scholarly journals Ramsay Hunt Syndrome associated with central nervous system involvement in an adult: a case report

2015 ◽  
Vol 42 (S1) ◽  
pp. S29-S30
Author(s):  
L Chan ◽  
A Cartagena ◽  
SM Hosseini ◽  
A Bombassaro
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Case Report ◽  
Varicella Zoster Virus ◽  
External Auditory Canal ◽  
Facial Palsy ◽  
Varicella Zoster ◽  
Ramsay Hunt Syndrome ◽  
Hunt Syndrome ◽  
The Central Nervous System

Background: Ramsay Hunt Syndrome with cerebellar encephalitis is rare in adult. Case Report: We describe a 55-year-old diabetic female who presented with truncal ataxia, right peripheral facial palsy and right ear pain associated with erythematous vesicular lesions in her external auditory canal. Later, she developed dysmetria, fluctuating diplopia and dysarthria. No facial lesions were identified and lesions were limited to the external auditory canal. Cerebral spinal fluid tested positive for varicella zoster virus polymerase chain reaction. She was diagnosed with Ramsay Hunt Syndrome with spread to the central nervous system and treated with acyclovir intravenous therapy (10 mg/kg every 8 hours). Her facial palsy completely resolved within 48 hours of acyclovir treatment, however, vesicular lesions, imbalance and cerebellar symptoms remained; a tapering course of high dose prednisone was then added.Discussion: Prognosis for facial palsy is poor in Ramsay Hunt Syndrome: Only 10% of patients will have complete resolution of their facial palsy. Improvement of facial palsy may be a good marker for response to treatment. Conclusion: Varicella zoster virus reactivation affecting the central nervous system in adults is rare. Knowledge of Ramsay Hunt syndrome with brainstem and/or cerebellar involvement is important for diagnosis and for consideration of antiviral and prednisone treatment.

scholarly journals Ramsay Hunt Syndrome Associated with Central Nervous System Involvement in an Adult

2016 ◽  
Vol 2016 ◽  
pp. 1-4 ◽  
Author(s):  
Tommy L. H. Chan ◽  
Ana M. Cartagena ◽  
Anne Marie Bombassaro ◽  
Seyed M. Hosseini-Moghaddam
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Varicella Zoster Virus ◽  
Facial Palsy ◽  
Central Nervous System Involvement ◽  
Varicella Zoster ◽  
Ramsay Hunt Syndrome ◽  
Hunt Syndrome ◽  
Intravenous Acyclovir ◽  
The Central Nervous System

Ramsay Hunt syndrome associated with varicella zoster virus reactivation affecting the central nervous system is rare. We describe a 55-year-old diabetic female who presented with gait ataxia, right peripheral facial palsy, and painful vesicular lesions involving her right ear. Later, she developed dysmetria, fluctuating diplopia, and dysarthria. Varicella zoster virus was detected in the cerebrospinal fluid by polymerase chain reaction. She was diagnosed with Ramsay Hunt syndrome associated with spread to the central nervous system. Her facial palsy completely resolved within 48 hours of treatment with intravenous acyclovir 10 mg/kg every 8 hours. However, cerebellar symptoms did not improve until a tapering course of steroid therapy was initiated.

scholarly journals Infection of the central nervous system caused by varicella zoster virus reactivation: a retrospective case series study

2013 ◽  
Vol 17 (7) ◽  
pp. e529-e534 ◽  
Author(s):  
Juan Carlos Lozano Becerra ◽  
Robert Sieber ◽  
Gladys Martinetti ◽  
Silvia Tschuor Costa ◽  
Pascal Meylan ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Varicella Zoster Virus ◽  
Case Series ◽  
Virus Reactivation ◽  
Retrospective Case ◽  
Varicella Zoster ◽  
Case Series Study ◽  
The Central Nervous System ◽  
Series Study

scholarly journals Varicella zoster virus infection of the central nervous system – 10 year experience from a tertiary hospital in South India

2017 ◽  
Vol 20 (2) ◽  
pp. 149
Author(s):  
RonaldAlbert Benton Carey ◽  
VigneshKumar Chandiraseharan ◽  
Anitha Jasper ◽  
Tunny Sebastian ◽  
Chrusolitha Gujjarlamudi ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Virus Infection ◽  
Varicella Zoster Virus ◽  
South India ◽  
Tertiary Hospital ◽  
Varicella Zoster Virus Infection ◽  
Varicella Zoster ◽  
The Central Nervous System

scholarly journals Defensive Perimeter in the Central Nervous System: Predominance of Astrocytes and Astrogliosis during Recovery from Varicella-Zoster Virus Encephalitis

2015 ◽  
Vol 90 (1) ◽  
pp. 379-391 ◽  
Author(s):  
John E. Carpenter ◽  
Amy C. Clayton ◽  
Kevin C. Halling ◽  
Daniel J. Bonthius ◽  
Erin M. Buckingham ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Human Brain ◽  
Varicella Zoster Virus ◽  
Peripheral Nervous System ◽  
Cellular Response ◽  
Cell Types ◽  
Varicella Zoster ◽  
Human Host ◽  
The Central Nervous System

ABSTRACTVaricella-zoster virus (VZV) is a highly neurotropic virus that can cause infections in both the peripheral nervous system and the central nervous system. Several studies of VZV reactivation in the peripheral nervous system (herpes zoster) have been published, while exceedingly few investigations have been carried out in a human brain. Notably, there is no animal model for VZV infection of the central nervous system. In this report, we characterized the cellular environment in the temporal lobe of a human subject who recovered from focal VZV encephalitis. The approach included not only VZV DNA/RNA analyses but also a delineation of infected cell types (neurons, microglia, oligodendrocytes, and astrocytes). The average VZV genome copy number per cell was 5. Several VZV regulatory and structural gene transcripts and products were detected. When colocalization studies were performed to determine which cell types harbored the viral proteins, the majority of infected cells were astrocytes, including aggregates of astrocytes. Evidence of syncytium formation within the aggregates included the continuity of cytoplasm positive for the VZV glycoprotein H (gH) fusion-complex protein within a cellular profile with as many as 80 distinct nuclei. As with other causes of brain injury, these results suggested that astrocytes likely formed a defensive perimeter around foci of VZV infection (astrogliosis). Because of the rarity of brain samples from living humans with VZV encephalitis, we compared our VZV results with those found in a rat encephalitis model following infection with the closely related pseudorabies virus and observed similar perimeters of gliosis.IMPORTANCEInvestigations of VZV-infected human brain from living immunocompetent human subjects are exceedingly rare. Therefore, much of our knowledge of VZV neuropathogenesis is gained from studies of VZV-infected brains obtained at autopsy from immunocompromised patients. These are not optimal samples with which to investigate a response by a human host to VZV infection. In this report, we examined both flash-frozen and paraffin-embedded formalin-fixed brain tissue of an otherwise healthy young male with focal VZV encephalitis, most likely acquired from VZV reactivation in the trigeminal ganglion. Of note, the cellular response to VZV infection mimicked the response to other causes of trauma to the brain, namely, an ingress of astrocytes and astrogliosis around an infectious focus. Many of the astrocytes themselves were infected; astrocytes aggregated in clusters. We postulate that astrogliosis represents a successful defense mechanism by an immunocompetent human host to eliminate VZV reactivation within neurons.

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