A 65-year-old immunocompetent patient develops severe burning pain and vesicular eruption following the T4 dermatome on the left side. He is started on antiviral therapy. Despite adequate antiviral therapy, he develops severe persistent pain (>10/10 on VAS) 6 weeks after the rash has healed. Which mechanism is responsible for this complication?
- A Ongoing viral replication in the skin causing continued tissue damage
- B Autoimmune nerve destruction by anti-VZV antibodies
- C Central and peripheral sensitisation with glial activation, altered ion channel expression, and ectopic discharge from damaged nociceptors in dorsal root ganglia ✓
- D Secondary bacterial superinfection of nerve sheaths
Explanation
Post-herpetic neuralgia (PHN) — the most common serious complication of herpes zoster — is caused by neuropathic sensitisation rather than active viral replication. VZV reactivation causes acute inflammation and axonal injury in the dorsal root ganglion. This leads to peripheral sensitisation (ectopic discharge, reduced nociceptor thresholds, altered Na+ channel expression) and central sensitisation (spinal dorsal horn hyperexcitability, glial activation, loss of inhibitory interneurons). The self-perpetuating neuropathic pain persists long after virus clearance. Treatment with tricyclic antidepressants, gabapentinoids, or topical lidocaine targets these central/peripheral mechanisms.
Reference: Neena Khanna Illustrated Synopsis of Dermatology & STD, 6th ed.
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Written and medically reviewed by the StethoPrep medical team.