Unilateral vestibular deafferentation causes permanent impairment of the human vertical vestibulo-ocular reflex in the pitch plane.
Rapid, passive, unpredictable, low-amplitude (10-20 degrees), high-acceleration (3000-4000 degrees/s2) head rotations were used to study the vertical vestibulo-ocular reflex in the pitch plane (pitch-vVOR) after unilateral vestibular deafferentation. The results from 23 human subjects who had undergone therapeutic unilateral vestibular deafferentation were compared with those from 19 normals. All subjects were tested while seated in the upright position. Group means and two-tailed 95% confidence intervals are reported for the pitch-vVOR gains in normal and unilateral vestibular deafferented subjects. In normal subjects, at a head velocity of 125 degrees/s the pitch-vVOR gains were: upward 0.89 +/- 0.06, downward 0.91 +/- 0.04. At a head velocity of 200 degrees/s, the pitch-vVOR gains were: upward 0.92 +/- 0.06, downward 0.96 +/- 0.04. There was no significant up-down asymmetry. In the 15 unilateral vestibular deafferented subjects who were studied more than 1 year after unilateral vestibular deafferentation, the pitch-vVOR was significantly impaired. At a head velocity of 125 degrees/s, the pitch-vVOR gains were: upward 0.67 +/- 0.11, downward 0.63 +/- 0.07. At a head velocity of 200 degrees/s, the pitch-vVOR gains were: upward 0.67 +/- 0.07, downward 0.58 +/- 0.06. There was no significant up-down asymmetry. The pitch-vVOR gain in unilateral vestibular deafferented subjects was significantly lower (P < 0.05) than the pitch-vVOR gain in normal subjects at the same head velocities. These results show that total, permanent unilateral loss of vestibular function produces a permanent symmetrical 30% (approximately) decrease in pitch-vVOR gain. This pitch-vVOR deficit is still present more than 1 year after deafferentation despite retinal slip velocities greater than 30 degrees/s in response to head accelerations in the physiological range, indicating that compensation of pitch-vVOR function following unilateral vestibular deafferentation remains incomplete.
Aw
S T
ST
Neurology Department, Royal Prince Alfred Hospital, Camperdown, Sydney, NSW, Australia.
Halmagyi
G M
GM
Curthoys
I S
IS
Todd
M J
MJ
Yavor
R A
RA
D000328:Adult; D000344:Afferent Pathways / Q000502:physiology; D000368:Aged; D016477:Artifacts; D005133:Eye Movements; D006257:Head; D006801:Humans; D008575:Meniere Disease / Q000601:surgery; D008875:Middle Aged; D009068:Movement; D009464:Neuroma, Acoustic / Q000601:surgery; D012016:Reference Values; D012027:Reflex, Vestibulo-Ocular; D013997:Time Factors; D014722:Vestibule, Labyrinth / Q000294:innervation*; D000159:Vestibulocochlear Nerve / Q000502:physiology / Q000601:surgery*