Pain
-
Comparative Study
The effects of prior pain experience on neural correlates of empathy for pain: An fMRI study.
Neuroimaging studies have revealed partially shared neural substrates for both the actual experience of pain and empathy elicited by the pain of others. We examined whether prior pain exposure increased neural activity in the anterior midcingulate cortex (aMCC) and bilateral anterior insula (AI) as a correlate of empathy for pain. Participants (N=64: 32 women, 32 men) viewed pictures displaying exposure to pressure pain (pain pictures) and pictures without any cue of pain (neutral pictures). ⋯ Based on the entire sample, whole brain analyses revealed stronger activation in the retrosplenial cortex, dorsomedial prefrontal cortex, and medial prefrontal cortex in the pain exposure condition. In conclusion, prior pain exposure did not increase, but decreased activity in regions regularly associated with empathy for pain. However, pain experience increased activity in regions associated with memory retrieval, perspective taking, and top-down emotion regulation, which might facilitate empathizing with others.
-
Fatty acid ethanolamides (FAEs), which include palmitoylethanolamide (PEA) and oleoylethanolamide (OEA), are endogenous agonists of peroxisome proliferator-activated receptor-α (PPAR-α) and important regulators of the inflammatory response. They are degraded in macrophages by the lysosomal cysteine amidase, N-acylethanolamine acid amidase (NAAA). Previous studies have shown that pharmacological inhibition of NAAA activity suppresses macrophage activation in vitro and causes marked anti-inflammatory effects in vivo, which is suggestive of a role for NAAA in the control of inflammation. ⋯ ARN077 reversed these biochemical effects. The results identify ARN077 as a potent inhibitor of intracellular NAAA activity, which is active in vivo by topical administration. The findings further suggest that NAAA regulates peripheral pain initiation by interrupting endogenous FAE signaling at PPAR-α.
-
Human unmyelinated (C) tactile afferents signal the pleasantness of gentle skin stroking on hairy (nonglabrous) skin. After neuronal injury, that same type of touch can elicit unpleasant sensations: tactile allodynia. The prevailing pathophysiological explanation is a spinal cord sensitization, triggered by nerve injury, which enables Aβ afferents to access pain pathways. ⋯ In addition, reduced activation in the medial prefrontal cortices, key areas for C-tactile hedonic processing, was identified. These findings suggest that dynamic tactile allodynia is associated with reduced C-tactile mediated hedonic touch processing. Nevertheless, because the patients did not develop allodynic pain, this seems dependent on Aβ signaling, at least under these experimental conditions.
-
Randomized Controlled Trial
Impact of being primed with social deception upon observer responses to others' pain.
This study examined whether priming with social deception affects responses (pain estimates, self-reported sympathy, inclination to help) towards others' pain. We further explored whether the priming effect is mediated by the valence of the patients (positive/negative), as indicated by the participants. First, participants (N=55) took part in an 'independent' delayed memory study in which they read either a neutral text about the use of the health care system (neutral condition) or a text about its misuse (social deception condition). ⋯ Results revealed no direct effect of priming with social deception. However, priming with social deception was related to less positive rating of the valence of the patients, that were related to lower ratings on pain and sympathy, and to larger discrepancies between the ratings of the patients and the observers. The results indicate that observers attribute less pain, feel less sympathy, and take patients' self-reported pain intensity less into account when the patients are evaluated less positively, which is likely to occur when a cognitive scheme of social deception is primed.