CINAC-Hospital Universitario HM Puerta del Sur, Móstoles, Universidad CEU San Pablo, Madrid, Spain.
Movement Disorders Unit, CHU Grenoble Alpes, Grenoble, France.
Hum Brain Mapp. 2018 Dec;39(12):5014-5027. doi: 10.1002/hbm.24341. Epub 2018 Sep 26.
Parkinson's disease impairs the decoding of emotional stimuli reflecting alterations of the limbic cortico-subcortical network. The objective of this study was to assess and compare the behavioral and electrophysiological effects of both levodopa and subthalamic stimulation on emotional processing in Parkinson's disease. Operated patients (n =16) and matched healthy subjects performed an emotional Stroop task, in which the emotion expressed by a face must be recognized while ignoring an emotional distractive word and that includes a neutral control sub-task. Patients were tested in the four possible treatment conditions (off stim/off med; on stim/off med; off stim/on med; and on stim/on med). High-resolution electroencephalography was recorded while performing the task. Patients made significantly more mistakes in facial emotion recognition than healthy subjects (p < .005). Untreated patients performed worse in the emotional trials than in the control sub-task (p < .05). Fearful faces induced significantly slower reaction times than happy faces in patients (p = .0002), but not in the healthy subjects. The emotional Stroop effect with levodopa was significantly higher than with subthalamic stimulation when fearful faces were assessed (p = .0243). Conversely, treatments did not modulate the Stroop effect of the control sub-task. EEG demonstrated that, compared with the untreated state, levodopa but not subthalamic stimulation significantly increases the amplitude of the event-related potential N170 (p = .002 vs. p = .1, respectively), an electrophysiological biomarker of early aspects of facial processing. The activity of the N170 cortical sources within the right fusiform gyrus was increased by levodopa (p < .05) but not by stimulation. While levodopa normalizes the recognition of emotional facial expression and early EEG markers of emotional processing, subthalamic stimulation does not. Thus, operated patients require dopaminergic medication in addition to stimulation to treat emotional symptoms of Parkinson's disease.
帕金森病损害了情绪刺激的解码，反映了边缘皮质下网络的改变。本研究的目的是评估和比较左旋多巴和丘脑下刺激对帕金森病患者情绪处理的行为和电生理影响。手术患者（n=16）和匹配的健康受试者进行了情绪斯特鲁普任务，在该任务中，必须在忽略情绪干扰词的同时识别出面部所表达的情绪，并且包括一个中性控制子任务。患者在四种可能的治疗条件下（关刺激/关药物；开刺激/关药物；关刺激/开药物；开刺激/开药物）进行测试。在执行任务时记录高分辨率脑电图。患者对面部情绪识别的错误明显多于健康受试者（p<0.005）。未经治疗的患者在情绪试验中的表现比在控制子任务中差（p<0.05）。与健康受试者相比，恐惧面孔会导致患者的反应时间明显变慢（p=0.0002）。情绪斯特鲁普效应，当评估恐惧面孔时，左旋多巴的效果明显高于丘脑下刺激（p=0.0243）。相反，治疗方法并没有调节控制子任务的斯特鲁普效应。脑电图显示，与未治疗状态相比，左旋多巴而非丘脑下刺激显著增加了事件相关电位 N170 的振幅（p=0.002 与 p=0.1，分别），这是面部处理早期方面的电生理生物标志物。右侧梭状回的 N170 皮质源的活动因左旋多巴而增加（p<0.05），但因刺激而不增加。虽然左旋多巴可以使情绪面部表情的识别和情绪处理的早期脑电图标志物正常化，但丘脑下刺激却不能。因此，手术患者除了刺激外还需要多巴胺药物来治疗帕金森病的情绪症状。
