Pain
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Following nociceptive heat or laser stimulation, an early contralateral and later vertex potential can be recorded. Although more indicative of the nociceptive input, the acquisition of the contralateral N1 after contact heat stimulation (contact heat-evoked potentials [CHEPs]) remains difficult. An advantage of contact heat is that the baseline skin temperature preceding peak stimulation can be controlled. ⋯ Based on standard averaging, N2/P2 amplitudes were also significantly increased with and without an accompanying change in the rating of perceived pain when the baseline temperature was increased (P<.05). In contrast, automated single-trial averaging revealed no significant difference in N2 amplitude when the baseline temperature was increased to 42°C and the peak temperature reduced. These findings suggest that 2 mechanisms underlie the improved acquisition of CHEPs: increased synchronization of afferent volley, yielding larger-amplitude evoked potentials in response to the same rating of intensity; and reduced inter-trial variability.
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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.
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Inflammatory pain severely affects the quality of life of millions of individuals worldwide. Prostaglandin E2 (PGE2), a pain mediator enriched in inflamed tissues, plays a pivotal role in nociceptor sensitization and in the genesis of inflammatory pain. Its EP4 receptor mainly mediates its role in inflammatory pain. ⋯ Intraplantar injection of complete Freud's adjuvant increases both total and cell-surface EP4 levels of L4-6 DRG neurons, an event suppressed by a cyclooxygenase-2 inhibitor or a selective EP4 antagonist, suggesting that PGE2/EP4 signalling in inflamed paw contributes to EP4 synthesis and export in DRG neurons, thus sensitizing nociceptors during inflammation. We conclude that PGE2/EP4 signalling-induced EP4 externalization in DRG neuron is a novel mechanism underlying nociceptor sensitization and inflammatory pain. Blocking EP4 externalization could open a novel therapeutic avenue to treat inflammatory pain.
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Patient-reported outcome measures are being developed for more relevant assessments of pain management. The patient acceptable symptom state (PASS) ("feeling well") and the minimal clinically important improvement (MCII) ("feeling better") have been determined in clinical trials, but not in daily pain management. We carried out a national multicenter cohort study of patients over the age of 50years with painful knee osteoarthritis (KOA) or hip osteoarthritis (HOA) who had visited their general practitioner and required treatment for more than 7days. ⋯ This improvement is smaller than that recorded in randomized controlled trials, and was the same for both sites, both at rest and on movement. In conclusion, patient-reported outcome values in daily practice differ from those in clinical trials, and their determinant factors may depend on the site of osteoarthritis. Assessments of the treatment of painful osteoarthritis should be adapted to the characteristics and daily life of the patient, to personalize patient management.
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Resting blood pressure (BP) is inversely related to pain sensitivity in individuals free of chronic pain, reflecting homeostatic interactions between cardiovascular and pain modulatory systems. Several laboratory studies indicate that BP-related hypoalgesia is diminished in chronic pain patients, suggesting dysfunction in these interacting systems. Separate epidemiological findings reveal elevated hypertension prevalence in the chronic pain population. ⋯ Presence of chronic pain was associated with significantly increased odds of comorbid hypertension (P<.001). Within the chronic pain group, higher chronic pain intensity was a significant predictor of positive hypertension status beyond the effects of traditional demographic risk factors (P<.05). Results are consistent with the hypothesis that increased hypertension risk in the chronic pain population might be linked in part to chronic pain-related dysfunction in interacting cardiovascular-pain modulatory systems.