Xu Zisheng, Jiang Yifei, Mu Weidong, Li Wenlong, Zhang Guanjun, Jiang Shichao, Xu Peng
Department of Orthopedic Trauma, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China.
Department of Orthopaedic trauma, Shandong Provincial Hospital affiliated to Shandong First Medical University, Jinan, China.
Front Bioeng Biotechnol. 2022 Sep 21;10:920991. doi: 10.3389/fbioe.2022.920991. eCollection 2022.
We aimed to study the mechanism of sacral nerve injury caused by sacral fractures and the relationship between nerve decompression and nerve function. First, we observed the anatomical features of lumbosacral nerve root region in Sprague-Dawley rats. Next, the rats were divided into the sham, 10 g, 30 g, and 60 g groups for electrophysiological studies on nerve root constriction injury. Then we studied the biomechanical properties of rat nerve roots, lumbosacral trunk, and sacrum. Finally, we established a finite element analysis model of sacral nerve roots injury in rats and determined the correlation between sacral deformation and the degree of sacral nerve roots injury. Anatomical study showed L5 constitutes sciatic nerve, the length of the L5 nerve root is 3.67 ± 0.15 mm, which is suitable for electrophysiological research on nerve root compression injury. After a series of electrophysiological study of L5 nerve roots, our results showed that nerve root function was almost unaffected at a low degree of compression (10 g). Nerve root function loss began at 30 g compression, and was severe at 60 g compression. The degree of neurological loss was therefore positively correlated with the degree of compression. Combining biomechanical testing of the lumbosacral nerve roots, finite element analysis and neuroelectrophysiological research, we concluded when the sacral foramina deformation is >22.94%, the sacral nerves lose function. When the compression exceeds 33.16%, early recovery of nerve function is difficult even after decompression. In this study, we found that the neurological loss was positively correlated with the degree of compression. After early decompression, nerve root function recovery is possible after moderate compression; however, in severe compression group, the nerve function would not recover. Furthermore, FEA was used to simulate nerve compression during sacral fracture, as well as calculate force loading on nerve with different deformation rates. The relationship between sacral fractures and neurological loss can be analyzed in combination with neurophysiological test results.
我们旨在研究骶骨骨折导致骶神经损伤的机制以及神经减压与神经功能之间的关系。首先,我们观察了Sprague-Dawley大鼠腰骶神经根区域的解剖特征。接下来,将大鼠分为假手术组、10克、30克和60克组,进行神经根压迫损伤的电生理研究。然后我们研究了大鼠神经根、腰骶干和骶骨的生物力学特性。最后,我们建立了大鼠骶神经根损伤的有限元分析模型,并确定了骶骨变形与骶神经根损伤程度之间的相关性。解剖学研究表明,L5构成坐骨神经,L5神经根长度为3.67±0.15毫米,适合进行神经根压迫损伤的电生理研究。对L5神经根进行一系列电生理研究后,我们的结果表明,在低压迫程度(10克)时神经根功能几乎未受影响。在30克压迫时神经根功能开始丧失,在60克压迫时则很严重。因此,神经功能丧失程度与压迫程度呈正相关。结合腰骶神经根的生物力学测试、有限元分析和神经电生理研究,我们得出结论,当骶骨孔变形>22.94%时,骶神经失去功能。当压迫超过33.16%时,即使减压后神经功能也难以早期恢复。在本研究中,我们发现神经功能丧失与压迫程度呈正相关。早期减压后,中度压迫后神经根功能有可能恢复;然而,在重度压迫组中,神经功能无法恢复。此外,有限元分析用于模拟骶骨骨折期间的神经压迫,以及计算不同变形率下神经上的力加载。结合神经生理学测试结果可以分析骶骨骨折与神经功能丧失之间的关系。