Latent Herpes Simplex Virus Type 1 in Human Vestibular Ganglia

Furuta, Yasushi; Takasu, Toshiyuki; Fukuda, Satoshi; Inuyama, Yukio; Sato, Kazuko; Nagashima, Kazuo

doi:10.3109/00016489309128081

Cited by 83 publications

(60 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Several studies have suggested that a viral agent may be the underlying cause of VN, either by demonstrating the presence of herpes simplex virus DNA within vestibular nerve fibers and "Scarpa's" ganglion or by demonstrating histologic changes within the vestibular nerve suggestive of viral-induced atrophy and inflammation. [11][12][13][14][15] On the other hand, an uncertain proportion of acute peripheral vestibular disorders are likely due to a vascular lesion of the nerve, and patients with such lesions may be at increased risk for future vascular events. [16] One study has suggested that age difference (50 years) plays an important role in differentiating between these two possible pathologies, however we were not able to confirm these results.…”

Section: Discussionmentioning

confidence: 99%

Incidence, seasonality and comorbidity in vestibular neuritis

et al. 2014

View full text Add to dashboard Cite

Source of funding: None other than the author's own institution. 1 Incidence, seasonality and comorbidity in vestibular neuritis AbstractAims of the present study were: 1) to assess the incidence of vestibular neuritis (VN) in the adult population in two cities in Croatia, 2) to identify distribution of new VN cases in the different months and seasons by years, and 3) to identify comorbidities associated with VN. This is a prospective, population-based study conducted in the cities of Zagreb and Velika Gorica, Croatia in the 2011-2012 period. All diagnoses were confirmed either with caloric test or vestibular evoked myogenic potentials within 7 days of symptom onset. Following clinical parameters were collected from all patients: age, gender, side of the lesion, month and season of symptoms onset and comorbidities. We identified 79 new cases of VN (34 in 2011VN (34 in , 45 in 2012. The male to female ratio was 1.1:1. The mean age at the onset of the disease was 52.3 (range 20-86) years. The average annual incidence was 11.7 per 100,000 (95% CI 7,8 -15,6) in the 2011 period and 15.5 per 100,000 (95% CI 11,0 -20,0) in the 2012 period.For both years there was no statistically significant uneven distribution in the different months or seasons by years. The most frequent comorbidities present in VN patients were hypertension (30.4%), diabetes mellitus (8.9%), hyperlipidemia (7.5%) and hypothyreosis (6.3%). Our study has shown higher incidence of VN than previously reported. We have found no evidence of seasonality of VN and significant proportion of VN patients older than 50 years who had vascular risk factors present.

show abstract

Section: Discussionmentioning

confidence: 99%

Incidence, seasonality and comorbidity in vestibular neuritis

et al. 2014

View full text Add to dashboard Cite

show abstract

“…Recent studies have suggested a viral etiology of VN (Schuknecht and Kitamura 1981), most likely a reactivation of latent herpes simplex virus type 1 (Furuta et al 1993;Schulz et al 1998;Arbusow et al l999, 2000).…”

Section: Introductionmentioning

confidence: 99%

Recovery of the High-Acceleration Vestibulo-ocular Reflex After Vestibular Neuritis

Palla

Straumann

2004

JARO

View full text Add to dashboard Cite

Vestibular neuritis (VN) usually leads to a sudden gain asymmetry of the high-acceleration horizontal vestibulo-ocular reflex (VOR). We asked whether this asymmetry decreases over time indicating peripheral recovery and/or central compensation. The horizontal VOR during rapid rotational head impulses to both sides was recorded with search coils in 37 patients at different time periods (1-240 weeks) after the onset of VN. In ten patients, sequential measurements were performed. Gains of the VOR during head impulses toward the ipsilesional side significantly increased after the initial drop (average gains: < 1 week: 0.35; 1-4 weeks: 0.33; 4-40 weeks: 0.55; 40-240 weeks: 0.50). Gains on the contralesional side, however, were only slightly reduced and showed no significant change. We conclude that, in contrast to patients after hemilabyrinthectomy or unilateral vestibular neurectomy, the ocular response to ipsilesional rotations in patients after VN improves over time. This finding suggests that ipsilesional recovery is peripheral or, if central, depends on spared peripheral function. The physiology of linear and nonlinear VOR pathways predicts a considerable gain reduction for contralesional head impulses if central compensation mechanisms are not engaged. Thus, the relatively preserved gain on the contralesional side can be explained only by central ''upregulation''. Apparently, for high accelerations of the head, effective central compensation after VN does not aim to balance the gains of the VOR but tries to boost the contralesional gain close to normal.

show abstract

“…The many terms -vestibular neuritis / neuronitis / neuropathy / neuronopathy, acute vestibulopathy, acute vestibular neurolabyrinthitis, acute labyrinthitis 1 -often used interchangeably to describe PVP, testify to the fact that there is still much to be discovered about the nature of the disease.A less disputed issue is the fact that PVP is often preceded by a viral infection of the upper respiratory tract [37] or the higher prevalence (compared to controls) of Herpes viruses in the eighth and other cranial nerves and their neurons [1,12,17,41] as well as in the saliva of patients with PVP [33]. One animal study also supports the etiopathogenetic role of Herpes viruses, but points to histopathological changes in both the vestibular nerve and labyrinth [13].…”

Section: Etiology and Pathogenesis Of Pvp: The Evidence So Farmentioning

confidence: 75%