Generalized Anxiety Disorder and Social Anxiety Disorder:

广泛性焦虑症和社交焦虑症：

• 批准号: 8556952
• 负责人: james r blair
• 金额: $ 13.7万
• 依托单位: NATIONAL INSTITUTE OF MENTAL HEALTH
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/8556952
• 关键词: Accidents; Affect; Affective; Alcohol abuse; Amygdaloid structure; Anxiety Disorders; Attention; Choking; Decision Making; Development; Disease; Drug abuse; Emotional; Emotions; Face Processing; Food; Fright; Functional Magnetic Resonance Imaging; Functional disorder; General Population; Generalized Anxiety Disorder; Impairment; Individual; Intervention; Life; Magnetic Resonance; Medial; Mediating; Mental Depression; Nature; Neurobiology; Participant; Pathology; Patients; Prefrontal Cortex; Prevalence; Process; Punishment; Rewards; Risk; Role; Social Phobia; Stimulus; Suggestion; Suicide; Symptoms; System; Systems Development; Time; Work; base; cognitive neuroscience; economic cost; functional disability; high risk; neuromechanism; relating to nervous system; response; showing emotion; social; therapeutic target

There are three important strands to our work with patients with GSP and GAD: The first of these strands is determining the degree to which the pathology seen in GAD differs from that seen in GSP. In previous work, we were the first to demonstrate that patients with GSP and GAD differ in their responsiveness to emotional expression stimuli. Specifically, we showed that the heightened amygdala response to fearful expressions seen in GSP is not seen in patients with GAD. Indeed, they show indications of hypo-responsiveness. Over the past year, we have extended these results in two important ways: (a) In the first developmental study of its kind, we have demonstrated that the heightened response to fearful expressions seen in GAD is present early in life and is not modulated by neural changes in the development of systems mediating face processing; and (b) We have also demonstrated, for the first time, that patients with GSP and GAD share a common deficit in the recruitment of systems involved in top down attention. This deficit results in heightened processing of emotional distracters and thus, presumably, increases the risk of the development of these disorders in affected individuals. The second strand concerns the specific nature of the functional impairment seen in GSP. In previous work, we have shown that GSP does not simply represent a heightened amygdala response to social threats. Instead, there appears additionally to be atypical self referential processing of social information. In short, our earlier work had indicated an important role for not only the amygdala but also medial prefrontal cortex (MPFC a region critical for self referential processing) in GSP. This year, we extended this work by showing highly atypical processing of social interactional vignettes in patients with GSP. Specifically, while healthy participants show heightened recruitment of MPFC when processing social transgressions (intentional spitting out unpalatable food at dinner table), patients with GSP show heightened recruitment of this region when processing social accidents (unintentionally spitting out food when choking). Importantly, the emotion most associated with social accidents is embarrassment. An important symptom shown by patients with GSP is a heightened level of embarrassment. The third strand of work concerns the specific nature of the functional impairment seen in GAD. In particular, we have been examining whether some of the problems in emotional responding in GAD that we observed in our preliminary work with patients with this disorder might manifest in difficulties on decision making tasks. Following on from our previous results, we have further demonstrated that patients with GAD show significant impairment when performing reward/ punishment based decision making tasks. Notably, such impairments were not seen in patients with GSP. Our on-going work is following up these results and using functional magnetic resonance imagingto determine their neural basis.

我们与 GSP 和 GAD 患者的合作分为三个重要部分： 第一条是确定 GAD 中所见病理学与 GSP 中所见病理学的不同程度。在之前的工作中，我们首先证明了 GSP 和 GAD 患者对情绪表达刺激的反应不同。 具体来说，我们发现，在 GSP 中观察到的杏仁核对恐惧表达的反应增强，在 GAD 患者中却没有出现。 事实上，它们表现出反应低下的迹象。 在过去的一年里，我们以两种重要方式扩展了这些结果：(a) 在第一项此类发展研究中，我们证明了广泛性焦虑症中对恐惧表达的强烈反应存在于生命早期，并且不受以下因素的调节：介导面部处理的系统发展中的神经变化； (b) 我们还首次证明，GSP 和 GAD 患者在招募自上而下注意力系统方面存在共同缺陷。 这种缺陷会导致情绪干扰的处理增强，因此可能会增加受影响个体患这些疾病的风险。 第二条涉及 GSP 中所见功能损伤的具体性质。 在之前的工作中，我们已经表明，普惠制不仅仅代表杏仁核对社会威胁的增强反应。 相反，似乎还存在对社会信息的非典型自我参照处理。 简而言之，我们早期的工作表明，在 GSP 中，杏仁核和内侧前额叶皮层（MPFC 是自我参照处理的关键区域）都发挥着重要作用。 今年，我们扩展了这项工作，展示了 GSP 患者社交互动小插曲的高度非典型处理。 具体来说，健康参与者在处理社交越轨行为（在餐桌上故意吐出难吃的食物）时，MPFC 区域的募集量增加，而患有 GSP 的患者在处理社会事故（窒息时无意中吐出食物）时，该区域的募集量增加。 重要的是，与社交事故最相关的情绪是尴尬。 GSP 患者表现出的一个重要症状是高度尴尬。 第三部分工作涉及广泛性焦虑症中所见功能障碍的具体性质。特别是，我们一直在研究我们在对广泛性焦虑症患者的初步研究中观察到的一些情绪反应问题是否可能表现为决策任务的困难。根据我们之前的结果，我们进一步证明，广泛性焦虑症患者在执行基于奖励/惩罚的决策任务时表现出明显的障碍。 值得注意的是，在 GSP 患者中并未发现此类损伤。我们正在进行的工作是跟踪这些结果并使用功能磁共振成像来确定它们的神经基础。