Tesarz Jonas, Gerhardt Andreas, Leisner Sabine, Janke Susanne, Treede Rolf-Detlef, Eich Wolfgang
Department of General Internal Medicine and Psychosomatics, Medical Hospital, University of Heidelberg, Heidelberg, Germany Department of Neurophysiology, Centre for Biomedicine and Medical Technology Mannheim (CBTM), University of Heidelberg, Heidelberg, Germany.
Pain. 2015 Apr;156(4):577-586. doi: 10.1097/01.j.pain.0000460350.30707.8d.
Psychological trauma is associated with an increased risk for chronification of nonspecific chronic back pain (nsCLBP) independent of posttraumatic stress disorder (PTSD). However, the mechanisms underlying the role of psychological trauma in nsCLBP are less clear than in PTSD. Therefore, this study considered whether psychological trauma exposure (TE) is accompanied by specific alterations in pain perception. The study included 56 participants with nsCLBP and TE (nsCLBP-TE), 93 participants with nsCLBP without TE (nsCLBP-W-TE), and 31 pain-free controls. All participants underwent a thorough clinical evaluation. The standardized quantitative sensory testing protocol of the "German Research Network on Neuropathic Pain" was used to obtain comprehensive profiles on somatosensory functions in painful (back) and non-painful areas (hand). The protocol consisted of thermal and mechanical detection as well as pain thresholds, vibration thresholds, and pain sensitivity to sharp and blunt mechanical stimuli. Psychological trauma was validated by structured clinical interview. Trauma-associated symptom severity, anxiety, and depressive symptomatology were assessed by self-report questionnaires. Differences in somatosensory function were seen only for pressure pain thresholds. Compared with controls, nsCLBP-TE revealed hyperalgesia generalized in space with lower thresholds in painful and non-painful areas, whereas nsCLBP-W-TE demonstrated localized alterations with decreased thresholds only in the pain-affected area of the back (P ≤ 0.006). Our findings suggest an augmented central pain processing in nsCLBP-TE (alterations in painful and non-painful areas), whereas nsCLBP-W-TE show only local changes (alterations only in the painful area) suggesting regional sensitization processes. This finding might explain why TE without PTSD is associated with an increased prevalence of chronic pain.
心理创伤与非特异性慢性背痛（nsCLBP）慢性化风险增加相关，且独立于创伤后应激障碍（PTSD）。然而，心理创伤在nsCLBP中作用的潜在机制不如在PTSD中那么清晰。因此，本研究探讨心理创伤暴露（TE）是否伴有痛觉的特定改变。该研究纳入了56名患有nsCLBP且有TE的参与者（nsCLBP - TE）、93名患有nsCLBP但无TE的参与者（nsCLBP - W - TE）以及31名无疼痛的对照者。所有参与者均接受了全面的临床评估。采用“德国神经性疼痛研究网络”的标准化定量感觉测试方案，以获取疼痛（背部）和非疼痛区域（手部）体感功能的综合概况。该方案包括热觉和机械觉检测以及疼痛阈值、振动阈值，以及对尖锐和钝性机械刺激的疼痛敏感性。通过结构化临床访谈验证心理创伤。通过自我报告问卷评估创伤相关症状严重程度、焦虑和抑郁症状。仅在压力疼痛阈值方面观察到体感功能的差异。与对照组相比，nsCLBP - TE表现出在空间上广泛的痛觉过敏，疼痛和非疼痛区域的阈值较低，而nsCLBP - W - TE仅表现出局部改变，仅在背部疼痛影响区域阈值降低（P≤0.006）。我们的研究结果表明，nsCLBP - TE存在增强的中枢性疼痛处理（疼痛和非疼痛区域均有改变），而nsCLBP - W - TE仅表现出局部变化（仅在疼痛区域有改变），提示区域致敏过程。这一发现可能解释了为何无PTSD的TE与慢性疼痛患病率增加相关。
