Cases reported "Herpes Zoster Oticus"

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1/10. Ramsay Hunt syndrome associated with brain stem enhancement.

    Postcontrast T1-weighted MR images in a patient with Ramsay Hunt syndrome showed an enhancing lesion in the region of the nucleus of the pontine facial nerve and abnormal enhancement of the intrameatal, labyrinthine, and tympanic facial nerve segments and of the geniculate ganglion, as well as enhancement of the vestibulocochlear nerve and parts of the membranous labyrinth. This enhancement most probably resulted from a primary neuritis of the intrameatal nerve trunks of the seventh and eighth cranial nerves.
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2/10. 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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3/10. 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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4/10. 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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5/10. 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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6/10. Enhanced MRI in patients with Ramsay-Hunt's syndrome.

    Enhanced MRI was performed in 14 patients with Ramsay-Hunt's syndrome to investigate the pathogenesis of this syndrome. All MRI studies were performed on a 0.5T superconductivity MRI system using a head coil with Gd-DTPA. Enhancement was observed in the areas of the distal internal auditory canal and labyrinthine segment in many patients, and was especially prominent in patients suffering from vertigo, tinnitus, and hearing loss. In some patients it involved not only the facial nerve of the internal auditory canal but also the cochlear nerve and vestibular nerves. Since histological changes of the facial nerve in patients with Ramsay-Hunt's syndrome are assumed to occur in the distal internal auditory canal and labyrinthine segment, which is more proximal than the geniculate ganglion, and the possibility is suggested that inflammation may spread to the vestibular and cochlear nerve via the internal auditory canal.
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7/10. Correlation of MRI, clinical, and electroneuronographic findings in acute facial nerve palsy.

    Intratemporal enhancement of (Gd-DTPA) was investigated by an interleaved-overlapping magnetic resonance imaging (MRI) technique in 35 cases of acute facial palsy. In a reference group (normal facial function), enhancement was localized from the ganglion geniculi to the stylomastoid foramen. In cases of acute palsy, the facial nerve enhanced in the meatal fundus independent of etiology (idiopathic, herpetic, or traumatic). In 70% of those with Ramsay-Hunt syndrome, the vestibular and cochlear nerves, the labyrinth, and the sheets of the internal and external auditory canal additionally enhanced. No correlation was found between intensity, extension, and duration of the enhancement and the clinical, intraoperative, or electroneuronographic degree of the facial palsy. The pathogenesis of the Gd-DTPA enhancement of the facial nerve appears to be closely connected with the vascular supply of the fallopian canal and the permeability of the neural sheets.
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8/10. Surgical management of geniculate neuralgia.

    BACKGROUND: geniculate ganglion or nervus intermedius neuraigia is an unusual condition resulting in deep ear pain with or without signs of atypical trigeminal neuralgia, deep face, or throat pain. This article describes an experience with 14 patients who came to the neurosurgical service at the University of Pittsburgh Medical Center with a diagnosis of geniculate neuralgia. methods: After failing conservative treatment and after undergoing neurologic, otologic, and dental evaluations, these 14 patients underwent 20 intracranial procedures consisting of retromastoid craniectomies with microvascular decompression of cranial nerves V, IX, and X with section of the nervus intermedius in most cases. RESULTS: At operation, vascular compression of the nerves and nervus intermedius was found, which implicated vascular compression as an etiology of this disorder. Initially, 10 of 14 patients had an excellent outcome (71.5%), 3 experienced partial relief (21.5%), and there was 1 failure (7%). Ten patients were available for long-term (> 12 months) follow-up. Of these 10, 3 retained the excellent result (30%), 6 experienced partial relief (60%), and there was 1 failure (10%). Complications included one transient facial paresis, one facial numbness, one paresis of cranial nerves IX and X, one chemical meningitis, two cerebrospinal fluid leaks, and one superficial wound infection. Of those that fell from the excellent to partial category, this usually involved a return of atypical facial pain, but otalgia remained resolved. CONCLUSIONS: overall, good results (with excellent or partial relief) were found long term for 90% of patients in this series. The authors recommend microvascular decompression of cranial nerves V, IX, and X with nervus intermedius section for the treatment of geniculate neuralgia.
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9/10. 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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10/10. herpes zoster oticus: correlations between clinical and MRI findings.

    Many gadolinium-enhanced magnetic resonance imaging (MRI) studies focusing on the anatomy and pathology of the 7th cranial nerve have already been published. However, only scattered cases of herpes zoster oticus (HZO) have been described and only the MRI appearance of the soft temporal bone structures has been reported. Enhanced MRI was performed in 4 patients with HZO observed at the Department of Otorhinolaryngology of the University of Pisa. A good correlation was found between the clinical data and MRI findings in both the acute and chronic stages of the disease. The 2 cases with complete facial palsy presented prominent and diffuse enhancement of the 7th and 8th cranial nerves on postcontrast MRI, while the patient with grade III facial palsy showed more limited nerve enhancement. The patient with grade II facial palsy presented no MRI abnormalities. In our series, enhancement limited to the geniculate ganglion and to the labyrinthine segment of the facial nerve indicates a good prognosis while a widespread enhancement correlates with a poor prognosis. In conclusion, MRI with contrast may be useful during the acute stage of HZO because it can confirm the diagnosis and can provide prognostic information on the facial function.
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