242 Figure 5. The loci of all significant fMRI results represented in a 3D model. Horizontal (A), sagittal (B), and coronal (C) views are displayed. As compared to control, nocebo trials and nocebo-augmented pain were characterized by differential BOLD activations in the vlPFC (light green), ACC (dark green), amygdala (red), and operculum/insula (orange). Discussion This study investigated the role of DCS on the acquisition and extinction of nocebo hyperalgesia in an fMRI study. Significant nocebo effects were induced but DCS did not influence nocebo magnitudes or brain activation, suggesting that the pharmacological manipulation did not influence learning in this nocebo paradigm. Results of the fMRI analyses indicated that in acquisition and extinction phases, there were significantly increased BOLD activations bilaterally in the amygdala, ACC, and insula, during nocebo compared to control trials. Nocebo acquisition trials also showed increased vlPFC activation. Increased opercular activation further differentiated nocebo-augmented pain aggravation from baseline high pain. These results are in line with previous nocebo studies and provide support for the involvement of specific cognitive processes in nocebo hyperalgesia.
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