Spatial patterns of gray and white matter compromise relate to age of seizure onset in temporal lobe epilepsy.
Spatial patterns of gray and white matter compromise relate to age of seizure onset in temporal lobe epilepsy.
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颞叶癫痫中灰质和白质损害的空间模式与发病年龄有关。
DOI：
10.1016/j.nicl.2023.103473
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发表时间：
2023
影响因子：
4.2
通讯作者：
Mcdonald, Carrie R.
中科院分区：
文献类型：
--
作者：
Ballerini, Alice;Arienzo, Donatello;Stasenko, Alena;Schadler, Adam;Vaudano, Anna Elisabetta;Meletti, Stefano;Kaestner, Erik;Mcdonald, Carrie R.
我们探讨了颞叶癫痫 (TLE) 患者群体中皮质-皮质下灰质和白质损伤的空间模式。我们的结果支持 TLE 中皮质萎缩和浅表白质 (SWM) 微观结构损伤的独特空间模式。根据癫痫发作的时间，这些特征似乎彼此相关。儿童期发生 TLE 导致海马损伤和癫痫病灶同侧大部分半球的 SWM 损伤之间存在相关性。成年期发生 TLE 会导致癫痫病灶同侧的内侧颞叶同时出现皮质厚度和 SWM 损伤。颞叶癫痫 (TLE) 通常是一种神经发育障碍，涉及皮质下体积损失、皮质萎缩和白质 (WM) 破坏。然而，很少有研究探讨 TLE 的这些病理变化如何相互关联。在这项研究中，我们研究了 TLE 中灰质和白质变性的空间模式，并评估了这些模式之间的关系随着癫痫发作开始年龄的变化而变化的假设。 82 名 TLE 患者和 59 名健康对照者入组。 T1 加权图像用于获取海马体积和皮质厚度估计值。扩散加权成像用于获得浅层 WM (SWM) 和深层 WM 束的分数各向异性 (FA) 和平均扩散率 (MD)。协方差分析用于检查 WM 模式和 TLE 中灰质相对于对照组的改变，并控制了年龄和性别。然后进行滑动窗口相关性检查 SWM 变性、皮质变薄和海马萎缩与癫痫发作年龄之间的关系。与对照组相比，TLE 中的皮质变薄遵循广泛的双侧模式，在后中央顶叶区域明显，而 SWM 和深部 WM 损失主要发生在同侧颞边缘区域。窗口相关性揭示了儿童期癫痫患者的海马体积损失与全脑 SWM 破坏之间的关系。另一方面，在成人发病的 TLE 患者中，在癫痫病灶同侧的内侧颞叶观察到同时发生的皮质和 SWM 改变。我们的结果表明，尽管皮质、海马和 WM 的改变在群体水平上看起来在空间上不一致，但这些特征之间的关系取决于癫痫发作的年龄。 TLE 的神经发育方面可能会导致致痫区附近同时发生 WM 和海马变性，而成年期癫痫发作可能会引发一连串 SWM 微结构损失和神经退行性皮层萎缩。
We explored the spatial patterns of cortico-subcortical gray and white matter injury in a population of temporal lobe epilepsy (TLE) patients. Our results supported unique spatial patterns of cortical atrophy and superficial white matter (SWM) microstructural damage in TLE. Those features seemed to be related to each other based on when the seizures began. Developing TLE during childhood lead to a relationship between hippocampal damage and SWM injury of the majority of the hemisphere ipsilateral to the seizure focus. Developing TLE during adulthood causes co-occurring cortical thickness and SWM injury in the medial temporal lobe ipsilateral to the epileptogenic focus. Temporal Lobe Epilepsy (TLE) is frequently a neurodevelopmental disorder, involving subcortical volume loss, cortical atrophy, and white matter (WM) disruption. However, few studies have addressed how these pathological changes in TLE relate to one another. In this study, we investigate spatial patterns of gray and white matter degeneration in TLE and evaluate the hypothesis that the relationship among these patterns varies as a function of the age at which seizures begin. Eighty-two patients with TLE and 59 healthy controls were enrolled. T1-weighted images were used to obtain hippocampal volumes and cortical thickness estimates. Diffusion-weighted imaging was used to obtain fractional anisotropy (FA) and mean diffusivity (MD) of the superficial WM (SWM) and deep WM tracts. Analysis of covariance was used to examine patterns of WM and gray matter alterations in TLE relative to controls, controlling for age and sex. Sliding window correlations were then performed to examine the relationships between SWM degeneration, cortical thinning, and hippocampal atrophy across ages of seizure onset. Cortical thinning in TLE followed a widespread, bilateral pattern that was pronounced in posterior centroparietal regions, whereas SWM and deep WM loss occurred mostly in ipsilateral, temporolimbic regions compared to controls. Window correlations revealed a relationship between hippocampal volume loss and whole brain SWM disruption in patients who developed epilepsy during childhood. On the other hand, in patients with adult-onset TLE, co-occurring cortical and SWM alterations were observed in the medial temporal lobe ipsilateral to the seizure focus. Our results suggest that although cortical, hippocampal and WM alterations appear spatially discordant at the group level, the relationship among these features depends on the age at which seizures begin. Whereas neurodevelopmental aspects of TLE may result in co-occurring WM and hippocampal degeneration near the epileptogenic zone, the onset of seizures in adulthood may set off a cascade of SWM microstructural loss and cortical atrophy of a neurodegenerative nature.
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64.8
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Bonilha L;Edwards JC;Kinsman SL;Morgan PS;Fridriksson J;Rorden C;Rumboldt Z;Roberts DR;Eckert MA;Halford JJ
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