Herpes zoster results from reactivation of varicella virus that has lain dormant in the cerebral ganglia (extramedullary ganglia of the cranial nerves) or in the ganglia of posterior nerve roots since a previous episode of chickenpox. Exactly how or why this reactivation occurs isn’t clear. Some believe that the virus multiplies as it is reactivated and that antibodies remaining from the initial infection neutralize it. However, if effective antibodies aren’t present, the virus continues to multiply in the ganglia, destroy the host neuron, and spread down the sensory nerves to the skin.

In rare cases, herpes zoster infection leads to generalized central nervous system infection, muscle atrophy, motor paralysis (usually transient), acute transverse myelitis, and ascending myelitis. More commonly, generalized infection causes acute urine retention and unilateral diaphragm paralysis. In postherpetic neuralgia, which is most common in elderly persons, intractable neurologic pain may persist for years. Scars may be permanent.

Herpes zoster infection begins with fever and malaise. Within 2 to 4 days, severe deep pain, pruritus, and paresthesia or hyperesthesia develop, usually on the trunk and occasionally on the arms and legs in a dermatomal distribution. Pain may be continuous or intermittent and usually lasts from 1 to 4 weeks. In some cases, small, red, nodular skin lesions erupt on the painful areas up to 2 weeks after the first symptoms. These lesions typically spread unilaterally around the thorax or vertically over the arms or legs. When these nodules appear, they quickly become vesicles filled with clear fluid or pus. About 10 days later, the vesicles dry and form scabs. Intense pain may occur before the rash appears and after the scabs form.