European journal of pain : EJP
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The aetiology of Complex Regional Pain Syndrome (CRPS) is unknown. Recent evidence suggests that there may be autoantibodies directed against peripheral nerves, but it is unclear whether such autoantibodies are merely biomarkers or whether they cause or contribute to the underlying pathology. The transfer of disease after injection of a patient's serum or IgG fraction into mice ('passive transfer') is the classic way to demonstrate a functional role of autoantibodies. ⋯ These results lend support to a pathophysiological role for IgG autoantibodies in CRPS.
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Among 385 female kitchen workers, we examined (1) whether mental stress and psychosocial factors at work (job control, skill discretion, supervisor support, co-worker relationships, and hurry) predict multiple-site musculoskeletal pain (MSP; defined as pain at ≥ 3 of seven sites) and (2) reversedly, whether MSP predicts these psychosocial factors. Data were collected by questionnaire at 3-month intervals during 2 years. Trajectory analysis was applied. ⋯ In generalized estimating equations, time-lagged by 3 months, all psychosocial factors but two predicted MSP (1.4-2.1), allowing, e.g. for MSP at baseline, and vice versa, MSP predicted low job control, low supervisor support, and mental stress (1.4-2.0), after adjustment for e.g. the relevant psychosocial factor at baseline. In conclusion, we found that several psychosocial factors predicted MSP and that MSP predicted several psychosocial factors. The results suggest a cumulative process in which adverse psychosocial factors and MSP influence each other.
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Randomized Controlled Trial
The role of depression and catastrophizing in musculoskeletal pain.
Many patients with musculoskeletal pain also suffer from a depressed mood. Catastrophizing is one process that may link depression and pain since it is a key concept in models of both problems. Earlier research has suggested that catastrophizing measures something above and beyond depression. ⋯ Further, having one or the other of the entities was associated with current pain problems and outcome, while having both increased the associations substantially. The replication showed very similar results Our data demonstrate that pain catastrophizing and heightened depressed mood have an additive and adverse effect on the impact of pain, relative to either alone. It suggests that each should be assessed in the clinic and that future research should focus on treatments specifically designed to tackle both depressed mood and catastrophizing.
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This study examined the relationship between microglia activation in the cuneate nucleus (CN) and behavioral hypersensitivity after chronic constriction injury (CCI) of the median nerve. We also investigated effects of local lidocaine pre- and post-treatment on microglia activation and development of hypersensitivity in this model. By immunohistochemistry and immunoblotting, little immunoreactivity of OX-42, a microglia activation marker, was detected in the CN of normal rats. ⋯ Late post-treatment with 1%, 2%, or 5% lidocaine failed to decrease OX-42 immunoreactivity and mechanical hypersensitivity in CCI rats. In conclusion, median nerve injury-induced microglia activation in the CN modulated development of behavioral hypersensitivity. High-concentration lidocaine was effective in decreasing microglia activation in the CN and in attenuating neuropathic pain sensations at the early stage following nerve injury, when microglia had not yet been activated.