Pain
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Evidence from randomized controlled studies shows that reconceptualizing pain improves patients' knowledge of pain biology, reduces catastrophizing thoughts, and improves pain and function. However, causal relationships between these variables remain untested. It is hypothesized that reductions in catastrophizing could mediate the relationship between improvements in pain knowledge and improvements in pain and function. ⋯ Similar trends were found in models with function as the outcome. Our findings indicate that change in catastrophizing did not mediate the effect of pain knowledge acquisition on change in pain or function. The strength of this conclusion is moderated, however, if patient-clinician relational factors are conceptualized as a consequence of catastrophizing, rather than a cause.
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Little is known about long-term pain and function outcomes among patients with chronic noncancer pain initiating chronic opioid therapy (COT). In the Middle-Aged/Seniors Chronic Opioid Therapy study of patients identified through electronic pharmacy records as initiating COT for chronic noncancer pain, we examined the relationships between level of opioid use (over the 120 days before outcome assessment) and pain and activity interference outcomes at 4- and 12-month follow-ups. Patients aged 45+ years (N = 1477) completed a baseline interview; 1311 and 1157 of these comprised the 4- and 12-month analysis samples, respectively. ⋯ A similar pattern was observed for pain intensity at 4 months and for activity interference at both time points. Better outcomes in the minimal/no use group could reflect pain improvement leading to opioid discontinuation. The similarity in outcomes of regular/higher-dose and intermittent/lower-dose opioid users suggests that intermittent and/or lower-dose use vs higher-dose use may confer risk reduction without reducing benefits.
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Multicenter Study
COMPLEXITY, COMORBIDITY AND HEALTHCARE COSTS ASSOCIATED WITH CHRONIC WIDESPREAD PAIN IN PRIMARY CARE.
The objective was to estimate the prevalence of chronic widespread pain (CWP) and compare the quality-of-life (QoL), cardiovascular risk factors, comorbidity, complexity, and health costs with the reference population. A multicenter case-control study was conducted at 3 primary care centers in Barcelona between January and December 2012: 3048 randomized patients were evaluated for CWP according to the American College of Rheumatology definition. Questionnaires on pain, QoL, disability, fatigue, anxiety, depression, and sleep quality were administered. ⋯ In conclusion, the average patient with CWP has a worse QoL and a greater burden of mental health disorders and cardiovascular risk. The average annual cost associated with CWP is nearly 3 times higher than that of patients without CWP, controlling for other clinical factors. These findings have implications for disease management and budgetary considerations.
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Colonoscopy is an invaluable tool for the screening and diagnosis of many colonic diseases. For most colonoscopies, moderate sedation is used during the procedure. However, insufflation of the colon produces a nociceptive stimulus that is usually accompanied by facial grimacing/groaning while under sedation. ⋯ The pattern of the activation is similar to that previously observed during nociceptive stimuli in awake healthy individuals, suggesting that this approach may be used to evaluate brain activity evoked by nociceptive stimuli under sedation, when there is incomplete analgesia. Although some patients report recollection of procedural pain after the procedure, the effects of repeated nociceptive stimuli in surgical patients may contribute to postoperative changes including chronic pain. The results from this study indicate that NIRS may be a suitable technology for continuous nociceptive afferent monitoring in patients undergoing sedation and could have applications under sedation or anesthesia.
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Changes in the nerve's microenvironment and local inflammation resulting from peripheral nerve injury participate in nerve sensitization and neuropathic pain development. Taking part in these early changes, disruption of the blood-nerve barrier (BNB) allows for infiltration of immunocytes and promotes the neuroinflammation. However, molecular mechanisms engaged in vascular endothelial cells (VEC) dysfunction and BNB alterations remain unclear. ⋯ In vitro, activation of Toll-like receptor 4 in VEC downregulated the components of Hh pathway and altered the endothelial functional state. Inhibition of Hh signaling in the ScN of naive rats mimicked the biochemical and functional alterations observed after CCI and was, on its own, sufficient to evoke local neuroinflammation and sustained mechanical allodynia. Alteration of the Hh signaling pathway in VEC associated with peripheral nerve injury, is involved in BNB disruption and local inflammation, and could thus participate in the early changes leading to the peripheral nerve sensitization and, ultimately, neuropathic pain development.