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1The aim of this study was to determine how context and on‐line sensory information are combined to control posture in seated subjects submitted to high‐jerk, passive linear accelerations. Subjects were seated with eyes closed on a servo‐controlled linear sled. They were asked to relax and received brief accelerations either sideways or in the fore‐aft direction. The stimuli had an abrupt onset, comparable to the jerk experienced during a minor car collision.2Rotation and translation of the head and body were measured using an Optotrak system. In some of the subjects, surface electromyographic (EMG) responses of selected neck and/or back muscles were recorded simultaneously. For each subject, responses were highly stereotyped from the first trial, and showed little sign of habituation or sensitisation.3Comparable results were obtained with sideways and fore‐aft accelerations. During each impulse, the head lagged behind the trunk for several tens of milliseconds. The subjects' head movement responses were distributed as a continuum in between two extreme categories. The ‘stiff’ subjects showed little rotation or translation of the head relative to the trunk for the whole duration of the impulse. In contrast, the ‘floppy’ subjects showed a large roll or pitch of the head relative to the trunk in the direction opposite to the sled movement. This response appeared as an exaggerated ‘inertial’ response to the impulse.4Surface EMG recordings showed that most of the stiff subjects were not contracting their superficial neck or back muscles. We think they relied on bilateral contractions of their deep, axial musculature to keep the head‐neck ensemble in line with the trunk during the movement.5About half of the floppy subjects displayed reflex activation of the neck muscles on the side opposite to the direction of acceleration, which occurred before or during the head movement and tended to exaggerate it. The other floppy subjects seemed to rely on only the passive biomechanical properties of their head‐neck ensemble to compensate for the perturbation.6In our study, proprioception was the sole source of sensory information as long as the head did not move. We therefore presume that the EMG responses and head movements we observed were mainly triggered by the activation of stretch receptors in the hips, trunk and/or neck.7The visualisation of an imaginary reference in space during sideways impulses significantly reduced the head roll exhibited by floppy subjects. This suggests that the adoption by the central nervous system of an extrinsic, ‘allocentric’ frame of reference instead of an intrinsic, ‘egocentric’ one may be instrumental for the selection of the stiff strategy.8The response of floppy subjects appeared to be maladaptive and likely to increase the risk of whiplash injury during motor vehicle accidents. Evolution of postural control may not have taken into account the implications of passive, high‐acceleration perturbations affecting seated subjects.

We have recently shown in vivo that N-Methyl-D-Aspartate (NMDA) receptors are present in the guinea-pig vestibular complex and demonstrated that they are involved in the regulation of the resting discharge of vestibular neurones. A parallel in vitro study has identified in the guinea-pig medial vestibular nuclei (MVN) two main neuronal cell types, A and B MVNn, differing by their intrinsic membrane properties. One subtype of B MVNn was further characterized by the presence of a low threshold calcium spike (LTS). The present study investigated in vitro the responses of these different cell types to NMDA. Both A and B MVNn were depolarized by NMDA, which also induced a decrease in membrane resistance and an increase in the spontaneous firing rate. These effects could be blocked by D-AP5, a specific antagonist of NMDA receptors. Following a 10–30 mV hyperpolarization, a long-lasting oscillatory behavior could be induced in presence of NMDA. These oscillations were however restricted to the subtype of B MVNn without LTS. The NMDA-induced oscillations were tetrodotoxine-resistant, but could be eliminated by D-AP5 or by replacing sodium with choline. Functional implications of this oscillatory behavior are discussed.

This review focuses on the neurochemistry of the central vestibular pathways. The main emphasis will be on the analysis of the central vestibular nuclei neurons, since several papers published in the past 5 years have provided important information on the role that neurotransmitter-dependent conductances play in the central processing of vestibular inputs. Indeed, increasing evidence suggests that both the non-linear intrinsic membrane properties of the neurons and the nature of the different neurotransmitters and neuromodulators involved in the vestibular network contribute to the various operations required for stabilising gaze and posture. It has also been demonstrated that the neurotransmitter-dependent conductances together with the ionic voltage-dependent conductances may determine the firing patterns of the medial vestibular neurons and interfere with their integrative properties. We hope that this review will show that by combining in vitro and in vivo electrophysiological approaches and the new powerful neuropharmacological techniques developed from the recent advances of molecular biology, the vestibular system can be used as a good model to elucidate some of the basic properties of the brain including learning, neural computation, network reconfiguration and post-lesional plasticity.

1. In the guinea‐pig, a unilateral labyrinthectomy induces postural disturbances and an ocular nystagmus which abate or disappear over time. These behavioural changes are accompanied by an initial collapse and a subsequent restoration of the spontaneous activity in the neurones of the ipsilateral vestibular nuclei. Recently, it has been shown that the vestibular neuronal activity remained collapsed over at least 10 h whereas its restoration was complete 1 week after the lesion. The aims of this study were to determine when restoration of spontaneous activity in the partially deafferented vestibular neurones started and to compare the time courses of the behavioural and neuronal recoveries in guinea‐pigs that had undergone a unilateral labyrinthectomy. 2. Neuronal discharge measurements were made using chronic extracellular recording of single unit activity. After a left labyrinthectomy, electrodes, were placed on the site of the destroyed labyrinth to enable stimulation of the left vestibular nerve. Behavioural measurements included chronic recording of eye movements by the scleral search coli technique. After a left labyrinthectomy, lateral deviation of the head, twisting of the head, and eye velocity of the slow phases of the nystagmus were measured. 3. The neuronal activity of the rostral part of the vestibular nuclear complex on the lesioned side was recorded in alert guinea‐pigs over 4 h recording sessions between 12 and 72 h after the lesion. 4. The criterion used to select vestibular neurones for analysis was their recruitment by an electric shock on the vestibular nerve. In addition, in order to explore a uniform population, we focused on neurones recruited at monosynaptic latencies (0.85‐1.15 ms). 5. For each recording period, the mean resting rate was calculated animal by animal and the grand mean of these individual resting rate means was calculated. Previously, a decline in the grand mean resting rate from 35.8 +/‐ 6.0 spikes s‐1 (control state) to 7.1 +/‐ 4.2 spikes s‐1 during the first 4 h after labyrinthectomy has been shown. In the present study, the first sign of recovery was observed during the 12‐16 h recording period when the resting rate grand mean increased to 16.3 +/‐ 3.9 spikes s‐1. This grand mean activity did not change significantly during the following 12 h. Thereafter, restoration of neuronal activity improved and was complete 1 week after the lesion. 6. Although the abatement of the vestibular symptoms roughly paralleled the restoration of neuronal activity in the vestibular nuclei, some discrepancies between the time courses of both phenomena emerged. An important step in postural recovery (the animals managed to stand up) and a major part of the abatement of the nystagmus occurred before the recovery of vestibular neuronal activity. In addition, lateral deviation of the head disappeared while restoration of the neuronal activity was incomplete, but significant head twisting was still evident when vestibular resting rates had recovered completely. 7. We conclude that restoration of neuronal activity in the ipsilateral vestibular nuclei starts 12 h after the lesion and that restoration of neuronal activity in the ipsilateral vestibular nuclei is not the only mechanism underlying behavioural vestibular compensation.

1. Neuronal activity was investigated in the left superior vestibular nucleus (SVN), lateral vestibular nucleus (LVN), and rostral part of the medial vestibular nucleus (MVN) in the alert guinea pig after a unilateral (left) labyrinthectomy was performed. Vestibular neurons were recorded either immediately (just-postoperative group, n = 6) or 1 wk after labyrinthectomy (1-wk-postoperative group, n = 6) and compared with the activity recorded in intact animals (control group, n = 6). 2. Animals were prepared for extracellular recording of single-unit activity and for eye movement recording (scleral search coil technique). To enable stimulation of the left vestibular nerve, bipolar silver ball electrodes were chronically implanted either in contact with the bony labyrinth in the control group or close to the stump of the vestibular nerve after labyrinthectomy. Complete labyrinthectomy was performed under halothane anesthesia. 3. The criterion used to select vestibular neurons for analysis was their recruitment by an electric shock on the vestibular nerve. Of the 589 recorded neurons, 424, defined as second-order vestibular neurons, were recruited at monosynaptic latencies (0.85-1.15 ms) and 165 were recruited at polysynaptic latencies. One hundred three second-order vestibular neurons were recorded in the control group, 173 in the just-postoperative group, and 148 in the 1-wk-postoperative group. 4. The activity of the electrically recruited neurons was recorded during sinusoidal horizontal head rotation in the dark (0.3 Hz, 40 degrees/s peak velocity). The behavior of the neurons was analyzed by plotting their firing rate against head velocity. The Y-intercept of the regression line was used to express spontaneous firing rate (resting discharge), and its slope was used to express the sensitivity of the neuron-to-head velocity. 5. In the absence of statistically significant difference between the characteristics of the neuronal discharge of the second-order vestibular neurons recorded in the SVN, LVN, and rostral MVN, the data were pooled. The Resting discharge of these cells amounted to 41.0 +/- 24.7 (SD) spikes/s in the control state, fell to 7.2 +/- 13.9 spikes/s just after labyrinthectomy, and completely returned to normal values 1 wk after surgery (42.5 +/- 21.6 spikes/s). Among the monosynaptically recruited neurons, the percentage of silent units was 0% in the control group, 69% in the just-postoperative group, and 0% in the 1-wk-postoperative group. 6. By contrast, the sensitivity to head velocity of the second-order vestibular neurons, which was 0.69 +/- 0.48 (SD) spikes.s-1/deg.s-1 in the control state and which fell to 0.03 +/- 0.11 spikes.s-1/deg.s-1 just after labyrinthectomy, remained low 1 wk after injury (0.21 +/- 0.26 spikes.s-1/deg.s-1). Moreover, the slight recovery of sensitivity to head rotation was due only to units behaving as type II neurons. 7. The mean resting discharge of the polysynaptically recruited neurons (pooled from the 3 explored nuclei) was 31.6 +/- 19.3 spikes/s in the control group. It decreased to 11.6 +/- 12.1 spikes/s in the just-postoperative group and recovered to 39.8 +/- 20.2 spikes/s in the 1-wk-postoperative group. No neuron was silent at rest either in the control group or in the 1-wk-postoperative group. Just after labyrinthectomy, 35% of the neurons had a null resting activity. The mean sensitivity to head velocity of these neurons was 0.55 +/- 0.42 spikes.s-1/deg.s-1 in the control group. It decreased to 0.05 +/- 0.12 spikes.s-1/deg.s-1 in the just-postoperative group and recovered to 0.22 +/- 0.17 spikes.s-1/deg.s-1 in the 1-wk-postoperative group. 8. We conclude that, at least in the guinea pig, the restoration of the spontaneous activity of the deafferented neurons is complete 1 wk after a unilateral labyrinthectomy and thus probably plays an important role in vestibular compensation...

The authors treated 22 patients with intratympanic gentamicin. Vestibular function was measured using caloric and head impulse tests and vestibular evoked myogenic potentials induced by high amplitude sounds and short duration galvanic currents. Roughly one-third of the patients, after initially losing their caloric responses and displaying refixation saccades to head impulse tests, recovered within 2 years of the lesion. Vertigo did not recur in patients in whom the galvanic response was abolished.