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Psychotherapy in Social Anxiety Disorder and alterations in neural processing (PANDA)

Psychotherapy in Social Anxiety Disorder and alterations in neural processing (PANDA)
社交焦虑症的心理治疗和神经处理的改变(PANDA)
批准号:
426604649
负责人:
Professor Dr. Stephan Heinzel
金额:
$0.0万
依托单位国家:
德国
项目类别:
Research Grants
财政年份:
2019
资助国家:
德国
项目状态:
已结题
起止时间:
2018-12-31 至 2023-12-31

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中文摘要
翻译
社交焦虑症(SAD)的特征是对因尴尬或羞辱行为而产生的负面社会评价产生强烈的恐惧。如果没有适当的治疗,SAD的病程通常是慢性的,并导致生活质量的显著下降。消极的自我信念对SAD症状的发展和维持起着关键作用。在神经生物学水平上,SAD与突显网络的高反应性和执行控制网络的失调有关。虽然认知行为疗法(CBT)的效果已经通过几个Meta分析进行了评估,但关于CBT的心理和神经生物学机制的研究仍然很少。在这项拟议的研究中,CBT的心理变化模型将在80名SAD患者中进行测试,并与神经生物学机制相关。具体地说,我们将通过功能磁共振成像的方法,在行为和神经水平上研究CBT相关的负面自我信念和对社会评价的恐惧的变化。第一次,负面自我信念的范式将与CBT前后社会评价情境中的执行功能范式相结合进行测试。因此,我们将能够第一次通过动态因果模型来测试CBT引起的有效(方向性)额叶到边缘连接(自上而下和自下而上的调制)的变化的假设。此外,我们将研究是否可以通过杏仁核到前扣带回皮质的异常高连接来预测CBT无反应。对CBT神经生物学机制的深入了解和对CBT结局的预测可能解释CBT无反应的潜在原因机制,并有助于开发更有效和个性化的SAD治疗策略。
英文摘要
Social Anxiety Disorder (SAD) is characterized by an intense fear of negative social evaluation due to embarrassing or humiliating behavior. Without adequate treatment, the course of SAD is often chronic and leads to a significant reduction in quality of life. Negative self-beliefs play a key role for the development and maintenance of SAD symptoms. On a neurobiological level, SAD is associated with a hyperreactivity of the salience network and a dysregulation of the executive control network. While effects of a cognitive behavioral therapy (CBT) have been evaluated by several meta-analyses, research on psychological and neurobiological mechanisms of CBT is still sparse. In the proposed study, a psychological change model of CBT will be tested in 80 patients with SAD and associated with neurobiological mechanisms. Specifically, we will investigate CBT-associated changes in negative self-beliefs and fear of social evaluation on a behavioral and neural level by means of functional Magnetic Resonance Imaging. For the first time, a paradigm on negative self-beliefs will be tested in combination with a paradigm on executive functions in a social-evaluative situation before and after CBT. Thus, we will be able to test assumptions on CBT-induced changes in effective (directional) fronto-limbic connectivity (top-down and bottom-up modulations) by means of Dynamic Causal Modelling for the first time. Furthermore, we will investigate if CBT-non-response can be predicted by abnormally high connectivity from Amygdala to Anterior Cingulate Cortex. An improved understanding of neurobiological mechanisms of CBT and the prediction of CBT outcome may explain underlying causal mechanisms for CBT-non-response and may contribute to the development of more effective and individualized treatment strategies for SAD.
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