Oral Concurrent Session 3 – Ultrasound and Genetics: Thursday, January 30, 2025 1:30 PM – 4:00 PM.

Herpes zoster (HZ) results from reactivation of latent varicella–zoster virus and affects about 1/3 people over a lifetime, with roughly one million cases annually in the United States (). The most frequent and debilitating complication is zoster-related pain (ZRP), which may evolve into postherpetic neuralgia (PHN). Published estimates suggest that PHN develops in approximately 5–30% of patients with HZ overall, approximately 12.5% of patients aged ≥50 years, and an even higher proportion of older or high-risk patients (). Clinically, ZRP progresses through acute, subacute, and chronic phases. PHN is conventionally defined as pain persisting for ≥90 days after rash onset (). In the acute/subacute phase, when nociceptive and neuropathic mechanisms overlap, peripheral and central sensitization may contribute to pain chronification. This window represents a critical therapeutic opportunity, highlighting the rationale for early and mechanism-targeted interventions (). Current standard care primarily includes prompt antiviral therapy—ideally within 72 h of rash onset—alongside analgesics and adjuvant neuropathic agents. While antivirals accelerate lesion healing and modestly alleviate acute pain, they have limited efficacy in preventing PHN (). Consequently, many patients continue to experience significant pain despite optimized pharmacological management, underscoring the need for interventional strategies.