Plasticity of Language Networks in Childhood Epilepsy

描述（由申请人提供）：本研究将研究癫痫发作对早期和慢性癫痫儿童语言技能功能解剖的影响。这个群体提供了一个机会来深入了解慢性神经元功能障碍对人类语言能力发展及其大脑表征的影响。我们假设癫痫发作会导致神经元损伤，并迫使基本认知技能（如语言）的再现重组。早发癫痫患者在fMRI语言激活模式上比晚发癫痫患者有更大的差异；这些变化只有在癫痫发作数年后才会发生。儿童将通过高分辨率结构1.5特斯拉MR.1和功能性MRI进行评估。图像数据也将被转换成标准的脑图谱，以方便受试者内部区域比较，以及解释受试者之间语言激活模式的可变性。将三组进行比较：1)定位相关性癫痫发作后一年内的儿童2)慢性定位相关性癫痫患儿（> ~ 3年）3)正常对照人群。由于这项研究的结果，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还是一种常见的脑部病理是大脑可塑性背后的驱动力。这些信息对于制定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影响是很重要的。与急性和有限的神经元损伤（如头部创伤和中风）不同，癫痫是一个慢性过程，具有持续但阵发性的神经元后遗症。此外，可以在疾病过程开始时识别和评估患者，以便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.