再活化病毒引发神经炎性病变导致外周和中枢神经可逆和不可逆损害分别是带状疱疹急性期（HZ）和后遗神经痛（PHN）本质所在。尽管临床观察到长期存在触诱发痛可促进HZ向PHN转化，但其发生的病生机制并不清楚。本组前期也发现PHN患者有更为广泛的脑结构、功能损害及功能重塑。由此假设：长期疼痛触诱发在HZ向PHN转化起重要作用，参与其中枢调控。本项目拟采用①静息状态＋触诱发状态功能MRI，观测HZ和PHN患者疼痛中枢的BOLD信号的变异性及内源性活动的网络基础，以期获取动态疼痛网络系统与疼痛体验的相关性；②对比健康志愿者并结合磁共振波谱、高分辨T1WI、弥散张量成像、临床评估用于探讨患者触诱发痛的中枢网络调控及其代谢、形态、结构基础，寻找HZ向PHN转化的可能影像标记。为理解疼痛触诱发在HZ向PHN发展中的作用提供重要理论依据，为临床治疗及预后提供新思路。

The reactivation of viral-induced neuroinflammation causes reversible and irreversible damage to the peripheral and central nerves is the essence of herpes zoster (HZ) and postherpetic neuralgia (PHN). Although clinical observations have shown that HZ patients with long-term allodynia are more tend to PHN conversion, the factors that affect the transformation of HZ to PHN still not clear. Our previous study reverified the clinical observations: PHN patientshave more extensive brain structure and function damage or remodeling. Based on these，we hypothesized that long-term allodynia plays an important role in the transformation of HZ to PHN and participates in the central regulation. This project intends to: ①use a resting state and allodynia state functional MRI to observe the variability of the BOLD signal and the network foundation of endogenous activities in pain centers in patients with HZ and PHN in order to obtain the correlation between dynamic pain network system and pain experience; ②compared with healthy controls using magnetic resonance spectroscopy, high-resolution T1WI, diffusion tensor imaging, and clinical assessment to explore the central network regulation mechanism and its metabolic, morphological, and structural basis of allodynia in patients and to seek possible image markers of HZ-to-PHN conversion. To provide important theoretical basis for understanding the role of allodynia in the process of HZ to PHN, and to provide new ideas for clinical treatment and prognosis.