Absent vestibular evoked myogenic potentials in vestibular neurolabyrinthitis - An indicator of inferior vestibular nerve involvement?

Absent vestibular evoked myogenic potentials in vestibular neurolabyrinthitis - An indicator of inferior vestibular nerve involvement?
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DOI:
10.1001/archotol.1996.01890200035008
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发表时间:
1996-08-01
影响因子:
--
通讯作者:
Colebatch, JG
Colebatch, JG
中科院分区:
其他
文献类型:
--
作者:
Murofushi, T;Halmagyi, GM;Colebatch, JG

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背景资料:良性阵发性定位性眩晕(BPPV)通常被认为是由后半规管结石引起的,后半规管是由前庭下神经支配的器官。我们假设,前庭诱发肌源性电位(VEMPs)的缺失提示前庭下神经受累,并且在VEMPs缺失的患者中,前庭神经炎(VNL)后不会发生后半规管型BPPV。目的:探讨VEMPs是否有助于评估急性VNL中前庭下神经受累。设计:我们回顾了47例患者的VEMP结果34例男性和13例女性急性VNL,其中10例随后发展为后半规管型BPPV。而p13-n23(VEMP的第一个正负峰)在所有患者的健侧刺激时均出现在同侧,16例(34%)患者患侧无此点。p13-n23的存在或缺失与冷热试验、纯音测听和听性脑干反应的结果无关。47例VNL急性发作后出现典型的后半规管BPPV者10例,均与神经根炎同侧。在所有10例BPPV患者的受影响的耳朵的刺激的p13-n23电位被保存。结论:这些结果表明,如果VEMPs是从一个耳朵,遭受急性VNL缺席,然后后半规管BPPV是不太可能发展的VNL的后果。其原因似乎是VEMPs的缺乏是由于前庭下神经或其支配的结构的参与。
Background: Benign paroxysmal positioning vertigo (BPPV) is generally thought to be caused by canalolithiasis in the posterior semicircular canal, an organ that is innervated by the inferior vestibular nerve. We hypothesized that absent vestibular evoked myogenic potentials (VEMPs) would indicate involvement of the inferior vestibular nerve and that posterior semicircular canal-type BPPV could not develop after vestibular neurolabyrinthitis (VNL) in patients with absent VEMPs.Objective: To find out if VEMPs could be helpful in evaluating involvement of the inferior vestibular nerve in acute VNL.Design: We reviewed the VEMP findings in 47 patients (34 men and 13 women) with acute VNL, 10 of whom had then developed posterior semicircular canal-type BPPV.Results: While p13-n23, the first positive-negative peak of the VEMP, was ipsilaterally present on stimulation of the unaffected side in all patients, it was absent on the affected side in 16 patients (34%). The absence or presence of p13-n23 was independent of the results of caloric tests, pure tone audiometry, and auditory brain-stem responses. Typical posterior semicircular canal BPPV developed in 10 of the 47 patients after the acute attack of VNL, always on the same side as the neurolabyrinthitis. The p13-n23 potentials were preserved on stimulation of the affected ear in all 10 patients with BPPV.Conclusions: These results suggest that if VEMPs are absent from an ear that has suffered acute VNL, then posterior semicircular canal BPPV is unlikely to develop as a consequence of the VNL. The reason for this appears to be that the absence of VEMPs is due to involvement of the inferior vestibular nerve or involvement of the structures that it innervates.