Pain
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The processing of reward and reinforcement learning seems to be important determinants of pain chronicity. However, reward processing is already altered early in life and if this is related to the development of pain symptoms later on is not known. The aim of this study was first to examine whether behavioural and brain-related indicators of reward processing at the age of 14 to 15 years are significant predictors of pain complaints 2 years later, at 16 to 17 years. ⋯ The relationship of pain complaints and activation in the periaqueductal gray and ventral striatum depended on the T-allele of rs563649. Carriers of this allele also showed more pain complaints than CC-allele carriers. Therefore, brain responses to reward outcomes and higher sensitivity to pain might be related already early in life and may thus set the course for pain complaints later in life, partly depending on a specific opioidergic genetic predisposition.
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Existing estimates of sociodemographic disparities in chronic pain in the United States are based on cross-sectional data, often treat pain as a binary construct, and rarely test for nonresponse or other types of bias. This study uses 7 biennial waves of national data from the Health and Retirement Study (1998-2010; n = 19,776) to describe long-term pain disparities among older (age 51+) American adults. It also investigates whether pain severity, reporting heterogeneity, survey nonresponse, and/or mortality selection might bias estimates of social disparities in pain. ⋯ No evidence of pain-related survey attrition is found, but surveys not accounting for pain severity and reporting heterogeneity are likely to underestimate socioeconomic disparities in pain. The lack of minority disadvantage (net of socioeconomic status) appears genuine. However, the age-related plateauing of pain observed cross-sectionally is not replicated longitudinally, and seems partially attributable to mortality selection, as well as to rising pain levels by birth cohort.
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Prior studies have documented an association of obesity with chronic pain, but the mechanism explaining the association remains unknown. This study evaluated the degree to which dietary intake of foods with anti-inflammatory effects mediates the relationship of body fat to body pain. Ninety-eight community-residing healthy adults (60% women; mean age = 43.2 ± 15.3 years; range: 20-78 years) participated in a home-based study of home environment, food-related behaviors, health, and adiposity. ⋯ Modeling in PROCESS revealed that Healthy Eating Index-2010 scores mediated the relationship between BMI and BP (bindirect = -0.34, 95% confidence interval = -0.68 to -0.13). The mediation model remained significant when controlling for biomechanical factors (arthritis/joint pain), medication use, psychological distress, age, and education, and models remained significant using the other 2 body fat measures. Thus, the data indicate that dietary intake of foods with anti-inflammatory effects mediates the relationship of body fat to body pain in healthy men and women.
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Widespread hyperalgesia has been found in patients with painful hip osteoarthritis (OA) which can be normalized after total hip arthroplasty (THA) if patients have no residual postoperative pain. This study characterized the preoperative somatosensory profiles and provided possible interpretation of underlying pain mechanisms that might influence the development of postoperative pain. Forty hip OA patients with unilateral pain were assessed before and 6 weeks post-THA and compared with 40 asymptomatic control subjects. ⋯ Postoperative hip pain VAS scores correlated with preoperative ipsilateral TSP (r = 0.44, P < 0.05). Bilateral pressure pain hypersensitivity and facilitated TSP were demonstrated in patients with preoperative hip OA. Although persistent postoperative pain is known as multifactorial, greater preoperative TSP was associated with greater pain and less reduction in pain after THA.