We have located links that may give you full text access.
CASE REPORTS
ENGLISH ABSTRACT
JOURNAL ARTICLE
[Otogenic herpes zoster--the Ramsay-Hunt syndrome].
Medicinski Pregled 2000
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.
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.
Full text links
Related Resources
Trending Papers
Challenges in Septic Shock: From New Hemodynamics to Blood Purification Therapies.Journal of Personalized Medicine 2024 Februrary 4
Molecular Targets of Novel Therapeutics for Diabetic Kidney Disease: A New Era of Nephroprotection.International Journal of Molecular Sciences 2024 April 4
Perioperative echocardiographic strain analysis: what anesthesiologists should know.Canadian Journal of Anaesthesia 2024 April 11
The 'Ten Commandments' for the 2023 European Society of Cardiology guidelines for the management of endocarditis.European Heart Journal 2024 April 18
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app