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PubMed1996

A proposal for introducing a modified vestibular index in neurotology. The classification of vestibular neuronitis.

The parameters for vestibular dysfunction were modified after our own studies. This index includes the degree of vertigo present, spontaneous nystagmus, dysfunction of the vestibulospinal reflexes and caloric and postrotatory side differences. The index is applicable for defining the extent of a lesion, follow-up, defining its stage and the results of therapy. Introduction of the modified vestibular index is proposed for use in clinical diagnosis. Classification of vestibular neuronitis into groups A, B and C is suggested on the basis of the reversibility of spontaneous nystagmus after caloric stimulation.

Caloric Tests↗
PubMed2002

Morphology of physiologically identified otolith-related vestibular neurons in cats.

The morphology of physiologically identified otolith nerve-activated vestibular neurons was investigated using intracellular injections of horseradish peroxidase (HRP). Eleven utricular, 11 saccular and three utricular/saccular nerve-activated vestibular neurons were labeled with HRP. All of these neurons except one were secondary neurons, the exception being a convergent neuron. The labeled neurons were pyramidal, elongated and ovoidal in shape. Most of the labeled cells were medium to large (mean diameter: > or =30 micro m). There was no apparent correlation between morphology and the different types of otolith nerve-activated vestibular neurons. Thus, it seems likely that the functional type of vestibular neurons cannot be presumed on the basis of their morphology alone.

Animals↗
PubMed1989

Vestibular neuronitis. Pathogenesis in the view of virological study of CSF.

Cerebrospinal fluid (CSF) samples from 15 patients with vestibular neuronitis were virologically examined and analyzed, and compared to those from 16 patients with Hunt's syndrome. The results were as follows: The CSF protein in vestibular neuronitis showed an increase, beginning about two weeks after the onset of vertigo, while the cell count remained normal. The CSF protein in Hunt's syndrome rose, but its progress was different from that in vestibular neuronitis. In both diseases, the increase in CSF protein seemed to be due to protein originating in the blood; the increase was probably caused by a disorder of the blood-CSF barrier. There was no direct evidence of an increase in IgG nor viral antibody titers in the CSF in vestibular neuronitis. In cases of Hunt's syndrome with CSF pleocytosis, intrathecal IgG synthesis was detected. It might be possible that HSV or EBV infection can be confirmed serologically in some cases of vestibular neuronitis and that, in those cases, pathogenesis of vestibular neuronitis is similar to that of Hunt's syndrome.

Adolescent↗
PubMed1983

Vestibular neuronitis--its clinical characteristics.

Several parts of a nationwide survey of the epidemiology of vestibular neuronitis were reported. Follow-up studies of vestibular neuronitis were made. The computed galvanic body-sway test (Yamaguchi University) obtained from 10 patients with vestibular neuronitis showed a peculiar 'slow and sluggish' pattern. In the course of the illness, this slow and sluggish pattern changed its appearance and soon resembled the pattern obtained from the opposite, healthy side. Improvement of the abnormal pattern was observed in 7 patients (observation period 6 months to 6 years, averaging 33 months). 3 other patients (observation period 1 month to 1 year, averaging 5.3 months) showed no improvement in the pattern. These findings suggest that the conductivity of the vestibular nerve affected by vestibular neuronitis has an increasing chance for recovery.

Adolescent↗
PubMed1993

Serum viral antibody titer in vestibular neuronitis.

Fifty-seven cases of vestibular neuronitis were evaluated for viral infection by means of serum antibody titer. The viruses tested were herpes simplex virus, varicella-zoster virus, cytomegalovirus, EB virus, adenovirus, influenza virus A, influenza virus B, parainfluenza virus 3, mumps virus, rubella virus and measles virus. Paired sera were examined in 49 cases among 57 cases, 26 cases showed significant change (four-fold or greater change) in viral antibody titer. Only one case (53-year old female) showed high HSV 1 IgM antibody level by ELISA method, so the vestibular neuronitis in this case was assumed to have a close relation to viral infection.

Adolescent↗
PubMed1993

Vestibular neuronitis in children.

Seventeen cases of vestibular neuronitis in children, including 11 cases from the questionnaires of an epidemiological survey in Japan and 6 patients in our clinic, were examined. Sex and age distribution was 11 males and 6 females, ranging in age from 3 to 15 years. Bilateral and recurrent cases were not encountered. Fifty-three percent of children had had a preceding episode of an upper respiratory tract infection and this ratio was higher than that in adults. The etiology of vestibular neuronitis is probably many-faceted, but it is thought that upper respiratory tract infections play an important role especially in children. Vertiginous symptoms had almost subsided among children at the last visit. However, among adults, 24% of patients felt persisting unsteadiness. The disappearance of positional and positioning nystagmus was observed in 71% of children at the last visit. Caloric CP failed to recover in only 14% of all cases who were re-examined. As shown in this study, the prognosis in children is better than in adults for nystagmus and caloric response. The results of this study thus indicate that not only central compensation but also recovery of the peripheral vestibular function is more effective for bringing recovery from the vestibular disorder in children than in adults.

Adolescent↗
PubMed2000

Saccular and utricular inputs to single vestibular neurons in cats.

Saccular and utricular organs are essential for postural stability and gaze control. Although saccular and utricular inputs are known to terminate on vestibular neurons, few previous studies have precisely elucidated the origin of these inputs. We investigated the saccular and utricular inputs to single vestibular neurons in whole vestibular nuclei of decerebrated cats. Postsynaptic potentials were recorded from vestibular neurons after electrical stimulation of the saccular and utricular nerves. Ascending and descending axonal projections were examined by stimulating the oculomotor/trochlear nuclei and the cervical segment of the spinal cord, respectively. After each experiment, locations of recorded neurons were identified. The recorded neurons (140) were classified into vestibulo-spinal (79), vestibulo-oculo-spinal (9), and vestibulo-ocular (3) neurons based on antidromic responses; 49 other vestibular neurons were unidentified. The majority of recorded neurons were mainly located in the lateral vestibular nucleus. Most of the otolith-activated vestibular nuclei neurons seemed to participate in vestibulospinal reflexes. Of the total 140 neurons recorded, approximately one third (51) received saccular and utricular inputs (convergent neurons). The properties of these 51 convergent neurons were further investigated. Most (33/51) received excitatory postsynaptic potentials (EPSPs) after saccular and utricular nerve stimulation. These results implied that most of the convergent neurons in this study additively coded mixed information for vertical and horizontal linear acceleration. Based on the latencies of convergent neurons, we found that an early integration process for vertical and horizontal linear acceleration existed at the second-order level.

Acceleration↗
PubMed1989

The firing properties of second-order vestibular neurons in correlation with the far-field recorded vestibular-evoked response.

Action potentials of the second-order vestibular neurons of ten cats were recorded, both in rest and responding to sinusoidal and intense impulse acceleration stimuli. The data were compared with the far-field recorded vestibular-evoked response induced by the same impulse stimuli. It was found that the irregular (kinetic) neurons, which had a phase lead relative to head velocity, were capable of responding to these impulses with a latency as short as 3.5 msec after the start of head acceleration. It is assumed, therefore, that these neurons are the generators of the second wave of the vestibular-evoked response, having a similar latency. A high correlation was found between the latency of the first peak in the poststimulus time histogram in response to acceleration impulses and the phase of the response to sinusoidal rotations. The regular (tonic) vestibular neurons did not respond to acceleration impulses and probably did not contribute to the vestibular-evoked response.

Animals↗
PubMed2004

[Some characteristics of vertigo in vestibular neuronitis].

The authors present a detailed clinical analysis of objective neurological symptoms and vertigo in patients with vestibular neuronitis. Diagnostic criteria are specified allowing differentiation between vertigo and dizziness, pathognomonic signs of vestibular neuronitis are outlined. Peripheral location of the pathological process in vestibular neuronitis is suggested. How rotating vertigo is forming in patients with vestibular neuronitis is hypothesized.

Adult↗
PubMed1997

Contributions of regularly and irregularly discharging vestibular-nerve inputs to the discharge of central vestibular neurons in the alert squirrel monkey.

The discharge of neurons in the vestibular nuclei was recorded in alert squirrel monkeys while they were being sinusoidally rotated at 2 Hz. Type I position-vestibular-pause (PVP I) and vestibular-only (V I) neurons, as well as a smaller number of other type I and type II eye-plus-vestibular neurons were studied. Many of the neurons were monosynaptically related to the ipsilateral vestibular nerve. Eye-position and vestibular components of the rotation response were separated by multiple regression. Anodal currents, simultaneously delivered to both ears, were used to eliminate the head-rotation signals of irregularly discharging (I) vestibular-nerve afferents, presumably without affecting the corresponding signals of regularly discharging (R) afferents. R and I inputs to individual central neurons were determined by comparing rotation responses with and without the anodal currents. The bilateral currents, while reducing the background discharge of all types of neurons, did not affect the mean vestibular gain or phase calculated from a population of PVP I neurons or from a mixed population consisting of all type I units. From this result, it is concluded that I inputs are canceled at the level of secondary neurons. The cancellation may explain why the ablating currents do not affect the gain and phase of the vestibulo-ocular reflex. While cancellation was nearly perfect on a population basis, it was less so in individual neurons. For some neurons, the ablating currents decreased vestibular gain, while for other neurons the vestibular gain was increased. The former neurons are interpreted as receiving a net excitatory (I-EXC) I input, the latter neurons, a net inhibitory (I-INH) input. When compared with the corresponding R inputs, the I inputs were usually small and phase advanced. Phase advances were larger for I-EXC than for I-INH inputs. The sign and magnitude of the I inputs were unrelated to other discharge properties of individual neurons, including discharge regularity and the phase of vestibular responses measured in the absence of the ablating currents. Unilateral currents were used to assess the efficacy of ipsilateral and contralateral pathways. Ipsilateral pathways were responsible for almost all of the effects seen with bilateral currents. The results suggest that the vestibular signals carried by central neurons, even by those neurons receiving a monosynaptic vestibular-nerve input, are modified by polysynaptic pathways.

Animals↗
PubMed1993

Vestibular neuronitis: a review of a common cause of vertigo in general practice.

Vestibular neuronitis is an interesting condition characterized by the acute onset of vertigo, nausea and vomiting, in the absence of hearing loss or tinnitus. There is often evidence of a recent or concurrent upper respiratory tract infection. The disease follows a benign course of between two days and six weeks. It often occurs in epidemics. Following the acute attack, mild transitory episodes of dizziness may recur over a period of 12 to 18 months. Clinical and histopathological evidence suggests that it is caused by an isolated lesion of the vestibular nerve, although the exact aetiology remains obscure. Vestibular neuronitis is a relatively common condition in general practice, but has lacked clear definition, partly as a result of confusion over its nomenclature. Current knowledge of vestibular neuronitis is reviewed. Clinical diagnostic criteria are described, and the diagnosis and differential diagnosis of the syndrome in general practice are outlined. There remains a need to describe the occurrence of vestibular neuronitis in general practice in greater detail.

Adult↗
PubMed1995

[Diagnostic and therapeutic problems in vestibular neuronitis: clinical implications for sudden vertigo].

We defined sudden vertigo as a sudden, unilateral peripheral vestibular dysfunction. The criterion for its diagnosis is a single episode of vertigo without cochlear and central symptoms. Among 20 patients with sudden vertigo there was no difference in clinical aspects between those with CP (canal paresis) (CP% > or = 25%) and those without CP (CP% < 25%). This suggests that sudden vertigo with CP is due to sudden vestibular dysfunction with predominant involvement of the lateral semicircular canal. Basically, vestibular neuronitis is considered to be due to acute unilateral neuropathy of the vestibular nerve. However, since we have no routine examination for evaluating vestibular nerve function, sudden vertigo with CP should be diagnosed as vestibular neuronitis. We then assessed the prognosis of sudden vertigo with CP (vestibular neuronitis). About two years after the onset of CP 4 of 10 patients had recovered. However, patients with persistent CP had a handicap in their everyday life because of the dizziness induced by head movements. The possibility of recovery of vestibular function in response to steroid therapy may improve the prognosis in vestibular neuronitis.

Adult↗
PubMed1996

Degeneration of vestibular neurons in late embryogenesis of both heterozygous and homozygous BDNF null mutant mice.

The generation of mice lacking specific neurotrophins permits evaluation of the trophic requirements of particular neuronal populations throughout development. In the present study, we examined the developing vestibulocochlear system to determine the time course of neurotrophin dependence and to determine whether competition occurred among developing cochlear or vestibular neurons for available amounts of either brain-derived neurotrophic factor (BDNF) or neurotrophin-4/5 (NT-4/5). Both cochlear and vestibular neurons were present in mice lacking NT-4/5. In contrast, vestibular neurons decreased in number beginning at mid-stages of inner ear development, in mice lacking BDNF. Early in development (E12.5-13), the size of the vestibular ganglion was normal in bdnf -/- mice. Decreased innervation to vestibular sensory epithelia was detected at E13.5-15, when progressive loss of all afferent innervation to the semicircular canals and reduced innervation to the utricle and saccule were observed. At E16.5-17, there was a reduction in the number of vestibular neurons in bdnf -/- mice. A further decrease in vestibular neurons was observed at P1 and P15. Compared to bdnf -/- mice, mice heterozygous for the BDNF null mutation (bdnf +/-) showed an intermediate decrease in the number of vestibular neurons from E16.5-P15. These data indicate a late developmental requirement of vestibular neurons for BDNF and suggest competition among these neurons for limited supplies of this factor.

Animals↗
PubMed1980

Eye movement related activity and morphology of second order vestibular neurons terminating in the cat abducens nucleus.

Intracellular records were obtained from axons of second order vestibular neurons in, and around, the left abducens nucleus in alert cats implanted with stimulating electrodes on both vestibular nerves and the left VIth nerve. Twelve secondary vestibular neurons were identified by their increase in firing rate with horizontal head rotation to the left and/or increasing eye position to the right. Following HRP injection, somatic location, axonal trajectory and termination sites were determined. Each of the above cells collateralized extensively in the abducens nucleus in a fashion consistent with their being either inhibitory (n = 7; left) or excitatory (n = 6; right) vestibular neurons in the disynaptic horizontal vestibulo-ocular reflex pathway. These vestibular neurons also arborized extensively in other posterior brainstem eye-movement related areas as well as sending an axon to the spinal cord.

Abducens Nerve↗
PubMed1977

The contribution of the contralateral labyrinth to second order vestibular neuronal activity in the cat.

Vestibular brain stem units of the horizontal canal in the awake C1 transected cat were examined in acute experiments before and after the contralateral vestibular nerve was cut. The latter procedure resulted in an immediate increase in mean resting rate from 19 to 45 spikes/sec and greater spontaneous fluctuations in firing rate. Mean sensitivity to constant accelerations from 2 to 16 degrees/sec2 was significantly reduced. In the 4-6 degrees/sec2 range, for example, mean sensitivity fell from 5.7 +/- 3.2 spike/sec/deg/sec2 (range 0.7-13.6, n = 107) to 2.8 +/- 1.4 (range 0.2-5.5, n = 29). Mean sensitivity to 4-6 degrees/sec2 deceleration was reduced from about 4.5 to 3.0. On the other hand, time constants and the ratio of adapting to non-adapting units was unchanged. Removal of the midline cerebellum, including the vermis and fastigial nuclei in a portion of the animals, did not materially alter the above results. It is concluded that the contralateral labyrinth, acting via the vestibular brain stem commissural pathway, not only exerts a powerful effect on the resting activity of brain stem canal vestibular neurons, but also on their response to acceleration.

Action Potentials↗
PubMed1980

Response of central vestibular neurons to horizontal linear acceleration in the rat.

Responses of central vestibular neurons to horizontal sinusoidal translation (F:0.25Hz) were recorded in albino rat. 57.5% of vestibular neurons were responding to this stimulation by a modulation of their firing rate, the mean phase angle of the response, averaged from the whole population being 22 +/- 79 deg. lag, relative to the peak of contralateral acceleration. Dynamic characteristics of phase and gain were studied and appeared to be different from previous reports on primary afferents: the gain decreased or was flat with increasing acceleration at one frequency, and the phase lag which was flat in the same conditions increased with increasing frequency. A phase lead of some units has been observed at low frequency (0.1 Hz). Regarding the convergence between otolith and canal inputs on nuclear vestibular neurons, it was shown that the major pattern of convergence is between canal and otolith inputs of same polarity.

Acceleration↗
PubMed1987

Anatomical and physiological characteristics of vestibular neurons mediating the horizontal vestibulo-ocular reflex of the squirrel monkey.

The anatomical characteristics of vestibular neurons, which are involved in controlling the horizontal vestibulo-ocular reflex, were studied by injecting horseradish peroxidase (HRP) into neurons whose response during spontaneous eye movements had been characterized in alert squirrel monkeys. Most of the vestibular neurons injected with HRP that had axons projecting to the abducens nucleus or the medial rectus subdivision of the oculomotor nucleus had discharge rates related to eye position and eye velocity. Three morphological types of cells were injected whose firing rates were related to horizontal eye movements. Two of the cell types were located in the ventral lateral vestibular nucleus and the ventral part of the medial vestibular nucleus (MV). These vestibular neurons could be activated at monosynaptic latencies following electrical stimulation of the vestibular nerve; increased their firing rate when the eye moved in the direction contralateral to the soma; had tonic firing rates that increased when the eye was held in contralateral positions; and had a pause in their firing rate during saccadic eye movements in the ipsilateral or vertical directions. Eleven of the above cells had axons that arborized exclusively on the contralateral side of the brainstem, terminating in the contralateral abducens nucleus, the dorsal paramedian pontine reticular formation, the prepositus nucleus, medial vestibular nucleus, dorsal medullary reticular formation, caudal interstitial nucleus of the medial longitudinal fasciculus, and raphé obscurus. Eight of the cells had axons that projected rostrally in the ascending tract of Deiters and arborized exclusively on the ipsilateral side of the brainstem, terminating in the ipsilateral medial rectus subdivision of the oculomotor nucleus and, in some cases, the dorsal paramedian pontine reticular formation or the caudal interstitial nucleus of the medial longitudinal fasciculus. Two MV neurons were injected that had discharge rates related to ipsilateral eye position, generated bursts of spikes during saccades in the ipsilateral direction, and paused during saccades in the contralateral direction. The axons of those cells arborized ipsilaterally, and terminated in the ipsilateral abducens nucleus, MV, prepositus nucleus, and the dorsal medullary reticular formation. The morphology of vestibular neurons that projected to the abducens nucleus whose discharge rate was not related to eye movements, or was related primarily to vertical eye movements, is also briefly presented.

Abducens Nerve↗
PubMed1997

Multiple voltage-dependent calcium currents in acutely isolated mouse vestibular neurons.

We investigated the presence of voltage-gated calcium currents in vestibular neurons acutely isolated from postnatal mice vestibular ganglions using the whole-cell patch-clamp technique. The neuronal origin of the recorded cells was confirmed by immunohistochemical detection of neurofilaments and calretinin. High and low voltage-activated calcium currents were recorded. High voltage-activated currents were present in all investigated neurons. Low voltage-activated currents were recorded in only a few large vestibular neurons. High and low voltage-activated currents were distinguished by their thresholds of activation and their ability to run-up during early recordings. Among high voltage-activated currents. L-, N- and P-type currents were identified by their sensitivity to, respectively, the dihydropyridines agonist Bay K 8644 (3 microM) and antagonist nitrendipine (3 microM), the co-conotoxin GVIA (3 microM) and the omega-agatoxin IVA at low concentration (50 nM). An inactivating current sensitive to 1 microM omega-agatoxin IVA with characteristics similar to those of the Q-type current was also recorded in vestibular neurons. When L-, N-, P-, Q-type barium currents were blocked, a residual high voltage-activated current defined by its resistance to saturating concentrations of all above blockers was detected. This residual current was completely blocked by 0.5 mM nickel and cadmium. Our results reveal that primary vestibular neurons express a variety of voltage-activated calcium currents with distinct physiological and pharmacological properties. This diversity could be related both with their functional synaptic characteristic, and with the intrinsic physiological properties of each class of vestibular afferents.

Animals↗