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In acute experiments in rabbits the influence of stimulation of the ventromedial hypothalamic nucleus on the activity of neurons of vestibular Deiters' nucleus was studied under conditions of 15-day exposure to vibration (60 Hz, 0.8 mm, 3 h daily). The mechanisms are discussed which underlie the observed phenomena.
Medial vestibular nucleus neurons develop a sustained increase in electrophysiological excitability after deafferentation, which may be an important component of 'vestibular compensation' (the behavioural recovery that follows peripheral vestibular lesions). We investigated the effects of gamma-aminobutyric acid, glutamate and glycine receptor blockade on the spontaneous activity of deafferented medial vestibular nucleus neurons in slices, to determine whether changes in synaptic inputs contribute to their increased excitability. Soon after deafferentation (4 h after labyrinthectomy) synaptic blockade had no effect on the elevated in-vitro firing of medial vestibular nucleus neurons, while later (48 h, 1 week), synaptic blockade reduced the elevated activity to normal. Intrinsic mechanisms therefore appear to mediate the elevated excitability of medial vestibular nucleus cells initially after deafferentation. Subsequently, changes in the efficacy of synaptic inputs are implicated, presumably involving intranuclear projections that are preserved in slices.
Opiates increase firing of rat medial vestibular nucleus neurons. We have attempted to determine the mechanism of these excitatory opiate actions by extracellular recording of neuronal activity with ionophoretic application of opiate agonists and bath application of antagonists. The spontaneous activity of approximately 30% of medial vestibular neurons, scattered throughout the nucleus, was increased by ionophoretic application of either morphine or [D-Ala2]leucine enkephalin, implicating the presence of both mu and delta opiate receptors. The responses to both were blocked by the opiate receptor antagonist, naloxone. In only a few neurons opiates decreased firing. Most previous reports of direct opiate excitation have proven to be due to disinhibition. This is not the case here, as indicated by three observations: 1) the excitatory opiate response was sustained when gamma-aminobutyric acid (GABA) receptors were blocked by bicuculline; 2) perfusion of a solution containing 0.1 mM Ca2+ and 6.3 mM Mg2+ blocks synaptic transmission, but does not block the excitatory responses to both opiates and 3) the opiate-induced depolarization and action potential generation was evident in neurons whose spontaneous firing was almost totally depressed by adenosine. These results indicate that the excitation is neither due to disinhibition nor to a presynaptic opiate action. We conclude that medial vestibular neurons have postsynaptic opiate receptors that mediate direct neuronal excitation.
1) The responses of single units in the pretectum (Pt) and in the n. reticularis tegmenti pontis (NRTP) to constant velocity horizontal rotation (0.25--60 deg/s) of a large-field visual pattern were studied in immobilized, non-anesthetized DA-HAN rats. In addition, responses of Pt and NRTP neurons to pure vestibular stimuli (rotation in the dark) were studied. 2) Pt neurons showed seven response types to optokinetic stimulation (Table 1). The most frequent response (48%) consisted of a very rapid increase in firing to steady state on temporonasal motion stimulation of the contralateral eye; nasotemporal stimuli yielded no change in resting rate as did stimulation of the ipsilateral eye. The response maximum occurred at a retinal slip velocity of 1 deg/s. None of the Pt units tested responded to pure vestibular stimuli. 3) NRTP neurons - as Pt units - most frequently (43%) increased their discharge rate on temporonasal stimulation of the contralateral eye and maintained a constant resting rate during nasotemporal motion. Peak response amplitudes also occurred with retinal slip velocites of 1 deg/s. Contrary to the fast time-to-peak of the responses of Pt neurons NRTP units showed a slow rise in frequency of firing to peak response levels. 4) NRTP neurons responded to pure vestibular stimuli (horizontal angular acceleration in the dark). The vestibular responses were synergistic with those evoked in the same neurons by optokinetic stimuli. Thus, the most frequently encountered type of optokinetic response (s. above) showed a type II vestibular response. 5) Comp]arison of OKN and Vn optokinetic responses with those of Pt and NRTP suggests that the unidirectional-selective Pt and NRTP neurons are important links in the central optokinetic path. In addition, the NRTP may represent the site at which the retinal slip signal and the eye velocity signal converge. This convergence has been postulated in models of the system [12].
Effects of viewing distance on the responses of horizontal canal-related secondary vestibular neurons during angular head rotation. The eye movements generated by the horizontal canal-related angular vestibuloocular reflex (AVOR) depend on the distance of the image from the head and the axis of head rotation. The effects of viewing distance on the responses of 105 horizontal canal-related central vestibular neurons were examined in two squirrel monkeys that were trained to fixate small, earth-stationary targets at different distances (10 and 150 cm) from their eyes. The majority of these cells (77/105) were identified as secondary vestibular neurons by synaptic activation following electrical stimulation of the vestibular nerve. All of the viewing distance-sensitive units were also sensitive to eye movements in the absence of head movements. Some classes of eye movement-related vestibular units were more sensitive to viewing distance than others. For example, the average increase in rotational gain (discharge rate/head velocity) of position-vestibular-pause units was 20%, whereas the gain increase of eye-head-velocity units was 44%. The concomitant change in gain of the AVOR was 11%. Near viewing responses of units phase lagged the responses they generated during far target viewing by 6-25 degrees. A similar phase lag was not observed in either the near AVOR eye movements or in the firing behavior of burst-position units in the vestibular nuclei whose firing behavior was only related to eye movements. The viewing distance-related increase in the evoked eye movements and in the rotational gain of all unit classes declined progressively as stimulus frequency increased from 0.7 to 4.0 Hz. When monkeys canceled their VOR by fixating head-stationary targets, the responses recorded during near and far target viewing were comparable. However, the viewing distance-related response changes exhibited by central units were not directly attributable to the eye movement signals they generated. Subtraction of static eye position signals reduced, but did not abolish viewing distance gain changes in most units. Smooth pursuit eye velocity sensitivity and viewing distance sensitivity were not well correlated. We conclude that the central premotor pathways that mediate the AVOR also mediate viewing distance-related changes in the reflex. Because irregular vestibular nerve afferents are necessary for viewing distance-related gain changes in the AVOR, we suggest that a central estimate of viewing distance is used to parametrically modify vestibular afferent inputs to secondary vestibuloocular reflex pathways.
OBJECTIVE: To investigate the effect and distribution of cholinergic efferent vestibular neurons in normal wistar rat. METHOD: HPR retrograde tracer and Immunocytochemical techniques were used. RESULT: Results show that AchT immunoreactive neurons locate in dorsolateral and dorsomedial to genu of the facial. Few neurons scatter in the parvocellular nucleus. CONCLUSION: As a neural transmitter, acetylcholine distribute in efferent vestibular neurons and play an important role.
A follow-up study of 26 patients with vestibular neuronitis is reported. The disease is characterized by an acute attack of severe vertigo with complete loss of unilateral caloric response. The following results were obtained: 1) The average period of spontaneous nystagmus was 136 days and the standard error was 39 days. 2) No correlation could be found between age and the period of spontaneous nystagmus. 3) Six patients showed direction reversal in their spontaneous nystagmus (recovery nystagmus), and their outcome was good. 4) On the most recent caloric test, 42% of the patients had bilateral normal responses, 27% displayed partial improvement on the affected side, and no reaction was observed in 31% of patients. We suggest that three types of clinical courses may occur in vestibular neuronitis: i) complete recovery of the function of the affected vestibular nerve, ii) partial recovery of vestibular function, and iii) no recovery of the affected vestibular nerve, but central nervous system compensates for the vestibular imbalance.
1. Vestibular neurones projecting to the upper cervical grey matter (vestibulocollic neurones) were identified by localized microstimulation in the C3 segment of the cat spinal cord.2. The neurones were found in the lateral (Deiters'), medial and descending nuclei bilaterally and projected to the spinal cord in the lateral and medial vestibulospinal tracts (LVST and MVST). Ipsilateral axons of Deiters' neurones were mostly in the LVST, axons of medial and descending neurones in the MVST; a few Deiters' neurones had axons in the MVST; some descending neurones had axons in the LVST. Most axons of contralateral neurones were in the MVST.3. The axons of 62% of ipsilateral vestibulocollic Deiters' neurones not only gave off a collateral to C3, but also extended as far as the cervical enlargement (;branching'); some of these neurones projected as far as the upper thoracic cord, almost none to the lumbar cord. Ipsilateral descending nucleus neurones branch in the same fashion, but there is no branching in the relatively small medial nucleus population.4. A large majority of vestibulocollic neurones receive monosynaptic excitation from the ipsilateral labyrinth and a number are inhibited by stimulation of the contralateral labyrinth (commissural inhibition). It is possible that commissural inhibition acts on a broad population of vestibular neurones involved in the control of eye, head and trunk movement.5. Vestibulocollic neurones do not make up a homogeneous population acting only on the neck. Instead it is likely that subpopulations, for example branching and non-branching neurones, have different functions.
Potassium channels are involved in the control of neuronal excitability by fixing the membrane potential, shaping the action potential, and setting firing rates. Recently, attention has been focused on identifying the factors influencing excitability in second-order auditory and vestibular neurons. Located in the brainstem, second-order auditory and vestibular neurons are sites for convergence of inputs from first-order auditory or vestibular ganglionic cells with other sensory systems and also motor areas. Typically, second-order auditory neurons exhibit two distinct firing patterns in response to depolarization: tonic, with a repetitive firing of action potentials, and phasic, characterized by only one or a few action potentials. In contrast, all mature vestibular second-order neurons fire tonically on depolarization. Already, certain fundamental roles have emerged for potassium currents in these neurons. In mature auditory and vestibular neurons, I(K), the delayed rectifier, is required for the fast repolarization of action potentials. In tonically firing auditory neurons, I(A), the transient outward rectifier, defines the discharge pattern. I(DS), a delayed rectifier-like current distinguished by its low threshold of activation, is found in phasically firing auditory and some developing vestibular neurons where it limits firing to one or a few spikes, and also may contribute to forming short-duration excitatory postsynaptic potential (EPSPs). Also, I(DS) sets the threshold for action potential generation rather high, which may prevent spontaneous discharge in phasically firing cells. During development, there is a gradual acquisition and loss of some potassium conductances, suggesting developmental regulation. As there are similarities in membrane properties of second-order auditory and vestibular neurons, investigations on firing pattern and its underlying mechanisms in one system should help to uncover fundamental properties of the other.
We evaluated the vestibular functions, especially for positional nystagmus and caloric nystagmus, in 43 cases of vestibular neuronitis for long periods after its onset. It is shown that in the cases of vestibular neuronitis that were studied more than 10 years after the onset of the disease, the completed vestibular compensation changed or the vestibular compensation was still incomplete.
We have studied the influence of intravenously administered diazepam on the activity of single secondary vestibular neurons in unanesthetized, paralyzed rabbits evoked by sinusoidal angular accelerations about the vertical and longitudinal axes. Intravenous injections of diazepam (20-100 micrograms/kg) caused a decreased sensitivity of all secondary vestibular neurons which were tested. The reduction in sensitivity was sometimes preceded by a transient increase in excitability which lasted 10-40 sec. The duration of the decreased sensitivity to vestibular stimulation following intravenous injections of diazepam was dose-dependent, lasting 15-60 min. These data suggest that the diazepam-induced reduction of vestibuloocular reflexes is caused, at least in part, by the depressant action of diazepam upon secondary vestibular neurons.
The authors have studied four cases of vestibular neuronitis. General and special ENT exploration were performed and repeated every month. The observation period was three months. ABR and ENG were used for evaluation. The cochlear part of the VIII cranial nerve ist affected without subjective clinical expression. So the patients were diagnosed as having vestibular neuronitis.
The pattern of development of several subpopulations of second-order vestibular neurons was investigated by using intracellular recordings from chicken brain slices to define the timing of morphological and electrophysiological changes occurring at 3 critical ages. Two embryonic stages, embryonic day 13 (E13) and E15-16, and also newborn chicks were selected according to previous anatomical findings showing the differentiation of primary vestibular afferents and their synapses within a distinctive brainstem vestibular nucleus, the tangential nucleus. The responses of these cells to depolarizing and hyperpolarizing current pulses and their postsynaptic responses to vestibular nerve stimulation were recorded, while simultaneously biocytin was injected for subsequent morphogenetic analysis. From this study, developmental schedules of membrane properties, synaptic responses, and dendritic differentiation were established for the 2 cell populations of the tangential nucleus and other neurons located in the surrounding vestibular nuclei. Compared with all other second-order vestibular neurons, the principal cells of the tangential nucleus exhibited a distinctive schedule. Mainly, this includes their pattern of firing on depolarization, the shape and duration of the vestibular-evoked excitatory postsynaptic potential, and the time of onset of dendritic outgrowth. In regard to these observations, E15-16 appears to be a turning point in principal cell ontogeny, whereas these features occur earlier in development for other second-order vestibular neurons. These findings, which indicate that the principal cells may have distinct membrane properties at specific ages, are discussed in light of their unique vestibular innervation and the possible consequences for vestibular signal processing.
We studied 28 patients with vestibular neuronitis treated at our hospital between 1997 and 1999. To determine the effects of steroid therapy on long-term canal prognosis and daily activity, we examined caloric tests and gave questionnaires to 12 steroid-treated and 16 nonsteroid-treated patients 2 years after onset. We found that canal improvement was 50% in the nonsteroid-treated group and 75% in the steroid-treated one. In cases with severe canal paresis (CP > or = 60%), canal improvement was 33% in the nonsteroid-treated group and 67% in the steroid-treated one. Steroid therapy at the acute stage of this disease significantly reduced the duration of spontaneous nystagmus and handicap in daily life due to dizziness induced by head and body movement, decreasing mood disturbance.
Optokinetic reflex was studied in 20 patients aged 20-58 years with vestibular neuronitis. In 16 decompensated patients the direction of the optokinetic nystagmus was inversed. This inversion disappeared in development of the compensation. Mean values of the amplitude and speed of the slow phase of optokinetic nystagmus are presented for patients with vestibular neuronitis and 20 healthy subjects in mono- and binocular optokinetic stimulation of various intensity.
OBJECTIVES To report our experience over the past 12 years with the evaluation and follow-up of pilots with vestibular neuronitis and to discuss points relevant to flight safety and the resumption of flying duties. STUDY DESIGN A retrospective, consecutive case series.METHODS Eighteen military pilots with vestibular neuronitis were examined and followed up. A complete otoneurological workup was performed, including both physical examination and laboratory evaluation. The latter included electro-oculography (EOG) and a rotatory chair test using the smooth harmonic acceleration protocol. RESULTS The mean patient age was 35 +/- 6 years (range, 23 to 42 y), and the average follow-up period was 20.5 +/- 12.8 months (mean +/- standard deviation [SD]; (range, 11 to 48 mo). Electro-oculography caloric test on presentation documented significant unilateral hypofunction in all patients. Thirteen of the 18 patients (72%) had abnormal smooth harmonic acceleration test results. None of the pilots reported any symptoms on follow-up. However, five (28%) had positive otoneurological examination findings, and eight (44%) still had significant caloric lateralization (>25%). The average caloric hypofunction was reduced from 67.8% +/- 29.3% at onset to 40% +/- 16% (mean +/- SD, <.05, paired test). Seven of the patients (39%) had additional electro-oculography findings beyond caloric hypofunction. These included spontaneous, positional, and positioning nystagmus. Smooth harmonic acceleration disease on follow-up was documented in eight patients (44%), five of whom had canal paresis. Eleven patients (61%) demonstrated residual vestibular damage on follow-up. In 6 of these 11 cases (55%), the laboratory evaluation revealed vestibular deficits otherwise undiagnosed by the bedside test battery. CONCLUSIONS The vestibular system plays a central role in orientation awareness and is often challenged by flying conditions. The finding that approximately 60% of pilots who have had vestibular neuronitis continue to show signs of vestibular malfunction, despite apparent clinical recovery, emphasizes the need for a complete vestibular evaluation, including specific bedside testing and laboratory examinations, before flying duties can be resumed.
The responses of central vestibular neurons in the decerebrate cat subjected to whole-body tilt were examined as a function both of stimulus orientation (with respect to the cat's head) and frequency, with the aim of understanding the neural processing responsible for producing the observed response patterns. Responses to whole-body tilt were recorded from vestibular neurons in and around the lateral vestibular nucleus (LVN). By plugging all six semicircular canals, the otolith contribution was studied in isolation. For each neuron, a response vector was defined as having three components: orientation, gain, and phase. These components were examined using sinusoidal stimulus frequencies of 0.01 to 2 Hz. The orientation component of the neural response vector does not vary as a function of stimulus frequency. Thus response dynamics previously described with a fixed (roll) axis cannot be explained by changes in the angle between the response vector orientation and a fixed stimulus axis. Two major classes of neural responses were observed. One class had a phase lead at low frequencies and gain that showed a modest increase with frequency. It could be described by a model that included a fractional s exponent operator. These response dynamics resemble that of otolith afferents, suggesting that these neurons may be acting as simple relays. The other major response class was characterized by a large gain increase and a phase lag of as much as 180 degrees as frequency increased; such response dynamics have been previously observed in otolith-evoked neck and forelimb reflexes. A more complex model, consisting of a parallel excitatory and high-pass-filtered inhibitory limb, was necessary to describe these responses. The orientation component of the response vector of most of the neurons whose dynamics were best described by the parallel pathway model pointed toward the contralateral side, implying they would be excited by side-up tilt (at low frequencies). Most other neurons had ipsilateral vectors.
The spontaneous activity of primary vestibular neurons was studied during postnatal development in the cat. Activities were categorized as regular, intermediate and irregular on the basis of the coefficient of variation. At birth, few regularly firing units were found while the percentage of intermediate and irregular units was high. During development, the percentage of units meeting the criterion of regularity increased steadily with age. At the same time the number of intermediate and irregular units decreased. The average resting rate of all categories of unit showed an increase in firing from birth up to the adult stage, i. e., around the second postnatal month. The mean firing rate of regularly firing units was always higher than the two other categories throughout all the stages of development. These results were compared with similar work performed in the rat.