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Results for “Endolymphatic Hydrops”

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PubMed1991

[Mechanisms of development of endolymphatic hydrops following secondary immune response in the endolymphatic sac of guinea pigs].

Previously the author reported the immediate development of endolymphatic hydrops (e. hydrops) following direct challenge of secondary antigen to the endolymphatic sac (ES) in guinea pigs, during the early phases of postchallenge, ranging from 1 to 5 weeks. The present study reports the results of specimens taken up to 10 weeks postchallenge, and correlation of e.hydrops to perilymph in antigen-specific antibody levels. From the present results, mechanisms of e.hydrops induced ES immune reaction are suggested as follows. 1) In the early stage of e.hydrops, an acute inflammatory reaction in the ES may produce endolymph by an increased vascular permeability of the inner ear and may impair endolymph absorption from the ES. 2) In the latter stage of e.hydrops, the moderate cellular infiltration in the ES may cause chronic impairment of endolymph absorption in the ES.

Animals↗

PubMed2004

[Quantification of endolymphatic hydrops in experimental animal model].

OBJECTIVE: To investigate a method of quantification of the endolymphatic hydrops in experimental animal model. METHODS: Thirty guinea pigs were divided into three groups at random. In control group, there were ten guinea pigs without operation on both ears. Endolymphatic hydrops was induced by endolymphatic sac obliteration through extradural posterior cranial fossa approach in right ear, including 4-week postoperative group(n = 10) and 8-week postoperative group(n = 10). The area of scala vestibuli (SV) and scala media(SM) of each turn on both cochlear midmodiolar sections was measured, respectively, using auto computer aided design(AutoCAD R14) software combined with digital camera, and then the maximum scala media area(SMA) ratio was calculated and compared. RESULTS: No endolymphatic hydrops was observed in all non-operated ears, however, variety degree of hydrops was present in all operated ears. The average maximum SMA ratio in the 4-week group (2.2231 +/- 0.1996) was greater than that in the control group (1.0971 +/- 0.0644). The average maximum SMA ratio of the 8-week group (4.0142 +/- 0.5218) was greater than that in the 4-weekgroup. There was significant difference between the two groups(P < 0.05). CONCLUSION: It is convenience and reliable to be used to quantify the experimental endolymphatic hydrops with the present method. This study provides a reliable methodological base for the experimental study of Meniere's disease.

Animals↗

PubMed2002

[Endolymphatic hydrops of both ears of guinea pig produced by aldosterone].

OBJECTIVE: To develop endolymphatic hydrops in both ears of guinea pigs by aldosterone. METHODS: Thirty animals were divided into 3 groups with 10 in each group. Group A received left ears operation following Kimura', with right ears non-operated as control; group B received introperitonal injection of aldosterone (0.1 mg.0.1 kg-1.d-1) for continuous 5 days; group C received introperitonal injection of 0.5 ml 0.9% NS. Five out of group A,B and C were killed 1 month and 2 months later respectively for analysis of blood K+, Ca2+, Na+ and pathological examination of inner ear, heart, lung, brain, liver and kidney. RESULTS: In group A' moderate to severe endolymphatic hydrops developed in the operated ears during 1 and 2 months. In group B, mild endolymphatic hydrops developed in the both ears during 1 month, and within 2 months it was moderate and severe. No endolymphatic hydrops developed in group C. In contrast to group C, No significant changes could be found in blood analysis of group A, but the concentrations of K+ and Ca2+ were declined, and that of Na+ were increased in group B. The heart, lung, brain, liver, and kidney of all animals were normal. CONCLUSIONS: Aldosterone may induce endolymphatic hydrops in both ears.

Aldosterone↗

PubMedDate not supplied

Experimental endolymphatic hydrops under action of a type II nitric oxide synthase inhibitor: otoacoustic emissions evaluation and electrocochleography.

UNLABELLED: In experimental endolymphatic hydrops distortion-products otoacoustic emission (dpoae) amplitudes decrease and there is elevation on electrocochleographic thresholds. Some authors found type ii nitric oxide synthase (nos ii) expression in hydropic cochleas and they suggest nitric oxide (no) may be involved in endolymphatic hydrops pathogenesis. The aim of this study was to evaluate the action of a nos ii inhibitor on dpoae and electrocochleography in experimental endolymphatic hydrops. MATERIAL AND METHODS: endolymphatic hydrops was induced in 16 guinea pigs by obliterating the endolymphatic duct and sac in the right ear. They were divided in two groups: eigth guinea pigs under the action of aminoguanidine, a nos ii inhibitor and eigth control guinea pigs. We compared dpoae amplitudes at geometric means of frequencies 1062, 2187, 4375 and 7000 hz, compound action potential threshold at 1000, 2000, 4000 and 6000 hz and summating potential to action potential (sp/ap) ratio between the groups during the postoperative observation period of 16 weeks. RESULTS: there were no significant changes in the dpoae amplitudes and in the sp/ap ratio. The group that received aminoguanidine had a lower degree of threshold increase at 2000 (p<0.05) And 6000 hz (p<0.05) In 12th postoperative week and at 1000 (p<0.05), 2000 (P<0.001), 4000 (P<0.001) And 6000 hz (p<0.001) At 16th postoperative week. CONCLUSIONS: nos ii inhibitor decreased the electrocochleography threshold elevation on experimental endolymphatic hydrops.

Animals↗

PubMed2003

In vivo visualization of endolymphatic hydrops in guinea pigs: magnetic resonance imaging evaluation at 4.7 tesla.

In order to find out whether it is possible to visualize experimental endolymphatic hydrops in the cochlea with magnetic resonance imaging (MRI) at 4.7 T, we used 11 guinea pigs. Five normal guinea pigs were used as controls. Early manifestation of endolymphatic hydrops was evaluated in endolymphatic sac (ES)-intact animals (n = 6), and advanced manifestation in ES-damaged animals (n = 5) by means of MRI with gadolinium-diethylenetriaminepentaacetate-bismethylamide (Gd-DTPA-BMA) contrast agent. Hearing was tested with electrocochleography. The surface area of 3 partitions of the cochlea was used to quantify endolymphatic hydrops. The fine structure of the 3 partitions of the cochlea was visualized with MRI in all animals, as Gd-DTPA-BMA appeared mainly in the scala tympani and scala vestibuli. As early as 5 days after endolymphatic sac surgery, endolymphatic hydrops started to appear as visualized by MRI and also verified with histology. Severe damage to the inner ear barrier with Gd-DTPA-BMA leakage into the scala media was detected with MRI in 1 ES-damaged animal that had a 60-dB hearing loss. To conclude, endolymphatic hydrops can be visualized with high-resolution MRI by means of Gd-DTPA-BMA, and it is possible to quantify the extent of endolymphatic hydrops. Damage to the inner ear barrier or possible rupture of membranes can be shown with the assistance of Gd-DTPA-BMA.

Animals↗

PubMed1993

Functional changes associated with experimentally induced endolymphatic hydrops.

A guinea pig model with surgically induced endolymphatic hydrops of the inner ear has been developed and studied over the past thirty years. The aim of such studies is to obtain insight into physiological processes associated with endolymphatic hydrops in man and in particular in Menière's disease where endolymphatic hydrops is systematically encountered at post-mortem examination of the temporal bones. The present review attempts to draw together the data pertaining to functional modifications of inner ear function in the animal model. For simplicity the data are categorised under five main titles: electrochemical modifications, electrophysiological modifications, pressure and hydrops, sensitivity to other insults and vestibular dysfunction. One of the most striking observations that can be made is that the data originating from different authors are very variable. There is, however, some evidence suggesting that the evolution of the auditory dysfunction could be considered as consisting of a series of different phases. This kind of information could serve as a basic framework for future research on the animal model.

Aminoglycosides↗

PubMed1981

Changes of the action potential, the summating potential and cochlear microphonics in experimental endolymphatic hydrops.

The changes of the action potential (AP), the summating potential (SP) and cochlear microphonics (CM) were investigated in reference to the grade of endolymphatic hydrops produced by endolymphatic sac obliteration in guinea pigs. In a few cases with minimum endolymphatic hydrops, super-normal AP was obtained. With an increase of endolymphatic hydrops, CM responses were reduced although AP responses at intensive stimulation were maintained relatively well. It is thought that the polarity of positive SP, as observed in control, was influenced to deflect towards negative SP by an interaction between the increased degree of endolymphatic hydrops and the changes of the biochemical components of the inner ear fluids.

Action Potentials↗

PubMed1994

Changes in immunostaining of cochleas with experimentally induced endolymphatic hydrops.

Cochleas with experimentally induced endolymphatic hydrops were immunostained for Na+,K(+)-ATPase, intracellular Ca(++)-ATPase, carbonic anhydrase, aldehyde dehydrogenase, calcium-binding proteins, vimentin, and the gap junction protein, connexin 26. No changes in immunostaining of hydropic ears were observed 1 week after blockage of the endolymphatic duct. Two weeks to 1 month after the operation, immunostaining of type I fibrocytes in the spiral ligament, which are positive for all but Na+,K(+)-ATPase, was slightly decreased on the operated side. These changes became more pronounced 3 months after the operation. However, staining for Na+,K(+)-ATPase of the stria vascularis and of type II fibrocytes of the spiral ligament was not reduced until 6 months postoperative. The reduction of enzymes and other cell constituents that may be involved in ion balance of cochlear fluids indicates that cells in the spiral ligament play an important role in cochlear homeostasis and that they merit further study in animal and human otopathology.

Adenosine Triphosphatases↗

PubMed2001

Endolymphatic hydrops in asymptomatic ears in unilateral Ménière's disease.

OBJECTIVES/HYPOTHESIS: The aim of our study was the objective assessment of endolymphatic hydrops in asymptomatic ears in unilateral Ménière's disease with a noninvasive electrophysiological test and investigation of significant clinical signs. The null hypothesis was that there would be no signs of endolymphatic hydrops in the asymptomatic ear. STUDY DESIGN: Prospective study using the traveling wave velocity test for endolymphatic hydrops. METHODS: The traveling wave velocity test was used in conjunction with standard audiological tests to investigate both ears of 181 Ménière's patients attending the Medical Research Council Institute of Hearing Research in Southampton, United Kingdom. The test uses derived auditory brainstem responses to estimate the velocity of the cochlear traveling wave that is altered in endolymphatic hydrops. Ménière's disease was assessed using Arenberg's five staging criteria. Significant correlations were evaluated using standard statistical methods. RESULTS: Of 100 patients with clinically unilateral Ménière's disease, 27% showed evidence of endolymphatic hydrops in their asymptomatic ear. There was a significant correlation between signs of hydrops and the mean air-conduction threshold at 500 Hz. CONCLUSIONS: We recommend that a full assessment of incipient disease in the asymptomatic ear in unilateral Ménière's disease should be undertaken before offering any treatment options to patients. Any suspicion of early disease in the asymptomatic ear in unilateral Ménière's disease should lead to full electrophysiological assessment to assess the evidence of endolymphatic hydrops in that ear.

Endolymphatic Hydrops↗

PubMed1992

Endolymphatic hydrops induced by immune response of the endolymphatic sac: relation to perilymph antibody levels.

This study investigated the effect of a secondary immune response in the endolymphatic sac on the development of endolymphatic hydrops in guinea pigs. Following secondary keyhole limpet hemocyanin (KLH) challenge directly to the sac in systemically presensitized animals, hydrops rapidly developed within 1 week, then gradually reduced by 4 weeks. After 5 weeks, hydrops gradually recurred and developed again. Mean perilymph anti-KLH antibody levels rose from day 1 to 4 weeks and then decreased. The elevation of perilymph anti-KLH antibody levels on day 2 was due to an increased vascular permeability and there was a local regeneration by the challenge of the sac after day 7. The development of hydrops correlated well with mean perilymph anti-KLH antibody levels in the period from day 1 to day 7. After 2 weeks, there was no correlation between them. These results suggest that an immune response of the sac may induce an excess secretion of endolymph in the initial stage and may further lead to irreversible dysfunction of the sac at a later stage.

Animals↗

PubMed2005

Diameter of the cochlear nerve in endolymphatic hydrops: implications for the etiology of hearing loss in Ménière's disease.

OBJECTIVE/HYPOTHESIS: Endolymphatic hydrops (ELH) is an important histopathological hallmark of Ménière's disease. Experimental data from human temporal bones as well as animal models of the disorder have generally failed to determine the mechanism by which ELH or related pathology causes hearing loss. Hair cell and spiral ganglion cell counts in both human and animal case studies have not, for the most part, shown severe enough deterioration to explain associated severe sensorineural hearing loss. However a limited number of detailed ultrastructural studies have demonstrated significant reductions in dendritic innervation densities, raising the possibility that neurotoxicity plays an important role in the pathology of Ménière's disease (MD) as well as experimental endolymphatic hydrops (ELH). This study tests the hypothesis that neurotoxicity is an important primary mediator of injury to the hydropic ear and is reflected in measurable deterioration of the cochlear nerve in the animal model of ELH. This study also explores the previously presented hypothesis that cochlear injury in ELH is mediated through the actions of nitric oxide (NO) by evaluating whether hearing loss or various measures of cochlear damage can be ameliorated by administration of an agent that limits excess production of NO. STUDY DESIGN: Part one of the project involves the surgical induction of endolymphatic hydrops and correlation of long term hearing loss with histological parameters of ELH severity as well as cochlear nerve and eighth cranial nerve diameter measurements. In part two, aminoguanidine is administered orally to a separate set of hydropic animals in an attempt to limit cochlear injury presumably mediated by NO. METHODS: Guinea pigs are subjected to surgical induction of unilateral endolymphatic hydrops after establishing baseline ABR thresholds at 2, 4, 8, 16, and 32 kHz. Threshold shifts are established prior to sacrifice at 4 to 6 months and temporal bones processed for light microscopy. Measurements of cochlear nerve and eighth cranial nerve maximal diameters as well as average maximal diameters are carried out and correlated to hearing loss and a semi-quantitative measure of hydrops severity. The identical experiments are carried out in animals treated with aminoguanidine, an inhibitor of inducible nitric oxide synthase. RESULTS: : The mean maximal diameter (n = 14) of the hydropic cochlear nerve was significantly reduced (432.14 +/- 43.18 vs. 479.28 +/- 49.22 microns, P = .0025) as compared to the control nerve. This was also seen in measures of the eighth cranial nerve (855.71 +/- 108.82 vs. 929 +/- 81.53 microns, P = 0.0003). Correlation studies failed to show correlation between hydrops severity and a cochlear nerve deterioration index (r = -0.0614, P = .8348). Similarly, hearing loss severity failed to correlate with cochlear nerve deterioration (r = 0.1300, P = .6577). There was a significant correlation between hearing loss and hydrops severity (r = 0.6148, P = .0193). Aminoguanidine treated animals (n = 5) also sustained nerve deterioration to the same degree as non-treated animals and there appeared to be no protective effect (at the dosage administered) against ELH related hearing loss, hydrops formation, or nerve deterioration. CONCLUSION: ELH results in significant deterioration of cochlear nerve and eighth cranial nerve maximal diameters in the guinea pig model. These findings are in accord with previous studies which detected ultrastructural evidence of dendritic damage and indicate that neural injury is of sufficient severity to result in light microscopic evidence of cochlear nerve and eighth cranial nerve deterioration. These data support the concept that the principle pathological insult in ELH is a form of neurotoxicity, especially in light of previous studies which indicate relative preservation of hair cells at similar points in time. The lack of correlation between the severity of hydrops and nerve deterioration suggests that nerve deterioration is independent of hydrops severity.

Animals↗

PubMedDate not supplied

Audiovestibular findings in patients with delayed and idiopathic endolymphatic hydrops: a comparative study.

OBJECTIVE: The objective of this study was to analyze the neuro-otological findings in patients with delayed endolymphatic hydrops and compare them with audiovestibular abnormalities found in patients with idiopathic endolymphatic hydrops. Study design A retrospective open case study. SETTING: A referral ambulatory dizziness clinic. PATIENTS: Medical records of 30 patients with delayed endolymphatic hydrops and of 33 patients with idiopathic hydrops were analyzed. Outcome measures Clinical, electronystagmographic, caloric, and audiometric results in both groups of patients. RESULTS: No differences in the prevalence of abnormalities on clinical testing, electronystagmography (including rotatory chair), or caloric testing were found between the groups. The clinical outcome of conservative therapy was better in patients with idiopathic endolymphatic hydrops (P =.03). CONCLUSIONS: These findings are in keeping with the presumed common pathophysiology of delayed and idiopathic endolymphatic hydrops. However, it is important to identify patients with delayed hydrops in view of the chance of the potential poor response to medical therapy.

Adolescent↗

PubMedDate not supplied

Electrocochleographic changes in relation to cochlear histopathology in experimental endolymphatic hydrops.

The relation between electrocochleographic and histological changes in experimental endolymphatic hydrops was studied 1, 2, 4, or 8 months after obliteration of the endolymphatic sac. An increase in the compound Action Potential (AP) threshold was found 2, 4, and 8 months after obliteration. This increase was strongly correlated with loss of outer hair cells, nerve fibres and spiral ganglion cells. An enhanced negative Summating Potential (SP) and an enhanced SP-AP ratio were found mainly in animals with an endolymphatic hydrops without further cochlear pathology. A normal or decreased SP and SP-AP ratio was regularly recorded in animals with both an endolymphatic hydrops and a variety of other histopathological changes in the inner ear. An increased second peak (N2) in the AP waveform was recorded from 63% (15/24) of the hydropic ears, equally divided over the four groups. There was no obvious correlation between the increased N2 and other electrophysiological or histological findings.

Action Potentials↗

PubMed1995

Delayed endolymphatic hydrops: clinical manifestations and treatment outcome.

The clinical entity of delayed endolymphatic hydrops was first defined by Schuknecht in 1978. It constitutes the development of symptoms consistent with endolymphatic hydrops either ipsilateral or contralateral to an ear with a profound hearing loss. We report our experience with this condition amongst 394 patients with Meniére's syndrome followed prospectively. Of 24 patients with the ipsilateral condition, nearly half responded to medical treatment. Thirteen patients underwent vestibular nerve section and the outcome, as assessed by a disability grading system, was very satisfactory. The proportion of patients undergoing vestibular nerve section (54.9%) was substantially higher than patients with classical Meniére's syndrome during the same period (5.4%) reflecting the increased severity of the symptoms. The contralateral form was less frequently seen and patients were more refractory to treatment. The audiological definition of delayed endolymphatic hydrops appears somewhat arbitrary, as these patients form a continuous spectrum with other Meniére's syndrome cases, occurring in association with less marked degrees of sensorineural hearing loss.

Adolescent↗

PubMed1995

[Diagnosis of endolymphatic hydrops with low tone masked otoacoustic emissions].

BACKGROUND: A new method of diagnosis of endolymphatic hydrops by recording low-tone masked evoked otoacoustic emissions (TEOAE) is presented. METHODS: A short acoustic stimulus and a masker tone of 30 Hz are applied in an adjustable phase relation simultaneously to the same ear. In the normal hearing ear the masker shows little influence on the TEOAE at 0 degrees, whereas the suppression at phase 270 degrees (maximal rarefaction at the eardrum) is nearly complete. However, in cases of endolymphatic hydrops this masking effect is reduced or absent, indicating impaired mobility of the basilar membrane. RESULTS: The masked TEOAE were recorded of patients with normal hearing, Menière's disease, and sudden hearing loss without vertigo. In Menière cases with supposed endolymphatic hydrops, the amplitude modulation of the emissions was found to be much less than in the other groups. CONCLUSIONS: Where TEOAE can be recorded, low-tone masking is a quick, objective, and noninvasive method for the diagnosis of endolymphatic hydrops.

Acoustic Stimulation↗

PubMed1997

Two-phase endolymphatic hydrops: a new dynamic guinea pig model.

The classical guinea pig model for Meniere's disease, in which endolymphatic hydrops was achieved by destruction of the endolymphatic sac and obliteration of the endolymphatic duct, is a non-physiological profound model with shortcomings in relation to Meniere's disease as seen in patients. We developed a more subtle animal model; the two-phase endolymphatic hydrops. This model is based on a combination of chronic endolymphatic sac dysfunction, induced by slight destruction of the most distal part of the endolymphatic sac, and acute stress-induced endolymph production by stimulation of the Na/K-ATPase in the stria vascularis with aldosterone. Light microscopy of the fluid compartments of four groups of cochleas was used to examine them for the presence of endolymphatic hydrops: i) Normal (control) cochleas showed no hydrops; ii) some of the non-operated (no destruction) aldosterone-treated cochleas showed small degrees of hydrops mainly present in the basal turns; iii) mild dissection of the endolymphatic sac without administration of aldosterone produced a hydrops which was mainly present in the cochlear apex; iv) combination of chronic endolymphatic sac dysfunction and acute attacks of endolymph production by aldosterone administration revealed the most severe degrees of hydrops in all cochlear windings, damage to cochlear structures, and cellular disturbances of the epithelial lining of the endolymphatic sac. This new model may represent a more physiologic and dynamic approach to Meniere's disease and may explain the etiology of many symptoms in patients such as the fluctuant nature and the types of sensoneuronal hearing losses.

Aldosterone↗

PubMed2006

[Diagnosis of delayed endolymphatic hydrops].

OBJECTIVE: To investigate the diagnostic methods and significance of several tests for delayed endolymphatic hydrops (DEH). METHOD: Fifteen patients with delayed endolymphatic hydrops were tested with pure tone threshold, ECochG, bithermal caloric test and vestibular evoked myogenic potentials test to detect the lesioned side and the extent of hydrops. RESULT: All of the 15 patients had sensorineural hearing loss to the medium-severe extent at least. Ten were the ipsilateral type, four contralateral type and one bilateral type. Five cases had abnormal horizontal semicircular canal (HSCC) hydrops and saccular hydrops; six cases had abnormal HSCC function and normal saccular function; two cases had abnormal saccular function and normal HSCC function. The seven abnormal VEMP took the forms of loss of p13-n23, elongation of the latency of p13 or depressed amplitude cases with of p13-n23. CONCLUSION: ECochG, bithermal caloric test and VEMP may play a major role in the diagnosis of delayed endolymphatic hydrops and they should be utilized as the routine tests.

Adolescent↗

PubMed2002

Vestibular evoked myogenic potentials in delayed endolymphatic hydrops.

OBJECTIVE/HYPOTHESIS: Vestibular evoked myogenic potential (VEMP) has become an established test to explore the sacculo-collic reflex. The study aims to investigate the VEMPs in cases of delayed endolymphatic hydrops because greatly dilated saccule was observed in histopathological specimens of delayed endolymphatic hydrops. STUDY DESIGN: Prospective study. METHODS: Twenty patients with delayed endolymphatic hydrops were subjected to pure-tone audiometry, caloric testing, and VEMP test. Delayed VEMP was defined as the latency of peak I exceeding 22.6 milliseconds or of peak II exceeding 33.1 milliseconds. Interaural amplitude difference over the sum of amplitudes of both ears was measured, and when the ratio exceeded 0.36, it was identified as augmented VEMP or depressed VEMP depending on whether the amplitude of the lesioned side was greater or less than the opposite side. RESULTS: The VEMP test revealed that 9 patients (45%) were normal, 6 (30%) exhibited absent VEMPs, and 5 (25%) displayed abnormal VEMPs, including delayed VEMPs in 2, depressed VEMPs in 2, and augmented VEMPs in 1. The caloric test indicated that 9 (47%) of the 19 ears exhibited normal caloric response, whereas 10 ears displayed abnormal caloric responses including canal paresis in 8 and absent caloric response in 2. Six ears had preserved both the caloric response and the VEMPs, whereas no ear demonstrated both absent caloric response and absent VEMPs. CONCLUSIONS: The residual caloric as well as saccular functions after ear insult may determine whether delayed endolymphatic hydrops will occur. These findings suggest that patients with sudden deafness or juvenile unilateral total deafness should undergo caloric testing and VEMP test to predict the occurrence of delayed endolymphatic hydrops in the future.

Adult↗