Pain
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Controlled Clinical Trial
Catechol-O-methyltransferase gene polymorphisms are associated with multiple pain-evoking stimuli.
Variations in the gene encoding catechol-O-methyltransferase (COMT) are linked to individual differences in pain sensitivity. A single nucleotide polymorphism (SNP) in codon 158 (val(158)met), which affects COMT protein stability, has been associated with the human experience of pain. We recently demonstrated that three common COMT haplotypes, which affect the efficiency of COMT translation, are strongly associated with a global measure of pain sensitivity derived from individuals' responses to noxious thermal, ischemic, and pressure stimuli. ⋯ In contrast, the val(158)met genotype was associated with the rate of temporal summation of heat pain, but not with the other pain measures. This suggests that the val(158)met SNP plays a primary role in variation in temporal summation of pain, but that other SNPs of the COMT haplotype exert a greater influence on resting nociceptive sensitivity. Here, we propose a mechanism whereby these two genetic polymorphisms differentially affect pain perception.
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The influence of potential prognostic factors (occupant- and crash-related factors, initial neck pain intensity and headache, whiplash injury severity, helplessness, locus of control, socioeconomic status) on neck pain intensity (VAS), disability (DRI), anxiety and depression (HADS) was estimated in a cohort of 3704 subjects with whiplash injury following a motor vehicle crash. Questionnaires were administered (baseline, 1-, 6-, 12-, 24-month follow-ups). VAS was trichotomized; "low" (0-30), "moderate" (31-54), "severe" (55-100). ⋯ Locus of control was not a factor of importance. In contrast, helplessness was related to all outcomes, but was most pronounced regarding neck pain intensity and depression for subjects with severe initial neck pain (OR 4.8; 95% CI 2.9-7.8; OR 6.6; 95% CI 2.6-17.0). Associations seem to be established early, and then to be relatively constant over time.
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While animal studies suggest that neonatal pain experiences induce long-term alterations in pain sensitivity, no such data exist in humans. Changes in pain sensitivity in school-aged children (9-14 years) who were born preterm or fullterm, had been hospitalized for a prolonged period of time after birth and had undergone repeated painful procedures while being treated in a Neonatal Intensive Care Unit (NICU) were determined. A retrospective cohort study of 19 preterm (