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Previous studies have found that the pathology of post-stroke aphasia might be related to abnormalities in the white matter connectivity. However, it is still unclear about the neural mechanism of white matter impairment in the post-stroke aphasia. The present study attempted to detect the alteration of the brain white matter structural network in the post-stroke aphasia. We recruited 16 PSA patients who suffered from post-stroke aphasia and 14 healthy controls and acquired their diffusion-tensor imaging data. We performed a deterministic white matter fiber tracking to construct white matter structural network and estimated network topological properties by using graph theory. We also assessed the between-group differences in these parameters and estimated the correlations between the abnormal parameters and clinical assessments in the patients. The patients showed higher shortest path length, higher normalized clustering coefficient, and lower global efficiency than the controls. We found abnormal nodal parameters in the frontal, parietal, basal ganglia, and limbic regions in the patient group. From the rich-club analysis, we found that the patient group showed higher rich-club connections and lower feeder connections than the control group, and had a new rich-club region, the right fusiform gyrus. In summary, this study detected the abnormal both nodal and global parameters of the brain white matter structural network in the post-stroke aphasia. These findings may provide insights into understanding the abnormal brain network and impairment of language function in the post-stroke aphasia.