The journal of pain : official journal of the American Pain Society
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Clinical Trial
Psychologic influence on experimental pain sensitivity and clinical pain intensity for patients with shoulder pain.
Pain-related fear and pain catastrophizing are 2 central psychologic factors in fear-avoidance models. Our previous studies in healthy subjects indicated that pain-related fear, but not pain catastrophizing, was associated with cold pressor pain outcomes. The current study extends previous work by investigating pain-related fear and pain catastrophizing in a group of subjects with shoulder pain, and included concurrent measures of experimental and clinical pain. Fifty nine consecutive subjects seeking operative treatment of shoulder pain were enrolled in this study (24 women, mean age = 50.4, SD = 14.9). Subjects completed validated measures of pain-related fear, pain catastrophizing, and clinical pain intensity and then underwent a cold pressor task to determine experimental pain sensitivity. Multivariate regression models used sex, age, pain-related fear, and pain catastrophizing to predict experimental pain sensitivity and clinical pain intensity. Results indicated that only pain-related fear uniquely contributed to variance in experimental pain sensitivity (beta = -.42, P < .01). In contrast, sex (beta = -.29, P = .02) and pain catastrophizing (beta = .43, P < .01) uniquely contributed to variance in clinical pain intensity. These data provide additional support for application of fear-avoidance models to subjects with shoulder pain. Our results also suggest that pain-related fear and pain catastrophizing may influence different components of the pain experience, providing preliminary support for recent theoretical conceptualizations of the role of pain catastrophizing. ⋯ This study provided additional information on how specific psychological variables potentially influence experimental and clinical pain. In this sample of subjects with shoulder pain, we replicated findings from our previous studies involving healthy subjects, as fear of pain was uniquely associated with experimental pain sensitivity. In contrast, pain catastrophizing emerged as the sole psychological variable related to clinical pain intensity.
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Previous research indicates that exposure to shock decreases thermal pain sensitivity in humans. This hypoalgesia has been attributed to a centrally mediated fear state that activates descending inhibitory pathways. Animal research suggests that distraction alters the activation of these hypoalgesic systems. To determine whether the pain memory alters the activation of hypoalgesic systems in humans, the present study examined whether a post-shock distractor attenuates shock-induced hypoalgesia. If fear-inducing shocks are represented by a limited capacity working memory system, then a distractor should speed the decay of the hypoalgesia. Healthy men were randomly assigned to 1 of 4 groups: shock-distraction, shock-no distraction, no shock-distraction, and no shock-no distraction. Following baseline pain tests, participants in the shock groups were presented with 3 brief shocks. Immediately following shock, an unexpected vibration stimulus was presented to participants in the distraction groups. Both self-report and physiological (SCL, HR) measures indicated that shock exposure resulted in fear, arousal, and decreased pain sensitivity. Consistent with prior animal studies, presentation of a post-shock distractor sped the decay of shock-induced hypoalgesia. Specifically, the distraction group exhibited significantly less shock-induced hypoalgesia compared to the no-distraction group. These findings provide additional evidence for the involvement of memory processes in the activation of descending pain inhibitory pathways. ⋯ This study demonstrated that the presentation of a distracting stimulus immediately following 3 brief shocks attenuated shock-induced hypoalgesia in healthy human subjects. Understanding the impact of post-pain distraction on pain processing may have important clinical implications because it may influence patients' willingness to undergo future painful medical procedures.
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This observational study aimed to determine whether pain sensitivity in patients with noncancer chronic pain, taking either methadone or morphine, is similar to patients maintained on methadone for dependence therapy, compared with a control group. Nociceptive thresholds were measured on a single occasion with von Frey hairs, electrical stimulation, and cold pressor tests. In all subjects receiving methadone or morphine, nociceptive testing occurred just before a scheduled dose. Cold pressor tolerance values in patients with noncancer, chronic pain, treated with morphine and methadone, were 18.1 +/- 2.6 seconds (mean +/- SEM) and 19.7 +/- 2.3 seconds, respectively; in methadone-maintained subjects it was 18.9 +/- 1.9 seconds, with all values being significantly (P < .05) lower than opioid-naïve subjects (30.7 +/- 3.9 seconds). These results indicate that patients with chronic pain managed with opioids and methadone-maintained subjects are hyperalgesic when assessed by the cold pressor test but not by the electrical stimulation test. None of the groups exhibited allodynia as measured using the von Frey hairs. These results add to the growing body of evidence that chronic opioid exposure increases sensitivity to some types of pain. They also demonstrate that in humans, this hyperalgesia is not associated with allodynia. ⋯ This article presents an observational study whereby the pain sensitivity of patients with chronic pain managed with opioids and opioid-maintained patients were compared with opioid-naïve patients. The results suggest that opioid use may contribute to an increase in the sensitivity to certain pain experimental stimuli.
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There is evidence that pain patients demonstrate attentional biases toward some pain-related stimuli (eg, sensory words) and not others (eg, affective words). However, whether individuals in chronic pain caused by rheumatoid arthritis (RA) also demonstrate this bias has not been investigated. Further, within the pain literature, whether these biases reflect hypervigilance or difficulty disengaging from stimuli remains contentious. The present study aimed to determine (a) whether RA patients demonstrate an attentional bias to sensory pain words; and (b) whether this bias is a result of hypervigilance or failure to disengage from the stimuli. RA patients showed a bias toward sensory words and away from threat-related words. The effect for sensory words resulted from slowed performance on incongruent trials (ie, difficulty disengaging), whereas the bias away from threat words resulted from faster responses on incongruent trials (ie, avoidance of threat). The pattern of attention biases in RA patients is very similar to those found in patients with chronic pain. At least in RA, attentional biases appear to be related to a failure to disengage from pain-related words rather than hypervigilance. ⋯ There is continued debate about whether these biases are caused by hypervigilance toward pain stimuli or difficulty disengaging from pain stimuli. This study shows that in a group of RA patients, attentional biases toward pain are caused by difficulty disengaging rather than hypervigilance.
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Evidence implicating Nav1.8 and TRPV1 ion channels in various chronic pain states is extensive. In this study, we used isobolographic analysis to examine the in vivo effects of the combination of the Nav1.8 blocker A-803467 [5-(4-Chloro-phenyl)-furan-2-carboxylic acid (3,5-dimethoxy-phenyl)-amide] with 2 structurally distinct TRPV1 antagonists, A-840257 [1-(1H-Indazol-4-yl)-3-([R]-4-piperidin-1-yl-indan-1-yl)-urea] or A-425619 [1-Isoquinolin-5-yl-3-(4-trifluoromethyl-benzyl)-urea]. The antinociceptive effects of the Nav1.8 blocker alone and in combination with each TRPV1 antagonist were examined in an inflammatory (complete Freund's adjuvant, CFA) and a neuropathic (spinal nerve ligation, SNL) pain model after systemic (intraperitoneal) administration. Alone, A-803467 was efficacious in both CFA and SNL models with ED(50) values of 70 (54.2 to 95.8) mg/kg and 70 (38.1 to 111.9) mg/kg, respectively. The ED(50) values of the TRPV1 antagonists A-840257 and A-425619 alone in the CFA model were 10 (3.6 to 14.9) mg/kg and 43 (24.1 to 62.2) mg/kg, respectively; both were without significant effect in the SNL model. A series of experiments incorporating 1:1, 3:1, or 0.3:1 ED(50) dose-ratio combinations of A-840257 and A-803467, or A-425619 and A-803467 were performed in both pain models, and the effective doses of mixtures that produced 50% antinociception (ED(50, mix)) were determined by isobolographic analysis. The ED(50, mix) in each case was not found to be statistically different than ED(50, add), the theoretical ED(50) calculated assuming additive effects. These data demonstrate that Nav1.8 blockers and TRPV1 antagonists administered in combination produce an additive effect in rat pain models. Using such a combination strategy to produce analgesia may potentially provide an improved therapeutic separation from unwanted in vivo side effects associated with blockade of either Nav1.8 or TRPV1 alone. ⋯ In this report, effects of coadministration of TRPV1 antagonists and A-803467, a Nav1.8 blocker, were investigated in preclinical rodent models of neuropathic and inflammatory pain. The 2 classes of novel antinociceptive agents produced an additive interaction in attenuating CFA-induced thermal hyperalgesia, providing a rationale for their use as a combination strategy in the clinic for treating inflammatory pain.