Pain
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Inflammation enhances release of neuropeptides from sensory nerve terminals in the spinal cord, and this may contribute to the development of hyperalgesia. In a similar manner, proinflammatory prostaglandins also augment peptide release from sensory neurons. To ascertain whether the inflammation-induced increase in peptide release from spinal cord slices is mediated by production of these eicosanoids, we examined whether intrathecal administration of nonsteroidal antiinflammatory drugs (NSAIDS) could attenuate the effects of inflammation. ⋯ Systemic administration of the same amount of ketorolac did not attenuate the effect of inflammation on peptide release. Intrathecal administration of 16 nmol/h (S)-ibuprofen, before and throughout the inflammation, also significantly attenuated the increase in evoked neuropeptide release associated with inflammation, whereas (R)-ibuprofen was ineffective. These results suggest that inhibition of cyclooxygenase at the level of the spinal cord attenuates the augmentation of neuropeptide release induced by peripheral inflammation, and provide further evidence for an action of prostaglandins at central terminals of sensory neurons during inflammation.
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Randomized Controlled Trial Clinical Trial
An intrusive impact of anchors in children's faces pain scales.
The numerous pain rating scales using faces depicting varying degrees of distress to elicit reports of pain from children fall into two categories; those with a neutral face as the 'no pain' anchor, and those with a smiling face as the 'no pain' anchor. This study examined the potentially biasing impact of these anchor types on children's self-reports of pain in response to a series of vignettes. Participants were 100 children stratified by age (5-6 years, 7-8 years, 9-12 years) and randomly assigned to one of three groups: (1) neutral scale/sensory instructions; (2) smiling scale/sensory instructions; (3) smiling scale/affective instructions. ⋯ Group differences in children's ratings with the VAS and emotions measure suggested that rating pain with a smiling faces scale may alter a child's concept of pain. Age differences indicated the younger children rated the negative emotion vignettes as more painful than the older children. These findings suggest that children's pain ratings vary depending on the types of faces scale used, and that faces scales with smiling anchors may confound affective states with pain ratings.
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To provide a better understanding of the prevalence, correlates and quality of phantom sensations and phantom pain in child and adolescent amputees. ⋯ Less than half of the sample experienced phantom sensations and phantom pain; however, the loss of a limb due to surgery is associated with an increase in the likelihood of experiencing these phenomena.
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Opinions are divided on the use of the term cervicogenic headache (CGH) in cases with no evidence of cervical damage. According to Sjaastad et al. (1990), CGH is diagnosed from three features: (1) unilateral headache triggered by head/neck movements or posture; (2) unilateral headache triggered by pressure on the neck; (3) unilateral headache spreading to the neck and the homolateral shoulder/arm. Other characteristics are not essential for CGH diagnosis, including pain improvement after greater occipital nerve (GON)/C2 block. ⋯ The lack of specificity of GON/C2 block as a treatment for CGH adds further difficulties to the diagnosis of this headache. We conclude that, although neck structures play a role in the pathophysiology of some headaches, clinical patterns indicating a neck-headache relationship have still not been adequately defined. We believe that further rigorous studies are needed to definitively confirm the validity of CGH as a nosological entity.
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We examined two possible mechanisms of neuropathic pain: contribution of adjacent intact nerves and decrease in presynaptic inhibition at the central terminal of the injured primary afferent. To this end, we examined the effects of unilateral L5 spinal nerve ligation, which causes mechanical allodynia and heat hyperalgesia in the ipsilateral hind paw, on gene expression in L4 and L5 dorsal root ganglion (DRG) neurons using in situ hybridization (ISH). Specifically, we examined changes in the expression of messenger RNAs (mRNAs) for neuropeptides which have been reported to be up- or down-regulated in the axotomized DRG neurons and for gamma-aminobutyric acid (GABA)A receptor (GABA(A)-R) subunits which contribute to presynaptic inhibition at the primary afferent terminals. ⋯ There was no difference in mRNAs between the bilateral L4 DRGs. These data suggest that the presynaptic disinhibition of the ipsilateral L5 primary afferent terminals may be explained at least partly by the down-regulation of GABA(A)-R following L5 spinal nerve ligation. Thus, both the up-regulation of CGRP in adjacent intact nerves and the decrease in presynaptic inhibition at the central terminal of the injured primary afferent could cause the hyper-excitability of dorsal horn neurons and contribute to the molecular mechanisms of this neuropathic pain model.