This study examines the effect of normal aging on temporal summation (TS) of pain and the nociceptive flexion reflex (RIII). Two groups of healthy volunteers, young and elderly, received transcutaneous electrical stimulation applied to the right sural nerve to assess pain and the nociceptive flexion reflex (RIII-reflex). Stimulus intensity was adjusted individually to 120% of RIII-reflex threshold, and shocks were delivered as a single stimulus or as a series of 5 stimuli to assess TS at 5 different frequencies (0.17, 0.33, 0.66, 1, and 2 Hz). This study shows that robust TS of pain and RIII-reflex is observable in individuals aged between 18 and 75 years and indicates that these effects are comparable between young and older individuals. These results contrast with some previous findings and imply that at least some pain regulatory processes, including TS, may not be affected by normal aging, although this may vary depending on the method.

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.

The shared-representation model of empathy suggests that vicarious pain processes rely partly on the activation of brain systems underlying self-pain in the observer. Here, we tested the hypothesis that self-pain may be facilitated by the vicarious priming of neural systems underlying pain perception. Pictures illustrating painful agents applied to the hand or the foot (sensory information), or painful facial expressions (emotional information) were shown to 43 participants to test the effects of vicarious pain on the nociceptive flexion reflex (NFR) of the lower limb and pain intensity and unpleasantness produced by transcutaneous electrical stimulation applied over the sural nerve. Results confirmed the expected priming effects of vicarious pain on spinal and perceptual processes. However, for comparable pain intensity and arousal evoked by the pain pictures, the facilitation of the NFR and the self-pain unpleasantness measurements was more robust in response to pictures depicting pain sensory compared to emotional information. Furthermore, the facilitation of the NFR by pain pictures was positively correlated with the empathy trait of the observer. In contrast, the change in perceived shock-pain intensity was negatively correlated with empathic traits. This dissociation implies that low-level vicarious priming processes underlying pain facilitation may be downregulated at higher pain-processing stages in individuals reporting higher levels of empathy. We speculate that this process contributes to reducing self-other assimilation and is necessary to adopt higher-order empathic responses and altruistic behaviors.

Heterotopic noxious counterstimulation (HNCS) by the application of a sustained noxious stimulus has been shown to inhibit nociceptive processes and decrease pain induced by a competing noxious stimulus. However, it is still not clear how attentional processes contribute to these effects. The main objective of this study was to compare the analgesic effects of HNCS in 2 sessions during which top-down attention was manipulated. Acute shock pain and the nociceptive flexion reflex were evoked by transcutaneous electrical stimulations of the right sural nerve in 4 blocks (15 stimuli/block): baseline, heterotopic innocuous counterstimulation (HICS), HNCS, and recovery. Counterstimulation was applied on the left upper limb with a thermode (HICS) or a cold pack (HNCS). Attention was manipulated between sessions by instructing participants to focus their attention on shock pain or counterstimulation. Shock pain ratings decreased significantly during counterstimulation (P<.001) with stronger effects of HNCS vs HICS in both sessions (P<.01). Furthermore, shock pain inhibition during HNCS relative to baseline was stronger with attention focusing on counterstimulation compared to attention focusing on shocks (P = .015). However, the relative decrease in pain ratings during HNCS vs HICS was not significantly affected by the direction of attention (P = .7). As for spinal nociceptive processes, nociceptive flexion reflex amplitude was significantly decreased during counterstimulation (P<.001) with larger reductions during HNCS compared to HICS (P = .03). However, these effects were not altered by attention (P = .35). Together, these results demonstrate that top-down attention and HNCS produce additive analgesic effects. However, attentional modulation of HNCS analgesia seems to depend on supraspinal processes.

The observation of others' facial expressions of pain has been shown to facilitate the observer's nociceptive responses and to increase pain perception. We investigated how this vicarious facilitation effect is modulated by directing the observer's attention toward the meaning of pain expression or the facial movements. In separate trials, participants were instructed to assess the "intensity of the pain expression"(meaning) or to "discriminate the facial movements" in the upper vs lower part of the face shown in 1-second dynamic clips displaying mild, moderate, or strong pain expressions or a neutral control. In 50% of the trials, participants received a painful electrical stimulation to the sural nerve immediately after the presentation of the expression. Low-level nociceptive reactivity was measured with the RIII-response, and pain perception was assessed using pain ratings. Pain induced by the electrical stimulation increased after viewing stronger pain expressions in both tasks, but the RIII-response showed this vicarious facilitation effect only in the movement discrimination task at the strongest expression intensity. These findings are consistent with the notion that vicarious processes facilitate self-pain and may prime automatic nociceptive responses. However, this priming effect is influenced by top-down attentional processes. These results provide another case of dissociation between reflexive and perceptual processes, consistent with the involvement of partly separate brain networks in the regulation of cortical and lower-level nociceptive responses. Combined with previous results, these findings suggest that vicarious pain facilitation is an automatic process that may be diminished by top-down attentional processes directed at the meaning of the expression.

The voluntary control of respiration is used as a common means to regulate pain and emotions and is fundamental to various relaxation and meditation techniques. The aim of the present study was to examine how breathing frequency and phase affect pain perception, spinal nociceptive activity (RIII-reflex) and brain activity (scalp somatosensory-evoked potentials - SEP's). In 20 healthy volunteers, painful electric shocks individually adjusted to 120% of the RIII-reflex threshold were delivered to the sural nerve near the end of inspiration or expiration phases, during three cued-breathing conditions: (1) slow breathing (0.1 Hz) with slow (4s) inspiration (0.1Hz-SlowIns), (2) slow breathing (0.1 Hz) with fast (2s) inspiration (0.1 Hz-FastIns), and (3) normal breathing (0.2 Hz) with fast (2s) inspiration (0.2 Hz). Pain ratings were not affected by breathing patterns (p=0.3), but were significantly lower during inspiration compared with expiration (p=0.02). This phase effect was also observed on the N100 component of SEP's, but only in the 0.1-Hz-FastIns condition (p=0.03). In contrast, RIII-reflex amplitude was greater during inspiration compared with expiration (p=0.02). It was also decreased in the 0.1-Hz-SlowIns compared with the 0.2-Hz condition (p=0.01). Slow breathing also increased the amplitude of respiratory sinus arrhythmia (RSA), although these changes were not significantly associated with changes in pain responses. In conclusion, this study shows that pain and pain-related brain activity may be reduced during inspiration but these changes are dissociated from spinal nociceptive transmission. The small amplitude of these effects suggests that factors other than respiration contribute to the analgesic effects of relaxation and meditation techniques.