Sympathetic blockade in acute and subacute shingles: A long term follow up study

Abstract

This chapter discusses the pathogenesis of primary varicella zoster virus (VZV) infection, clinical aspects of VZV reactivation and treatment, vaccination studies, recent advances in the molecular aspects of VZV infection, latency and apoptosis, and animal models for studying varicella biology. VZV is an exclusively human neurotropic alphaherpesvirus. Primary infection causes varicella (chicken pox), after which the virus becomes latent in cranial nerve ganglia, dorsal root ganglia (DRG), and autonomic ganglia along the entire neuraxis. As cell-mediated immunity to VZV declines with age or immunosuppression, VZV reactivates to cause zoster (shingles), often followed by chronic pain (postherpetic neuralgia [PHN]) as well as vasculopathy, meningoencephalitis, myelopathy, cerebellitis, and various ocular disorders, the most serious of which is retinal necrosis. VZV reactivation can also produce radicular pain without rash (zoster sine herpete), although it has now become clear that all of the neurologic and ocular complications of VZV reactivation identified earlier can occur without rash. VZV is highly infectious and transmission occurs by direct contact with skin lesions or by respiratory aerosols. Immunosuppression increases the risk of disseminated zoster. In most patients, the disappearance of skin lesions is accompanied by decreased pain and complete resolution of pain in 4–6 weeks. Widespread, aggressive VZV vaccination has reduced the total number of varicella cases by ∼85% and the number of moderate to severe cases by 95–100%. Like the live varicella vaccine for children, there is now a live zoster vaccine that appears to be safe and effective clinically.