Vestibular Paralysis Research Articles

Distribution of herpes simplex virus type 1 in human geniculate and vestibular ganglia: implications for vestibular neuritis.

Vestibular neuritis is a common cause of partial unilateral vestibular paralysis, which usually spares posterior semicircular canal function. The cause is assumed to be a viral reactivation of latent herpes simplex virus type 1 (HSV-1) in human vestibular ganglia. The existence of an anastomosis between the intermediate nerve and the superior vestibular nerve suggests the question of whether selective affliction of the superior vestibular nerve is the result of migration of HSV-1 from the geniculate ganglion along this faciovestibular anastomosis. We determined the distribution of HSV-1 among geniculate ganglia, vestibular ganglia, and within Scarpa's ganglion by examining 35 human temporal bones by polymerase chain reaction. HSV-1 was found in 66% of geniculate ganglia and 60% of vestibular ganglia; all examined parts of vestibular ganglia were almost equally HSV-1 infected. Our data provided no support for viral migration along this anastomosis or for a preferential latency of HSV-1 in the superior vestibular nerve. We suggest that the common double innervation of the posterior ampulla by two nerves running in two separate bony canals could offer an alternative explanation for the regular sparing of posterior canal function in vestibular neuritis.

Vestibulo-Ocular Responses During Static Head Roll and Three-Dimensional Head Impulses After Vestibular Neuritis

This study aimed to investigate whether unilateral vestibular neuritis (VN) causes the same deficits of ocular counter-roll during static head roll (OCRS) and dynamic vestibulo-ocular reflex gains during head impulses (VORHI) as unilateral vestibular deafferentation (VD). Ten patients with acute and 14 patients with chronic vestibular paralysis after VN were examined. The testing battery included fundus photography of both eyes with the head upright (binocular cyclorotation) and dual search coil recordings in a three-field magnetic frame. With one dual search coil on the right eye and the other on the forehead, the following stimuli were given: i) Halmagyi-Curthoys head impulses about the vertical, horizontal and torsional axes. ii) Static roll positions of the head up to 20° right- and left-ear-down by movement of the neck. The comparison group consisted of 19 healthy subjects. Compared with the VD-patients, as reported in the literature, acute VN-patients showed the same pattern of OCRS gain reduction and binocular cyclorotation (CRb). The main feature that distinguished chronic VN-patients from chronic VD-patients was the normalization of the torsional VORHI gain to the affected side, whereas the VORHI gains in the horizontal and vertical directions did not show recovery (as in the patients with chronic VD). Chronic VN-patients differed from acute VN-patients by: i) symmetrical OCRS gains, ii) a less pronounced CRb toward the affected side, and iii) a normal torsional VORHI gain toward the affected side. Since the ipsilesional torsional VORHI gain did not recover in VD-patients, the normalization of this gain in our VN-patients can only be explained by a (partial) recovery of otolith function on the side of the lesion after the neuritis.

MAN IN MOTION

This is a review of selected aspects of the history of the vestibular system (J. E. Purkyne, E. Mach, A. Crum-Brown) and of our current understanding of vestibular malfunction in clinical vertigo syndromes. Evidence is presented for a preliminary classification of central vestibular brainstem syndromes according to the three major planes of action of the vestibulo-ocular reflex (VOR): (1) disorders of the VOR in the horizontal (yaw) plane (horizontal nystagmus, pseudo 'vestibular neuritis'); (2) disorders of the VOR in the sagittal (pitch) plane (downbeat nystagmus; upbeat nystagmus); (3) disorders of the VOR in the frontal (roll) plane (ocular tilt reaction; lateropulsion). The pathophysiology of peripheral vestibular disorders is discussed: a specific gravity differential between the cupula fluid and the endolymph (buoyancy mechanism) causes vertigo in benign paroxysmal positioning vertigo and positional alcohol nystagmus. Vestibular neuritis is probably a partial unilateral vestibular paralysis due to viral infection of the superior division of the nerve trunk. The common post-traumatic vertigo is explained by otolith dysfunction secondary to dislodged otoconia resulting in unequal loads on the macula beds and a tonus imbalance between the two otoliths.

Long-term modifications of vertical and horizontal vestibulo-ocular reflex dynamics in man. I. After acute unilateral peripheral vestibular paralysis.

Horizontal (HOR) and vertical (VERT) vestibulo-ocular reflex (VOR) responses to whole-body triangular velocity profiles with constant accelerations of 10, 15 and 20 deg/s2 were studied in two populations: normals, and patients with acute unilateral peripheral vestibular paralysis. The effect of this type of unilateral deficit on VOR gain and long time constant were determined as well as the time course of the compensation processes for HOR and VERT VOR dynamics. In the patient population, HOR VOR gain was asymmetric post deficit, being, on average, 50% and 75% of normal for rotations toward and away from the deficit, respectively. For the VERT VOR, on average, a symmetric 66% reduction occurred. The VERT VOR time constant was marginally affected by the deficit. HOR time constants were reduced for both directions of rotation. HOR and VERT VOR gain was within normal limits 1-3 months following an acute paralysis; time constants required a longer recovery period. Our results indicate that a unilateral deficit causes a markedly different alteration for HOR VOR dynamics compared to the effect on VERT VOR.

頭振を負荷した足踏検査の有用性

Fukuda's stepping test was modified and made more sensitive to detect latent imbalance of labyrinthine function. The subject was asked to shake his head 7 times at one hertz in about 90 degrees in a horizontal plane and to step in the same position with both arms stretched straight before him. This test was applied to 12 patients whose vestibular function as tested by Romberg, Mann and Fukuda's method had become normal after an attack of vertigo due to unilateral vestibular paralysis. All these patients showed deviation and a tendency to fall to the affected side.

A Clinical Study of Acute Genuine Vestibular Paralysis, So-called Vestibular Neuronitis

A Clinical Study of Acute Genuine Vestibular Paralysis, So-called Vestibular Neuronitis

Vestibular paralysis and cochlear impairment due to streptomycin intoxication.

Streptomycin toxicity has been studied by many observers who reported disturbances arising from therapeutic use of the antibiotic. When streptomycin is administered in high dosage or over prolonged periods of time, toxic reactions involving the vestibular and sometimes also cochlear functions are regularly encountered. Hinshaw and Feldman (1945) 1 presented the first report. These authors observed one case of deafness and three cases with vestibular disturbances subsequent to large doses of streptomycin. They ascribed these symptoms to a selective toxic effect on the eighth cranial nerve. The following year Brown and Hinshaw 2 reported similar observations in 23 cases during treatment with streptomycin. Disturbance of equilibrium with dizziness and lightheadedness appeared. The imbalance varied from gentle swaying to falling. The response to caloric stimulation and turning tests indicated a bilateral progressive decrease of vestibular function. In five patients they observed impairment of hearing when doses of 3 gm. a

SYNDROME OF BILATERAL VESTIBULAR PARALYSIS AND ITS OCCURRENCE FROM STREPTOMYCIN THERAPY

THE DISTURBANCE of equilibrium caused by bilateral loss of vestibular function from streptomycin therapy appears to be basically similar to that of bilateral vestibular paralysis from other causes, whether the site of the lesion is in the peripheral or the central components of the vestibular nervous system. The syndrome of bilateral vestibular paralysis has rarely been noted in the literature, and not before its happening as an untoward effect of streptomycin therapy has there been an opportunity to observe a considerable number of patients with this syndrome from its onset and through the stages of its regression. The practice of prescribing smaller doses of streptomycin than formerly and of substituting other antibiotics with less neurotoxic effects makes the study of the symptomatology of the toxicity of streptomycin, including its pathologic foci, of importance chiefly in obtaining a better understanding of disorders of the function of the acoustic nerve as an

Vertigo of vestibular paralysis

The LaryngoscopeVolume 21, Issue 10 p. 978-985 Article Vertigo of vestibular paralysis† Philip D. Krrrison M. D., Philip D. Krrrison M. D. 58 West Fifty-sixth Street, New YorkSearch for more papers by this author Philip D. Krrrison M. D., Philip D. Krrrison M. D. 58 West Fifty-sixth Street, New YorkSearch for more papers by this author First published: October 1911 https://doi.org/10.1288/00005537-191110000-00002 † ReAd before the Meeting of the American Otological Society, Atlantic City, N. T., June 27. 1911 AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Volume21, Issue10October 1911Pages 978-985 RelatedInformation