Abstract
Patients with bilateral vestibular failure (BVF) suffer from postural and gait unsteadiness with an increased risk of falls. The aim of this study was to elucidate the differential role of otolith, semicircular canal (SSC), visual, proprioceptive, and cognitive influences on the postural stability of BVF patients. Center-of-pressure displacements were recorded by posturography under six conditions: target visibility; tonic head positions in the pitch plane; horizontal head shaking; sensory deprivation; dual task; and tandem stance. Between-group analysis revealed larger postural sway in BVF patients on eye closure; but with the eyes open, BVF did not differ from healthy controls (HCs). Head tilts and horizontal head shaking increased sway but did not differ between groups. In the dual task condition, BVF patients maintained posture indistinguishable from controls. On foam and tandem stance, postural sway was larger in BVF, even with the eyes open. The best predictor for the severity of bilateral vestibulopathy was standing on foam with eyes closed. Postural control of our BVF was indistinguishable from HCs once visual and proprioceptive feedback is provided. This distinguishes them from patients with vestibulo-cerebellar disorders or functional dizziness. It confirms previous reports and explains that postural unsteadiness of BVF patients can be missed easily if not examined by conditions of visual and/or proprioceptive deprivation. In fact, the best predictor for vestibular hypofunction (VOR gain) was examining patients standing on foam with the eyes closed. Postural sway in that condition increased with the severity of vestibular impairment but not with disease duration. In the absence of visual control, impaired otolith input destabilizes BVF with head retroflexion. Stimulating deficient SSC does not distinguish patients from controls possibly reflecting a shift of intersensory weighing toward proprioceptive-guided postural control. Accordingly, proprioceptive deprivation heavily destabilizes BVF, even when visual control is provided.
Highlights
Bilateral vestibular failure (BVF) is characterized by unsteadiness of stance and gait and disabling oscillopsia during head movements [1]
The mean VOR gain was reduced to 0.26 ± 0.04 indicating severe bilateral vestibulopathy
Mean peak slow phase velocity (SPV) of caloric nystagmus was 4.5 ± 0.8°/s. oVEMP were recorded in patients and healthy controls (HCs) subjects; they were absent in 12 patients and revealed reduced amplitudes in the other 10 patients: peak amplitude differed significantly between groups (Mann–Withney U test, p = 0.003, median patients: 3.8 μV, median HC subjects: 6.95 μV). cVEMP were recorded in patients and HC subjects; they were absent in 17 patients and showed significantly reduced amplitudes in the other five patients
Summary
Bilateral vestibular failure (BVF) is characterized by unsteadiness of stance and gait and disabling oscillopsia during head movements [1]. Rarer causes include systemic autoimmune diseases, e.g., Cogan’s syndrome [14], in particular connective tissue disease, e.g., systemic lupus erythematosus, Behcet’s disease, neurosarcoidosis and infectious diseases (e.g., borreliosis), vitamine B1 deficiency [15], schwannoma, meningeosis, superficial siderosis [16] and it may present as part of neurodegenerative diseases, e.g., idiopathic cerebellar ataxia with BVF [17, 18] and additional polyneuropathy CANVAS syndrome [19]. Moderate vestibular hypofunction may come from cerebellar disease [20] which causes postural unsteadiness
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