Department of Psychological Sciences, Vanderbilt University, United States.
Department of Neurology, Vanderbilt University, United States.
Neuropsychologia. 2018 Mar;111:26-35. doi: 10.1016/j.neuropsychologia.2018.01.014. Epub 2018 Jan 29.
Basal ganglia dysfunction in Parkinson's disease (PD) is thought to generate deficits in action control, but the characterization of these deficits have been qualitative rather than quantitative. Patients with PD typically show prolonged response times on tasks that instantiate a conflict between goal-directed processing and automatic response tendencies. In the Simon task, for example, the irrelevant location of the stimulus automatically activates a corresponding lateralized response, generating a potential conflict with goal-directed choices. We applied a new computational model of conflict processing to two sets of behavioral data from the Simon task to quantify the effects of PD and dopaminergic (DA) medication on action control mechanisms. Compared to healthy controls (HC) matched in age gender and education, patients with PD showed a deficit in goal-directed processing, and the magnitude of this deficit positively correlated with cognitive symptoms. Analyses of the time-course of the location-based automatic activation yielded mixed findings. In both datasets, we found that the peak amplitude of the automatic activation was similar between PD and HC, demonstrating a similar degree of response capture. However, PD patients showed a prolonged automatic activation in only one dataset. This discrepancy was resolved by theoretical analyses of conflict resolution in the Simon task. The reduction of interference generated by the automatic activation appears to be driven by a mixture of passive decay and top-down inhibitory control, the contribution of each component being modulated by task demands. Our results suggest that PD selectively impairs the inhibitory control component, a deficit likely remediated by DA medication. This work advances our understanding of action control deficits in PD, and illustrates the benefit of using computational models to quantitatively measure cognitive processes in clinical populations.
基底神经节功能障碍被认为是帕金森病（PD）患者在动作控制中产生缺陷的原因，但这些缺陷的特征描述一直是定性的，而非定量的。PD 患者在体现目标导向加工与自动反应倾向之间冲突的任务中，通常表现出延长的反应时间。例如，在 Simon 任务中，刺激的无关位置会自动激活相应的侧化反应，从而与目标导向的选择产生潜在冲突。我们应用了一种新的冲突处理计算模型，对 Simon 任务中的两组行为数据进行了分析，以量化 PD 和多巴胺能（DA）药物对动作控制机制的影响。与年龄、性别和教育程度相匹配的健康对照组（HC）相比，PD 患者表现出目标导向加工的缺陷，并且这种缺陷的严重程度与认知症状呈正相关。对基于位置的自动激活的时程分析得出了混合的结果。在两个数据集，我们发现 PD 和 HC 之间的自动激活的峰值幅度相似，表明反应捕获程度相似。然而，PD 患者在仅一个数据集表现出自动激活的延长。通过对 Simon 任务中冲突解决的理论分析，解决了这一差异。自动激活产生的干扰减少似乎是由被动衰减和自上而下的抑制控制混合驱动的，每个成分的贡献受到任务需求的调节。我们的研究结果表明，PD 选择性地损害了抑制控制成分，这一缺陷可能通过 DA 药物得到缓解。这项工作推进了我们对 PD 患者动作控制缺陷的理解，并说明了在临床人群中使用计算模型来定量测量认知过程的益处。
