Vestibulocochlear implant (VCI) modulation improves mid and high frequency vestibulo-ocular reflex (VOR)

The vestibulo-ocular reflex (VOR) stabilizes gaze during head movements by generating compensatory eye movements. In bilateral vestibulopathy (BV), loss of vestibular function leads to loss of VOR and consequently, oscillopsia. Currently, no curative treatment exists. Vestibulocochlear implants (VCI) aim to restore vestibular function by modulating electrical stimulation of the ampullary nerves in response to head motion. Although prior studies have demonstrated partial VOR restoration, a comprehensive evaluation across different stimulation conditions remains limited. This study assessed the effects of multiple stimulation conditions on VOR gain in BV patients implanted with the latest VCI prototype.

Nine BV patients were unilaterally implanted with an intralabyrinthine VCI. VOR responses were assessed using rotatory chair testing (mid-frequency domain) and video head impulse testing (vHIT; high-frequency domain). Five stimulation conditions were evaluated: Reference (VI off), Baseline only (constant stimulation), Default (motion modulation around baseline), Lowered baseline (motion modulation around threshold level), and Boosted stimulation (maximized modulation). Subjects were classified into subgroup A (peak eye velocity, PEV, ≥ 30°/s) during lateral ampullary nerve block stimulation and subgroup B (PEV < 30°/s).

Six subjects were classified in subgroup A. In rotatory chair testing, excitatory VOR gain increased significantly under modulated stimulation at all tested frequencies (p < 0.05), with median gains rising from 0.09-0.20 (Reference) to 0.82 (Lowered baseline). No significant inhibitory improvements were observed. In vHIT, subgroup A demonstrated significant excitatory median gain improvements across all canal planes (p < 0.005). Lateral canal gains improved from 0.12 (Reference) to 0.69 (Boosted), and anterior canal median gains up to 0.74. Posterior gains improved but remained < 0.60. Inhibitory gains showed no changes. Subgroup B showed no meaningful gain improvements in any condition.

Motion-modulated stimulation enhanced excitatory VOR function at mid- and high frequencies in patients who demonstrated higher PEV during block stimulations. However, baseline stimulation alone was ineffective. Lowered baseline and Boosted conditions showed the largest improvements, with gains approaching functional levels in several subjects. However, inhibitory responses remained limited, reflecting physiological and technical constraints. These findings support individualized, frequency-dependent modulation strategies to optimize gaze stabilization and potentially reduce oscillopsia in daily life.