面肌痉挛面神经脱髓鞘的实验研究

Experimental study on demyelination of facial nerve in hemifacial spasm

目的 观察面肌痉挛家兔面神经-面肌的组织学变化,探讨面肌痉挛的发病机制。方法 选择健康成年家兔16只,随机分为对照组和模型组,每组8只;将模型组家兔面部软组织在茎乳孔处切开,找到面神经主干用硅胶夹压迫,对照组不予处理;术后3周,取两组家兔面神经以及面肌作HE染色及透射电镜切片观察。结果 (1)面神经:对照组面神经纤维轴索排列整齐,髓鞘连续完整;模型组面神经脱髓鞘明显,髓鞘松解脱失,轴突退行性变。(2)面肌:对照组HE染色见骨骼肌横纹明显,核数个,扁椭圆形,位居细胞周边部位,肌内膜、肌束膜明显;电镜下见肌原纤维上I带和A带明暗相间,I带中的Z线清晰可见,肌浆内可见线粒体、内质网等细胞器。模型组HE染色见面肌富含无髓神经纤维束,较对照组显著增多(P<0.01);肌内膜毛细血管丰富,较对照组显著增多(P<0.01)。电镜下见面肌肌丝较模糊,A带变浅,I带不明显,肌浆网扩张,线粒体变大或呈空泡状。结论 (1)面神经受压后发生脱髓鞘改变,为面肌痉挛发病的形态学基础和始动因素;(2)受压面神经所支配的面肌内出现较多无髓神经纤维束,可增多增强面肌内神经冲动的传导,从而增强面肌收缩,导致面肌痉挛发生;(3)受压面神经所支配的面肌肌内膜内出现丰富毛细血管,是面肌痉挛发生的密切相关因素。

Objective To observe the histological changes of facial nerve and facial muscle in hemifacial spasm and explore the pathogenesis of hemifacial spasm.Methods Sixteen adult rabbits were randomly divided into control group and model group,with 8 rabbits in each group.For model group.The facial soft tissue of rabbits was cut at the stylomastoid foramen,and the main trunk of facial nerve was found and compressed with silicone clamp.3 weeks after operation,the facial nerve and facial muscle of the control group and the model group were observed by HE staining and transmission electron microscope section.Results(1)Facial nerve:HE staining and transmission electron microscopy showed that the axons of facial nerve fibers in the control group were neatly arranged and myelin sheath was continuous and complete;In the model group,facial nerve demyelination was obvious and axons degeneration was observed.(2)Facial muscle:In the control group,HE staining showed obvious skeletal muscle stripes,several nuclei,oblate ovals,located in the peripheral parts of cells,and obvious intramuscular and fascicle membranes;Under electron microscope,the I band and A band on the myofibrillar fibers alternated between light and dark,the Z line in the I band was clearly visible,and mitochondria,endoplasmic reticulum and other organelles were visible in the sarcasm.In the model group,HE staining showed that the facial muscle was rich in unmyelinated nerve fiber bundles(P<0.01),and the intramuscular capillaries were abundant(P<0.01).Under electron microscope,the myofilaments of facial muscle were blurred,the A band was shallow,the I band was not obvious,the sarcoplasmic reticulum was expanded,and the mitochondria were enlarged or vacuumed.Conclusion(1)The demyelinating changes occurred after facial nerve compression,and this histological change is the morphological basis and initiating factor of hemifacial spasm.(2)There are more unmyelinated nerve fiber bundles in the facial muscle innervated by the compressed facial nerve,which can increase and enhance the conduction of nerve impulse in the facial muscle,thus enhancing the contraction of the facial muscle,resulting in the occurrence of facial spasm.(3)There are abundant capillaries in the of the facial muscle innervated by the compressed facial nerve.It is believed that the increase of capillaries meets the needs of enhanced facial muscle contraction and is a closely cooperating factor in the occurrence of facial spasm.