Pain
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Although animal models have consistently demonstrated acute pain inhibitory effects of nicotine and tobacco, human experimental studies have yielded mixed results. The main goal of this meta-analysis was to quantify the effects of nicotine/tobacco administration on human experimental pain threshold and tolerance ratings. A search of PubMed and PsycINFO online databases identified 13 eligible articles, including k = 21 tests of pain tolerance (N = 393) and k = 15 tests of pain threshold (N = 339). ⋯ Current smoking has been associated with more severe chronic pain and physical impairment. Acute nicotine-induced analgesia could make smoking more rewarding and harder to give up. Future research should use dynamic measures of experimental pain reactivity and further explore biopsychosocial mechanisms of action.
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Randomized Controlled Trial
Brief Time-Based Activity Pacing Instruction as a Singular Behavioral Intervention was not Effective in Participants with Symptomatic Osteoarthritis.
Osteoarthritis (OA) of the lower extremities is a prevalent cause of disability in which symptoms interfere with mobility and activity participation. Behavioral self-management for OA symptomatology is commonly recommended; but these interventions are underutilized, unstandardized in application, and at times, unavailable in the context of clinical care. For people with chronic pain, rehabilitation professionals may select to apply activity pacing instruction as one behavioral strategy to manage symptoms. ⋯ Using linear mixed models, Western Ontario and McMaster Universities Osteoarthritis Index pain scores changed over time, decreasing the most in the general and usual care groups; only the usual care group had decreased pain over 6 months. The tailored and general activity pacing groups reported higher frequency of pacing behaviors than the usual care group at 10 weeks, but pacing was not sustained at 6 months. This trial does not support the use of time-based pacing as a singular behavioral strategy for people with knee or hip OA.
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The McGill pain questionnaire (MPQ) and its later derivative the short form-MPQ have been used widely both in experimental and clinical pain studies. They have been of considerable importance in stimulating research into the perception of pain and now, with the publication of its latest variant, the short form-MPQ-2, it is appropriate to appraise their utility in the light of subsequent research into the nature of pain and the purpose of pain assessment. Following a description of the content and development of the questionnaires, issues of validity, reliability, and utility are addressed, not only in terms of the individual pain descriptors and the scales, but also in terms of methods of quantification. ⋯ It is suggested that pain assessment needs to be cast in its social context. We need to understand the influences on pain expression using a socio-communication model of pain that recognizes the function of pain and the importance of both innate pain responses and the effects of social learning. The review concludes with recommendations for future use of the MPQ and identifies a number of research challenges which lie ahead.
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It seems that central neuropathic pain (CNP) is associated with altered abilities to modulate pain; whereas dysfunction in descending pain inhibition is associated with the extent of chronic pain distribution, enhanced pain excitation is associated with the intensity of chronic pain. We investigated the hypothesis that CNP is associated with decreased descending pain inhibition along with increased neuronal excitability and that both traits are associated with spinothalamic tract (STT) damage. Chronic spinal cord injury subjects with CNP (n = 27) and without CNP (n = 23) and healthy controls (n = 20) underwent the measurement of pain adaptation, conditioned pain modulation (CPM), tonic suprathreshold pain (TSP), and spatial summation of pain above injury level. ⋯ Thus, top-down processes may determine the spread of CNP, whereas bottom-up processes may determine CNP intensity. It also seems that the mechanisms of CNP may involve STT-induced hyperexcitability. Future, longitudinal studies may investigate the timeline of this scenario.