Abnormal alterations in structure-function coupling at the modular level in patients with postherpetic neuralgia.

To investigate the presence of modular loss of coupling and abnormal alterations in functional and structural networks in the brain networks of patients with postherpetic neuralgia (PHN). We collected resting-state functional magnetic resonance imaging data and diffusion tensor imaging data from 82 healthy controls (HCs) and 71 PHN patients, generated structural connectivity (SC) and functional connectivity (FC) networks, and assessed the corresponding clinical information assessment. Based on AAL(90) mapping, the brain network was divided into 9 modules, and the structural-functional connectivity (SC-FC) coupling was compared at the whole-brain level and within the modules, as well as alterations in the topological properties of the brain network in the patient group. Finally, correlation analyses were performed using the following clinical scales: Visual Analogue Scale (VAS), Hamilton Anxiety Scale (HAMA), and Hamilton Depression Scale (HAMD). Compared with HCs, patients with PHN had reduced global efficiency (Eg) and local efficiency (Eloc) of structural and functional networks. The FC in the PHN group presented abnormal node clustering coefficients (NCp), local node efficiencies (NLe), and node efficiencies (Ne), and the SC presented abnormal node degrees (Dc), NCp, NLe, characteristic path lengths (NLp), and Ne. In addition, SC-FC coupling was reduced in the patient default network (DMN), salient network (SN), and visual network (VIS). Moreover, the degree of impairment of graph theory indicators was significantly positively correlated with scales such as VAS scores, and the coupling of modules was significantly negatively correlated with the early course of the patient's disease. Large-scale impaired topological properties of the FC and SC networks were observed in patients with PHN, and SC-FC decoupling was detected in these modules of the DMN, SN, and VIS. These aberrant alterations may have led to over-transmission of pain information or central sensitization of pain.