The journal of pain : official journal of the American Pain Society
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Observational Study
Changes in opioid prescribing for Washington workers' compensation claimants after implementation of an opioid dosing guideline for chronic noncancer pain: 2004 to 2010.
An opioid overdose epidemic emerged in the United States following increased opioid prescribing for chronic noncancer pain. In 2007, Washington State agencies implemented an opioid dosing guideline on safe prescribing for chronic noncancer pain. The objective of this population-based observational study was to evaluate opioid use and dosing before and after guideline implementation. We identified 161,283 workers aged 18 to 64 years with ≥1 opioid prescriptions in Washington Workers' Compensation, April 1, 2004, to December 31, 2010. Prevalence and incidence rates of opioid use were assessed. We compared pre- and postguideline chronic and high-dose use (≥120 mg/d) among incident users. The mean monthly prevalence of opioid use declined by 25.6% between 2004 (14.4%) and 2010 (10.7%). Fewer incident users went on to chronic opioid therapy in the postguideline period (4.7%; 95% confidence interval [CI], 4.5-5.0%) than in the preguideline period (6.3%; 95% CI, 6.1-6.6%). Compared with preguideline incident users, postguideline incident users were 35% less likely to receive high doses (adjusted odds ratio = .65; 95% CI, .59-.71). Although the extent to which decreases were due to the guidelines is uncertain, to our knowledge, this is the first report of significant decreases in chronic and high-dose prescription opioid use among incident users. ⋯ Evidence-based strategies for opioid risk management are needed to help abate the epidemic of opioid-related morbidity and mortality. The study findings suggest that opioid dosing guidelines that specify a "yellow flag" dosing threshold may be a useful tool in preventing escalation of doses into ranges associated with increased mortality risk.
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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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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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To assess the longitudinal gray matter (GM) and white matter (WM) changes between repeated observations 1 year apart in a group of the early clinical stage of migraine patients without aura, and to explore the relationship of such structural changes with headache activity, we studied patients newly diagnosed with episodic migraine lasting 8 to 14 weeks. Optimized voxel-based morphometry and tract-based spatial statistical analyses were used to evaluate changes in GM and WM by using 3-dimensional T1-weighted and diffusion-tensor imaging, respectively. At the 1-year follow-up examination, GM reduction was observed in the dorsolateral and medial part of the superior frontal gyrus, orbitofrontal cortex, hippocampus, precuneus, and primary and secondary somatosensory cortices. No significant differences were found in the fractional anisotropy and longitudinal, radial, and mean diffusivity of WM in migraine patients without aura within a year. Negative results were found for the association between changes in headache activity parameters and GM. Our results indicated that the GM and WM changed in different pathophysiological conditions of migraine patients without aura. The WM probably evolves slowly in the course of migraine chronicity. ⋯ Our study found early involvement of GM reduction of sensory-discriminative brain regions in the pathologic process of migraine, but the WM did not exhibit significant changes in the same time interval. GM reduction in sensory-discriminative brain regions may characterize the pathophysiological features of migraine patients without aura in its early stage.
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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.