Abstract

Acute herpes zoster is a highly stereotyped condition of viral recrudescence producing inflammation in a dorsal root ganglion, a segmental vesicular rash, and pain. The long-term outcome is unpredictable. Those acute zoster patients that develop postherpetic neuralgia (PHN) fall into three subtypes: (1) an “irritable nociceptor” group with minimal deafferentation and touch-evoked allodynia due to peripheral nociceptor input, (2) a deafferentation group with marked sensory loss and no allodynia, and (3) a deafferentation group with sensory loss and allodynia due to central reorganization. Response to therapy also shows significant inhomogeneity. Some patients obtain nearly complete relief by either topical agents or oral monotherapy with opioids, antidepressants, or anticonvulsants. Other PHN sufferers are refractory to all measures, similar to patients with spinal cord injury and central poststroke pain. Because the clinical picture of PHN falls into distinct patterns based on differing pathophysiology, PHN should be thought of as several disorders, which may respond differently to therapeutic interventions and which may or may not coexist in the same patient.

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