Rethinking the causes of pain in herpes zoster and postherpetic neuralgia: The ectopic pacemaker hypothesis

Marshall Devor*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

57 Scopus citations

Abstract

Introduction: Pain in herpes zoster (HZ) and postherpetic neuralgia (PHN) is traditionally explained in terms of 2 processes: Irritable nociceptors in the rash-inflamed skin and, later, deafferentation due to destruction of sensory neurons in one virally infected dorsal root ganglion. Objectives and methods: Consideration of the evidence supporting this explanation in light of contemporary understanding of the pain system finds it wanting. An alternative hypothesis is proposed as a replacement. Results: This model, the ectopic pacemaker hypothesis of HZ and PHN, proposes that pain in both conditions is driven by hyperexcitable ectopic pacemaker sites at various locations in primary sensory neurons affected by the causative varicella zoster virus infection. This peripheral input is exacerbated by central sensitization induced and maintained by the ectopic activity. Conclusions: The shift in perspective regarding the pain mechanism in HZ/PHN has specific implications for clinical management.

Original languageEnglish
Article numbere702
JournalPain Reports
Volume3
Issue number6
DOIs
StatePublished - 1 Nov 2018

Bibliographical note

Publisher Copyright:
© 2018 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of The International Association for the Study of Pain.

Keywords

  • Deafferentation
  • Dorsal root ganglion
  • Dying-back
  • Ectopic discharge
  • Herpes zoster
  • Pain mechanism
  • Postherpetic neuralgia

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