Herpes Zoster

Encephalitis. Varicella-zoster virus encephalitis can develop associated with zoster, follow zoster by days to months, or may develop without any history of a vesicular rash. The symptoms of encephalitis include fever, headache, seizures, focal neurologic deficits, and an altered level of consciousness. Varicella-zoster virus encephalitis is due to ischemic and hemorrhagic infarctions in both cortical and subcortical gray matter and white matter. Small demyelinative lesions have been attributed to a small-vessel vasculopathy. Neuroimaging in patients with varicella-zoster virus encephalitis may demonstrate ischemic and hemorrhagic infarctions and demyelinative lesions. Zoster reactivation may also cause a ventriculitis and periventriculitis with hydrocephalus, altered mental status, and gait abnormalities.

Ophthalmic Herpes Zoster. Patients with reactivation of varicella-zoster virus in the trigeminal ganglion develop vesicular lesions in the ophthalmic division of the trigeminal nerve and are at risk for infarction in the distribution of the carotid, anterior, or middle cerebral arteries due to varicella zoster virus vasculopathy. There is also a risk of corneal scarring.

Cerebellitis. An acute cerebellar ataxia can complicate childhood varicella but may also occur in adulthood.

Ramsay Hunt Syndrome. Ramsay Hunt syndrome is due to the reactivation of varicella-zoster virus in the geniculate ganglion, resulting in a peripheral facial nerve palsy. Vesicular lesions may be found on the pinna or in the mouth.

Postherpetic Neuralgia. Postherpetic neuralgia is the most common neurologic complication of varicella-zoster virus. The pain of zoster tends to resolve as the lesions heal but may be associated with or followed by postherpetic neuralgia. Postherpetic neuralgia is defined as the presence of pain in the dermatomal distribution of the vesicular rash for more than 1 month after the onset of zoster, after the lesions have healed.

Zoster Sine Herpete. Zoster sine herpete is pain in a dermatomal distribution without the appearance of a vesicular rash. It is diagnosed by either a fourfold increase in serum antibodies to varicella-zoster virus between acute and convalescent serology obtained 4 weeks later, or by the demonstration of VZV IgM in CSF and/or VZV DNA in cerebrospinal fluid (CSF) by polymerase chain reaction (PCR).

The best diagnostic test for varicella-zoster virus encephalitis is the detection of varicella-zoster virus IgM antibodies in CSF. VZV DNA can also be detected in cerebrospinal fluid by PCR, but this is less sensitive than the antibody.

Varicella-zoster virus encephalitis is treated with intravenous acyclovir. Zoster is treated with oral valacyclovir, famciclovir, or acyclovir. Postherpetic neuralgia is treated with a combination of amitriptyline and gabapentin. The routine use of the varicella vaccine in childhood has decreased the incidence of chicken pox. Effectiveness declines with time, and a booster immunization is required. There is also a zoster vaccine that decreases the risk of zoster.

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