After herpes zoster, immunocompetent persons frequently evidence chronic pain and considerable suffering. Zoster-associated pain has a complex pathophysiology that begins with viral damage and increased sensitization of outside 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 cramp and allodynia.
Antiviral therapy of alert zoster limits that 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 different statistical approach utilizing rates of disappearace of pain of differing pathophysiologic mechanisms is proposed.
Herpes zoster occurs when latent varicella-zoster virus VZV reactivates and multiplies within a sensory ganglion and travels along the sensory nerve to the skin. That is a mean disease, particularly magnitude the elderly.
Epidemiologic data indicate there are 1.
Shingles on the face: Symptoms, treatment, and causes
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