Neuroanatomical correlates of cognitive phenotypes in temporal lobe epilepsy.
Neuroanatomical correlates of cognitive phenotypes in temporal lobe epilepsy.
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DOI：
10.1016/j.yebeh.2009.05.012
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发表时间：
2009-08
期刊：
影响因子：
--
通讯作者：
Hermann B
中科院分区：
文献类型：
--
作者：
Dabbs K;Jones J;Seidenberg M;Hermann B
先前的研究描述了颞叶癫痫的三种认知表型；每种表型都与不同的临床癫痫发作和人口学特征、大脑总体积(灰白色、白色、脑脊液)和海马体体积以及预期的认知轨迹有关。这项研究的目的是详细描述与每种认知表型相关的特定神经解剖异常。对健康对照组(n=53)和颞叶癫痫患者(n=55)的高分辨率MRI扫描，按认知表型分组(轻度受损；记忆力受损；记忆力、执行力和速度受损)，检查整个皮质外套膜灰质厚度的模式以及皮质下结构、胼胝体和小脑区域的体积。颞叶和颞外皮质厚度、皮质下结构(海马体、丘脑、基底节)、胼胝体所有区域和双侧小脑灰质的体积增加的异常通常以一种逐步的方式区分认知表型。最完整的解剖结构在轻度癫痫组观察到，最异常的解剖结构在癫痫组明显，记忆、执行和速度受损。根据经验得出的认知表型与广泛分布的皮质、皮质下、胼胝体和小脑网络中解剖异常的存在、严重程度和分布有关。
Previous research characterized three cognitive phenotypes in temporal lobe epilepsy; each associated with different profiles of clinical seizure and demographic characteristics, total cerebral (gray, white, CSF) and hippocampal volumes, and prospective cognitive trajectories. The objective of this investigation is to characterize in detail the specific neuroanatomical abnormalities associated with each cognitive phenotype. High resolution MRI scans from healthy controls (n=53) and temporal lobe epilepsy patients (n=55), grouped by cognitive phenotype (minimally impaired; memory impaired; memory, executive and speed impaired) are examined in regard to patterns of gray matter thickness throughout the cortical mantle as well as volumes of subcortical structures, corpus callosum, and regions of the cerebellum. Increasing abnormalities in temporal and extratemporal cortical thickness, volumes of subcortical structures (hippocampus, thalamus, basal ganglia), all regions of the corpus callosum, and bilateral cerebellar gray matter distinguish the cognitive phenotypes in a generally step-wise fashion. The most intact anatomy is observed in the minimally impaired epilepsy group and the most abnormal anatomy is evident in the epilepsy group with impairments in memory, executive and speed. Empirically derived cognitive phenotypes are associated with the presence, severity, and distribution of anatomic abnormalities in widely distributed cortical, subcortical, callosal, and cerebellar networks.
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