Plasticity of Language Networks in Childhood Epilepsy

描述(申请人提供)：这项研究将检查癫痫发作对早发性和慢性癫痫儿童语言技能的功能解剖的影响。这一人群提供了一个机会，可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的发展的影响。我们假设癫痫发作会导致神经元损伤，并迫使语言等基本认知技能的表征重组。早期癫痫发作的患者在功能磁共振语言激活模式上的差异预计比起病较晚的患者更大；这些变化预计只有在癫痫发作几年后才会发生。儿童将接受高分辨率结构1.5特斯拉MR.1和功能磁共振成像的评估。图像数据也将被转换成标准的脑图谱，以便于受试者内部的区域比较，以及解释受试者之间语言激活模式的差异。将比较三组：1)局部性癫痫发作后一年内的儿童，2)慢性局部性癫痫儿童(病程3年)，3)正常对照组。通过这项研究，我们将对语言在认知发展和神经元可塑性的关键时期的解剖结构有更深入的了解。我们将确定癫痫发作本身还是常见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，以减轻癫痫发病时的后遗症以及最易受其影响的儿童的后遗症非常重要。与头部创伤和中风等急性和有限的神经元损伤不同，癫痫是一个持续但发作性神经元后遗症的慢性过程。此外，可以在疾病过程的开始就识别和评估患者，以便可以评估和监测神经元的反应和可塑性程度。

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.