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Vestibulo-cochlear function in inflammatory neuropathies


Blanquet, Marisa; Petersen, Jens A; Palla, Antonella; Veraguth, Dorothe; Weber, Konrad P; Straumann, Dominik; Tarnutzer, Alexander A; Jung, Hans H (2018). Vestibulo-cochlear function in inflammatory neuropathies. Clinical Neurophysiology, 129(4):863-873.

Abstract

OBJECTIVE: We aimed to quantify peripheral-vestibular deficits that may contribute to imbalanced stance/gait in patients with inflammatory neuropathies.
METHODS: Twenty-one patients (58 ± 15 y [mean age ± 1SD]; chronic-inflammatory-demyelinating-polyneuropathy = 10, Guillain-Barré Syndrome = 5, Anti-MAG peripheral neuropathy = 2, multifocal-motor-neuropathy = 4) were compared with 26 healthy controls. All subjects received video-head-impulse testing (vHIT), caloric irrigation and cervical/ocular vestibular-evoked myogenic-potentials (VEMPs). The Yardley vertigo-symptom-scale (VSS) was used to rate vertigo/dizziness. Postural stability was assessed using the functional gait-assessment (FGA). Pure-tone audiograms (n = 18), otoacoustic emissions (n = 12) and auditory brainstem responses were obtained (n = 12).
RESULTS: Semicircular-canal hypofunction was noted in 9/21 (43%) patients (vHIT = 6; caloric irrigation = 5), whereas otolith function was impaired in 12/21 (57%) (oVEMPs = 8; cVEMPs = 5), resulting in vestibular impairment of at least one sensor in 13/21 (62%). On average, 2.4 ± 1.1 vestibular end organs (each side: anterior/posterior/horizontal canal, utriculus, sacculus; total = 10) were affected. The VSS-scores were higher in patients (16.8 ± 8.6 vs. 9.5 ± 6.2, p = 0.002) but did not correlate with the number of affected organs. Auditory neuropathy was found in 1/12 (8%) patients.
CONCLUSION: Impairment of one or more vestibular end organs was frequent, but usually mild, possibly contributing to imbalance of stance/gait in inflammatory neuropathies.
SIGNIFICANCE: While our data does not support routine vestibular testing in inflammatory neuropathies, this may be considered in selected cases.

Abstract

OBJECTIVE: We aimed to quantify peripheral-vestibular deficits that may contribute to imbalanced stance/gait in patients with inflammatory neuropathies.
METHODS: Twenty-one patients (58 ± 15 y [mean age ± 1SD]; chronic-inflammatory-demyelinating-polyneuropathy = 10, Guillain-Barré Syndrome = 5, Anti-MAG peripheral neuropathy = 2, multifocal-motor-neuropathy = 4) were compared with 26 healthy controls. All subjects received video-head-impulse testing (vHIT), caloric irrigation and cervical/ocular vestibular-evoked myogenic-potentials (VEMPs). The Yardley vertigo-symptom-scale (VSS) was used to rate vertigo/dizziness. Postural stability was assessed using the functional gait-assessment (FGA). Pure-tone audiograms (n = 18), otoacoustic emissions (n = 12) and auditory brainstem responses were obtained (n = 12).
RESULTS: Semicircular-canal hypofunction was noted in 9/21 (43%) patients (vHIT = 6; caloric irrigation = 5), whereas otolith function was impaired in 12/21 (57%) (oVEMPs = 8; cVEMPs = 5), resulting in vestibular impairment of at least one sensor in 13/21 (62%). On average, 2.4 ± 1.1 vestibular end organs (each side: anterior/posterior/horizontal canal, utriculus, sacculus; total = 10) were affected. The VSS-scores were higher in patients (16.8 ± 8.6 vs. 9.5 ± 6.2, p = 0.002) but did not correlate with the number of affected organs. Auditory neuropathy was found in 1/12 (8%) patients.
CONCLUSION: Impairment of one or more vestibular end organs was frequent, but usually mild, possibly contributing to imbalance of stance/gait in inflammatory neuropathies.
SIGNIFICANCE: While our data does not support routine vestibular testing in inflammatory neuropathies, this may be considered in selected cases.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Clinic for Otorhinolaryngology
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:2018
Deposited On:26 Feb 2018 20:47
Last Modified:14 Mar 2018 15:38
Publisher:Elsevier
ISSN:1388-2457
OA Status:Closed
Publisher DOI:https://doi.org/10.1016/j.clinph.2017.11.025
PubMed ID:29305208

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