Pain
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Comparative Study Clinical Trial Controlled Clinical Trial
Electrically evoked itch in humans.
We compared itch sensations and axon reflex flare induced by transcutaneous electrical (0.08-8 ms, 2-200 Hz) and chemical (histamine iontophoresis; 100 microC) stimulation. Stimuli were applied to non-lesional volar wrist skin in 20 healthy human subjects and 10 patients with atopic dermatitis. Intensity of evoked itch and pain sensations were rated on a numerical rating scale (NRS) of 0 (no sensation) to 10 (the maximum sensation imaginable). ⋯ Healthy subjects and patients with atopic dermatitis did not differ significantly in their response to either stimulation. We conclude that C-fiber activation underlies the electrically evoked itch sensation. The low electrical thresholds and the absence of an axon reflex flare suggest that these fibers are not identical with the previously described mechano-insensitive histamine responsive C fibers, but represent a separate peripheral neuronal system for the induction of itch.
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Comparative Study
Parent-child interactions among children with juvenile fibromyalgia, arthritis, and healthy controls.
Parent-child interactions during pain-inducing exercise tasks among children (11-17 years old) with fibromyalgia, juvenile rheumatoid arthritis, and pain-free controls were examined and the contribution of parent-child interactions to disability was tested. Fifteen children in each of the three diagnostic groups and their parents completed 5-min exercise tasks and completed questionnaire measures of disability (Functional Disability Inventory) and coping (Pain Coping Questionnaire). There were few group differences in parent-child interactions. ⋯ Across the groups, more pain and less time on task during the exercises were related to Functional Disability Inventory scores and more school absences. Parent-child interaction patterns influence children's adaptation to pain during experimental tasks. Parents' discouragement of coping in response to their children's negative statements related to the pain or the pain-evoking task are counter productive to children's ability to maintain activity in a mildly painful situation.
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Tumor necrosis factor alpha (TNFalpha) and interleukin 1beta (IL-1beta) are pro-inflammatory cytokines capable of altering the sensitivity of sensory neurons. Because sensitization elicited by IL-1beta and TNFalpha is blocked by inhibition of the inducible enzyme, cyclooxygenase-II (COX-2), we examined whether these cytokines could increase COX-2 expression in dorsal root ganglion (DRG) cultures. Treatment of cell cultures with either IL-1beta or TNFalpha increases immunoreactive COX-2, as measured by immunoblotting, in a time- and concentration-dependent manner. ⋯ IL-1beta and TNFalpha treatment for 24 h enhanced prostaglandin E2 (PGE2) production 2-4-fold, which was blocked by pretreatment with the COX-2 inhibitor, NS-398. Exposing cultures to PGE2, IL-1beta, or TNFalpha for 24 h did not alter PGE2 receptor (EP) mRNA levels. These results indicate that TNFalpha and IL-1beta induce the functional expression of COX-2 but not EP receptors in DRG cells in culture and suggest that cytokine-induced sensitization of sensory neurons is secondary to prostaglandin production and not alterations in EP receptors.
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Comparative Study
Activation of p38 MAPK in primary afferent neurons by noxious stimulation and its involvement in the development of thermal hyperalgesia.
Alterations in the intracellular signal transduction pathway in primary afferents may contribute to pain hypersensitivity. We demonstrated that very rapid phosphorylation of p38 mitogen-activated protein kinase occurred in dorsal root ganglion (DRG) neurons that were participating in the transmission of noxious signals. Capsaicin injection induced phosphorylated-p38 (p-p38) in small-to-medium diameter sensory neurons with a peak at 2 min after capsaicin injection. ⋯ Intrathecal administration of the p38 inhibitor, FR167653, reversed the thermal hyperalgesia produced by the capsaicin injection. Inhibition of p38 activation was confirmed by the decrease in the number of p-p38-IR neurons in the DRG following capsaicin injection. Taken together, these findings suggest that the activation of p38 pathways in primary afferents by noxious stimulation in vivo may be, at least in part, correlated with functional activity, and further, involved in the development of thermal hyperalgesia.