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： 第一条是确定GAD中所见病理与GSP中所见病理的不同程度。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不同。 具体来说，我们发现，在GSP中看到的杏仁核对恐惧表情的反应增强，在GAD患者中没有看到。 事实上，它们显示出低反应性的迹象。 在过去的一年里，我们以两种重要的方式扩展了这些结果：（a）在同类的第一次发展研究中，我们已经证明，在GAD中看到的对恐惧表情的高度反应在生命早期就存在，并且不受调节面部处理系统发展的神经变化的调节;（B）我们还首次证明，GSP和GAD患者在涉及自上而下注意的系统的募集方面存在共同缺陷。 这种缺陷会导致情绪干扰物的高度处理，因此，据推测，会增加受影响个体发展这些疾病的风险。 第二部分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并不仅仅代表了杏仁核对社会威胁的反应。 相反，似乎还存在非典型的社会信息的自我参照处理。 简而言之，我们早期的工作表明，不仅杏仁核，而且内侧前额叶皮层（MPFC是自我参照处理的关键区域）在GSP中起着重要作用。 今年，我们扩展了这项工作，展示了高度非典型的处理与GSP患者的社会干扰小插曲。 具体而言，虽然健康的参与者在处理社会违规行为（故意在餐桌上吐出不好吃的食物）时表现出MPFC的高度招募，但GSP患者在处理社会事故时表现出该区域的高度招募（窒息时无意中吐出食物）。 重要的是，与社会事故联系最紧密的情绪是尴尬。 GSP患者表现出的一个重要症状是高度的尴尬。 第三部分工作涉及GAD中所见的功能障碍的具体性质。特别是，我们一直在研究是否在GAD的情绪反应，我们观察到在我们的初步工作与这种疾病的患者的一些问题可能会表现在决策任务的困难。根据我们以前的结果，我们进一步证明了GAD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患者中未观察到此类损伤。我们正在进行的工作是跟进这些结果，并使用功能磁共振成像来确定其神经基础。

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.