The journal of pain : official journal of the American Pain Society
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The effects of minocycline or riluzole treatment on spinal root avulsion-induced pain in adult rats.
Spinal root avulsion produces tactile and thermal hypersensitivity, neurodegeneration, and microglial and astrocyte activation in both the deafferented and the adjacent intact spinal cord segments. Following avulsion of the fifth lumbar spinal root, immediate and prolonged treatment with riluzole or minocycline for 2 weeks altered the development of behavioral hypersensitivity. Riluzole delayed the onset of thermal and tactile hypersensitivity and partially reversed established pain behavior. Minocycline effectively prevented and reversed both types of behavioral change. Histologic analysis revealed that both drugs reduced microglial staining in the spinal cord, with minocycline being more effective than riluzole. Astrocyte activation was ameliorated to a lesser extent. Surprisingly, neither drug provided a neuroprotective effect on avulsed motoneurons. ⋯ Immediate treatment of spinal root avulsion injuries with minocycline or riluzole prevents the onset of evoked pain hypersensitivity by reducing microglial cell activation. When treatment is delayed, minocycline, but not riluzole, reverses pre-established hypersensitivity. Thus, these drugs may provide a new translational treatment option for chronic avulsion injury pain.
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Racial disparities in pain treatment pose a significant public health and scientific problem. Prior studies have demonstrated that clinicians and nonclinicians are less perceptive of, and suggest less treatment for, the pain of African Americans relative to European Americans. Here we investigate the effects of explicit/implicit patient race presentation, patient race, and perceiver race on pain perception and response. African American and European American participants rated pain perception, empathy, helping motivation, and treatment suggestion in response to vignettes about patients' pain. Vignettes were accompanied by a rapid (implicit) or static (explicit) presentation of an African or European American patient's face. Participants perceived and responded more to European American patients in the implicit prime condition, when the effect of patient race was below the level of conscious regulation. This effect was reversed when patient race was presented explicitly. Additionally, female participants perceived and responded more to the pain of all patients, relative to male participants, and in the implicit prime condition, African American participants were more perceptive and responsive than European Americans to the pain of all patients. Taken together, these results suggest that known disparities in pain treatment may be largely due to automatic (below the level of conscious regulation) rather than deliberate (subject to conscious regulation) biases. These biases were not associated with traditional implicit measures of racial attitudes, suggesting that biases in pain perception and response may be independent of general prejudice. ⋯ Results suggest that racial biases in pain perception and treatment are at least partially due to automatic processes. When the relevance of patient race is made explicit, however, biases are attenuated and even reversed. We also find preliminary evidence that African Americans may be more sensitive to the pain of others than are European Americans.
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Pain-related self-efficacy and pain-related fear have been proposed as opposing predictors of pain-related functional outcomes in youth with chronic pain. Self-efficacy is a potential resiliency factor that can mitigate the influence that pain-related fear has on outcomes in youth with chronic pain. Drawing from theoretical assertions tested among adults with chronic pain, this study aimed to determine whether pain-related self-efficacy mediates the adverse influence of pain-related fear on functional outcomes in a sample of youth with chronic headache. In a cross-sectional design of 199 youth with headache, self-efficacy was strongly associated with fear, disability, school impairment, and depressive symptoms. Pain intensity and self-efficacy were only modestly related, indicating that level of pain has less influence on one's confidence functioning with pain. Self-efficacy partially mediated relationships between pain-related fear and both functional disability and school functioning but did not mediate the relationship between pain-related fear and depressive symptoms. These results suggest that confidence in the ability to function despite pain and fear avoidance each uniquely contributes to pain-related outcomes in youth with chronic headache. These results further suggest that treatment for chronic headache in youth must focus not only on decreasing pain-related fear but also on enhancing a patient's pain-related self-efficacy. ⋯ Pain-related self-efficacy is an important resiliency factor impacting the influence of pain-related fear on functional disability and school functioning in youth with headache. Enhancing self-efficacy may be a key mechanism for improving behavioral outcomes. Clinicians can reduce pain-related fear and enhance pain-related self-efficacy through interventions that encourage accomplishment and self-confidence.
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Insights into mechanisms governing resolution of inflammatory pain are of great importance for many chronic pain-associated diseases. Here we investigate the role of macrophages/monocytes and the anti-inflammatory cytokine interleukin-10 (IL-10) in the resolution of transient inflammatory pain. Depletion of mice from peripheral monocytes/macrophages delayed resolution of intraplantar IL-1β- and carrageenan-induced inflammatory hyperalgesia from 1 to 3 days to >1 week. Intrathecal administration of a neutralizing IL-10 antibody also markedly delayed resolution of IL-1β- and carrageenan-induced inflammatory hyperalgesia. Recently, we showed that IL-1β- and carrageenan-induced hyperalgesia is significantly prolonged in LysM-GRK2(+/-) mice, which have reduced levels of G-protein-coupled receptor kinase 2 (GRK2) in LysM(+) myeloid cells. Here we show that adoptive transfer of wild-type, but not of GRK2(+/-), bone marrow-derived monocytes normalizes the resolution of IL-1β-induced hyperalgesia in LysM-GRK2(+/-) mice. Adoptive transfer of IL-10(-/-) bone marrow-derived monocytes failed to normalize the duration of IL-1β-induced hyperalgesia in LysM-GRK2(+/-) mice. Mechanistically, we show that GRK2(+/-) macrophages produce less IL-10 in vitro. In addition, intrathecal IL-10 administration attenuated IL-1β-induced hyperalgesia in LysM-GRK2(+/-) mice, whereas it had no effect in wild-type mice. Our data uncover a key role for monocytes/macrophages in promoting resolution of inflammatory hyperalgesia via a mechanism dependent on IL-10 signaling in dorsal root ganglia. ⋯ We show that IL-10-producing monocytes/macrophages promote resolution of transient inflammatory hyperalgesia. Additionally, we show that reduced monocyte/macrophage GRK2 impairs resolution of hyperalgesia and reduces IL-10 production. We propose that low GRK2 expression and/or impaired IL-10 production by monocytes/macrophages represent peripheral biomarkers for the risk of developing chronic pain after inflammation.
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Studies about clinical pain in schizophrenia are rare. Conclusions on pain sensitivity in people with schizophrenia are primarily based on experimental pain studies. This review attempts to assess clinical pain, that is, everyday pain without experimental manipulation, in people with schizophrenia. PubMed, PsycINFO, Embase.com, and Cochrane were searched with terms related to schizophrenia and pain. Methodological quality was assessed with the Mixed Methods Appraisal Tool. Fourteen studies were included. Persons with schizophrenia appear to have a diminished prevalence of pain, as well as a lower intensity of pain when compared to persons with other psychiatric diseases. When compared to healthy controls, both prevalence and intensity of pain appear to be diminished for persons with schizophrenia. However, it was found that this effect only applies to pain with an apparent medical cause, such as headache after lumbar puncture. For less severe situations, prevalence and intensity of pain appears to be comparable between people with schizophrenia and controls. Possible underlying mechanisms are discussed. Knowledge about pain in schizophrenia is important for adequate pain treatment in clinical practice. ⋯ This review presents a valuable insight into clinical pain in people with schizophrenia.