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At least 109 records · Page 6Linked to original sources
PubMed1993

Progress of caloric response of vestibular neuronitis.

Progress of caloric response and subjective symptoms of 60 patients with vestibular neuronitis was evaluated by a long term follow-up study. Normalization of caloric responses was confirmed in 25 (41.7%) out of 60 patients, 20 of whom had recovered within 2 years of the onset of vertigo. The rate of the patients with canal paresis was about 90% after 1 month of the onset, and 80% after 6 months, while 50% of them still showed canal paresis after 5 or 10 years had passed. Complete relief from subjective symptoms was recognized in 34 (56.7%) cases during the follow-up period. We conclude that the prognosis of vestibular neuronitis is not always good, because vestibular function did not recover within normal levels in about half of the patients in spite of complete relief from subjective symptoms in many of them.

Adolescent↗
PubMed1993

Vestibular neuronitis: epidemiological survey by questionnaire in Japan.

An epidemiological survey on vestibular neuronitis in Japan was conducted by means of a questionnaire filled in by major neuro-otology clinics (otolaryngologists) during 1988-1990 (3 years). The diagnostic criteria of vestibular neuronitis settled on in 1986 by the Standardization Committee of the Japan Society of Equilibrium Research were applied. Gross analysis of questionnaire answers showed that i) there was no sexual difference, ii) the peak of age distribution was between 40-50 years, iii) about 30% of all cases had had common colds prior to the disease, the rate being highest among children below 10 years, iv) disappearance of positional and positioning nystagmus appeared in about 60% of all cases within 3 months, and that v) caloric CP was observed in about half of the cases at the follow-up test. Progress was not as favorable when compared to previous studies.

Adolescent↗
PubMed2000

Convergence patterns of the posterior semicircular canal and utricular inputs in single vestibular neurons in cats.

The convergence of the posterior semicircular canal (PC) and utricular (UT) inputs in single vestibular nuclei neurons was studied intracellularly in decerebrate cats. A total of 160 vestibular neurons were orthodromically activated by selective stimulation of the PC and the UT nerve and classified according to whether or not they were antidromically activated from the spinal cord and oculomotor nuclei into vestibulospinal (VS), vestibulooculospinal (VOS), vestibuloocular (VO), and unidentified vestibular neurons. Fifty-three (33%) of 160 vestibular neurons received convergent inputs from both the PC and UT nerves. Seventy-nine (49%) vestibular neurons responded to PC inputs alone, and 28 (18%) neurons received inputs only from the UT nerve. Of 53 convergent neurons, 8 (15%) were monosynaptically excited from both nerves. Thirty-five (66%) received monosynaptic excitatory inputs from the PC nerve and polysynaptic excitatory or inhibitory inputs from the UT nerve, or vice versa. Approximately one-third of VS and VOS neurons received convergent inputs. A majority of the VS neurons descended to the spinal cord through the lateral vestibulospinal tract, while almost all the VOS neurons descended to the spinal cord through the medial vestibulospinal tract. The convergent neurons were found in all vestibular nuclei but more in the lateral nucleus and descending nucleus. The VS neurons were more numerous than VO neurons or VOS neurons.

Acceleration↗
PubMed2000

Vestibular compensation modifies the sensitivity of vestibular neurones to inhibitory amino acids.

The progressive disappearance of the postural and oculomotor syndrome triggered by unilateral labyrinthectomy (vestibular compensation) is a model of plasticity in the adult central nervous system. This recovery may involve modifications of the pharmacological profile of central vestibular neurones, in particular their sensitivity to inhibitory amino acids. We therefore compared the sensitivity of medial vestibular nucleus neurones to glycine and muscimol in slices taken either from control animals, or from guinea-pigs labyrinthectomized 3 days before. We demonstrate that the loss of excitatory inputs experienced by the ipsilesional vestibular neurones induces a decrease in their sensitivity to inhibitory amino acids. These pharmacological changes should facilitate the recovery of a normal balance between the average resting discharge of neurones in both vestibular nuclei.

Adaptation, Physiological↗
PubMed2000

Neuronal organization of the utricular macula concerned with innervation of single vestibular neurons in the cat.

We investigated whether cross-striolar inhibition, which may increase sensitivity to linear acceleration, contributed to utricular (UT) afferent innervation of single vestibular neurons (VNs). Excitatory and inhibitory postsynaptic potentials (EPSPs, IPSPs, respectively) were recorded from VNs after focal stimulation of the UT macula (M). From a total of 83 VNs, 25 (30%) neurons received inputs from both sides of the UTM, and the response patterns were opposite, i.e. cross-striolar inhibition was observed. In roughly 2/3 of these neurons, stimulation of the medial side of the UTM evoked EPSPs, while stimulation of the lateral side evoked IPSPs. In the remaining 1/3 neurons, the response patterns were opposite. Thirty-two (39%) of the 83 neurons received the identical pattern of inputs from both sides of the UTM: EPSPs in 26 neurons and IPSPs in six neurons. Twenty-six (31%) of the 83 neurons received inputs from either the medial or the lateral side of the UTM. These findings suggest that cross-striolar inhibition existed in the UT system, although it was not a dominant circuit that increased the sensitivity as in the saccular system [15].

Acoustic Maculae↗
PubMed1991

Postnatal developmental changes in the responses of mouse primary vestibular neurons to externally applied galvanic currents.

The ontogenesis of vestibular primary neuron sensitivity to depolarisation produced by galvanic current stimulations was studied in mouse inner ear explants maintained in vitro. Cathodal galvanic stimulations, which elicit an increase of the discharge frequencies, are assumed to act on the spike initiation site by depolarizing the neuron. The responses of neurons to galvanic currents at various developmental stages were recorded. The pattern of responses reflected the sensitivities of the neurons to depolarization. At birth, about 75% of the vestibular neurons responded weakly to high intensity galvanic currents thus indicating that they were able to generate action potentials. However, the very low gain of the response to the stimulation revealed the immaturity of the neurons at the spike generation site. Between the day of birth and the ninth postnatal day, an increase in the gain of the responses was observed, indicating the enhancement of the sensitivity of the vestibular neurons to the galvanic currents. This increase in sensitivity was more pronounced from the fourth postnatal day. The response of the neurons to galvanic stimulation increased gradually during postnatal development without reaching a plateau at postnatal day 9 indicating that a further physiological maturation occurs after this stage. These results are consistent with the morphological maturation of the vestibular primary afferents and with previous studies showing that the physiological maturation parallels myelination of the afferent fibers.

Animals↗
PubMed2001

Influence of serotonin on the glutamate-induced excitations of secondary vestibular neurons in the rat.

The excitatory responses evoked by glutamate and its agonists in secondary vestibular neurons of the rat were studied during microiontophoretic application of 5-hydroxytryptamine (5-HT). Ejection of 5-HT modified neuronal responsiveness to glutamate in 86% of the studied units, the effect being a depression of the excitatory responses in two-thirds of cases and an enhancement in the remaining third. 5-HT was also effective in modifying 94% of the responses evoked by N-methyl-d-aspartate (NMDA), inducing a depressive effect in 76% of cases and an enhancement in the remaining ones. Quisqualate-evoked effects were depressed and enhanced by 5-HT in about the same number of cases; in contrast, kainate-evoked responses were enhanced. The depressive action of 5-HT was mimicked by application of alpha-methyl-5-hydroxytryptamine (alpha-Me-5-HT), a 5-HT(2) receptor agonist, whereas the enhancing effect could be evoked by application of 8-hydroxy-2(di-n-propylamino)tetralin (8-OH-DPAT), a selective 5-HT(1A) receptor agonist. The 5-HT(2) receptor antagonist ketanserin was able to reduce, but not to block totally, the depressive action of 5-HT on glutamate- or NMDA-evoked responses. No significant difference was detected between neuronal responses in the lateral and the superior vestibular nucleus. These results indicate that 5-HT is able to modulate the responsiveness of secondary vestibular neurons to excitatory amino acids. Its action is mostly depressive, involves 5-HT(2) receptors, and is exerted on NMDA receptors. A minor involvement of other 5-HT receptors (at least 5-HT(1A)) and other glutamate receptors (for quisqualate and kainate) in the modulatory action of 5-HT is plausible.

Animals↗
PubMedDate not supplied

Response of first order vestibular neurons to lidocaine hydrochloride.

Changes in behavior and electrical activity of primary vestibular neurons were observed following injection of lidocaine hydrochloride into the middle ear of cats. After injection the cats exhibited head and ocular nystagmus, head and neck deviation and pupillary changes. Mean preinjection resting discharge rate for first order vestibular neurons was 46.0 spikes/sec. Two hours after lidocaine application the resting rate decreased to a mean of 22.2 spikes/sec and then recovered to 43.0 spikes/sec four hours, and 47.4 spikes/sec six hours after the experimental treatment. The increment sensitivity (increased rate of firing) of horizontal canal neurons to constant angular acceleration for the control period was 2.0 extra spikes/sec/deg/sec2; two hours after the application, 70% of the recorded neurons were unresponsive to angular acceleration or tilt. The sensitivity after four hours was 1.0 spikes/sec/deg/sec2 and 2.1 spikes/sec/deg/sec2 at six hours. The distinct depression of sensitivity by lidocaine at four hours compared to normal mean resting rate at this time suggests these functions may be governed by two modes of action in the receptor or first order afferents.

Animals↗
PubMed2001

Convergence of the horizontal semicircular canal and otolith afferents on cat single vestibular neurons.

We studied the convergence of two afferent pairs of single vestibular neurons by selective stimulation of the horizontal semicircular canal (HC) and saccular (SAC) nerves, and the HC and utricular (UT) nerves in decerebrate cats. All recorded neurons were classified as vestibulospinal (VS), vestibulo-oculospinal (VOS) or vestibulo-ocular (VO), by antidromic stimulation from the oculomotor/trochlear nuclei and the spinal cord: neurons that could not be activated from any test sites were classified as vestibular (V) neurons. Of a total of 125 neurons activated by stimulation of the HC/SAC nerves, 21(17%) received convergent inputs. Twelve of 21 neurons received monosynaptic excitatory inputs from both nerves. About half (9/21, 43%) of the convergent neurons were classified as VS neurons, the majority of which descended through the ipsilateral lateral vestibulospinal tract (i-LVST). The HC/SAC convergent neurons were located in the rostral part of the descending, the medial and the caudal-ventral part of the lateral vestibular nucleus. In 80 neurons studied by stimulation of the HC/UT nerves, both inputs converged in 12 (15%) neurons, more than half of which were VS neurons. Eight of 12 convergent neurons received excitatory inputs followed by inhibition from both the HC and UT nerves. A few convergent neurons (3/12) projected to the oculomotor/trochlear nucleus. Half of the convergent and non-convergent VS neurons descended to the spinal cord through the i-LVST, and the only one VOS convergent neuron via the medial vestibulospinal tract. Most of the convergent neurons were located in the lateral, the rostral part of the descending and medial vestibular nucleus. The percentages of HC/SAC and HC/UT convergence were half those of the posterior semicircular canal (PC), PC/SAC (33%) and PC/UT (33%) convergence, respectively. The convergent neurons receiving the HC and otolith inputs may contribute at least partly to the vestibulocollic reflex.

Afferent Pathways↗
PubMed1984

Responses to head tilt in cat central vestibular neurons. I. Direction of maximum sensitivity.

Responses to head tilt were recorded from vestibular neurons in and around the lateral vestibular nucleus (LVN) of the decerebrate cat. Each animal had all six semicircular canals rendered nonfunctional by a plugging procedure. Each cell was studied by slowly tilting the cat, using one or both of two paradigms. In the first method, sinusoidal tilts (0.05 or 0.1 Hz) were used to produce bidirectional stimuli in up to 12 pairs of directions, including left/right (roll tilt) and fore/aft (pitch). The second method imposed a constant 10 degree tilt; the direction of the tilt was rotated around the animal by an appropriate combination of roll and pitch motions. Neurons responded by maximally increasing their discharge frequency in a particular direction of head tilt from the horizontal. Each cell's response could be described by a vector in the animal's horizontal plane whose orientation is given by the direction of the most effective stimulus and whose length represents the neuron's maximal sensitivity to tilt. The two methods of stimulation yielded equivalent response vectors. Response vectors were obtained for 100 neurons. The distribution of vector directions for these vestibular neurons was not uniform; there was a conspicuous absence of neurons with fore/aft-directed vectors. The sensitivity of these cells (length of the response vector) ranged from 10 to 230 impulses X s-1 X g-1 (median 50). Neurons whose vectors lay in the ipsilateral half-plane (which would be excited by ear-down tilt) tended to be less sensitive than those with contralateral vectors. Neurons excited by ear-up tilt tended to be located ventrally in the LVN, while those excited by ear-down tilt were more evenly distributed. There was no other obvious correlation of vector orientation with the anatomical locus of the cell in the LVN. The directional selectivity of the responses of these neurons to head tilts are similar to those previously reported tin utricular afferents. The broad distribution of response vector orientations provides an appropriate substrate for vestibulospinal reflexes to a wide variety of head tilts.

Afferent Pathways↗
PubMed1993

Neuroborreliosis in the etiology of vestibular neuronitis.

Symptoms and incidence of neuroborreliosis (NB) were studied in ambulatory patients visiting the ENT clinic in Helsinki. Especially we tried to search for possible markers indicating the connection between vestibular neuronitis and NB. A total of 350 patients were screened with the enzyme-linked immunosorbent assay (ELISA) technique for possible antibodies against Borrelia burgdorferi (BB). Twelve patients had positive serological reactions for BB with sera titer levels ranging from 640-14700 (normal < 500). In 2 additional cases, NB was clinically confirmed. In 7 cases a history of tick bite and in 4 cases erythema chronicum migrans was confirmed. In 9 cases, vertigo was the predominant symptom, and in 3 cases the symptoms were linked to facial nerve paresis. Six patients suffered from hearing loss. In 7 cases, the diagnosis was initially settled as vestibular neuronitis. NB seems to be present in about 4% of cases with apparent otologic diseases in Finland. In the majority of the cases, the disease resembles vestibular neuronitis in the acute stage. Since NB is tractable, all patients visiting the ENT clinic, especially those with vertigo, should be screened.

Antibodies, Bacterial↗
PubMed1993

Vestibular neuronitis evaluated by the combined galvanic test.

Forty-two patients with unilateral vestibular neuronitis were examined by the combined galvanic test (CGT), consisting of the galvanic eye movement test (GEMT) and the galvanic body sway test (GBST). Results of the CGT were evaluated with respect to the time period from the onset of vestibular neuronitis. A favorable recovery was observed earlier with the GBST than the GEMT. We believe that this discrepancy may be due to the difference in compensation between the vestibulo-ocular reflex and the vestibulo-spinal reflex.

Adult↗
PubMed2003

Contribution of GABAergic inhibition to the responses of secondary vestibular neurons to head rotation in the rat.

To assess the contribution of GABAA receptor-mediated inputs in control of vestibular responses of secondary vestibular neurons, we examined the effects of the GABAA receptor antagonists, bicuculline and picrotoxin, on these neurons in anesthetized rats. Horizontal canal-related secondary vestibular neurons were identified by their monosynaptic excitation from the ipsilateral vestibular nerve and by the modulation of their firing rate for head rotation. Responses to sinusoidal head rotation were recorded before and during iontophoretic application of the drugs. Application of bicuculline increased DC level of the responses (mean firing rate in each cycle) in all of the 10 neurons examined. In seven of these, the gain was increased along with the DC level, but the phase was virtually unaffected. Similarly, picrotoxin increased both the DC level (4/4) and the gain (3/4), but did not affect the phase. In the 10 neurons that increased the gain, the mean percent increase in the gain was 31% (8-54%). These results indicate that the majority of neurons received inhibitory inputs that were in phase with the excitatory inputs from primary afferents. This suggests that these neurons received GABAergic input of non-commissural origin, most likely from the flocculus.

Action Potentials↗
PubMed1993

Effects of inferior olive inactivation and lesion on the activity of medial vestibular neurons in the rat.

In anaesthetized rats, the unitary activity from the medial vestibular nucleus had been recorded during horizontal sinusoidal rotation in the absence of visual stimulation. In the first series of experiments, the inferior olivary nuclei were selectively destroyed by means of 3-acetylpyridine. Unitary activity was recorded three to five days or one month after the lesion. A few days after the lesion, the average spontaneous activity, as well as the peak-to-peak amplitude of the modulation of the medial vestibular neurons during sinusoidal rotation, were significantly lower compared to those recorded in intact rats, and to those recorded one month after the lesion. In the second series of experiments, during reversible cooling of the inferior olive region of one side, in the contralateral medial vestibular nuclei 57% of units underwent a clear decrease in firing rate accompanied by a decrease in the amplitude of modulation. In rats whose inferior olivary nuclei had been destroyed by means of 3-acetylpyridine one month before, or whose cerebellum had been removed, there were few units that showed a decrease of the firing rate and modulation amplitude on cooling the same olivary region. Our experiments show that silencing the activity of the inferior olive causes a decrease both in the spontaneous firing rate and in the amplitude of the response of the vestibular neurons to natural labyrinthine stimulation. These results support the hypothesis that the inferior olive, by changing its firing rate, may regulate on-line the gain of reflexes which are under cerebellar control.

Animals↗