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Introduction
Ramsay Hunt syndrome (RHS) is first described by James Ramsay Hunt in 1907 [1]. It is caused by the reactivation of latent varicella-zoster virus (VZV) that has remained dormant within sensory root ganglia (commonly the geniculate ganglion) of the sensory branch of the facial nerve. Involvement of sensory branch of the geniculate ganglion of facial nerve leads Herpes zoster (HZ) oticus which is also known as RHS. Individuals with decreased cell-mediated immunity resulting from carcinoma, radiation therapy, chemotherapy or human immunodeficiency virus (HIV) infection are at greater risk for reactivation of latent VZV. Physical stress and emotional stress often are cited as precipitating factors. Incidence and clinical severity increases when host immunity is compromised. However it is uncommon to see Herpes zoster oticus in healthy individuals. In this report, we describe the clinical course of a patient who presented with Herpes zoster oticus in the absence of a known immunosuppressive condition. A brief review of literature on this topic is also presented.
Case Report
A previously healthy 65-year old man presented with a 3-days history of vesicular lesions with erythematous base on neck. It was followed by the spread of vesicular eruption to involve external external auditory meatus of right side, and pinna over next 2-days. These are fluid filled vesicular eruptions which bust and break down on 2nd-3rd day with subsequent scab formation. There is no facial weakness. On examination, there was no lower motor neuron facial palsy. A neurologic examination revealed no weakness in the marginal mandibular branch of the left facial nerve. There is no any sign of loss of ipsilateral nasolabial fold or weakness in the temporal branch of the facial nerve. There were painful adherent crusts and scabs...