目的:本研究旨在确定海马T2高强度是否可预测高热性癫痫持续状态的后遗症,包括海马萎缩,硬化症,和内侧颞叶癫痫。
方法:在高热状态后平均4.4(SD=5.5,中位数=2.0)天内获得了>200名婴儿的急性磁共振成像(MRI),并在大约1、5和10年进行了MRI随访。海马大小,形态学,和T2信号强度由不了解临床细节的神经放射科医师进行视觉评分。海马容积法提供了定量测量。在发生两次或更多次无缘无故的癫痫发作时,受试者被重新评估癫痫.使用总脑体积将海马体积标准化。
结果:22例急性海马T2高强度患者中有14例返回随访MRI,10人发展为明确的海马硬化,持续了10年的随访。最初看起来正常的海马在视觉检查中保持正常。然而,在海马体正常的受试者中,体积表明男性,但不是女性,海马比对照组小,但是在发热状态下没有看到海马不对称的增加。44名受试者发展为癫痫;六个发展为内侧颞叶癫痫,六个,两个有明确的,两个人模棱两可,两个没有海马硬化。只有一名受试者在没有初始高强度的情况下发展了内侧颞叶癫痫,那个受试者有海马旋转不良。所有类型癫痫的十年累积发病率,包括内侧颞叶癫痫,在初始T2高强度的受试者中最高,在信号正常且无其他脑异常的受试者中最低。
结论:高热性癫痫持续状态后海马T2高强度预测海马硬化和颞叶内侧癫痫的可能性。在急性发作后MRI中,海马外观正常,随后外观保持正常。对称增长,降低癫痫的风险。体积测量检测到发热状态男性海马体积轻度减少。
OBJECTIVE: This
study was undertaken to determine whether hippocampal T2 hyperintensity predicts sequelae of febrile status epilepticus, including hippocampal atrophy, sclerosis, and mesial temporal lobe epilepsy.
METHODS: Acute magnetic resonance imaging (MRI) was obtained within a mean of 4.4 (SD = 5.5, median = 2.0) days after febrile status on >200 infants with follow-up MRI at approximately 1, 5, and 10 years. Hippocampal size, morphology, and T2 signal intensity were scored visually by neuroradiologists blinded to clinical details. Hippocampal volumetry provided quantitative measurement. Upon the occurrence of two or more unprovoked seizures, subjects were reassessed for epilepsy. Hippocampal volumes were normalized using total brain volumes.
RESULTS: Fourteen of 22 subjects with acute hippocampal T2 hyperintensity returned for follow-up MRI, and 10 developed definite hippocampal sclerosis, which persisted through the 10-year follow-up. Hippocampi appearing normal initially remained normal on visual inspection. However, in subjects with normal-appearing hippocampi, volumetrics indicated that male, but not female, hippocampi were smaller than controls, but increasing hippocampal asymmetry was not seen following febrile status. Forty-four subjects developed epilepsy; six developed mesial temporal lobe epilepsy and, of the six, two had definite, two had equivocal, and two had no hippocampal sclerosis. Only one subject developed mesial temporal epilepsy without initial hyperintensity, and that subject had hippocampal malrotation. Ten-year cumulative incidence of all types of epilepsy, including mesial temporal epilepsy, was highest in subjects with initial T2 hyperintensity and lowest in those with normal signal and no other brain abnormalities.
CONCLUSIONS: Hippocampal T2 hyperintensity following febrile status epilepticus predicted hippocampal sclerosis and significant likelihood of mesial temporal lobe epilepsy. Normal hippocampal appearance in the acute postictal MRI was followed by maintained normal appearance, symmetric growth, and lower risk of epilepsy. Volumetric measurement detected mildly decreased hippocampal volume in males with febrile status.