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Background The treatment of post-facial palsy synkinesis (PFPS) remains inadequate. Previous studies have confirmed that brain plasticity is involved in the process of functional restoration. Isolated activation has been well studied, however, the brain works as an integrity of several isolated regions. This study aimed to assess the alteration of the brain network topology with overall and local characteristics of information dissemination. Understanding the neural mechanisms of PFPS could help to improve therapy options and prognosis. Methods Patients with facial synkinesis and healthy controls (HCs) were estimated using functional magnetic resonance imaging (fMRI) of resting-state. Subsequently, an independent component analysis (ICA) was used to extract four subnets from the whole brain. Then we used the measurements of graph theory and calculated in the whole-brain network and each sub-network. Results We found no significant difference between the patient group and the HCs on the whole-brain scale. Then we identified four subnetworks from the resting-state data. In the sub-network property analysis, patients' locally distributed properties in the sensorimotor network (SMN) and ventral default mode network (vDMN) were reduced. It revealed that γ (10,000 permutations, P=0.048) and S (10,000 permutations, P=0.022) within the SMN progressively decreased in patients with PFPS. For the analysis of vDMN, significant differences were found in γ (10,000 permutations, P=0.019), Elocal (10,000 permutations, P=0.008), and β (10,000 permutations, P=0.011) between the groups. Conclusions Our results demonstrated a reduction in local network processing efficiency in patients with PFPS. Therefore, we speculate that decreased characteristics in the intra-vDMN and intra-SMN, rather than the whole-brain network, may serve distinct symptoms such as facial nerve damage or more synkinetic movements. This finding of the alteration of network properties is a small step forward to help uncover the underlying mechanism.