Varicella zoster virus (VZV) is an exclusively human neurotropic alphaherpesvirus. Primary
infection causes
varicella (
chickenpox), after which virus becomes latent in ganglionic neurons along the entire neuraxis. With advancing age or immunosuppression, cell-mediated immunity to VZV declines and virus reactivates to cause
zoster (
shingles), which can occur anywhere on the body. Skin lesions resolve within 1-2 weeks, while complete cessation of
pain usually takes 4-6 weeks.
Zoster can be followed by
chronic pain (
postherpetic neuralgia),
cranial nerve palsies,
zoster paresis,
meningoencephalitis, cerebellitis,
myelopathy, multiple ocular disorders and vasculopathy that can mimic
giant cell arteritis. All of the neurological and ocular disorders listed above may also develop without
rash. Diagnosis of VZV-induced neurological disease may require examination of cerebrospinal fluid (CSF), serum and/ or ocular fluids. In the absence of
rash in a patient with neurological disease potentially due to VZV, CSF should be examined for VZV
DNA by PCR and for anti-VZV
IgG and
IgM. Detection of VZV
IgG antibody in CSF is superior to detection of VZV
DNA in CSF to diagnose vasculopathy, recurrent
myelopathy, and brainstem
encephalitis. Oral
antiviral drugs speed healing of
rash and shorten
acute pain. Immunocompromised patients require intravenous
acyclovir. First-line treatments for post-herpetic
neuralgia include
tricyclic antidepressants,
gabapentin,
pregabalin, and topical
lidocaine patches. VZV vasculopathy,
meningoencephalitis, and
myelitis are all treated with intravenous
acyclovir.