Previous studies on trigeminal neuragia(TN) have mainly focused on peripheral nerve damage, but little is known about the structural and functional changes in central nervous system(CNS) that can occur following trigeminal nerve dysfunction. Based on the theories concerning CNS pathogenesis^[1], we hypothesized that TN patients would show both structural plasticity and functional reorganization in brain areas concerning the sensory, cognitive-affective, and modulatory aspects of pain that progress to form pathologic algogenic system. Diffusion Kurtosis Imaging(DKI)^[2] were analyzed in 32 unilateral TN patients and 22 healthy controls to extract FA, RD, AD, MD, RK, AK, and MK from whole brain analysis. Functional connectivity density(FCD) mapping was used to explore the functional reorganization in hub regions^[3]. Group differences in DKI analysis were compared using Tract-Based Spatial Statistics (TBSS), and FCD differences were compared in a voxel-wise manner using two-sample t-tests (P ＜ 0.05, corrected). We also tested relations between these functional and structural changes in TN patients.We found white matter abnormalities in TN patients, mainly marked by lower AK, higher FA and AD in the internal capsule, cerebral peduncle, corticospinal tract, superior longitudinal fasciculus, inferior longitudinal fasciculus, inferior fronto-occipital fasciculus, posterior thalamic radiation, uncinate fasciculus, and splenium of corpus callosum (Figure 1). The FCDs with significant intergroup differences were shown in Figure 2-4. TN patients exhibited significantly increased FCDs in bilateral hippocampus, contralesional caudate nucleus, and contralesional orbitofrontal cortex. We also found FCDs reduction in TN patients in the posterior cingulate cortex, bilateral angular gyrus, and contralesional supramarginal gyrus. Otherwise, white matter and FCD changes were significantly correlated (Figure 5)We performed a comprehensive analysis to investigate structural and functional changes of CNS in TN patients. These white matter abnormalities located in tracts for transmiting and regulating pain information, characterized by lower AK and higher FA and AD, suggested an increase in the density and alignment of fibers. However, we found related FCD changes were rather complex, including not only highly connected hubs in the sensory, cognitive-affective, and modulatory aspects of pain, but also disrupted functional connections.This is the first study to demonstrate the correlations of white matter plasticity and functional reorganization underlying the central pathogenesis of TN. With higher density and alignment of fibers that increase nociceptive activity to the CNS, functional modulation disequilibrium in hub regions may contribute to pathologic algogenic system. These findings may be helpful guidance for systematic therapeutics in both peripheral and central nerves.