The journal of pain : official journal of the American Pain Society
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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.
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Randomized Controlled Trial
Reduction of bodily pain in response to an online positive activities intervention.
Inducing temporary positive states reduces pain and increases pain tolerance in laboratory studies. We tested whether completing positive activities in one's daily life produces long-term reductions in self-reported bodily pain in a randomized controlled trial of an online positive activities intervention. Participants recruited via the Web were randomly assigned to complete 0, 2, 4, or 6 positive activities administered online over a 6-week period. Follow-up assessments were collected at the end of 6 weeks and at 1, 3, and 6 months postintervention. We used linear mixed effects models to examine whether the intervention reduced pain over time among those who had a score <67 on the bodily pain subscale of the Short Form-36 at baseline (N = 417; pain scores range from 0 to 100; higher scores indicate less pain). Mean pain scores improved from baseline to 6 months in the 2-activity (55.7 to 67.4), 4-activity (54.2 to 71.0), and 6-activity (50.9 to 67.9) groups. Improvements were significantly greater (P < .05) in the 4-activity and 6-activity groups than in the 0-activity control group (54.1 to 62.2) in unadjusted and adjusted models. This study suggests that positive activities administered online can reduce bodily pain in adults with at least mild to moderate baseline pain. ⋯ This study demonstrates that teaching people simple positive activities can decrease reported levels of bodily pain; moreover, these activities can be administered over the internet, a potential avenue for broadly disseminating health interventions at relatively low costs and with high sustainability.
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Aromatase inhibitors (AIs), which are used to treat breast cancer, inhibit estrogen production in postmenopausal women. AI-associated musculoskeletal symptoms occur in approximately half of treated women and lead to treatment discontinuation in 20 to 30%. The etiology may be due in part to estrogen deprivation. In premenopausal women, lower estrogen levels have been associated with increased pain as well as with impairment of descending pain inhibitory pathways, which may be a risk factor for developing chronic pain. We prospectively tested whether AI-induced estrogen deprivation alters pain sensitivity, thereby increasing the risk of developing AI-associated musculoskeletal symptoms. Fifty postmenopausal breast cancer patients underwent pressure pain testing and conditioned pain modulation (CPM) assessment prior to AI initiation and after 3 and 6 months. At baseline, 26 of 40 (65%) assessed patients demonstrated impaired CPM, which was greater in those who had previously received chemotherapy (P = .006). No statistically significant change in pressure pain threshold or CPM was identified following estrogen deprivation. In addition, there was no association with either measure of pain sensitivity and change in patient-reported pain with AI therapy. AI-associated musculoskeletal symptoms are not likely due to decreased pain threshold or impaired CPM prior to treatment initiation, or to effects of estrogen depletion on pain sensitivity. ⋯ This article presents our findings of the effect of estrogen deprivation on objective measures of pain sensitivity. In postmenopausal women, medication-induced estrogen depletion did not result in an identifiable change in pressure pain threshold or CPM. Impaired CPM may be associated with chemotherapy.
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The pathogenesis of complex regional pain syndrome (CRPS) is unresolved, but tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) are elevated in experimental skin blister fluid from CRPS-affected limbs, as is tryptase, a marker for mast cells. In the rat fracture model of CRPS, exaggerated sensory and sympathetic neural signaling stimulate keratinocyte and mast cell proliferation, causing the local production of high levels of inflammatory cytokines leading to pain behavior. The current investigation used CRPS patient skin biopsies to determine whether keratinocyte and mast cell proliferation occur in CRPS skin and to identify the cellular source of the up-regulated TNF-α, IL-6, and tryptase observed in CRPS experimental skin blister fluid. Skin biopsies were collected from the affected skin and the contralateral mirror site in 55 CRPS patients and the biopsy sections were immunostained for keratinocyte, cell proliferation, mast cell markers, TNF-α, and IL-6. In early CRPS, keratinocytes were activated in the affected skin, resulting in proliferation, epidermal thickening, and up-regulated TNF-α and IL-6 expression. In chronic CRPS, there was reduced keratinocyte proliferation, leading to epidermal thinning in the affected skin. Acute CRPS patients also had increased mast cell accumulation in the affected skin, but there was no increase in mast cell numbers in chronic CRPS. ⋯ The results of this study support the hypotheses that CRPS involves activation of the innate immune system, with keratinocyte and mast cell activation and proliferation, inflammatory mediator release, and pain.
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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.