plasticity (response to excitatory paired associative stimulation protocol) in both hemispheres. All measurements were performed 6 mo and 12 mo after the baseline experiments.
Asymmetry in clinical motor symptoms was reflected in asymmetry of plasticity and inhibition. In the group as a whole, little change was seen in any of the parameters over 12 mo. However, analysis of within-individual data showed clear correlations between changes in clinical asymmetry and asymmetry of response to paired associative stimulation protocol and cortical silent period.
Longitudinal changes in cortical silent period and response to paired associative stimulation protocol in Parkinson's disease reflect dynamic effects on motor cortex that are related to progression of motor signs. They are useful objective markers of early disease progression that could be used to detect effects of disease-modifying therapies. The decline in heightened plasticity that was present at disease onset may reflect failure of compensatory mechanisms that maintained function in the preclinical state.
帕金森病患者存在许多神经生理异常，但很少有关于这些异常如何随疾病进展而变化的纵向研究报告。我们描述了 12 名患者在初始诊断时报告的 6 个月和 12 个月时运动皮层抑制和可塑性的测量值。鉴于这些测量值在个体间存在明显差异，我们特别关注随时间的个体内变化。
患者接受临床评估，并使用经颅磁刺激（TMS）测量双侧运动皮层兴奋性、抑制（短间隔内皮质抑制、皮质静息期）和可塑性（对兴奋性成对关联刺激方案的反应）。所有测量均在基线实验后 6 个月和 12 个月进行。
临床运动症状的不对称反映在可塑性和抑制的不对称中。在整个组中，在 12 个月内，任何参数都没有明显变化。然而，个体内数据分析显示，临床不对称性的变化与对成对关联刺激方案和皮质静息期反应的不对称性之间存在明显的相关性。
帕金森病患者皮质静息期和对成对关联刺激方案反应的纵向变化反映了对运动皮层的动态影响，这些影响与运动症状的进展有关。它们是早期疾病进展的有用客观标志物，可用于检测疾病修饰疗法的效果。在疾病发作时存在的高可塑性下降可能反映了维持临床前状态功能的代偿机制的失败。
