Pain
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Cancer and its treatment can have lasting consequences on somatosensation, including pain, which is often underrecognized and undertreated. Research characterizing the impact of cancer on pain and sensory processing in survivors of childhood cancer is scarce. This study aimed to quantify generalized differences in pain and sensory processing in survivors of childhood cancer compared with reference data using a standardized thermal and mechanical quantitative sensory testing (QST) protocol. ⋯ Several risk factors for changes in sensory processing were identified, including current age, history of leukemia, certain treatment exposures (eg, vincristine cumulative dose, major surgery, and bone marrow or stem cell transplant), time off treatment, and higher anxiety and pain catastrophizing scores. Overall, this study demonstrated that somatosensory changes are prevalent in survivors of childhood cancer years after the completion of treatment. Future research is needed to understand long-term implications of altered somatosensation in this complex population.
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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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Identifying the genetic determinants of pain is a scientific imperative given the magnitude of the global health burden that pain causes. Here, we report a genetic screen for nociception, performed under the auspices of the International Mouse Phenotyping Consortium. A biased set of 110 single-gene knockout mouse strains was screened for 1 or more nociception and hypersensitivity assays, including chemical nociception (formalin) and mechanical and thermal nociception (von Frey filaments and Hargreaves tests, respectively), with or without an inflammatory agent (complete Freund's adjuvant). ⋯ Two of the 13 genes (Gria1 and Htr3a) have been previously reported with nociception-related phenotypes in genetically engineered mouse strains and represent useful benchmarking standards. One of the 13 genes (Cnrip1) is known from human studies to play a role in pain modulation and the knockout mouse reported herein can be used to explore this function further. The remaining 10 genes (Abhd13, Alg6, BC048562, Cgnl1, Cp, Mmp16, Oxa1l, Tecpr2, Trim14, and Trim2) reveal novel pathways involved in nociception and may provide new knowledge to better understand genetic mechanisms of inflammatory pain and to serve as models for therapeutic target validation and drug development.