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°/s(2)) and head-on-body impulses (peak ~30°, 150°/s, 3,000°/s(2)). 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.