The journal of pain : official journal of the American Pain Society
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From a treatment perspective, it is highly relevant to pinpoint individual vulnerability factors for resistance to exposure treatment in highly fearful chronic pain patients. Previous fear conditioning research showed that healthy individuals scoring relatively high on trait anxiety display sustained fear to safety cues during extinction. In the context of fear of movement-related pain, this intriguing question has been largely neglected so far. Even more importantly, positive psychological traits such as trait positive affect may function as protective factors against the spreading of fear to safe movements and improve exposure treatment outcomes. In this study, healthy participants completed a trait anxiety and trait positive affect questionnaire and underwent acquisition and extinction of fear of movement-related pain using an experimental voluntary movement paradigm. During acquisition, one movement (CS+) was paired with a painful stimulus and another movement was not (CS-). During extinction, the CS+ was no longer reinforced. Results show failure of fear inhibition to the CS- during extinction in healthy individuals scoring relatively high on trait anxiety or relatively low on positive affect. These findings seem to suggest that safety learning is more vulnerable in healthy people with a high anxious disposition and/or relatively lower levels of positive affect. In addition, this is the first study to show that the negative impact of high trait anxiety on fear inhibition to safety cues during extinction can be countered by high levels of positive affect. These findings may have important clinical implications. ⋯ Both low positive affect and high trait anxiety are associated with impaired fear inhibition to nonpainful movements during fear extinction. Interestingly, high levels of positive affect buffer against the negative impact of trait anxiety. Increasing positive affect during exposure may counter the effects of trait vulnerabilities and improve treatment outcomes.
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The purpose of this study was to examine exercise-induced pain modulation in diabetic adults with painful diabetic neuropathy (PDN) compared to diabetic adults without PDN. Eighteen adults diagnosed with type 2 diabetes with and without PDN (mean age of 49 years) completed 2 sessions. During the familiarization session, participants completed questionnaires, were familiarized with the pain testing protocols, and completed maximal isometric contractions. During the exercise session, experimental pain testing was completed before and following exercise consisting of 3 minutes of isometric exercise performed at 25% maximal voluntary contraction. Ratings of perceived exertion and muscle pain were assessed every 30 seconds during exercise. Results indicated that ratings of perceived exertion and muscle pain during exercise were significantly higher (P < .05) for diabetic adults with PDN versus diabetic adults without PDN. Diabetic adults with PDN did not experience changes in thermal pain ratings following exercise, whereas diabetic adults without PDN reported significantly lower pain ratings following exercise. It is concluded that diabetic adults with PDN experienced high levels of muscle pain during exercise and a lack of exercise-induced hypoalgesia following exercise, in comparison to diabetic adults without PDN, who experienced lower levels of muscle pain during exercise and a hypoalgesic response following exercise. ⋯ Very little research has been conducted examining the impact of exercise on pain modulation in diabetic adults with PDN. This study provides support that adults with PDN exhibit exercise-induced endogenous pain modulatory system dysfunction.
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The aim of the present study was to analyze differences between men and women in the experience of chronic pain. Resilience, fear-avoidance of pain, and pain acceptance were included in a hypothetical model as variables involved in chronic pain adjustment. A sample of 400 chronic spinal pain patients (190 men and 210 women) attending primary care units participated in the study. Student's t-test analyses showed that the women's scores were significantly higher than men's scores on pain intensity, pain anxiety, and current functioning. A LISREL multisample analysis of the theoretical model across genders was conducted. As expected, statistically significant associations were found between resilience and confrontation in both samples. Thus, resilient people will probably develop accepting behavior when faced with chronic pain. Confrontation yielded 3 statistically significant path coefficients: to pain intensity, functional status, and negative mood. Statistically significant associations were found between fear-avoidance and negative mood in both samples, but no association was found between fear-avoidance and functional status in either sample. Finally, fear-avoidance was associated with pain intensity in the sample of men alone. Despite this difference, the results suggest that the theoretical model had an adequate fit across both groups. ⋯ In the context of fear-avoidance models, this article analyzed differences between men and women with spinal pain in relation to the pain experience. The fear-avoidance model appeared to be a good theoretical reference model in both men and women.
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Opioids are standard therapy for the treatment of pain; however, adverse effects limit their use. Voltage-gated calcium channel blockers may be used to increase opioid analgesia, but their effect on opioid-induced side effects is little known. Thus, the goal of this study was to evaluate the action of the peptide Phα1β, a voltage-gated calcium channel blocker, on the antinociceptive and adverse effects produced by morphine in mice. A single administration of morphine (3-10 mg/kg) was able to reduce heat nociception as well as decrease gastrointestinal transit. The antinociception caused by a single injection of morphine was slightly increased by an intrathecal injection of Phα1β (30 pmol/site). Repeated treatment with morphine caused tolerance, hyperalgesia, withdrawal syndrome, and constipation, and the Phα1β (.1-30 pmol/site, intrathecal) was able to reverse these effects. Finally, the effects produced by the native form of Phα1β were fully mimicked by a recombinant version of this peptide. Taken together, these data show that Phα1β was effective in potentiating the analgesia caused by a single dose of morphine as well as in reducing tolerance and the adverse effects induced by repeated administration of morphine, indicating its potential use as an adjuvant drug in combination with opioids. ⋯ This article presents preclinical evidence for a useful adjuvant drug in opioid treatment. Phα1β, a peptide calcium channel blocker, could be used not only to potentiate morphine analgesia but also to reduce the adverse effects caused by repeated administration of morphine.