Functional Neuroimaging Unit, Centre de Recherche, Institut Universitaire de Gériatrie de Montréal, 4545 Queen Mary, Montréal, QC, H3W 1W5, Canada.
Eur J Neurosci. 2012 Feb;35(4):572-83. doi: 10.1111/j.1460-9568.2011.07979.x. Epub 2012 Feb 3.
Motor studies of Parkinson's disease (PD) have shown cortical hypo-activity in relation to nigrostriatal dopamine depletion. Cognitive studies also identified increased cortical activity in PD. We have previously suggested that the hypo-activity/hyper-activity patterns observed in PD are related to the striatal contribution. Tasks that recruit the striatum in control participants are associated with cortical hypo-activity in patients with PD, whereas tasks that do not result in cortical hyper-activity. The putamen, a structure affected by the neurodegeneration observed in PD, shows increased activation for externally-triggered (ET) and self-initiated (SI) movements. The first goal of this study was to evaluate the effect of levodopa on the putamen's response to ET and SI movements. Our second goal was to assess the effect of levodopa on the hypo-activity/hyper-activity patterns in cortical areas. Patients with PD on and off levodopa and healthy volunteers performed SI, ET and control finger movements during functional magnetic resonance imaging. Healthy participants displayed significant differences in putamen activity in ET and SI movements. These differences were reduced in patients off medication, with non-task-specific increases in activity after levodopa administration. Furthermore, the ventrolateral prefrontal cortex showed significant increases in activity during SI movements in healthy controls, whereas it was hypo-active in PD. This region showed significantly increased activity during ET movements in patients off medication. Levodopa had no effect on this discrepancy. Our results suggest that dopamine replacement therapy has a non-task-specific effect on motor corticostriatal regions, and support the hypothesis that increases and decreases in cortical activity in PD are related to the mesocortical dopamine pathway imbalance.
帕金森病（PD）的运动研究表明，与黑质纹状体多巴胺耗竭有关的皮质活动低下。认知研究也确定了 PD 中皮质活动增加。我们之前曾提出，PD 中观察到的低活动/高活动模式与纹状体的贡献有关。在对照组参与者中招募纹状体的任务与 PD 患者的皮质低活动相关，而不会导致皮质高活动的任务。纹状体是受 PD 中观察到的神经退行性变影响的结构，对外源性触发（ET）和自我启动（SI）运动显示出增加的激活。本研究的第一个目标是评估左旋多巴对 ET 和 SI 运动中纹状体反应的影响。我们的第二个目标是评估左旋多巴对皮质区域低活动/高活动模式的影响。PD 患者在服用和未服用左旋多巴以及健康志愿者在功能磁共振成像期间进行 SI、ET 和对照手指运动。健康参与者在 ET 和 SI 运动中显示出纹状体活动的显著差异。这些差异在未服药的患者中减少，并且在左旋多巴给药后出现非任务特异性的活性增加。此外，腹外侧前额叶皮层在健康对照者的 SI 运动中显示出显著的活性增加，而在 PD 中则呈低活性。该区域在未服药的患者的 ET 运动中显示出显著增加的活性。左旋多巴对这种差异没有影响。我们的结果表明，多巴胺替代疗法对运动皮质纹状体区域具有非任务特异性影响，并支持 PD 中皮质活动增加和减少与中皮质多巴胺通路失衡有关的假设。
