88 the first session, indicating nocebo sensitization. When only nocebo responders (n=14) were contrasted to the control group, greater activations were found in the amygdala and secondary somatosensory cortex during pain anticipation. During the pain inductions, nocebo responders demonstrated significantly enhanced hyperactivation of the amygdala, thalamus, and insula. As a function of negative expectations, the insular cortex showed increased connectivity with the midcingulate cortex (MCC) extending to the posterior cingulate cortex (PCC) during pain stimulations. Schmid and colleagues stated that their findings highlighted an involvement of the MCC in visceral nocebo effects. In sum, visceral and somatic experimental models of nocebo hyperalgesia show a consistent involvement of cognitive-affective brain regions such as the hippocampus and amygdala. A consistent finding that seems to be prominent in visceral pain studies but also in somatic pain studies although somewhat less consistently, is the involvement of the insula in nocebo hyperalgesia. The insula is thought to be crucial for neural functions such as sensory integration and pain-related decision making 69–72. The insula may thus constitute a primary brain region for the cognitive modulation of visceral and somatic pain 73. Visceral pain studies have also found a role of the MCC in nocebo hyperalgesia, which was not observed in somatic pain studies. The MCC has been implicated in pain-related processes, including cognitive modulation and fear responses related to pain 74, central sensitization to visceral pain and pain modulation in patients with chronic abdominal pain 75–79. These findings suggest that nocebo effects on visceral pain show similarities to other types of pain. At the same time, these studies highlight a distinct implication of structures such as the MCC in visceral pain. Spinal imaging
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