The journal of pain : official journal of the American Pain Society
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Anxiety sensitivity (AS) or fear of anxiety sensations has been linked to childhood learning history for somatic symptoms, suggesting that parental AS may impact children's responses to pain. Using structural equation modeling, we tested a conceptual model in which parent AS predicted child AS, which in turn predicted a hypothesized latent construct consisting of children's pain intensity ratings for 3 laboratory pain tasks (cold pressor, thermal heat, and pressure). This conceptual model was tested in 211 nonclinical parent-child pairs (104 girls, 107 boys; mean age 12.4 years; 178 mothers, 33 fathers). Our model was supported in girls only, indicating that the sex of the child moderated the hypothesized relationships. Thus, parent AS was related to child laboratory pain intensity via its contribution to child AS in girls but not in boys. In girls, 42% of the effect of parent AS on laboratory pain intensity was explained via child AS. In boys, there was no clear link between parent AS and child AS, although child AS was predictive of experimental pain intensity across sex. Our results are consistent with the notion that parent AS may operate via healthy girls' own fear of anxiety symptoms to influence their responses to laboratory pain stimuli. ⋯ The present study highlights sex differences in the links among parent and child anxiety sensitivity (fear of anxiety sensations) and children's experimental pain responses. Among girls, childhood learning history related to somatic symptoms may be a particularly salient factor in the development of anxiety sensitivity and pain responsivity.
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The aim of this study was to translate and cross-culturally adapt the American version of the Coping Strategies Questionnaire (CSQ) and to test the reliability and validity of the German version (CSQ-D). The CSQ was translated and cross-culturally adapted following international guidelines. Reliability and validity were tested in 62 individuals with chronic musculoskeletal pain syndromes. For the concurrent criterion-related validity the CSQ-D scales were compared with the German Pain Coping Questionnaire (FESV-BW), and for the construct validity with the German Short Form 36 (SF-36). The translation process proceeded without major difficulties. In testing for reliability, the CSQ-D as a whole had a Cronbach's alpha of .94 and an intraclass correlation coefficient of .89 (95% CI .86-.98). The total CSQ-D score was correlated to the FESV-BW scales with scores of r = 0.32-0.55 and with the SF-36 Mental Component Summary with scores of r = 0.32-0.53. The CSQ-D is a precisely translated and highly reliable instrument in the assessment of chronic pain coping strategies. Its concurrent criterion-related validity and construct validity are low. The main reason for the low level of agreement between the CSQ-D and the FESV-BW was revealed by factor analysis. ⋯ This paper presents the German version of the Coping Strategies Questionnaire (CSQ-D) together with the results of clinimetric testing. The CSQ-D is a feasible and reliable outcome measure to be used in trials with German-speaking patients or large multicenter multinational trials to assess pain coping strategies in patients with chronic musculoskeletal pain.
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This study examined effects of age (young rats, approximately 35 days, vs mature rats, approximately 75-110 days) on spinal nerve ligation (SNL)-induced tactile allodynia and phosphorylation of p38 (as measured by phospho-p38 MAP kinase [P-p38]) in dorsal root ganglia and spinal cord. Effects of SNL combined with spinal nerve transection also were assessed. Mature rats displayed milder SNL-induced allodynia than young rats. Addition of spinal nerve transection distal to the ligation in older animals resulted in an allodynia comparable to that seen in young animals. In DRG, both groups displayed early (5 h) and late (10 days) peaks in P-p38 following surgery as compared to naïve rats. Tight nerve ligation plus transection had no additional effect on P-p38 levels in DRG. In spinal cord, young rats had increased levels of P-p38 from 5 h to 3 days after SNL. Phosphorylated p38 levels then decreased, with a second peak at 10 days. In contrast, spinal cord from mature rats showed less early p38 phosphorylation, although they also displayed a late 10-day peak. Addition of a transection to the ligation produced restoration of the early peak along with intensification of allodynia. Alterations of spinal P-p38 at early time points thus seem to covary with intensity of tactile allodynia. ⋯ Age and modifications to spinal nerve ligation, a common model of neuropathic pain, influence spinal p38 phosphorylation and allodynia. Early levels of spinal P-p38 seem to covary with allodynia intensity. This may mean that small variations of an injury could affect the therapeutic window of a p38 antagonist.
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Progress in the understanding of chronic pain with neuropathic features has been hindered by a lack of epidemiologic research in the general population. The Leeds Assessment of Neuropathic Symptoms and Signs score (S-LANSS) was recently validated for use in postal surveys, making the identification of pain of predominantly neuropathic origin possible. Six family practices in 3 UK cities (Aberdeen, Leeds, and London) generated a total random sample of 6,000 adults. The mailed questionnaire included demographic items, chronic pain identification, and intensity questions, the S-LANSS, the Level of Expressed Needs questionnaire, and the Neuropathic Pain Scale. With a corrected response rate of 52%, the prevalence of any chronic pain was 48% and the prevalence of pain of predominantly neuropathic origin was 8%. Respondents with this chronic neuropathic pain were significantly more likely to be female, slightly older, no longer married, living in council rented accommodation, unable to work, have no educational qualifications, and be smokers than all other respondents. Multiple logistic regression modeling found that pain of predominantly neuropathic origin was independently associated with older age, gender, employment (being unable to work), and lower educational attainment. Respondents with this pain type also reported significantly greater pain intensity, higher scores on the NPS, higher levels of expressed need, and longer duration of pain. This is the first estimate of the prevalence and distribution of pain of predominantly neuropathic origin in the general population, using a previously validated and reliable data collection instrument. ⋯ Chronic pain with neuropathic features appears to be more common in the general population than previously suggested. This type of pain is more severe than other chronic pain but distributed similarly throughout sociodemographic groups.
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The aim of this study was to examine whether treatments based on different theories change pain catastrophizing and internal control of pain, and whether changes in these factors mediate treatment outcome. Participants were 211 patients with nonspecific chronic low back pain (CLBP) participating in a randomized controlled trial, attending active physical treatment (APT, n = 52), cognitive-behavioral treatment (CBT, n = 55), treatment combining the APT and CBT (CT, n = 55), or waiting list (WL, n = 49). Pain catastrophizing decreased in all 3 active treatment groups and not in the WL. There was no difference in the change in internal control across all 4 groups. In all the active treatment groups, patients improved regarding perceived disability, main complaints, and current pain at post-treatment, and no changes were observed in the WL group. Depression only changed significantly in the APT group. Change in pain catastrophizing mediated the reduction of disability, main complaints, and pain intensity. In the APT condition, pain catastrophizing also mediated the reduction of depression. Not only cognitive-behavioral treatments but also a physical treatment produced changes in pain catastrophizing that seemed to mediate the outcome of the treatment significantly. The implications and limitations of these results are discussed. ⋯ This article shows that treatment elements that do not deliberately target cognitive factors can reduce pain catastrophizing. Reduction in pain catastrophizing seemed to mediate the improvement of functioning in patients with chronic low back pain. The results might contribute to the development of more effective interventions.