The journal of pain : official journal of the American Pain Society
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Persistent stressors associated with sociodemographic disadvantage exert a physiologic toll, labeled "allostatic load," that contributes to disparities in some health conditions. We investigated the contribution of allostatic load to pain prevalence in U.S. adults. Interviews with 14,184 adults in the 1999-2004 National Health and Nutrition Examination Survey asked about severe headache, pain that lasted >24 hours, and widespread pain. Ten biomarkers of allostatic load were quantified from blood (glycated hemoglobin), serum (C-reactive protein, homocysteine, cholesterol, triglycerides), urine (creatinine, albumin), and physical measurements (body mass index, systolic and diastolic blood pressure). Log-binomial regression models estimated prevalence ratios (PRs) and 95% confidence intervals (95% CIs). Prevalence ranged from 3.4% for widespread pain to 26.9% for pain >24 hours. After adjustment for demographic characteristics, low income was associated with greater prevalence of pain >24 hours (PR = 1.65, 95% CI = 1.49, 1.83), severe headache (PR = 2.05, 95% CI = 1.68, 2.50), and widespread pain (PR = 3.67, 95% CI = 2.56, 5.27). Racial/ethnic minorities had lower prevalence of all 3 pain conditions than non-Hispanic whites. While greater allostatic load was associated with elevated prevalence of pain, allostatic load did not meaningfully attenuate PRs associated with income or race/ethnicity. We conclude that greater pain prevalence among low-income groups is not explained by greater allostatic load. ⋯ In U.S. adults, pain occurs more frequently in lower-income groups, although the relationship is not attributable to their experience of greater allostatic load. While allostatic load contributes to population variation in pain, other etiologic mechanisms contributing to pain are needed to account for income disparities in pain.
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Evoked potentials (EPs) to radiant or contact heat pain stimuli reflect the synchronization of brain activity to noxious inputs. However, we do not know how they relate to conscious awareness (AW) of a sensation. In healthy volunteers, we determined the time of AW for thermal noxious and non-noxious sensory inputs and examined its correlation to parametric measures of vertex EPs. Subjects had to report the position of the hand of a Libet's clock at the moment they perceived either a laser or a thermode stimulus. AW was determined after subtracting the position of the clock hand at the moment of stimulus delivery from the one reported by the subject, in ms. Subjects estimated AW in all single trials, including those in which no EPs could be identified. Mean AW was estimated earlier than the corresponding EP latency for both types and intensities of stimuli. There was a weak but significant negative correlation of AW to EPs amplitude, which was higher than the correlation of AW to EPs latency. Our results indicate that the timing of AW is influenced by the subjective relevance of sensory inputs. This feature could be used for the analysis of cognitive aspects of pain processing. ⋯ This article presents a way to measure the subjective awareness of the sensation induced by a noxious heat stimulus, either radiant or contact, in healthy human subjects. This method could be used for the analysis of cognitive aspects of pain processing.
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While self-pain motivates protective behaviors and self-oriented feelings, the perception of others' pain often motivates concern and prosocial behaviors toward the person suffering. The conflicting consequences of these 2 states raise the question of how pain is perceived in others when one is actually in pain. Two conflicting hypotheses could predict the interaction between these 2 signals: the threat value of pain hypothesis and the shared-representation model of pain empathy. Here, we asked 33 healthy volunteers exposed to acute experimental pain to judge the intensity of the pain felt by models expressing different levels of pain in video clips. Results showed that compared to a control warm stimulus, a stimulus causing self-pain increased the perception of others' pain for clips depicting male pain expressions but decreased the perceived intensity of female high pain expressions in both male and female participants. These results show that one's own pain state influences the perception of pain in others and that the gender of the person observed influences this interaction. ⋯ By documenting the effects of self-pain on pain perception in others, this study provides a better understanding of the shared mechanisms between self-pain and others' pain processing. It could ultimately provide clues as to how the health status of health care professionals could affect their ability to assess their patients' pain.
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This study investigated if conditioned pain modulation (CPM) varies across the menstrual cycle in healthy, normally menstruating women and investigated correlations between sex hormone levels and CPM across the menstrual cycle. Thirty-six normally menstruating women were tested during 3 phases of the menstrual cycle: early follicular, ovulatory, and midluteal, confirmed by hormone determinations. Mechanical pressure (test stimulus) was applied to the masseter muscle and the induced pain assessed before, during, and after immersion of the hand into ice water (conditioning stimulus) to activate CPM or tepid water (control). Conditioning pain, ie, pain in the hand during CPM/control experiment, and tolerance time were also measured. Test pain intensity was suppressed during CPM in all phases (P < .001), but with more effective suppression during the ovulatry than during the early follicular phase (P < .05). There were no changes in test pain intensity during the control experiment and no significant differences in conditioning pain, or tolerance time between phases. In conclusion, our results showed more effective pain modulation in the ovulatory phase of the menstrual cycle, when estradiol levels are high and progesterone levels are low, than in the early follicular phase when both these hormones are low. ⋯ Deficient pain modulation is believed to be an important pathogenic factor in many chronic pain conditions that affect women. This article shows that sex hormones modulate conditioned pain modulation, because pain inhibition was more effective in the ovulatory phase of the menstrual cycle than in the early follicular phase.
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Several lines of evidence indicate that brain-derived neurotrophic factor (BDNF) plays a key role as a central pronociceptive modulator of pain, acting through postsynaptic TrkB receptors that trigger intracellular signaling cascades leading to central sensitization. The overall aim of this study was to investigate to what extent BDNF could participate in the generation and maintenance of trigeminal neuropathic pain. The results showed that acute intracisternal administration of nanogram doses of BDNF in naïve mice elicited long-lasting, dose-related, cold allodynic responses to topical application of acetone onto vibrissal pad skin. The systemic administration of cyclotraxin-B (CTX-B), a new TrkB receptor antagonist, or propentofylline, an inhibitor of glial activation, was able to either prevent or reverse the effects of intracisternal BDNF on cold nociception. In addition, the blockade of TrkB receptor by CTX-B inhibited the mechanisms that either initiate or maintain cold allodynia in the ipsilateral vibrissal pad skin after unilateral constriction of the infraorbital nerve. These observations raise the possibility that BDNF is capable on its own of conveying many features of the signaling mechanisms that underlie central sensitization caused by nerve constriction. ⋯ Although further studies are necessary to examine in detail the mechanisms underlying the strong anti-allodynic action of CTX-B, this compound may represent an interesting lead for the development of novel therapeutic strategies aimed at preventing and/or suppressing central sensitization associated with neuropathic pain.