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 posterior cingulated cortex/precuneus to medial prefrontal cortex were negatively correlated with the epilepsy duration (P=0.006). These findings might reflect the structural basis of the altered functional connectivity in DMN about absence epilepsy. Given that functional connectivity abnormality in our previous work, it is implied that the abnormal fiber connectivity from posterior cingulated cortex/precuneus to medial prefrontal cortex plays an important role in absence epilepsy. This may open up new avenues to understand the pathophysiological mechanisms of absence epilepsy.