Postherpetic neuralgia (PHN) Herpes zoster is a common clinical condition with a high incidence, especially in immunocompromised groups, and is often associated with neuralgia of varying degrees in addition to skin lesions. In some patients, painful symptoms may persist for weeks or even months or years after the rash subsides. The pain can be severe, even to the point of being triggered by touch, and is called “postherpetic neuralgia (PHN)”. The pain associated with herpes zoster is generally considered to fall into three categories: acute herpetic pain, which occurs with the rash and lasts about 30 days; subacute herpetic pain, which lasts 30-120 days after the onset of the rash; and PHN, which lasts more than 120 days after the onset of the rash. The clinical features of postherpetic neuralgia The herpes zoster rash occurs as a result of the multiplication and replication of varicella-zoster virus (VZV) in the infected sensory ganglia and peripheral sensory nerve fibers VZV can also reach the corresponding dorsal root ganglia and adjacent spinal cords along the nerve pathways and even enter the circulation Activation of VZV induces cellular immunity in the body and can also cause neuronal inflammation, hemorrhage, and structural destruction of neurons. During this period, the patient may experience prodromal pain or discomfort in the skin area corresponding to the affected nerve, which usually lasts for several days. In addition to age, the severity of the rash and pain during the acute phase are risk factors for the development of PHN. Most patients with PHN complain of several different types of pain and sensory abnormalities: drilling pain, stabbing pain, flashing pain, burning pain, electric shock-like pain, abnormal pain, pain that gradually increases in response to repeated stimuli, sensory hypersensitivity, and unbearable itching. The mechanism of PHN PHN is the same as the acute phase pain of herpes zoster, which is neuropathic pain. It is not only the result of peripheral nerve damage, but is also associated with changes in signal processing in the central nervous system. In the peripheral nervous system, on the one hand, the ectopic impulses generated by virus-induced nerve injury are accompanied by enhanced expression of mRNA for certain voltage-gated sodium channels in primary afferent neurons. The aggregation of sodium channels at the site of ectopic impulse generation results in a decrease in action potential threshold. On the other hand, the cytokine TNF-α produced by activated macrophages induces ectopic activity in primary afferent injury receptors, causing acute inflammation of the peripheral nerve trunk, resulting in pain and nociceptive hypersensitivity in patients. In the CNS, VZV activation leads to inflammation of the dorsal root ganglion, important changes in the CNS pathways for sensing injury, and afferent nerve block. These changes result in abnormally high activity of CNS pain signaling neurons; degeneration of unmyelinated primary afferent central terminals causes regeneration of synapses within the posterior horn, leading to misdirected connections between Aβ2 mechanoreceptor fibers and posterior root neurons, thus preventing normal input to injury receptors; and hyperfunction of injury receptors sensitizes the center. The pharmacological entry pathway for PHN treatment is threefold: first, local drugs that act on the affected skin; second, drugs that affect the excitability and conductivity of sensory axonal nerves; and third, drugs that act on synaptic changes associated with nerve injury. the criteria for effective PHN drug therapy are that the patient feels > 30% pain relief, the side effects are tolerable, and the patient’s vitality and function are enhanced accordingly. 1.Pharmacological treatment: anticonvulsant drugs such as gabapentin and pregabalin are effective for PHN and are the first-line drugs for PHN, in addition to tricyclic antidepressants and nonsteroidal anti-inflammatory and analgesic drugs also have certain efficacy. Local application of local anesthetics and capsaicin preparations can also effectively relieve pain symptoms. The effect of opioids is more limited. 2.Intradermal receptor block or nerve block: blocking the conduction pathway of pain can effectively relieve pain symptoms, generally after three to five times of intradermal receptor block treatment, can effectively reduce the pain caused by PHN. 3. For patients with poor results of the above treatments, intracanal block, nerve destruction, intrathecal continuous drug injection and spinal cord electrical stimulation can be considered. Prevention of PHN For the prevention of PHN, the current consensus is that early detection, consultation and treatment are important prerequisites for the active prevention of PHN. Treatments used during the acute phase of herpes zoster may help reduce the risk of PHN and should be administered early after the onset of the rash. Antivirals may reduce the duration of herpes zoster pain, and antivirals, such as acyclovir, famciclovir, and valacyclovir, are now advocated to reduce the duration of herpes zoster pain and the risk of PHN. Older patients (over 50 years of age) who do not receive antivirals have more severe symptoms and longer duration of PHN. The efficacy of vaxilovir appears to be better than that of acyclovir. Patients with herpes zoster often receive a short course of oral, intravenous, or topical corticosteroids to prevent the onset of PHN, and the often recommended regimen is oral prednisone for 3 consecutive weeks, with a dose of 60 mg/d for the first week and 30 mg/d and 15 mg/d for the next 2 weeks. Some studies seem to show that corticosteroids can reduce early pain symptoms in PHN, but do not relieve chronic neuralgia. Other studies have shown no difference in the duration and intensity of PHN in the treatment group receiving prednisone compared to the control group. A recent large, randomized, controlled trial showed that combining prednisone with acyclovir significantly shortened the duration of acute neuritis and the course of pain medication, but was ineffective for pain lasting more than 6 months after a herpes zoster episode. And in elderly patients, the application of high-dose corticosteroids should be weighed against the possible benefits and potential risks.