Neuroscience Research Australia (NeuRA), Sydney, NSW, Australia Prince of Wales Clinical School, University of New South Wales, Sydney, NSW, Australia EMGO+ Institute, VU University Medical Centre, Amsterdam, the Netherlands The George Institute for Global Health, University of Sydney, Sydney, NSW, Australia Sansom Institute for Health Research, University of South Australia, Adelaide, SA, Australia.
Pain. 2016 Apr;157(4):922-930. doi: 10.1097/j.pain.0000000000000472.
Evidence from randomized controlled studies shows that reconceptualizing pain improves patients' knowledge of pain biology, reduces catastrophizing thoughts, and improves pain and function. However, causal relationships between these variables remain untested. It is hypothesized that reductions in catastrophizing could mediate the relationship between improvements in pain knowledge and improvements in pain and function. To test this causal mechanism, we conducted longitudinal mediation analyses on a cohort of 799 patients who were exposed to a pain education intervention. Patients provided responses to the neurophysiology of pain questionnaire, catastrophic thoughts about pain scale, visual analogue pain scale, and the patient specific functional scale, at baseline, 1-month, 6-month, and 12-month follow-up. With adjustment for potential confounding variables, an improvement in pain biology knowledge was significantly associated with a reduction in pain intensity (total effect = -2.20, 95% confidence interval [CI] = -2.96 to -1.44). However, this effect was not mediated by a reduction in catastrophizing (indirect effect = -0.16, 95% CI = -0.36 to 0.02). This might be due to a weak, nonsignificant relationship between changes in catastrophizing and pain intensity (path b = 0.19, 95% CI = -0.03 to 0.41). Similar trends were found in models with function as the outcome. Our findings indicate that change in catastrophizing did not mediate the effect of pain knowledge acquisition on change in pain or function. The strength of this conclusion is moderated, however, if patient-clinician relational factors are conceptualized as a consequence of catastrophizing, rather than a cause.
随机对照研究的证据表明,重新概念化疼痛可以改善患者对疼痛生物学的认识,减少灾难化思维,并改善疼痛和功能。然而,这些变量之间的因果关系尚未得到检验。据推测,灾难化思维的减少可以介导疼痛知识改善与疼痛和功能改善之间的关系。为了检验这种因果机制,我们对 799 名接受疼痛教育干预的患者进行了纵向中介分析。患者在基线、1 个月、6 个月和 12 个月随访时,对疼痛的神经生理学问卷、对疼痛的灾难化思维量表、视觉模拟疼痛量表和患者特定功能量表做出了回应。在调整了潜在的混杂变量后,疼痛生物学知识的改善与疼痛强度的降低显著相关(总效应=-2.20,95%置信区间[CI]:-2.96 至-1.44)。然而,这种效应并没有通过灾难化思维的减少来介导(间接效应=-0.16,95%CI:-0.36 至 0.02)。这可能是由于灾难化思维的变化与疼痛强度之间的关系较弱且无统计学意义(路径 b = 0.19,95%CI:-0.03 至 0.41)。在以功能为结果的模型中也发现了类似的趋势。我们的研究结果表明,灾难化思维的变化并没有介导疼痛知识获取对疼痛或功能变化的影响。然而,如果将医患关系因素视为灾难化思维的后果而不是原因,那么这一结论的强度就会受到限制。