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精神疾病患者快感缺失与动机缺乏的跨诊断研究
Alternative TitleA Transdiagnostic Studv of Anhedonia and Amotivation in Patients with Mental Disorders
王艳郁
Subtype博士
Thesis Advisor陈楚侨
2019-05
Degree Grantor中国科学院大学
Place of Conferral中国科学院心理研究所
Degree Name理学硕士
Degree Discipline认知神经科学
Keyword精神分裂症 抑郁症 双相障碍 快感缺失 动机缺乏
Abstract

快感缺失和动机缺乏普遍存在于精神分裂症(SCZ)、抑郁症(MDD)及双相障碍(BD)患者中,对其行为和神经机制的探索将会对患者个体化治疗方案的制定及社会功能的康复起着至关重要的作用。研究表明,精神疾病患者快感缺失的实质可能并不单纯是对愉快刺激的反应下降或者对奖赏寻求的动机减弱这两个成分中某一个成分的缺陷,而是从愉快体验转化到动机行为这一过程的失败。以往的研究通常局限于某一疾病群体,采用单一的测评方法在快感缺失的某一成分上进行探讨,从而使得研究结论不一。函需采用相同的行为测评工具,对这一情绪一行为的分离过程及其神经机制开展跨诊断对比研究,从而揭示不同精神疾病患者快感缺失共同的病理机制及各自的独特性。本论文通过两个研究,系统使用自我报告、临床评估、行为学实验以及基于任务的脑成像方法,对SCZ,MDD以及BD患者快感缺失和动机缺乏的临床表现、行为及神经机制进行了跨诊断的对比。

在研究一中,我们采用一系列快感缺失自评量表、临床评估工具以及期待性与即时性愉快体验计算机任务(ACP)对41名SCZ患者,44名MDD患者,43名BD患者以及43名健康被试的快感缺失和动机缺乏及情绪一行为分离模式进行了对比。结果发现,SCZ, MDD和BD患者均在自我报告中表现出一定程度的快感缺失和动机缺乏。在ACP任务中,SCZ患者无论是在愉悦寻求还是在厌恶回避过程中,图片引起的动机行为都更少。MDD和BD患者在负性图片下的情绪一行为分离既表现在表征反应阶段也表现在唤起反应阶段,而在正性图片下的情绪一行为分离仅表现在唤起反应阶段。本研究揭示了SCZ, MDD和BD患者快感缺失与动机缺乏在行为加工过程上的缺损均表现为情绪一行为的分离,但模式有所不同。

在研究二中,我们进一步采用基于努力的奖赏任务(EEfRT)进行脑成像实验,对研究一中的20名SCZ患者、23名MDD患者、17名BD患者及30名健康被试的快感缺失与动机缺乏的神经机制进行了对比。结果发现,SCZ, MDD以及BD患者在EEfRT任务下共同激活了奖赏加工相关的脑区,如后扣带回、额内侧回、额中回、楔前叶等。在这些脑区的激活和功能连接的改变上既有相似又有所不同。scz患者主要表现为右侧尾状核体部、楔前叶、后扣带回等脑区激活的减弱以及尾状核与杏仁核、海马等脑区功能连接的增强。从而提示了SCZ患者在高奖赏高概率任务下的动机缺损可能主要来自于同时并存的对无关刺激的注意过度分配以及皮层价值表征或付出一收益计算相关脑区功能的减弱。对于MDD患者来说,尾状核与扣带回、中央后回、顶下小叶等脑区的功能连接随着奖赏金额的增加而减弱;而右侧颗上回的活动却随着奖赏金额的增加而增加。从而暗示了MDD患者可能通过提升与冲突控制有关的皮层区域的高反应性代偿性地弥补了中脑多巴胺通路的低反应性,进而在付出一收益计算中维持了和健康被试相似的任务成绩。BD患者在高奖赏高概率条件下的动机缺损则主要与其不稳定的奖赏敏感性有关,主要体现为增强的左侧楔前叶的脑活动以及减弱的背外侧前额叶的脑活动。

综上所述,我们的研究发现了SCZ, MDD以及BD患者均存在着一定程度的快感缺失和动机缺乏。这一症状在行为上的共性特征体现在SCZ, MDD以及BD患者均存在着不同程度的情绪一行为的分离。但三类患者情绪一行为分离的模式有所不同。在神经机制上,SCZ, MDD以及BD患者在基于努力的奖赏加工过程中有共同的脑区的激活,但在这些脑区的激活模式和功能连接的改变上又具有各自的独特性。该研究对于精神疾病患者快感缺失和动机缺乏的心理病理机制提供了生物学标记上的证据,同时也为三类患者的临床精准治疗和康复提供了更具针对性的治疗靶点,从而有着潜在的临床推广意义和价值。

Other Abstract

Anhedonia and amotivation are common symptoms in patients with schizophrenia (SCZ), major depressive disorer (MDD) and bipolar disorder (BD), suggesting a necessity to explore the underlying behavioural and neural mechnisms to facilitate the development of effective therapeutic programmes and social function rehabilitation. Accumulating evidences indicated that the nature of anhedonia may not only due to deficits in pleasure experience or reward pursuit motivation, but may also be related to failure in translating emotional salience into effortful behaviour. Results from previous studies on anhedonia have been inconsistent because most only recruited participants from one diagnostic group and comparing them with healthy controls. Investigating the underlying mechanisms of emotion-behaviour decoupling using a transdiagnostic sample and the same measurements could reveal the common and unique features of anhedonia among different disorders and facilitate the development of novel interventions. Using this approach, we compared the phenomenological, behavioural and neural features of anhedonia/amotivation in patients with SCZ, MDD and BD in two studies, using self-reported questionnaires, clinical assessment instruments, behavioural tasks and functional brain imaging.

Study 1 aimed to compare the patterns of emotion-behaviour decoupling among patients with SCZ, MDD and BD. In this study, 42 patients with SCZ, 44 patients with MDD, 43 patients with BD and 43 healthy controls were recruited. A computerized `Anticipatory and Consummatory Pleasure' (ACP) task and a set of checklists were used to evaluate different facets of anhedonia. We found that participants with SCZ,MDD and BD exhibited a certain degree of physical and social anhedonia, as well as emotion-behaviour decoupfing. In SCZ participants, both desirable and undesirable images elicited lower correspondence between self-report liking and behaviour in both representational responding and evoked responding. In individuals with MDD and BD deficits in emotion-behaviour coupling under undesirable conditions were observed in both representational and evoked responding, while deficits in emotion-behaviour coupling under desirable conditions were only observed in evoked responding. Our results suggest that emotion-behaviour decoupling may be the common behavioural mechanism of anhedonia/amotivation in patients with SCZ, MDD and BD, with different diagnostic groups exhibiting different patterns of decoupling.

Study 2 aimed to investigate the neural mechanisms of anhedonia and amotivation in patients with SCZ, MDD and BD using task-based functional brain imaging. In this study, 20 patients with SCZ, 23 patients with MDD, 17 patients with BD and 30 healthy controls were scanned while performing the Effort Expenditure for Reward Task (EEfRT). We found that brain regions related to reward processing, such as the posterior cingulate gyrus, the medial frontal gyrus and the precuneus, were activated when participants with SCZ, MDD, BD and healthy participants were performing the EEfRT. However, participants with different disorders exhibited unique activation patterns and changes of functional connections in these brain regions. In SCZ participants, we observed reduced activation at the right caudate body, the precuneus and the posterior cingulate gyrus and enhanced functional connectivity between the caudate and the amygdala and the hippocampus, suggesting that motivational deficits observed in SCZ participants under higher reward and higher probability conditions may be due to excessive allocation of efforts to irrelevant stimuli and a decreased ativation of the cortex related to value representation or effort-benefit computation. In MDD participants, we observed decreased functional connectivity between the caudate and the cingulate, the postcentral gyrus and the inferior parietal lobule when the magnitude of reward increased. We also observed increased activation at the right superior temporal gyrus with an increase in reward magnitude. Our results suggest that the similar task performance during cost-benefit computation of MDD participants with healthy controls may be related to increased responsivity of cortical regions related to conflict control, which compensated the lowered responsivity of midbrain dopamine pathway. The unique mechanism of the motivational deficits under higher reward magnitude and higher reward probability in BD patients was speculated to be related to the unstable sensitivity to rewards, manifesting as increased activation of the left precuneus and reduced activation at the dorsolateral prefrontal cortex.

Taken together, participants with SCZ, MDD and BD all exhibited a certain degree of anhedonia and amotivation. The common behavioural mechanism of anhedonia /amotivation in SCZ, MDD and BD is emotion-behaviour decoupling, but the pattern of decoupling is different among these diagnostic groups. In terms of neural correlates, common brain regions appears to be consistently activated during the EEfRT in patients with SCZ, MDD and BD, with each diagnostic group exhibiting unique patterns. In this study, we have identified potential biomarkers of anhedonia/amotivation, which may be potential therapeutic targets for the development of novel interventions.

Pages112
Language中文
Document Type学位论文
Identifierhttp://ir.psych.ac.cn/handle/311026/29319
Collection健康与遗传心理学研究室
Recommended Citation
GB/T 7714
王艳郁. 精神疾病患者快感缺失与动机缺乏的跨诊断研究[D]. 中国科学院心理研究所. 中国科学院大学,2019.
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