Relation between perception of vertical axis rotation and vestibulo-ocular reflex symmetry

Subjects seated in a vertical axis rotation chair controlled their rotational velocity by adjusting a potentiometer. Their goal was to null out pseudorandom rotational perturbations in order to remain perceptually stationary. Most subjects showed a slow linear drift of velocity (a constant acceleration) to one side when they were deprived of an earth-fixed visual reference. The amplitude and direction of this drift can be considered a measure of a static bias in the subject's perception of rotation. The presence of a perceptual bias is consistent with a small, constant imbalance of vestibular function which could be of either central or peripheral origin. Deviations from perfect vestibulocular reflex (VOR) symmetry are also assumed to be related to imbalances in either peripheral or central vestibular function. Researchers looked for correlations between perceptual bias and various measures of vestibular reflex symmetry that might suggest a common source for both reflective and perceptual imbalances. No correlations were found. Measurement errors could not account for these results since repeated tests on the same subjects of both perceptual bias and VOR symmetry were well correlated

Role of somatosensory and vestibular cues in attenuating visually induced human postural sway

The purpose was to determine the contribution of visual, vestibular, and somatosensory cues to the maintenance of stance in humans. Postural sway was induced by full field, sinusoidal visual surround rotations about an axis at the level of the ankle joints. The influences of vestibular and somatosensory cues were characterized by comparing postural sway in normal and bilateral vestibular absent subjects in conditions that provided either accurate or inaccurate somatosensory orientation information. In normal subjects, the amplitude of visually induced sway reached a saturation level as stimulus amplitude increased. The saturation amplitude decreased with increasing stimulus frequency. No saturation phenomena was observed in subjects with vestibular loss, implying that vestibular cues were responsible for the saturation phenomenon. For visually induced sways below the saturation level, the stimulus-response curves for both normal and vestibular loss subjects were nearly identical implying that (1) normal subjects were not using vestibular information to attenuate their visually induced sway, possibly because sway was below a vestibular-related threshold level, and (2) vestibular loss subjects did not utilize visual cues to a greater extent than normal subjects; that is, a fundamental change in visual system 'gain' was not used to compensate for a vestibular deficit. An unexpected finding was that the amplitude of body sway induced by visual surround motion could be almost three times greater than the amplitude of the visual stimulus in normals and vestibular loss subjects. This occurred in conditions where somatosensory cues were inaccurate and at low stimulus amplitudes. A control system model of visually induced postural sway was developed to explain this finding. For both subject groups, the amplitude of visually induced sway was smaller by a factor of about four in tests where somatosensory cues provided accurate versus inaccurate orientation information. This implied that (1) the vestibular loss subjects did not utilize somatosensory cues to a greater extent than normal subjects; that is, changes in somatosensory system 'gain' were not used to compensate for a vestibular deficit, and (2) the threshold for the use of vestibular cues in normals was apparently lower in test conditions where somatosensory cues were providing accurate orientation information