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At least 19 recordsLinked to original sources
PubMed2003

Central vestibular system: vestibular nuclei and posterior cerebellum.

The vestibular nuclei and posterior cerebellum are the destination of vestibular primary afferents and the subject of this review. The vestibular nuclei include four major nuclei (medial, descending, superior and lateral). In addition, smaller vestibular nuclei include: Y-group, parasolitary nucleus, and nucleus intercalatus. Each of the major nuclei can be subdivided further based primarily on cytological and immunohistochemical histological criteria or differences in afferent and/or efferent projections. The primary afferent projections of vestibular end organs are distributed to several ipsilateral vestibular nuclei. Vestibular nuclei communicate bilaterally through a commissural system that is predominantly inhibitory. Secondary vestibular neurons also receive convergent sensory information from optokinetic circuitry, central visual system and neck proprioceptive systems. Secondary vestibular neurons cannot distinguish between sources of afferent activity. However, the discharge of secondary vestibular neurons can distinguish between "active" and "passive" movements. The posterior cerebellum has extensive afferent and efferent connections with vestibular nuclei. Vestibular primary afferents are distributed to the ipsilateral uvula-nodulus as mossy fibers. Vestibular secondary afferents are distributed bilaterally. Climbing fibers to the cerebellum originate from two subnuclei of the contralateral inferior olive; the dorsomedial cell column and beta-nucleus. Vestibular climbing fibers carry information only from the vertical semicircular canals and otoliths. They establish a coordinate map, arrayed in sagittal zones on the surface of the uvula-nodulus. Purkinje cells respond to vestibular stimulation with antiphasic modulation of climbing fiber responses (CFRs) and simple spikes (SSs). The modulation of SSs is out of phase with the modulation of vestibular primary afferents. Modulation of SSs persists, even after vestibular primary afferents are destroyed by a unilateral labyrinthectomy, suggesting that an interneuronal network, triggered by CFRs is responsible for SS modulation. The vestibulo-cerebellum, imposes a vestibular coordinate system on postural responses and permits adaptive guidance of movement.

Acoustic Stimulation↗
PubMed1999

Effect of noise on the vestibular system - Vestibular evoked potential studies in rats.

Studies have shown that in order for sound to affect the vestibular end organs in the inner ear, very high intensities are required. Furthermore, in patients with noise induced hearing loss, vestibular signs, if present, are subclinical. In order to study possible auditory-vestibular interactions in a more controlled fashion, using physiological sound intensities, the present study used short latency vestibular evoked potentials (VsEPs) to impulses of angular (15,000 degrees /sec(2), risetime 1.5 msec) and linear (3-5 g, risetime 1.5 msec) acceleration were used to study the possible effects of sound on peripheral vestibular function in rats. Four different paradigms were used: a - an intense (135 dB pe SPL) click stimulus was presented 5 msec before the linear acceleration impulse and the VsEP to 128 stimuli were recorded with and without this click stimulus. There was no effect of the preceding intense click on the first wave (reflecting end organ activity) of the linear VsEP. b - 113 dB SPL white noise "masking" was presented while the VsEPs were elicited. A 10-20% reduction in the amplitude of the first VsEP wave was seen during the noise exposure, but 5 minutes after this exposure, there was almost complete recovery to pre-exposure amplitude. c - 113 dB SPL noise was presented for one hour and VsEPs were recorded within 15 minutes of cessation of the noise. The auditory nerve-brainstem-evoked response showed a temporary threshold shift while there was no effect on the VsEP. d - 113 dB SPL white noise was presented for 12 hours per day for 21 consecutive days. Auditory nerve-brainstem-evoked responses and vestibular (VsEPs) function were studied one week after the conclusion of the noise exposure. Auditory function was severely permanently depressed (40 dB threshold elevation and clear histological damage) while the amplitude of wave 1 of the VsEP was not affected. It seems therefore that even though intense noise clearly affects the cochlea and may have a "masking" effect on the vestibular end organs, the intensities used in this study (113 dB SPL) are not able to produce a long-term noise induced vestibular disorder in the initially normal ear. These differences between the response of the cochlear and vestibular end organs to noise may be due to dissimilarities in their acoustic impedances and/or their electrical resting potential.

Journal Article↗
PubMed1999

[Calcitonin gene-related peptide changes in efferent vestibular system during vestibular compensation].

OBJECTIVE: To investigate the calcitonin gene-related peptide (CGRP) effect on efferent vestibular system during pathological state of vestibular afferent system. METHODS: An animal model of vestibular compensation was made by administration of streptomycin to rat vestibular organ to destroy unilateral vestibular function. Change of CGRP in efferent vestibular neurons in all processes from vestibular disorder to vestibular compensation was observed utilizing ABC method of immunohistochemical technique. RESULTS: Efferent vestibular neurons of normal animals showed low immunoreactivity to CGRP. The number of CGRP immunoreactivity neurons and level of CGRP immunoreactivity increased in efferent vestibular system during vestibular disorder, and these changes decreased with vestibular compensation. CONCLUSION: Activity of CGRP in efferent vestibular system plays a regular role on accelerating vestibular compensation.

Animals↗
PubMed2000

Temporal bone studies of the human peripheral vestibular system. Normative vestibular hair cell data.

Quantitative studies of the vestibular system with serially sectioned human temporal bones have been limited because of difficulty in distinguishing hair cells from supporting cells and type I from type II hair cells. In addition, there is only a limited amount of normative data available regarding vestibular hair cell counts in humans. In this study, archival temporal bone sections were examined by Nomarski (differential interference contrast) microscopy, which permitted visualization of the cuticular plate and stereociliary bundle so as to allow unambiguous identification of hair cells. The density of type I, type II, and total numbers of vestibular hair cells in each of the 5 sense organs was determined in a set of 67 normal temporal bones that ranged from birth through 100 years of age. The mean total densities at birth were 76 to 79 cells per 0.01 mm2 in the cristae, 68 cells per 0.01 mm2 in the utricle, and 61 cells per 0.01 mm2 in the saccule. The ratio of type I to type II hair cells at birth was 2.4:1 in the cristae and 1.3:1 in the maculae. There was a highly significant age-related decline in all sense organs for total, type I, and type II hair cell densities that was best fit by a linear regression model. The cristae lost type I cells with advancing age at a significantly greater rate than the maculae, whereas age-related losses for type II cells occurred at the same rate for all 5 sense organs. Hair cell densities in the cristae were significantly higher at the periphery than at the center. There were no significant sex or interaural differences for any of the counts. Mathematical models were developed to calculate the mean and 95% prediction intervals for the total, type I, and type II hair cell densities in each sense organ on the basis of age. There was overall good agreement between the hair cell densities determined in this study and those reported by others using surface preparation techniques. Our data and related models will serve as a normative database that will be useful for comparison to counts made from subjects with known vestibular disorders.

Adolescent↗
PubMed1996

Histopathology of the peripheral vestibular system in small vestibular schwannomas.

Gadolinium-enhanced magnetic resonance imaging can be used to detect small vestibular schwannomas/acoustic neuromas. Early detection raises the question of the necessity of their surgical removal. Do all tumors induce lesions in the vestibule and to what extent? We thus investigated the ultrastructure of peripheral vestibular systems in grades I and II schwannomas. Vestibular tissues were fixed as soon as they were removed during the resection of tumors, by the translabyrinthine approach, and then processed for transmission electron microscope observations. In neurosensory epithelia, hair cells lost stereocilia, whereas cuticular plates disaggregated. The cytoplasm of hair cells degenerated in either a dense or vacuolated manner, and cytoplasmic blisters extended into the endolymph. In some cases, supporting cells extended processes covering the apical surface of hair cells. Nerve fibers massively disappeared from epithelia, only few nerve fibers contacted type I and type II hair cells, and both afferent and efferent terminals were abnormal. In vestibular nerves, axons degenerated, and myelin sheaths disaggregated. Glycogen was present in both intracellular and extracellular spaces. Luse bodies associated with collagen bundles were found between fibers. Scarpa ganglion neurons contained lysosomes/lipofuscin granules and vacuoles. Tumor cells were found in both the ganglion and the vestibular nerve. Thus small tumors induce extensive degeneration of vestibular tissues. The various hallmarks of schwannomas are already present in small acoustic neuromas. Moreover, different types of degeneration of hair cells and neurons were observed, together with the covering of hair cells by supporting cells and the accumulation of glycogen in the vestibular nerve.

Adult↗
PubMedDate not supplied

Parallel auditory vestibular evoked neurogenic and myogenic potential results in a case of peripheral vestibular dysfunction, showing that the former originates from the vestibular system.

PURPOSE: Vestibular evoked myogenic potentials (VEMPs) uses high intensity clicks with recording from the tonically active sternocleidomastoid muscle, taking advantage of the close proximity of the saccule to the oval window. Our group has used the same stimulus to record Vestibular Evoked Neurogenic Potentials (VENPs) directly from the brain. VEMPs are now regarded the electrophysiological gold standard in peripheral vestibular system examination. We present a case of peripheral vestibular dysfunction to show that both VEMPs and VENPs provide similar results during recovery. METHODS: A case of Meniere's Disease in recovery is examined. VEMPs were recorded using a 105 dB nHL click stimulus from the ipsilateral sternocleidomastoid muscle. VENPs were recorded using an ipsilateral parietal to Fpz montage and a 1 kHz tone-pip stimulus. Standard BAEPs and threshold latency series (TLS) were performed. RESULTS: VEMP and VENP were unobtainable from the left side at initial presentation in a patient with Meniere's Disease, with normal BAEP and TLS bilaterally. After one month of therapy both the VEMP and VENP normalized. CONCLUSIONS: As VEMPs are known to originate from the vestibular system, the parallel VENP result suggests the same for the latter VENP may prove to be useful and complement VEMP in determining vestibular dysfunction.

Evoked Potentials, Auditory↗
PubMed1975

[Lesions of the vertical and horizontal systems in the optokinetic vestibular system].

Symptoms of vestibulo-ocular disturbances may be classified into two major groups; i.e., vertical plane and horizontal plane disturbances. Vertical plane symptoms arise from midline lesions of the cerebellum or the brainstem and also from diffuse or symmetrical lesions to either. Vertical plane symptoms also arise from lesions which simultaneously effect both peripheral vestibular systems. Horizontal plane symptoms originate from a unilateral disturbance in the vestibular system. Thus, vertical plane symptoms indicate bilateral disturbances and the symptoms appear symmetrically in the eyes, trunk or extremities. Vertical plane symptoms appear in the sagittal plane, or the plane of the vertical semicircular canals. On the other hand, horizontal plane symptoms appear in the horizontal plane, or the plane of the horizontal semicircular canals.

Cerebellar Ataxia↗
PubMed2006

Intrinsic and synaptic plasticity in the vestibular system.

The vestibular system provides an attractive model for understanding how changes in cellular and synaptic activity influence learning and memory in a quantifiable behavior, the vestibulo-ocular reflex. The vestibulo-ocular reflex produces eye movements that compensate for head motion; simple yet powerful forms of motor learning calibrate the circuit throughout life. Learning in the vestibulo-ocular reflex depends initially on the activity of Purkinje cells in the cerebellar flocculus, but consolidated memories appear to be stored downstream of Purkinje cells, probably in the vestibular nuclei. Recent studies have demonstrated that the neurons of the vestibular nucleus possess the capacity for both synaptic and intrinsic plasticity. Mechanistic analyses of a novel form of firing rate potentiation in neurons of the vestibular nucleus have revealed new rules of plasticity that could apply to spontaneously firing neurons in other parts of the brain.

Action Potentials↗
PubMed1998

Molecular mechanisms of vestibular compensation in the central vestibular system--review.

Vestibular compensation consists of two stages: the inhibition of the contralesional medial vestibular nucleus (contra-MVe) activities at the acute stage after unilateral labyrinthectomy (UL) and the recovery and maintenance of the ipsilesional MVe (ipsi-MVe) spontaneous activities at the chronic stage after UL. In this paper, we reviewed molecular mechanisms of vestibular compensation in the central vestibular system using several morphological and pharmacological approaches in rats. Based on our examinations, we propose the following hypotheses: i) at the acute stage after UL, the activated neurons in the ipsi-MVe project their axons into the flocculus to inhibit the contra-MVe neurons via the NMDA receptor, nitric oxide (NO) and/or GABA-mediated signalling, resulting in the restoration of balance between intervestibular nuclear activities. ii) At the chronic stage after UL, the flocculus depresses the inhibitory effects on the ipsi-MVe neurons via protein phosphatase 2A (PP2A) beta, protein kinase C (PKC) and glutamate receptor (GluR) delta-2, to help the recovery and maintenance of ipsi-MVe activities.

Animals↗
PubMed1986

The effect of loop diuretics on the vestibular system. Assessment by recording the vestibular evoked response.

Whether or to what extent loop diuretics, e.g., ethacrynic acid and furosemide, affect the vestibular system is controversial. We studied this problem by recording in cats the short-latency vestibular evoked response (VsER) to acceleration stimuli by skin electrodes before and after local or systemic administration of loop diuretics. The effect on the VsER was minimal in contrast to the major changes that appeared in the auditory evoked response, in which, among the waves known to originate from the brain stem, the most affected was N1. These findings suggest that the vestibular end-organ function is minimally affected by loop diuretics and that the changes in the vestibulo-ocular reflex reported by several authors might be due to the effect of the drugs on the central nervous system. Thus, recording of the VsER in experimental animal models might serve as a useful tool for direct evaluation of the effect of certain drugs and conditions on the vestibular system.

Animals↗
PubMed1991

Distribution of histaminergic neurons and fibers in rat brain. Comparison with noradrenergic and serotonergic innervation of the vestibular system.

Histamine-immunoreactive cell bodies are strictly confined to the ventral part of the posterior hypothalamus and the region of the mamillary nuclei. They can be divided into two main cell groups with two major ascending projections and one minor descending projection. The ascending histaminergic fiber tracts innervate almost all regions of the di- and telencephalon with high numbers in for instance the median eminence, the nucleus of the diagonal tract of Broca, the caudate-putamen complex and cortical structures. The arrangement of the histaminergic neuronal system, i.e. a compact cell group with a widespread distribution of fibers, resembles that of other monoaminergic (i.e. serotonergic and catecholaminergic) systems. The vestibular system receives a high innervation of serotonergic fibers, a moderate density of noradrenergic fibers and only scattered histaminergic fibers.

Animals↗
PubMedDate not supplied

Neurogenic vestibular evoked potentials in three cases of vestibular system dysfunction.

OBJECTIVES: To demonstrate that neurogenic vestibular evoked potentials (NVsEP) may be specific to the vestibular system using three cases of vestibular system dysfunction and normal auditory function, METHODS: Neurogenic vestibular evoked potentials were performed by recording from the parietal areas of the scalp using a tone-pip auditory stimulus via headphones. Brainstem auditory evoked potentials (BAEPs) and NVsEP were performed in all three cases. RESULTS: Brainstem auditory evoked potentials were within normal limits in all three cases. All three patients showed abnormalities in their NVsEP In the third case, the responses normalized after treatment. CONCLUSIONS: The findings support further the hypothesis that NVsEP are specific to the vestibular system and are a separate response from the BAEP SIGNIFICANCE: Neurogenic vestibular evoked potentials is an easy examination to carry out and can be performed in any clinical neurophysiological laboratory that is familiar with BAEPs. Examinations used to diagnose vestibular system disorders at present include the glycerol dehydration test, electrocochleography, myogenic vestibular evoked potentials and electronystagmography. Neurogenic vestibular evoked potentials may also prove to be useful.

Adult↗
PubMedDate not supplied

Clinical evidence that the vestibular system participates in autonomic control.

The vestibular system, including both the peripheral vestibular system, that is, the labyrinth, and the central vestibular system, is known to influence autonomic function in several ways that have clinical implications. This paper discusses evidence for vestibular influences on autonomic control from normal human subjects, evidence for vestibular influences on autonomic control from patients, clinical implications of vestibulo-autonomic regulation, and speculations regarding possible clinical implications of vestibulo-autonomic control. Situations that provoke vestibular-induced autonomic responses in normal subjects include vestibular laboratory testing, vehicular motion, simulators, and, possibly, exposure to microgravity. Patients with peripheral and central vestibular abnormalities manifest both symptoms and signs of autonomic dysfunction presumably via vestibulo-autonomic connections. Vestibulo-autonomic regulation impacts vestibular diagnostic testing, clinical diagnosis of balance disorders, and treatment of balance disorders. In addition to well-recognized peripheral and central vestibular disorders, anxiety disorders have recently been linked to vestibular dysfunction in a subset of patients. In particular, vestibular dysfunction has been linked to panic disorder and agoraphobia. Vestibular-autonomic connections may form a basis for an association between vestibular dysfunction and panic attacks. The importance of vestibulo-autonomic regulation in the clinical arena is not fully known. Two speculative areas discussed in this paper include vestibular-induced orthostatic intolerance and the role of vestibular-respiratory pathways on sleep apnea.

Autonomic Nervous System↗
PubMed1985

Directional asymmetries of optokinetic nystagmus: developmental changes and relation to the accessory optic system and to the vestibular system.

To investigate the relation of the directional organization of the accessory optic system (AOS) to that of its principal behavioral output, optokinetic nystagmus (OKN), we measured the eye velocity during OKN in response to 14 directions of stimulus motion, including horizontal, vertical, cyclorotational (rotations about the optic axis), and intermediate directions in both neonatal and older chickens. We found substantial and consistent OKN asymmetries between opposite directions of stimulus motion when the stimuli were viewed monocularly; the asymmetries were largest to combinations of cyclorotational and vertical stimulus motion and to horizontal stimulus motion. The highest gain of OKN in the older animals was in response to two directions of stimulus motion: horizontal temporal-to-nasal and a combination of excyclorotation and downward. In addition, OKN to upward moving stimuli was consistently better than to downward stimuli. The association of high OKN gain in the older animals with the pattern of visual motion produced by head movements exciting the contralateral anterior semicircular canal suggests a possible vestibular organization of the optokinetic system. The response pattern of the newly hatched chickens differed in three ways from that of the older animals: in the non-horizontal stimulus directions the best direction was to upward and excyclorotational stimulus motion; the horizontal asymmetry was somewhat less strong; and the OKN gain to high velocity horizontal stimulus motion was lower. The change in directional pattern of OKN over the first weeks of life appears related to a corresponding change in anatomy of the AOS.

Animals↗
PubMed1999

Dizziness in the elderly and age-related degeneration of the vestibular system.

The peripheral and central vestibular systems exhibit an age-related structural deterioration which may be responsible for vestibular reflex deficits and dizziness in the elderly. However, it seems likely that the central nervous system is capable of compensating for a certain degree of decline in function, since not all elderly people are impaired to the extent that the clinical signs of vestibular dysfunction are apparent. Dizziness and other vestibular disorders may develop only when the degree of deterioration of the vestibular system exceeds the ability of the nervous system to compensate. If dizziness does eventuate, it can have profound psychological consequences, particularly in terms of loss of confidence in independent activity, and may lead to the development of anxiety disorders. Vestibular rehabilitation programs may help to minimise the effects of age-related deterioration of the vestibular system and its psychological impact.

Aged↗