Horizontal (HOR) and vertical (VERT) vestibulo-ocular reflex (VOR) responses to whole-body triangular velocity profiles with constant accelerations of 10, 15 and 20 deg/s2 were studied in two populations: normals, and patients with acute unilateral peripheral vestibular paralysis. The effect of this type of unilateral deficit on VOR gain and long time constant were determined as well as the time course of the compensation processes for HOR and VERT VOR dynamics. In the patient population, HOR VOR gain was asymmetric post deficit, being, on average, 50% and 75% of normal for rotations toward and away from the deficit, respectively. For the VERT VOR, on average, a symmetric 66% reduction occurred. The VERT VOR time constant was marginally affected by the deficit. HOR time constants were reduced for both directions of rotation. HOR and VERT VOR gain was within normal limits 1-3 months following an acute paralysis; time constants required a longer recovery period. Our results indicate that a unilateral deficit causes a markedly different alteration for HOR VOR dynamics compared to the effect on VERT VOR.

This review describes the effect of unilateral peripheral vestibular deficit (UPVD) on balance control for stance and gait tests. Because a UPVD is normally defined based on vestibular ocular reflex (VOR) tests, we compared recovery observed in balance control with patterns of recovery in VOR function. Two general types of UPVD are considered; acute vestibular neuritis (AVN) and vestibular neurectomy. The latter was subdivided into vestibular loss after cerebellar pontine angle tumor surgery during which a vestibular neurectomy was performed, and vestibular loss following neurectomy to eliminate disabling Ménière’s disease. To measure balance control, body-worn gyroscopes, mounted near the body’s center of mass (CoM), were used. Measurement variables were the pitch (anterior–posterior) and roll (lateral) sway angles and angular velocities of the lower trunk/pelvis. Both patient groups showed balance deficits during stance tasks on foam, especially with eyes closed when stable balance control is normally highly dependent on vestibular inputs. Deficits during gait were also present and were more profound for complex gait tasks such as tandem gait than simple gait tasks. Major differences emerged between the groups concerning the severity of the deficit and its recovery. Generally, the effects of acute neuritis on balance control were more severe but recovered rapidly. Deficits due to vestibular neurectomy were less severe, but longer lasting. These results mostly paralleled recovery of deficits in VOR function. However, questions need to be raised about the effect on balance control of the two modes of neural plasticity occurring in the vestibular system following vestibular loss due to neuritis: one mode being the limited central compensation for the loss, and the second mode being some restoration of peripheral vestibular function. Future work will need to correlate deficits in balance control during stance and gait more exactly with VOR deficits and carefully consider the differences between insufficient central compensation compared to inadequate peripheral restoration of function.

The responses of vestibular nuclei neurons of relaxed unanaesthetized goldfish have been examined with trapezoid velocity stimuli under three conditions. Responses to horizontal body rotation in the dark (pure vestibular stimulation) resemble those observed in vestibular nerve afferents. Optokinetic responses to exclusive visual surround-motion are also direction-specific and, in contrast to vestibular responses, exhibit a tonic response to constant velocity. They show three different response profiles, classified A,B or C, based on the neuron's discharge rate: either increasing, decreasing or remaining constant once surround motion is maintained at constant velocity. Following these dynamic effects, optokinetic responses have a maintained modulation of resting discharge until deceleration commences. The time constants associated with the dynamic effects vary between 1 and 11 seconds. Steady-state modulation of optokinetic responses shows a weak relation to stimulus velocities exceeding 10 deg/sec. Responses to body rotation in the light were found to linearly combine the weighted vestibular and optokinetic responses so that accurate velocity information is available for sensory and motor functions independent of the neuron's vestibular (I,II) or optokinetic (A,B,C) response type. The principle of this visual-vestibular interaction is discussed with respect to multisensory processing within the vestibular nuclei.

The influence of vestibular and visual (optokinetic) stimuli on the nystagmus slow phase velocity (SPV) in man was studied using different combinations of visual horizon and/or passive body rotations (velocity trapezoids). The interactions of combined stimulation were evaluated in comparison to pure optokinetic and pure vestibular reactions. The results indicate that retinal image stabilization and vestibular systems simultaneously activate ocular reflexes during passive body accelerations in the light. Results:1. Exclusive vestibular stimulation by passive body -This work was supported by the Deutsche Forschungsgemeinschaft sFB 70 r'Hirnforschung und physiologie").

The present report is based on the analysis of clinical data collected from 80 patients with cerebellopontine-angle tumors. Special reference is made to the history of the patient, the neurootologic test battery, particularly to the sensitivity and specificity of audiological and vestibular diagnostic procedures. The postoperative findings are evaluated especially with respect to postoperative morbidity and the preservation of facial nerve and auditory functions.