Pain
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In our prospective cross-sectional study, we comprehensively characterized Parkinson disease (PD)-related pain in monocentrically recruited patients with PD using standardized tools of pain assessment and categorization. One hundred fifty patients were systematically interviewed and filled in questionnaires for pain, depression, motor, and nonmotor symptoms. Patients with PD-related pain (PD pain), patients without PD-related pain (no PD pain), and patients without pain (no pain) were compared. ⋯ Parkinson disease-related pain was most frequently located in the feet (51/90, 57%), mainly at the toe joints (22/51, 43%). 38/90 (42%) patients with PD-related pain received analgesic medication with nonsteroidal anti-inflammatory drugs being the most frequently used (31/42, 82%) and opioids most effective (70% pain reduction of individual maximum pain intensities, range 22%-100%, confidence interval 50%-90%). All patients received oral PD treatment; however, levodopa equivalent dose showed no correlation with mean pain intensities (Spearman ρ = 0.027, P > 0.05). Our data provide a comprehensive analysis of PD-related pain, giving evidence for mainly non-neuropathic podalgia, which bears the potential to rethink assessment and analgesic treatment of pain in PD in clinical practice.
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Research on the geographic distribution of pain and arthritis outcomes, especially at the county level, is limited. This is a high-priority topic, however, given the heterogeneity of subnational and substate regions and the importance of county-level governments in shaping population health. Our study provides the most fine-grained picture to date of the geography of pain in the United States. ⋯ Severe joint pain is also more common in counties with more female individuals, separated or divorced residents, more high school noncompleters, fewer chiropractors, and higher opioid prescribing rates. Activity limitations are more common in counties with higher percentages of uninsured people. Our findings show that different spatial processes shape the distribution of different arthritis-related pain outcomes, which may inform local policies and programs to reduce the risk of arthritis and its consequences.
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Recent evidence highlights the importance of the neuroimmune interface, including periphery-to-central nervous system (CNS) neuroimmune crosstalk, in chronic pain. Although neuroinflammatory processes have been implicated in central sensitization for a long time, their potential neuroprotective and analgesic effects remain relatively elusive. We have explored the relationships between cytokine expression and symptom severity, and candidates for periphery-to-CNS crosstalk. ⋯ The cytokines CCL11, CD5, IL8, and MMP-10 were elevated in the CSF, had positive correlations between CSF and serum levels, and associated in a nonlinear manner with back, but not leg, pain intensity in the LDH, but not the DDD, group. In conclusion, we found evidence for neuroimmune activation in the CNS of both patient groups in the absence of systemic inflammation and signs of a communication between CSF and serum. Complex and disease-specific associations were found between cytokines in CSF and back pain intensity.
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Visceral pain is a leading cause of morbidity in inflammatory bowel disease (IBD), contributing significantly to reduced quality of life. Currently available analgesics often lack efficacy or have intolerable side effects, driving the need for a more complete understanding of the mechanisms causing pain. Whole transcriptome gene expression analysis was performed by bulk RNA sequencing of colonic biopsies from patients with ulcerative colitis (UC) and Crohn's disease (CD) reporting abdominal pain and compared with noninflamed control biopsies. ⋯ These effects were inhibited by the AT 1 receptor antagonist valsartan. Findings from our study identify AT 1 receptor-mediated colonic nociceptor activation as a novel pathway of visceral nociception in patients with UC. This work highlights the potential utility of angiotensin receptor blockers, such as valsartan, as treatments for pain in IBD.
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Metabolism is inextricably linked to every aspect of cellular function. In addition to energy production and biosynthesis, metabolism plays a crucial role in regulating signal transduction and gene expression. Altered metabolic states have been shown to maintain aberrant signaling and transcription, contributing to diseases like cancer, cardiovascular disease, and neurodegeneration. ⋯ By linking metabolic disturbance of dorsal root ganglia to transcriptome reprogramming, this study enhances our understanding of the mechanisms underlying persistent nociceptive sensitization. These findings imply that impaired mitochondrial pyruvate oxidation may drive chronic pain, possibly by impacting transcriptomic regulation. Exploring these metabolite-driven mechanisms further might reveal novel therapeutic targets for intractable pain.