Sterling Michele, Head Jessica, Cabot Peter J, Farrell Michael
Centre of National Research on Disability and Rehabilitation Medicine (CONROD), CRE in Road Traffic Injury, Menzies Health Institute Queensland, Griffith University, Parklands, Australia.
School of Health and Rehabilitation Sciences, The University of Queensland, St Lucia, Australia.
Scand J Pain. 2016 Apr;11:19-26. doi: 10.1016/j.sjpain.2015.11.003. Epub 2015 Dec 2.
Whiplash Associated Disorders (WAD) are a costly health burden. The condition is characterised by sensory disturbances such as widespread hyperalgesia likely indicative of central hyperexcitability. Recently elevated levels of pro-inflammatory biomarkers have also found in acute and chronic WAD. The aim of this cross-sectional study was to investigate the relationship between inflammatory biomarkers and pain processing in people with persistent whiplash associated disorders (WAD).
Twenty one participants with chronic whiplash (>3 months) were recruited. Venous blood samples were collected and assays performed for C-reactive protein (CRP) and TNF-α. Blood oxygen level-dependent (BOLD) contrast images of the brain were acquired with a Siemens 1.5T MRI scanner during repeated 24s stimulus blocks of innocuous or painful stimuli (thumbnail pressure and cold stimulation of dorsum of hand) separated by 36s inter-stimulus intervals. Stimulus intensities used during scanning were at the level of participants' thresholds for moderate pain. Parameter estimates representing BOLD signal increases during painful events from each participant were tested for associations with inflammatory biomarkers.
Clinically relevant levels of CRP and TNF-α were found in 33% and 38% of participants. Levels of CRP showed a positive correlation with levels of cold pain activation in brain regions including the anterior insula, posterior parietal cortex, caudate and thalamus (p<0.05). Levels of TNF-α were not related to activation levels during either noxious pressure or cold. Pressure pain activations also did not show a relationship with CRP levels.
Shared variance between inflammation and increased levels of regional pain-related activation in people with persistent whiplash symptoms is apparent for cold, but not pressure stimuli.
The results highlight cold pain processing as an important aspect of whiplash chronicity, although the implications of this modality-specific effect are not readily apparent.
挥鞭样损伤相关疾病（WAD）是一种代价高昂的健康负担。该病症的特征是感觉障碍，如广泛的痛觉过敏，这可能表明中枢兴奋性过高。最近在急性和慢性WAD中也发现促炎生物标志物水平升高。这项横断面研究的目的是调查持续性挥鞭样损伤相关疾病（WAD）患者炎症生物标志物与疼痛处理之间的关系。
招募了21名患有慢性挥鞭样损伤（超过3个月）的参与者。采集静脉血样并检测C反应蛋白（CRP）和肿瘤坏死因子-α（TNF-α）。在重复的24秒刺激块（无害或疼痛刺激，即拇指按压和手背冷刺激）期间，使用西门子1.5T MRI扫描仪采集大脑的血氧水平依赖（BOLD）对比图像，刺激间隔为36秒。扫描期间使用的刺激强度为参与者中度疼痛阈值水平。测试代表每个参与者疼痛事件期间BOLD信号增加的参数估计值与炎症生物标志物的相关性。
33%的参与者CRP水平及38%的参与者TNF-α水平具有临床相关性。CRP水平与包括前脑岛、顶叶后皮质、尾状核和丘脑在内的脑区冷痛激活水平呈正相关（p<0.05）。TNF-α水平与有害压力或冷刺激期间的激活水平无关。压力性疼痛激活也与CRP水平无关。
对于持续性挥鞭样损伤症状患者，炎症与局部疼痛相关激活水平增加之间的共同差异在冷刺激方面明显，但在压力刺激方面不明显。
结果突出了冷痛处理是挥鞭样损伤慢性化的一个重要方面，尽管这种模式特异性效应的影响尚不清楚。
