Department of Orthopaedics and Rehabilitation Medicine, Fukui University Faculty of Medical Sciences, Matsuoka Shimoaizuki 23, Eiheiji, Fukui 910-1193, Japan.
J Clin Neurosci. 2010 Apr;17(4):501-5. doi: 10.1016/j.jocn.2009.07.110. Epub 2010 Feb 1.
Entrapment neuropathy is a frequent clinical problem that can be caused by, among other factors, mechanical compression; however, exactly how a compressive force affects the peripheral nerves remains poorly understood. In this study, using a rabbit model of sciatic nerve injury (n=12), we evaluated the time-course of changes in intraneural blood flow, compound nerve action potentials, and functioning of the blood-nerve barrier during graded mechanical compression. Nerve injury was applied using a compressor equipped with a custom-made pressure transducer. Cessation of intraneural blood flow was noted at a mean compressive force of 0.457+/-0.022 N (+/-SEM), and the compound action potential became zero at 0.486+/-0.031 N. Marked extravasation of Evans blue albumin was noted after 20 min of intraneural ischemia. The functional changes induced by compression are likely due to intraneural edema, which could subsequently result in impairment of nerve function. These changes may be critical factors in the development of symptoms associated with nerve compression.
神经嵌压症是一种常见的临床问题，可由多种因素引起，包括机械压迫；然而，确切的压迫力如何影响周围神经仍知之甚少。在这项研究中，我们使用兔坐骨神经损伤模型（n=12），评估了在分级机械压迫过程中神经内血流、复合神经动作电位和血神经屏障功能的时程变化。神经损伤是通过配备定制压力传感器的压缩机施加的。在平均压缩力为 0.457+/-0.022 N（+/-SEM）时，观察到神经内血流停止，而复合动作电位在 0.486+/-0.031 N 时变为零。在神经内缺血 20 分钟后，观察到 Evans 蓝白蛋白明显外渗。压迫引起的功能变化可能是由于神经内水肿引起的，随后可能导致神经功能障碍。这些变化可能是与神经压迫相关症状发展的关键因素。
