Cases reported "Herpes Zoster Oticus"

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1/10. Sympathetic contralateral vestibulopathy after unilateral zoster oticus.

    A unique case of initially right sided varicella zoster induced Ramsay-Hunt syndrome with complete vestibular loss is reported. The patient subsequently developed deficits of the left vestibule 5 months later. An autoimmune pathogenesis of the left vestibular failure rather than bilateral varicella zoster infection was suggested by the following data: (1) no evidence of vesicular eruptions on the left auricle and the virtual absence of antiviral antibodies after onset of bilateral vestibulopathy; (2) prompt response of the left vestibule to immunosuppressive therapy with corticosteroids; and (3) presence of atypical nervous tissue specific autoantibodies against a 45 kDa protein.
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2/10. Ramsay-Hunt syndrome in a 4-year-old child.

    The Ramsay-Hunt syndrome mostly affects adults, but a small number of children with herpes zoster oticus have been reported. We describe a case of Ramsay Hunt syndrome in a healthy 4-year-old boy. He developed varicella at 7 months of age. At the age of 4 years, he complained of pain in his right ear, and herpes zoster vesicles were noted on his right pinna. Three days later, he developed right facial paralysis. He was treated with intravenous acyclovir and methylprednisolone. One month later, his facial paralysis had fully resolved.
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3/10. Delayed facial palsy after middle-ear surgery due to reactivation of varicella-zoster virus.

    Viral reactivation is thought to be an important cause of post-operative facial palsy of delayed onset. We present an unusual case of Ramsay-Hunt syndrome that occurred as a consequence of middle-ear surgery by triggering varicella-zoster virus reactivation. As a pathognomonic auricular eruption was not seen, the patient was initially misdiagnosed as iatrogenic facial palsy. Clinical features, diagnosis and management are discussed.
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keywords = varicella
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4/10. Detection of varicella zoster virus dna in tear fluid and saliva of patients with Ramsay Hunt syndrome.

    OBJECTIVE: To clarify the dynamics of the reactivation of the varicella zoster virus in Ramsay Hunt syndrome. SUBJECTS AND methods: Varicella zoster virus dna in the tear fluid, submandibular gland saliva, and parotid gland saliva of 15 patients with Ramsay Hunt syndrome was studied. The presence of varicella zoster virus dna was detected quantitatively by the use of polymerase chain reaction and a microplate hybridization method. RESULTS: Of 102 specimens of the tear fluid and saliva collected from 15 patients, varicella zoster virus dna was detected in 40 specimens (39%) from 12 patients (80%). The detection rate was 72% in the submandibular saliva, 57% in the parotid saliva, and 27% in the tear fluid. Varicella zoster virus dna was detected not only in specimens from the affected side but also in specimens from the unaffected side at the same rate of detection, and at nearly the same number of dna copies. Regarding the parotid saliva, varicella zoster virus dna was detected in samples collected at an early stage of the disease. In the tear fluid and submandibular saliva, however, the detection rate was high in samples collected 2 weeks after the onset of disease or later. CONCLUSIONS: Secretion of varicella zoster virus dna into the tear fluid and saliva was confirmed in the patient with Ramsay Hunt syndrome. The increase and decrease in the detection rate and the number of varicella zoster virus dna copies detected in samples collected at different times was considered to substantiate varicella zoster virus reactivation in Ramsay Hunt syndrome. Varicella zoster virus reactivation was thought to occur in the unaffected side at the same level as in the affected side, and some of the secreted varicella zoster virus dna was suspected to be derived from the ganglion trigeminale.
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keywords = varicella
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5/10. Corneal epithelial keratitis in herpes zoster ophthalmicus: "delayed" and "sine herpete". A non-contact photomicrographic in vivo study in the human cornea.

    PURPOSE: To investigate the origin of corneal epithelial keratitis occurring without accompanying herpes zoster ophthalmicus (HZO) cutaneous rash. methods: Corneal epithelial lesions in seven patients (four with a history of classical HZO with cutaneous rash, one of herpes zoster oticus, and two with no history of herpes zoster, were examined with the slit lamp and photographed by non-contact in vivo photomicrography. The findings were compared with lesions in classical acute HZO. polymerase chain reaction (PCR) was done in three patients. RESULTS: Slit lamp appearance, morphology at higher magnification, and kinetics of the lesions were indistinguishable from classical acute HZO. PCR was positive for varicella-zoster virus dna in all three samples. CONCLUSIONS: The findings strongly suggest that HZO typical corneal epithelial lesions occurring in the absence of cutaneous rash are in fact recurrent episodes of virus shedding.
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6/10. Ramsay Hunt syndrome: pathophysiology of cochleovestibular symptoms.

    Ramsay Hunt's hypothesis that herpes zoster oticus results from reactivation of the varicella zoster virus (VZV) in the geniculate ganglion is supported by the detection of viral genome in archival temporal bones of normals and Ramsay Hunt patients by the polymerase chain reaction. Ramsay Hunt syndrome is characterized by the presence of cochleovestibular symptoms in association with facial paralysis. VZV has also been demonstrated in the spiral and/or vestibular ganglion. Two cases are reported in which cochleovestibular symptoms outweighed the facial nerve symptoms, presumably representing VZV reactivation in the spiral and/or vestibular ganglion. From these observations and the known dormancy of VZV in non-neuronal satellite cells, it is argued that the cochleovestibular symptoms in Ramsay Hunt syndrome may result from VZV transmission across the nerves inside the internal auditory canal and that prompt treatment with an antiviral-corticosteroid combination might be justified in the management of any acute non-hydropic cochleovestibular syndrome.
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7/10. Chronic varicella-zoster virus ganglionitis--a possible cause of postherpetic neuralgia.

    Postherpetic neuralgia (PHN) is dermatomal distribution pain that persists for months to years after the resolution of herpes zoster rash. The cause of PHN is unknown. Herein, we report clinical, molecular virological, and immunological findings over an 11-year period in an immunocompetent elderly woman with PHN. Initially, blood mononuclear cells (MNCs) contained varicella-zoster virus (VZV) dna on two consecutive occasions. Random testing after treatment with famciclovir to relieve pain did not detect VZV dna. However, the patient was reluctant to continue famciclovir indefinitely and voluntarily stopped drug treatment five times. pain always recurred within 1 week, and blood MNCs contained many, but not all, regions of the VZV genome on all five occasions. Immunological analysis revealed increased cell-mediated immunity to VZV. Chronic VZV ganglionitis-induced PHN best explains the recurrence of VZV dna in MNCs whenever famciclovir was discontinued; the detection of only some regions of the viral genome in MNCs, compared to the detection of all regions of the VZV genome in latently infected ganglia; the increased cell-mediated immunity to VZV; and a gratifying clinical response to famciclovir. The presence of fragments of VZV dna in MNCs likely represents partial degradation of viral dna in MNCs that trafficked through ganglia during productive infection.
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8/10. Varicella zoster virus: beyond facial paralysis.

    J. Ramsay Hunt's hypothesis that herpes zoster oticus results from a reactivation of the herpes zoster virus in the geniculate ganglion, has been supported by the demonstration of varicella zoster viral dna in the geniculate ganglion of the side with facial paralysis in patients with Ramsay Hunt syndrome, with the use of the polymerase chain reaction. Similarly, dna of the varicella zoster virus has been identified in the spiral and vestibular ganglion as well. We report on three patients with cochleovestibular symptoms as the first manifestations of Ramsay Hunt syndrome. A 64-year old woman and a 72-year old man presented with vertigo and an auricular herpetiform eruption. Only the woman developed later on a mild facial paralysis. A 58-year old man presented with an acute cochleovestibular syndrome, serologically proven to be a varicella zoster viral reactivation, which was followed three weeks later by the typical cutaneous recrudescence. We believe that these cases result from reactivation of latent varicella zoster virus in the spiral and/or vestibular ganglion. As the varicella zoster virus is dormant in the non-neuronal satellite cells, the facial symptoms in our patients as well as the high incidence of cochleovestibular symptoms in classical Ramsay Hunt syndrome can be explained by viral transmission across the nerves inside the internal auditory canal. Therefore, we think there are grounds to recommend a prompt treatment with an antiviral and a corticosteroid agent, not only in case of an acute facial paralysis but also when confronted with an acute cochleovestibular syndrome.
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keywords = varicella
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9/10. Cranial polyneuropathy--Ramsay Hunt's syndrome: case report and discussion.

    Ramsay Hunt's syndrome is an infectious cranial polyneuropathy caused by varicella zoster, the herpetic virus that also causes chickenpox and shingles. Its symptoms include facial paralysis, ear pain, and an auricular rash. Oral lesions are also present in most cases. This syndrome can affect any cranial nerve and usually affects multiple nerves, causing central, cervical, and peripheral effects. This article reports the case of a 35-year-old white female who was treated by the oral surgery service of a large urban hospital, after first reporting to the emergency clinic. Her reported symptoms of unilateral left-side facial paralysis, auricular pain, and trigeminal hyperesthesia were confirmed by clinical examination. An initial short low-dose steroid regimen was unsuccessful. A second daily dosage of 50 mg of prednisone was successful in 21 days. No permanent sequelae were evident or reported after treatment.
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10/10. Molecular temporal bone pathology: II. Ramsay Hunt syndrome (herpes zoster oticus).

    In 1907 J. Ramsay Hunt suggested that herpes zoster oticus resulted from a geniculate ganglionitis; however, many contemporary authors believe that this disorder represents a neuritis or polycranial neuropathy. Herpes varicella-zoster viral (VZV) dna was identified, using the polymerase chain reaction, in archival celloidin-embedded temporal bone sections from two patients who clinically had Ramsay Hunt syndrome (herpes zoster oticus). The presence of VZV was confirmed by sequencing the PCR products. These experiments demonstrated that VZV genomic dna was present in the geniculate ganglion of the side with facial paralysis and cutaneous recrudescence in both patients and in the clinically unaffected side in patient 1. In addition, patient 2 had a sudden hearing loss and was found to have VZV genomic dna in sections from the affected side containing the spiral ganglion, Scarpa's ganglion, organ of corti, and macula of the saccule. No VZV genomic dna was identified in temporal bone sections from five patients with Bell's palsy and ten patients without evidence of otologic disease. In this study, the histopathology of these two cases yielded complementary information regarding the role of VZV in herpes zoster oticus. These data suggest that in patients with Ramsay Hunt syndrome, latent VZV is located in the geniculate ganglia and may be present in the auditory and vestibular primary afferent ganglia in some patients.
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