Transmastoid galvanic stimulation does not affect the vergence-mediated gain increase of the human angular vestibulo-ocular reflex

Vergence is one of several viewing contexts that require an increase in the angular vestibular-ocular reflex (aVOR) response. A previous monkey study found that the vergence-mediated gain (eye/head velocity) increase of the aVOR was attenuated by 64 % when anodic currents, which preferentially lower the activity of irregularly firing vestibular afferents, were delivered to both labyrinths. We sought to determine whether there was similar evidence implicating a role for irregular afferents in the vergence-mediated gain increase of the human aVOR. Our study is based upon analysis of the aVOR evoked by head rotations, delivered passively while subjects viewed a near (15 cm) or far (124 cm) target and applying galvanic vestibular stimulation (GVS) via surface electrodes. We tested 12 subjects during 2–3 sessions each. Vestibular stimuli consisted of passive whole-body rotations (sinusoids from 0.05–3 Hz and 12–25°/s, and transients with peak ~15°, 50°/s, 500°/s²) and head-on-body impulses (peak ~30°, 150°/s, 3,000°/s²). GVS was on for 10 s every 20 s. All polarity combinations were tested, with emphasis on uni- and bi-lateral anodic inhibition. The average stimulus current was 5.9 ± 1.6 mA (range: 3–9.5 mA), vergence angle (during near viewing) was 22.6 ± 2.8° and slow-phase eye velocity caused by left anodic current stimulation with head stationary was −3.4 ± 1.1°/s, −0.2 ± 0.6°/s and 2.5 ± 1.4°/s (torsion, vertical, horizontal). No statistically significant GVS effects were observed, suggesting that surface electrode GVS has no effect on the vergence-mediated gain increase of the aVOR at the current levels (~6 mA) tolerated by most humans. We conclude that clinically practical transmastoid GVS does not effectively silence irregular afferents and hypothesize that currents >10 mA are needed to reproduce the monkey results.