Distribution of herpes simplex virus type 1 in human geniculate and vestibular ganglia: Implications for vestibular neuritis

Arbusow, Viktor; Schulz, Peter; Strupp, Michael; Dieterich, Marianne; Reinhardstoettner, A. Von; Rauch, E.; Brandt, Thomas

doi:10.1002/1531-8249(199909)46:3<416::aid-ana20>3.0.co;2-w

Cited by 174 publications

(118 citation statements)

References 15 publications

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“…28 A recent study also reported the presence of herpes simplex virus type one in vestibular nuclei, indicating that viral migration can also occur via the vestibular nerve to the pontomedullary brainstem. 29 A more recent paper suggests the possibility of viral migration from the vestibular ganglia to the labyrinth, provoking vestibular deafferentation. Different mechanisms could explain such viral distribution: viral migration along anastomoses; haematogenic infection by herpes simplex virus type one infected T lymphocytes; or direct infection of the vestibular labyrinth.…”

Section: Discussionmentioning

confidence: 97%

Otoneurological findings in human immunodeficiency virus positive patients

et al. 2008

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Objective: To investigate vestibular function in human immunodeficiency virus positive subjects.Methods: We studied vestibular function in 60 human immunodeficiency virus positive subjects reporting dizziness. All three Center for Disease Control and Prevention categories of human immunodeficiency virus infection were represented in the study group (30 patients in class A, 20 in class B and 10 in class C). Subjects had had no previous history of acute vertigo. All subjects underwent: neurotological screening for spontaneous, positional and positioning nystagmus, using head-shaking and head-thrust (Halmagyi) tests; audiometrical examination; and electronystagmography with bithermal stimulation (Freyss' method). The results of the 30 class A subjects were compared with those of 30 human immunodeficiency virus negative patients reporting dizziness.Results: Abnormal otoneurological findings increased progressively from the A to C categories, particularly regarding increased central damage (3.3 per cent of class A, 35 per cent of class B and 100 per cent of class C subjects). In contrast, the incidence of peripheral vestibular disorders remained almost the same, comparing the three categories (33.3 per cent in class A and 50 per cent in classes B and C subjects). Moreover, a higher number of human immunodeficiency virus positive subjects showed abnormal otoneurological findings, compared with the dizzy, human immunodeficiency virus negative subjects.Conclusions: In our opinion, a vestibular disorder may occur in human immunodeficiency virus positive patients as a result of direct viral damage, even in the early phase of infection. Central vestibular damage may be established later on, and may be linked to different causes (e.g. superinfections, vascular causes and drug toxicity).

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Section: Discussionmentioning

confidence: 97%

Otoneurological findings in human immunodeficiency virus positive patients

et al. 2008

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“…AUV is caused by a sudden unilateral vestibular loss of function causing an asymmetry in the resting tone of the vestibular nerves that is responsible for the nystagmus and ensuing perception of vertigo. The symptoms of AUV gradually improve over time as a result of a process of vestibular compensation with eventual restitution of vestibular function in the majority of patients [1].…”

Section: Introductionmentioning

confidence: 99%

Glucocorticoids improve acute dizziness symptoms following acute unilateral vestibulopathy

et al. 2015

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“…32 These findings indicate latent infection of the vestibular ganglia with HSV-1. 33 Furthermore, inoculation of HSV induces vestibular dysfunction with infected vestibular ganglion cells in mice.…”

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confidence: 99%