Patients with irritable bowel syndrome (IBS) are affected by chronic abdominal pain and show decreased pain inhibition. Moreover, they exhibit differences in brain morphology compared with healthy volunteers. The aim of this study was to examine whether decreased pain inhibition is associated with altered brain morphology in IBS patients. Structural magnetic resonance imaging scans were acquired in 14 female patients with diarrhea-predominant IBS and 14 controls. Pain and anxiety modulation were characterized using electrical stimulation of the sural nerve and heterotopic noxious counterstimulation. IBS patients reported decreased pain inhibition (P = .02) as well as increased shock anxiety, pain catastrophizing, depressive symptoms, and trait anxiety (P's ≤ .05). IBS patients also showed a thicker right posterior insula (pINS), associated with longer IBS duration (r = .67, P = .02). In addition, thicker right lateral orbitofrontal cortex was strongly associated with less pain inhibition in both IBS patients (r = .70, P = .02) and controls (r = .68, P = .01). Results are consistent with the role of the insula in interoception and pain and suggest that IBS may induce thickening of the pINS. Reduced pain inhibition may further involve a modification of the regulatory influence of the orbitofrontal cortex on pain-related processes.

Vicarious pain has been shown to enhance observers' nociceptive reactivity and pain perception. We exposed healthy participants to specific parts of facial pain expressions in order to investigate which components are required to induce this modulation. We created 2 classes of stimuli: one containing the most useful information for identification of pain expressions (diagnostic) and one containing the least useful information (antidiagnostic). Twenty-eight normal volunteers received electrical stimulation of the sural nerve immediately after they viewed these stimuli. Subjective ratings (intensity and unpleasantness) as well as the nociceptive flexion reflex (NFR) evoked by the shock were recorded. Results show that diagnostic stimuli lead to higher subjective ratings of shock pain than the antidiagnostic stimuli, but the stimuli classes had no significant impact on the NFR. A control experiment showed that our facial stimuli were given very low valence and arousal ratings compared to stimuli previously used to demonstrate the effect of emotional pictures on pain. Thus, the results are unlikely to be explained by emotions felt by the observer and suggest a vicarious facilitation of supraspinal pain processing induced by key features underlying pain expressions recognition. Results provide further support to the perception-action model of empathy.

The present study examined the contribution of expectations to analgesia induced by heterotopic noxious counter-stimulation (HNCS) in healthy volunteers assigned to a control group or 1 of 3 experimental groups in which expectations were either assessed (a priori expectations) or manipulated using suggestions (hyperalgesia and analgesia). Acute shock-pain, the nociceptive flexion reflex (RIII-reflex), and shock-related anxiety were measured in response to electrical stimulations of the right sural nerve in the baseline, HNCS, and recovery periods. Counter-stimulation was applied on the contralateral forearm using a flexible cold pack. A priori expectations were strongly associated with the actual magnitude of the analgesia induced by HNCS. In comparison to the control condition, suggestions of hyperalgesia led to an increase in RIII-reflex amplitude and shock-pain, while suggestions of analgesia resulted in a greater decrease in RIII-reflex amplitude, which confirms that the analgesic process normally activated by HNCS can be blocked or enhanced by the verbal induction of expectations through suggestions. Changes in shock-anxiety induced by these suggestions were correlated to changes in shock-pain and RIII-reflex, but these changes did not emerge as a mediator of the association between manipulated expectations and HNCS analgesia. Overall, the results demonstrate that HNCS analgesia is modulated by expectations, either from a priori beliefs or suggestions, and this appears to be independent of anxiety processes.