文章摘要
胡秀秀,董靖德,王小姗,卢孝鹏,胡 正.血清神经元特异性烯醇化酶与儿童失神癫■关系的研究[J].南京医科大学学报,2010,(6):837~840
血清神经元特异性烯醇化酶与儿童失神癫■关系的研究
Study of relationship between serum neuron-specific enolase and childhood absence epilepsy
投稿时间:2010-02-10  
DOI:10.7655
中文关键词: 儿童失神癫■  神经元特异性烯醇化酶  酶联免疫法
英文关键词: childhood absence epilepsy  neuron-specific enolase  enzyme-linked immunosorbent assay
基金项目:南京市医学科技发展基金资助(ZKM05033)
作者单位
胡秀秀 南京医科大学附属脑科医院老年神经科,江苏 南京〓210029 
董靖德 南京医科大学附属脑科医院老年神经科,江苏 南京〓210029 
王小姗 南京医科大学附属脑科医院老年神经科,江苏 南京〓210029 
卢孝鹏 南京医科大学附属南京儿童医院神经内科,江苏 南京 210029 
胡 正 南京医科大学附属南京儿童医院神经内科,江苏 南京 210029 
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中文摘要:
      目的:探讨血清神经元特异性烯醇化酶(NSE)在失神癫■儿童癫■发作后水平的变化及其与脑损伤的关系?方法:选择失神癫■儿童22例,根据过度换气是否能诱发失神癫■发作分为2个亚组:失神发作组10例,失神非发作组12例;正常对照组20例?应用酶联免疫法(ELISA)测定各组血清NSE水平?结果:失神发作组癫■发作后30 min内,血清NSE水平显著高于失神非发作组及正常对照组,差异有统计学意义(P < 0.01);而失神非发作组与正常对照组相比,差异无统计学意义(P > 0.05)?结论:失神癫■发作后血清NSE水平明显升高,提示失神癫■发作后存在一定程度的脑神经元损伤,NSE可作为早期检测失神癫痫发作后神经元损伤的一个重要特异性生化指标?
英文摘要:
      Objective:To investigate the levels of neuron-specific enolase(NSE)in serum and to explore neuronal damage in absence epilepsy children after seizures. Methods:Twenty two children with absence epilepsy were enrolled,according to whether the hyperventilation induced absence seizures or not. The children were divided into two subgroups:10 cases of absence seizures group/12 cases of non-seizure group. and twenty healthy children served as normal control group. The blood samples were collected within 30 minutes after seizure. An enzyme-linked immunosorbent assay(ELISA)was used to detect the serum NSE in all the children. Results:The serum levels of NSE in the absence seizures group were significantly higher than those in non-seizure group and normal control group(P < 0.01);but there was no significant difference between non- seizures group and normal control group (P > 0.05). Conclusion:The levels of serum NSE in children with absence epilepsy were markedly increased after seizures. suggesting that a certain degree of neuronal damage may result from absence seizures. Neuron-specific enolase may server as an important specificity of biochemical marker in the early detection of neuronal damage after absence seizures.
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