| 1. |
- Aw, S T, et al.
(författare)
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Individual semicircular canal function in superior and inferior vestibular neuritis
- 2001
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Ingår i: Neurology. - 1526-632X. ; 57:5, s. 768-774
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: To examine the concept of selective superior and inferior vestibular nerve involvement in vestibular neuritis by studying the distribution of semicircular canal (SCC) involvement in such patients. BACKGROUND: Vestibular neuritis was traditionally thought to involve the superior and inferior vestibular nerves. Recent work suggests that in some patients, only the superior nerve is involved. So far there are no reported cases of selective involvement of the inferior vestibular nerve. METHODS: The authors measured the vestibuloocular reflex from individual SCC at natural head accelerations using the head impulse test. The authors studied 33 patients with acute unilateral peripheral vestibulopathy, including 29 with classic vestibular neuritis and 4 with simultaneous ipsilateral hearing loss, 18 healthy subjects and 15 surgical unilateral vestibular deafferented patients. RESULTS: In patients with preserved hearing, eight had deficits in all three SCC, suggesting involvement of the superior and inferior vestibular nerves. Twenty-one had a lateral SCC deficit or a combined lateral and anterior SCC deficit consistent with selective involvement of the superior vestibular nerve. Two patients with ipsilateral hearing loss had normal caloric responses and an isolated posterior SCC deficit on impulsive testing. The authors propose that these two patients had a selective loss of inferior vestibular nerve function. CONCLUSION: Vestibular neuritis can affect the superior and inferior vestibular nerves together or can selectively affect the superior vestibular nerve.
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| 2. |
- Halmagyi, G M, et al.
(författare)
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Inferior vestibular neuritis
- 2002
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Ingår i: Annals of the New York Academy of Sciences. - 0077-8923. ; 956, s. 306-313
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Tidskriftsartikel (refereegranskat)abstract
- Sudden, spontaneous, unilateral loss of vestibular function without simultaneous hearing loss or brain stem signs is generally attributed to a viral infection involving the vestibular nerve and is called acute vestibular neuritis. The clinical hallmarks of acute vestibular neuritis are vertigo, spontaneous nystagmus, and unilateral loss of lateral semicircular function as shown by impulsive and caloric testing. In some patients with vestibular neuritis the process appears to involve only anterior and lateral semicircular function, and these patients are considered to have selective superior vestibular neuritis. Here we report on two patients with acute vertigo, normal lateral semicircular canal function as shown by both impulsive and caloric testing, but selective loss of posterior semicircular canal function as shown by impulsive testing and of saccular function as shown by vestibular evoked myogenic potential testing. We suggest that these patients had selective inferior vestibular neuritis and that contrary to conventional teaching, in a patient with acute spontaneous vertigo, unilateral loss of lateral semicircular canal function is not essential for a diagnosis of acute vestibular neuritis.
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| 3. |
- Karlberg, Mikael, et al.
(författare)
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The effects of galvanic stimulation on the human vestibulo-ocular reflex
- 2000
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Ingår i: NeuroReport. - 1473-558X. ; 11:17, s. 3897-3901
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Tidskriftsartikel (refereegranskat)abstract
- We studied the effects of 5 mA bilateral or unilateral, bipolar or monopolar, galvanic stimulation on the horizontal vestibulo-ocular reflex (hVOR) in six normal subjects during 0.01, 0.05, 0.1, 0.5 and 1 Hz yaw rotations and in two subjects during high-acceleration, low-amplitude yaw head rotations (head impulses). Bipolar galvanic stimulation induced horizontal nystagmus in all subjects and an asymmetry of the hVOR only during rotations below 0.1 Hz. Monopolar stimulation had no significant effect. The findings suggest that in humans galvanic stimulation affects those primary horizontal semicircular canal neurons that mediate the hVOR via indirect pathways through the velocity storage mechanism.
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