Generalized Anxiety Disorder and Social Anxiety Disorder:

我们对GSP和GAD患者的工作有三个重要方面： 这些线索中的第一条是确定在GAD中看到的病理与在GSP中看到的不同程度。在之前的工作中，我们首次证明了GSP和GAD患者对情绪表达刺激的反应不同。具体地说，我们发现在GAD患者中没有看到GSP对恐惧表达的杏仁核反应增强。事实上，它们显示出反应迟钝的迹象。在过去的一年里，我们在两个重要方面推广了这些结果：(A)在第一个此类发育研究中，我们证明了GAD患者对恐惧表情的高反应存在于生命早期，并且不受调节面孔加工的系统发育的神经变化的调节；(B)我们还首次证明，GSP和GAD患者在招募参与自上而下注意的系统方面存在共同的缺陷。这种缺陷导致对情绪干扰的高度处理，因此可能增加了受影响个体发生这些疾病的风险。 第二条线索涉及普惠制中所见的功能损害的具体性质。在以前的工作中，我们已经表明，GSP不仅仅代表杏仁核对社会威胁的高度反应。相反，似乎还有一种非典型的社会信息自我参照加工。简而言之，我们早期的工作表明，不仅杏仁核，而且内侧前额叶皮质(MPFC，自我参照加工的关键区域)在GSP中起着重要作用。今年，我们扩展了这项工作，展示了GSP患者社交互动片段的高度非典型加工。具体地说，健康受试者在处理社会违法行为(故意在餐桌上吐出难吃的食物)时表现出对MPFC的高度招募，而GSP患者在处理社会事故(在窒息时无意地吐出食物)时表现出对这一区域的高度招募。重要的是，与社交意外联系最密切的情绪是尴尬。GSP患者表现出的一个重要症状是高度的尴尬。 第三项工作涉及GAD中所见的功能障碍的具体性质。特别是，我们一直在研究我们在对患有这种疾病的患者的初步工作中观察到的GAD在情绪反应方面的一些问题是否可能表现为决策任务中的困难。根据我们之前的结果，我们进一步证明了广泛性焦虑症患者在执行基于奖惩的决策任务时表现出显著的损害。值得注意的是，这种损害在GSP患者中未见。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。

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.