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PubMedDate not supplied

Menière's disease and endolymphatic hydrops: clinical-histopathological correlations.

The clinical-histopathological correlation between Menière's disease and endolymphatic hydrops was done to explain, as much as possible, causes of symptoms of Menière's disease. Twenty-three temporal bones with endolymphatic hydrops from 17 patients were reviewed and clinical and histopathological findings were correlated. Histopathological examination revealed frequent, severe deformities in the labyrinthine walls and permanent changes in Reissner's membranes. Evidence of rupture was difficult to assess. Of 21 ears of patients with the clinical diagnosis of Menière's disease, 93% had endolymphatic hydrops. A statistical correlation between increased area of the cochlear duct and hearing loss was found. Some correlation was also found between frequency of vertigo and results of electronystagmography with histopathological findings. Consequently, the mechanical effect of endolymphatic hydrops seems to have greater significance in the production of symptoms of Menière's disease than the biochemical effect of ruptures. In a review of ten unusual cases from this series of 17 patients, traumatic neuromas or remnants of vestibular structures were found after an incomplete labyrinthectomy. Histopathological findings of four patients who had undergone endolymphatic subarachnoid shunt surgery are described.

Adult↗

PubMed1996

A human temporal bone study of changes in the basilar membrane of the apical turn in endolymphatic hydrops.

We observed that some temporal bones with endolymphatic hydrops (EH) showed varying degrees of basalward displacement (towards the scala tympani) of the basilar membrane (BM) in the apical turn of the cochlea. In some, the BM was adherent to the bony wall of the scala tympani (i.e., the interscalar septum). Such mechanical distortion of the BM could conceivably alter cochlear mechanics and lead to sensorineural hearing loss. The results of a systematic evaluation of 234 temporal bones to characterize, quantify and determine the functional significance of this observation are presented. Four groups of bones were evaluated: normal (N = 78), presbycusis (N = 96), Ménière's disease (N = 23), and EH secondary to labyrinthitis (N = 37). The incidence of extreme displacement of the BM in the apical turn such that it adhered to the interscalar septum was 52% in Ménière's disease, 57% in EH secondary to labyrinthitis, 10% in presbycusis, and 1% in normals. These differences were significant and could not be explained on the basis of age, sex, postmortem time, or artifact of technique or processing. Displacement of the BM was not observed in other turns of the cochlea. Its pathogenesis is not known, but may be related to atrophy of the spiral ligament. It is likely that such BM displacement results in sensorineural hearing loss. However, our data and theoretical analyses both indicate that such a loss will be restricted to frequencies below 100 Hz and that this pathologic change alone is not likely to cause appreciable hearing loss at clinically tested frequencies of 250 HZ and higher. Hence, even though this pathologic finding is common in endolymphatic hydrops, it cannot explain the low-frequency hearing lost observed in Ménière's disease.

Adult↗

PubMed1987

Induction of experimental endolymphatic hydrops by immunologic techniques.

Immunologic techniques have been used by many investigators to produce experimental endolymphatic hydrops models. These techniques, however, have achieved little success in producing models simulating the idiopathic endolymphatic hydrops of Meniere's disease, in which no inflammatory changes occur in the perilymphatic spaces. In this study, the antigen horseradish peroxidase (HRP) was injected into the endolymphatic sacs of ninety guinea pigs that had been systematically sensitized to this antigen. Endolymphatic hydrops was induced in sixty-seven of the subjects, sixty-four of which showed no inflammatory changes in the perilymphatic spaces. The endolymphatic sacs of the affected guinea pigs were packed with soft granulation tissue induced by immunologic mechanisms; it is felt that the hydrops was caused by disturbances in endolymph absorption resulting from these tissue formations. Our results suggest that the introduction of antigens into the endolymphatic sac may prove useful in producing endolymphatic hydrops with characteristics similar to those occurring in Meniere's disease.

Animals↗

PubMed2001

Sensory cell damage in two-phase endolymphatic hydrops: a morphologic evaluation of a new experimental model by low-voltage scanning techniques.

HYPOTHESIS: The aim of this study was to create a more dynamic animal model of Ménière's disease combining multiple causes, such as the role of endocrine factors and endolymphatic sac dysfunction, that may mimic the fluctuant characteristics of Ménière's disease. BACKGROUND: Endolymphatic hydrops remains to be considered a pathologic substrate in the etiology of Ménière's disease. The classic guinea pig model of inducing hydrops by total destruction of the endolymphatic sac is a nonphysiologic rigid model of Ménière's disease. METHODS: The authors developed the two-phase endolymphatic hydrops model by inducing hydrops by mild chronic endolymphatic sac dysfunction, in combination with increased endolymph production by aldosterone. Sensory cell damage was evaluated by low-voltage field emission scanning microscopy. RESULTS: This study describes a wide spectrum of morphologic effects of the outer hair cells in radial gradients, in which most effects were observed in the third to second row of outer hair cells, and longitudinal gradients in which the most severe effects were observed in the apical turns. Most affected were the ears that underwent distal endolymphatic sac dissection followed by the administration of aldosterone. Damaging effects proceeded from degeneration and absence of short stereocilia of outer hair cells and even some inner hair cells in the apical turns, to stereociliary disarrangement and atrophy, followed by degeneration and absence of outer hair cells, which were replaced by supporting cells. CONCLUSION: The two-phase endolymphatic hydrops model seems to represent a functional model that may mimic the fluctuant characteristics of Ménière's disease and emphasizes the influence of multiple and coexisting hydrops-inducing influences.

Animals↗

PubMed2002

Changes in Ca2+-ATPase in a guinea pig endolymphatic hydrops model.

OBJECTIVE: To investigate the localization of Ca(2+)-ATPase (Ca(2+) pump) in the cochlear and its change after endolymphatic hydrops, and to study the relationship between compound action potential (CAP) threshold and the Ca(2+)-ATPase activety. METHODS: The left endolymphatic sac was ablated to induce endolymphatic hydrops in fourteen healthy guinea pigs with normal action potential thresholds measured after a sliver ball electrode placed on the round window. Ca(2+)-ATPase activity was studied cytochemically using a lead citrate reaction in control and hydropic ears. The reaction product was lead phosphate particles as an expression of Ca(2+)-ATPase activity, observed with an eletron microscope. RESULTS: Ca(2+)-ATPase activity is mainly found on the endolymphatic surface of Reis sner's membrane, the stereocilia and cuticular plate of inner and outer hair cells, and along the infolded plasma membrane of strial marginal cells. CAP thresholds of filtered click are increased and Ca(2+)-ATPase activity significantly decreased after endolymphatic hydrops in the mentioned locations. CONCLUSIONS: CAP thresholds are increased and Ca(2+)-ATPase activity are significantly decreased in the cochlea after endolymphatic hydrops. These results suggest that there is a negative correlation between them.

Action Potentials↗

PubMed2001

Spontaneous otoacoustic emissions in humans with endolymphatic hydrops.

OBJECTIVE/METHODS: The origin and clinical implications of spontaneous otoacoustic emissions (SOAEs) have not been well revealed. To investigate the relationship between the ear with endolymphatic hydrops and SOAE, SOAEs were measured in 31 patients with unilateral endolymphatic hydrops and 10 volunteers with normal hearing levels that had less than 25 dB hearing level (HL) on average for five frequencies (0.25, 0.5, 1, 2, and 4 kHz). RESULTS: SOAEs were detected in 18 (58%) of the 31 ears with hydrops. In 15 hydropic ears in which the hearing levels were less than 25 dB HL on average, SOAEs were observed in 11 (73%). The results of examining the relationship between changes in hearing level after administering the glycerol test and SOAE frequency showed that four (50%) of eight hydropic ears had SOAEs that were detectable between the frequency in which hearing level improved more than 5 dB and the frequency with no hearing level change in the audiogram. In 28 contralateral ears, except for three cases of delayed endolymphatic hydrops, SOAEs were detected in 17 (61%). In 14 contralateral ears in which the hearing levels were less than 25 dB HL on average for the five frequencies noted above, SOAEs were observed in nine ears (64%). In 20 normal ears, SOAEs were detected in eight (40%). Prevalence of SOAEs in hydropic ears and contralateral ears of the patients with unilateral hydrops tended to be greater than that in normal ears; however, there was no significant statistical difference between them. CONCLUSION: The present results suggest that it is not possible to mention the characteristics of SOAE in the hydropic ear only in terms of the prevalence of SOAEs. SOAEs may occur in a specific portion of the basilar membrane corresponding to the frequency in which hearing levels improve after the glycerol test, in some cases with endolymphatic hydrops.

Adult↗

PubMed1998

Low-frequency masking for detection of endolymphatic hydrops in patients with glaucoma.

The coincidence of various eye and ear abnormalities has been described in the literature. Some authors discuss the possible existence of endolymphatic hydrops in patients with glaucoma. Whereas the current diagnostic tests for glaucoma are well-defined and evident, those for endolymphatic hydrops are not so reliable. This has made it difficult to accurately study the coincidence of endolymphatic hydrops and glaucoma. For better detection of endolymphatic hydrops, we performed low-frequency masking tests in 23 patients with primary open-angle glaucoma without signs of Ménìere's disease. The phase dependent sensitivity of the organ of Corti to a short test stimulus can be measured by applying a low-frequency masker tone to determine the modulation depth. Whereas the modulation depth in the normal hearing population is around 20-35 dB, the modulation depth in patients with Ménière's disease may be significantly decreased (5-10 dB), depending on the stage of disease. A decreased modulation depth was found in at least one ear in 19 of our 23 patients with glaucoma. Correlations between homeostatic mechanisms and their histological characteristics, e.g. melanocytes and their hormonal and enzymatic regulation, will be discussed. If the common pathogenesis of eye and ear lesions is better understood, it may be possible to develop new and more effective strategies for prevention and therapy.

Acoustic Stimulation↗

PubMed2003

Correlation between hearing loss and scala media area in guinea pigs with long-standing endolymphatic hydrops.

HYPOTHESIS: Histologic analysis of the hydropic and normal guinea pig cochleae was undertaken to assess a potential correlation between the magnitude of endolymphatic hydrops and hearing loss. It was hypothesized that a greater correlation than previously reported might be found by looking at long-standing endolymphatic hydrops and high-frequency range hearing. BACKGROUND: Surgically induced endolymphatic hydrops in guinea pigs is the most widely used animal model for the study of human Ménière's Disease and recapitulates both endolymphatic hydrops and progressive sensorineural hearing loss. A strong correlation between the magnitude of hydrops and severity of hearing loss has been reported in the human condition, but not in the animal model. METHODS: Nine albino guinea pigs were each subjected to surgical obstruction of the endolymphatic sac and duct of the right ear. The left ears remained as internal histologic controls. Hearing was assessed from 2 kHz to 32 kHz by auditory brain stem response testing for 16 to 25 weeks after surgery. Histologic morphometry after the animals were killed was used to quantify both turn-specific and weighted overall hydrops. These measures were correlated with hearing loss in each animal at all tested frequencies. RESULTS: A statistically significant correlation between the magnitude of hydrops and the severity of hearing loss was observed for 2 kHz and 16 kHz. These frequencies correlated with both turn-specific hydrops and overall hydrops. However, turn-specific hydrops did not reliably correlate with the magnitude of hearing loss at anatomically appropriate frequency ranges. Where such a correlation did exist, it might well have been simply part of an expression of an overall correlation between hydrops and hearing loss. CONCLUSIONS: There may be a greater correlation between hydrops and hearing loss in guinea pigs with long-standing surgically induced hydrops than has previously been reported in animals with less advanced disease. These findings help to validate continued use of the model for hearing loss related to Ménière's Disease, verify the rationale of treatment modalities aimed at reducing hydrops in the human condition, and may indicate that efforts at reducing hydrops in such patients has benefits toward long-term hearing preservation.

Animals↗

PubMedDate not supplied

Classification of endolymphatic hydrops.

Ménière's disease is but one member of a family of disorders linked by the common pathophysiologic substrate of endolymphatic hydrops. The authors evaluated both clinical cases and temporal bone specimens and conclude that endolymphatic hydrops is a pathologic condition that is the final common manifestation of a variety of otologic insults. They present a logical classification which, on the basis of clinical data, distinguishes symptomatic and asymptomatic forms. The hallmarks of the symptomatic form are fluctuating hearing loss and episodic vertigo. The asymptomatic form is clinically silent. Each form may be further subclassified into embryopathic, acquired, and idiopathic types. The embryopathic type comprises those cases in which a noxious influence disrupts labyrinthine development in utero. The acquired type includes those cases in which a documented insult, either inflammatory or traumatic, is suffered by a previously normal labyrinth. The idiopathic type encompasses all those cases in which the event precipitating the endolymphatic hydrops is unknown. Ménière's disease is redefined as idiopathic, symptomatic endolymphatic hydrops.

Adolescent↗

PubMed1999

Ultrastructure of the endolymphatic sac in two-phase endolymphatic hydrops in the guinea pig.

Two-phase endolymphatic hydrops is a subtle experimental model for Meniere's disease. Chronic dysfunction of the endolymphatic sac, induced by dissection of the most distal part without causing damage to the intermediate part, is combined with increased endolymph production induced by administration of aldosterone which stimulates the N/K-ATPase in the stria vascularis. A transmission electron microscopic study was performed on the endolymphatic sacs of four groups of guinea pig cochleas: controls: non-operated aldosterone-treated cochleas; operated (dissection of the endolymphatic sac) cochleas; operated and aldosterone-treated cochleas. Light and electron microscopy showed a normal morphology in the controls. Aldosterone treatment had no visible effect. Dissected ears revealed severe deviations. The epithelium of the intermediate sac was low, showed dilated lateral intercellular spaces indicating elevated fluid transport and displayed serious degenerative processes. Distally, the endolymphatic sac was completely blocked by newly formed bone. Additional aldosterone treatment had no cumulative effect on the dissected ears.

Aldosterone↗

PubMed1998

[Clinical features in patients with delayed endolymphatic hydrops].

We report clinical features in patients with delayed endolymphatic hydrops (DEH) with juvenile unilateral deafness. Among 23 patients with DEH, 15 cases were diagnosed as ipsilateral DEH and 8 cases as contralateral DEH. The distribution of onset age showed two peaks at ages of < 30 years and > 40 years. In 80% of the ipsilateral DEH cases, the onset of episodic vertigo was at younger ages. On the other hand, in 75% of the contralateral DEH cases, the onset of fluctuation hearing loss of the contralateral ear was at older ages. Ispilateral DEH and Meniere's disease may show different pathophysiologies. The incidence of dominant negative summating potential in the better-hearing ear was 20% in the ispilateral DEH cases and 60% in the contralateral DEH cases. It is suggested that endolymphatic hydrops is in the better-hearing ear of contralateral DEH.

Adult↗

PubMed1979

The vestibular aqueduct and endolymphatic sac and duct in endolymphatic hydrops.

The histologic features of the endolymphatic sac and duct in 23 serially sectioned temporal bones with idiopathic or secondary endolymphatic hydrops were blindly compared with 22 randomly selected, normal temporal bones. In idiopathic hydrops, the pars rugosa of the endolymphatic sac extended out of the vestibular aqueduct into the dura in 29% of bones, compared with none of normal bones (P less than .01). In the other 71%, the pars rugosa in the vestibular aqueduct was surrounded by dura more commonly than normal. Functional studies are required to assess the relationship of these findings to hydrops. In secondary hydrops (eg, due to labyrinthitis), the endolymphatic duct was obliterated in the isthmus of the vestibular aqueduct by bone or fibrosis in seven of nine bones. Because of similar ossification and fibrosis elsewhere in the vestibular labyrinth, a direct relationship with hydrops cannot be assumed.

Adult↗

PubMed2003

[Aural fullness and endolymphatic hydrops].

BACKGROUND: Low-frequency modulated DPOAEs were registrated to investigate whether the subjective symptom of aural fullness can indicate an endolymphatic hydrops. METHOD: The cochlear partition is periodically moved towards scala vestibuli and scala tympani by a low-frequency suppressor tone. The level of simultaneously registrated DPOAEs is modulated depending on the phase of the suppressor. This modulation may be reduced when the displacement of the organ of Corti is inhibited by mechanical stiffening of the basilar membrane (e. g. in endolymphatic hydrops). SUBJECTS: Low-frequency modulated DPOAEs were registrated in 15 patients with Menière's disease, in 8 patients with aural fullness and tinnitus, but without vertigo, and in 21 normal hearing adults. RESULTS: In both patient groups the modulation depth is high significantly lower than in the control group. The results do not differ significantly in the patients with and without vertigo. CONCLUSION: The reduction of the modulation depth can be interpreted as a sign of an endolymphatic hydrops. In the group of patients with aural fullness a cochlear hydrops can be assumed. The measurement of low-frequency modulated DPOAEs is a new tool to diagnose and monitor the course of endolymphatic hydrops and to evaluate the effectiveness of therapeutic methods.

Audiometry, Pure-Tone↗

PubMed1991

Cellular changes in Reissner's membrane in endolymphatic hydrops.

A quantitative morphologic study of the cellular changes in human Reissner's membrane (RM) was performed under light microscopy on 30 normal temporal bones from 15 subjects, and on 20 temporal bones from 10 subjects with endolymphatic hydrops. The cellular density of the epithelial and mesothelial layers of normal RMs decreased with increasing age. In endolymphatic hydrops, cellular proliferation and decreased cellular density of a distended RM were observed, and these changes occurred more remarkably in epithelial cells. Decreased cellular density in RM was correlated to the degree of endolymphatic hydrops. These findings indicate an involvement of the epithelial cellular changes in the pathogenesis of endolymphatic hydrops. Our results suggest that cellular changes in RM may cause dysfunction of radial flow leading to ionic disturbance of endolymph, which provides a possible mechanism of hearing loss in endolymphatic hydrops.

Adolescent↗

PubMedDate not supplied

Unilateral endolymphatic hydrops and associated abnormalities.

A case of unilateral endolymphatic hydrops is presented in which several significant histopathological findings are observed in the affected inner ear and are absent in the opposite ear. Moderate endolymphatic hydrops is present in all cochlear turns on the involved side. Atrophic changes in the cochlear and vestibular end-organs, partial collapse and infolding of Reissner's and the saccular membranes, and collapse of the posterior canal membrane are also seen. There is also marked narrowing of the proximal rugose portion of the endolymphatic sac, associated with a flattened, epithelial lining, dense fibrotic connective tissue, brown pigment deposition, and poor vascularity in a relatively narrowed and straightened vestibular aqueduct. Fibrosis, loss of vascularity, and brown pigment deposition are also observed in the bony channels surrounding the vestibular aqueduct.

Cochlea↗

PubMed1995

Vascular permeability of the stria vascularis and morphology of the endolymphatic sac in two types of experimental endolymphatic hydrops.

We produced two kinds of experimental endolymphatic hydrops. One was induced by obliteration of the endolymphatic sac (ES), and the other was induced by both systemic keyhole limpet hemocyanin immunization and secondary keyhole limpet hemocyanin challenge into the ES. The vascular permeability of the stria vascularis in acute and chronic phases was compared between both models by light and electron microscopy using the tracer method of horseradish peroxidase. Both models showed that the number of strial capillaries showing horseradish peroxidase leakage was significantly higher in the acute phase than in the chronic phase. In the acute phase, the ES showed acute inflammation in both models. In the chronic phase, extensive fibrosis occurred in the ES obliteration model, whereas the ES appeared to have a normal shape in the immunologically induced model. The mechanism of hydrops formation will be compared between the two models.

Acute Disease↗

PubMed1991

Vestibular aqueduct in Menière's disease and non-Menière's disease with endolymphatic hydrops: a computer aided volumetric study.

The volume of the vestibular aqueduct was studied by a computer-aided volumetric method in 9 temporal bones with endolymphatic hydrops from individuals with Menière's disease (MD), 7 temporal bones with endolymphatic hydrops from individuals without a history of Meniere's disease (non-MD hydrops), and 10 normal temporal bones (controls) to investigate the cause of endolymphatic hydrops in both MD and non-MD hydrops. A hypoplastic vestibular aqueduct was found significantly more often in the MD group than in either the non-MD hydrops group (chi 2-test, chi 2 = 4.063, p less than 0.05) or the control group (chi 2-test, chi 2 = 6.363, p less than 0.05). The difference in volume between the non-MD hydrops group and the control group was not significant. It is speculated that a small vestibular aqueduct (presumably containing a small endolymphatic sac) might be a predisposing factor in Menière's disease. In contrast, in non-MD hydrops, there seems to be no correlation of endolymphatic hydrops with a hypoplastic vestibular aqueduct and endolymphatic sac.

Adult↗

PubMed1999

Meniere's disease and endolymphatic hydrops without Meniere's symptoms: temporal bone histopathology.

We studied temporal bone histopathology in 21 ears with Meniere's disease and 24 ears with endolymphatic hydrops without Meniere's symptoms and compared the findings to those in 10 ears with presbycusis and 11 ears with normal hearing. Normal hearing ears showed less degeneration of cochlear structures than the other ears. In ears with endolymphatic hydrops without Meniere's symptoms, the degeneration of spiral ligament, hair cells, dendrites (peripheral processes) and apical spiral ganglion cells was more severe than in the other three groups. In ears with Meniere's disease and endolymphatic hydrops without Meniere's symptoms, the hair cells and dendrites were more affected than ganglion cells and there was no correlation between hair cell and ganglion cell degeneration. These findings suggest that a permanent threshold shift in late stage endolymphatic hydrops is not related to ganglion cell loss but rather to degeneration of sensory elements.

Aged↗