Pain
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No validated screening tasks exist to distinguish children who can accurately use self-report pain measures from those who cannot. Children aged 3-7 years (n=108), each with a parent, provided data before and after day surgery. Parents rated how well they thought their child could understand the Faces Pain Scale-Revised (FPS-R), and children completed 4 screening tasks in counterbalanced order, such as rating pain in vignettes and selecting a middle-sized cup. ⋯ We failed to identify a screening tool that was better than chronological age in identifying which children could accurately self-report pain using the FPS-R. Future research should explore other screening tasks, training methods, and simplified approaches to pain assessment for young children. The ability to use self-report pain scales usually develops from age 3 to 7 years, but no valid screening method exists to identify this achievement.
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Excessive medication intake is a risk factor for the development of medication-overuse headache (MOH), a condition characterized by an increase of headache frequency to a daily or near-daily pattern. As yet, it is largely unknown why some patients overuse medication. In this study, we examined to what extent attitudes about pain medication, especially perceived need and concerns, and problem-solving are related to MOH. ⋯ Results are discussed in terms of how repeated attempts to solve pain may trigger overuse of medication, even in the presence of clear negative consequences. Repeated attempts at solving pain may increase the need for analgesic medication, despite obvious costs. This mechanism might contribute to the problem of medication-overuse headache.
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Insomnia is a common problem for people with chronic pain. Cortical GABAergic neurons are part of the neurobiological substrate that underlies homeostatic sleep regulation. In the present study, we confirmed that sciatic nerve ligation caused thermal hyperalgesia and tactile allodynia in mice. ⋯ These findings provide novel evidence that sciatic nerve ligation decreases extracellular-released GABA in the cingulate cortex of mice. These phenomena may, at least in part, explain the insomnia in patients with neuropathic pain. Neuropathic pain-like stimuli suppress the GABAergic transmission with increased GABA (γ-aminobutyric acid) transporters located on activated astrocytes in the cingulate cortex related to sleep disturbance.
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This study compared individuals with fibromyalgia (FM) and individuals with chronic low back pain (CLBP) on repetition-induced summation of activity-related pain (RISP). Fear of movement, pain catastrophizing and depression were examined as potential mediators of group differences. The sample consisted of 50 women with FM and 50 women with CLBP who were matched on age, pain severity and pain duration. ⋯ Discussion addresses the processes by which individuals with FM might have increased RISP responses. The findings of this study point to possible neurophysiological mechanisms that could help explain the high levels of pain-related disability seen in individuals with FM. Patients with fibromyalgia showed greater activity-related summation of pain than patients with chronic low back pain.
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Recent studies have shown that leptin (an adipocytokine) played an important role in nociceptive behavior induced by nerve injury, but the cellular mechanism of this action remains unclear. Using the whole-cell patch-clamp recording from rat's spinal cord slices, we showed that superfusion of leptin onto spinal cord slices dose-dependently enhanced N-methyl-d-aspartate (NMDA) receptor-mediated currents in spinal cord lamina II neurons. At the cellular level, the effect of leptin on spinal NMDA-induced currents was mediated through the leptin receptor and the JAK2/STAT3 (but not PI3K or MAPK) pathway, as the leptin effect was abolished in leptin receptor-deficient (db/db) mice and inhibited by a JAK/STAT inhibitor. ⋯ Our data demonstrate a relationship between leptin and NMDA receptor-mediated spinal neuronal excitation and its functional role in nociceptive behavior. Since leptin contributes to nociceptive behavior induced by nerve injury, the present findings suggest an important cellular link between the leptin's spinal effect and the NMDA receptor-mediated cellular mechanism of neuropathic pain. A functional link is demonstrated between leptin, an adipocytokine, and the cellular mechanisms of neuropathic pain via enhancement of function and expression of spinal N-methyl-d-aspartate receptors.