Goswami Ruma, Anastakis Dimitri J, Katz Joel, Davis Karen D
Division of Brain, Imaging, and Behaviour, Systems Neuroscience, Krembil Research Institute, Toronto Western Hospital, University Health Network, Toronto, ON, Canada Institute of Medical Science, University of Toronto, Toronto, ON, Canada Department of Surgery, University of Toronto, Toronto, ON, Canada Department of Psychology, York University, Toronto, ON, Canada Department of Anesthesia, University of Toronto, Toronto, ON, Canada Department of Anesthesia and Pain Management, Toronto General Hospital, University Health Network, Toronto, ON, Canada.
Pain. 2016 Mar;157(3):729-739. doi: 10.1097/j.pain.0000000000000430.
We do not know precisely why pain develops and becomes chronic after peripheral nerve injury (PNI), but it is likely due to biological and psychological factors. Here, we tested the hypotheses that (1) high Pain Catastrophizing Scale (PCS) scores at the time of injury and repair are associated with pain and cold sensitivity after 1-year recovery and (2) insula gray matter changes reflect the course of injury and improvements over time. Ten patients with complete median and/or ulnar nerve transections and surgical repair were tested ∼3 weeks after surgical nerve repair (time 1) and ∼1 year later for 6 of the 10 patients (time 2). Patients and 10 age-/sex-matched healthy controls completed questionnaires that assessed pain (patients) and personality and underwent quantitative sensory testing and 3T MRI to assess cortical thickness. In patients, pain intensity and neuropathic pain correlated with pain catastrophizing. Time 1 pain catastrophizing trended toward predicting cold pain thresholds at time 2, and at time 1 cortical thickness of the right insula was reduced. At time 2, chronic pain was related to the time 1 pain-PCS relationship and cold sensitivity, pain catastrophizing correlated with cold pain threshold, and insula thickness reversed to control levels. This study highlights the interplay between personality, sensory function, and pain in patients following PNI and repair. The PCS-pain association suggests that a focus on affective or negative components of pain could render patients vulnerable to chronic pain. Cold sensitivity and structural insula changes may reflect altered thermosensory or sensorimotor awareness representations.
我们并不确切知道为什么在周围神经损伤(PNI)后疼痛会产生并发展为慢性疼痛,但这可能是由生物学和心理因素导致的。在此,我们检验了以下假设:(1)损伤和修复时疼痛灾难化量表(PCS)得分高与1年恢复后的疼痛及冷敏感相关;(2)脑岛灰质变化反映损伤过程及随时间的改善情况。对10例正中神经和/或尺神经完全横断并接受手术修复的患者,在手术神经修复后约3周(时间1)进行测试,10例患者中的6例在约1年后(时间2)再次测试。患者和10名年龄及性别匹配的健康对照完成了评估疼痛(患者)和性格的问卷,并接受了定量感觉测试和3T磁共振成像以评估皮质厚度。在患者中,疼痛强度和神经性疼痛与疼痛灾难化相关。时间1的疼痛灾难化倾向于预测时间2的冷痛阈值,且在时间1时右侧脑岛的皮质厚度减小。在时间2时,慢性疼痛与时间1的疼痛-PCS关系及冷敏感相关,疼痛灾难化与冷痛阈值相关,且脑岛厚度恢复至对照水平。本研究强调了PNI及修复后患者的性格、感觉功能和疼痛之间的相互作用。PCS与疼痛的关联表明,关注疼痛的情感或负面成分可能使患者易患慢性疼痛。冷敏感和脑岛结构变化可能反映了热感觉或感觉运动意识表征的改变。