The journal of pain : official journal of the American Pain Society
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Observational Study
Multivariable modeling of phenotypic risk factors for first-onset TMD: the OPPERA prospective cohort study.
Incidence of temporomandibular disorder (TMD) was predicted with multivariable models that used putative risk factors collected from initially TMD-free individuals in the Orofacial Pain: Prospective Evaluation and Risk Assessment (OPPERA) study. The 202 baseline risk factors included sociodemographic and clinical characteristics, measures of general health status, experimental pain sensitivity, autonomic function, and psychological distress. Study participants (n = 2,737) were then followed prospectively for a median of 2.8 years to ascertain cases of first-onset TMD. Lasso regression and random forest models were used to predict incidence of first-onset TMD using all of the aforementioned measures. Variable importance scores identified the most important risk factors, and their relationship with TMD incidence was illustrated graphically using partial dependence plots. Two of the most important risk factors for elevated TMD incidence were greater numbers of comorbid pain conditions and greater extent of nonspecific orofacial symptoms. Other important baseline risk factors were preexisting bodily pain, heightened somatic awareness, and greater extent of pain in response to examiners' palpation of the head, neck, and body. Several demographic variables persisted as risk factors even after adjusting for other OPPERA variables, suggesting that environmental variables not measured in OPPERA may also contribute to first-onset TMD. ⋯ Multivariable methods were used to identify the most important predictors of first-onset TMD in the OPPERA study. Important variables included comorbid pain conditions, preexisting pain, and somatic awareness. Demographic characteristics, which probably reflect environmental variables not measured in OPPERA, also appear to play an important role in the etiology of TMD.
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Neurotoxicity is the limiting side effect of the anticancer agent oxaliplatin. A tangled panel of symptoms, sensory loss, paresthesia, dysesthesia, and pain may be disabling for patients and adversely affect their quality of life. To elucidate the morphologic and molecular alterations that occur in the nervous system during neuropathy, rats were daily injected with 2.4 mg kg(-1) oxaliplatin intraperitoneally. A progressive decrease in the pain threshold and hypersensitivity to noxious and nonnoxious stimuli were evidenced during the treatment (7, 14, 21 days). On day 21, morphometric alterations were detectable exclusively in the dorsal root ganglia, whereas the activating transcription factor 3 and neurofilament (heavy-chain) expression changed dramatically in both the nerves and ganglia. Inflammatory features were not highlighted. Interestingly, satellite cells exhibited signs of activation. Glial modulation was characterized in the spinal cord and brain areas involved in pain signaling. On the 21st day, spinal astrocytes increased numerically whereas the microglial population was unaltered. The number of glial cells in the brain differed according to the zone and treatment time points. In particular, on day 21, a significant astrocyte increase was measured in the anterior cingulate cortex, somatosensory area 1, neostriatum, ventrolateral periaqueductal gray, and nucleus raphe magnus. ⋯ These data highlight the relevance of glial cells in chemotherapy-induced neurotoxicity as part of the investigation of the role that specific brain areas play in neuropathy.
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Observational Study
Pain sensitivity and autonomic factors associated with development of TMD: the OPPERA prospective cohort study.
Multiple studies report that individuals with chronic temporomandibular disorder (TMD) have enhanced sensitivity to experimental pain. Additionally, chronic TMD cases show altered autonomic function, including elevated heart rate and reduced heart rate variability. However, causal inferences regarding the association between TMD and pain sensitivity and autonomic function cannot be drawn from these cross-sectional observations. The prospective Orofacial Pain: Prospective Evaluation and Risk Assessment (OPPERA) study examines whether measures of pain sensitivity or cardiac autonomic function provide predictive value in TMD incidence. A cohort of 2,737 initially TMD-free participants was followed for up to 5.2 years, during which time 260 developed first-onset TMD. Fourteen of 39 experimental pain measures produced significant hazard ratios, such that greater pain sensitivity was associated with greater TMD incidence. A single autonomic measure-heart rate at rest-was also associated significantly with greater TMD incidence. In contrast, using the same measures of pain sensitivity and cardiac autonomic function, we previously reported a larger group of variables that was significantly associated with chronic TMD in the OPPERA case-control study. Future studies should investigate whether premorbid pain sensitivity or autonomic function more specifically predicts risk of developing chronic TMD than first-onset TMD. ⋯ Our previous case-control studies showed that associations with both pain sensitivity and cardiac autonomic function are profound in chronic TMD cases. Here we show that some measures of enhanced pain sensitivity contribute modestly to the risk of developing TMD whereas autonomic dysregulation appears to confer little or no risk for TMD incidence.
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To improve U.S. pain education and promote interinstitutional and interprofessional collaborations, the National Institutes of Health Pain Consortium has funded 12 sites to develop Centers of Excellence in Pain Education (CoEPEs). Each site was given the tasks of development, evaluation, integration, and promotion of pain management curriculum resources, including case studies that will be shared nationally. Collaborations among schools of medicine, dentistry, nursing, pharmacy, and others were encouraged. The John D. Loeser CoEPE is unique in that it represents extensive regionalization of health science education, in this case in the region covering the states of Washington, Wyoming, Alaska, Montana, and Idaho. This paper describes a blueprint of pain content and teaching methods across the University of Washington's 6 health sciences schools and provides recommendations for improvement in pain education at the prelicensure level. The Schools of Dentistry and Physician Assistant provide the highest percentage of total required curriculum hours devoted to pain compared with the Schools of Medicine, Nursing, Pharmacy, and Social Work. The findings confirm the paucity of pain content in health sciences curricula, missing International Association for the Study of Pain curriculum topics, and limited use of innovative teaching methods such as problem-based and team-based learning. ⋯ Findings confirm the paucity of pain education across the health sciences curriculum in a CoEPE that serves a large region in the United States. The data provide a pain curriculum blueprint that can be used to recommend added pain content in health sciences programs across the country.
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The temporal dynamics of the blood oxygen level-dependent (BOLD) signal, especially for painful stimulations, is not completely understood. In this study, the BOLD signal response to a long painful electrical stimulation (a continuous painful stimulation of 2 minutes) is directly compared to that of a short painful stimulation (four 30-second periods of painful stimulation interleaved with 30-second rest) in an effort to further probe the relationship between the temporal dynamics of the BOLD signal during constant-intensity pain stimulation. Time course analysis showed that both stimulation protocols produced 3 similarly timed peaks in both data sets, suggesting an early and delayed BOLD response to painful stimulation initiation, and a response related to stimulus termination. Despite the continuous stimulation, the BOLD signal returned to baseline in the 2-minute task. Even with this signal discrepancy, however, the activation maps of the 2 pain tasks differed only slightly, suggesting that the bulk of the activation is determined by the sharp rise in BOLD signal with stimulus onset. These findings imply that the BOLD signal response time course is not directly reflective of pain perception. ⋯ This article demonstrates that the BOLD signal for a painful stimulation contains multiple peaks and does not maintain the constant level during stimulation that is assumed in typical analysis. Although these dynamics should be accounted for in future studies because of their ability to confound results, their presence did not significantly alter the overall group maps.