Complications of Varicella Zoster Virus Reactivation.
ABSTRACT 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.
Article: [Postherpetic neuralgia].Nippon Hifuka Gakkai zasshi. The Japanese journal of dermatology 12/1990; 100(13):1352-4.
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ABSTRACT: Two otherwise healthy immunocompetent men, ages 62 and 66 years, experienced years of radicular pain without zoster rash. An extensive search for systemic disease and malignancy was negative. Varicella-zoster virus DNA, but not herpes simplex virus DNA, was found in the cerebrospinal fluid of the first patient 5 months after the onset of pain, and in the second patient 8 months after the onset of pain. Prolonged radicular pain without zoster rash combined with the presence of varicella-zoster virus in the cerebrospinal fluid indicates that both men had zoster sine herpete, and strongly supports this syndrome as a clinical variant.Annals of Neurology 06/1994; 35(5):530-3. · 11.19 Impact Factor
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ABSTRACT: Severe loss of vision and bilateral optic disc edema occurred in a 10-year-old girl 38 days after the rash of varicella first appeared and subsequent encephalitis developed. Recovery of visual function was nearly complete, but optic atrophy persisted. Parainfectious optic neuritis following other viral infections, with the exception of herpes zoster, has a similar clinical profile: delayed onset, severe visual loss, optic disc edema, bilaterality, good recovery, and residual optic atrophy. Conduction delays in our patient's patterned visual evoked potentials implicated demyelination within the optic nerves. The often favorable recovery, frequency of delayed onset, and bilateral involvement of the optic nerves support an autoimmune process in the pathogenesis of parainfectious optic neuritis.JAMA Neurology 07/1983; 40(6):347-50. · 7.58 Impact Factor