Next, we examined the contrast of postcongruent in¬congruent trials minus postincongruent incongruent tri¬als in the dorsomedial prefrontal cortex and amygdala in both groups and found a significant cluster in the dor¬somedial prefrontal cortex (x=-1, y=36, z=38; z=3.26; 568 mm3; d=1.15; see Figure 3C) but not in the amygdala. Ex¬traction of average signal within this cluster revealed that the group difference was driven by the expected greater activity in postcongruent incongruent trials in healthy comparison subjects (t=2.36, df=23, p<0.05; d=0.48) and by the opposite effect in patients (t=2.66, df=16, p<0.05; d=0.64; see Figure 3D). Note that the inability of patients to decrease dorsomedial prefrontal activity in postincon¬gruent incongruent trials paralleled patients’ inability to improve reaction times during these trials compared to healthy comparison subjects. No group differences were observed in any of the regions of interest for the contrast of postcongruent congruent trials with postincongruent congruent trials. Finally, comparing across all trial types, we found significantly greater activation in patients than in comparison subjects in the left amygdala (x=-22, y=-2, z=-18; z=3.04; 232 mm3; d=1.04). Using cytoarchitectonic probability maps of the basolateral, centromedial, and su¬perficial amygdalar subregions (47, 48), we found that 78% of this cluster corresponded to the superficial amygdala and 21.1% to the basolateral amygdala.
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