大脑结构连接是其功能连接的物质基础.已有研究表明,失神癫痫患者默认模式网络(default mode network,DMN)中的功能连接发生了改变.为了探索这些改变相应的结构基础,对11名儿童失神癫痫患者和12名正常对照,使用基于弥散张量成像(diffusion tensor imaging,DTI)的纤维束追踪技术,构建了每个被试DMN脑区间的纤维束连接.结果表明,在所有被试的DMN网络中一致发现后扣带/楔前叶到内侧前额叶、后扣带/楔前叶到左右双侧的内侧颞叶都存在纤维束连接.通过两组间统计比较这些纤维束连接的平均长度、连接强度、平均部分各向异性(fractional anisotropic,FA)值和平均弥散度(mean diffusivity,MD)值等参数,发现患者组的后扣带/楔前叶到内侧前额叶纤维束连接上的平均FA值及连接强度都显著降低,而平均MD值显著增加,并且其FA值与癫痫病程呈显著的负相关关系,这些改变可能影响了患者DMN网络的功能连接.本研究结果为DMN功能连接异常提供了相关的结构上的依据,提示后扣带/楔前叶到内侧前额叶的连接异常可能在儿童失神癫痫中起着非常重要的作用.
The structural connectivity patterns of human brain are the underlying basis of functional connectivity. Abnormal functional connectivity in default mode network (DMN) has been uncovered in electroencephalography (EEG) and functional magnetic resonance imaging (fMRI) studies, which suggests that the abnormality might be related to the cognitive mental impairment and unconsciousness during absence seizures. However, so far, little is known about the structural connectivity in DMN about childhood absence epilepsy (CAE). In the present study, we hypothesize that the structural connectivity in DMN should be disrupted to respond to the altered brain function in CAE. To test the hypothesis, 11 patients with CAE and 12 age- and gender- matched healthy controls were recruited. We utilized diffusion tensor imaging tractography to map the anatomical structural connectivity of DMN. The fiber bundles among regions of DMN were built for each subject. Then, mean length, fractional anisotropic (FA), mean diffusivity (MD) and connection strength on fibers linking two brain regions were calculated. Further, these parameters were executed two-sample t-test between CAE group and health control group. Finally, we used Pearson's correlation coefficient to evaluate the relationship between these parameters and epilepsy duration (year). Both CAE and healthy control groups showed similar structural connectivity patterns in DMN. Among these fiber bundles, three were identified in all subjects, with one linking posterior cingulate cortex/precuneus to medial prefrontal cortex, and another two linking posterior cingulate cortex/precuneus to bilateral medial temporal lobes. Furthermore, the significantly decreased FA and connection strength, and increased MD in fiber bundles linking posterior cingulated cortex/precuneus to medial prefrontal cortex, were found in patients compared with the cases in healthy controls (P 〈 0.05,Bonferroni corrected). Predominantly, the FA values in fiber bundles linking poster