Pain
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Numerous studies have shown an association between smoking and pain, with smokers reporting more pain and worse functioning. However, little is known about factors that impact this complex relationship. This study investigated the association between smoking, pain, and depressive symptoms. ⋯ Additionally, among former smokers, longer quit duration was associated with less pain severity. In conclusion, smoking rates were high and smoking was associated with a worse chronic pain phenotype. Importantly, depressive symptoms emerged as a critical mediating factor in helping to explain the relationship between smoking and pain.
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Multicenter Study
Assessment and validation of prognostic models for poor functional recovery 12 months after whiplash injury: a multicentre inception cohort study.
Uncertainty surrounds prognostic factors after whiplash injury. Previously we identified a prognostic model for 6-month pain-related disability in a cohort of 80 participants with acute whiplash. Predictors included initial disability, older age, decreased cold pain thresholds, decreased neck rotation movement, posttraumatic stress symptoms and decreased sympathetic vasoconstriction. ⋯ After adjusting for site, age and Impact of Events Scale scores regained significance (r(2) = 0.56, 95% confidence interval 0.48 to 0.64). The tested model was not precise in predicting NDI as a continuous variable. However, it found good accuracy to discriminate participants with moderate to severe disability at 12 months (area under the receiver operating characteristic curve 0.89 [95% confidence interval 0.84-0.94], P<.001) which is clinically useful.
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Randomized Controlled Trial
Ethnicity interacts with the OPRM1 gene in experimental pain sensitivity.
Robust interindividual variation in pain sensitivity has been observed, and recent evidence suggests that some of the variability may be genetically mediated. Our previous data revealed significantly higher pressure pain thresholds among individuals possessing the minor G allele of the A118G SNP of the mu-opioid receptor gene (OPRM1) compared with those with 2 consensus alleles. Moreover, ethnic differences in pain sensitivity have been widely reported. ⋯ The reasons for this dichotomy are unclear; they may involve ethnic differences in haplotypic structure, or A118G may be a tag-SNP linked to other functional polymorphisms. These findings demonstrate an ethnicity-dependent association of OPRM1 genotype with pain sensitivity. Additional research is warranted to uncover the mechanisms influencing these relationships.
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Inflammatory thermal hyperalgesia is principally mediated through transient receptor potential vanilloid 1 (TRPV1) channels, as demonstrated by prior studies using models of cutaneous inflammation. Muscle pain is significantly different from cutaneous pain, and the involvement of TRPV1 in hyperalgesia induced by muscle inflammation is unknown. We tested whether TRPV1 contributes to the development of mechanical and heat hypersensitivity of the paw in TRPV1(-/-) mice after muscle inflammation. ⋯ Heat hypersensitivity induced by muscle inflammation did not develop in TRPV1(-/-) mice; mechanical hypersensitivity was similar between TRPV1(-/-) and TRPV1(+/+) mice. Heat hypersensitivity induced by muscle inflammation was restored by reexpression of TRPV1 into both muscle and skin of TRPV1(-/-) mice. These results suggest that TRPV1 serves as both a mediator of nociceptor sensitization at the site of inflammation and as a heat sensor at the paw.