Address for correspondence: Dr. Lloyd Minor, Department of Otolaryngology-Head & Neck Surgery, Johns Hopkins University School of Medicine, 601 N. Caroline St., Rm. 6253, Baltimore, MD 21287-0910. Voice: 410-955-3403; fax: 410-955-0035.
lminor{at}jhmi.edu
Ann. N.Y. Acad. Sci. 956: 324-337 (2002).
The horizontal vestibulo-ocular reflex (VOR) evoked by passive,
high-acceleration, head-on-body rotations (head thrusts) while
viewing a far (124-cm) or near (15-cm) target was recorded (scleral
search coil) in four subjects with normal vestibular function
and in one subject with unilateral vestibular hypofunction.
For responses in the subjects with normal vestibular function,
the latency of responses relative to the onset of head movement
was 7.5 ± 1.5 ms for the VOR and 21.6 ± 1.2 ms
for the vergence-mediated increase in VOR gain. The gain of
the VOR at the peak of the velocity response while viewing a
far target was 1.01 ± 0.06; while viewing a near target,
it was 1.25 ± 0.08 (
p <0.003). The responses were
modeled with two pathways based on the different latencies.
The "far-viewing" pathway was represented by a constant gain
term. The "near-viewing" pathway was represented by a first-order
lead term, a gain that was dependent on viewing distance, and
a delay. Analysis of the responses revealed that the lead term
was greater for the adducting than the abducting eye. In the
subject with unilateral vestibular hypofunction, ipsilesional
responses showed no change in VOR gain with respect to viewing
distance. Contralesional responses retained the vergence-dependent
increase in gain. A bilateral model was developed based on the
data from the subjects with normal vestibular function. Simulations
of this model when inputs were eliminated from one side predict
the changes observed in the subject with unilateral vestibular
hypofunction. The response asymmetries arise because the near-viewing
pathway is more susceptible to inhibitory cutoff than is the
far-viewing pathway.
