磁共振成像对点燃模型癫痫进行性发展的研究

Epilepsy is one of the most common neurological disorders in the world, it is difficult to cure, and the pathogenic mechanism of epilepsy is still unclear. Brain dysfunction and the white matter disease are the common clinical manifestation and pathological changes of epileptic, such as cognitive dysfunction, brain function plasticity, the reduced white matter and decreased neuronal connection of the focus. Most objects of the previous studies are definitive epileptic or models, and the work focus on epileptogenesis process is still very rare. Study of epileptogenesis is important to understand the pathogenic mechanism of epilepsy. In view of this, this subject is aimed at using the pentylenetetrazole-induced kindling to study the development of epileptogenesis, manganese enhanced magnetic resonance imaging (MEMRI) and diffusion tensor imaging (DTI) are used to detect the changes of brain functional activity and white matter during the kindling, and combining with pathological and behavioral testing to explore the pathological basis of these changes and their behavioral responses. The overall aim of this study is to gain insights into the neuropathology of the pathogenic mechanism of epilepsy, and it may also play a role in promoting the establishment of early diagnosis and treatment of epilepsy.

癫痫是国内外发病率较高的神经系统疾病，难治愈，且致病机理复杂。脑功能异常和白质病变是癫痫常见的临床表现与病理改变，包括脑认知功能障碍或脑功能可塑性重组，病灶区脑白质减少，与其它脑区白质连接减弱等。目前有关癫痫的研究主要是针对已致痫的对象，而着眼于癫痫形成的进行性发展过程的研究还很少见。立足于癫痫化过程的动态研究对于探讨癫痫发病机制具有重要的意义。鉴于此，本课题拟利用戊四氮点燃大鼠模型，主要针对癫痫的进行性发展过程，采用锰离子增强磁共振成像（MEMRI）和扩散张量磁共振成像（DTI）方法，动态地研究脑功能活动及白质连接在癫痫进行性发展过程中的变化，并结合病理和行为学检测，探索这种变化的病理基础及其与行为反应的相关性。本项目的研究成果有望为阐明癫痫致病机理的研究提供神经病理学方面的信息，将为癫痫早期诊断与治疗方法的建立提供研究基础。

癫痫是临床常见的神经疾病之一，其致病机制和治疗方法是目前医学研究的重要课题。磁共振成像（MRI）是临床癫痫诊断和癫痫灶定位的重要手段。由于临床研究的局限性，动物模型被广泛应用于癫痫研究当中，戊四氮（PTZ）常用于诱导慢性点燃癫痫。研究运用MRI免疫组化方法从组织形态、白质病变及病理改变方面对PTZ慢性致癫痫大鼠进行研究，探讨了这种模型中癫痫致病机制、发展过程中的一些基础问题。.根据造模过程中动物模型的行为学检测结果，将实验动物分为对照组、未点燃组和点燃组。MRI结果显示点燃和未点燃动物在扣带皮质FA值显著增高，纹状体和苍白球区域FA值则显著降低，且点燃动物感觉运动皮质、黒质的FA值降低，内嗅皮质、海马齿状回区域FA值显著增高。组化结果显示点燃动物海马有明显的胶质细胞和小胶质细胞增生。.结果分析认为，扣带皮质、纹状体和苍白球可能是PTZ致点燃的一个易感区域，内嗅皮质和海马功能的变化是点燃的标志。神经链接在纹状体-苍白球-底丘脑核-黑质通路上减弱，在内嗅皮质-海马通路上增强，这两条神经通路的活动可能与PTZ诱导癫痫的致病机制有关。