癫痫症患者脑细胞线粒体代谢功能研究

目的:探讨人类大脑中主要的抑制性神经递质GABA(γ-氨基丁酸)对癫痫患者大脑代谢的作用。方法:二组接受癫痫部位颅内监测的患者:手术治疗的海马区癫痫症患者(MTLE)和新皮质区(非海马区癫痫)癫痫症患者。在颅内监测过程中使用体内微量透析法监测胞外GABA(ec GABA)。术前使用体内核磁共振成像技术检测N-乙酰天冬氨酸(NAA)与肌酸(NAA/Cr)的比例。使用标准方法进行神经病理学和海马体积检测。结果:在新皮质区组的海马区内,ec GABA的升高与NAA/Cr的升高相关(R=+0.70,P0.015,n=12),而在MTLE组的海马区中,ec GABA的升高是由NAA/Cr的下降所引起的(R=0.94,P0.001,n=8)。在MTLE组,ec GABA的升高和NAA/Cr的降低皆与神经胶质细胞数的增多有关(分别为R=+0.71,P0.01,n=12和R=0.76,P0.03)。二组中ec GABA的浓度和海马体积均没有明显的相关性。结论:在癫痫症中,ec GABA的升高是由一系列的代谢功能变化引起的。在癫痫部位以外,ec GABA和NAA/Cr同步升高;而在癫痫部位,线粒体功能的下降却伴随着ec GABA的升高。

Study on the Metabolismof Brain Cells Mitochondria Function in Epilepsy Patients

Objective:To investigate the inhibitory neurotransmitter GABA mainly in the human brain (GABA) on cerebral metabolismin patients with epilepsy. Methods:2 groups of patients with epilepsy received intracranial monitoring: operation treatment of hippocampal epilepsy (MTLE) and cortex (non hippocampal epilepsy) in patients with epilepsy. In vivo microdialysis monitoring of extracellular GABA (ecGABA) was applied in the process of intracranial monitoring. In vivo nuclear magnetic resonance imaging technique was used for the detection of N- acetyl aspartic acid(NAA) and creatinine(NAA/Cr) ratio. While standard method was used to detect neuropathology and hippocampal volume.Results:In the group of new cortex hippocampus, the evaluation of NAA/Cr was associated with that of ecGABA(R =+0.70, P<0.015, namely, n=12), while in group MTLE of the hippocampus, the increase of ecGABA was caused by the decrease of NAA/Cr (R= 0.94, P<0.001, n=8). In MTLE group, both the evaluation of ecGABA and the reduction of NAA/Cr were related to the increase of glial cell number(R''s +0.71=P<0.01, namely, n=12 and R''s = 0.76, P<0.03). The concentration of EcGABA had no obvious correlation with hippocampal volume in either group.Conclusion:In epilepsy, the increase of ecGABA is caused by a change in a series of metabolic function. In epilepsy outside the site, ecGABA and NAA/Cr synchronously increase; and in epilepsy parts, decrease of mitochondrial function is accompanied by the increase of ecGABA.