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Peripheral Facial Palsy in an Adolescent: A Ramsay Hunt Syndrome Diagnosis

 

Vasco Carvalho* and Sofia Martins

Paediatrics Service, Hospital de Braga, Portugal

*Corresponding author: Vasco Carvalho, Paediatrics Service, Hospital de Braga, Portugal, Tel: 967109619; E-mail: vascofonscacarvalh1@gmail.com

Received: May 19, 2021; Accepted: June 02, 2021; Published: June 14, 2021

Citation: Vasco Carvalho, Sofia Martins, et al. Peripheral Facial Palsy in an Adolescent: A Ramsay Hunt Syndrome Diagnosis. Clin Image Case Rep J. 2021; 3(6): 173.

Abstract

An 11-year-old girl presented to our emergency department with a 2-day history of nausea, vomiting and headache. Her medical history included varicella infection at 5 years of age. Physical examination revealed a deviation of the left lip commissure, incapacity for total occlusion of the right eye and asymmetry of the wrinkles in the forehead (House-Brackmann Facial Nerve Grading Scale (HB FGS) V). She had crusting vesicular lesions on the right ear pinna (Figure 1,2 and 3). Meningeal signs were negative. CT scan and blood analysis were unremarkable. Cerebrospinal Fluid (CSF) showed an elevated white cell count (210 u/L) but normal glucose and protein levels. Based on clinical and analytical findings, Ramsay Hunt Syndrome complicated with viral meningitis was diagnosed at this point. The patient started oral prednisolone (60 mg/day), intravenous acyclovir (1500 mg/m2 /day) and physical rehabilitation. Subsequent molecular testing of CSF detected Varicella Zoster Virus (VZV) RNA by reverse transcriptase PCR. The follow-up showed disappearance of the earache and vesicular rash, as well as the improvement of facial paralysis, becoming a grade III HBFGS (Figure 4,5 and 6). The one-year follow-up showed no relapse of the syndrome (Figure 7 and 8). Ramsay-Hunt Syndrome is a rare disease characterized by facial paralysis, inner ear dysfunction, periauricular pain, and herpetiform vesicles (zoster oticus). The reported incidence in children is 2.7/100,000 and it´s caused by the reactivation of latent VZV in the geniculate ganglion [1-3].

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