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Original Research ARTICLE Provisionally accepted The full-text will be published soon. Notify me

Front. Neurol. | doi: 10.3389/fneur.2018.00046


  • 1Neurology, University of Illinois at Peoria, United States

Background: Previous series of bilateral vestibular loss (BVL) identified numerous etiologies, but surprisingly, a cause in a significant number of cases remains unknown. In an effort to understand possible etiology and management strategies, a global effort is currently in progress. Here I contribute my ten-year experience with both acute and chronic BVL during the 2007-2017 decade.
Methods: This is a retrospective review of the charts and EMR of patients diagnosed with BVL in the last ten years. Following Institutional IRB approval, we identified 57 patients with a diagnosis of BVL, and utilized the current diagnostic criteria listed by the Barany society (1). The inclusion criteria included patients with BVL of any cause, within an age span older than 18 and a neuro-otologic examination supporting the clinical impression of BVL.
During the current decade 2007-2017 I identified two broad categories of BVL (acute and chronic) in 57 patients; only 41 of them had records available. The etiology includes: Idiopathic: n= 9, Wernicke’s encephalopathy n= 11, superficial siderosis n= 3, paraneoplastic syndrome: n=3, bilateral vestibular neuritis (recurrent AVS lasting days without cochlear symptoms) n= 3, simultaneous ototoxicity of aminoglycoside and chemotherapy toxicity n= 2 ,MELAS n= 2, Meniere’s disease treated with intra-tympanic streptomycin in one ear n = 1, acute phenytoin intoxication: n=1 , combined chronic unilateral tumor related vestibulopathy and new contralateral vestibular neuritis (this patient presented with Betcherew’s phenomenon) n=1, bilateral AICA stroke n= 1, mixed spinocerebellar ataxia type 3, n= 2 and CANVAS n= 2 .
This cohort included a 28% overall incidence of acute and subacute BVL; among them 65% improved with intervention. In the thiamine deficiency group specifically, the vestibular function improved in 80% of the patients. Even though acute, subacute or chronic showed slightly asymmetric horizontal-VOR gain loss, it never did cause spontaneous, primary straight gaze horizontal nystagmus. n=39/41 patients had abnormal manual HIT, n=26/41 BVL patients tested with vHIT immediately after manual testing showed decreased VOR gain ,including two with covert saccades. Two thiamine patients with positive bedside pre-treatment manual HIT, tested after treatment with high-dose thiamine showed improved VOR.

Keywords: Vestibular loss, Acute bilaeral vestibular loss, Thiamine Deficiency, abnormal head ipmpulse test, paraneoplastic bilateral vestibualr loss

Received: 01 Dec 2017; Accepted: 18 Jan 2018.

Edited by:

Alexander A. Tarnutzer, University of Zurich, Switzerland

Reviewed by:

Konrad P. Weber, University of Zurich, Switzerland
Klaus Jahn, Schön Klinik, Germany  

Copyright: © 2018 Kattah. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Dr. Jorge Kattah, C., University of Illinois at Peoria, Neurology, 530 North GlenOak Avenue, Peoria, 61637, United States,