Varicella zoster virus-related myelitis: a case series and literature review

Varicella zoster virus (VZV) is a human neurotropic herpesvirus that remains latent in the dorsal root ganglia and can reactivate to cause herpes zoster. In immunocompromised patients, reactivation may lead to severe neurological complications such as encephalitis, meningitis, myelitis, and neuropathy. However, varicella zoster virus-related myelitis (VZVM) is relatively rare, particularly in immunocompetent adults. The pathogenesis may involve direct viral invasion of the spinal cord parenchyma during the acute phase or a postinfectious immune-mediated inflammatory response.

This report describes three patients with VZVM(one woman ages 49 years and two men age 60 and 56 years), none of whom presented with a typical rash. Two patients (cases 1 and 2) developed encephalomyelitis at disease onset, characterized by fever, impaired consciousness, and long-segment spinal cord lesions. Metagenomic next-generation sequencing (mNGS) of cerebrospinal fluid (CSF) detected VZV nucleic acid in both cases. In case 3, the patient initially developed VZVM complicated by cerebral venous sinus thrombosis. After an interval of approximately 40 days, delayed thoracic myelitis developed, and repeated CSF mNGS testing yielded negative results. All three patients received intravenous antiviral therapy; two additionally received low-dose corticosteroids combined with intravenous immunoglobulin, and one received intravenous methylprednisolone. During follow-up, one patient achieved full recovery of lower-limb motor function, whereas two patients remained paraplegic.

VZVM presents with diverse clinical manifestations and may occur without the typical vesicular rash. It can develop either during the initial phase of VZV infection or as a delayed complication. Early magnetic resonance imaging and CSF molecular testing support timely diagnosis. Prompt and adequate antiviral therapy combined with immunomodulatory treatment may improve neurological outcomes.