Abstract
Pain in herpes zoster and postherpetic neuralgia is classically ascribed to irritable, inflammation-sensitized nociceptors in the cutaneous rash and to spinal cord deafferentation. After considering weaknesses in the evidence base underlying this view an alternative explanation is offered, based on hyperexcitability at ectopic pacemaker sites in affected primary sensory neurons, and central sensitization induced and maintained by the ectopic activity.
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