Central Lesions With Selective Semicircular Canal Involvement Mimicking Bilateral Vestibulopathy

Bilateral vestibulopathy (BVP), which is due to peripheral lesions, may selectively involve certain semicircular canal (SCC). Recent eye movement recordings with search coil and video head impulse test (HIT) have provided insight in central lesions that can cause bilateral and selective SCC deficit...

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Main Authors: Luke Chen, G. Michael Halmagyi
Format: Article
Language:English
Published: Frontiers Media S.A. 2018-04-01
Series:Frontiers in Neurology
Subjects:
Online Access:http://journal.frontiersin.org/article/10.3389/fneur.2018.00264/full
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author Luke Chen
G. Michael Halmagyi
author_facet Luke Chen
G. Michael Halmagyi
author_sort Luke Chen
collection DOAJ
description Bilateral vestibulopathy (BVP), which is due to peripheral lesions, may selectively involve certain semicircular canal (SCC). Recent eye movement recordings with search coil and video head impulse test (HIT) have provided insight in central lesions that can cause bilateral and selective SCC deficit mimicking BVP. Since neurological signs or ocular motor deficits maybe subtle or absent, it is critical to recognize central lesions correctly since there is prognostic and treatment implication. Acute floccular lesions cause bilateral horizontal SCC (HC) impairment while leaving vertical SCC function unaffected. Vestibular nuclear lesions affect bilateral HC and posterior SCC (PC) function, but anterior SCC (AC) function is spared. When both eyes are recorded, medial longitudinal fasciculus lesions cause horizontal dysconjugacy in HC function and catch-up saccades, as well as selective deficiency of PC over AC function. Combined peripheral and central lesions may be difficult to distinguish from BVP. Anterior inferior cerebellar artery stroke causes two types of deficits: 1. ipsilateral pan-SCC deficits and contralateral HC deficit and 2. bilateral HC deficit with vertical SCC sparing. Metabolic disorders such as Wernicke encephalopathy characteristically involve HC but not AC or PC function. Gaucher disease causes uniform loss of all SCC function but with minimal horizontal catch-up saccades. Genetic cerebellar ataxias and cerebellar-ataxia neuropathy vestibular areflexia syndrome typically do not spare AC function. While video HIT does not replace the gold-standard, search coil HIT, clinicians are now able to rapidly and accurately identify specific pattern of SCC deficits, which can aid differentiation of central lesions from BVP.
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spelling doaj.art-1cbdcbad776d4fd1a6acde5d2cde49ce2022-12-22T00:41:37ZengFrontiers Media S.A.Frontiers in Neurology1664-22952018-04-01910.3389/fneur.2018.00264376463Central Lesions With Selective Semicircular Canal Involvement Mimicking Bilateral VestibulopathyLuke Chen0G. Michael Halmagyi1Faculty of Medicine, University of New South Wales, Sydney, NSW, AustraliaNeurology Department, Royal Prince Alfred Hospital, Sydney, NSW, AustraliaBilateral vestibulopathy (BVP), which is due to peripheral lesions, may selectively involve certain semicircular canal (SCC). Recent eye movement recordings with search coil and video head impulse test (HIT) have provided insight in central lesions that can cause bilateral and selective SCC deficit mimicking BVP. Since neurological signs or ocular motor deficits maybe subtle or absent, it is critical to recognize central lesions correctly since there is prognostic and treatment implication. Acute floccular lesions cause bilateral horizontal SCC (HC) impairment while leaving vertical SCC function unaffected. Vestibular nuclear lesions affect bilateral HC and posterior SCC (PC) function, but anterior SCC (AC) function is spared. When both eyes are recorded, medial longitudinal fasciculus lesions cause horizontal dysconjugacy in HC function and catch-up saccades, as well as selective deficiency of PC over AC function. Combined peripheral and central lesions may be difficult to distinguish from BVP. Anterior inferior cerebellar artery stroke causes two types of deficits: 1. ipsilateral pan-SCC deficits and contralateral HC deficit and 2. bilateral HC deficit with vertical SCC sparing. Metabolic disorders such as Wernicke encephalopathy characteristically involve HC but not AC or PC function. Gaucher disease causes uniform loss of all SCC function but with minimal horizontal catch-up saccades. Genetic cerebellar ataxias and cerebellar-ataxia neuropathy vestibular areflexia syndrome typically do not spare AC function. While video HIT does not replace the gold-standard, search coil HIT, clinicians are now able to rapidly and accurately identify specific pattern of SCC deficits, which can aid differentiation of central lesions from BVP.http://journal.frontiersin.org/article/10.3389/fneur.2018.00264/fullbilateral vestibulopathycentral vestibular disorderssemicircular canalhead impulse testeye movements
spellingShingle Luke Chen
G. Michael Halmagyi
Central Lesions With Selective Semicircular Canal Involvement Mimicking Bilateral Vestibulopathy
Frontiers in Neurology
bilateral vestibulopathy
central vestibular disorders
semicircular canal
head impulse test
eye movements
title Central Lesions With Selective Semicircular Canal Involvement Mimicking Bilateral Vestibulopathy
title_full Central Lesions With Selective Semicircular Canal Involvement Mimicking Bilateral Vestibulopathy
title_fullStr Central Lesions With Selective Semicircular Canal Involvement Mimicking Bilateral Vestibulopathy
title_full_unstemmed Central Lesions With Selective Semicircular Canal Involvement Mimicking Bilateral Vestibulopathy
title_short Central Lesions With Selective Semicircular Canal Involvement Mimicking Bilateral Vestibulopathy
title_sort central lesions with selective semicircular canal involvement mimicking bilateral vestibulopathy
topic bilateral vestibulopathy
central vestibular disorders
semicircular canal
head impulse test
eye movements
url http://journal.frontiersin.org/article/10.3389/fneur.2018.00264/full
work_keys_str_mv AT lukechen centrallesionswithselectivesemicircularcanalinvolvementmimickingbilateralvestibulopathy
AT gmichaelhalmagyi centrallesionswithselectivesemicircularcanalinvolvementmimickingbilateralvestibulopathy