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目的探讨神经源性大便失禁患儿提肛肌功能障碍的发病机制。方法取22例神经源性大便失禁患儿的提肛肌标本,另取8例排便正常儿童的提肛肌标本作为对照,采用免疫组化染色(NCAM、S-100蛋白和MBP)进行病理学观察分析。结果脊髓脊膜膨出术后组和隐性脊柱裂患儿组,其NCAM、S-100蛋白和MBP染色强度均较弱,与正常对照组比较明显减弱,但脊髓脊膜膨出术后组和隐性脊柱裂患儿组之间NCAM、S-100蛋白和MBP指标无明显差异。结论神经源性大便失禁患儿的提肛肌明显缺乏NCAM和神经胶质细胞,这对神经细胞的分化、诱导、神经肌肉接头的形成产生不利影响,使提肛肌无法形成正常的神经支配和神经损伤后无法有效再生,严重影响提肛肌功能。
Objective To investigate the pathogenesis of levator ani dysfunction in children with neurogenic fecal incontinence. Methods Twenty-two cases of levator ani muscle from children with neurogenic fecal incontinence were enrolled in this study. Eight other levator ani specimens from normal defecation children were used as control. Immunohistochemical staining (NCAM, S-100 protein and MBP) Observation and analysis. Results The myelodysplastic group and recessive spina bifida group had weaker staining intensity of NCAM, S-100 protein and MBP than those of the normal control group, but the group of meningomyelia There was no significant difference in NCAM, S-100 protein and MBP between children with and without the recessive spina bifida. Conclusions The absence of NCAM and glial cells in the levator ani muscle of children with neurogenic fecal incontinence has an adverse effect on the differentiation and induction of nerve cells and the formation of neuromuscular junctions and prevents the levator ani muscle from forming normal innervation and Nerve injury can not be effectively regenerated, seriously affecting the levator ani muscle function.