Effect of unilateral vestibular deafferentation on the initial human vestibulo-ocular reflex to surge translation.

Transient whole-body surge (fore-aft) translation at 0.5 G peak acceleration was administered to six subjects with unilateral vestibular deafferentation (UVD), and eight age-matched controls. Subjects viewed eccentric targets to determine if linear vestibulo-ocular reflex (LVOR) asymmetry might lateralize otolith deficits. Eye rotation was measured using magnetic search coils. Immediately before surge, subjects viewed a luminous target 50 cm away, centered or displaced 10 degrees horizontally or vertically. The target was extinguished during randomly directed surges. LVOR gain relative to ideal velocity in subjects with UVD for the contralesional horizontally eccentric target (0.59 +/- 0.08, mean +/- SEM) did not differ significantly from normal (0.50 +/- 0.04), but gain for the ipsilesional eccentric target (0.35 +/- 0.02) was significantly less than normal (0.48 +/- 0.03, P < 0.05). Normal subjects had mean gain asymmetry for horizontally eccentric targets of 0.17 +/- 0.03, but asymmetry in UVD was significantly increased to 0.35 +/- 0.05 (P < 0.05). Four of six subjects with UVD had maximum gain asymmetry outside normal 95% confidence limits. Asymmetry did not correlate with UVD duration. Gain for 10 degrees vertically eccentric targets averaged 0.38 +/- 0.14 for subjects with UVD, insignificantly lower than the normal value of 0.75 +/- 0.15 (P > 0.05). Surge LVOR latency was symmetrical in UVD, and did not differ significantly from normal. There was no significant difference in response between dark and visible target conditions until 200 ms after surge onset. Chronic human UVD, on average, significantly impairs the surge LVOR for horizontally eccentric targets placed ipsilesionally, but this asymmetry is small relative to interindividual variation.

Benign positional nystagmus: a study of its three-dimensional spatio-temporal characteristics.

OBJECTIVE: To describe the spatial and temporal characteristics of benign positional nystagmus (BPN) subtypes in benign positional vertigo (BPV) due to vestibular lithiasis affecting one or more semicircular canals (SCCs). BACKGROUND: Activation of SCC receptors by sequestered otoconia, either freely moving (canalithiasis) or cupula-adherent (cupulolithiasis) during head position changes with respect to gravity, is the accepted cause of BPV. Although accurate identification and interpretation of BPN is critical to BPV therapy, no rigorous, kinematically correct three-dimensional spatio-temporal analysis of BPN in all its forms exists. METHODS: Using dual-search scleral coils, the authors recorded BPN provoked by Dix-Hallpike or supine ear-down test in a two-axis whole-body rotator in 44 patients with refractory BPV. To localize the SCC affected, BPN rotation axes were compared to SCC axes, axes orthogonal to average SCC planes. RESULTS: Sixteen patients had upbeat, geotropic-torsional BPN in the Dix-Hallpike test to one side and five to both sides, with BPN rotation axes clustered around the lowermost posterior SCC axis. Seven had direction-changing horizontal BPN, three geotropic (canalithiasis) and four apogeotropic (cupulolithiasis), with rotation axes around the lowermost and uppermost horizontal SCC axis. Seven had predominantly downbeating BPN with rotation axes clustered around one superior SCC axis. Nine had upbeat, horizontal-torsional BPN with rotation axes located between posterior and horizontal SCC axes of the lowermost ear suggesting simultaneous lithiasis in both SCCs. BPN vector-guided repositioning therapy was successful in 43 patients. CONCLUSION: Benign positional vertigo can affect one or more semicircular canals and three-dimensional recording with vector analysis of the benign positional nystagmus (BPN) can guide canalith repositioning therapy especially in refractory cases with atypical BPN.

[Towards a cellular pathophysiology of Meniere's disease]. / Neue Konzepte zu einer Pathophysiologie des M. Menière auf zellulärer Ebene.

BACKGROUND: A modest increase in the hydrostatic pressure within the endolymphatic space may induce an endolymphatic hydrops which in turn is typically associated with Meniere's disease. However, there is no convincing pathophysiological model that might explain, on a cellular level, how a pressure increases may cause disturbed functions of vestibular hair cells and vertigo attacks. METHODS: So far, models involve osmotic mechanisms leading to electrolyte imbalances in the endolymphatic space. Alternatively, impaired longitudinal flow in the endolymphatic space is considered important. RESULTS: Recently, a pressure-sensitive potassium current was identified and characterized in vestibular hair cells. CONCLUSIONS: This current may modify the frequency behavior of a cell and may be the "missing link" in a cellular pathophysiology of the hydrops. Ion currents in hair cells offer attractive targets for pharmacological interventions in Meniere's disease.

[The patterns of cell proliferation in the chick basilar papilla following severe acoustic trauma].

OBJECTIVE: To investigate the characteristics of cell proliferation in chick basilar papilla (BP) following severe acoustic trauma, and the orgin of precursor cell that can generate into new hair cell. METHOD: Chicks were continuously exposed to a 1.5 kHz pure tone at 120 dB SPL for 48 h, and they were intraperitoneally injected with bromodeoxyuridine (BrdU) at 40 h, 48 h after the onset of exposure. Then, cochlea were immunocytochemically labeled to detect BrdU, and examined the cell proliferative activity in BP. RESULT: 1. Labeled cells presented in the mid-proximal region of BP where hair cells have been damaged and lost following noise overstimulation; 2. The most cells in S phase were detected at 48 h after the onset of exposure; and 3. Both labeled hair cells and supporting cells can be seen in BP; In addition, the supporting cells may act as precursor cells that can generate into new hair cells. CONCLUSION: These findings suggest that auditory epithelial cells can be regenerated in chick cochlea after acoustic trauma, even though ongoing production of hair cells don't occur in BP, and supporting cells may be a source of newly generated hair cells under pathological conditions.

Vestibulo-ocular, optokinetic and postural function in humans with rheumatoid arthritis.

The present study investigated vestibulo-ocular reflex (VOR), optokinetic reflex (OKR) and postural function in patients with rheumatoid arthritis (RA). Compared with controls, no differences in gaze-holding, VOR gain or phase, OKR slow phase velocity (SPV) or quick phase amplitude, optokinetic afternystagmus SPV or duration, or latency to the illusion of circularvection, were found. RA patients did exhibit greater sway in the leftward direction (P<0.01), however, this was no greater in the conditions of the Clinical Test of Sensory Interaction and Balance that increase reliance upon vestibular information. We conclude that RA patients do not exhibit substantial deficits in visual-vestibular function.

Effects of hypergravity on the morphological properties of the vestibular sensory epithelium. I. Long-term exposure of rats after full maturation of the labyrinths.

The effect of prolonged exposure to hypergravity on the morphology of vestibular epithelia of rats was investigated. At the age of 1 month, i.e., when vestibular end organs are fully maturated, three rats were transferred to a hypergravity environment of 2.5 g inside a large radius centrifuge. After 9 months, vestibular epithelia of these animals and of three control animals were immunohistochemically labeled for actin and tubulin. The apical cross-sectional area of epithelial cells of hypergravity exposed rats appeared to be smaller in all end organs. Area reduction was 1.9% in the saccule (not significant), 5.0% in the utricle (p < 0.005), and 11.6% in the crista (p<<0.001). No indications for a deterioration of vestibular functioning were observed.

Study of the gerbil utricular macula following treatment with gentamicin, by use of bromodeoxyuridine and calmodulin immunohistochemical labelling.

Effects of ototoxic drugs on the gerbil vestibular sensory epithelium were probed by use of immunocytochemical labelling with antibodies to both a mitogenic marker (bromodeoxyuridine) and a hair cell specific protein (calmodulin). Nine animals had gentamicin administered once daily for 5 days, as a transtympanic injection into the right middle ear. They additionally were given a daily intraperitoneal injection of bromodeoxyuridine, starting on the same day as the gentamicin injection and continuing until the day of sacrifice. Nine other animals, serving as controls for bromodeoxyuridine incorporation, received only the intraperitoneal injections of bromodeoxyuridine. The inner ears from three gerbils were obtained at 1, 2 or 4 weeks following the last gentamicin injection and utricles from the injected ears were processed for immunohistochemical analysis. In specimens where gentamicin was administered, we found evidence of bromodeoxyuridine incorporation in 17 cells (10 single cells and 7 pairs of cells) in a total of 216 sections taken from the central regions of the 9 utricles. However, in control specimens, no bromodeoxyuridine labelling was found in any cells of the 216 sections examined. Of 10 single cells labelled with bromodeoxyuridine, two cells in the hair cell layer were labelled with antibodies against calmodulin. One had a faint labelling in the nucleus and the other in the stereocilia, but not in the cell bodies. Of 7 pairs of cells, two pairs with nuclei localized in the hair cell layer had faint labelling for calmodulin in the nuclei, but no labelling in any other part of the cell. The other 13 cells labelled with antibodies to bromodeoxyuridine were not labelled with antibodies to calmodulin. Our results suggest that the bromodeoxyuridine-labelled cells could not be positively identified as hair cells based on immunohistochemical labelling for calmodulin.

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.