Herpes Zoster and Postherpetic Neuralgia: Prevention and Management

Abstract

Herpes zoster, or shingles, is caused by reactivation of varicella zoster virus, which causes chickenpox. There are an estimated 1 million cases in the Unites States annually, with an individual lifetime risk of 30%. Patients with conditions that decrease cell-mediated immunity are 20 to 100 times more likely to develop herpes zoster. Patients may present with malaise, headache, low-grade fever, and abnormal skin sensations for two to three days before the classic maculopapular rash appears. The rash is usually unilateral, confined to a single dermatome, and typically progresses to clear vesicles that become cloudy and crust over in seven to 10 days. Herpes zoster can be treated with acyclovir, valacyclovir, or famciclovir, ideally within 72 hours of the development of the rash. Postherpetic neuralgia is the most common complication, occurring in about one in five patients. It is defined as pain in a dermatomal distribution sustained for at least 90 days after acute herpes zoster. Treatment is focused on symptom control and includes topical lidocaine or capsaicin and oral gabapentin, pregabalin, or tricyclic antidepressants. The varicella zoster virus vaccine decreases the incidence of herpes zoster and is approved for adults 50 years and older. The Centers for Disease Control and Prevention's Advisory Committee on Immunization Practices recommends this vaccine for adults 60 years and older, except for certain immunosuppressed patients.