Herpes zoster neuralgia is a persistent disease and a worldwide problem. Postherpetic neuralgia has a complex clinical spectrum of pain types, concomitant clinical symptoms and multiple subtypes. Postherpetic neuralgia is primarily the result of viral invasion and damage to the sensory nervous system, but the currently accepted treatments are only on analgesia. These mainly include some of the following treatments: 1. non-steroidal anti-inflammatory and analgesic drugs. 2.Promote nerve damage repair drugs. 3, antidepressants. 4.Anti-epileptic drugs. 5.Narcotic analgesics and narcotics. 6.Topical topical drugs. 7.Nerve block, hormone and other closed treatment. 8, nerve destruction treatment, etc. The existence of multiple methods in itself indicates the complexity of the pathological mechanism of this disease and the difficulty of treatment. Postherpetic neuralgia is insensitive to general neuropathic pain treatment methods, such as the best analgesic developed for herpes zoster neuralgia – Pregabalin, a 2013 study report suggests that only less than 50% of patients are effective, and more than 50% of patients also need to use other central The clinical use process should also pay attention to side effects, especially in elderly patients and patients on long-term medication should be monitored for liver and kidney function and white blood cell count. The effect of nerve block therapy, nerve destruction and even the more popular spinal cord electrical stimulation is not satisfactory. The pain of PHN only involves one or two adjacent spinal nerves, but the damage to sensory nerves destroyed by the virus is extensive, so only nerve block or nerve destruction of sensory nerves is not helpful for blocking or destroying the pain signal caused by neuropathy in the central segment of the point. Moreover, the destruction of damaged nerves is only adding to the pain and quenching the thirst in terms of pathological mechanisms. Therefore, in many cases it is not yet possible to achieve good therapeutic results. The pathological mechanism of this disease is mainly the resurgence and massive replication of the VZV virus latent in the sensory ganglia and its transfer along the nerve axons to the peripheral innervation sites, resulting in a series of pathological changes in the peripheral nerve fibers. In layman’s terms, this means that the destruction of nerve fibers causes severe and intractable pain, which is excruciating and seriously affects the patient’s mood and quality of life.