Pain
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Comparative Study
Acute and persistent pain modulation of attention-related anterior cingulate fMRI activations.
The anterior cingulate cortex (ACC) has been implicated in both sustained attention (SA) and pain perception. Nonetheless, only a small body of literature has examined the relationship between SA and pain perception. This study utilized fMRI to examine activation patterns that emerged in the ACC in healthy participants and participants with chronic pain (due to osteoarthritis (OA) of the knee) while completing a sustained attention task with and without exposure to an acute painful stimulus. ⋯ In the healthy group, there were broadly distributed clusters of voxels within the ACC that were modulated by painful stimulation. But in the chronic pain group, a discrete focal region of the ACC was modulated by pain. These results demonstrate that ACC activity is modulated differently during tasks of SA and pain, and that acute pain in healthy participants and participants with chronic pain result in significantly different ACC activation patterns.
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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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NaV1.8 is a voltage-gated sodium channel expressed only in a subset of sensory neurons of which more than 85% are nociceptors. In order to delete genes in nociceptive neurons, we generated heterozygous transgenic mice expressing Cre recombinase under the control of the NaV1.8 promoter. Functional Cre recombinase expression replicated precisely the expression pattern of NaV1.8. ⋯ Sodium channel subtypes were normal in isolated DRG neurons. Pain behaviour in response to mechanical or thermal stimuli, and in acute, inflammatory and neuropathic pain was also normal. These data demonstrate that the heterozygous NaV1.8-Cre mouse line is a useful tool to analyse the effects of deleting floxed genes on pain behaviour.
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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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Comparative Study Clinical Trial
Gender differences in pain modulation evoked by repeated injections of glutamate into the human trapezius muscle.
Gender differences in pain habituation, temporal summation, and pressure hyperalgesia evoked by repeated injections of glutamate into the dominant trapezius muscle were investigated. The glutamate-evoked muscle pain intensity and pressure pain threshold (PPT) were assessed. The PPTs were measured bilaterally in the trapezius muscles (local pain area) and posterolateral neck muscles (referred pain area) after glutamate injection in healthy and age-matched males and females (each n=14). ⋯ No PPTs changes were observed either in the contralateral trapezius muscle or bilaterally in the referred pain areas in either sex. These results suggest that a less efficient pain habituation and a greater susceptibility to the development of temporal summation of muscle pain in females, but not in males, might be one of the contributing factors to the higher incidence of neck shoulder pain in females. In addition, the reduction of PPTs in the local pain area evoked by intramuscular glutamate injection may represent an early process of peripheral pressure hyperalgesia, which is most likely gender independent.