Ramsay Hunt syndrome in children

Hato, Naohito; Kisaki, Hisanobu; Honda, Nobumitsu; Gyo, Kiyofumi; Murakami, Shingo; Yanagihara, Naoaki

doi:10.1002/1531-8249(200008)48:2<254::aid-ana17>3.3.co;2-m

Cited by 30 publications

(52 citation statements)

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“…The counterpart among patients with Ramsay Hunt syndrome is characterised by peripheral facial paralysis without ear or mouth rash, and the presence of either a fourfold rise in antibody to VZV or the detection of VZV DNA in skin, blood mononuclear cells, or middle ear fluid. In the retrospective study by Hato et al ,19 of 1705 patients with ipsilateral facial palsy without vesicles, the data imply that 42 (2.4%) had zoster sine herpete. In a study of 32 patients with isolated peripheral facial palsy, Murakami et al 25identified zoster sine herpete in six (19%) of the patients based on a fourfold rise in serum antibody titre to VZV.…”

Section: Ramsay Hunt Syndrome Zoster Sine Herpetementioning

confidence: 96%

“…A retrospective review of 2076 patients presenting with unilateral facial palsy, with or without vesicles, from 1976 to 1996 in Japan19 disclosed a similar incidence of Ramsay Hunt syndrome in adults and children over age 6 years. In that study, the syndrome was defined as unilateral facial palsy, herpetic vesicles on the ear or oral mucosa, and vestibulocochlear dysfunction.…”

Section: Epidemiologymentioning

confidence: 99%

“…Facial strength was evaluated with the House-Brackmann grading system used by Hato et al 19 in their retrospective review of Ramsay Hunt syndrome in children and adults. Complete recovery occurred in 85/173 (49%) adults, and in 33/42 (78%) patients younger than 16.…”

Section: Natural Historymentioning

confidence: 99%

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NOSOLOGICAL ENTITIES?: Ramsay Hunt syndrome

Sweeney

2001

Journal of Neurology, Neurosurgery &Amp; Psychiatry

367

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The strict definition of the Ramsay Hunt syndrome is peripheral facial nerve palsy accompanied by an erythematous vesicular rash on the ear (zoster oticus) or in the mouth. J Ramsay Hunt, who described various clinical presentations of facial paralysis and rash, also recognised other frequent symptoms and signs such as tinnitus, hearing loss, nausea, vomiting, vertigo, and nystagmus. He explained these eighth nerve features by the close proximity of the geniculate ganglion to the vestibulocochlear nerve within the bony facial canal. Hunt's analysis of clinical variations of the syndrome now bearing his name led to his recognition of the general somatic sensory function of the facial nerve and his defining of the geniculate zone of the ear. It is now known that varicella zoster virus (VZV) causes Ramsay Hunt syndrome.Compared with Bell's palsy (facial paralysis without rash), patients with Ramsay Hunt syndrome often have more severe paralysis at onset and are less likely to recover completely. Studies suggest that treatment with prednisone and acyclovir may improve outcome, although a prospective randomised treatment trial remains to be undertaken. In the only prospective study of patients with Ramsay Hunt syndrome, 14% developed vesicles after the onset of facial weakness. Thus, Ramsay Hunt syndrome may initially be indistinguishable from Bell's palsy. Further, Bell's palsy is significantly associated with herpes simplex virus (HSV) infection. In the light of the known safety and eVectiveness of antiviral drugs against VZV or HSV, consideration should be given to early treatment of all patients with Ramsay Hunt syndrome or Bell's palsy with a 7-10 day course of famciclovir (500 mg, three times daily) or acyclovir (800 mg, five times daily), as well as oral prednisone (60 mg daily for 3-5 days).Finally, some patients develop peripheral facial paralysis without ear or mouth rash, associated with either a fourfold rise in antibody to VZV or the presence of VZV DNA in auricular skin, blood mononuclear cells, middle ear fluid, or saliva. This indicates that a proportion of patients with "Bell's palsy" have Ramsay Hunt syndrome zoster sine herpete. Treatment of these patients with acyclovir and prednisone within 7 days of onset has been shown to improve the outcome of recovery from facial palsy. (J Neurol Neurosurg Psychiatry 2001;71:149-154)

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Section: Ramsay Hunt Syndrome Zoster Sine Herpetementioning

confidence: 96%

Section: Epidemiologymentioning

confidence: 99%

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NOSOLOGICAL ENTITIES?: Ramsay Hunt syndrome

Sweeney

2001

Journal of Neurology, Neurosurgery &Amp; Psychiatry

367

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“…VZV causes the RHS. Some patients develop peripheral facial paralysis without ear or mouth rash associated with either a fourfold rise in antibody to VZV or the presence of VZV DNA in auricular skin, blood MNCs, middle ear fluid, or saliva (Hato et al 2000). In a study of 32 patients with isolated peripheral facial palsy, Murakami et al (1998) identified RHS zoster sine herpete in six (19%) of the patients based on a fourfold rise in serum antibody titer to VZV; four of these six patients were positive for VZV DNA by PCR when geniculate zone skin scrapings were studied.…”

Section: Ramsay Hunt Syndromementioning

confidence: 99%

Neurological Disease Produced by Varicella Zoster Virus Reactivation Without Rash

Gilden

Cohrs

Mahalingam

et al. 2010

Current Topics in Microbiology and Immunology

123

111

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Reactivation of varicella zoster virus (VZV) from latently infected human ganglia usually produces herpes zoster (shingles), characterized by dermatomal distribution pain and rash. Zoster is often followed by chronic pain (postherpetic neuralgia or PHN) as well as meningitis or meningoencephalitis, cerebellitts, isolated cranial nerve palsies that produce ophthalmoplegia or the Ramsay Hunt syndrome, multiple cranial nerve palsies (polyneuritis cranialis), vasculopathy. myelopathy, and various inflammatory disorders of the eye. Importantly, VZV reactivation can produce chronic radicular pain without rash (zoster sine herpete), as well as all the neurological disorders listed above without rash. The protean neurological and ocular disorders produced by VZV in the absence of rash are a challenge to the practicing clinician. The presentation of these conditions vanes from acute to subacute to chronic. Virological confirmation requires the demonstration of amplifiable VZV DNA in cerebrospinal fluid (CSF) or in blood mononuclear cells, or the presence of anti-VZV IgG antibody in CSF or of anti-VZV IgM antibody in CSF or serum.

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“…The rash can also affect the face and the omolateral two-thirds anterior part of the tongue and palate 2 3. Remarkably, not all the symptoms may be present; in the early phase of the disease, especially in children, vesicular rash may be absent (ie, zoster sine herpete), and pain and hyperaemia cutis along the affected nerve are typical clinical features 4. VZV reactivation should also be considered without facial palsy as affecting only the sensory portion of cranial nerve VII5; besides, VZV is responsible for one-third of isolated palsy and can be misdiagnosed as idiopathic Bell’s palsy 6.…”

Section: Answer To Questionmentioning

confidence: 99%