White matter abnormalities across different epilepsy syndromes in adults: an ENIGMA-Epilepsy study
White matter abnormalities across different epilepsy syndromes in adults: an ENIGMA-Epilepsy study
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DOI：
10.1093/brain/awaa200
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发表时间：
2020-08-01
期刊：
影响因子：
14.5
通讯作者：
McDonald, Carrie R.
中科院分区：
文献类型：
--
作者：
Hatton, Sean N.;Huynh, Khoa H.;McDonald, Carrie R.
Hatton等人分析了来自大型国际成像数据集的弥散张量成像数据，包括1，069名对照和1，249名癫痫患者。他们发现双侧胼胝体、扣带回和外囊存在明显的白色异常，癫痫综合征的严重程度不同，癫痫通常伴有广泛的大脑白色异常。ENIGMA-Epilepsy是一个大型定量脑成像联盟，聚集数据以研究常见癫痫综合征中的神经成像异常模式，包括颞叶癫痫，颞外癫痫和遗传性全身性癫痫。我们的目标是在一个多中心的成人癫痫患者样本中，对综合征之间和综合征内最强大的白色物质显微结构差异进行排名。分析了1069例健康对照和1249例患者的弥散加权MRI数据：颞叶癫痫伴海马硬化（n = 599），颞叶癫痫伴正常MRI（n = 275），遗传性全身性癫痫（n = 182）和非病灶性颞外癫痫（n = 193）。使用基于束的空间统计的协调协议被用于导出每个参与者的分数各向异性和平均扩散率的归一化图，并且使用扩散MRI图谱分割纤维束。数据进行了协调，以纠正扫描仪特定的扩散措施的变化，使用批量效应校正工具（ComBat）。协方差分析，调整年龄和性别，检查每种癫痫综合征和对照组之间的差异，为每个白色物质束（Bonferroni校正P < 0.001）。在所有癫痫患者中，在大多数具有小到中等效应大小的纤维束中观察到较低的各向异性分数，特别是在胼胝体、扣带和外囊中。平均扩散率的增加也不那么强劲。症状特异性各向异性分数和平均扩散率差异在同侧海马旁扣带和外囊的海马硬化患者中最明显，对大多数其他通道的影响较小。颞叶癫痫和正常MRI的个人表现出类似的模式，更大的同侧比对侧的异常，但不显着比海马硬化患者。全身性和颞外癫痫患者的胼胝体、放射冠和外囊的各向异性分数显著降低，前放射冠的平均扩散率增加。海马硬化患者癫痫发作年龄越早，病程越长，弥散异常程度越大。我们在一项大型多中心癫痫研究中证实了主要联合、连合和投射纤维的显微结构异常。总体而言，癫痫患者在胼胝体、扣带回和外囊中显示出白色异常，不同癫痫综合征的严重程度不同。这些数据进一步定义了常见癫痫综合征中白色物质异常的谱，产生了对病理基质的更详细的见解，这些病理基质可以解释认知和精神共病，并用于指导治疗结局的生物标志物研究和/或遗传研究。
Hatton et al. analyze diffusion tensor imaging data from a large, international imaging dataset, including 1,069 controls and 1,249 patients with epilepsy. They find robust white matter abnormalities in the corpus callosum, cingulum and external capsule bilaterally, with differing severity across epilepsy syndromes.The epilepsies are commonly accompanied by widespread abnormalities in cerebral white matter. ENIGMA-Epilepsy is a large quantitative brain imaging consortium, aggregating data to investigate patterns of neuroimaging abnormalities in common epilepsy syndromes, including temporal lobe epilepsy, extratemporal epilepsy, and genetic generalized epilepsy. Our goal was to rank the most robust white matter microstructural differences across and within syndromes in a multicentre sample of adult epilepsy patients. Diffusion-weighted MRI data were analysed from 1069 healthy controls and 1249 patients: temporal lobe epilepsy with hippocampal sclerosis (n = 599), temporal lobe epilepsy with normal MRI (n = 275), genetic generalized epilepsy (n = 182) and non-lesional extratemporal epilepsy (n = 193). A harmonized protocol using tract-based spatial statistics was used to derive skeletonized maps of fractional anisotropy and mean diffusivity for each participant, and fibre tracts were segmented using a diffusion MRI atlas. Data were harmonized to correct for scanner-specific variations in diffusion measures using a batch-effect correction tool (ComBat). Analyses of covariance, adjusting for age and sex, examined differences between each epilepsy syndrome and controls for each white matter tract (Bonferroni corrected at P < 0.001). Across 'all epilepsies' lower fractional anisotropy was observed in most fibre tracts with small to medium effect sizes, especially in the corpus callosum, cingulum and external capsule. There were also less robust increases in mean diffusivity. Syndrome-specific fractional anisotropy and mean diffusivity differences were most pronounced in patients with hippocampal sclerosis in the ipsilateral parahippocampal cingulum and external capsule, with smaller effects across most other tracts. Individuals with temporal lobe epilepsy and normal MRI showed a similar pattern of greater ipsilateral than contralateral abnormalities, but less marked than those in patients with hippocampal sclerosis. Patients with generalized and extratemporal epilepsies had pronounced reductions in fractional anisotropy in the corpus callosum, corona radiata and external capsule, and increased mean diffusivity of the anterior corona radiata. Earlier age of seizure onset and longer disease duration were associated with a greater extent of diffusion abnormalities in patients with hippocampal sclerosis. We demonstrate microstructural abnormalities across major association, commissural, and projection fibres in a large multicentre study of epilepsy. Overall, patients with epilepsy showed white matter abnormalities in the corpus callosum, cingulum and external capsule, with differing severity across epilepsy syndromes. These data further define the spectrum of white matter abnormalities in common epilepsy syndromes, yielding more detailed insights into pathological substrates that may explain cognitive and psychiatric co-morbidities and be used to guide biomarker studies of treatment outcomes and/or genetic research.