Pain
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Chronic pain associated with inflammation is a major clinical problem, but the underlying mechanisms are incompletely understood. Recently, we reported that GRK2(+/-) mice with a approximately 50% reduction of GRK2 develop prolonged hyperalgesia following a single intraplantar injection of the pro-inflammatory cytokine interleukin-1beta (IL-1beta). Here we show that spinal microglia/macrophage GRK2 is reduced during chronic inflammation-induced hyperalgesia. ⋯ These data establish that chronic inflammatory hyperalgesia is associated with reduced GRK2 in microglia/macrophages and that low GRK2 in these cells is sufficient to markedly prolong hyperalgesia after a single intraplantar injection of IL-1beta. Ongoing hyperalgesia is maintained by spinal microglial/macrophage activity, fractalkine signaling, p38 activation and IL-1 signaling. We propose that chronic inflammation decreases spinal microglial/macrophage GRK2, which prevents silencing of microglia/macrophage activity and thereby contributes to prolonged hyperalgesia.
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Functional abdominal pain in childhood and adolescence increases risk for chronic pain in adulthood.
A few studies of long-term outcomes for pediatric functional abdominal pain (FAP) have assessed acute non-abdominal pain at follow-up, but none has assessed chronic pain. We followed a cohort of pediatric patients with FAP (n=155) and a well control group (n=45) prospectively for up to 15 years. Participants ranged in age from 18 to 32 years at a follow-up telephone interview. ⋯ One-third of the Unresolved group reported both headache and one or more sites of chronic non-abdominal pain at follow-up, compared to 17.8% of the Resolved group and 4.4% of controls. Youth with FAP that persists into adulthood may be at increased risk for chronic pain and headache. Examination of central mechanisms that are common across chronic pain disorders may enhance understanding of this subgroup of FAP.
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Using latent class analysis (LCA), a previous study on patients attending primary care identified four courses of low back pain (LBP) over the subsequent 6 months. To date, no studies have used longitudinal pain recordings to examine the "natural" course of recurrent and chronic LBP in a population-based sample of individuals. This study examines the course of LBP in the general population and elaborates on the stability and criterion-related validity of the clusters derived. ⋯ Three of the four clusters describing the typical course of pain matched the clusters described previously for patients in primary care. Due to the population-based design, this study achieves, for the first time, a close insight into the "natural" course of chronic and recurrent low back pain, including individuals that did not necessarily visit the general practitioner. The findings will help to understand better the nature of this pain in the general population.