Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Vestibular Neuronitis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,477 records · Page 82Linked to original sources

Immunochemical and immunohistochemical localization of parvalbumin in rat nervous tissues.

The contents of parvalbumin in various nervous tissues of the rat were measured by radioimmunoassay (RIA) and its cellular distribution was immunohistochemically examined by peroxidase-antiperoxidase methods. The antibody, raised in rabbits using rat skeletal muscle parvalbumin, did not cross-react with other Ca2+-binding proteins such as calmodulin or S-100 proteins. The RIA demonstrated the wide distribution of the antigen, with very high levels in the cerebellum (3,217 +/- 519 ng/mg protein). The immunohistochemical description by Celio and Heizmann [Nature 293, 300-302 (1981)] was confirmed concerning the existence of the antigen in Purkinje cells of the cerebellum; nonpyramidal neurons of the cerebral cortex; and medium-sized cells of the olfactory bulb, hippocampus, and reticular nucleus of the thalamus. In addition to these neurons, we found the parvalbumin-like immunoreactivity in the large neurons of the superior vestibular nucleus and the neurons of the medial superior olive nucleus. In the gamma-aminobutyric acid (GABA)-containing nuclei such as substantia nigra, caudatoputamen, and globus pallidus, parvalbumin-positive cells and fibers were rare. In the medial lemniscus of the midbrain which contains no GABA, parvalbumin-immunoreactive fibers were prominent. The possibility was discussed that parvalbumin exists in a specific population of neurons that differ from those containing GABA.

Animals↗

Functional organization of primate translational vestibulo-ocular reflexes and effects of unilateral labyrinthectomy.

Translational vestibulo-ocular reflexes (trVORs) are characterized by distinct spatio-temporal properties and sensitivities that are proportional to the inverse of viewing distance. Anodal (inhibitory) labyrinthine stimulation (100 microA, < 2 s) during motion decreased the high-pass filtered dynamics, as well as horizontal trVOR sensitivity and its dependence on viewing distance. Cathodal (excitatory) currents had opposite effects. Translational VORs were also affected after unilateral labyrinthectomy. Animals lost their ability to modulate trVOR sensitivity as a function of viewing distance acutely after the lesion. These deficits partially recovered over time, albeit a significant reduction in trVOR sensitivity as a function of viewing distance remained in compensated animals. During fore-aft motion, the effects of unilateral labyrinthectomy were more dramatic. Both acute and compensated animals permanently lost their ability to modulate fore-aft trVOR responses as a function of target eccentricity. These results suggest that (1) the dynamics and viewing distance-dependent properties of the trVORs are very sensitive to changes in the resting firing rate of vestibular afferents and, consequently, vestibular nuclei neurons; (2) the most irregularly firing primary otolith afferents that are most sensitive to labyrinthine electrical stimulation might contribute to reflex dynamics and sensitivity; (3) inputs from both labyrinths are necessary for the generation of the translational VORs.

Adaptation, Physiological↗

Exercise and drug therapy alter recovery from labyrinth lesion in humans.

Acute unilateral vestibular failure is characterized by rotatory vertigo, horizontal-rotatory nystagmus, and postural imbalance, all of which last from days to weeks. These signs and symptoms are caused by a vestibular tone imbalance between the two labyrinths. Recovery results from a combination of peripheral restoration of labyrinthine function (usually incomplete) and central vestibular compensation (CVC) of the vestibular tone imbalance. Acute unilateral failure is most often caused by vestibular neuritis, which is most likely due to the reactivation of a latent HSV-1 infection. Therefore, therapeutic strategies to improve the outcome of VN are theoretically based on two principles: (a) vestibular exercises and drugs to improve CVC and (b) drug treatment of the assumed viral inflammation. The following conclusions can be drawn from studies in animals and/or humans: (1) There is strong evidence that vestibular exercises may improve vestibulo-spinal compensation. These exercises should begin as early as possible after symptom onset. Moreover, slower exercises are likely to be more effective than faster exercises because slower ones seem to depend more on the vestibular system. (2) Despite extensive data from animal experiments indicating that drugs have a favorable effect on CVC, this has not been clinically proven and thus cannot be recommended yet. (3) Preliminary results of an interim analysis from an ongoing randomized, prospective study showed that methylprednisolone (plus an antiviral agent?) may be useful for improving peripheral vestibular function in vestibular neuritis.

Acyclovir↗

Impulsive testing of individual semicircular canal function.

In order to test the human angular vestibulo-ocular reflex in the dynamic range of normal head movements, we measured 3-dimensional compensatory eye-movement responses to low-amplitude (10-12 degrees), high-acceleration (3000-4000 degrees/s/s), passive, manually delivered head rotations (head "impulses") in the three planes of the semicircular canals in normal subjects, in subjects who had recovered from surgical unilateral vestibular deafferentation, and in patients after acute unilateral peripheral vestibulopathy, that is, from vestibular "neuritis." We found that canal-plane head impulses away from an intact semicircular canal, that is, toward a lesioned semicircular canal, invariably produce a vestibulo-ocular reflex with permanently low gain, typically less that 0.4 if the lesion is complete. These results are a necessary consequence of primary semicircular canal afferents being driven into inhibitory saturation by rapid angular accelerations. With practice, clinicians can learn to recognize the telltale compensatory saccades that patients with unilateral loss of semicircular canal function will make if asked to look at an earth-fixed target during head impulses in any one of the three semicircular canal planes.

Head Movements↗

Simulations of cochlear nucleus neural circuitry: excitatory-inhibitory response-area types I-IV.

Several circuitry schemes have been explored among model stellate and fusiform cochlear nucleus neurons in an effort to reproduce excitatory-inhibitory response-area (EIRA scheme) types I-IV. Single cell models incorporated known nonlinear membrane properties and spike-discharge characteristics, as described in previous modeling and intracellular recording. In addition, a unique method of implementing dendritic electrotonic distance processing was developed that provides greater computational efficiency, but with results similar to compartmental models. As an initial simple case, results were examined for a kHz pure tone. Auditory nerve (AN) population responses across characteristic frequencies from 200 Hz to 50 kHz based on actual single unit recordings were incorporated into the model as input. The findings and conclusions are (1) relatively simple inhibitory connections among stellate and fusiform cells, all of which receive AN excitatory inputs, can account for the salient features of EIRA-scheme types I-IV; (2) both types III and IV may be obtained using fusiform cells with small adjustments in the anatomical connections; (3) if stellate cells laterally inhibit their own neighbors, they can create inhibitory sidebands, but may have difficulty avoiding multiple sidebands; (4) in the model, type II cells are not responsive to broadband noise but rather to pure tones, and the reason for this was partly because the type II cells were inhibited by other CN units, and partly because the simulated AN fiber response to broadband noise was near their threshold; and (5) the type IV complex response areas may actually arise not necessarily because of elaborate circuitry, but as a result of a complex AN fiber population profile at high stimulus levels in conjunction with the type II inhibitory input to the type IV cells.

Acoustic Stimulation↗

Gangliosides in isolated neurons and glial cells.

Gangliosides occur in much greater amounts in clean isolated neurons and in the neuropil teased from immediately around the neuron cell body and dendrites than in isolated clumps of glial cells. Since the zone of neuropil adjacent to neurons is richest in terminal axons and synaptic endings, these findings indicate a specific concentration of these sialoglycolipids in synaptic membranes.

Animals↗

Interaction of somatoform and vestibular disorders.

BACKGROUND: The high coincidence of organic vestibular and somatoform vertigo syndromes has appeared to support pathogenic models showing a strong linkage between them. It was hypothesised that a persisting vestibular dysfunction causes the development of anxiety disorders. OBJECTIVE: To determine the relation between vestibular deficits and somatoform vertigo disorders in an interdisciplinary prospective study. METHODS: Participants were divided into eight diagnostic groups: healthy volunteers (n=26) and patients with benign paroxysmal positioning vertigo (BPPV, n=11), vestibular neuritis (n=11), Menière's disease (n=7), vestibular migraine (n=15), anxiety (n=23), depression (n=12), or somatoform disorders (n=22). Neuro-otological diagnostic procedures included electro-oculography with rotatory and caloric testing, orthoptic examination with measurements of subjective visual vertical (SVV) and ocular torsion, and a neurological examination. Psychosomatic diagnostic procedures comprised interviews and psychometric instruments. RESULTS: Patients with BPPV (35.3%) and with vestibular neuritis (52.2%) had pathological test values on caloric irrigation (p<0.001). Otolith dysfunction with pathological tilts of SVV and ocular torsion was found only in patients with vestibular neuritis (p<0.001). Patients with Menière's disease, vestibular migraine, and psychiatric disorders showed normal parameters for vestibular testing but pathological values for psychometric measures. There was no correlation between pathological neurological and pathological psychometric parameters. CONCLUSIONS: High anxiety scores are not a result of vestibular deficits or dysfunction. Patients with Menière's disease and vestibular migraine but not vestibular deficits showed the highest psychiatric comorbidity. Thus the course of vertigo syndromes and the possibility of a pre-existing psychopathological personality should be considered pathogenic factors in any linkage between organic and psychometric vertigo syndromes.

Adult↗

Absence of nystagmus during REM sleep in patients with vestibular neuritis.

Saccades, including fast phases of nystagmus, disappear during drowsiness and non-rapid eye movement (NREM) sleep, but are present during the alert state and REM sleep. The purpose of this study was to determine whether spontaneous nystagmus is present in patients with vestibular neuritis during REM sleep. Eight patients with spontaneous nystagmus due to vestibular neuritis and eight control patients without any nystagmus underwent at least one night of polysomnography. Fast phases of nystagmus were analyzed. The number of right and left horizontal saccades were counted, first during 3-5 minute samples of the awake state before sleep onset, then during the first REM episode and the last REM episode of nocturnal sleep, and finally during the alert state in the morning after nocturnal sleep. All patients with vestibular neuritis showed significantly more saccades (fast phases) towards the side contralateral to their vestibular lesion in the awake state before and after the polysomnography. This reflects their spontaneous nystagmus. By contrast, during REM sleep the patients with vestibular neuritis showed no preponderance in saccade direction. The eye movement pattern in REM was the same for patients and controls. In conclusion, peripheral vestibular imbalance producing nystagmus in vestibular neuritis in the awake state is not active at the brain stem level during REM sleep.

Aged↗

Effects of postural changes and vestibular lesions on genioglossal muscle activity in conscious cats.

Previous studies in humans showed that genioglossal muscle activity is higher when individuals are supine than when they are upright, and prior experiments in anesthetized or decerebrate animals suggested that vestibular inputs might participate in triggering these alterations in muscle firing. The present study determined the effects of whole body tilts in the pitch (nose-up) plane on genioglossal activity in a conscious feline model and compared these responses with those generated by roll (ear-down) tilts. We also ascertained the effects of a bilateral vestibular neurectomy on the alterations in genioglossal activity elicited by changes in body position. Both pitch and roll body tilts produced modifications in muscle firing that were dependent on the amplitude of the rotation; however, the relative effects of ear-down and nose-up tilts on genioglossal activity were variable from animal to animal. The response variability observed might reflect the fact that genioglossus has a complex organization and participates in a variety of tongue movements; in each animal, electromyographic recordings presumably sampled the firing of different proportions of fibers in the various compartments and subcompartments of the muscle. Furthermore, removal of labyrinthine inputs resulted in alterations in genioglossal responses to postural changes that persisted until recordings were discontinued approximately 1 mo later, demonstrating that the vestibular system participates in regulating the muscle's activity. Peripheral vestibular lesions were subsequently demonstrated to be complete through the postmortem inspection of temporal bone sections or by observing that vestibular nucleus neurons did not respond to rotations in vertical planes.

Animals↗

Transmission between type II hair cells and bouton afferents in the turtle posterior crista.

Synaptic activity was recorded with sharp microelectrodes during rest and during 0.3-Hz sinusoidal stimulation from bouton afferents identified by their efferent-mediated inhibitory responses. A glutamate antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) decreased quantal size (qsize) while lowering external Ca(2+) decreased quantal rate (qrate). Miniature excitatory postsynaptic potentials (mEPSPs) had effective durations (qdur) of 3.5-5 ms. Their timing was consistent with Poisson statistics. Mean qsizes ranged in different units from 0.25 to 0.73 mV and mean qrates from 200 to 1,500/s; there was an inverse relation across the afferent population between qrate and qsize. qsize distributions were consistent with the independent release of variable-sized quanta. Channel noise, measured during AMPA-induced depolarizations, was small compared with quantal noise. Excitatory responses were larger than inhibitory responses. Peak qrates, which could approach 3,000/s, led peak excitatory mechanical stimulation by 40 degrees . Quantal parameters varied with stimulation phase with qdur and qsize being maximal during inhibitory stimulation. Voltage modulation (vmod) was in phase with qrate and had a peak depolarization of 1.5-3 mV. On average, 80% of vmod was accounted for by quantal activity; the remaining 20% was a nonquantal component that persisted in the absence of quantal activity. The extracellular accumulation of glutamate and K(+) are potential sources of nonquantal transmission and may provide a basis for the inverse relation between qrate and qsize. Comparison of the phases of synaptic and spike activity suggests that both presynaptic and postsynaptic mechanisms contribute to variations across afferents in the timing of spikes during sinusoidal stimulation.

Action Potentials↗

Frequency-response analysis of vestibular-induced neck reflex in cat. I. Characteristics of neural transmission from horizontal semicircular canal to neck motoneurons.

1. Vestibular-induced neck muscle reflexes (vestibulocollic reflexes) were studied with frequency-response methods in unanesthetized, decerebrate cats. The horizontal semicircular canals were stimulated by oscillation of the turntable and EMG activity was recorded from neck extensor muscles. 2. The maximum firing rate of each motor unit was less than 40 spikes/s. The motor units were classified by their maximum firing rates into two groups: HF (high frequency) units which could fire above 20 spikes/s and LF (low frequency) units which could not exceed 20 spikes/s of firing. The HF units had larger gains than the LF units on the average. 3. Compound EMGs, which presumably represent activity of the whole muscle, were examined at different frequencies of stimulation. The gain of compound EMG responses depended on the spontaneous activity. When the spontaneous activity was low or too high, the gain was small. There was an intermediate spontaneous activity level at which the gain became maximal. 4. The phase lag and the gain of the frequency response were represented in a Bode diagram with respect to angular acceleration. The transfer function of the system from the vestibular nuclei to neck EMG activity was estimated by assuming a first-order lag-lead system. A phase lag of 70-80 degrees (0.05 Hz) was found between the averaged activity of vestibular nucleus neurons and cervical motor activity. A positive correlation was observed between the phase lag and the gain of each motor unit. These results cannot be attributed solely to the action of the vestibulospinal tract, but suggest the existence of a neural intergrator in the vestibulocollic reflex arc.

Action Potentials↗

HSV-1 not only in human vestibular ganglia but also in the vestibular labyrinth.

Reactivation of herpes simplex virus type 1 (HSV-1) in the vestibular ganglion (VG) is the suspected cause of vestibular neuritis (VN). Recent studies reported the presence of HSV-1 DNA not only in human VGs but also in vestibular nuclei, a finding that indicates the possibility of viral migration to the human vestibular labyrinth. Distribution of HSV-1 DNA was determined in geniculate ganglia, VGs, semicircular canals, and macula organs of 21 randomly obtained human temporal bones by nested PCR. Viral DNA was detected in 48% of the labyrinths, 62% of the VGs, and 57% of the geniculate ganglia. The potential significance of this finding is twofold: (1) Inflammation in VN could also involve the labyrinth and thereby cause acute unilateral vestibular deafferentation. (2) As benign paroxysmal positional vertigo often occurs in patients who have had VN, it could also be a sequel of viral labyrinthitis.

Adult↗