NEUROPSYCHOLOGICAL PROGESSION IN NEW ONSET EPILEPSY

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 我们先前对患有慢性定位相关(颞叶)癫痫的成年人和健康对照组的研究表明，儿童期癫痫发作与对大脑结构和认知功能的普遍不利神经发育影响有关(NS-37738)。这项建议的目的是直接描述这种不利的神经发育影响的时间、原因和后果。采用横断面和纵向相结合的设计，将75名新发的定位相关癫痫儿童(年龄8-18岁)与75名年龄和性别匹配的对照组进行比较。对神经心理状态和神经成像(定量MRI、扩散张量成像和磁化传递成像)的横断面和两年纵向评估将与有关神经发育史、临床癫痫特征和精神疾病的信息相结合，以阐明大脑结构和认知明显异常的时间、病因和后果。我们假设如下：(1)与对照组相比，新发定位相关癫痫儿童将表现出全身性认知障碍，脑组织总体积(尤其是脑白质体积)普遍减少，以及脑白质微结构异常；(2)与对照组相比，新发癫痫儿童原有神经发育异常的频率将显著增加，并与癫痫发作时的神经成像和认知异常有关；(3)与对照组相比，持续的儿童期癫痫将与正常认知和脑发育(尤其是脑白质)的发育滞后和精神障碍的增加有关。(4)癫痫发病年龄越早，大脑发育和认知发育滞后的预测作用越强，而癫痫的严重程度与精神疾病发病率的增加关系最大。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Our prior investigation of adults with chronic localization-related (temporal lobe) epilepsy and healthy controls has shown childhood onset epilepsy to be associated with a generalized adverse neurodevelopmental impact on brain structure and cognitive function (NS-37738). The purpose of this proposal is to directly characterize the timing, cause and consequences of this adverse neurodevelopmental impact. Using a combined cross-sectional and longitudinal design, 75 children (age 8-18) with new onset localization-related epilepsy will be compared to 75 age and gender matched controls. Cross-sectional and two-year longitudinal assessment of neuropsychological status and neuroimaging (quantitative MRI, diffusion tensor imaging, and magnetization transfer imaging) will be integrated with information regarding neurodevelopmental history, clinical epilepsy characteristics and psychiatric morbidity in order to clarify the timing, etiology and consequences of evident abnormalities in brain structure and cognition. We hypothesize the following: (1) children with new onset localization-related epilepsy will exhibit generalized cognitive impairment, generalized reduction in total brain tissue volumes (especially cerebral white matter volumes), and microstructural abnormalities in cerebral white matter compared to controls, (2) frequency of preexisting neurodevelopmental abnormalities will be significantly increased in children with new onset epilepsy compared to controls and will be associated with neuroimaging and cognitive abnormalities at epilepsy onset, (3) ongoing childhood onset epilepsy will be associated with lags in normal cognitive and brain development (especially cerebral white matter) and increased psychiatric morbidity compared to controls, and (4) earlier age of epilepsy onset will be the strongest predictor of lags in brain growth and cognitive development while seizure severity will be most strongly associated with increased psychiatric morbidity.