The Clinical journal of pain
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Progress in advancing understanding of the role of "catastrophizing" in pain and associated physical and psychosocial disability may be furthered by (1) consideration of the construct of catastrophizing, (2) evaluation of the extent to which currently available measures of pain catastrophizing tap into that construct, (3) investigation of the relation of catastrophizing to personal trait variables (e.g., neuroticism and worry), and (4) identification of the conditions (or states) under which catastrophizing is most likely to occur. In this article, the authors discuss these issues and suggest directions for future research.
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The authors aimed to provide an educational update on the current evidence of the effectiveness of drug therapy in the treatment of musculoskeletal pain and to offer a perspective of possible future developments. ⋯ The effectiveness of the currently available drugs in the treatment of musculoskeletal pain conditions is disappointing. Recent developments may open new perspectives in this area of pain medicine.
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The tendency to "catastrophize" during painful stimulation contributes to more intense pain experience and increased emotional distress. Catastrophizing has been broadly conceived as an exaggerated negative "mental set" brought to bear during painful experiences. Although findings have been consistent in showing a relation between catastrophizing and pain, research in this area has proceeded in the relative absence of a guiding theoretical framework. ⋯ The article evaluates the explanatory power of a schema activation model, an appraisal model, an attention model, and a communal coping model of pain perception. It is suggested that catastrophizing might best be viewed from the perspective of hierarchical levels of analysis, where social factors and social goals may play a role in the development and maintenance of catastrophizing, whereas appraisal-related processes may point to the mechanisms that link catastrophizing to pain experience. Directions for future research are suggested.
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Randomized Controlled Trial Clinical Trial
Plasma levels of interleukin-6 and interleukin-10 are affected by ketorolac as an adjunct to patient-controlled morphine after abdominal hysterectomy.
Because morphine affects various immune functions, patient-controlled analgesia with morphine may further deteriorate the immune mechanisms after surgery. Therefore, the purpose of this study was to determine differences between morphine patient-controlled analgesia and a combination of morphine and ketorolac in interleukin-6 and interleukin-10 responses, and in analgesia and morphine-related side effects. ⋯ The authors conclude that supplementation using ketorolac plus administration of morphine modifies cytokine responses and may contribute to immune augmentations during postoperative periods.
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The peripheral apparatus of muscle pain consists of nociceptors that can be excited by endogenous substances and mechanical stimuli. Histologically, the nociceptors are free nerve endings supplied by group III (thin myelinated) and group IV (nonmyelinated) afferents with conduction velocities less than 30 m/s. At the molecular level, nociceptors have receptors for algesic substances, such as bradykinin, serotonin, and prostagladin E2. ⋯ For example, animal studies showed that serotonin sensitizes muscle nociceptors to chemical and mechanical stimuli. Later, human studies showed that serotonin combined with bradykinin induces muscle hyperalgesia to pressure. The sensitization process by endogenous substances that are likely to be released during trauma or inflammatory injury is probably the best established peripheral mechanism for muscle tenderness and hyperalgesia.