Pain
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Pain can be modulated by contextual stimuli, such as emotions, social factors, or specific bodily perceptions. We presented painful laser stimuli together with body-related masochistic visual stimuli to persons with and without preferred masochistic sexual behavior and used neutral, positive, and negative pictures with and without painful stimuli as control. Masochists reported substantially reduced pain intensity and unpleasantness in the masochistic context compared with controls but had unaltered pain perception in the other conditions. ⋯ Masochists additionally showed negative correlations between the duration of interest in masochistic activities and activation of areas involved in motor activity and affective processing. We propose that the parietal operculum serves as an important relay station that attenuates the affective-motivational aspects of pain in masochists. This novel mechanism of pain modulation might be related to multisensory integration and has important implications for the assessment and treatment of pain.
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Adolescents who experience pain often face competing goals and have to choose whether to approach (confront) or avoid pain. This study investigates the decisions adolescents make when their pain conflicts with a valued goal. Adolescents between the ages of 15 and 18 years (N = 170) completed questionnaires on general and pain-specific anxiety, courage, and dispositional avoidance. ⋯ In addition, we compared approach-avoidance of adolescents with and without chronic pain; analyses revealed no differences in approach-avoidance behaviour. We also found that behavioural endurance was predictive of approach and dispositional avoidance predicted higher avoidance, but courage was not predictive of behaviour in this task. We adopt a motivational perspective when interpreting the findings and consider whether the fear-avoidance model should be extended to include the function of avoidance or approach in the pursuit of a desired goal.
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Human surrogate models of neuropathic pain in healthy subjects are used to study symptoms, signs, and the hypothesized underlying mechanisms. Although different models are available, different spontaneous and evoked symptoms and signs are inducible; 2 key questions need to be answered: are human surrogate models conceptually valid, ie, do they share the sensory phenotype of neuropathic pain states, and are they sufficiently reliable to allow consistent translational research?
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The information from nociceptors is processed in the dorsal horn of the spinal cord by complex circuits involving excitatory and inhibitory interneurons. It is well documented that GluN2B and ERK1/2 phosphorylation contributes to central sensitization. Striatal-enriched protein tyrosine phosphatase (STEP) dephosphorylates GluN2B and ERK1/2, promoting internalization of GluN2B and inactivation of ERK1/2. ⋯ Consistently, STEP knockout mice failed to show age-related thermal hyperalgesia, although gender-related differences were preserved. Moreover, in a model of inflammatory pain, hyperalgesia was associated with increased phosphorylation-mediated STEP(61) inactivation and increased pGluN2B(Tyr1472) and pERK1/2(Thr202/Tyr204)levels in the lumbar spinal cord. Collectively, the present results underscore an important role of spinal STEP activity in the modulation of nociception.
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Unpredictable threat amplifies pain and spinal nociception (as measured by the nociceptive flexion reflex, NFR), but it is unknown whether pain catastrophizing mediates this threat-related amplification. To examine this, the present study experimentally reduced catastrophizing and examined the effect on threat-evoked pain/NFR facilitation. Healthy pain-free participants (N = 113) were randomly assigned to a brief 30-minute intervention designed to reduce catastrophic thoughts or a control intervention that involved education about pain neurobiology. ⋯ However, this threat-related pain/NFR amplification was not attenuated by the catastrophizing reduction intervention at the group level, although the intervention generally led to lower pain ratings (but not reduced NFR), regardless of the context. Nonetheless, bootstrapped mediation analyses found that reductions in catastrophizing mediated reductions in threat-related amplification of pain, but not NFR. This suggests that catastrophizing is partly responsible for threat-evoked pain amplification and provides further evidence that catastrophizing does not amplify pain at the spinal level.