Neurometabolism in human epilepsy
Neurometabolism in human epilepsy
复制标题
DOI：
10.1111/j.1528-1167.2008.01508.x
复制
发表时间：
2008-01-01
期刊：
影响因子：
5.6
通讯作者：
Spencer, Dennis D.
中科院分区：
文献类型：
--
作者：
Pan, Jullie W.;Williamson, Anne;Spencer, Dennis D.
目的：由于大脑功能需要大量且持续的能量，神经代谢功能障碍是癫痫脑的一个关键病理生理学方面。此外，神经代谢功能障碍具有许多自我传播的特征，这些特征是癫痫发生过程的典型特征，也就是说，每次发生都使进一步线粒体和能量损伤的可能性更大。因此，神经代谢异常可能不仅是癫痫大脑的慢性伴随物，而且也是癫痫发生的直接因素。方法：我们综合代谢成像、电生理学、微透析以及颅内脑电图和神经病理学的人体研究，检查癫痫神经代谢功能障碍的证据。结果：作为一种无创功能成像方法，定量磁共振波谱成像（MRSI）测量了线粒体和能量功能障碍的异常（通过1H或31P光谱）与癫痫功能障碍的几种病理生理指标有关。对于接受海马切除术的患者，术中 13C-葡萄糖周转研究显示，与硬化海马中的氧化相比，神经递质（谷氨酸-谷氨酰胺）循环显着减少。细胞外谷氨酸的增加（长期以来与癫痫发作可能性增加有关）与 31P MR 测量的能量下降以及 Teager 能量的 EEG 测量增加显着相关，进一步论证了谷氨酸对过度兴奋性的直接作用。讨论：鉴于代谢性能对大脑兴奋性的重要贡献，线粒体和能量状态的许多方面与人类的电生理和微透析测量显着相关也就不足为奇了。癫痫。这可能与线粒体损伤的自我传播性质特别相关，但也可能有助于确定可能制定干预措施的条件。
Purpose: Because of the large and continuous energetic requirements of brain function, neurometabolic dysfunction is a key pathophysiologic aspect of the epileptic brain. Additionally, neurometabolic dysfunction has many self-propagating features that are typical of epileptogenic processes, that is, where each occurrence makes the likelihood of further mitochondrial and energetic injury more probable. Thus abnormal neurometabolism may be not only a chronic accompaniment of the epileptic brain, but also a direct contributor to epileptogenesis.Methods: We examine the evidence for neurometabolic dysfunction in epilepsy, integrating human studies of metabolic imaging, electrophysiology, microdialysis, as well as intracranial EEG and neuropathology.Results: As an approach of noninvasive functional imaging, quantitative magnetic resonance spectroscopic imaging (MRSI) measured abnormalities of mitochondrial and energetic dysfunction (via 1H or 31P spectroscopy) are related to several pathophysiologic indices of epileptic dysfunction. With patients undergoing hippocampal resection, intraoperative 13C-glucose turnover studies show a profound decrease in neurotransmitter (glutamate-glutamine) cycling relative to oxidation in the sclerotic hippocampus. Increased extracellular glutamate (which has long been associated with increased seizure likelihood) is significantly linked with declining energetics as measured by 31P MR, as well as with increased EEG measures of Teager energy, further arguing for a direct role of glutamate with hyperexcitability.Discussion: Given the important contribution that metabolic performance makes toward excitability in brain, it is not surprising that numerous aspects of mitochondrial and energetic state link significantly with electrophysiologic and microdialysis measures in human epilepsy. This may be of particular relevance with the self-propagating nature of mitochondrial injury, but may also help define the conditions for which interventions may be developed.