[Otogenic herpes zoster--the Ramsay-Hunt syndrome].

INTRODUCTION

Herpes zoster is a viral disease caused by a specific neurotropic virus-varicella zoster, similar to varicella virus, but not identical. Herpes zoster oticus was described by Letulle in 1882 and Körner in 1884, but particularly studied by Ramsay Hunt who reported it as a herpetic disease of ganglion geniculi in 1907. Herpes zoster oticus associated with facial nerve paralysis is most commonly called the Ramsay-Hunt syndrome.

MATERIAL AND METHODS

In this work, cases of herpes zoster oticus associated with facial nerve paralysis are shown. At the ORL Clinic in Novi Sad, in the period from 1996-1997, 5 cases with Ramsay-Hunt syndrome were treated. The diagnostic procedure involved analysis of anamnestic data, clinical examination, complete cochleovestibular investigation with electronystagmography (ENG), topodiagnostic investigation of facial nerve (Schirmer's test, stapedial reflex, electrogustometry), electromyographic investigation (EMG), laboratory and virusologic investigations. According to many statistical data, paralysis of facial nerve due to herpes zoster is after Bell's paralysis the most common cause of the disease. The efflorescence of auricula, face and neck, which are typical manifestations of the disease, may precede facial nerve paralysis for about a week or more, and therefore may be disregarded and misdiagnosed with Bell's paralysis. The peripheral paralysis of this nerve in herpes zoster has an unfavorable course. More than 75% of patients have consequences of paralysis (paresis, hemispasm, synkinesia etc.). Regarding the unfavorable recovery period in herpes zoster, we managed our patients accordingly.

CONCLUSION

Herpes zoster oticus is a common cause of peripheral facial nerve paralysis. The clinical course is not as favorable as in Bell's paralysis. It may be associated with sensorineural hearing disorder, vertigo and paralysis of other cranial nerves. The therapeutic procedures in Ramsay-Hunt syndrome include administration of conservative therapy and surgical intervention. We performed surgery in 2 and conservative therapy in 3 patients. Facial nerve decompression is indicated in persistent paralyses, or in cases without clear clinical signs of recovery after 6 weeks-2 months from the onset of the disease. The site of decompression is determined by topodiagnostic investigations.