期刊文献+

脑出血后早发癫癎患者血清氨基酸类神经递质测定分析 被引量:1

Analysis of Amino Acid Neurotransmitters of Blood in Patients with Early Developed Epilepsy after Intracerebral Haemorrhage
下载PDF
导出
摘要 目的:探讨脑出血后早发癫癎的发病机制。方法:将50例年龄、性别等一般情况相匹配的脑出血患者分为脑出血后早发癫癎(A)组和脑出血(B)组各25例,A组再根据出血部位不同分为皮质亚组18例与非皮质亚组7例,均运用反相高效液相色谱分析法测定血清兴奋性氨基酸递质(Glu、Asp)及抑制性氨基酸递质(GABA、Gly、Ala)水平。结果:A组血清Glu、Asp、GABA浓度升高,Gly、Ala浓度降低,与B组比较差异有统计学意义(P<0.05),皮质亚组血清Glu、Asp浓度较非皮质亚组高,差异有统计学意义(P<0.05),血清GABA、Gly、Ala浓度与非皮质亚组比较,差异无统计学意义。结论:脑出血后早发癫癎的机制可能与癎性发作时兴奋性氨基酸的兴奋毒性导致神经细胞损伤,致使机体自我调节机制改变,GABA代偿性释放增加有关。脑出血的部位位于皮质时更容易发生癫癎,且皮质部位脑出血癎性发作与兴奋性氨基酸的兴奋毒性作用的关系更加密切。 Objective: To investigate the pathogenesis of early developed epilepsy after intracerebral haemorrhage. Method:Fifty intracerehral haemorrhagic patients with the similar ages and gender were divided into epileptic group (n = 25) and intracerebral haemorrhage group (n= 25) according to with/without early epilepsy. The epileptic group were further divided into 2 subgroups: cortex subgroup (18 cases) and non-cortex subgroup (7 cases). The concentrations of amino acid transmitters(Glu, Asp, GABA, Gly, Ala) in serum in the both groups were analyzed by reversed-phase high performance liquid chromatography method. Results: The concentrations of Glu, Asp, and GABA in the epileptic group were significantly increased when compared with those in the intracerebral haemorrhage group,while the concentrations of Gly and Ala were significantly reduced in the epileptic group (P〈0. 05). The concentrations of Glu and Asp in the cortex subgroup were significantly higher than those in the non-cortex subgroup (P〈0. 05), while the concentrations of GABA, Gly and Ala in both the cortex and non-cortex subgroups showed no difference. Conclusion: The enhanced exitotoxicity might play an important role in the pathological process of early epilepsy after intracerebral haemorrhage.
出处 《神经损伤与功能重建》 2009年第3期181-184,共4页 Neural Injury and Functional Reconstruction
关键词 脑出血 癫癎 氨基酸类神经递质 intracerebral haemorrhage epilepsy amino acid neurotransmitters
  • 相关文献

参考文献16

二级参考文献46

共引文献249

同被引文献11

引证文献1

二级引证文献4

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部