Concurrent Central and Autonomic Nervous System Involvement in Varicella-Zoster Virus Infection in an Immunocompetent Patient: A Case-Based Mechanistic Analysis

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Abstract

Background/Objectives: Varicella-zoster virus (VZV) is a neurotropic alphaherpesvirus capable of causing a wide spectrum of neurologic complications. While central nervous system involvement and autonomic dysfunction have each been described, their concurrent occurrence in immunocompetent individuals is rarely reported. We describe a case of VZV meningoencephalitis with simultaneous autonomic dysfunction and explore the underlying pathophysiologic mechanisms. Methods: Clinical data were obtained through retrospective review of the patient’s hospitalization, including clinical presentation, laboratory studies, imaging, and treatment course. Cerebrospinal fluid (CSF) analysis included cell count, protein, glucose, and polymerase chain reaction (PCR) testing for viral pathogens. Radiographic evaluation included computed tomography (CT), magnetic resonance imaging (MRI), and abdominal radiography. This study represents a descriptive clinical case analysis based on retrospective review. Results: A 66-year-old previously healthy man presented with fever, severe headache, photophobia, and low back pain and was initially misdiagnosed. He subsequently developed a sacral dermatomal vesicular rash followed by encephalopathy with meningeal signs. CSF analysis demonstrated lymphocytic pleocytosis, markedly elevated protein, and positive VZV PCR, confirming VZV meningoencephalitis. Concurrent findings of significant urinary retention (~ 1100 mL) and bowel distention without mechanical obstruction indicated autonomic dysfunction. Treatment with intravenous acyclovir and supportive measures, including erythromycin for prokinetic therapy, resulted in recovery of neurologic and autonomic function. Conclusions: This case demonstrates concurrent involvement of the central and autonomic nervous systems, likely reflecting viral reactivation within sacral dorsal root ganglia with extension to adjacent autonomic pathways. Mechanisms including VZV neurotropism, latency, and host immune modulation—particularly interferon signaling and JAK–STAT pathway interactions—provide a framework for understanding atypical or multifocal disease. Recognition of these presentations is essential, as early diagnosis and prompt antiviral therapy may improve clinical outcomes.

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