[Vestibular neuronitis. Vestibular paralysis with special characteristics].
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Adult↗
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Response of vestibular neurons to head rotations in vertical planes. III. Response of vestibulocollic neurons to vestibular and neck stimulation.
1. To compare the properties of the vestibulocollic reflex (VCR) with those of vestibular neurons projecting to the neck [vestibulocollic (VC) neurons], we have studied the behavior of the latter in the decerebrate cat. Neurons were identified by their antidromic responses to stimulation in C1-C2, but not C5. Responses to stimulation of vestibular and neck receptors were produced by rotation of the body and head in vertical planes. 2. We determined the plane of whole body (vestibular) or body with head counter-rotated (neck) rotation, which produced the maximal modulation of each neuron (response vector orientation). Neuron dynamics were then studied with sinusoidal (0.02-2 Hz) stimuli aligned with this orientation. 3. On the basis of dynamics and vector orientation, the neuron was assigned a vestibular input classification of otolith, vertical canal, otolith + canal, or spatial-temporal convergence (STC). 4. The properties of this sample of VC neurons are similar to those of a larger population of vestibular neurons whose projection was not identified. For example, the distributions of cells with different types of vestibular inputs were roughly the same; in particular, few cells showed STC responses. In addition, there was no evidence of significant convergence of like canals across the midline (e.g., right anterior + left anterior). 5. Also similar to the larger unidentified population, 80% of VC neurons tested for neck input received such an input. The neck and vestibular responses tended to be antagonistic; the vector orientations were usually opposite, and the response gains and phases similar.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Behavior of primate vestibulo-ocular reflex neurons and vestibular neurons during head-free gaze shifts.
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Abducens Nerve↗
Prolonged dysequilibrium in three cases with vestibular neuronitis: efficacy of vestibular rehabilitation.
The clinical course of acute unilateral vestibular disturbance in 3 cases with vestibular neuronitis and a case with labyrinthine destruction was surveyed for a long-term period. Vestibular training with a modified Cawthorne-Cooksey's exercise was done in 2 of 3 cases with vestibular neuronitis and a case of labyrinthine destruction. All had no severe troubles in activities of their daily lives over one year after the onset of the disease, but the central compensation was not completed, even in a young patient, in a case of labyrinthine destruction and in a well trained case. Spontaneous nystagmus to the affected side and increase of body sway with eyes closed were revealed by examinations in all cases. Physical exercise was found to be effective for relief from vestibular ataxia, but it was difficult to keep the effect even after training.
Adult↗
Vestibular neuronal function during ischemia. Response of vestibular neurons to vertebral and carotid artery occlusion in rabbits.
The relation between ischemia experimentally produced by occlusion of arteries injecting to the brain and the changes in vestibular excitability was examined in 102 rabbit vestibular neurons responding to sinusoidal rotation. During occlusion of ipsilateral and/or contralateral vertebral and common carotid arteries, the neuronal activity took on three different patterns with respect to the frequency of neuronal discharge. The incidence of alteration of neuronal activities reflected vestibular excitability dependent on hemodynamic changes due to occlusion of the ipsilateral vertebral artery rather than due to occlusion of the contralateral artery. Occlusion of common carotid arteries caused no significant difference between the right and left vessels in the resultant change of the neuronal activity, and differed little, either, from occlusion of vertebral arteries in the incidence of the changes. A supplementary experiment, in which the four arteries were only partially occluded, clearly showed that the resultant changes in neuronal activity reflect the role of Willis' circle in the maintenance of blood flow to vestibular nuclei.
Animals↗
Vestibular neuronitis. Proceedings of an international symposium on vestibular ganglia and vestibular neuronitis. Yamaguchi, Japan, 14-16 September, 1991.
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Animals↗
Postsynaptic inhibition underlying spike suppression of secondary vestibular neurons during quick phases of vestibular nystagmus.
Synaptic mechanisms of spike suppression of vestibular neurons during quick phases of vestibular nystagmus were investigated by intracellular recording in the rostrolateral part of the cat medial vestibular nucleus. When repetitive spike discharges of vestibular neurons were abruptly suppressed at the quick phase, the membrane potential shifted steeply in the hyperpolarizing direction. After the commissural IPSP was inverted into depolarization by intracellular injection of Cl-ions, the hyperpolarizing deflection of the membrane potential at the quick phase was also inverted into a depolarizing potential. The results indicate that an abrupt generation of IPSPs in vestibular neurons underlies the quick phase suppression of spike activity in these neurons.
Abducens Nerve↗
Bilateral vestibular neuronitis.
Bilateral vestibular neuronitis with a different onset time for each affected side was reported in two cases among 74 cases observed. The first case appeared 3 weeks and the other 5 years before involvement of the second ear. In the case with a short period before the second attack, the direction of nystagmus was unchanged throughout the clinical course. It is suggested that the direction of nystagmus depends upon the severity of each vestibular dysfunction. In the case with a long period when the vestibular compensation has been completed, paralytic nystagmus was observed and its direction corresponded with the side affected by canal.
Adolescent↗
Properties of utricular-activated vestibular neurons that project to the contralateral vestibular nuclei in the cat.
The properties of utricular (UT)-activated vestibular neurons that send axons to the contralateral vestibular nuclei (commissural neurons) were investigated intracellularly or extracellularly in decerebrate cats. A total of 27 vestibular neurons were orthodromically activated by stimulation of UT nerves and antidromically activated by stimulation of the contralateral vestibular nuclei. All neurons tested were classified as vestibulospinal (VS), vestibulooculospinal (VOS), vestibuloocular (VO), and unidentified vestibular neurons (V) after antidromic stimulation of the spinal cord and oculomotor/trochlear nuclei. Most UT-activated commissural neurons (20/27) received monosynaptic inputs. Twelve of 27 commissural neurons were located in the medial vestibular nucleus, 5 were in the lateral vestibular nucleus, 10 were in the descending vestibular nucleus, and no commissural neurons were recorded in the superior vestibular nucleus. Seven of 27 neurons were commissural VS neurons, 9 of 27 were commissural VOS neurons, and 11 of 27 were commissural V neurons. No commissural VO neurons were found. All VOS neurons and 3 VS neurons issued descending axons via the medial vestibulospinal tract. We also studied convergent inputs from the posterior semicircular canal (PC) nerve onto UT-activated commissural neurons. Five of 27 UT-activated commissural neurons received converging inputs from the PC nerves.
Animals↗
Modification of the pacemaker activity of vestibular neurons in brainstem slices during vestibular compensation in the guinea pig.
In the guinea pig, unilateral labyrinthectomy causes an immediate and severe depression of the spontaneous activity of the ipsilateral central vestibular neurons, which subsequently recovers completely within one week. A possible underlying mechanism could be an increase in the endogenous activity of the neurons deprived of their labyrinthine input. Here, we addressed this hypothesis. The endogenous activity of the neurons was assessed by their spontaneous activity recorded extracellularly in brainstem slices in the presence of a cocktail of neurotransmitter blockers (CNQX, D-APV, bicuculline and strychnine) which freed them from their main synaptic influences. The left medial vestibular nucleus (MVN) was explored in a very systematic way and strict methodological precautions were taken in order to validate comparisons between the numbers of spontaneously active neurons recorded in the MVN of distinct slices. In the presence of neurotransmitter antagonists, the mean number of spontaneously active neurons detected in a single MVN increased dramatically from 9.5 in slices from control guinea pigs to 26.3 in slices from animals labyrinthectomized on the left side one week beforehand. The mean firing rate of the recorded neurons also increased from 7.5 +/- 5.6 spikes/s in slices from control animals to 12.3 +/- 7.6 spikes/s in slices from guinea pigs labyrinthectomized one week beforehand. These results show that deprivation of the vestibular neurons of their labyrinthine input caused a change in the deprived neurons themselves. They suggest that an increase in pacemaker activity might be a factor responsible for the restoration of spontaneous activity in the vestibular neurons after labyrinthectomy.
2-Amino-5-phosphonovalerate↗
Convergence pattern of uncrossed excitatory and inhibitory semicircular canal-specific inputs onto second-order vestibular neurons of frogs. Organization of vestibular side loops.
Second-order vestibular neurons of frogs receive converging monosynaptic excitatory and disynaptic excitatory and inhibitory inputs following electrical pulse stimulation of an individual semicircular canal nerve on the ipsilateral side. Here we revealed, in the in vitro frog brain, disynaptic inhibitory postsynaptic potentials (IPSPs) by bath application of antagonists specific for glycine or gamma-aminobutyric acid-A (GABA(A)) receptors. Differences in the response parameters between disynaptic IPSPs and excitatory postsynaptic potentials (EPSPs) suggested that disynaptic IPSPs originated from a more homogeneous subpopulation of thicker vestibular nerve afferent fibers than mono- or disynaptic EPSPs. To investigate a possible size-related organization of these canal-specific, parallel pathways, we combined long-lasting anodal currents of variable intensities with strong cathodal test pulses, to block pulse-evoked responses reversibly in a graded manner according to the size-related sensitivity of vestibular nerve afferent fibers. The anodal current intensity required to block a particular response component was about 15 times lower than the strength of the cathodal test pulse that activated this response component. These large threshold differences were exploited for a selective anodal suppression of the responses from thick vestibular nerve afferent fibers. In fact, response components known to originate exclusively from thick-caliber afferent fibers such as the electrically transmitted monosynaptic EPSP component exhibited the lowest thresholds for cathodal test pulses and were the first to disappear in the presence of small anodal polarization steps. Thresholds for the activation/inactivation of responses and current intensities required for response saturation/blockade were used to assess the fiber spectrum that evoked the different response components. Mono- and disynaptic EPSPs appeared to originate from a broad spectrum of thick and thin vestibular nerve afferent fibers. The spectrum of afferent fibers that activated disynaptic IPSPs on the other hand was more homogeneous and consisted of thick and intermediate fibers. Such a canal-specific and fiber type-related organization of converging inputs of second-order vestibular neurons via feedforward projections was shown for the first time by this study in frogs, but might also prevail in mammals. Similar differences in these feedforward pathways have been proposed earlier in a vestibular side-loop model. Our results are consistent with the basic assumptions of this model and relate to the processing and tuning of dynamic vestibular signals.
Animals↗
Functional connections of tonic and kinetic vestibular neurons with primary vestibular afferents.
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Acceleration↗
Effects of viewing distance on the responses of vestibular neurons to combined angular and linear vestibular stimulation.
Effects of viewing distance on the responses of vestibular neurons to combined angular and linear vestibular stimulation. The firing behavior of 59 horizontal canal-related secondary vestibular neurons was studied in alert squirrel monkeys during the combined angular and linear vestibuloocular reflex (CVOR). The CVOR was evoked by positioning the animal's head 20 cm in front of, or behind, the axis of rotation during whole body rotation (0.7, 1.9, and 4.0 Hz). The effect of viewing distance was studied by having the monkeys fixate small targets that were either near (10 cm) or far (1.3-1.7 m) from the eyes. Most units (50/59) were sensitive to eye movements and were monosynaptically activated after electrical stimulation of the vestibular nerve (51/56 tested). The responses of eye movement-related units were significantly affected by viewing distance. The viewing distance-related change in response gain of many eye-head-velocity and burst-position units was comparable with the change in eye movement gain. On the other hand, position-vestibular-pause units were approximately half as sensitive to changes in viewing distance as were eye movements. The sensitivity of units to the linear vestibuloocular reflex (LVOR) was estimated by subtraction of angular vestibuloocular reflex (AVOR)-related responses recorded with the head in the center of the axis of rotation from CVOR responses. During far target viewing, unit sensitivity to linear translation was small, but during near target viewing the firing rate of many units was strongly modulated. The LVOR responses and viewing distance-related LVOR responses of most units were nearly in phase with linear head velocity. The signals generated by secondary vestibular units during voluntary cancellation of the AVOR and CVOR were comparable. However, unit sensitivity to linear translation and angular rotation were not well correlated either during far or near target viewing. Unit LVOR responses were also not well correlated with their sensitivity to smooth pursuit eye movements or their sensitivity to viewing distance during the AVOR. On the other hand there was a significant correlation between static eye position sensitivity and sensitivity to viewing distance. We conclude that secondary horizontal canal-related vestibuloocular pathways are an important part of the premotor neural substrate that produces the LVOR. The otolith sensory signals that appear on these pathways have been spatially and temporally transformed to match the angular eye movement commands required to stabilize images at different distances. We suggest that this transformation may be performed by the circuits related to temporal integration of the LVOR.
Animals↗
Canal and otolith inputs to single vestibular neurons in cats.
Convergence of both afferents from the PC and saccular macula, and those from the PC and utricular macula on single vestibular neurons was noted by use of intercellular recording from vestibular neurons. Vestibular neurons were classified VO neurons (vestibulo-ocular proper neurons), VOS (Vestibulo-oculo-spinal neurons sending axon collaterals both to the extraocular motoneuron pools and to the spinal cord), VS neurons (vestibulospinal proper neurons) and V neurons (vestibular neurons without axons to the oculomotor nuclei or the spinal cord) on the basis of whether or not they responded antidromically to stimulation of the oculomotor nuclei and the spinal cord. Of the total 143 vestibular neurons recorded in the series of experiments on convergence of the PC and saccular afferents, 47 neurons (33%) were received inputs from both the PC and saccular nerves. Twenty-six of the 47 convergent neurons were identified as having the nature of VS neurons. Half (13/26) of those were activated monosynaptically from both the PC and saccular nerves. Only one saccular-activated neuron without PC inputs sent an axon to the oculomotor nuclei. In the other series of experiments on the convergence of the PC and utricular afferents, 41 (37%) of 111 vestibular neurons were proved to converge on inputs from both nerves. The majority (35/41) of the neurons received monosynaptic inputs from the PC nerve and polysynaptic EPSP-IPSP sequences from the utricular nerve, or vice versa. The ratio of PC-otolith convergent neurons among utricular-activated neurons (41/54, 76%) was higher than that among saccular activated neurons (47/88, 53%). The percentage of utricular alone neurons without PC inputs (13/111, 12%) was less than that of the saccular alone without PC inputs (41/145, 28%). In conclusion, the convergence of canal and otolith inputs likely contribute mainly to vestibulospinal reflexes including the vestibulocollic reflex, by sending inputs to the neck and other muscles during head inclination which creates the combined stimuli of angular and linear acceleration.
Animals↗
Cerebellar control of vestibular neurons of the frog.
Intra- and extracellular potentials were recorded from vestibular neurons of the frog following stimulation of the ipsilateral cerebellar cortex (auricular lobe). Single neurons were identified as vestibular neurons by their location within the borders of the vestibular nuclei and by their activation via stimulation of the anterior branch of the VIIIth nerve. 2. Stimulation of the cerebellar auricular lobe provoked in some vestibular neurons apparently pure IPSPs with latencies as short as 1.5 msec suggesting a monosynaptic linkage between Purkinje cells and vestibular neuron. Vestibular-evoked responses were inhibited by cerebellar conditioning stimuli for as long as 50 msec. 3. Cerebellar stimulation also elicited an EPSP-IPSP sequence or occasionally pure EPSPs in vestibular neurons. These EPSPs were probably generated by axon reflex activation via the excitation of axons of primary and secondary vestibular neurons terminating in the cerebellum since they persisted after chronic VIIIth nerve section. Some vestibular evoked resonses were facilitated by cerebellar stimuli for 40-50 msec. 4. Occasionally an inhibitory effect was also induced in vestibular neurons by paired ipsilateral VIIIth nerve stimulation; it's latency of onset and time course suggested that a vestibulo-cerebello-vestibular loop was mainly responsible for the inhibition.
Animals↗
Uncrossed disynaptic inhibition of second-order vestibular neurons and its interaction with monosynaptic excitation from vestibular nerve afferent fibers in the frog.
1. Eighth nerve evoked responses in central vestibular neurons (n = 146) were studied in the isolated brain stem of frogs. Ninety percent of these neurons responded with a monosynaptic excitatory postsynaptic potential (EPSP) after electrical stimulation of the ipsilateral VIIIth nerve. In 5% of these neurons, the EPSP was truncated by a disynaptic inhibitory postsynaptic potential (IPSP), and in 5% of these neurons a pure disynaptic IPSP was evoked. 2. Disynaptic IPSPs superimposed upon apparently pure EPSPs were revealed by bath application of the glycine receptor antagonist strychnine (0.5-5 microM) or of the gamma-aminobutyric acid-A (GABAA) receptor antagonist bicuculline (0.5-2 microM). The evoked EPSP increased in most central vestibular neurons (strychnine: 15 out of 16 neurons; bicuculline 26 out of 29 neurons). At higher stimulus intensities, the evoked spike discharge increased from 2 to 3 spikes before up to 8-10 spikes per electrical pulse during the application of blocking agents. The unmasked disynaptic inhibitory component increased with stimulus intensity to a different extent in different neurons. 3. Lesion studies demonstrated that these inhibitory components were generated ipsilaterally with respect to the recording side. The disynaptic strychnine-sensitive inhibition was mediated by neurons located either in the ventral vestibular nuclear complex (VNC) or in the adjacent reticular formation. The spatial distribution of the disynaptic inhibition was investigated by simultaneous recordings of VIIIth nerve-evoked field potentials at different rostrocaudal locations of the VNC. A significant strychnine-sensitive component was detected in the middle and caudal parts but not in the rostral part of the VNC. A bicuculline-sensitive component was detected in the rostral and in the caudal parts but not in the middle part of the VNC. In view of a similar rostrocaudal distribution of glycineor GABA-immunoreactive neurons in the VNC of frogs, our results suggest that part of the disynaptic inhibition is mediated by local interneurons with a spatially restricted projection area. 4. The monosynaptic EPSP of second-order vestibular neurons was mediated in part by N-methyl-D-aspartate (NMDA) and in part by non-NMDA receptors. The relative contribution of the NMDA receptor-mediated component of the EPSP decreased with stronger stimuli. This negative correlation could have resulted from a preferential activation of NMDA receptors via thick vestibular nerve afferent fibers. Alternatively, the activation of NMDA receptors became disfacilitated at higher stimulus intensities due to the recruitment of disynaptic inhibitory inputs. Comparison of data obtained in the presence and in the absence of these glycine and GABAA receptor blockers indicates a preferential activation of NMDA receptors via larger-diameter vestibular nerve afferent fibers. 5. The kinetics of NMDA receptors (delay, rise time) activated by afferent nerve inputs were relatively fast. These fast kinetics were independent of superimposed IPSPs. The association of these receptors with large-diameter vestibular nerve afferent fibers suggests that fast NMDA receptor kinetics might be matched to the more phasic response dynamics of the large diameter vestibular afferent neurons to natural head accelerations.
Afferent Pathways↗
Excitatory and inhibitory inputs from saccular afferents to single vestibular neurons in the cat.
Connections from saccular afferents to vestibular neurons were studied by means of intracellular recordings of excitatory (E) and inhibitory (I) postsynaptic potentials (PSPs) in vestibular neurons after focal stimulation of the saccular macula in decerebrated cats. Focal stimulation was given to the saccular macula in two ways, in which the polarity of stimulus current via a pair of electrodes was changed. In group A, one of the electrodes was inserted into the ventral and the other into the dorsal edge of the saccular macula. The focal stimulation was across the striola so that the reversal of morphological polarization in hair cells was bridged by the pulse stimulus. In 22/36 vestibular neurons tested, the stimulation of the saccular macula evoked monosynaptic (</=1.2 ms) EPSPs, including EPSP-IPSP sequences, with one polarity of stimulation, and disynaptic (>/=1.5 ms) IPSPs when the polarity of the stimulus current was changed. In 14/36 neurons, the response pattern was the same regardless of the stimulus polarity; EPSPs (12/36) or IPSPs (2/36). In group B, a pair of electrodes was inserted into the dorsal edge of the saccular macula, so that the striola was not bridged by the current stimulus. In all of the vestibular neurons tested, the response pattern was always the same regardless of the polarity: mono- (22/31) and disynaptic (3/31) EPSPs or disynaptic IPSPs (6/31). In addition, the saccular nerve was stimulated after removing the macula in some cats (group C). The stimulation of the saccular nerve evoked EPSPs in 62 vestibular neurons (including EPSP-IPSP sequences in 31 neurons) and IPSPs in 19 vestibular neurons. Convergence between the saccular nerve and other vestibular nerves was studied by the intracellular recording of PSPs. Fifty-six percent (18/32) of the saccular-activated neurons had excitatory and/or inhibitory potentials evoked after stimulation of the utricular nerve and the horizontal and anterior semicircular canal nerves, and 44% (19/43) of the neurons received inputs from the posterior semicircular canal nerve. The results support the hypothesis that saccular afferents from one population of hair cells activate vestibular neurons monosynaptically and that afferents from another population of hair cells located on the opposite side of the striola appear to project to the same vestibular neurons disynaptically via inhibitory interneurons. Neural circuits from saccular afferents to vestibular neurons, which we term cross-striolar inhibition, thus may provide a mechanism for increasing the sensitivity to vertical linear acceleration. The circuit described is provided not only with high sensitivity but also with input noise-resistant characteristics.
Afferent Pathways↗
Firing behavior of brain stem neurons during voluntary cancellation of the horizontal vestibuloocular reflex. I. Secondary vestibular neurons.
1. The single-unit activity of vestibular neurons was recorded in alert squirrel monkeys. The monkeys had been trained to track a small visual target by generating smooth pursuit eye movements and to cancel their vestibuloocular reflex (VOR) by fixating a head stationary target. The monkeys were seated on a vestibular turntable, and their heads were held in the plane of the horizontal semicircular canals. The responses of 45 type I vestibular neurons whose activity was related to ipsilateral horizontal head movements were recorded. In 19 of 30 cells tested, electrical stimulation (0.1-ms monophasic pulses, < or = 800 microA) of the ipsilateral vestibular nerve evoked a spike at a monosynaptic latency (0.7-1.3 ms). 2. The spiking behavior of each cell was recorded during several behavioral paradigms: 1) spontaneous eye movements, 2) horizontal smooth pursuit of a target that was moved sinusoidally +/- 20 degrees/s at 0.5 Hz, 3) horizontal VOR during 0.5-Hz sinusoidal turntable rotations +/- 40 degrees/s (VORs), and 4) voluntary cancellation of the sinusoidal VOR by fixation of a head-stationary target during 0.5-Hz sinusoidal turntable rotation at +/- 40 degrees/s in the light (VORCs). 3. The response of most (34) of the units was recorded during unpredictable 100-ms steps in head acceleration (400 degrees/s2) that were generated while the monkey was fixating a target light. The acceleration steps were generated either when the monkey was stationary (VORt paradigm) or when the turntable was already rotating, and the monkey was canceling its VOR (VORCt paradigm). Smaller eye movements were evoked when the acceleration step was generated during VOR cancellation. 4. Type I vestibular units were grouped into two classes on the basis of the relationship of their firing rate to eye movements. The discharge rate of 20 "pure vestibular" units was not clearly related to eye movements. The remaining 25 units were classified as position-vestibular-pause (PVP) neurons. PVP neurons increased their firing rate during contralateral eye movements and during ipsilateral turntable rotations, and paused during saccadic eye movements. 5. Most (17/20) pure vestibular neurons generated the same response to vestibular stimuli when the monkeys canceled their VOR as they did during the VOR in both the sinusoidal and acceleration step paradigms. 6. The head velocity sensitivity of most (19/24) PVP neurons was reduced by 20-60% during VORCs, compared with their response during the VORs. The PVP neurons whose sensitivity of head movements was reduced during VORCs also exhibited a reduced vestibular sensitivity during VORCt.(ABSTRACT TRUNCATED AT 400 WORDS)
Afferent Pathways↗