Abstract：
BACKGROUND: Idiopathic trigeminal neuralgia (TN) cases encountered frequently in daily practice indicate significant gaps that still need to be illuminated in the etiopathogenesis. In this study, a novel TN animal model was developed by compressing the dorsal horn (DH) of the upper cervical spinal cord.
METHODS: Eighteen rabbits were equally divided into three groups, namely control (CG), sham (SG), and spinal cord compression (SCC) groups. External pressure was applied to the left side at the C3 level in the SCC group. Dorsal hemilaminectomy was performed in the SG, and the operative side was closed without compression. No procedure was implemented in the control group. Samples from the SC, TG, and ION were taken after seven days. For the histochemical staining, damage and axons with myelin were scored using Hematoxylin and Eosin and Toluidine Blue, respectively. Immunohistochemistry, nuclei, apoptotic index, astrocyte activity, microglial labeling, and CD11b were evaluated.
RESULTS: Mechanical allodynia was observed on the ipsilateral side in the SCC group. In addition, both the TG and ION were partially damaged from SC compression, which resulted in significant histopathological changes and increased the expression of all markers in both the SG and SCC groups compared to that in the CG. There was a notable increase in tissue damage, an increase in the number of apoptotic nuclei, an increase in the apoptotic index, an indication of astrocytic gliosis, and an upsurge in microglial cells. Significant increases were noted in the SG group, whereas more pronounced significant increases were observed in the SCC group. Transmission electron microscopy revealed myelin damage, mitochondrial disruption, and increased anchoring particles. Similar changes were observed to a lesser extent in the contralateral spinal cord.
CONCLUSIONS: Ipsilateral trigeminal neuropathic pain was developed due to upper cervical SCC. The clinical finding is supported by immunohistochemical and ultrastructural changes. Thus, alterations in the DH due to compression of the upper cervical region should be considered as a potential cause of idiopathic TN.
METHODS: Eighteen rabbits were equally divided into three groups, namely control (CG), sham (SG), and spinal cord compression (SCC) groups. External pressure was applied to the left side at the C3 level in the SCC group. Dorsal hemilaminectomy was performed in the SG, and the operative side was closed without compression. No procedure was implemented in the control group. Samples from the SC, TG, and ION were taken after seven days. For the histochemical staining, damage and axons with myelin were scored using Hematoxylin and Eosin and Toluidine Blue, respectively. Immunohistochemistry, nuclei, apoptotic index, astrocyte activity, microglial labeling, and CD11b were evaluated.
RESULTS: Mechanical allodynia was observed on the ipsilateral side in the SCC group. In addition, both the TG and ION were partially damaged from SC compression, which resulted in significant histopathological changes and increased the expression of all markers in both the SG and SCC groups compared to that in the CG. There was a notable increase in tissue damage, an increase in the number of apoptotic nuclei, an increase in the apoptotic index, an indication of astrocytic gliosis, and an upsurge in microglial cells. Significant increases were noted in the SG group, whereas more pronounced significant increases were observed in the SCC group. Transmission electron microscopy revealed myelin damage, mitochondrial disruption, and increased anchoring particles. Similar changes were observed to a lesser extent in the contralateral spinal cord.
CONCLUSIONS: Ipsilateral trigeminal neuropathic pain was developed due to upper cervical SCC. The clinical finding is supported by immunohistochemical and ultrastructural changes. Thus, alterations in the DH due to compression of the upper cervical region should be considered as a potential cause of idiopathic TN.
摘要：
背景：在日常实践中经常遇到的特发性三叉神经痛（TN）病例表明在病因发病机制中仍然需要阐明的重要差距。在这项研究中,通过压缩上颈脊髓的背角（DH），开发了一种新型的TN动物模型。
方法:18只大白兔平均分为3组,即控制(CG)，sham(SG),脊髓压迫（SCC）组。在SCC组中，在C3水平向左侧施加外部压力。在SG中进行了背侧半椎板切除术，手术侧关闭，没有压迫。对照组未实施任何程序。SC的样本，TG,离子是在七天后服用的。对于组织化学染色，使用苏木精、伊红和甲苯胺蓝对髓鞘损伤和轴突进行评分，分别。免疫组织化学,原子核,凋亡指数，星形胶质细胞活性，小胶质细胞标记，和CD11b进行评估。
结果：在SCC组中，在同侧观察到机械性异常性疼痛。此外,TG和ION均因SC压缩而部分受损，与CG相比，这导致了显着的组织病理学变化，并增加了SG和SCC组的所有标志物的表达。组织损伤明显增加，凋亡细胞核数量的增加，凋亡指数的增加，星形胶质细胞增生的迹象,和小胶质细胞的激增。SG组显著增加，而在SCC组中观察到更明显的显著增加.透射电镜显示髓鞘损伤,线粒体破坏，和增加锚定颗粒。在对侧脊髓中观察到较小程度的类似变化。
结论：同侧三叉神经疼痛是由于上颈椎SCC引起的。临床发现得到免疫组织化学和超微结构变化的支持。因此，由于上子宫颈受压而引起的DH改变应被视为特发性TN的潜在原因。
方法:18只大白兔平均分为3组,即控制(CG)，sham(SG),脊髓压迫（SCC）组。在SCC组中，在C3水平向左侧施加外部压力。在SG中进行了背侧半椎板切除术，手术侧关闭，没有压迫。对照组未实施任何程序。SC的样本，TG,离子是在七天后服用的。对于组织化学染色，使用苏木精、伊红和甲苯胺蓝对髓鞘损伤和轴突进行评分，分别。免疫组织化学,原子核,凋亡指数，星形胶质细胞活性，小胶质细胞标记，和CD11b进行评估。
结果：在SCC组中，在同侧观察到机械性异常性疼痛。此外,TG和ION均因SC压缩而部分受损，与CG相比，这导致了显着的组织病理学变化，并增加了SG和SCC组的所有标志物的表达。组织损伤明显增加，凋亡细胞核数量的增加，凋亡指数的增加，星形胶质细胞增生的迹象,和小胶质细胞的激增。SG组显著增加，而在SCC组中观察到更明显的显著增加.透射电镜显示髓鞘损伤,线粒体破坏，和增加锚定颗粒。在对侧脊髓中观察到较小程度的类似变化。
结论：同侧三叉神经疼痛是由于上颈椎SCC引起的。临床发现得到免疫组织化学和超微结构变化的支持。因此，由于上子宫颈受压而引起的DH改变应被视为特发性TN的潜在原因。
