Emotion Regulation, Executive Function, and Parkinson Disease

描述(由申请者提供)：当前项目的首要目标是增加对帕金森氏症患者情绪过程的了解。帕金森病(Parkinson‘s Disease，PD)是最常见的老年神经退行性疾病之一。它是由递进性多巴胺能耗竭伴随运动、认知和情绪变化引起的。虽然在运动症状方面取得了进展，但情绪和神经精神变化(抑郁、冷漠、焦虑)很普遍，可能是该疾病最令人不安、最致残和最复杂的一些方面。最近四项关于情绪反应的研究发现，没有精神疾病共病的非痴呆性帕金森患者对厌恶的图片表现出迟钝的生理反应，以惊吓为指标。 眨眼反应(Bowers等人，2006；Miller等人，2009；Zahodne等人，2011)或动机注意的事件相关电位成分，LPP(Dietz等人， 2011a)。这种对令人不快的刺激的反应性降低不是由于药物、抑郁、知觉困难或未能产生基本的惊吓或皮层活动。对这种情绪迟钝的一种解释与多巴胺能门控和杏仁核的抑制有关，杏仁核是情绪处理级联中的关键边缘结构。根据这些发现，本研究的目的是了解帕金森患者是否能够上调他们对情绪刺激的反应，以及这样做的成功是否与额叶-执行功能的完整性有关。为了达到这个目的，将采取两种方法来放大情绪反应，一种是更主动和自我定向的(自我唤起)，另一种是更被动的(外部唤起)。这两种方法都与健康对照组中增加的生理反应性有关，以皮层反应为指标(Moser等人，2009,2010；Foti&Hajcak，2008；McNamara等人，2009)。在目前的研究中，非痴呆、非抑郁的帕金森患者和健康对照将参与两项独立的研究。帕金森患者将根据神经认知测量方法被分成两个认知亚组：执行障碍(PD-EXEC)和认知正常(PD)。在测试过程中，参与者将观看标准化的中性和情绪图片集，同时记录惊吓眨眼反应和脑电。一项研究将使用自我导向调节策略来增加对情绪图片的反应性，另一项研究将涉及被动倾听会改变后续语义意义的叙述。主要的因变量将是LPP的幅度、惊吓的眨眼以及对效价和唤醒的言语评级。主要的假设是帕金森病患者对情绪刺激的生理反应的有效调节将取决于额叶执行系统的完整性。认知正常亚组中的帕金森病患者无论采用主动或被动调节方式，情绪反应性都会发生改变，而有执行障碍的帕金森病患者只有在被动状态下才能受益。将研究疾病变量和神经精神因素(冷漠、焦虑)之间的关系。这项拟议的研究将首次测试帕金森患者是否可以从增强他们的生理和情感反应的技术中受益。如果预测得到满足，所获得的发现可能会对帕金森病患者的情绪增强产生广泛的影响。

DESCRIPTION (provided by applicant): The overarching goal of the current project is increased understanding of emotional processes in Parkinson's disease. Parkinson's disease (PD) is one of the most common neurodegenerative disorders of late life. It is caused by progressive dopaminergic depletion with motor, cognitive, and emotional changes. While advances have been made with respect to motor symptoms, emotional and neuropsychiatric changes (depression, apathy, anxiety) are prevalent and can be the some of the most disturbing, disabling, and complex aspects of the disorder. Findings from four recent studies of emotional responding have found that non-demented Parkinson patients without psychiatric co-morbidities exhibited blunted physiologic reactivity to aversive pictures as indexed by the startle eyeblink response (Bowers et al., 2006; Miller et al., 2009; Zahodne et al., 2011) or an event related potential component of motivated attention, the late positive potential, LPP (Dietz et al., 2011a). This reduced reactivity to unpleasant stimuli was not due to medication, depression, perceptual difficulties, or failure to generate basic startle or electrocortical activity. One interpretation of this emotional blunting relates to dopaminergic gating and inhibition of the amygdala, a key limbic structure in the emotion processing cascade. In light of these findings, the aims of the present study are to learn whether Parkinson patients can upregulate their responses to emotional stimuli and whether success in doing so is related to integrity of frontal-executive function. To address this aim, two approaches for amplifying emotional reactivity will be taken, one that is more active and self-directed (auto-evoked) and another that is more passive (exo-evoked). Both approaches have been associated with increased physiologic reactivity in healthy controls, as indexed by electrocortical responses (Moser et al., 2009, 2010; Foti & Hajcak, 2008; McNamara et al., 2009). In the current research, non-demented, non-depressed Parkinson patients and healthy controls will participate in two separate studies. Parkinson patients will be psychometrically classified into two cognitive subgroups based on neurocognitive measures: executively impaired (PD-exec) and cognitively normal (PD). During testing, participants will view standardized sets of neutral and emotional pictures while startle eyeblink responses and EEG are recorded. One study will involve use of self-directed regulation strategies to increase reactivity to emotional pictures, and the other study will involve passive listening to narratives that alter subsequent semantic meaning. Primary dependent variables will be amplitude of LPP, startle eyeblink and verbal ratings of valence and arousal. The major hypothesis is that effective regulation of physiologic reactivity to emotional stimuli by PD patients will depend on the integrity of frontal-executive systems. Parkinson patients in the cognitively normal subgroup will show changes in emotional reactivity regardless of active or more passive regulation approaches, whereas PD patients with executive disturbance will benefit only in the passive condition. Relationship to disease variables and neuropsychiatric factors (apathy, anxiety) will be examined. The proposed research will be the first to test whether Parkinson patients can benefit from techniques for bolstering their physiological and emotional reactivity. If predictions are met, the obtained findings may have broad implications for emotional enhancement in Parkinson disease.