Pain
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Current fear-avoidance models consider fear of pain as a key factor in the development of chronic musculoskeletal pain. Generally, the idea is that by virtue of the formation of associations or acquired propositional knowledge about the relation between neutral movements and pain, these movements may signal pain, and hence start to elicit defensive fear responses (eg, avoidance behavior). This assumption has never been investigated experimentally. ⋯ Participants were slower initiating a CS+ movement than a CS- movement, while response latencies to CSs in the control condition did not differ. These data support the acquisition of fear of movement-related pain by associative learning. Results are discussed in the broader context of the acquisition of pain-related fear in patients with musculoskeletal pain.
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Clinical Trial
Evaluation of the fear-avoidance model with health care workers experiencing acute/subacute pain.
Studies in the literature do not show clear evidence supporting the relationship between pain and depressive symptoms in individuals experiencing acute/subacute pain compared to those experiencing chronic pain. However, more information is needed about which variables act as mediators in the pain-depression relationship in people having acute/subacute pain, before pain becomes chronic. ⋯ The catastrophizing concept was most closely associated with depressive symptoms, while pain self-efficacy was directly associated with fear-avoidance beliefs and indirectly to work outcomes. Assessing and modifying pain self-efficacy in acute/subacute pain patients is important for interventions aiming to decrease fear-avoidance and improve work outcomes.
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Randomized Controlled Trial
Escitalopram is associated with reductions in pain severity and pain interference in opioid dependent patients with depressive symptoms.
Pain is common among opioid-dependent patients, yet pharmacologic strategies are limited. The aim of this study was to explore whether escitalopram, a selective serotonin reuptake inhibitor, was associated with reductions in pain. The study used longitudinal data from a randomized, controlled trial that evaluated the effects of escitalopram on treatment retention in patients with depressive symptoms who were initiating buprenorphine/naloxone for treatment of opioid dependence. ⋯ In this sample of 147 adults, we found that participants randomized to escitalopram had significantly larger reductions on both pain severity (b=-14.34, t=-2.66, P<.01) and pain interference (b=-1.20, t=-2.23, P<.05) between baseline and follow-up. After adjusting for within-subject changes in depression, the estimated effects of escitalopram on pain severity and pain interference were virtually identical to the unadjusted effects. This study of opioid-dependent patients with depressive symptoms found that treatment with escitalopram was associated with clinically meaningful reductions in pain severity and pain interference during the first 3 months of therapy.
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Forebrain medial septum region facilitates nociception in a rat formalin model of inflammatory pain.
The medial septum is anatomically and functionally linked to the hippocampus, a region implicated in nociception. However, the role of medial septum in nociception remains unclear. To investigate the role of the region in nociception in rats, muscimol, a GABA agonist, or zolpidem, a positive allosteric modulator of GABA(A) receptors, was microinjected into medial septum to attenuate the activity of neurons in the region. ⋯ The reduction was accompanied by a decrease in formalin-induced expression of spinal c-Fos protein that serves as an index of spinal nociceptive processing. The drug effects on nociceptive behaviors were without overt sedation and were distinct from the effects observed after septal lateral microinjections. Taken together, these findings suggest that the activation of medial septum is pro-nociceptive and facilitates aspects of central neural processing underlying nociception.