Varicella zoster virus and central nervous system syndromes

Abstract

Varicella zoster virus (VZV) causes chicken pox (varicella) after which it establishes latency and can subsequently reactivate to cause herpes zoster. Central nervous system (CNS) complications can follow both primary infection and reactivation of VZV. The more serious manifestations arise when VZV invades the spinal cord or cerebral arteries after reactivation of the virus, causing diseases such as myelitis and focal vasculopathies. The International Herpes Management Forum (IHMF) has developed guidelines to aid in the diagnosis and management of CNS syndromes associated with VZV and these have focused on VZV vasculopathy. The new guidelines recommend that where VZV vasculopathy is suspected, cerebrospinal fluid (CSF) should be analysed by polymerase chain reaction (PCR) for VZV DNA. As VZV antibodies may be present in the CSF in the presence or absence of detectable VZV DNA, CSF should also be analysed for VZV-specific antibody if there is a high likelihood of CNS disease. Early diagnosis of these serious complications is important, as aggressive antiviral treatment can be effective. Patients with VZV focal vasculopathy should be treated with intravenous aciclovir (10 mg/kg every 8 h for adults, 500 mg/m2 body surface area for children) for 7 days. The immunocompromised patient may require longer treatment. However, treatment should be discontinued if negative results are obtained for both VZV DNA and anti-VZV antibody in CSF. Steroid therapy (prednisone 60-80 mg/day for 3-5 days) should be considered in VZV vasculopathy to reduce inflammation.