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PubMed1991

The influence of noise exposure on endolymphatic hydrops. An experimental study.

The influence of noise exposure on endolymphatic hydrops was examined morphologically. Endolymphatic hydrops was produced experimentally in guinea pigs by means of endolymphatic sac obliteration. Approximately 2 months later, the animals were subjected to noise exposure for 2 h and, as a result, the following findings were obtained: Vascular and circulatory disturbances in the 3rd and 4th turns of cochlea, i.e., vasoconstriction-like changes in the upper coiled arterioles and capillaries in the stria vascularis, as well as blood cell sludge. In addition, the outer hair cells in Corti's organ at the same turns disappeared sporadically. No changes were observed in the opposite, control, ear of the same animal which was free from endolymphatic hydrops. On the basis of these results, it is argued that endolymphatic hydropic ears are highly vulnerable to noise exposure.

Animals↗

PubMed1988

Delayed endolymphatic hydrops: a review of 15 cases.

Delayed endolymphatic hydrops is a disease entity that can be differentiated from Meniere's disease. This condition was first reported simultaneously by Nadol, et al. and Wolfson and Leiberman, with further clarification by Schuknecht. The disease is characterized by a profound sensorineural hearing loss in one ear, with the onset of episodic vertigo from that ear after a prolonged period of time (ipsilateral delayed endolymphatic hydrops) or the development of fluctuating hearing loss and/or episodic vertigo in the opposite ear after a prolonged period of time (contralateral delayed endolymphatic hydrops). This paper is a review of 15 cases of delayed endolymphatic hydrops, eight ipsilateral and seven contralateral. The results of this study indicate that surgical treatment for the ipsilateral form of the disease gave the best results. For the contralateral variant, it appears that medical measures should be the therapy of choice resorting, in the event of their failure, to conservative surgical intervention on what may be the only hearing ear to preserve hearing and control vertigo.

Adolescent↗

PubMed1984

Detection of delayed endolymphatic hydrops by the furosemide test.

Delayed endolymphatic hydrops, an entity which can be differentiated from Meniere's disease, was first reported simultaneously by Nadol et al. (1975) and Wolfson & Leiberman (1975) and specified by Schuknecht (1978). They diagnosed it from the anamnesis of patients and confirmed the hydropic condition of the labyrinth solely by evidence obtained from surgical procedures such as labyrinthectomy. The aim of the present study was to emphasize the usefulness of the furosemide test for distinguishing this entity before surgery by detecting the hydropic condition in the labyrinth. In these 3 years, we encountered 11 cases of endolymphatic hydrops, 9 ipsilateral and 2 contralateral, in our clinic (Univ. of Tokyo Hospital). Among the ipsilateral cases, the estimated genesis of pre-existing hearing loss was most frequent in mumps (44%). The result of the furosemide test in this group was 89% positive. On the basis of this result, we have been able to choose the method of treatment, i.e. 4 cases treated by epidural shunt operation on the endolymphatic sac, 2 by labyrinthectomy, one by cochleosacculotomy and 2 by medication with steroids and diuretics. In the 2 contralateral cases, one was treated by epidural shunt and the other by medication. The authors are therefore able to confirm the usefulness of the furosemide test for detecting delayed endolymphatic hydrops.

Adult↗

PubMed1990

[Pathohistological study on active endolymphatic hydrops in guinea pig--with stress stimulations].

Recently Meniere's disease is believed to show a pathological features of endolymphatic hydrops, but the etiology of this disease has not yet been ascertained. Many investigators tried to create animal models with endolymphatic hydrops by obliterating endolymphatic sac and duct. However, these methods have not been adequate to explain the mechanism of development of Meniere's disease, because it gives mechanical damage to destroy endolymphatic sac and duct. On the other hand, Meniere's disease is thought to develop even as a result of stress. The present paper reported the conduction of an acute experiment, creating active endolymphatic hydrops by stress load, to study the occurrence rate of endolymphatic hydrops and the pathological findings of inner ears by a light microscope. This was followed by a light and electron microscopic study on the changes in permeability of the cochlear lateral wall with horseradish peroxidase and a study of the development mechanism of endolymphatic hydrops. Results obtained were as follows: 1. Although it was impossible to cause endolymphatic hydrops with a single stimulation, four kinds of stress stimulations could cause endolymphatic hydrops with the rate of 37.8%. 2. Judging from the different pathological findings between the group with four kinds of stress stimulations and the untreated control group, vessel permeability in the stria vascularis was highly changeable, while that in the spiral ligament was not. 3. It was found out that increased permeability of the stria vascularis vessels was by increased pinocytotic vesicular transport and through tight junctions from vessel lumen to basal lamina and that it was presumably only by increased pinocytotic vesicular transport beyond basal lamina. 4. It was assumed that increased permeability of the stria vascularis vessels was one of the causes of endolymphatic hydrops which were believed to be pathological features of Meniere's disease.

Animals↗

PubMed1994

Endolymphatic hydrops associated with otosclerosis.

Endolymphatic hydrops (EH) associated with otosclerosis has been noted for many years. However, the causal relationship of these two entities remains controversial. Having reviewed the records of patients with otosclerosis describing fluctuant hearing loss and vertiginous symptoms, the authors found the EH may coexist with otosclerosis preoperatively; they may be two separate diseases that exist coincidentally; or EH may be caused by the otosclerotic process. Secondly, EH may occur with a fistula after surgery. Occurring after stapedectomy, EH may be caused by fistulization of the bony labyrinth, which is effectively treated by surgery to seal the fistula, which may cause EH to subside and hearing to improve. Thirdly, delayed EH may occur months or years after stapedectomy, possibly as a result of otosclerotic foci or surgical insult to the labyrinth. Dexamethasone, diuretics, and a room air rebreather can be used in the treatment of delayed EH. Hearing may be maintained or may deteriorate, but there usually is no dizziness. The clinical manifestations of EH associated with otosclerosis include a conductive or mixed type of hearing loss; the presence of fullness, tinnitus, fluctuation of hearing, episodic vertigo, an elevated negative summating potential (SP), and an increased summating potential:action potential (SP:AP) ratio shown by ECoG. This report presents five cases of EH associated with otosclerosis.

Adult↗

PubMed1990

[Results of trapezoid rotation test in guinea pigs with unilateral endolymphatic hydrops].

Obliteration of the right endolymphatic sac was performed by Kimura's method in 57 guinea pigs with normal hearing and vestibular function. However, 43 animals exhibited postoperative cerebellopontile disturbance and labyrinthitis detected by gait test, ABR test and histological examination. The remaining 14 guinea pigs were evaluated periodically by the trapezoid rotation test. Two weeks after the operation, 11 of these 14 guinea pigs exhibited prolonged right beating nystagmus based on the labyrinthine preponderance of impaired side (Lpi). In addition, endolymphatic hydrops was histological detected in the labyrinth on the operation side. A positive relation was observed between the degree of endolymphatic hydrops and the degree of Lpi. Lpi at 4 weeks after the operation was markedly lower than that at 2 weeks (P = 0.05). Therefore, the degree of Lpi was thought to be influenced by the rate of hydrops development. These results corresponded with the clinical findings that the degree of Lpi increases prior to vertiginous episodes in Meniere's patients.

Animals↗

PubMed1990

Experimental endolymphatic hydrops: are cochlear and vestibular symptoms caused by increased endolymphatic pressure?

The correlation between inner ear pressure and cochlear function was investigated in guinea pigs with unilaterally obliterated endolymphatic sacs and ducts. In 11 animals that developed endolymphatic hydrops, auditory thresholds as monitored by auditory evoked action potentials had increased with recruitment. Most of these animals also experienced episodes of spontaneous nystagmus. In control ears endolymphatic pressure did not differ more than 0.5 cm H2O from perilymphatic pressure. In six of 11 hydropic ears, endolymphatic pressure was more than 0.5 cm H2O higher than perilympathic pressure; auditory thresholds in all these ears had deteriorated within 2 weeks before pressure recording. No further hearing deterioration within this period was noted in five hydropic ears with endolymphatic pressure equal to or lower than perilymphatic pressure. Endolympathic-perilymphatic pressure gradients may contribute to auditory threshold increase in endolymphatic hydrops, but are not its only cause.

Animals↗

PubMed2004

The quantification of endolymphatic hydrops in an experimental animal model with guinea pigs.

To better quantify endolymphatic hydrops in experimental guinea pigs, endolymphatic hydrops was induced by endolymphatic sac obliteration through an extradural posterior cranial fossa approach in the right ear. The area of the scala vestibuli and scala media of each turn on both cochlear midmodiolar sections was measured, using an automated computer-aided design (AutoCAD R14) software combined with a digital camera. No endolymphatic hydrops was observed in all nonoperated ears; however, various degrees of hydrops were present in all operated ears. The average maximum SMA (scala media area) ratio in the 4-week group (2.22 +/- 0.20) was greater than that in the control group (1.10 +/- 0.06). The average maximum SMA ratio of the 8-week group (4.04 +/- 0.52) was greater than that of the 4-week group (p < 0.05). This study provides a reliable methodologic base for the experimental study of Ménière's disease.

Animals↗

PubMed2005

Changes in distortion of two-tone cochlear microphonic and otoacoustic emission signals during an acute endolymphatic hydrops in the guinea pig.

An acute endolymphatic hydrops was induced by the injection of 1.1 mul of artificial endolymph into the scala media of guinea pig cochleas. This volume corresponds with an acute endolymphatic hydrops of 23%. During and after the injection, cochlear function was assessed by measuring the 2f(1)-f(2 )and f(2)-f(1) distortion products in cochlear microphonics (CMDP) and the 2f(1)-f(2) distortion product otoacoustic emission (DPOAE). A reversible pressure increase of 23 Pa and a relatively stable endocochlear potential (EP) were accompanied by a mean decrease in 2f(1)-f(2) DPOAE of only 3.4 dB. Similarly, the 2f(1)-f(2) CMDP amplitude change was minimal during and after the injection. The only substantial change was measured in the f(2)-f(1) CMDP amplitude. The measured range of distortion amplitudes during an acute endolymphatic hydrops can be related to small changes in the cochlear transducer operating point.

Acute Disease↗

PubMed2001

Distortion-product otoacoustic emissions and glycerol testing in endolymphatic hydrops.

OBJECTIVES/HYPOTHESIS: Aural fullness is a frequent symptom of endolymphatic hydrops. Its evaluation may provide valuable information on the initial stage of development of endolymphatic hydrops. STUDY DESIGN: The present investigation was specifically designed to ascertain the ability of the glycerol test, combined with pure tone audiometry and distortion product otoacoustic emissions (DPOAEs) testing, to diagnose endolymphatic hydrops early and to identify patients who may evolve toward Meniere's disease. For these purposes, patients who complained about aural fullness as their only audiologic symptom were selected. METHODS: This investigation consisted of 19 consecutive patients with unilateral or bilateral aural fullness who received no treatment. Each patient underwent glycerol testing measured with conventional pure tone audiometry and with both DPOAEs. For the traditional pure-tone glycerol test, a hearing improvement of at least 10 dB, at the lower two or three frequencies (125, 250, and 500 Hz), was judged as a positive result. For the DPOAE glycerol test, a smaller positive difference (5 dB) for at least three frequencies was interpreted as an ameliorative fluctuation. RESULTS: The outcomes of the glycerol tests (24 ears examined) showed variable patterns. Seven ears showed no significant changes of either the pure-tone audiogram or DPOAE. In seven other ears, the comparison of the traditional glycerol test and the DPOAE glycerol test indicated an improvement in both measures. Another seven ears showed negative glycerol tests, whereas DPOAE responses gradually recovered reaching levels significantly higher than those recorded before glycerol administration. The three remaining ears showed contrasting results. CONCLUSIONS: Patients with aural fullness in the absence of other associated symptoms may potentially be in the initial stages of Meniere's disease. This notion is confirmed by the present findings showing a high rate (58%) of positive glycerol tests in the selected patients. The importance of DPOAE testing is supported by their ability to detect minimal dysfunction, possibly representing endolymphatic hydrops that goes undetected by routine pure-tone audiometry.

Adult↗

PubMed1982

Apical endolymphatic hydrops.

The incidence of apical endolymphatic hydrops was determined in 495 temporal bones from 300 subjects in whom the otopathologic diagnoses were presbycusis, otosclerosis, otitis media, and nonpathologic cochlea. The overall incidence was 15.8% and was not significantly different in the four diagnostic groups. These findings indicate that apical endolymphatic hydrops is of no pathologic or functional significance.

Adolescent↗

PubMed2005

Morphology of the endolymphatic sac in the guinea pig after an acute endolymphatic hydrops.

The role of the endolymphatic sac (ES) in endolymph volume homeostasis is speculative. The present study investigates changes of the ES's epithelia and luminal filling after induction of an acute endolymphatic hydrops. After microinjection of 1.1 mul artificial endolymph into scala media of the cochlea, guinea pigs were terminated immediately (n = 6) or after different time intervals ; 1/2 h (n = 3), 1 h (n = 4) and 2 h (n = 4). Inner ear specimens were processed for light and/or transmission electron microscopy. The non-injected contralateral ear served as a histological control. Correct injection was confirmed by detection of microspheres in the endolymphatic compartment after the same microinjection procedure. In all specimens, ribosome rich cells and intraluminal macrophages appeared to be actively involved in degradation of homogeneous substance (HS) by secreting lytic enzymes and digestion, respectively. Amazingly, in our study no ES differences were found between injected and non-injected ears and no distinct changes were observed in guinea pigs terminated after different time intervals. The ES's luminal HS was always present and often to a large extent. This is in contrast with [Hear. Res. 138, 81] dramatic changes were observed. Endolymph volume homeostasis is a complex mechanism, in which the role of HS remains obscure.

Acute Disease↗

PubMed2002

Cochlear ultrastructure in two-phase endolymphatic hydrops in the guinea-pig.

Endolymphatic hydrops continues to be considered as a pathological factor in the etiology of Meniere's disease. We have developed the two-phase endolymphatic hydrops model, which seems to represent a functional model combining multiple etiologies, and which may resemble the fluctuating characteristics of Meniere's disease. A transmission electron microscopic study was performed on the endolymphatic sacs of four groups of guinea-pig cochleas: (1) controls, (2) non-operated, aldosterone-treated cochleas, (3) operated (dissection of the endolymphatic sac) cochleas, (4) operated and aldosterone-treated cochleas. Light and electron microscopy showed a normal morphology in the controls. Aldosterone as a single treatment resulted in an increased activity of the marginal cells in the stria vascularis. Dissection induced a gradient of degenerative effects and cell loss in the intracellular and extracellular structures of the sensory cells, the stria vascularis and Reissner's membrane, which may be reversible. Subsequent administration of aldosterone induced severe damage and increased cell loss, which may be irreversible. Our findings demonstrate changes that may be reversible due to the compromising effect of a single treatment, and irreversible changes due to interaction of both compromising factors. These findings support our two-phase concept.

Animals↗

PubMed1991

Endolymphatic hydrops in animal experiments. A confirmation of mechanical and immunological methods of inducement.

The etiology underlying endolymphatic hydrops is scarcely understood. It is generally accepted, however, that the primary cause of endolymphatic hydrops is the malfunction and malabsorption of the endolymphatic sac. This has already been proven by animal experiments as well as by histopathological studies of human temporal bone. In this study, we attempted to induce endolymphatic hydrops by utilizing both mechanical and immunological methods. An obliterative procedure was performed on the endolymphatic sac and duct of 14 guinea pigs, 12 of which showed extensive endolymphatic hydrops after a variable period of time. The immunological method employed was to inject the antigen horseradish peroxidase into the endolymphatic sac of 22 guinea pigs that had been systemically sensitized to this antigen. Endolymphatic hydrops was induced in 11 of these subjects. Thus, this study lends further support to the fact that endolymphatic hydrops is caused by malfunction of the endolymphatic sac, resulting from either mechanical obliteration or immunological reaction.

Animals↗

PubMed1995

Microvascular disorder of the stria vascularis in endolymphatic hydrops.

To investigate the role of pathology of the stria vascularis in endolymphatic hydrops, the vascularity and atrophy of the stria were examined by histological observation in guinea pig temporal bones affected by experimental endolymphatic hydrops. Blood cell sludge and vasoconstriction accompanied by strial atrophy were observed in the coiled arteriole and capillary of the stria vascularis of the ear with endolymphatic hydrops after exposure to noise, suggesting the development of inner ear circulatory disturbance. Furthermore, these findings were observed around the upper turn of the cochlea. The effect of glycerol and difenidol hydrochloride on endolymphatic hydrops was also examined. Vasoconstriction and blood cell sludge disappeared following administration of these agents, accompanied by collapse. These findings suggest the possibility that the circulatory disturbance might be the cause of endolymphatic hydrops, followed by strial atrophy.

Animals↗

PubMed2001

Diagnosis of endolymphatic hydrops in vivo with magnetic resonance imaging.

HYPOTHESIS: High-resolution magnetic resonance imaging (MRI) at 1.5 T preferentially enhances the perilymph over endolymph after administration of contrast with gadodiamide, which allows for differentiation of the membranous labyrinth. Furthermore, this imaging allows for the detection of endolymphatic hydrops. BACKGROUND: Endolymphatic hydrops is believed to be associated with a number of ear diseases, including Ménière's disease. Although the pathologic changes of overaccumulation of endolymph in the inner ear are obvious on postmortem histologic examination of the temporal bone, they have yet to be observed in a living organism. Previous attempts to visualize this condition with high-resolution contrast-enhanced computed tomographic imaging and MRI have been unsuccessful. METHODS: Healthy pigmented guinea pigs underwent a unilateral surgical ablation of the endolymphatic sac to create endolymphatic hydrops in the ear. High-resolution temporal bone imaging was performed by use of a 1.5-T MRI system. Two-dimensional images were acquired by a spin-echo technique with and without contrast enhancement by gadodiamide. RESULTS: T1-weighted gadodiamide contrast-enhanced MRI of the midmodiolar level of the cochlea demonstrated that the perilymph appeared to be preferentially enhanced relative to the endolymph, resulting in a clear distinction between the scalae of the inner ear. The contrast-enhanced T1-weighted MRI of the midmodiolar level of the hydropic cochlea demonstrated a significantly enlarged scala media in comparison with the normal cochlea in the same animal. CONCLUSION: The demonstration of endolymphatic hydrops has been possible for the first time in vivo by the use of a standard 1.5-T MRI system. This research has important clinical implications: Specifically, this technique may allow for the noninvasive diagnosis of Ménière's disease.

Animals↗

PubMed1997

Treatment of ipsilateral delayed endolymphatic hydrops.

Nine patients with ipsilateral delayed endolymphatic hydrops were treated. All cases were initially treated by conservative therapy using isosorbide or other drugs and 4 patients have been doing well without surgical intervention, though they occasionally have slight dizziness. Five patients required surgery to control vertigo. Three patients first underwent cochleosacculotomy to maintain the vestibular function in the diseased ear, but vertigo recurred after 6 months in all 3 cases. These 3 patients and another patient who wanted definitive treatment right from the start underwent transmastoid labyrinthectomy which resulted in complete control of vertigo. One patient received chorda tympani nerve section because he did not want his vestibule destroyed. After the nerve section, he has had no vertigo though sometimes dizziness. Transmastoid labyrinthectomy seems to be the best treatment for ipsilateral delayed endolymphatic hydrops.

Adult↗

PubMed2005

Frequency dynamics shift of vestibular evoked myogenic potentials in patients with endolymphatic hydrops.

OBJECTIVE: To measure the frequency dynamics of the vestibular evoked myogenic potential in patients with endolymphatic hydrops. STUDY DESIGN: A prospective study. SETTING: A university hospital. SUBJECTS: The endolymphatic hydrops group consisted of 28 affected ears of patients with definite unilateral Ménière's disease and a control group of 36 ears of 20 healthy volunteers. INTERVENTIONS: Vestibular evoked myogenic potentials generated by tone bursts at 250, 500, 700, 1,000, 1,500, 2,000, and 4,000 Hz were measured in both groups. Vestibular evoked myogenic potentials were also measured after furosemide administration in six patients in the endolymphatic hydrops group. MAIN OUTCOME MEASURE: The frequency sensitivity of vestibular evoked myogenic potential, as evaluated by p13-n23 normalized amplitude. RESULTS: Peak amplitudes were noted at 500 Hz in the control group and at 1,000 Hz in the endolymphatic hydrops group. After furosemide loading, peak amplitude shifted to a lower frequency in four of six ears. CONCLUSION: The peak amplitude of vestibular evoked myogenic potentials in the endolymphatic hydrops group was at a higher frequency than in the control group. The frequency of the saccule (nu) should be proportional to radical(tau/sigma), where tau is the tension of membrane and sigma is its density. We advocate the hypothesis that the shift in frequency dynamics of vestibular evoked myogenic potential in patients with endolymphatic hydrops originates from the morphologic features of the saccule, analogous to an expanded balloon.

Acoustic Stimulation↗