Pain
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Although multimodal management of chronic noncancer pain (CNCP) is recommended, long-term treatment utilization patterns among people using opioids are not well known. The Pain and Opioids IN Treatment study recruited Australian adults receiving opioids for CNCP for more than 6 weeks from community pharmacies. Pharmacological (opioid and nonopioid analgesics and psychotropic medicines) and nonpharmacological (physical, mental health, and specialized) treatments used in the previous 12 months and 30 days were collected annually over 4 years (2015-2018). ⋯ This study demonstrates that many Australians taking opioids long-term for CNCP also use nonopioid pharmacological and nonpharmacological treatments. The use of pharmacological treatments including nonsteroidal anti-inflammatory drugs, psychotropic medicines, and gabapentinoids, outside guidelines, warrants review. Furthermore, despite Australia's universal healthcare scheme subsidising some nonpharmacological treatments, overall use of these treatments was associated with having private health insurance, highlighting a need for more equitable service provision.
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Chronic pain is a highly debilitating and difficult to treat condition, which affects the structure of the brain. Although the development of chronic pain is moderately heritable, how disease-related alterations at the microscopic genetic architecture drive macroscopic brain abnormalities is currently largely unknown. Here, we examined alterations in morphometric similarity (MS) and applied an integrative imaging transcriptomics approach to identify transcriptional and cellular correlates of these MS changes, in 3 independent small cohorts of patients with distinct chronic pain syndromes (knee osteoarthritis, low back pain, and fibromyalgia) and age-matched and sex-matched pain-free controls. ⋯ By leveraging transcriptomic data from Allen Human Brain Atlas, we show that cortical MS remodelling in chronic pain spatially correlates with the brain-wide expression of genes related to pain and broadly involved in the glial immune response and neuronal plasticity. Our findings bridge levels to connect genes, cell classes, and biological pathways to in vivo imaging correlates of chronic pain. Although correlational, our data suggest that cortical remodelling in chronic pain might be shaped by multiple elements of the cellular architecture of the brain and identifies several pathways that could be prioritized in future genetic association or drug development studies.
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The lack of a reliable approach to assess quality of pain care hinders quality improvement initiatives. Rule-based natural language processing algorithms were used to extract pain care quality (PCQ) indicators from documents of Veterans Health Administration primary care providers for veterans diagnosed within the past year with musculoskeletal disorders with moderate-to-severe pain intensity across 2 time periods 2013 to 2014 (fiscal year [FY] 2013) and 2017 to 2018 (FY 2017). Patterns of documentation of PCQ indicators for 64,444 veterans and 124,408 unique visits (FY 2013) and 63,427 veterans and 146,507 visits (FY 2017) are described. ⋯ The mean PCQ indicator scores across patient characteristics and types of healthcare facilities were highly stable. Estimates of the frequency of documentation of PCQ indicators have face validity and encourage further evaluation of the reliability, validity, and utility of the measure. A reliable measure of PCQ fills an important scientific knowledge and practice gap.
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Mean pain intensity alone is insufficient to describe pain phenotypes in sickle cell disease (SCD). The objective of this study was to determine impact of day-to-day intraindividual pain variability on patient outcomes in SCD. We calculated metrics of pain variability and pain intensity for 139 participants with <10% missing data in the first 28 days of the Pain in Sickle Cell Epidemiology Study. ⋯ Cluster 2 included individuals with the highest mean pain, highest temporal dependency, highest proportion of days with pain and opioid use, and lowest physical function. Cluster 3 included individuals with high levels of mean pain, highest temporal instability, but with lower temporal dependency, proportion of days with pain and opioid use, and physical function compared with cluster 2. We conclude that intraindividual pain variability is associated with patient outcomes and psychological characteristics in SCD and is useful in delineating phenotypes of pain in SCD.
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We modelled the effects of pain intensity inclusion thresholds (3/10, 4/10, and 5/10 on a 0- to 10-point numerical pain rating scale) on the magnitude of the regression to the mean effect under conditions that were consistent with the sample mean and variance, and intermeasurement correlation observed in clinical trials for the management of chronic pain. All data were modelled on a hypothetical placebo control group. We found a progressive increase in the mean pain intensity as the pain inclusion threshold increased, but this increase was not uniform, having an increasing effect on baseline measurements compared with study endpoint measurements as the threshold was increased. ⋯ At its smallest, the regression to the mean effect was 0.13/10 (95% confidence interval: 0.03/10-0.24/10; threshold: 3/10, baseline mean pain: 6.5/10, SD: 1.6/10, and correlation: 0.44), and at its greatest, it was 0.78/10 (95% confidence interval: 0.63/10-0.94/10; threshold: 5/10, baseline mean pain: 6/10, SD: 1.8/10, and correlation: 0.19). We have shown that using pain inclusion thresholds in clinical trials drives progressively larger regression to the mean effects. We believe that a threshold of 3/10 offers the best compromise between maintaining assay sensitivity (the goal of thresholds) and the size of the regression to the mean effect.