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PubMed2004

The use of antiserotonin drugs in the nucleoreticular vestibular syndrome: preliminary observations.

Vestibular neuronitis was described in 1949 and 1952 by Dix and Hallpike. Two groups of patients were described, those with sudden seizures and sensations of blackout (since identified as having vestibular neuritis) and a second group with symptoms of disequilibrium and feelings of top-heaviness or imbalance. The pathology was believed to be central to the inner ear. Arslan labeled these groups as having nucleoreticular vestibular syndrome. Using a suprathreshold stapedial reflex test, Bosatra localized the pathophysiology in the brainstem, an area rich in serotonergic neurons. This author has used antiserotonergic drugs, with success, in treating patients having the symptoms identified by Dix and Hallpike in their second group (which now should be labeled nucleoreticular vestibular syndrome), properly identified as a brainstem affliction. This study describes the characteristics of this disorder, the methods of diagnosis and treatment, and the outcomes in two groups of patients studied. The study concluded that antiserotonin drugs, specifically affecting 5-hydroxytryptamine2, should be considered in the management of nucleoreticular vestibular syndrome.

Brain Stem↗
PubMed2006

Vertigo: few new spins on a common problem.

Vertigo is a common balance deregulation symptom among elders. Its etiology may be peripheral vestibular disease or a central vestibular disorder. Symptom onset, severity, and duration are distinguishing characteristics. The majority of peripheral vestibular disorders include benign paroxysmal positional vertigo, vestibular neuronitis, Meniere's disease, and perilymph fistula. Medication regimen review is necessary to identify possible drug-induced etiology. Treatment options include pharmacotherapy, canalith repositioning procedures, surgery, vestibular rehabilitation therapy, and dietary interventions.

Diet↗
PubMed1995

Neuronal activity in the ipsilateral vestibular nucleus following unilateral labyrinthectomy in the alert guinea pig.

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

Animals↗
PubMed1996

Evidence for reactive astrocytes in rat vestibular and cochlear nuclei following unilateral inner ear lesion.

We investigated whether unilateral removal of the labyrinthine and cochlear receptors induces a macroglial reaction in rat vestibular and cochlear nuclei using vimentin and glial fibrillary acidic protein (GFAP) immunochemical markers. Antibody binding was visualized using the avidin-biotin method and 3,3'-diaminobenzidine as the peroxidase substrate. In addition, double-labelling experiments were performed using specific secondary fluorescent antibodies. Potentially degenerating axon terminals were also studied using a silver impregnation method. In normal adult rats, vimentin was found only in ependymal cells, tanicytes around the fourth ventricle, endothelial cells in the blood vessels and Bergmann glia in the molecular layer of the cerebellum. In lesioned rats, all deafferented vestibular and ventral cochlear nuclei showed strong vimentin immunoreactivity. Furthermore, double-labelling experiments demonstrated that these vimentin-positive cells were also GFAP-positive. The reaction became evident on the second day after the lesion, was intense for 3-8 days and then declined until day 21. No vimentin immunoreactivity could be detected at the level of the ipsilateral dorsal cochlear nucleus. Therefore, unilateral inner ear lesion induced an astroglial reaction within the deafferented vestibular and cochlear nuclei. The decrease in the resting discharge of the primary vestibular afferents and/or in the deafferented central vestibular neurons may induce the glial reaction in the vestibular complex, whereas both degeneration and silence of the cochlear nerve and central cochlear neurons are most probably responsible for the cochlear vimentin-immunoreactive staining. The role of the reactive astrocytes in the vestibular compensation process remains to be determined.

Animals↗
PubMed1996

GABAergic inhibitory response of locus coeruleus neurons to caloric vestibular stimulation in rats.

We examined the effects of caloric vestibular stimulation on the neuronal activity of the locus coeruleus (LC) in urethane-anesthetized rats. The middle ear cavity was irrigated with hot (44 degrees C) or cold (30 degrees C) water through a polyethylene tube. Most neurons (hot water: 76%, 55/72; cold water: 90%, 19/21) exhibited suppression of neuronal discharge in response to caloric stimulation. The suppression of LC neuronal discharge following caloric stimulation occurred with a long latency (approximately 80 s), and lasted a long period of time (approximately 3 min). Neither caloric stimulation of the auricle, nor irrigation of the middle ear with water at 37 degrees C, nor caloric stimulation of the middle ear after labyrinthectomy inhibited LC neuronal discharge. The caloric stimulation-induced LC neuronal inhibition was significantly attenuated by the intravenous injection of picrotoxin and by the iontophoretic application of bicuculline methiodide. These findings indicate that the predominant effect of caloric vestibular stimulation on LC neuronal discharge is inhibitory, and that the caloric stimulation-induced LC neuronal inhibition is mediated by GABAA receptors located on the membrane of LC neurons. It is suggested that the suppressed activity of noradrenergic LC neurons is involved in the vestibulo-autonomic reflex.

Action Potentials↗
PubMed2006

Histopathology of the peripheral vestibular system after cochlear implantation in the human.

OBJECTIVES: The objective of this study was to describe the histology of the peripheral vestibular system in temporal bones from patients who in life had undergone cochlear implantation and to correlate the findings with previous reports of vestibular dysfunction after cochlear implantation. This is the first quantitative report of the impact of implantation on the vestibular neuronal end organ. METHODSThere were 19 temporal bones available for histologic study. Of these, 17 were suitable for the description of the morphology of the membranous labyrinth, 8 for counting Scarpa's ganglion cells, and 6 for measuring the densities of vestibular hair cells. The bones were fixed, cut, and stained according to previously published methods. Preferably, the implanted electrode was left in situ. Vestibular hair cells were counted with Nomarski's optics. RESULTS: Differences in Scarpa's ganglion cell counts and hair cell densities between the implanted and nonimplanted sides were not statistically significant. In 59% of the implanted bones, the cochlea was hydropic, and in the majority of these bones the saccule was collapsed. CONCLUSION: Cochlear implantation does not cause deafferentation of the peripheral vestibular system. Cochlear hydrops accompanied by saccular collapse is common and may cause attacks of vertigo of delayed onset, similar to Ménière's syndrome as previously reported in several clinical series. Hydrops could be caused by obstruction of endolymphatic flow in the ductus reuniens or in the hook portion of the cochlea or by damage to the lateral cochlear wall caused by implantation.

Aged↗
PubMed2002

Altered cupular mechanics: a cause of peripheral vestibular disorders?

It has taken many decades to arrive at today's concept of cupula mechanics in the stimulation of endolymphatic flows on the hair cells in the ampullae of the semicircular canal. While Steinhausen assumed free swing-door movement of the cupula in the 1930s, Hillman was the first to demonstrate firm cupula attachment to the ampulla wall as a physiological necessity in the 1970s. In contrast to the present clinical concepts of acute peripheral vestibular functional disorders (circulatory disturbances, viral or bacterial infection, altered electrolytes in the endolymph), this study examines the extent to which an impaired attachment mechanism can trigger peripheral vestibular disorders. For this purpose, we used a pigeon model (n = 8), in which mechanical detachment of the cupula from the ampulla wall was achieved by means of a targeted pressure increase in the ampulla of the lateral semicircular canal. In two additional animals the labyrinth was completely destroyed on one side in order to directly compare partial and complete vestibular disorders. In this way partial damage to the lateral semicircular canal ampulla presents a clinical picture whose symptoms are very similar to those of an idiopathic vestibular disorder in humans. Their intensity and course of compensation differ markedly from the symptoms of complete vestibular destruction. Subsequent histological examination revealed that the hair cells remained intact during the experimental detachment of the cupula. Our results thus show that only altered cupula mechanics seem to trigger the clinical picture of a peripheral vestibular disorder. This may result in completely new approaches to differential diagnosis and the therapy of vestibular neuronitis.

Animals↗
PubMed2003

Plurisegmental vestibulocerebellar projections and other hindbrain cerebellar afferents in midterm chick embryos: biotinylated dextranamine experiments in vitro.

The vestibular neuronal groups that project to the cerebellum were mapped in midterm chick embryos (10-11 days in "ovo") through "in vitro " retrograde tracing experiments. Massive unilateral deposits of biotin-dextranamine were placed at the basis of the cerebellum to label the cerebellar peduncles. Separate rostral and caudal vestibulo-cerebellar groups were identified, with predominance of contralateral neurons. We tentatively identified the rhombomeric location of both groups, as well as their topography within the conventional cytoarchitectonically-defined vestibular nuclei, by comparison with previously established segmental fate maps. The rostral group extended from rhombomeres 1-4 (r1-r4) and was restricted mainly to the superior vestibular nucleus. The caudal group stretched from r6 to pseudorhombomere "r8" and was related to the descending and medial vestibular nuclei. The less abundant ipsilateral vestibulocerebellar neurons had a similar topography. The crossing axons of the rostral vestibulocerebellar neurons formed a distinct rostral vestibulocerebellar decussation, restricted to the floorplate of rhombomere 2. The axons of the caudal vestibulocerebellar population mostly decussated associated to the deep cochlear commissure. The present results extend the "segmental hodological mosaic" of defined projection-neuron groups identified within the avian vestibular nuclear complex: The vestibulocerebellar projecting neurons as a type appear iterated from r1 to r4 and from r6 to pseudorhombomere "r8," albeit showing in their arrangement peculiarities related to single segmental domains, particularly rostrally. In contrast, the vestibulospinal groups are located more restrictedly in r4-r6, while the vestibulo-ocular projecting neurons extend from r1 to "r7." Only r4 and r6 contain elements of all three hodological types. The organization of the three vestibular projection populations studied to date seems comparable in chicken and frogs and may be a conserved feature in vertebrates.

Afferent Pathways↗
PubMed1992

Neurotransmitters in the vestibular commissural system of the cat.

The present study focused on the transmitters that control the vestibular neural activity and, in particular, that regulate commissural inhibition. Extracellular spikes of a single vestibular neuron were recorded in decerebrate cats. The seven barrels of the electrode, with the exception of the center barrel, were filled with transmitter candidates and their specific antagonists, while the center barrel was filled with 2 M NaCl for extracellular recording. After isolation of a type 1 neuron, chemicals were iontophoretically applied to examine their effects on its activity. The results were as follows: (1) GABA and glycine markedly decreased spontaneous firing of the neurons, while serotonin did not affect their activity. (2) Bicuculline abolished the inhibitory effects of GABA on the neurons. (3) Strychine abolished the effects of glycine. (4) Commissural inhibition induced by electrical stimulation of the contralateral labyrinth was not abolished by strychine but was abolished by bicuculline. We conclude that (1) vestibular type 1 neurons are controlled by GABAergic and glycinergic but not serotoninergic neurons, and (2) commissural inhibition is activated by the GABAA receptor, but not by the GABAB receptor.

Animals↗
PubMed1977

Ipsilateral utricular and semicircular canal interactions from electrical stimulation of individual vestibular nerve branches recorded in the descending medial longitudinal fasciculus.

Interactions from electrical stimulation of individual vestibular end organ nerves recorded from second order vestibular neurons projecting caudally in the medial longitudinal fasciculus (MLF) have been investigated in unanesthetized, decerebrate decerebellate cats. Canal-canal and utricle-canal interactions were recorded using various condition-test parameters. The brain stem was sectioned to eliminate influence of the contralateral vestibular nuclei, and the condition-test experiments were repeated. The type of interaction observed (inhibition or facilitation) and the degree to which it occurred were dependent on the MLF recording site. Also, in the case of utricular interactions, these were dependent on the site of utricular stimulation. These dependencies indicate a topological arrangement from receptor cell through the second order neuronal projection pathways. Sectioning of the brain stem produced changes in the interaction patterns, indicating masking and/or balancing of the ipsilateral interactions. In interactions between the anterior and posterior canals, instances of no apparent interaction occurring before sectioning converted to inhibition after sectioning. This indicates that some facilitative interaction occurs involving feedback from the contralateral vestibular nuclei, and this facilitation masks or balances ipsilateral inhibition. In interactions between the anterior and horizontal canals, contralateral inhibitory influence masks ipsilateral facilitatory interactions. Contralateral facilitatory influence again balances ipsilateral inhibition in interactions between the horizontal and posterior canals. The degree of inhibition and facilitation observed indicates that considerably more polysynaptic ipsilateral convergence on second order vestibular neurons occurs than has been demonstrated in intracellular studies. Only inhibition was observed when the anterior canal was conditioned by stimulation of the utricular nerve after sectioning. In all other pairings, mixed effects were observed. It is suggested that this is related to known functional connections of semicircular canal second order neurons with neck motoneurons. Not only is canal output affected by utricular activity, but each canal affects utricular output in a different manner.

Afferent Pathways↗
PubMed2002

The three faces of vestibular ganglionitis.

We present temporal bone and clinical evidence that common syndromes of recurrent vertigo are caused by a viral infection of the vestibular ganglion. In the present series, histopathologic and radiologic changes in the vestibular ganglion and meatal ganglion were consistent with a viral inflammation of ganglion cells in cases of Meniere's disease, benign paroxysmal positional vertigo, and vestibular neuronitis. Clinical observations of multiple neuropathies involving cranial nerves V, VII, and VIII on the same side in patients with recurrent vertigo are best explained by a cranial polyganglionitis caused by a neurotrophic virus, which is reactivated by a stressful event later in life. The reactivation of the latent virus may manifest as one of the above vertigo syndromes, depending on the part of the vestibular ganglion that is inflamed, the type and strain of the virus, and host resistance.

Adult↗
PubMed2006

Spatial coding capacity of central otolith neurons.

This review focuses on recent approaches to unravel the capacity of otolith-related brainstem neurons for coding head orientations. In the first section, the spatiotemporal features of central vestibular neurons in response to natural otolithic stimulation are reviewed. Experiments that reveal convergent inputs from bilateral vestibular end organs bear important implications on the processing of spatiotemporal signals and integration of head orientational signals within central otolith neurons. Another section covers the maturation profile of central otolith neurons in the recognition of spatial information. Postnatal changes in the distribution pattern of neuronal subpopulations that subserve the horizontal and vertical otolith systems are highlighted. Lastly, the expression pattern of glutamate receptor subunits and neurotrophin receptors in otolith-related neurons within the vestibular nuclear complex are reviewed in relation to the potential roles of these receptors in the development of vestibular function.

Head Movements↗
PubMedDate not supplied

Effect of hemilabyrinthectomy on monoamine metabolism in the medial vestibular nucleus, locus coeruleus, and other brainstem nuclei of albino and pigmented rats.

We compared in albino and pigmented rats the early effect of unilateral labyrinthectomy (UL) on the concentrations of monoamines (norepinephrine, dopamine, serotonin) and their respective metabolites--3-methoxy,4-hydroxyphenylglycol (MHPG), 3,4-dihydroxy-phenylacetic acid (DOPAC), and 5-hydroxyindoleacetic acid (5HIAA)--in medial vestibular nuclei (MVN), locus coeruleus, raphe dorsalis, and cochlear nuclei. The study was conducted 6 hours after UL in both strains, differing by the functional optokinetic responses of their central vestibular neurons and the time-course of their vestibular compensation. The results show that the monoaminergic changes are different in the two rat strains. In the MVN of albino rats, there was a bilateral increase of MHPG and an ipsilateral increase of dopamine suggesting activation of norepinephrine synthesis and metabolism, whereas no such changes were observed in the MVN of pigmented rats. On the other hand, the simultaneous increase of norepinephrine and DOPAC observed in the contralateral locus coeruleus of albino rats suggested enhanced norepinephrine synthesis, whereas in pigmented rats the decreased norepinephrine content found in the ipsilateral locus coeruleus might reflect an earlier strong stimulation of NE release. These biochemical results confirm the relevant role of locus coeruleus noradrenergic innervation in vestibular compensation and also point out the involvement of norepinephrine of the MVN in the early stages of this process. The different strain-related noradrenergic responses observed on the 6th hour suggest that the involvement of central norepinephrine, particularly from locus coeruleus innervation, may be more crucial and more sustained in the albino than in pigmented rats. No serotonin and 5HIAA changes were found in either brainstem nuclei of albino rats. In contrast, the increase of the ratio 5HIAA/5HT observed in raphe dorsalis, in ipsilateral locus coeruleus, and in both sides of MVN of pigmented rats suggested that UL induced an extended and enhanced utilization of 5HT in this strain.

Albinism↗
PubMed2002

[Effect of pathologic and induced peripheral vestibular balance disturbance on the central nervous system].

The authors investigated the central projection of excitement in acute stage vestibular neuronitis using positron emission tomography. The changes in the pattern of regional cerebral blood flow caused by the disease were compared with the effect of cold caloric stimulation known to provoke similar signs. It was concluded that the involved brain regions overlapped each other only partially. The mismatch could be explained by the compensatory processes developing during the disease. These processes do not normally develop during the caloric vestibular stimulation because of its short duration.

Adult↗
PubMed2002

Effectiveness of the particle repositioning maneuver in benign paroxysmal positional vertigo with and without additional vestibular pathology.

OBJECTIVE: We compared the treatment outcome of patients with benign paroxysmal positional vertigo unassociated with additional objective evidence of vestibular pathology (BPPV) with that in patients who did demonstrate additional vestibular pathology on standard neurotologic testing (BPPV+). STUDY DESIGN: An open, retrospective, record-based study. SETTING: Specialized outpatient dizziness clinic. PATIENTS AND METHODS: We reviewed 58 unselected patients with a Dix-Hallpike test demonstrating positioning nystagmus characteristic of BPPV, who were treated during the past 4 years with the particle repositioning maneuver. Before treatment, all patients underwent detailed clinical and laboratory neurotological testing. MAIN OUTCOME MEASURES: The treatment outcome was assessed with regard to persistence of symptoms and the presence of positioning nystagmus on Dix-Hallpike testing. RESULTS: Seventy-eight percent of patients with BPPV no longer demonstrated characteristic positional nystagmus after 1 particle repositioning maneuver compared with 71% of patients with BPPV+ (p = 0.56) who did, whereas 13% of the BPPV and 14% of the BPPV+ group required more than 1 treatment to be rendered nystagmus negative on Dix-Hallpike testing (p = 0.89). However, 14% of patients with BPPV remained dizzy, compared with 63% patients from the BPPV+ group, despite a negative Dix-Hallpike test after treatment (p = 0.0018). Patients with horizontal canal paresis (n = 15) had a better outcome than patients with central vestibular dysfunction (n = 7, p = 0.006). Etiologic factors seemed to affect outcome-patients with idiopathic BPPV and those with a preceding acute vestibular neuronitis had a tendency for a better outcome than BPPV patients with any other etiology (p = 0.058). CONCLUSION: Our study demonstrates that patients with BPPV+ do not have a worse prognosis with respect to resolution of positional nystagmus, on performing the particle repositioning procedure, compared with patients with uncomplicated BPPV. However, they do suffer incomplete resolution of symptoms because of a coincidental anterior or horizontal canal dysfunction and otolithic or central vestibular dysfunction. It appears that the majority of patients with BPPV+ need further vestibular rehabilitation after the particle repositioning maneuver.

Acute Disease↗
PubMed1993

Neurogenetical segregation of the vestibulospinal neurons in the rat.

The time of origin of the vestibulospinal projection neurons was determined by a double-labeling method using 5-bromodeoxyuridine (BrdU), the thymidine analogue, and Fluoro-Gold (FG), a retrograde fluorescent tracer. Rat fetuses were exposed to BrdU in utero to label the vestibular neurons on one of the embryonic (E) days between E12 and E15. Upon reaching adulthood, the rats were given unilateral injections of FG into the cervical cord to identify the spinal projection neurons. Brainstem sections were immunohistochemically processed for BrdU and then examined for neurons that were both BrdU-positive and FG-positive in the vestibular nuclei. In the lateral vestibular nucleus (LVe), most of the vestibulospinal neurons were generated on E12. In the inferior vestibular nucleus (IVe), the vestibulospinal neurons were produced almost equally on both E12 and E13. In the medial vestibular nucleus (MVe), the vestibulospinal neurons were generated consistently on days between E12 and E14 with a mild peak on E13. The present results thus demonstrate that genesis of the vestibulospinal neurons occurs sequentially in the following order: firstly in the LVe, secondly in the IVe, and finally in the MVe. The different sequential generation of vestibulospinal neurons among the LVe, MVe and IVe may reflect the fact that the vestibulospinal projections are differentially organized depending on the nature of each subnucleus.

Animals↗
PubMed2001

Visuo-vestibular biofeedback in patients with peripheral vestibular disorders.

It is well known that diseases of the vestibular system can be compensated by increased spontaneous activity of other systems engaged in maintaining equilibrium, i.e. proprioceptive and visual systems. A complex approach using multisensory stimulation is the optimal way to achieve vestibular compensation. The aim of our study was to determine the effect of vestibular rehabilitation therapy as measured by posturography in a group of 72 patients suffering from vestibular disorders: Ménière's disease (n = 31), neuritis vestibularis (n = 21) and vertebrobasilar insufficiency (n = 20). Patients underwent the following examinations: electronystagmography; caloric, rotatory and optokinetic tests; computed posturography; craniocorpography; pure-tone audiometry; speech audiometry; and tinnitometry (tinnitus loudness, pitch). The instability in patients with Ménière's disease decreased 3 weeks after starting the therapy; nevertheless, the decrease in area (the surface formed by the movement of the patient's equilibrium point during a defined time) was transitory because of the increase in area values obtained between the 3rd and 6th weeks when measured with closed eyes. In the vestibular neuronitis patients, the measured values of area and the velocity of the patient's movement decreased continuously. The values measured in the patients suffering from vertebrobasilar insufficiency decreased continuously, the absolute values remaining pathological.

Adolescent↗
PubMed1998

Neurotransmitters of vestibular commissural inhibition in the cat.

The present study examined transmitters that regulate commissural inhibition. Extracellular spikes of a single vestibular neuron were recorded in decerebrated cats. Multibarreled electrodes were filled with transmitter candidates (GABA and glycine), their specific antagonists (bicuculline, strychnine) and 2 M NaCl for extracellular recording. After isolation of a type I neuron, chemicals were iontophoretically applied to examine their effects on the activity of the neuron. The results were as follows. Commissural inhibition caused by electrical stimulation of the contralateral labyrinth was not abolished by the application of strychnine (a glycine antagonist), but was abolished by bicuculline (a GABA antagonist). Commissural inhibition was not abolished by phaclofen. Some bicuculline-sensitive neurons, with a short-latency commissural inhibition (presumably disynaptic inhibition), showed spacial summation when the conditioning stimulation (contralateral vestibular nerve stimulation) was applied with the test stimulation (vestibular nucleus stimulation). It was concluded that commissural inhibition was activated by the GABAA receptor, but not by the GABAB receptor, that the inhibitory type I neurons located in the contralateral vestibular nucleus were GABAergic, and that inhibitory type II neurons were also GABAergic neurons.

Animals↗