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首页> 外文期刊>Spine >Experimental spinal stenosis: relationship between degree of cauda equina compression, neuropathology, and pain.
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Experimental spinal stenosis: relationship between degree of cauda equina compression, neuropathology, and pain.

机译：实验性椎管狭窄：马尾神经受压程度，神经病理学和疼痛之间的关系。

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STUDY DESIGN: An analysis of pathologic changes after different degrees of cauda equina compression. OBJECTIVES: To explore the association between the degree of the cauda equina compression and the extent of pathologic change, expression of tumor necrosis factor (TNF-alpha), and neuropathic pain. To compare with distal nerve compression injury. SUMMARY OF BACKGROUND DATA: Compression of the cauda equina reduces blood flow in compressed nerve roots and causes TNF-alpha expression and neuropathological change. In peripheral nerve, expression of TNF-alpha in Schwann cells is associated with primary demyelination without pain while TNF-alpha expression by macrophages is associated with axonal (Wallerian) degeneration and pain. METHODS: Two square-shaped pieces of silicon were placed into the fourth and sixth epidural space in rats. Various sized silicon was used in each group (mild, moderate, and strong compression groups), while no silicon was used in the sham-operated group. Mechanical allodynia was determined by the von Frey test. Comparisons of the number of TNF-alpha- and apoptosis-positive cells were made using immunohistochemistry. RESULTS: There was no significant mechanical allodynia observed in any group. Some nerve roots showed demyelination following mild cauda equina compression. Axonal degeneration was observed in the moderate and strong cauda equina compression groups. TNF-alpha-immunoreactive cells were increased in all compression groups. Apoptosis of dorsal root ganglion cells was less than apoptosis in the spinal cord. CONCLUSION: Mild cauda equina compression induces TNF-alpha expression and demyelination. Moderate and strong cauda equina compression induces TNF-alpha expression and degeneration associated with macrophage invasion. Neither demyelination nor degeneration in the cauda equina induced mechanical allodynia. Nerve lesions proximal to the dorsal root ganglion do not produce significant mechanical allodynia. Dorsal root ganglion apoptosis may be important for pain.
机译：研究设计：分析不同程度的马尾神经受压后的病理变化。目的：探讨马尾神经受压程度与病理改变，肿瘤坏死因子（TNF-α）表达和神经性疼痛之间的关系。与远端神经受压比较。背景数据摘要：马尾神经受压会减少受压神经根的血流量，并导致TNF-α表达和神经病理改变。在周围神经中，雪旺细胞中TNF-α的表达与无疼痛的原发性脱髓鞘有关，而巨噬细胞的TNF-α的表达与轴突（瓦勒氏）变性和疼痛有关。方法：将两个方形硅片分别置于大鼠的第四和第六硬膜外腔。每个组（轻度，中度和强压缩组）中使用各种尺寸的硅，而假手术组中不使用硅。机械性异常性疼痛通过冯·弗雷（von Frey）试验确定。使用免疫组织化学比较TNF-α和凋亡阳性细胞的数量。结果：在任何组中均未观察到明显的机械性异常性疼痛。轻度马尾神经受压后，一些神经根显示脱髓鞘。在中等和强马尾压迫组中观察到轴突变性。在所有压缩组中，TNF-α免疫反应性细胞均增加。脊髓背根神经节细胞的凋亡少于凋亡。结论：马尾轻度压迫诱导TNF-α表达和脱髓鞘。中度和强烈的马尾马受压诱导巨噬细胞侵袭相关的TNF-α表达和变性。马尾脱髓鞘或变性均不会引起机械性异常性疼痛。背根神经节近端的神经病变不会产生明显的机械性异常性疼痛。背根神经节凋亡对于疼痛可能很重要。

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