Vestibulo-ocular reflex gain improvements at peak head acceleration and velocity following onset of unilateral vestibular neuritis: Insights into neural compensation mechanisms.

Background and aims: An acute unilateral peripheral vestibular deficit (aUPVD) due to vestibular neuritis causes deficient yaw axis vestibular ocular reflex (VOR) gains. Using video head impulse tests (vHITs), we examined phasic and tonic velocity gains of the VOR over time to determine if these differed at onset and during subsequent improvement.

Methods: The VOR responses of 61 patients were examined within 5 days of aUPVD onset, and 3 and 7 weeks later using vHIT with mean peak yaw angular velocities of 177°/s (sd 45°/s) and mean peak accelerations of 3660°/s2 (sd 1300°/s2). The phasic velocity or acceleration gain (aG) was computed as the ratio of eye to head velocity around peak head acceleration, and the tonic velocity gain (vG) was calculated as the same ratio around peak head velocity.

Results: aG increased ipsi-deficit from 0.45 at onset to 0.67 at 3 weeks and 7 weeks later, and vG increased ipsi-deficit from 0.29 to 0.51 and 0.53, respectively, yielding a significant time effect (p < 0.001). Deficit side aG was significantly greater (p < 0.001) than vG at all time points. Deficit side gain improvements in aG and vG were similar. Contra-deficit aG increased from 0.86 to 0.95 and 0.94 at 3 weeks and 7 weeks, and vG contra-deficit increased from 0.84, to 0.89 and 0.87, respectively, also yielding a significant time effect (p = 0.004). Contra-deficit aG and vG were normal at 3 weeks. Mean canal paresis values improved from 91% to 67% over the 7 weeks.

Conclusions: Acceleration and velocity VOR gains on the deficit side are reduced by aUPVD and improve most in the first 3 weeks after aUPVD onset. Deficit side aG is consistently higher than deficit side vG following an aUPVD, suggesting that acceleration rather than velocity sensitive compensatory neural mechanisms are predominant during the compensation process for aUPVD.