Pain
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Functional magnetic resonance imaging (fMRI) of blood oxygen level dependent (BOLD) haemodynamic responses was used to study the effects of the noxious substance capsaicin on whole brain activation in isofluorane anaesthetised rats. Rats (n=8) received intradermal injection of capsaicin (30 microg/5 microl), or topical cream (0.1%) capsaicin and BOLD responses were acquired for up to 120 min. Effects of capsaicin versus placebo cream treatment on the BOLD response to a 15 g mechanical stimulus applied adjacent to the site of cream application were also studied. ⋯ Capsaicin also produced increases in BOLD signal intensity in other regions that contribute to pain processing, such as the parabrachial nucleus and superior colliculus. Mechanical stimulation in capsaicin-treated rats, but not placebo-treated rats, induced a significant decrease in BOLD signal intensity in the PAG (p<0.001). These data demonstrate that the noxious substance capsaicin produces brain activation in the midbrain regions and reveals the importance of the PAG in central sensitization.
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The aims of this study were to explore: (a) the interrelation between spatial summation (SS) and spatial discrimination (SD) of pain, (b) whether the two phenomena are subserved by different sensory channels. SS and SD of pain were measured with contact heat stimuli delivered at slow (0.50 degrees C/s) and fast (40 degrees C/s) rise times. Pressure nerve block of the radial nerve was employed to assess whether differential activation of C and A delta fibers is obtained by these different rates of rise. ⋯ Stimulation rate did not affect SS or SD. Following nerve block, thresholds obtained with the fast rise stimulation increased significantly (HPT rose from 46.2 to 50.5 degrees C) but those obtained with slow rise stimuli were not affected by the block, indicating that C and A delta fibers were activated selectively. The results suggest that: (a) SS and SD are mutually exclusive functions of the nociceptive systems, (b) C and A delta nociceptors are probably similarly involved in these functions.
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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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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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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 (
or=37 weeks gestational age) treated at least 3 days in a NICU at a University Hospital and 20 fullterm control children without NICU experience was performed. ⋯ Mechanical pain threshold and perceptual sensitization did not differ between groups. Consistent with findings in animals, repeated pain experiences during the neonatal period were associated with alterations in thermal pain responsivity in school-aged preterm and fullterm children that was characterized by enhanced perceptual sensitization to prolonged painful stimulation and hypoalgesia to brief heat pain stimuli. Our findings suggest that repeated pain experiences in neonates may induce activity-induced changes in the functioning of pain pathways that persist well beyond infancy.