Normal subjects standing on an earth-fixed force platform inside a movable room displaced at velocities comparable to those accompanying spontaneous body sway, exhibit a visually evoked postural response (VEPR) some 600 ms after the start of the room movement. It consists of a displacement of the centre of force of the body in the direction of the stimulus (primary component), followed shortly by a corrective displacement in the opposite (secondary component). On second presentation of the stimulus VEPR is markedly reduced, but only if full proprioceptive information from the lower limbs is available to the subjects. A patient deprived of this information showed much enhanced VEPR which he was unable to suppress, in contrast to a patient with absent vestibular function who presented normal VEPR. The results show that in the presence of conflict between different sensory clues, vision is initially dominant in sway control, although adaptive processes can quickly rearrange this hierarchy.

Eight patients with absent vestibular function categorized into four grades according to the disability they suffered from oscillopsia have been studied with a view to correlating its severity with the development of gaze stabilizing compensatory mechanisms. Eye movements were recorded while the following sinusoidal rotational stimuli were delivered: 1) trunk on head oscillation in the dark (COR); 2) head on trunk oscillation in the dark; 3) head on trunk and whole body (head and trunk) oscillation in the light in the presence of optic fixation. The COR was potentiated in all the patients regardless of their clinical status. Velocity gains (peak slow phase eye velocity/peak head velocity) during whole body rotation were significantly lower than head on trunk gains in the light in the better compensated patients. Since in the absence of vestibular function whole body rotation involves only the otokinetic system (OKN), this finding implies a depression of the OKN in these patients which can be corrected during head on trunk movements by virtue of a dynamic input from the neck. The results suggest that the processes of recovery from oscillopsia are dependent, in the main, upon the development of central mechanisms by means of which undesirable image movement across the retina is perceptually suppressed. Depression of OKN may be secondary to this perceptual rearrangement.

No abstract