Effect of unilateral vestibular deafferentation on the initial human vestibulo-ocular reflex to surge translation

Abstract

Transient whole-body surge (fore-aft) translation at 0.5 G peak acceleration was administered to six subjects with unilateral vestibular deafferentation (UVD), and eight age-matched controls. Subjects viewed eccentric targets to determine if linear vestibulo-ocular reflex (LVOR) asymmetry might lateralize otolith deficits. Eye rotation was measured using magnetic search coils. Immediately before surge, subjects viewed a luminous target 50 cm away, centered or displaced 10° horizontally or vertically. The target was extinguished during randomly directed surges. LVOR gain relative to ideal velocity in subjects with UVD for the contralesional horizontally eccentric target (0.59 ± 0.08, mean ± SEM) did not differ significantly from normal (0.50 ± 0.04), but gain for the ipsilesional eccentric target (0.35 ± 0.02) was significantly less than normal (0.48 ± 0.03, P < 0.05). Normal subjects had mean gain asymmetry for horizontally eccentric targets of 0.17 ± 0.03, but asymmetry in UVD was significantly increased to 0.35 ± 0.05 (P < 0.05). Four of six subjects with UVD had maximum gain asymmetry outside normal 95% confidence limits. Asymmetry did not correlate with UVD duration. Gain for 10° vertically eccentric targets averaged 0.38 ± 0.14 for subjects with UVD, insignificantly lower than the normal value of 0.75 ± 0.15 (P > 0.05). Surge LVOR latency was symmetrical in UVD, and did not differ significantly from normal. There was no significant difference in response between dark and visible target conditions until 200 ms after surge onset. Chronic human UVD, on average, significantly impairs the surge LVOR for horizontally eccentric targets placed ipsilesionally, but this asymmetry is small relative to interindividual variation.

Temporal dynamics of semicircular canal and otolith function following acute unilateral vestibular deafferentation in humans

“…The small and symmetric magnitude of the LVOR deficit in UVD has made it difficult to lateralize otolith pathology based on test findings. Exceptions have involved the anteroposterior otolith VOR with an eccentric visual target in monkey UVD (Angelaki et al 2000) and human UVD (Tian et al 2006). However, in contrast to the modest otolith VOR deficits during pure linear acceleration, the current study found that the otolith VOR evoked by eccentric yaw rotation with near target viewing was profoundly and asymmetrically ablated during ipsilesional rotation at high acceleration.…”

“…Testing of the VOR during pure translation appears insufficiently robust to be a practical lateralizing test of otolith function (Tian et al 2006). However, high acceleration eccentric yaw rotation with a near target in the current study disclosed a profound, immediate, enduring and lateralizing deficit in the otolith VOR in UVD.…”

“…Deficits in the transient otolith VOR to pure linear acceleration following chronic UVD are usually modest (Aw et al 2003;Bronstein et al 1991;Crane et al 2005;Lempert et al 1998;Tian et al 2006) and directionally symmetrical (Aw et al 2003;Bronstein et al 1991;Crane et al 2005;Lempert et al 1998). It has been supposed that otolith VOR deficits revealed during eccentric yaw rotation with near target viewing might better lateralize otolith pathology than would the modest and directionally symmetrical effect during pure translational acceleration (Paige 2002;Seidman et al 2002;Takeda et al 1991).…”

The Anatomical and Physiological Basis of Clinical Tests of Otolith Function. A Tribute to Yoshio Uchino

“…However, these asymmetries reduce over time such that long term patients (6-10 weeks) show no consistent asymmetry to rolltilt stimuli (7). Similarly, patients 6 weeks after surgery show no asymmetry for linear lateral translations (81,107). This is in sharp contrast to the semicircular canal system where response asymmetries after unilateral loss are permanent as shown by the head impulse test (108)(109)(110).…”

“…This horizontal eye movement to lateral linear acceleration (80) has been used to try to identify the unilateral utricular loss, by analogy with the success of the horizontal eye movement to angular acceleration identifying the side of unilateral semicircular canal loss (81). A horizontal angular acceleration toward the affected ear results in a reduced horizontal compensatory eye velocity response and so permanently identifies the affected semicircular canal (82).…”