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We studied horizontal eye movements evoked by lateral whole body translation in nine patients who underwent vestibular nerve section. Preoperatively, all had preserved caloric function on both sides. Testing was performed before, 1 week and 6-10 weeks after surgery. Patients were seated upright in an electrically powered car running on a linear track. The car executed acceleration steps of 0.24 g, randomly to the left and right in the dark. The normal response consisted of a bidirectionally symmetrical nystagmus with compensatory slow phases. Response asymmetry of the slow-phase velocity of the desaccaded and averaged eye position signal was less than 13% in normals (n = 21). Before surgery, patients' responses were mostly symmetrical. Postoperatively, responses were diminished or absent with head acceleration towards the operated ear in all patients, causing a marked asymmetry which averaged 56% after correction for spontaneous nystagmus. On follow-up, responses regained symmetry. Thus, early after vestibular nerve section, a single utricle produces a normal LVOR only with ipsilateral head translation. Therefore, afferents for the LVOR seem to originate from the mid-lateral area of the macula, where hair cells are stimulated in their on-direction during ipsilateral head translation. Compensation may depend on recovery of the off-directional responses from lateral hair cells of the remaining utricle.

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Patients with Waardenburg syndrome may experience primarily vestibular symptoms without hearing loss. Electrocochleography and vestibular function tests appear to be the most sensitive measures of otologic abnormalities in such patients.

Visual symptoms emerging after the loss of vestibular function are usually attributed to the dysfunction of semicircular canal vestibulo-ocular reflexes, as they have been shown to stabilize vision during angular head movements. However, natural head displacements involve both angular and linear motion, and therefore visual instability may occur because of defective otolith-ocular reflexes (OORs) which are the eye movements evoked by linear head acceleration. In this paper, the relationship between OORs and visual acuity during linear head motion was studied in normal subjects and 14 patients with bilateral loss of caloric responses. OORs were elicited in darkness by step acceleration (0.24 g) of the whole body along the interaural axis. Latency, slow phase velocity and asymmetry of the OOR were measured from the desaccaded and averaged electrooculographic trace. Visual acuity was assessed during sinusoidal lateral oscillation of the subject viewing an earth-fixed target, and vice versa with the subject stationary and the target moving at 0.5, 1.0 and 1.5 Hz. The task was to recognize numbers flashing up on a three digit light-emitting diode visual display. Normal subjects had symmetrical OORs with short latencies (< 130 ms). In patients, OORs were either absent (n = 2) or abnormal with asymmetries (n = 8), diminished velocities (n = 4) or prolonged latencies (n = 6). At high frequency oscillation (1.5 Hz), normal subjects invariably recognized more numbers during self-motion compared with target motion, whereas most patients did not. In patients, abnormal dynamic visual acuity was correlated with absent or delayed OOR responses. This is the first demonstration of a functional role of the OORs in that they contribute to visual stabilization during high frequency linear head motion. Bilateral vestibular failure commonly affects the OORs and thereby compromises dynamic visual acuity.

Eye movement responses were obtained from six normal subjects exposed to randomly ordered rightwards/leftwards linear acceleration steps of 0.05 g, 0.1 g or 0.24 g amplitude and 650 ms duration along the interaural axis. With the instruction to gaze passively into the darkness, compensatory nystagmus was evoked with slow-phase velocity sensitivity of 49 degrees s(-1) g(-1). When subjects viewed earth-fixed targets at 30 cm, 60 cm or 280 cm, eye movements at 130 ms from motion onset were proportional to acceleration and inversely proportional to target distance, before the onset of visually guided eye movements. Our results show that a modulation with viewing distances of the earliest human otolith-ocular reflexes occurs in the presence of pure linear acceleration. However, full compensation was not attained for the nearer targets and higher accelerations.

The possibility of synergistic interaction between the canal and otolith components of the horizontal vestibulo-ocular reflex (VOR) was evaluated in human subjects by subtracting the response to pure angular rotation (AVOR) from the response to combined angular and translational motion (ALVOR) and comparing this difference with the VOR to isolated linear motion (LVOR). Assessments were made with target fixation at 60 cm and in darkness. Linear stimuli were acceleration steps attaining 0.25 g in less than 80 ms. To elicit responses to combined translational and angular head movements, the subjects were seated on a Barany chair with the head displaced forwards 40 cm from the axis of rotation. The chair was accelerated at approximately 300 deg/s2 to 127 deg/s peak angular velocity, the tangential acceleration of the head being comparable with that of isolated translation. Estimates of the contribution of smooth pursuit to responses in the light were made from comparisons of isolated pursuit of similar target trajectories. In the dark the slow phase eye movements evoked by combined canal-otolith stimuli were higher in magnitude by approximately a third than the sum of those produced by translation and rotation alone. In the light, the relative target displacement during isolated linear motion was similar to the difference in relative target displacements during eccentric and centred rotation. However, the gain of the translational component of compensatory eye movement during combined translational and angular motion was approximately unity, in contrast to the gain of the response to isolated linear motion, which was approximately a half. Pursuit performance was always poorer than target following during self-motion. The LVOR responses in the light were greater than the sum of the LVOR responses in the dark with pursuit eye movements. We conclude that, in response to transient motion, there is a synergistic enhancement of the translational VOR with concurrent canal stimulation and that the enhancement of the LVOR in the light is not due solely to pursuit.

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