The journal of pain : official journal of the American Pain Society
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Effective management of patients with pain requires accurate information about the prevalence, outcomes, and co-occurrence of common pain conditions. However, the transition from ICD-9-CM to ICD-10-CM diagnostic coding in 2015 left researchers without methods for comparing the prevalence of pain conditions before and after the transition. In this study, we developed and assessed a diagnostic framework to serve as a crosswalk between ICD-9-CM and ICD-10-CM diagnosis codes for common pain-related health conditions. ⋯ This allows the tool to serve as a foundation for a broad array of pain-related health services research utilizing electronic databases. PERSPECTIVE: This article details the development and assessment of the Pain Condition ICD-9-CM to ICD-10-CM Crosswalk, a diagnostic framework for assessing pain condition prevalence across the ICD-9-CM to ICD-10-CM transition. This framework can serve as a standardized tool for research on pain conditions, including health services and epidemiologic research.
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Using the EEG recordings of patients with endometriosis-related chronic pelvic pain, we have examined the effective connectivity within the cortical pain-related network during rest and during pain-related imagery. During rest, an altered connectivity was hypothesized between cortical somatosensory pain areas and regions involved in emotional and cognitive modulation of pain. During pain-related imagery, alterations in prefrontal-temporal connectivity were expected. ⋯ Results of this study open up new directions in chronic pain research aimed at exploring the beta band connectivity alterations. PERSPECTIVE: This study examined the pain system's dynamics in endometriosis patients with chronic pelvic pain during resting-state and pain-related mental imagery. The results could contribute to the development of new therapies using guided mental imagery.
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Our preliminary experiment indicated the activation of with-nolysine kinases 1 (WNK1) in bone cancer pain (BCP) rats. This study aimed to investigate the underlying mechanisms via which WNK1 contributed to BCP. A rat model of BCP was induced by Walker-256 tumor cell implantation. ⋯ PERSPECTIVE: Our findings demonstrated that the WNK1-SPAK/OSR1 signaling contributed to BCP in rats via regulating NKCC1 and KCC2. Suppressing this pathway reduced pain behaviors. Based on these findings, the WNK1-SPAK/OSR1 signaling may be a potential target for BCP therapy.