Pain
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There exists currently a fair degree of introspection in the pain research community about the value of animal research. This review represents a defense of animal research in pain. ⋯ Finally, we discuss recent developments in animal models of pain that should improve the relevance and translatability of findings using laboratory animals. We believe that pain research using animal models is a continuing necessity-to understand fundamental mechanisms, identify new analgesic targets, and inform, guide and follow up human studies-if novel analgesics are to be developed for the treatment of chronic pain.
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To determine the impact of occupational psychological/social and mechanical factors on neck pain, a prospective cohort study with a follow-up period of 2 years was conducted with a sample of Norwegian employees. The following designs were tested: (i) cross-sectional analyses at baseline (n=4569) and follow-up (n=4122), (ii) prospective analyses with baseline predictors, (iii) prospective analyses with average exposure over time [(T1+T2)/2] as predictor, and (iv) prospective analyses with measures of change in exposure from T1 to T2 as predictors. A total of 2419 employees responded to both the baseline and follow-up questionnaire. ⋯ The most consistent protective factors were empowering leadership (lowest OR 0.53, 99% CI: 0.35-0.81) and decision control (lowest OR 0.60, 99% CI: 0.36-1.00). Hence, psychological and social factors are important precursors of neck pain, along with mechanical factors. Although traditional factors such as quantitative demands and decision control play a part in the etiology of neck pain at work, in this study several new factors emerged as more important.
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The mechanisms of neuropathic pain (NP) in Guillain Barré syndrome (GBS) are currently unknown. It has recently been shown that acute neuropathy of GBS not only affects large myelinated fibres but also small nociceptive fibres. In this prospective longitudinal 18 months study, we investigated the role of small fibre impairment in NP in GBS (n=30). ⋯ Large fibre dysfunction and motor disability were similar between groups. Small fibre sensory impairment at the acute stage was correlated with the intensity of burning pain (Rho: -0.72; p=0.01 for cold detection; Rho: 0.72; p=0.02 for heat pain) and predicted residual NP (odds 4.1 p=0.04 for heat pain). These findings emphasize the importance of nociceptive fibre impairment in NP in GBS at both acute and chronic stages and suggest similarities between the mechanisms of NP in GBS and those of small fibre painful sensory polyneuropathies.
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Spinal cord injury (SCI) is a major cause of persistent neuropathic pain of central origin. Recent evidence suggests neuropathic pain in clinically complete SCI patients correlates with limited sensory function below the lesion (sensory discomplete). On this basis we examined if the onset of mechanical hyperalgesia was different in rodents after a severe incomplete clip-compression SCI versus a complete spinal cord transection at thoracic segment T13. ⋯ Evidence of central sensitization in cervical spinal cord segments that receive sensory projections from the forelimbs was provided by immunohistochemistry for Zif268, a functional marker of neuroplasticity. Zif268-immunoreactive neurons in laminae I/II increased in response to repetitive noxious forepaw stimulation in the incomplete SCI group, and this response was reduced in the complete transection and sham-operated groups. These data are consistent with the hypothesis that neuropathic pain of cord origin is more likely to develop after SCI when there is an incomplete loss of axons traversing the lesion.
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Despite utilization concerns, little information is available on opioid prescribing for acute, disabling low back pain (LBP) and how opioid features (purity, strength, and length of action) and dose change over time. This information is important in targeting guideline implementation efforts and identifying risks for inappropriate prescribing. Using 2002-2003 United States' workers compensation claims, a cohort of 2868 cases with a new episode of work-related LBP and at least one opioid prescription was followed for 2 years. ⋯ Dose escalation was greater with pure formulations, and was not related to clinical severity or surgery. In contrast to previous and current guideline recommendations, opioid prescribing for acute LBP was often prolonged, and longer for surgical cases. These results reinforce recommendations to limit opioid duration, and suggest that consideration of opioid features, purity as an important one, can be part of a strategy to prevent escalating dosages.