The journal of pain : official journal of the American Pain Society
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There is growing interest in the role that positive aspects of psychological adjustment, such as pain acceptance, hope, and optimism, may play in explaining adjustment in persons suffering from persistent pain. This study conducted in obese patients with persistent musculoskeletal pain (N = 89) examined the degree to which pain acceptance and hope explained pain intensity, pain unpleasantness, psychological distress, and pain-related disability, after controlling for the effects of optimism. In correlational analyses, pain acceptance and optimism were associated with psychological distress and pain disability with hope being related to only psychological distress. Pain acceptance, optimism, and hope were not significantly associated with pain. Hierarchical linear regression (HLR) analyses found that pain acceptance remained a significant predictor of psychological distress and pain disability after controlling for optimism, demographic, and medical variables. HLR analyses found that hope was not a significant predictor of psychological distress after controlling for optimism, pain acceptance, and demographic and medical variables. The results of this study are important because they indicate that pain acceptance, hope, and optimism are all related to pain adjustment. They also highlight the importance of controlling for optimism when examining the effects of pain acceptance and hope on pain adjustment. ⋯ In a sample of obese patients with persistent musculoskeletal pain, pain acceptance was a significant predictor of psychological distress and pain disability even after controlling for optimism, demographic, and medical variables. These results add to the growing literature on the importance of pain acceptance in understanding adjustment to persistent pain.
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Several case-control studies have been conducted that examine the association between autonomic variables and persistent pain conditions; however, there is a surprising dearth of published studies in this area that have focused on temporomandibular disorders (TMD). The current study presents autonomic findings from the baseline case-control study of the OPPERA (Orofacial Pain: Prospective Evaluation and Risk Assessment) cooperative agreement. Measures of arterial blood pressure, heart rate, heart rate variability, and indirect measures of baroreflex sensitivity were assessed at rest and in response to a physical (orthostatic) and psychological (Stroop) stressors in 1,633 TMD-free controls and 185 TMD cases. In bivariate and demographically adjusted analyses, greater odds of TMD case status were associated with elevated heart rates, reduced heart rate variability, and reduced surrogate measures of baroreflex sensitivity across all experimental procedures. Principal component analysis was undertaken to identify latent constructs revealing 5 components. These findings provide evidence of associations between autonomic factors and TMD. Future prospective analyses in the OPPERA cohort will determine if the presence of these autonomic factors predicts increased risk for developing new onset TMD. ⋯ This article reports autonomic findings from the OPPERA Study, a large prospective cohort study designed to discover causal determinants of TMD pain. Findings indicate statistically significant differences between TMD cases and controls across multiple autonomic constructs at rest and during both physical and psychologically challenging conditions. Future analyses will determine whether these autonomic factors increase risk for new onset TMD.
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Glial cell line-derived neurotrophic factor (GDNF), a survival-promoting factor for a subset of nociceptive small-diameter neurons, has been shown to exert analgesic effects on neuropathic pain. However, its detailed mechanisms of action are still unknown. In the present study, we investigated the site-specific analgesic effects of GDNF in the neuropathic pain state using lentiviral vector-mediated GDNF overexpression in mice with left fifth lumbar (L5) spinal nerve ligation (SNL) as a neuropathic pain model. A lentiviral vector expressing both GDNF and enhanced green fluorescent protein (EGFP) was constructed and injected into the left dorsal spinal cord, uninjured fourth lumbar (L4) dorsal root ganglion (DRG), injured L5 DRG, or plantar skin of mice. In SNL mice, injection of the GDNF-EGFP-expressing lentivirus into the dorsal spinal cord or uninjured L4 DRG partially but significantly reduced the mechanical allodynia in association with an increase in GDNF protein expression in each virus injection site, whereas injection into the injured L5 DRG or plantar skin had no effects. These results suggest that GDNF exerts its analgesic effects in the neuropathic pain state by acting on the central terminals of uninjured DRG neurons and/or on the spinal cells targeted by the uninjured DRG neurons. ⋯ This article shows that GDNF exerts its analgesic effects on neuropathic pain by acting on the central terminals of uninjured DRG neurons and/or on the spinal cells targeted by these neurons. Therefore, research focusing on these GDNF-dependent neurons in the uninjured DRG would provide a new strategy for treating neuropathic pain.
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Genetic factors play a role in the etiology of persistent pain conditions, putatively by modulating underlying processes such as nociceptive sensitivity, psychological well-being, inflammation, and autonomic response. However, to date, only a few genes have been associated with temporomandibular disorders (TMD). This study evaluated 358 genes involved in pain processes, comparing allelic frequencies between 166 cases with chronic TMD and 1,442 controls enrolled in the OPPERA (Orofacial Pain: Prospective Evaluation and Risk Assessment) study cooperative agreement. To enhance statistical power, 182 TMD cases and 170 controls from a similar study were included in the analysis. Genotyping was performed using the Pain Research Panel, an Affymetrix gene chip representing 3,295 single nucleotide polymorphisms, including ancestry-informative markers that were used to adjust for population stratification. Adjusted associations between genetic markers and TMD case status were evaluated using logistic regression. The OPPERA findings provided evidence supporting previously reported associations between TMD and 2 genes: HTR2A and COMT. Other genes were revealed as potential new genetic risk factors for TMD, including NR3C1, CAMK4, CHRM2, IFRD1, and GRK5. While these findings need to be replicated in independent cohorts, the genes potentially represent important markers of risk for TMD, and they identify potential targets for therapeutic intervention. ⋯ Genetic risk factors for TMD pain were explored in the case-control component of the OPPERA cooperative agreement, a large population-based prospective cohort study. Over 350 candidate pain genes were assessed using a candidate gene panel, with several genes displaying preliminary evidence for association with TMD status.