Pain
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Randomized Controlled Trial Clinical Trial
Tailored cognitive-behavioral therapy in early rheumatoid arthritis for patients at risk: a randomized controlled trial.
Recent developments in chronic pain research suggest that effectiveness of cognitive-behavioral therapy (CBT) may be optimized when applying early, customized treatments to patients at risk. For this purpose, a randomized, controlled trial with tailor-made treatment modules was conducted among patients with relatively early rheumatoid arthritis (RA disease duration of <8 years), who had been screened for psychosocial risk profiles. All participants received standard medical care from a rheumatologist and rheumatology nurse consultant. ⋯ Specifically, fatigue and depression were significantly reduced at post-treatment and at the 6-month follow-up in the CBT condition in comparison to the control condition, while perceived support increased at follow-up assessment. In addition, helplessness decreased at post-treatment and follow-up assessment, active coping with stress increased at post-treatment, and compliance with medication increased at follow-up assessment in the CBT condition in comparison to the control condition. Results indicate the effectiveness of tailor-made CBT for patients at risk in relatively early RA, and supply preliminary support for the idea that customizing treatments to patient characteristics may be a way to optimize CBT effectiveness in RA patients.
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A purported pathogenic mechanism for the development of fibromyalgia, a medically unexplained syndrome involving widespread pain, is stress and associated psychiatric disorder. The major stressor of recent World Trade Center terrorist attacks provides a natural experiment for evaluating this mechanism. This study sought to determine whether symptoms consistent with fibromyalgia increased post-September 11 and whether exposure to specific terrorism-related events or prior depression predicted symptom increase. ⋯ Event exposure did not relate to FM-L onset at follow-up, nor did depressive symptoms at baseline interact with event exposure. Depressive symptoms did not predict new onsets better than the extent of their comorbidity with FM-L at baseline. The failure to detect a significant increase in symptoms consistent with a diagnosis of fibromyalgia and the failure of new onsets of such symptoms to be accounted for by exposure to major stressors or prior depressive symptoms suggests that these hypothesized risk factors are unlikely to be of major importance in the pathogenesis of fibromyalgia.
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The present study examined the value of a measure of catastrophizing as a predictor of activity intolerance in response to delayed onset muscle soreness (DOMS). A sample of 50 (17 men, 33 women) sedentary undergraduates participated in an exercise protocol designed to induce muscle soreness and were asked to return 2 days later to perform the same physical maneuvers. Participants performed five strength exercises that emphasized the eccentric component of the muscle contraction in order to induce DOMS. ⋯ Regression analyses revealed that catastrophizing predicted reductions in weight lifted even after controlling for pain and negative mood. These findings extend previous research in demonstrating that catastrophizing is associated with objective indices of activity intolerance associated with pain. Implications of these findings for understanding pain-related disability are addressed.
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Neuropathic pain syndromes are characterized by spontaneous pain and by stimulus-evoked allodynia and hyperalgesia. Stimulus-induced pain, i.e. the capacity of external stimuli to alter sensory processing so as to generate a pain hypersensitivity that outlasts the initiating stimulus, is usually present only after intense activation of nociceptors. In abnormal pain states, however, such as after capsaicin injection or inflammation, a stimulus-induced incremental pain can be generated by repetitive light touch, termed progressive tactile hypersensitivity (PTH). ⋯ However, 10 weeks and after, the same repeated stimulation induced a progressive tactile hypersensitivity that persisted after discontinuation of the tactile stimulation. Following SNI, repeated stimulation of the hypersensitive skin territory, corresponding to the intact spared sural nerve, never induced PTH. Tactile stimulation of regenerating afferents but not spared non-injured afferents, can induce, therefore, PTH and such a stimulus-induced alteration in pain processing may contribute to clinical neuropathic pain.