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患者的工作有三个重要的链接： 这些链中的第一个是确定GAD中看到的病理与GSP中看到的病理的程度。在以前的工作中，我们是第一个证明GSP和GAD患者对情绪表达刺激的反应性不同的人。 具体而言，我们表明，在GAD患者中未见杏仁核对GSP中可怕表达的反应增强。 确实，它们显示出表现不佳的迹象。 在过去的一年中，我们以两种重要的方式扩展了这些结果：（a）在同类产品的首次发展研究中，我们证明，对GAD中看到的恐惧表达的反应增强存在于生命的早期，并且不受介导面部处理的系统发展的神经变化的调节； （b）我们还首次证明了患有GSP和GAD的患者在募集中自上而下的系统方面存在共同的赤字。 这种赤字导致情绪干扰者的处理加剧，因此，大概会增加受影响个体中这些疾病的风险。 第二链涉及在GSP中看到的功能障碍的特定性质。 在以前的工作中，我们已经表明，GSP不仅代表了对社会威胁的杏仁核的增强反应。 取而代之的是，似乎还有非典型的社会信息自我参考处理。 简而言之，我们较早的工作表明，不仅是杏仁核，而且对GSP中的内侧前额叶皮层（MPFC一个至关重要的区域）的重要作用。 今年，我们通过在GSP患者中显示出高度非典型的社交互动式小插曲来扩展这项工作。 具体而言，尽管健康的参与者在处理社交违法行为时表现出MPFC的招募增强（故意在餐桌上吐出不可避免的食物），但GSP患者在处理社交事故时显示了该地区的招募增强（无意中吐出食物时，cho住食物）。 重要的是，与社会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尴尬水平提高。 第三组工作涉及GAD中看到的功能障碍的特定性质。特别是，我们一直在研究我们在与这种疾病患者的初步工作中观察到的情感反应中的一些问题可能在决策任务上遇到困难。从以前的结果开始，我们进一步证明，在执行基于奖励/惩罚的决策任务时，患有GAD的患者显示出严重的损害。 值得注意的是，在GSP患者中未见这种障碍。我们正在进行的工作正在跟踪这些结果，并使用功能磁共振成像来确定其神经基础。