Vestibular catch-up saccades augmenting the human transient heave linear vestibulo-ocular reflex.

Abstract

Vestibular catch-up saccades (VCUS) cued by the semicircular canals can supplement the deficient angular vestibulo-ocular reflex during transient rotations to stabilize gaze in people with unilateral vestibular deafferentation (Tian et al. 2000). However, a possible analogous role for VCUS to augment a deficient linear vestibulo-ocular reflex (LVOR) has not been carefully studied. We investigated VCUS in 9 younger, 8 older normal, and 12 vestibulopathic subjects undergoing directionally random heave (interaural) translations at 0.5 g peak acceleration. Eye and head movements were sampled at 1200 Hz using magnetic search coils and a cranial accelerometer. Subjects fixated visible targets 200, 50, or 15 cm distant immediately before unpredictable onset of translation in either darkness or light. Evoked slow phase eye rotations opposite to the direction of head translation accounted for only 19-70% of ideal eye position, being less for nearer targets, and VCUS commonly occurred to augment the deficiency. Eye position error relative to geometric ideal was highly correlated to VCUS amplitude ( P<0.001). This error was systematically corrected by VCUS whose latency decreased, and speed and frequency increased, with decreasing target distance. When targets remained visible, nearly all subjects made VCUS for nearer targets. In darkness, VCUS for the nearest target were significantly less common for older normal and vestibulopathic subjects than in younger normal subjects ( P<0.001). In older and vestibulopathic subjects, VCUS latency was significantly prolonged. We conclude that otolith-mediated VCUS calibrated to target distance assist LVOR slow phases, but the ability to generate VCUS in darkness is impaired in older normal and vestibulopathic subjects. In the presence of visual information, VCUS can be generated in older and vestibulopathic subjects, albeit at prolonged latency perhaps indicating visual augmentation of deficient vestibular input.