著者: V Arbusow, P Schulz, M Strupp, M Dieterich, A von Reinhardstoettner, E Rauch, T Brandt
雑誌名: Ann Neurol. 1999 Sep;46(3):416-9.
Abstract/Text
Vestibular neuritis is a common cause of partial unilateral vestibular paralysis, which usually spares posterior semicircular canal function. The cause is assumed to be a viral reactivation of latent herpes simplex virus type 1 (HSV-1) in human vestibular ganglia. The existence of an anastomosis between the intermediate nerve and the superior vestibular nerve suggests the question of whether selective affliction of the superior vestibular nerve is the result of migration of HSV-1 from the geniculate ganglion along this faciovestibular anastomosis. We determined the distribution of HSV-1 among geniculate ganglia, vestibular ganglia, and within Scarpa's ganglion by examining 35 human temporal bones by polymerase chain reaction. HSV-1 was found in 66% of geniculate ganglia and 60% of vestibular ganglia; all examined parts of vestibular ganglia were almost equally HSV-1 infected. Our data provided no support for viral migration along this anastomosis or for a preferential latency of HSV-1 in the superior vestibular nerve. We suggest that the common double innervation of the posterior ampulla by two nerves running in two separate bony canals could offer an alternative explanation for the regular sparing of posterior canal function in vestibular neuritis.
PMID
10482275 Ann Neurol. 1999 Sep;46(3):416-9.
著者: V Arbusow, D Theil, M Strupp, A Mascolo, T Brandt
雑誌名: Audiol Neurootol. 2001 Sep-Oct;6(5):259-62.
Abstract/Text
Reactivation of herpes simplex virus type 1 (HSV-1) in the vestibular ganglion (VG) is the suspected cause of vestibular neuritis (VN). Recent studies reported the presence of HSV-1 DNA not only in human VGs but also in vestibular nuclei, a finding that indicates the possibility of viral migration to the human vestibular labyrinth. Distribution of HSV-1 DNA was determined in geniculate ganglia, VGs, semicircular canals, and macula organs of 21 randomly obtained human temporal bones by nested PCR. Viral DNA was detected in 48% of the labyrinths, 62% of the VGs, and 57% of the geniculate ganglia. The potential significance of this finding is twofold: (1) Inflammation in VN could also involve the labyrinth and thereby cause acute unilateral vestibular deafferentation. (2) As benign paroxysmal positional vertigo often occurs in patients who have had VN, it could also be a sequel of viral labyrinthitis.
Copyright 2001 S. Karger AG, Basel
PMID
11729328 Audiol Neurootol. 2001 Sep-Oct;6(5):259-62.
著者: Michael Strupp, Vera Carina Zingler, Viktor Arbusow, Daniel Niklas, Klaus Peter Maag, Marianne Dieterich, Sandra Bense, Diethilde Theil, Klaus Jahn, Thomas Brandt
雑誌名: N Engl J Med. 2004 Jul 22;351(4):354-61. doi: 10.1056/NEJMoa033280.
Abstract/Text
BACKGROUND: Vestibular neuritis is the second most common cause of peripheral vestibular vertigo. Its assumed cause is a reactivation of herpes simplex virus type 1 infection. Therefore, corticosteroids, antiviral agents, or a combination of the two might improve the outcome in patients with vestibular neuritis.
METHODS: We performed a prospective, randomized, double-blind, two-by-two factorial trial in which patients with acute vestibular neuritis were randomly assigned to treatment with placebo, methylprednisolone, valacyclovir, or methylprednisolone plus valacyclovir. Vestibular function was determined by caloric irrigation, with the use of the vestibular paresis formula (to measure the extent of unilateral caloric paresis) within 3 days after the onset of symptoms and 12 months afterward.
RESULTS: Of a total of 141 patients who underwent randomization, 38 received placebo, 35 methylprednisolone, 33 valacyclovir, and 35 methylprednisolone plus valacyclovir. At the onset of symptoms there was no difference among the groups in the severity of vestibular paresis. The mean (+/-SD) improvement in peripheral vestibular function at the 12-month follow-up was 39.6+/-28.1 percentage points in the placebo group, 62.4+/-16.9 percentage points in the methylprednisolone group, 36.0+/-26.7 percentage points in the valacyclovir group, and 59.2+/-24.1 percentage points in the methylprednisolone-plus-valacyclovir group. Analysis of variance showed a significant effect of methylprednisolone (P<0.001) but not of valacyclovir (P=0.43). The combination of methylprednisolone and valacyclovir was not superior to corticosteroid monotherapy.
CONCLUSIONS: Methylprednisolone significantly improves the recovery of peripheral vestibular function in patients with vestibular neuritis, whereas valacyclovir does not.
Copyright 2004 Massachusetts Medical Society
PMID
15269315 N Engl J Med. 2004 Jul 22;351(4):354-61. doi: 10.1056/N･･･
著者: Mikael L-Å Karlberg, Måns Magnusson
雑誌名: Otol Neurotol. 2011 Sep;32(7):1140-3. doi: 10.1097/MAO.0b013e3182267e24.
Abstract/Text
OBJECTIVE: To report the effects of glucocorticoid treatment of acute vestibular neuronitis on recovery of vestibular function and length of hospital stay.
STUDY DESIGN: Prospective, consecutive case series compared with historic controls.
SETTING: Secondary referral academic hospital.
PATIENTS: Patients with acute vestibular neuronitis. One group treated with glucocorticoids within 3 days after symptom onset (n = 33) and 2 historic untreated control groups (n = 41 and n = 67).
INTERVENTIONS: Oral prednisolone 50 mg/d for 5 days with tapering of doses for the next 5 days, alternatively with intravenous betamethasone 8 mg on the first 1 to 2 days if nauseated.
MAIN OUTCOME MEASURES: Extent of unilateral vestibular paresis (%) in the caloric test at presentation and at 12 months of follow-up. Length of hospital stay (days).
RESULTS: The initial vestibular paresis value did not differ between the treatment group and the control group. At follow-up, the treatment group showed a lower value (22.8% versus 47.2%, p = 0.0003) and greater improvement (53.4% versus 35.6%, p = 0.002). At follow-up, 70% of the treatment group had a normal caloric test result compared to only 34% of the control group. The mean hospital stay of the treatment group was significantly shorter than that of the control group (1.8 versus 3.0 d, p = 0.001).
CONCLUSION: Glucocorticoids administered within 3 days after onset of vestibular neuronitis improves long-time recovery of vestibular function and reduces length of hospital stay.
PMID
21817947 Otol Neurotol. 2011 Sep;32(7):1140-3. doi: 10.1097/MAO.･･･
著者: Robert W Baloh
雑誌名: N Engl J Med. 2003 Mar 13;348(11):1027-32. doi: 10.1056/NEJMcp021154.
Abstract/Text
PMID
12637613 N Engl J Med. 2003 Mar 13;348(11):1027-32. doi: 10.1056･･･
