Plasticity of Language Networks in Childhood Epilepsy

描述（由申请人提供）：本研究将检查癫痫发作对早发性和慢性癫痫儿童语言技能功能解剖的影响。这一人群提供了一个机会，以深入了解慢性神经元功能障碍对人类语言能力及其大脑表征发展的影响。我们假设癫痫发作导致神经元损伤，并迫使基本认知技能（如语言）的表达重组。癫痫早期发作的患者，预计有更大的变化，在功能磁共振成像语言激活模式比那些晚发病，这些变化预计只会发生在几年后的癫痫。 将使用高分辨率结构1.5特斯拉MR 1和功能MRI对儿童进行评估。图像数据也将被转换成标准的大脑图谱，以促进受试者内的区域比较，以及考虑语言激活模式的受试者间的变异性。将比较三组：1）定位相关癫痫发作后1年内的儿童2）慢性定位相关癫痫儿童（持续时间>3年）3）正常对照人群。 作为这项研究的结果，在认知发展和神经元可塑性的关键时期，语言的解剖组织将获得更好的理解。我们将确定癫痫发作本身或共同的大脑病理是大脑可塑性背后的驱动力。这些信息对于规划干预战略以减轻癫痫病发作时的后遗症和最易受其影响的儿童的后遗症非常重要。与急性和有限的神经元损伤，如头部创伤和中风，癫痫是一种慢性过程，持续但阵发性神经元后遗症。此外，可以在疾病过程开始时识别和评估患者，从而可以评估和监测神经元反应和可塑性程度。

DESCRIPTION (provided by applicant): This study will examine the effects of seizures on the functional anatomy of language skills in children with both early onset and chronic epilepsy. This population provides an opportunity to gain insight into the effect of chronic neuronal dysfunction on the development of human language abilities and their brain representation. We hypothesize that seizures cause neuronal injury and force reorganization of the representation of essential cognitive skills, such as language. Patients with early epilepsy onset are expected to have greater variation in fMRI language activation patterns than those with later onset; these changes are expected to occur only after several years of epilepsy. Children will be evaluated with high resolution structural 1.5 Tesla MR.1, and functional MRI. Image data will also be transformed into a standard brain atlas to facilitate intra-subject regional comparison, as well as to account for inter-subject variability of language activation patterns. Three groups will be compared: 1) children within one year after localization related seizure onset 2) children with chronic localization related epilepsy (>3 years duration) 3) a normal control population. As a result of this study a greater understanding of the anatomic organization of language during critical periods of cognitive development and neuronal plasticity will be gained. We will determine whether seizures themselves or a common brain pathology is the driving force behind brain plasticity. Such information is important to plan intervention strategies to mitigate the sequelae of epilepsy at disease onset and in the most vulnerable children to its effects. Unlike acute and limited neuronal insults, such as head trauma and stroke, epilepsy is a chronic process with continuing but paroxysmal neuronal sequelae. Furthermore, patients may be identified and evaluated at the outset of the disease process so that the neuronal response and degree of plasticity may be assessed and monitored.