86 of the conditioned faces were accompanied by moderate pain stimulations. Both conscious and nonconscious exposure to the conditioned cues led to significant nocebo responses. Nocebo hyperalgesia, irrespective of exposure type, revealed increased activation in several regions involved in nociceptive processing, such as the ACC, insula, thalamus, and brainstem. As compared to conscious nocebo, nonconscious nocebo led to increased activation of the thalamus, amygdala, and hippocampus. Involvement of these subcortical structures may reflect processing and encoding of a perceived threat 67, given the aversive nature of pain. In a recent study, Egorova and collogues (2020), aimed to investigate the effects of administering an inert cream while providing neutral information regarding its effects on pain. This neutral condition was compared to a nocebo, in which negative suggestions were provided about the effects of a second cream. A conditioning paradigm was used in which increased pain was administered in the nocebo as compared to the neutral skin patches. The evocation phase took place inside the MRI scanner. While this study focused on how participants responded to pain following the administration of the neutral cream, connectivity analyses were conducted for the nocebo condition as well. These results showed increased connectivity between the left amygdala and the striatum and this increase was correlated with the magnitude of nocebo responses. With a particular focus on the amygdala, this study highlighted an involvement of the amygdala in modulating or reflecting the magnitude of nocebo responses. Taken together, fMRI studies that explored brain correlates of nocebo effects on somatic pain have provided some consistent findings. As expected, sensory-discriminative and descending processing has been implicated in the presentation of nocebo hyperalgesic responses, with brain areas such as the ACC, operculum, PAG, and the PFC being consistently involved in nocebo hyperalgesia 8,9,62. Studies consistently
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