Hubbard Raymond D, Quinn Kyle P, Martínez Joan J, Winkelstein Beth A
Spine Pain Research Lab, Department of Bioengineering & Neurosurgery, University of Pennsylvania, 240 Skirkanich Hall, 210 South 33rd Street, Philadelphia, PA 19104-6321, USA.
Stapp Car Crash J. 2008 Nov;52:33-58. doi: 10.4271/2008-22-0002.
Rapid neck motions can load cervical nerve roots and produce persistent pain. This study investigated the cellular basis of radicular pain and mechanical implications of tissue loading rate. A range of peak loads was applied in an in vivo rat model of dorsal root compression, and mechanical allodynia (i.e. pain) was measured. Axonal damage and nociceptive mediators were assessed in the axons and cell bodies of compressed dorsal roots in separate groups of rats at days 1 and 7 after injury. In the day 7 group, damage in the compressed axons, evaluated by decreased heavy chain neurofilament immunoreactivity, was increased for compressions above a load of 34.08 mN, which is similar to the load-threshold for producing persistent pain in that model. Also, the neuropeptide substance P and glial cell line-derived neurotrophic factor and its receptor significantly decreased (p < 0.02) with increasing load in the small nociceptive neurons of the dorsal root ganglion, suggesting that axonal damage may also decrease neurotrophic support in injured nociceptive afferent fibers. In a separate study, roots were compressed at 2mm/s, and held, to develop a quasi-linear viscoelastic model that was validated through comparisons to quasistatic loading. The model demonstrated that nearly 23% less displacement was required to reach the axonal injury load threshold during dynamic loading than for quasistatic rates. Together, these studies demonstrate that nerve root compressions that produce pain symptoms are sufficient to mediate nociceptive cellular changes, and that thresholds for pain and nociceptive pathophysiology may be lower for dynamic loading scenarios.
快速的颈部运动会使颈神经根负荷增加并产生持续性疼痛。本研究调查了神经根性疼痛的细胞基础以及组织负荷率的力学影响。在背根压迫的体内大鼠模型中施加一系列峰值负荷，并测量机械性异常性疼痛（即疼痛）。在损伤后第1天和第7天，分别对不同组大鼠受压背根的轴突和细胞体中的轴突损伤和伤害性介质进行评估。在第7天的组中，通过重链神经丝免疫反应性降低评估，当负荷超过34.08 mN时，受压轴突的损伤增加，这与该模型中产生持续性疼痛的负荷阈值相似。此外，随着背根神经节中小伤害性神经元负荷的增加，神经肽P物质、胶质细胞系源性神经营养因子及其受体显著减少（p < 0.02），这表明轴突损伤也可能减少受损伤害性传入纤维的神经营养支持。在另一项研究中，以2mm/s的速度压迫神经根并保持，以建立一个准线性粘弹性模型，该模型通过与准静态负荷的比较得到验证。该模型表明，在动态负荷下达到轴突损伤负荷阈值所需的位移比准静态负荷时少近23%。总之，这些研究表明，产生疼痛症状的神经根压迫足以介导伤害性细胞变化，并且在动态负荷情况下，疼痛和伤害性病理生理学的阈值可能更低。
