Kübel Stefanie, Stegmayer Katharina, Vanbellingen Tim, Pastore-Wapp Manuela, Bertschi Manuel, Burgunder Jean-Marc, Abela Eugenio, Weder Bruno, Walther Sebastian, Bohlhalter Stephan
Neurocenter, Luzerner Kantonsspital, Spitalstrasse 31, 6000 Luzern 16, Switzerland.
University Hospital of Psychiatry, Bolligenstrasse 111, 3000 Bern 60, Switzerland.
Neuroimage Clin. 2017 Jul 18;16:88-97. doi: 10.1016/j.nicl.2017.07.007. eCollection 2017.
Parkinson's disease (PD) patients frequently suffer from dexterous deficits impeding activities of daily living. There is controversy whether impaired fine motor skill may stem from limb kinetic apraxia (LKA) rather than bradykinesia. Based on classical models of limb praxis LKA is thought to result when premotor transmission of time-space information of skilled movements to primary motor representations is interrupted. Therefore, using functional magnetic resonance imaging (fMRI) we tested the hypothesis that dexterous deficits in PD are associated with altered activity and connectivity in left parieto-premotor praxis network. Whole-brain analysis of fMRI activity during a task for LKA (coin rotation) showed increased activation of superior and inferior parietal lobule (SPL, IPL) and ventral premotor cortex (vPM) in PD patients compared to controls. For bradykinesia (assessed by finger tapping) a decreased fMRI activity could be detected in patients. Additionally, psychophysical interaction analysis showed increased functional connectivity between IPL and the posterior hippocampi in patients with PD. By contrast, functional connectivity to the right dorsolateral prefrontal cortex was decreased in patients with PD compared to controls. In conclusion, our data demonstrates that dexterous deficits in PD were associated with enhanced fMRI activation of the left praxis network upstream to primary motor areas, mirroring a neural correlate for the behavioral dissociation of LKA and bradykinesia. Furthermore, the findings suggest that patients recruit temporal areas of motor memory as an attempt to compensate for impaired motor skills. Finally, dysexecutive function may contribute to the deficit.
帕金森病（PD）患者经常遭受灵巧性缺陷，这妨碍了他们的日常生活活动。关于精细运动技能受损是否源于肢体运动性失用症（LKA）而非运动迟缓，目前存在争议。基于肢体运用的经典模型，当熟练运动的时空信息从前运动区向初级运动表征的传递中断时，就会导致LKA。因此，我们使用功能磁共振成像（fMRI）来检验这一假设，即PD患者的灵巧性缺陷与左侧顶叶 - 前运动运用网络的活动和连接改变有关。在一项针对LKA（硬币旋转）的任务中，对fMRI活动进行全脑分析发现，与对照组相比，PD患者的顶上小叶和顶下小叶（SPL、IPL）以及腹侧前运动皮层（vPM）的激活增加。对于运动迟缓（通过手指敲击评估），在患者中可检测到fMRI活动减少。此外，心理物理学交互分析显示，PD患者的IPL与后海马之间的功能连接增加。相比之下，与对照组相比，PD患者与右侧背外侧前额叶皮层的功能连接减少。总之，我们的数据表明，PD患者的灵巧性缺陷与初级运动区上游左侧运用网络的fMRI激活增强有关，这反映了LKA和运动迟缓行为分离的神经关联。此外，研究结果表明，患者会调动运动记忆的颞叶区域，试图补偿受损的运动技能。最后，执行功能障碍可能导致这种缺陷。
