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Acyclovir responsive brain stem disease after the Ramsay Hunt syndrome.
Shuching Hu1, Melanie Walker, Todd Czartoski
1Department of Neurology, University of Washington, Box 356465, Seattle, WA 98195, USA.
Journal of the Neurological Sciences
|December 17, 2003
Summary
Varicella zoster virus (VZV) can cause Ramsay Hunt syndrome and subsequent brainstem disease in immunocompetent individuals. Prompt treatment with intravenous acyclovir effectively resolves neurological deficits, highlighting the importance of early antiviral therapy.
Area of Science:
- Neurology
- Virology
- Infectious Diseases
Background:
- Ramsay Hunt syndrome (RHS), a neurological condition caused by varicella zoster virus (VZV) reactivation, typically affects the facial nerve.
- While VZV is a known neurotropic virus, its potential to cause severe central nervous system disease in immunocompetent individuals requires further investigation.
Observation:
- An immunocompetent patient presented with Ramsay Hunt syndrome (RHS).
- Days following the initial presentation, the patient developed brainstem disease, indicating a potential progression of VZV infection.
- Virological studies confirmed varicella zoster virus (VZV) as the causative agent for both RHS and the subsequent brainstem involvement.
Findings:
- Intravenous acyclovir treatment led to rapid improvement in the patient's neurological deficits.
- Peripheral facial palsy was the only neurological deficit that did not fully resolve with antiviral therapy.
- This case underscores that VZV can cause brainstem disease even in immunocompetent hosts.
Implications:
- The findings suggest that brainstem disease is a potential complication of geniculate zoster (RHS) in immunocompetent individuals.
- Early initiation of antiviral therapy, such as intravenous acyclovir, can be curative for VZV-induced neurological complications.
- This case highlights the importance of considering VZV as a cause of neurological disease beyond peripheral facial nerve palsy.