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 the first study of its kind, we presented patients with GSP, patients with GAD, patients with both GSP and GAD and no pathology individuals with angry, fearful, and neutral facial expression stimuli. We demonstrated clear differences in the pathology of GAD and GSP. Patients with GSP showed significantly increased activation to fearful relative to neutral expressions in several regions, including the amygdala. In contrast, patients with GAD showed significantly reduced activation to fearful relative to neutral faces compared to healthy individuals and patients with GSP but this was coupled with anomalously and significantly increased responses in a lateral region of prefrontal cortex. Patients with comorbid GAD/GSP appeared to present with the pathology associated with the GAD, but not the GSP. Our on-going work has continued to follow this approach. Specifically, we have been examining differences in automatic and controlled emotional regulation across these patient groups. The second strand concerns the specific nature of the functional impairment seen in GSP. Patients with GSP show increased amygdala responses to socially threatening stimuli such as fearful and angry expressions. We followed this work up by examining the neural responses to receipt of praise or criticism in GSP. Participants were presented with positive, negative, and neutral statements (e.g., You are beautiful/ ugly/ human) that could be either about highly relevant and about themselves or less relevant about somebody else (e.g., He is beautiful). The results of this study indicated an important role for not only the amygdala but also medial prefrontal cortex (MPFC) in GSP. MPFC plays an important role in self-referential processing and it now appears that GSP reflects a particular sensitivity to self-referential information. Our on-going work has followed up on these results. In particular, we have been examining the specific nature of this sensitivity to self-referential information in patients with GSP. The third strand of work concerns the specific nature of the functional impairment seen in GAD. It was this third strand that has been the specific focus for the past 12 months. In particular, we wished to examine 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. Using several decision making paradigms where successful performance is based on the appropriate representation of reward and punishment expectances, we observed significant impairment in patients with GAD (Devido et al., 2009). Notably, such impairments were not seen in patients with GSP. Our on-going work is following up these results and using functional magnetic resonance imaging to determine their neural basis.
