Department of Anatomy & Neurosciences, VU University Medical Center (VUmc), Amsterdam, The Netherlands; Neuroscience Campus Amsterdam (NCA), Amsterdam, The Netherlands.
Department of Anatomy & Neurosciences, VU University Medical Center (VUmc), Amsterdam, The Netherlands; Netherlands Institute for Neuroscience, an Institute of the Royal Netherlands Academy of Arts and Sciences, Amsterdam, The Netherlands; Neuroscience Campus Amsterdam (NCA), Amsterdam, The Netherlands.
Neuropsychologia. 2015 Feb;68:107-16. doi: 10.1016/j.neuropsychologia.2014.12.022. Epub 2015 Jan 7.
Patients with Parkinson's disease (PD) often suffer from impairments in executive functions, such as mental rigidity, which can be measured as impaired set-shifting. Previous studies have shown that set-shifting deficits in patients with PD result from hypo-excitation of the caudate nucleus and lateral prefrontal cortices. The results of these studies may have been influenced by the inclusion of patients on dopaminergic medication, and by choosing set-shifting paradigms in which performance also depends on other cognitive mechanisms, such as matching-to-sample. To circumvent these potential confounding factors, we tested patients with PD that were not on dopamine replacement therapy, and we developed a new feedback-based paradigm to measure the cognitive construct set-shifting more accurately. In this case-control study, 18 patients with PD and 35 well-matched healthy controls performed the set-shifting task, while task-related neural activation was recorded using functional magnetic resonance imaging. Behaviourally, PD patients, compared with healthy controls, made more errors during repeat trials, but not set-shift trials. The patients, compared with controls, showed increased task-related activation of the bilateral inferior parietal cortex, and the right superior frontal gyrus, and decreased activation of the right ventrolateral prefrontal cortex during set-shift trials. Our findings suggest that, despite decreased task-related activation of the right ventrolateral prefrontal cortex, these early-stage unmedicated patients with PD do not yet suffer from set-shifting deficits due to compensatory hyperactivation in the inferior parietal cortex and the superior frontal gyrus.
帕金森病（PD）患者常存在执行功能障碍，如思维僵化，可表现为转换能力受损。既往研究显示 PD 患者的转换能力缺陷源于尾状核和外侧前额叶皮质的兴奋性降低。但这些研究结果可能受到纳入正在接受多巴胺能药物治疗的患者以及选择依赖其他认知机制（如样本匹配）的转换范式的影响。为了避免这些潜在的混杂因素，我们测试了未接受多巴胺替代治疗的 PD 患者，并开发了一种新的基于反馈的范式，以更准确地测量认知结构转换。在这项病例对照研究中，18 名 PD 患者和 35 名匹配良好的健康对照组进行了转换任务，同时使用功能磁共振成像记录任务相关的神经激活。行为上，与健康对照组相比，PD 患者在重复试验中犯了更多的错误，但在转换试验中没有。与对照组相比，患者在进行转换试验时双侧顶下小叶和右侧额上回的任务相关激活增加，右侧腹外侧前额叶皮质的激活减少。我们的发现表明，尽管右侧腹外侧前额叶皮质的任务相关激活减少，但这些未经药物治疗的早期 PD 患者尚未因顶下小叶和额上回的代偿性过度激活而出现转换缺陷。
