Postherpetic neuralgia is a kind of intractable pain, and the current methods for postherpetic neuralgia are mainly medication and closure therapy. The effect of these methods is not particularly obvious, mainly because the mechanism of postherpetic neuralgia is not very clear. Postherpetic neuralgia is a pain that persists 4 weeks after the acute herpes zoster has subsided. The mechanism of postherpetic neuralgia is still the focus of research in the medical community. The exact mechanism of postherpetic neuralgia is not fully elucidated, and possible mechanisms include: pathological sensitization and ectopic impulse generation in primary afferent injury receptor neurons after nerve injury; inflammation of the peripheral nerve trunk, with cytokines produced by macrophage activation (e.g., tumor necrosis factor) inducing ectopic activity in primary afferent injury receptors, which may be a potential cause of pain and nociceptive hypersensitivity; injury receptor degeneration and regeneration of central synapses; injury receptor hyperfunction sensitizes the center, and when the center is sensitized, mechanoreceptors have the function of activating central pain signaling neurons. In the same patient, one or several mechanisms may be involved together and may change during the course of disease development. Pain should be treated aggressively early in the course of shingles, and patients are very distressed when pain is not eliminated. The treatment of postherpetic neuralgia with shingles using minimally invasive radiofrequency has a very significant efficacy and patients should consult a pain unit.