Pain
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Late-life depression and pain more often co-occur than can be explained by chance. Determinants of pain in late-life depression are unknown, even though knowledge on possible determinants of pain in depression is important for clinical practice. Therefore, the objectives of the present study were 1) to describe pain characteristics of depressed older adults and a nondepressed comparison group, and 2) to explore physical, lifestyle, psychological, and social determinants of acute and chronic pain intensity, disability, and multisite pain in depressed older adults. ⋯ Adjusted for demographic, physical, and lifestyle characteristics, multinomial logistic regression analyses showed increased odds ratios (OR) for depression in acute pain (OR 3.010; P=0.005) and chronic pain (OR 4.544, P<0.001). In addition, linear regression analyses showed that acute and chronic pain intensity, disability, and multisite pain were associated with several biopsychosocial determinants, of which anxiety was most pronounced. Further research could focus on the temporal relationship between anxiety, late-life depression, and pain.
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Neuropathic pain affects millions of people worldwide, causing substantial disability and greatly impairing quality of life. Commonly used analgesics or antihyperalgesic compounds are generally characterized by limited therapeutic outcomes. Thus, there is a compelling need for novel therapeutic strategies able to prevent nervous tissue alterations responsible for chronic pain. ⋯ In L4-L5 dorsal root ganglia, RgIA prevented morphometric changes and reduced the inflammatory infiltrate consistent with a disease-modifying effect. In the dorsal horn of the spinal cord, RgIA prevented CCI-induced activation of microglia and astrocytes. These data suggest that RgIA-like compounds may represent a novel class of therapeutics for neuropathic pain that protects peripheral nervous tissues as well as prevents central maladaptive plasticity by inhibiting glial cell activation.
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In healthy individuals, emotions modulate pain and spinal nociception according to a valence linear trend (ie, pain/nociception is highest during negative emotions and lowest during positive emotions). However, emerging evidence suggests that emotional modulation of pain (but not spinal nociception) is disrupted in fibromyalgia and disorders associated with chronic pain risk (eg, major depression, insomnia). The present study attempted to extend this work and to examine whether women with premenstrual dysphoric disorder (PMDD), a cyclical syndrome associated with debilitating affective symptoms during the late-luteal (premenstrual) phase of the menstrual cycle, is also associated with disrupted emotional modulation of pain. ⋯ Statistically powerful linear mixed model analyses confirmed that pictures evoked the intended emotional states in both groups across all menstrual phases. Furthermore, emotion modulated pain and NFR according to a valence linear trend in both groups and across all menstrual phases. Thus, PMDD-related affective disturbance is not associated with a failure to emotionally modulate pain, suggesting that PMDD does not share this pain phenotype with major depression, insomnia, and fibromyalgia.
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Emerging evidence suggests that the appraisal of pain and disability in terms of justice-related themes contributes to adverse pain outcomes. To date, however, research on the relation between perceived injustice and pain outcomes has focused primarily on individuals with musculoskeletal injuries. The primary aim of this study was to investigate the role of perceived injustice in the prediction of pain and disability after total knee arthroplasty (TKA). ⋯ Pain catastrophizing contributed significant unique variance to the prediction of postsurgical disability. The current findings add to a growing body of evidence supporting the prognostic value of perceived injustice in the prediction of adverse pain outcomes. The results suggest that psychosocial interventions designed to target perceptions of injustice and pain catastrophizing before surgery might contribute to more positive recovery trajectories after TKA.
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The p38α mitogenous activated protein kinase (MAPK) cell signaling pathway is a key mechanism of microglia activation and has been studied as a target for neuropathic pain. The effect of UR13870, a p38α MAPK inhibitor, on microglia expression in the anterior cingulate cortex (ACC) and spinal dorsal horn was addressed after T9 contusion spinal cord injury (SCI) in the rat, in addition to behavioral testing of pain-related aversion and anxiety. Administration of intravenous UR13870 (1mg/kg i.v.) and pregabalin (30 mg/kg i.v.) reduced place escape avoidance paradigm (PEAP) but did not affect open-field anxiety behavior 42 days after SCI. ⋯ UR13870 (10mg/kg p.o.) treatment significantly reduced OX-42, metabotropic glutamate type 5 receptor (mGluR5), and NMDA (N-methyl-d-aspartate) 2B subunit receptor (NR2B) expression in the ACC after SCI. To conclude, oral treatment with a p38α MAPK inhibitor reduces the affective behavioral component of pain after SCI in association with a reduction of microglia and specific glutamate receptors within the ACC. Nevertheless the role of neuroinflammatory processes within the vicinity of the SCI site in the development of affective neuropathic pain cannot be excluded.