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Results for “VESTIBULAR APPARATUS”

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PubMed1994

[Vestibular neuritis].

Vestibular neuronitis is an acute disorder of the vestibular apparatus which manifests by sudden vertigo, without apparent cause, and without auditory or neurological symptoms. Clinically and by thermal stimulation tests, it is characterised by unilateral peripheral vestibular deficit. Evolution is favourable in several days to several weeks and prognosis is favourable, although disorders of moderate intensity may rather often persist, in the form of positional vertigo, sometimes paroxysmal, or disorders of equilibrium on abrupt movement. Careful history-taking and clinical examination, routine evaluation of the vestibular-cochlear apparatus and follow-up of the patient during the first days can eliminate the possibility of vascular cerebellar syndrome, which would require emergency imaging and possibly recuperation by surgery. The aetiology of vestibular neuronitis remains mysterious: inflammatory, viral, vascular? Sedatives acting on the vestibular system should be given for only a very limited time; they inhibit the mechanism of central compensation, which is on the contrary favoured by early vestibular function and rehabilitation.

Acute Disease↗

PubMed2004

Brain injury after head trauma: pathophysiology, diagnosis, and treatment.

Brain injury after impact to the head is due to both immediate mechanical effects and delayed responses of neural tissues. In horses, traumatic brain injury occurs in three main settings: (1) poll impact in horses that flip over backwards; (2) frontal/parietal impact in horses that run into a fixed object, and (3) injury to the vestibular apparatus secondary to temporohyoid osteoarthropathy. Distinct forebrain, vestibular, midbrain, hindbrain, or multifocal syndromes may be encountered in horses with traumatic brain injury. The most important components of treatment are those consistent with principles of "evidence-based medicine". Accordingly,secondary brain injury can most effectively be prevented by establishing normal blood pressure, temperature, blood glucose concentration, and tissue oxygenation. Pain must be controlled and brain swelling may be treated with infusions of hypertonic saline or mannitol. Surgical procedures, including unilateral hyoid bone transaction or elevation of skull fracture fragments, are indicated in selected cases. Optional additional treatments include use of anti-oxidants, conventional doses of corticosteroids, magnesium sulfate and drainage of CSE There is no indication for the use of massive doses of methyl prednisolone sodium succinate.

Animals↗

PubMed1976

[Effect of vestibular, somatic and autonomic afferent impulsation on the activity of individual neurons in the nuclei of the cat vestibular complex].

Responses of single vestibular neurons were studied in cats under adequate and electric stimulation of different afferent sources (labyrinths, mixed nerves, n. vagus, n. depressor, limb movements). Different types of responses to the employed stimulation as well as evoked activity as bursts followed by depression of background firing are described. The activity of vestibular neurons is shown to depend on extralabyrinthal stimulation. The role of muscle-joint receptors is distinguished from natural stimulation of the vestibular apparatus during the head tilting. Somatotopic organization of vestibular nuclei and convergence of different afferental impulses to the neurons forming the vestibulospinal tract are discussed.

Animals↗

PubMed1987

Lack of effects of astemizole on vestibular ocular reflex, motion sickness, and cognitive performance in man.

Astemizole was orally administered to 20 subjects in a randomized, double-blind design to assess the efficacy of this peripherally active antihistamine as an antimotion sickness drug possessing no central side-effects. Measures of vestibular ocular reflex (VOR) were made to evaluate the agent as a selective vestibular depressant. Following 1 week of orally administered astemizole (30 mg daily), a Staircase Profile Test, a VOR test, and a variety of tests of cognitive performance were administered. These tests revealed no statistically significant effects of astemizole. This leads us to conclude that, although the drug probably reaches the peripheral vestibular apparatus in man by crossing the blood-vestibular barrier, a selective peripheral antihistamine (H1) action is inadequate to control motion sickness induced through cross-coupled accelerative semicircular canal stimulation in a rotating chair.

Adolescent↗

PubMed1991

Head acceleration following linear translations in the freely-standing cat.

The aim of this study was to determine whether vestibular information related to head acceleration is available for triggering postural responses to perturbations of stance in the freely-standing cat. Linear accelerations of the head were recorded during postural responses evoked by linear translations of the support surface. A consistent initial peak of acceleration was observed at an average latency of 22 ms and magnitude of 0.03 g (g is acceleration due to gravity, 9.8 m/s/s). The acceleration peak preceded the first evoked EMG activity by an average of 24 ms. It was concluded that stimulation of the vestibular apparatus was both adequate and early enough for the vestibular system to have triggered the automatic postural response.

Animals↗

PubMed2003

Anodal vestibular stimulation does not suppress vestibular reflexes in human subjects.

Anodal current applied to the vestibular apparatus has previously been found to inhibit discharge from irregular vestibular afferents in squirrel monkeys. We wished to investigate whether anodal currents applied over the mastoid processes of human subjects would significantly reduce ongoing vestibular activity and thereby the size of galvanic-evoked vestibulospinal reflexes, measured by soleus electromyogram. Nine subjects were tested, of whom six subjects (five females, one male) provided data for the final analysis. Tonic anodal current was applied over one mastoid at 0 (baseline), 2, 4, 6 and 8 mA. The cathode was placed at C7. Superimposed on each intensity of tonic current were separate, short anodal currents of 4 mA, duration 20 ms, presented as 128 stimuli to the same side, and used to test vestibular responsiveness. These trials were then repeated with the anode overlying the contralateral mastoid. Short latency (SL) and medium latency (ML) reflexes were measured from the right soleus muscle. All six subjects used in the final analysis had readily identifiable reflexes to all stimuli. One-way ANOVA revealed no significant difference in the magnitude of the SL ( P=0.99) or ML ( P=0.96) components of the vestibulospinal reflexes across the group. Despite surface anodal currents of up to 8 mA, there was no consistent effect on the size of galvanic-evoked vestibulospinal reflexes. As 8 mA is close to the maximum intensity tolerated by volunteer subjects, our results indicate that anodal current applied over the mastoids is unlikely to be a useful means of suppressing vestibular function in human subjects.

Adult↗

PubMedDate not supplied

Sudden vertigo of central origin.

Intense vertiginous attacks with sudden onset and of several months' duration were observed in a group of patients following viral infection. Neurotological examination revealed different types of signs of involvement of the central vestibular apparatus. All of these patients became dizzier when medicated with vestibular depressor drugs, and could obtain symptomatic relief with corticosteroids. They became asymptomatic after a period of 3-4 months from the onset of the disease, but the signs of central vestibular involvement persisted for 6-12 months.

Adolescent↗

PubMed1994

Physiological properties of vestibular primary afferents that mediate motor learning and normal performance of the vestibulo-ocular reflex in monkeys.

We have used electrical stimulation of the vestibular apparatus to reveal parallels between the physiological responses of the vestibular afferents activated at different currents and the properties of the evoked eye movements before and after magnifying spectacles had been used to cause motor learning in the vestibulo-ocular reflex (VOR). Stimulation with the lowest currents caused little or no eye motion, but activated all the afferents with irregular spontaneous discharge, low sensitivities to head velocity, and highly phasic responses during rapid head turns. Stimulation with moderate currents caused substantial eye motion that was weakly affected by motor learning; these currents activated afferents with a wide range of physiological properties, including many that had intermediate discharge regularity, high sensitivity to head velocity, and clear phasic responses during rapid head turns. Stimulation at still higher currents caused still larger eye movements that were strongly altered by motor learning; these currents activated primarily afferents that had regular spontaneous discharge, lower sensitivities to head velocity, and tonic responses during rapid head turns. Stimulation at the highest currents did not cause any further increment in the amplitude of the evoked eye movement, but activated the afferents with the most regular spontaneous discharge and the lowest sensitivities to head velocity. The data imply that the VOR pathways receive substantial vestibular inputs from afferents with a middle range of thresholds for electrical stimulation. These afferents have a wide range of physiological properties, including a large group that shows substantial phasic responses during rapid head turns. The data also suggest that only a subset of these afferents, primarily those with more regular spontaneous discharge, project into the VOR pathways that are modified in association with motor learning.

Afferent Pathways↗

PubMed2002

What does galvanic vestibular stimulation stimulate?

The technique of galvanic vestibular stimulation (GVS) has been used for a long time. The stimulus produces stereotyped automatic postural and ocular responses. The mechanisms underlying these responses are not understood although they are commonly attributed to altered otolith output. Based on animal studies, it seems reasonable to assume that vestibular afferents from the otoliths and semicircular canals are affected similarly by GVS. With this assumption, and anatomical knowledge of the vestibular apparatus, a model is developed to describe the expected responses of vestibular afferents to percutaneous GVS and the physiological implications of this altered sensory signal. Bilateral bipolar GVS, the most commonly used technique, should produce a canal signal consistent with a strong ear-down roll towards the cathodal side, a smaller nose-to-cathode yaw, but no pitch signal. Bilateral bipolar GVS should also produce an otolith signal consistent with tilt towards the cathodal side or a translational acceleration towards the anodal side. The expected responses for other configurations of GVS are also described. The model appears consistent with published data on the ocular and postural responses to GVS, and suggests other testable hypotheses concerning postural, ocular and perceptual responses to GVS.

Animals↗

PubMed1997

Sound-evoked activity in primary afferent neurons of a mammalian vestibular system.

HYPOTHESIS: Some primary vestibular afferents in the cat respond to sound at moderately intense sound levels. BACKGROUND: In fish and amphibians, parts of the vestibular apparatus are involved in audition. The possibility was explored that the vestibular system in mammals is also acoustically responsive. METHODS: Microelectrodes were used to record from single afferent fibers in the inferior vestibular nerve of the cat; some acoustically responsive fibers were labeled intracellularly with biocytin. RESULTS: Vestibular afferents with regular spontaneous activity were unresponsive to sound, whereas a sizable fraction of vestibular afferents with irregular activity were acoustically responsive. Labeling experiments demonstrated that acoustically responsive afferents innervate the saccule, have cell bodies in Scarpa's ganglion, and project to central regions both inside and outside the traditional boundaries of the vestibular nuclei. Acoustically responsive vestibular afferents responded to sound with shorter latencies than cochlear afferents but had higher thresholds (> 90 dB sound pressure level) and responded only in the range 0.1-3.0 kHz. In contrast to cochlear afferents, efferent stimulation excited background activity and proportionately increased sound-evoked responses in these vestibular afferents, that is, there was centrally mediated enhancement of gain (gain = spike-rate/motion). CONCLUSIONS: The evolutionary conservation of a saccular auditory pathway in mammals suggests that it confers survival advantages. Recent evidence suggests that acoustically responsive saccular afferents trigger acoustic reflexes of the sternocleidomastoid muscle, and hence measurement of such reflexes may provide a relatively simple test for saccular dysfunction.

Acoustic Stimulation↗

PubMedDate not supplied

Body volume changes during simulated microgravity: auditory changes, segmental fluid redistribution, and regional hemodynamics.

Space adaptation syndrome (SAS), manifested by cephalad fluid shifts, spacial disorientation, nausea, and vomiting, is of varied expression and uncertain etiology. One theory is that fluid shift to the upper body alters the function of the vestibular apparatus to create an entity similar to Meniere's disease. Since clinical vestibular dysfunction syndromes are mirrored by altered cochlear function, this experiment was undertaken to study the relation between fluid redistribution and the auditory effects of initial antiorthostatic bed rest. Manual and bone audiometry, impedance tympanometry, and brain-stem evoked potentials were used to monitor auditory changes prior to, during, and following short term exposure to -6 degrees head down tilt. Impedance plethysmography was performed to assess the segmental and intracranial fluid redistribution and hemodynamic changes during short-term head down tilt simulated microgravity. Even though significant cephalad fluid shift produced marked intracranial congestion and the subjects exhibited SAS symptoms, no clinically significant changes in the auditory system could be detected.

Acoustic Impedance Tests↗

PubMed2006

Vestibular evoked potentials (VsEPs) in patients with severe to profound bilateral hearing loss.

OBJECTIVE: To confirm the exclusive vestibular dependence of the evoked potentials (P10 and N15) recorded in normal subjects, by recording the potentials evoked in response to bone-conducted sound stimulation in patients with bilateral hearing loss. METHODS: Fourteen patients with severe to profound bilateral hearing loss were stimulated via a B71 bone-vibrator above the mastoid with bone-conducted tone bursts (500 Hz, 6 ms) at fixed levels above their individual vestibular evoked myogenic potential (VEMP) thresholds. Surface potentials were recorded from scalp electrodes at F7, F3, Fpz, F4, F8, T3, Cz, and T4 and referred to linked earlobes. RESULTS: Seven of 14 patients had suitable VEMPs to the maximal stimulus. P10 and N15 potentials were present in each of these 7 patients, but were absent in patients with absent VEMP responses. The potentials were only detected above VEMP threshold, and were similar in size, shape and latency to those recorded in normal controls at a matched intensity above VEMP threshold. CONCLUSIONS: Normal P10 and N15 potentials can be recorded from patients with profound bilateral hearing loss using bone-conducted acoustic stimulation of the vestibular apparatus. SIGNIFICANCE: The P10 and N15 appear to be dependent purely upon vestibular activation.

Acoustic Stimulation↗

PubMed1988

Conditioned taste aversion induced by motion is prevented by selective vagotomy in the rat.

The role of the vagus nerve in motion-induced conditioned taste aversion (CTA) was studied in hooded rats. Animals with complete, selective gastric vagotomy failed to form conditioned taste aversion after multiple conditioning sessions in which the conditioned stimulus (a cider vinegar solution) was drunk immediately before a 30-min exposure to vertical axis rotation at 150 degrees/s. Results are discussed with reference to the use of CTA as a measure of motion-induced "sickness" or gastrointestinal disturbance, and, because motion-induced CTA requires that both the vagus nerve and the vestibular apparatus be intact, in light of the possible convergence of vagal and vestibular functions.

Afferent Pathways↗

PubMed1998

Motion sickness susceptibility correlates with otolith- and canal-ocular reflexes.

Since motion sickness (MS) never occurs in individuals who lack functional vestibular apparatus, it has been suggested that MS susceptible individuals have more sensitive vestibular systems than non-susceptible people. However, previous investigations involving only stimulation of the semi-circular canals have been inconclusive. We measured gain and time constant (TC) of horizontal canal-ocular reflex (COR) and magnitude of otolith-ocular reflex (OOR). We found that MS susceptibility was not correlated to COR gain but was negatively correlated to OOR magnitude. Thus, MS susceptible individuals do not have more sensitive vestibular systems. We also found a positive correlation between MS susceptibility and TC. We hypothesize that central vestibular integration (velocity storage mechanism), by increasing low frequency vestibular inputs, would favour MS.

Adult↗

PubMed1991

The influence of rotary vestibular stimulation upon motor development of nonhandicapped and Down syndrome infants.

The vestibular system plays a major role in the expression of early motor behavior. Previous research has cited extensive neural connections between the vestibular apparatus and the motor system. Accordingly, some therapists have implemented programs of supplemental vestibular stimulation to improve motor and cognitive abilities in children with delayed motor development. In the present study a quantifiable regimen of supplemental rotary vestibular stimulation was administered in a cross-over longitudinal design to nonhandicapped and Down syndrome infants. Time constants, considered a measure of habituation in the vestibular system, were derived from postrotary nystagmus. Results indicated that supplemental rotary vestibular stimulation produced no measurable gain in motor ability beyond that evident in control periods. In addition, it was determined that children exhibited greater gains in motor skills in the early phase of the study, regardless of experimental condition. A positive correlation was found between changes in time constant and motor development.

Down Syndrome↗

PubMed1998

Vestibular adaptation: how models can affect data interpretations.

Vestibular adaptation can be induced optically or by chemical or physical injury to the vestibular apparatus or the brain stem. In searching for the sites or mechanisms of vestibular adaptation, neurophysiologists often rely on comparing central resting (background) activities and central modulations (sensitivity) during vestibular stimulation, before and after motor learning or vestibular compensation. It is assumed that adapted central sites must exhibit modulation changes that parallel vestibulo-ocular reflex changes. Using model simulations and analysis, we will show that such presumptions may be misleading. First, using a simple schematic of interconnected cells or nuclei, one can show that modulation depth and background "tone" can be modified (or fixed) independently, using weightings on direct or indirect afferent projections. That is, if synaptic weights along all stimulus pathways are altered, one may fix or strongly modify central premotor characteristics in a manner apparently unrelated to global reflex changes. In the vestibulo-ocular reflex, the dominant premotor pathways contain position-vestibular-pause cells and eye-head-velocity cells (which are behaviorally similar to floccular-target neurons). Several experiments have reported negligible changes in the velocity sensitivity of position-vestibular-pause cells, despite large gain changes in the vestibulo-ocular reflex induced by training with visual-vestibular conflict. On the other hand, the modulation changes on floccular-target neurons (position-vestibular-pause) can be much larger than the changes in reflex gain. Using a bilateral vestibulo-ocular reflex model, we show that overall increases or decreases in reflex gain can be expressed (even overexpressed) in one particular subgroup of premotor neurons. Nevertheless, such observations are theoretically compatible with synaptic changes on all primary projections in a widely interconnected central network. Hence, stable neural responses during reflex adaptation are not sufficient to exclude a potential site of sensory-motor adaptation. Similarly, modified neural responses (as in cerebellum) need not necessarily imply a direct role in supporting the adapted state. Model predictions should help to design additional experimental protocols, to test hypotheses, and to refine diagnostic measures of recovery after vestibular lesions.

Adaptation, Physiological↗

PubMed2001

Morphological alterations in the inner ear of the arylsulfatase A-deficient mouse.

Metachromatic leukodystrophy of humans is an inherited sulfatide lipidosis due to deficiency of arylsulfatase A (ASA). As an animal model, ASA(-/-) mice have been generated. A previous study showed that the mice lose most of their spiral (acoustic) ganglion cells and develop deafness by the end of the first year of life. The present report describes the sulfatide histochemistry and ultrastructure of the inner ears of ASA(-/-) mice at 0.5-26 months of age. Lysosomal accumulation of sulfatides was observed in various cell types such as Schwann cells that maintain the myelin sheaths around the spiral and vestibular ganglion cells, periaxonal Schwann cells, macrophages, and spiral and vestibular ganglion cell perikarya. In the spiral ganglion, the only surviving neurons were those which are primarily non-myelinated (type 2 cells). However, the myelinated spiral neurons and their processes were rarely encountered within the process of dying, suggesting that this was a rather rapid process. Since the myelin sheaths around dying perikarya and axons appeared structurally normal, the primary cause of the neuronal cell death seems to reside in the neuron. In contrast to the spiral ganglion, the vestibular ganglion as a whole survived throughout the period of observation. The organ of Corti and the vestibular apparatus appeared preserved at the light microscopic level, despite massive sulfatide storage in the vestibular hair cells.

Animals↗

PubMed1996

Trigeminal motoneuron responses to vestibular stimulation in the guinea pig.

Experiments performed in the guinea pig were aimed at evaluating the effect of electric or caloric stimulations of the vestibular afferents on the electrical activity of the jaw-closing and jaw-opening trigeminal motoneurons. Results showed that masseter and digastric motoneurons mainly responded to vestibular ampullar activation with excitatory responses, with latencies being shorter for contralateral than ipsilateral ampullar stimulation. Differences in latencies between the jaw-closing and jaw-opening trigeminal motoneurons were observed: the masseter motoneurons constantly responded about 2 msec earlier than the digastric motoneurons. These results suggest that the vestibular-trigeminal relationship is quite complex and uses multiple systems to connect the vestibular apparatus with the trigeminal motor nuclei. From the functional point of view, the vestibular-trigeminal relationship may play a role in the dynamic control of the jaw muscle tone during head movements.

Animals↗