Shibukawa M, Shirai Y
Department of Orthopaedic Surgery, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan.
J Orthop Sci. 2001;6(3):262-8. doi: 10.1007/s007760100045.
Slow-speed elongation of the sciatic nerves was induced in 41 rabbits by lengthening the osteotomized femur by 2.1 mm/day with an external fixator. Time courses were monitored. About 2 weeks after elongation began, the amplitude of the compound nerve action potentials decreased, and delayed latency began. Histological observations showed that the wavy structure of the nerve fibers was lost during the stage at which reduction in the amplitude of action potentials occurred. In some nerve fibers, narrowing of the axons was observed. Further elongation caused delay in the percent latency. Histologically, collagen fibers were noted in the nerve fascicles, as well as narrowing in all the nerve fibers. When elongation ceased at the stage at which a reduction in the amplitude of action potential was noted, recovery from nerve damage followed. When elongation did not cease until the stage at which latency was delayed, however, recovery was not apparent, either histologically or electrophysiologically. The critical level of percent amplitude for recovery was at 82.4% of the original level (the critical rate for bone lengthening was 20.5%).
通过使用外固定器以每天2.1毫米的速度延长截骨的股骨，在41只兔子中诱导坐骨神经的低速延长。监测时间进程。延长开始约2周后，复合神经动作电位的幅度降低，潜伏期开始延迟。组织学观察表明，在动作电位幅度降低的阶段，神经纤维的波浪状结构消失。在一些神经纤维中，观察到轴突变窄。进一步延长导致潜伏期百分比延迟。组织学上，在神经束中发现胶原纤维，并且所有神经纤维都变窄。当在观察到动作电位幅度降低的阶段停止延长时，神经损伤随之恢复。然而，当延长直到潜伏期延迟的阶段才停止时，无论是组织学还是电生理学上，恢复都不明显。恢复的临界幅度百分比水平为原始水平的82.4%（骨延长的临界速率为20.5%）。
