Vestibular neuronitis

Morgenstein, Karl M.; Seung, Hong Il

doi:10.1288/00005537-197101000-00012

Cited by 32 publications

(10 citation statements)

References 6 publications

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“…The hypothesis that vestibular neuritis was caused by a reactivation of HSV-1 in the VG was based on data from temporal bone studies, which showed that changes in the vestibular nerve were similar to those normally seen in viral infections (31,32), and studies that detected HSV-1 DNA in the VG (6,33,34). Animal studies also reported that HSV-1 antigen was found in the VG and the vestibular nerve of mice experimentally infected with HSV-1 (35,36).…”

Section: Discussionmentioning

confidence: 99%

Differential Involvement during Latent Herpes Simplex Virus 1 Infection of the Superior and Inferior Divisions of the Vestibular Ganglia: Implications for Vestibular Neuritis

Himmelein

Lindemann

Sinicina

et al. 2017

J Virol

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Controversy still surrounds both the etiology and pathophysiology of vestibular neuritis (VN). Especially uncertain is why the superior vestibular nerve (SVN) is more frequently affected than the inferior vestibular nerve (IVN), which is partially or totally spared. To address this question, we developed an improved method for preparing human vestibular ganglia (VG) and nerve. Subsequently, macro-and microanatomical as well as PCR studies were performed on 38 human ganglia from 38 individuals. The SVN was 2.4 mm longer than the IVN, and in 65% of the cases, the IVN ran in two separate bony canals, which was not the case for the SVN. Anastomoses between the facial and cochlear nerves were more common for the SVN (14/38 and 9/38, respectively) than for the IVN (7/38 and 2/38, respectively). Using reverse transcription-quantitative PCR (RT-qPCR), we found only a few latently herpes simplex virus 1 (HSV-1)-infected VG (18.4%). In cases of two separate neuronal fields, infected neurons were located in the superior part only. In summary, these PCR and micro-and macroanatomical studies provide possible explanations for the high frequency of SVN infection in vestibular neuritis.IMPORTANCE Vestibular neuritis is known to affect the superior part of the vestibular nerve more frequently than the inferior part. The reason for this clinical phenomenon remains unclear. Anatomical differences may play a role, or if latent HSV-1 infection is assumed, the etiology may be due to the different distribution of the infection. To shed further light on this subject, we conducted different macro-and microanatomical studies. We also assessed the presence of HSV-1 in VG and in different sections of the VG. Our findings add new information on the macro-and microanatomy of the VG as well as the pathophysiology of vestibular neuritis. We also show that latent HSV-1 infection of VG neurons is less frequent than previously reported.KEYWORDS HSV-1 latency, human, vestibular ganglia, vestibular neuritis V estibular neuritis (VN) is a common cause of an "acute unilateral vestibulopathy." The main clinical symptoms of VN are acute onset of prolonged severe spinning vertigo with spontaneous horizontal torsional nystagmus toward the unaffected ear, postural imbalance, and nausea (1). Its annual incidence is reported to be 3.5 to 15.5 per population of 100,000 (2, 3). It is the third most common cause of peripheral vestibular

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Section: Discussionmentioning

confidence: 99%

Differential Involvement during Latent Herpes Simplex Virus 1 Infection of the Superior and Inferior Divisions of the Vestibular Ganglia: Implications for Vestibular Neuritis

Himmelein

Lindemann

Sinicina

et al. 2017

J Virol

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“…Vestibular neuritis might also damage the inferior vestibular nerve as reflected by lacking vestibular evoked myogenic potentials response (38). In addition, derangements of the sensory epithelium of the utricle, anterior, and posterior semicircular canals, in addition to that of the horizontal semicircular canal, have been demonstrated in temporal bone autopsies of patients diagnosed as having VN (39,40). These findings imply that if the functioning of the superior vestibular nerve returns to normal in the face of continuous dysfunction of the inferior vestibular nerve and the corresponding end organs, the patient might not recover the symptoms and clinical signs of VN.…”

Section: Fig 3 Electronystagmographic Caloric Test Lateralization Rmentioning

confidence: 99%

Prednisone Treatment for Vestibular Neuritis

Shupak

Issa²,

Golz³

et al. 2008

Otology &Amp; Neurotology

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“…This finding strengthens the hypothesis that vestibular neuritis is caused by a reactivation of latent HSV-1 from the VG. Until now this hypothesis was based only on temporal bone studies, which revealed that changes in the vestibular nerve were similar to those usually seen in viral infections (25,28), and on studies that detected genomic HSV-1 DNA in the VG (2,18). Additional support derives from animal studies that demonstrated HSV-1 antigen in the VG and vestibular nerve of mice experimentally infected with HSV-1 (12,19) and an electron microscopy study that found virus-like structures in the human VG (20).…”

Section: Latent Hsv-1 In the Vgmentioning

confidence: 99%

Prevalence of HSV‐1 LAT in Human Trigeminal, Geniculate, and Vestibular Ganglia and Its Implication for Cranial Nerve Syndromes

et al. 2001

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Herpes simplex virus type 1 (HSV-1) enters sensory neurons and can remain latent there until reactivation. During latency restricted HSV-1 gene expression takes place in the form of latency-associated transcripts (LAT). LAT has been demonstrated to be important not only for latency but also for reactivation, which may cause cranial nerve disorders. Tissue sections of the trigeminal ganglia (TG), geniculate ganglia (GG), and the vestibular ganglia (VG) from seven subjects were examined for the presence of LAT using the in situ hybridization technique. LAT was found on both sides in allTG (100%), on both sides of five subjects (70%) in the GG, and in none of the VG. Using a second more sensitive detection method (RT-PCR), we found LAT in the VG of seven of ten other persons (70%). This is the first study to demonstrate viral latency in the VG, a finding that supports the hypothesis that vestibular neuritis is caused by HSV-1 reactivation. The distribution of LAT in the cranial nerve ganglia indicates that primary infection occurs in the TG and GG and subsequently spreads along the faciovestibular anastomosis to the VG.

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Vestibular neuronitis

Cited by 32 publications

References 6 publications

Differential Involvement during Latent Herpes Simplex Virus 1 Infection of the Superior and Inferior Divisions of the Vestibular Ganglia: Implications for Vestibular Neuritis

Differential Involvement during Latent Herpes Simplex Virus 1 Infection of the Superior and Inferior Divisions of the Vestibular Ganglia: Implications for Vestibular Neuritis

Prednisone Treatment for Vestibular Neuritis

Prevalence of HSV‐1 LAT in Human Trigeminal, Geniculate, and Vestibular Ganglia and Its Implication for Cranial Nerve Syndromes

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