Pain
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Understanding, measuring, and mitigating pain-related suffering is a key challenge for both clinical care and pain research. However, there is no consensus on what exactly the concept of pain-related suffering includes, and it is often not precisely operationalized in empirical studies. Here, we (1) systematically review the conceptualization of pain-related suffering in the existing literature, (2) develop a definition and a conceptual framework, and (3) use machine learning to cross-validate the results. ⋯ We also offer a conceptual framework of pain-related suffering distinguishing 8 dimensions: social, physical, personal, spiritual, existential, cultural, cognitive, and affective. Our data show that pain-related suffering is a multidimensional phenomenon that is closely related to but distinct from pain itself. The present analysis provides a roadmap for further theoretical and empirical development.
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Botulinum toxin (BoNT), a presynaptic inhibitor of acetylcholine (Ach) release at the neuromuscular junction (NMJ), is a successful and safe drug for the treatment of several neurological disorders. However, a wide and recent literature review has demonstrated that BoNT exerts its effects not only at the "periphery" but also within the central nervous system (CNS). Studies from animal models, in fact, have shown a retrograde transport to the CNS, thus modulating synaptic function. ⋯ In this new light, BoNT might interfere with the activity of spinal, brain stem, and cortical circuitry, modulating excitability and the functional organization of CNS in healthy conditions. Botulinum toxins efficacy on CNP is the result of a wide and complex action on many and diverse mechanisms at the basis of the maladaptive plasticity, the core of the pathogenesis of CNP. This systematic review aims to discuss in detail the BoNT's mechanisms and effects on peripheral and central neuroplasticity, at the basis for the clinical efficacy in CNP syndromes.
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Some patients with back pain contribute disproportionately to high healthcare costs; however, characteristics of high-cost users with back pain are not well defined. We described high-cost healthcare users based on total costs among a population-based cohort of adults with back pain within the Ontario government's single-payer health system across sociodemographic, health, and behavioural characteristics. We conducted a population-based cohort study of Ontario adult (aged 18 years or older) respondents of the Canadian Community Health Survey (CCHS) with back pain (2003-2012), linked to administrative data (n = 36,605; weighted n = 2,076,937, representative of Ontario). ⋯ High-cost users tended to be current/former smokers, obese, and report fair/poor mental health. High-cost users (based on total costs) among adults with back pain account for nearly half of all healthcare spending over a 1-year period and are associated with older age, lower income, comorbidities, and fair/poor general health. Findings identify characteristics associated with a high-risk group for back pain to inform healthcare and public health strategies that target upstream determinants.
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Knowledge is needed regarding mechanisms acting between physical activity (PA) and chronic pain. We investigated whether cold pain tolerance mediates an effect of leisure-time physical activity on the risk of chronic pain 7 to 8 years later using consecutive surveys of the population-based Tromsø Study. We included participants with information on baseline leisure-time PA (LTPA) and the level of cold pressor-assessed cold pain tolerance, who reported chronic pain status at follow-up as any of the following: chronic pain for ≥3 months, widespread chronic pain, moderate-to-severe chronic pain, or widespread moderate-to-severe chronic pain. ⋯ Statistically significantly mediated RR for widespread moderate-to-severe chronic pain was 0.988 (0.977-0.999); total effect RR was 0.77 (0.64-0.94). This shows small mediation of the effect of LTPA through pain tolerance on 2 moderate-to-severe chronic pain types. This suggests pain tolerance to be one possible mechanism through which PA modifies the risk of moderate-to-severe chronic pain types with and without widespread pain.
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The pressing need for safer, more efficacious analgesics is felt worldwide. Preclinical tests in animal models of painful conditions represent one of the earliest checkpoints novel therapeutics must negotiate before consideration for human use. Traditionally, the pain status of laboratory animals has been inferred from evoked nociceptive assays that measure their responses to noxious stimuli. ⋯ The analgesia conferred by meloxicam and gabapentin was compared in the monosodium iodoacetate knee osteoarthritis model, with meloxicam more effectively ameliorating digging deficits, in line with human patients finding meloxicam more effective. Finally, in a visceral pain model, the decrease in digging behavior correlated with the extent of disease. Ultimately, we make a case for adopting ethological assays, such as digging, in studies of pain in laboratory animals, which we believe to be more representative of the human experience of pain and thus valuable in assessing clinical potential of novel analgesics in animals.