Abstract
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.
Highlights
Bilateral vestibulopathy (BVP) is a chronic vestibular syndrome defined by bilaterally impaired vestibulo-ocular reflex, variably involving semicircular canal (SCC) and otolith function [1], as typically assessed by individual SCC head impulse test (HIT) [2, 3] and vestibular evoked myogenic potential [4], respectively
While search coil HIT (scHIT) is the gold-standard for evaluating individual SCC function [3], it is time consuming and semi-invasive, and, with the advent of modern video-oculography, rapid and reliable assessment of each SCC function is possible in the clinic with video HIT (vHIT) [12, 13]
VHIT has shown that anterior SCC (AC) function may be selectively spared compared to posterior canal (PC) function in BVP due to gentamicin vestibulotoxicity and bilateral Meniere’s disease, whereas such sparing does not occur with idiopathic cases, those associated with sudden hearing loss and infection [11, 16]
Summary
Bilateral vestibulopathy (BVP) is a chronic vestibular syndrome defined by bilaterally impaired vestibulo-ocular reflex, variably involving semicircular canal (SCC) and otolith function [1], as typically assessed by individual SCC head impulse test (HIT) [2, 3] and vestibular evoked myogenic potential [4], respectively. Peripheral lesions, such as gentamicin vestibulotoxicity, autoimmune inner ear diseases, bilateral Meniere’s disease, and bilateral vestibular schwannomas are well recognized in BVP [5, 6]. We discuss current understanding of pattern of SCC abnormality in central lesions that can mimic BVP, drawing data from both scHIT and vHIT studies
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