White matter impairment in the basal ganglia-thalamocortical circuit of drug-na茂ve childhood absence epilepsy

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• 作者：Tianhua Yang^a ; Zhiwei Guo^b ; Cheng Luo^b ; Qifu Li^a ; Bo Yan^a ; Ling Liu^a ; Qiyong Gong^c ; Dezhong Yao^b ; Dong Zhou^a ; ^{zhoudong66@yahoo.de}
• 关键词：Childhood absence epilepsy ; Diffusion tensor imaging ; White matter ; Voxel based analysis
• 刊名：Epilepsy Research
• 出版年：2012
• 期刊代码：87_09201211
• 类别：med
• 出版时间：May, 2012
• 卷：99
• 期：3
• 页码：267-273
• 文件大小：734 K

摘要

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Summary

Purpose

It is unknown whether white matter abnormalities exist in childhood absence epilepsy (CAE), a syndrome of idiopathic epilepsy (IGE). Diffusion tensor imaging (DTI) can noninvasively quantify white matter integrity. This study used DTI to investigate abnormal changes in white matter of untreated CAE patients.

Methods

Subjects included nine patients with untreated CAE and nine age-and sex-matched healthy controls. Diffusion tensor imaging parameters were voxel based and statistically compared between patients and controls. The correlations between DTI parameters in regions of interest (ROIs) and age of seizure onset or duration of epilepsy were analyzed.

Results

Untreated CAE patients had a significantly higher fractional anisotropy (FA) value in the bilateral thalamus, anterior corpus callosum and upper brainstem, while also displaying a lower FA value in prefrontal white matter, anterior cingulate, and bilateral posterior limbs of the internal capsule compared to control subjects. An increase in mean diffusivity (MD) value was observed in parietal lobe white matter, prefrontal white matter, and posterior cerebellar hemispheres, in addition to subcortical structures including bilateral putamen and posterior limb of internal capsule. MD significant correlations between ROI diffusion parameters and the duration of the disease or the age of onset.

Conclusions

The results showed white matter integrity impairment in the basal ganglia-thalamocortical circuit of drug-na茂ve CAE patients. These abnormalities in white matter may be related to increased cortical excitability and cause cognitive, linguistic, and behavioral/emotional deficits both during and between seizures.