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In Vivo Cervical Facet Capsule Distraction: Mechanical Implications for Whiplash and Neck Pain

机译:体内宫颈面孔胶囊分散:鞭打和颈部疼痛的机械影响

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While extensive research points to mechanical injury of the cervical facet joint as a mechanism of whiplash injury, findings remain speculative regarding its potential for causing pain. The purpose of this study was to examine the relationship between facet joint distraction, capsular ligament strain, cellular nociceptive responses, and pain. A novel rat model of in vivo facet joint injury was used to impose C6/C7 joint distraction in separate studies of subcatastrophic and physiologic vertebral distraction, as well as sham procedures. A common clinical measure of behavioral hypersensitivity (allodynia) was measured for 14 days after injury, as quantification of resulting pain symptoms. Also, on day 14, spinal activation of microglia and astrocytes was quantified to examine the potential role of glial activation as a physiologic mechanism of facet-mediated painful injury. Vertebral distractions of 0.90±0.53 mm across the rat facet joint reliably produced symptoms of persistent pain. Allodynia results showed immediate and sustained behavioral sensitivity following subcatastrophic vertebral distractions; pain symptoms were significantly greater (p<0.008) than those for other injury groups. Further, spinal astrocytic activation was also greater (p=0.049) for subcatastrophic injuries compared to lower distraction magnitudes. The mean maximum principal strain in the capsular ligament for joint distractions of 0.57±0.11 mm was 27.7±11.9%. Findings suggest that facet capsule strains comparable to those previously reported for whiplash kinematics and subcatastrophic failures of this ligament have the potential to produce pain symptoms and alter one element of nociception. Results further suggest that a mechanical threshold likely exists for painful joint distraction, providing behavioral and physiologic evidence of the cervical facet joint's mechanical injury as a source of neck pain.
机译:尽管广泛的研究指向颈椎小关节如颈椎损伤的机制的机械性损伤,发现关于其引起疼痛的潜力仍然投机。这项研究的目的是审查小关节撑开,囊韧带拉伤,蜂窝伤害性反应和疼痛之间的关系。体内小关节损伤是用来强加C6 / C7在subcatastrophic和生理椎骨撑开的独立研究关节牵引,以及假程序的一种新的大鼠模型。行为超敏反应(异常性疼痛)的一个常见的临床措施是14天测得的损伤后,作为所得的疼痛症状的定量。此外,第14天,小胶质细胞和星形胶质细胞的活化脊椎定量研究神经胶质细胞活化为小介导的痛苦伤害的生理机制的潜在作用。横跨鼠小面关节的0.90±0.53毫米椎骨分心可靠地生产的持续性疼痛的症状。异常性疼痛结果表明立即和持续的以下subcatastrophic椎分心行为的敏感性;疼痛症状显著高于(P <0.008)比其他损伤的基团。此外,脊髓星形细胞活化也变大(P = 0.049),用于相比subcatastrophic损伤降低分心的量值。在为0.57±0.11毫米关节分心的囊韧带的平均最大主应变为27.7±11.9%。研究结果表明,小胶囊菌株堪比以前的挥鞭运动,这韧带subcatastrophic故障报告必须产生疼痛症状和伤害性的改变一个元素的潜力的。结果进一步表明,机械门槛可能存在疼痛的关节撑开,提供颈椎小关节的机械性损伤的行为和生理证据的颈部疼痛的来源。

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