postherpetic neuralgia

PHN results from VZV reactivation causing neuronal damage, demyelination, and scarring in the affected dorsal root ganglion and peripheral nerve, leading to aberrant pain signaling (peripheral and central sensitization) even after the rash heals. Risk factors include older age (>50-60 years), greater acute pain/rash severity, ophthalmic (V1) involvement, and immunocompromised state. Clinically, patients experience burning, aching, or lancinating pain, allodynia, and hyperalgesia in the dermatomal distribution of prior rash. Diagnosis is clinical, based on history of zoster and persistent pain >90 days post-rash. Prevention is key: the recombinant zoster vaccine (Shingrix) significantly reduces incidence of both zoster and PHN; early antiviral therapy (acyclovir, valacyclovir, famciclovir) during acute zoster may reduce PHN risk and severity. First-line treatments for PHN include anticonvulsants (gabapentin, pregabalin), tricyclic antidepressants (amitriptyline, nortriptyline), and topical agents (lidocaine patches, capsaicin cream/patch). Opioids and tramadol are second-line due to side effects and dependence risk. PHN is a classic board topic linking virology (VZV latency in dorsal root ganglia), neurology (neuropathic pain mechanisms), and pharmacology (choice of analgesics for neuropathic vs nociceptive pain).