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Understanding pain in herpes zoster: an essential for optimizing treatment Wood MJ Infect Dis 2002[Oct]; 186 Suppl 1 (ä): S78-82After herpes zoster, immunocompetent persons frequently experience chronic pain and considerable suffering. Zoster-associated pain has a complex pathophysiology that begins with viral damage and increased sensitization of peripheral sensory neurons. The enhanced afferent barrage from these neurons sensitizes spinal neurons and leads to loss of synapses from descending inhibitory fibers, resulting in central neuropathic pain and allodynia. Antiviral therapy of acute zoster limits this sequence of pathophysiologic mechanisms. There is no clear consensus regarding the optimal means of determining the benefits of antiviral therapy in the management of pain of herpes zoster. A novel statistical approach utilizing rates of disappearance of pain of differing pathophysiologic mechanisms is proposed.|*Herpesvirus 3, Human[MESH]|2-Aminopurine/*analogs & derivatives/therapeutic use[MESH]|Acyclovir/*analogs & derivatives/therapeutic use[MESH]|Analgesics/*therapeutic use[MESH]|Antiviral Agents/*therapeutic use[MESH]|Chronic Disease[MESH]|Clinical Trials as Topic[MESH]|Famciclovir[MESH]|Herpes Zoster/*drug therapy/physiopathology[MESH]|Humans[MESH]|Meta-Analysis as Topic[MESH]|Pain Measurement[MESH]|Pain/*drug therapy/physiopathology[MESH]|Proportional Hazards Models[MESH]|Treatment Outcome[MESH]|Valacyclovir[MESH]|Valine/*analogs & derivatives/therapeutic use[MESH] |
