Provenzale James M, Barboriak Daniel P, VanLandingham Kevan, MacFall James, Delong David, Lewis Darrell V
Department of Radiology, Duke University Medical Center, Box 3808, Durham, NC 27710, USA.
AJR Am J Roentgenol. 2008 Apr;190(4):976-83. doi: 10.2214/AJR.07.2407.
The objective of our study was to test the hypothesis that the finding of hyperintense hippocampal signal intensity on T2-weighted MR images soon after febrile status epilepticus is associated with subsequent hippocampal volume loss and persistent abnormal signal intensity on T2-weighted images (i.e., mesial temporal sclerosis).
Eleven children (mean age, 25 months) underwent initial MRI that included coronal temporal lobe imaging within 72 hours of febrile status epilepticus and follow-up imaging from 3 to 23 months later (mean, 9 months). A neuroradiologist blinded to clinical history graded initial and follow-up hippocampal signal intensity on a scale from 0 (normal) to 4 (markedly increased). Two blinded observers measured hippocampal volumes on initial and follow-up MR studies using commercially available software and volumes from 30 healthy children (mean age, 6.3 years). Initial signal intensity and hippocampal volume changes were compared using Kendall tau correlation coefficients.
On initial imaging, hyperintense signal intensity ranging from 1 (minimally increased) to 4 (markedly increased) was seen in seven children. Four children had at least one hippocampus with moderate or marked signal abnormality, three children had a hippocampus with mild or minimal abnormality, and four children had normal signal intensity. The Kendall tau correlation coefficient between signal intensity increase and volume change was -0.68 (p < 0.01). Five children (two with temporal lobe epilepsy and two with complex partial seizures) had hippocampal volume loss and increased signal intensity on follow-up imaging, meeting the criteria for mesial temporal sclerosis.
MRI findings of a markedly hyperintense hippocampus in children with febrile status epilepticus was highly associated with subsequent mesial temporal sclerosis.
我们研究的目的是检验以下假设,即热性惊厥状态后不久在T2加权磁共振成像(MRI)上发现海马高信号强度与随后的海马体积缩小以及T2加权图像上持续的异常信号强度(即内侧颞叶硬化)相关。
11名儿童(平均年龄25个月)在热性惊厥状态发作72小时内接受了首次MRI检查,其中包括冠状位颞叶成像,并在3至23个月后(平均9个月)进行了随访成像。一名对临床病史不知情的神经放射科医生将首次和随访时的海马信号强度按0(正常)至4(明显增加)的等级进行评分。两名不知情的观察者使用商用软件测量首次和随访MRI研究中的海马体积,并测量了30名健康儿童(平均年龄6.3岁)的海马体积。使用肯德尔tau相关系数比较初始信号强度和海马体积变化。
在首次成像时,7名儿童出现了1(轻度增加)至4(明显增加)的高信号强度。4名儿童至少有一个海马出现中度或明显信号异常,3名儿童有一个海马出现轻度或轻微异常,4名儿童信号强度正常。信号强度增加与体积变化之间的肯德尔tau相关系数为-0.68(p<0.01)。5名儿童(2名患有颞叶癫痫,2名患有复杂部分性发作)在随访成像时出现海马体积缩小和信号强度增加,符合内侧颞叶硬化的标准。
热性惊厥儿童海马明显高信号的MRI表现与随后的内侧颞叶硬化高度相关。