Postherpetic neuralgia presents as chronic pain with skin changes lasting for more than 3 months, in the distribution of one or more sensory roots after herpes zoster infection. Also known as shingles, it is due to the reactivation of varicella zoster virus. The reactivation may be triggered by disease (lymphoma, HIV infection), immunosuppression (organ transplant, autoimmune disease) or management of malignancy. Twenty percent of patients with herpes zoster develop PHN.

It includes degeneration of affected primary afferent neuronal cell bodies and axons, atrophy of the spinal cord dorsal horn, scarring of dorsal root ganglion and loss of epidermal innervations. Continuous pain is seen due to intrinsic changes in the central nervous system, and paroxysmal pain is due to demyelinated Aβ fibres. Sensitization of intact C nociceptors leads to allodynia and reduced thermal threshold.

Risk factors are older age, female, more intense acute pain, more severe rash developing within 3 days after the onset of herpes zoster, prodrome of dermatomal pain before the rash (if associated with fever >38 °C) and psychosocial predictors (anxiety, poor coping strategies).

It can be an acute pain (<30 days), subacute pain (30–120 days) and chronic pain (>3 months). Prodrome lasts for 2–3 weeks and comprises of pain with skin lesions most commonly involving thoracic dermatomes. Allodynia may be accompanied by weight loss, chronic fatigue, anorexia, sleep disturbance, depression and concentration deficit. Other manifestations include sensory deficit or itch, skin pigmentation, scarring after the rash, motor weakness and autonomic dysfunction.