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PubMed1993

Ultrastructural features of human Reissner's membrane.

Ultrastructural features of human Reissner's membrane were investigated in two groups of similarly aged patients. Five patients had age-related normal hearing (ARNH) and four patients had acquired sensorineural hearing loss (SNHL) from causes other than age. The membrane consisted of a mesothelium facing the perilymph and an epithelium facing the endolymph. The two cell layers were separated by a basement membrane. The mesothelium was formed by wide spread thin cells with a smooth surface. The epithelial cells assumed two different shapes, flat and rounded. Both epithelial cell types were covered with many short microvilli. In all specimens, the rounded cells were arranged in bands, strands, whorls and clusters. The size of bands and whorls was larger in the lower half of the basal turn and decreased gradually towards the apex. Bands and whorls were both larger in specimens from patients with SNHL than in those with ARNH and expanded up to the middle turn. In patients with SNHL, some flat cells had relatively few long microvilli. The epithelium showed more pronounced cellular changes in patients with SNHL than in those with ARNH and these alterations are discussed in relation to sensorineural degeneration.

Aged↗
PubMed1993

Review: morphological changes associated with endolymphatic hydrops.

Endolymphatic hydrops of the inner ear is identified as a swelling of the endolymphatic spaces. This morphopathology in man can only be confirmed at post-mortem examination although it is believed to underlie the auditory dysfunction and vestibular disturbances associated with Menière's disease. This is an illusive inner ear disorder characterized typically by the fluctuant hearing loss, tinnitus and episodes of vertigo. Menière's disease remains a major problem in otorhinolaryngology since the cause of the disease is not known and various treatments are recommended, often with unsatisfactory results. Experimentally induced endolymphatic hydrops in the animal model has been developed in order to understand better the consequences of this morphopathology on inner ear structure and function. Further investigations on the model might, in the future, lead to a more efficient management of the disorder.

Animals↗
PubMed1995

Auditory impairment in guinea pigs treated with isepamicin.

Groups of adult guinea pigs were treated intramuscularly with isepamicin at doses of 100, 150 and 225 mg/kg/day for 21 days. For comparison, two other groups were administered either saline or amikacin 225 mg/kg/day. Auditory function, as measured by the Preyer pinna reflex and the brain stem evoked response, was impaired in both the isepamicin and amikacin groups treated with 225 mg/kg/day, and to a lesser extent in the group receiving isepamicin 150 mg/kg/day. Morphological evaluation of the organ in Corti, performed either by scanning electron microscopy or by light microscopy, showed the typical pattern of damage associated with the aminoglycosides. The greatest damage was observed at 225 mg/kg/day, with no difference between isepamicin and amikacin. Isepamicin 100 mg/kg/day produced no impairment in auditory function and very little change in the morphology of the organ of Corti.

Amikacin↗
PubMed1996

Reconstructions and cross-sectional area measurements from magnetic resonance microscopic images of the cochlea.

In this study, magnetic resonance (MR) microscopy was used to obtain serial sections through the cochleae of mustached bats. As previously reported, 25 microns isotropic voxels can be obtained. Specific areas in each slice were segmented and then three-dimensional (3-D) reconstructions of the perilymphatic and endolymphatic spaces and spiral ligament were obtained. Quantitative measurements of the cross-sectional areas were made with customized macros written for the public-domain software, NIH Image. Results of this study revealed enlargements of the scalae and spiral ligament in areas known to be involved with processing of the animal's biosonar and fine-frequency analysis.

Animals↗
PubMed1996

Dexamethasone perfusion of the labyrinth plus intravenous dexamethasone for Ménière's disease.

Recent clinical and laboratory evidence indicates that Meniere's disease is an immune-mediated disease. Dexamethasone perfusion of the inner ear through the round window plus intravenous dexamethasone often will stop the dizzy spells, reduce the fullness and low-frequency tinnitus, and sometimes improve the hearing in patients with Meniere's disease. The dexamethasone must act mostly on the endolymphatic sac and, to a lesser extent, on the stria vascularis and spiral ligament, the known targets of immune response in the inner ear, to reduce the endolymphatic hydrops and restore the fluid dynamics of the endolymph. Despite the good results with streptomycin perfusion, the number of patients with further hearing loss is large, so dexamethasone perfusion with intravenous dexamethasone should be tried first. The initial response to dexamethasone perfusion plus intravenous dexamethasone has been very good, with very little risk of further hearing loss, and it holds great promise for the future.

Administration, Topical↗
PubMed1997

An ATP-dependent inwardly rectifying potassium channel, KAB-2 (Kir4. 1), in cochlear stria vascularis of inner ear: its specific subcellular localization and correlation with the formation of endocochlear potential.

Cochlear endolymph has a highly positive potential of approximately +80 mV. This so-called endocochlear potential (EP) is essential for hearing. Although pivotal roles of K+ channels in the formation of EP have been suggested, the types and distribution of K+ channels in cochlea have not been characterized. Because EP was depressed by vascular perfusion of Ba2+, an inhibitor of inwardly rectifying K+ (Kir) channels, but not by either 4-aminopyridine or tetraethylammonium, we examined the expression of Kir channel subunits in cochlear stria vascularis, the tissue that is supposed to play the central role in the generation of positive EP. Of 11 members of the Kir channel family examined with reverse transcription-PCR, we could detect only expression of KAB-2 (Kir4.1) mRNA in stria vascularis. KAB-2 immunoreactivity was specifically localized at the basolateral membrane of marginal cells but not in either basal or intermediate cells. Developmental expression of KAB-2 in marginal cells paralleled formation of EP. Furthermore, deaf mutant mice (viable dominant spotting; WV/WV) expressed no KAB-2 in their marginal cells. These results suggest that KAB-2 in marginal cells may be critically involved in the generation of positive EP.

4-Aminopyridine↗
PubMed1997

Measurement of pressure and displacement of the membranous labyrinth in endolymphatic hydrops by the tensile test.

We measured the mechanical characteristics, particularly the strength of various regions of the membranous labyrinth by the penetration test with a specially designed machine. A load-displacement curve was drawn by the tensile test for the Reissner's and basement membranes. Additionally, a stress-strain curve was drawn. The modulus of elasticity was measured showing a straight line in the stress-strain curve: 1.5 x 10(2) mN/mm2 for Reissner's membrane and 9.3 x 10(2)-1.3 x 10(3) mN/mm2 for the basement membrane. Furthermore, the endolymphatic pressure was calculated at the point in time when the maximum strain as the limit of elasticity was 0.2. It was 81 Pa. The displacement of Reissner's membrane was 0.2 mm when the initial tension was taken as 0 in the formula, and that of the basement membrane was 3 to 37 microns when the initial tension was 0, 0.1, 0.2 and 0.3.

Aged↗
PubMed1996

[Computer image analysis in the study of endolymphatic hydrops].

In search for an objective method to be used to judge the extent of hydrops, computer image analysis system was used in the study on guinea pig endolymphatic hydrops. The image information of the whole cochlea was collected, then the length of Reissener's membrane and section area of scala media were calculated based upon parameters such as ratio factors and point values. The results were as follows: 1) Hydrops observed with light microscope had no statistical difference. 2) Within 55 days postoperatively, the hydrops grew more obvious with time. 3) The hydrops was more extensive in the basal turn than in the apical turn, though more conspicuous cytopathologic change was found in the apical turn. The conclusions: 1) The current technique is objective, accurate and reliable. 2) Both the length of Reissener's membrane and section area of scala media can be used to measure the extent of hydrops.

Animals↗
PubMed2000

MR imaging of the enlarged endolymphatic duct and sac syndrome by use of a 3D fast asymmetric spin-echo sequence: volume and signal-intensity measurement of the endolymphatic duct and sac and area measurement of the cochlear modiolus.

BACKGROUND AND PURPOSE: In enlarged endolymphatic duct (EED) and sac (EES) syndrome, deformity of the EED and EES is congenital; however, hearing loss is acquired. To investigate the pathophysiology of progressive sensorineural hearing loss in EED and EES syndrome, we measured the volume of the EED and EES, the diameter of the EED and EES, the area of the cochlear modiolus, and the signal intensity of the EES and compared our findings against degree of hearing loss. METHODS: Thin-section MR images of 33 ears in 17 patients with EED and EES syndrome were studied. All studies were obtained on a 1.5-T MR unit using a quadrature surface phased-array coil. Heavily T2-weighted 3D fast asymmetric spin-echo images were obtained with a voxel size of 0.3 x 0.3 x 0.8 mm without zero-fill interpolation. Two radiologists traced the areas of the EED and EES manually, and the volume was calculated. The area of the cochlear modiolus, diameter of the EED and EES, and signal intensity of the EES were also measured by drawing regions of interest manually. The signal intensity ratio of EES/CSF was calculated. These measured values were compared against audiographic data, and the degree of linear correlation was determined. RESULTS: The volume of the EED and EES, the area of the modiolus, the diameter of the EED and EES, and the signal intensity of the EES did not show significant correlation with degree of hearing loss. CONCLUSION: These findings suggest that there is a microscopic area of damage or fragility in the inner ear not visible even with thin-section heavily T2-weighted MR imaging.

Adolescent↗
PubMed2004

The role of Pax2 in mouse inner ear development.

The paired box transcription factor, Pax2, is important for cochlear development in the mouse inner ear. Two mutant alleles of Pax2, a knockout and a frameshift mutation (Pax21Neu), show either agenesis or severe malformation of the cochlea, respectively. In humans, mutations in the PAX2 gene cause renal coloboma syndrome that is characterized by kidney abnormalities, optic nerve colobomas and mild sensorineural deafness. To better understand the role of Pax2 in inner ear development, we examined the inner ear phenotype in the Pax2 knockout mice using paint-fill and gene expression analyses. We show that Pax2-/- ears often lack a distinct saccule, and the endolymphatic duct and common crus are invariably fused. However, a rudimentary cochlea is always present in all Pax2 knockout inner ears. Cochlear outgrowth in the mutants is arrested at an early stage due to apoptosis of cells that normally express Pax2 in the cochlear anlage. Lack of Pax2 affects tissue specification within the cochlear duct, particularly regions between the sensory tissue and the stria vascularis. Because the cochlear phenotypes observed in Pax2 mutants are more severe than those observed in mice lacking Otx1 and Otx2, we postulate that Pax2 plays a key role in regulating the differential growth within the cochlear duct and thus, its proper outgrowth and coiling.

Animals↗
PubMed1999

MR imaging of the cochlear modiolus: area measurement in healthy subjects and in patients with a large endolymphatic duct and sac.

PURPOSE: To evaluate the cochlear modiolus with thin-section magnetic resonance (MR) imaging in healthy subjects and patients with a large endolymphatic duct and sac, and to assess whether the cochlea is normal or abnormal in patients with a large endolymphatic duct and sac. MATERIALS AND METHODS: MR images were obtained in 10 ears in five volunteers (group 1), 40 ears in 20 patients with bilateral sensory hearing loss (group 2), three ears in two patients with Mondini malformation (group 3), and 12 ears in seven patients with a large endolymphatic duct and sac (group 4). RESULTS: In groups 1 and 2, all modiolar areas were larger than 4.0 mm2. In group 3, each modiolus was smaller than 2.0 mm2. In group 4, modiolar areas were smaller than 2.0 mm2 in eight ears and were larger than 4.0 mm2 in four ears. CONCLUSION: Findings in this study confirm that a large endolymphatic duct and sac is frequently associated with modiolar deficiency, but the modiolar area is normal in some cases. This result does not support the recently proposed hypothesis that hearing loss with a large endolymphatic duct and sac is caused by the transmission of subarachnoid pressure forces into the labyrinth through a deficient modiolus.

Adolescent↗
PubMed2001

[Retraction of the endolymphatic membranes in temporal bones of the Wittmaack and Tufts collections].

BACKGROUND: In histologic studies, the volumetric status of the intralabyrinthine fluids is judged by the position of the endolymphatic membranes. Bulging of the membranes, commonly known as endolymphatic hydrops, is assumed to be caused by excess of endolymph. The opposite situation, retraction of the membranes is, however, only incidentally described and relatively little attention has been paid to its significance. Almost one hundred years ago Wittmaack described retraction of the endolymphatic membranes, which has since been considered to be preparation artifact--a concept that essentially remains unchallenged. To test the validity of this long premise, we examined two sets of temporal bones from different centers. MATERIAL AND METHODS: We studied the following collections: 1. The Wittmaack collection in Hamburg, Germany. The original material of 67 temporal bones (patient ages 0-92 years, average age 35.2 years) on which Wittmaack based his opinions. 2. For comparison and to exclude age related phenomena, 125 temporal bones from 73 children between the ages newborn to ten years (average age 13.4 months, median 1.5 months) from the temporal bone collection of the Department of Otolaryngology Tufts University School of Medicine. All specimens were studied by light microscopy. Retraction was defined as depression of Reissner's membrane toward the stria vascularis and the Organ of Corti in more than one cochlear turn and was graded into mild, moderate and severe. Additionally the saccule, utricle and semicircular ducts were examined for collapse. RESULTS: The reevaluation of the 67 temporal bones described by Wittmaack, including those of 7 children below the age of 10 years, showed retraction of Reissner's membrane in 81% compared to 33% of the temporal bones from the Tufts collection. In contrast to the high incidence of retraction in the cochlear duct, fewer saccules (12%) and utricles (4%) were collapsed in the Tufts collection. In the Wittmaack collection no significant differences between the underlying diseases were found, however in the Tufts collection the group of children who suffered from extracochlear infections and malignancies had a higher frequency of retraction. CONCLUSION: Mild retraction might be to some extent physiologic or even artifactual. Severe retraction, however, is a definitive finding that is a part of a local or regional otopathologic process. Of material, it is quite possible that Wittmaack's original observations of what he called "hypotonic collapse" was of viral origin (viruses were not known during Wittmaack's time), ototoxicity or even of genetic origin.

Adolescent↗
PubMed2004

[Muscle dystrophies].

BACKGROUND: In histologic studies, the volumetric status of the intralabyrinthine fluids is judged by the position of the endolymphatic membranes. Bulging of the membranes, commonly known as endolymphatic hydrops, is assumed to be caused by excess of endolymph. The opposite situation, retraction of the membranes is, however, only incidentally described and relatively little attention has been paid to its significance. Almost one hundred years ago Wittmaack described retraction of the endolymphatic membranes, which has since been considered to be preparation artifact - a concept that essentially remains unchallenged. To test the validity of this long held premise, we examined two sets of temporal bones from different centers. MATERIAL AND METHODS: We studied the following collections: 1. The Wittmaack collection in Hamburg, Germany. The original material of 67 temporal bones (patient ages 0-92 years, average age 35.2 years) on which Wittmaack based his opinions. 2. For comparison and to exclude age related phenomena, 125 temporal bones from 73 children between the ages newborn to ten years (average age 13.4 months, median 1.5 months) from the temporal bone collection of the Department of Otolaryngology Tufts University School of Medicine. All specimens were studied by light microscopy. Retraction was defined as depression of Reissner's membrane toward the stria vascularis and the Organ of Corti in more than one cochlear turn and was graded into mild, moderate and severe. Additionally the saccule, utricle and semicircular ducts were examined for collapse. RESULTS: The reevaluation of the 67 temporal bones described by Wittmaack, including those of 7 children below the age of 10 years, showed retraction of Reissner's membrane in 81% compared to 33% of the temporal bones from the Tufts collection. In contrast to the high incidence of retraction in the cochlear duct, fewer saccules (12%) and utricles (4%) were collapsed in the Tufts collection. In the Wittmaack collection no significant differences between the underlying diseases were found, however in the Tufts collection the group of children who suffered from extracochlear infections and malignancies had a higher frequency of retraction. CONCLUSION: Mild retraction might be to some extent physiologic or even artifactual. Severe retraction, however, is a definitive finding that is a part of a local or regional otopathologic process. Of material, it is quite possible that Wittmaack's original observations of what he called "hypotonic collapse" was of viral origin (viruses were not known during Wittmaack's time), ototoxicity or even of genetic origin.

Diagnosis, Differential↗
PubMed1983

Endolymphatic hydrops in the rabbit: auditory brainstem responses and cochlear morphology.

A rabbit model of endolymphatic hydrops was studied using detailed functional and cytohistologic methods. Immediately following surgical destruction of the endolymphatic sac and the distal portion of the duct, measures of the evoked auditory brainstem response (ABR) revealed mild to profound losses specific to low- and high-frequency test stimuli while responses to mid-frequency signals remained unchanged for the majority of animals. Rabbits exhibited varying degrees of vestibular upset involving both overt behavior and reduced responses to caloric stimulation. Histologic processing of the plastic embedded cochleae demonstrated distended Reissner's membranes along with extensive damage to apical and basal turn sensory cells and myelinated afferent nerve fibers while the middle portion of the cochlear duct remained relatively unaltered. An atypical pattern of hair cell lesions involving a greater loss for inner than for outer hair cells was identified at the interface between damaged apical sensorineural elements and the normal appearing organ of Corti of the middle turns.

Animals↗
PubMed1980

Later stages of development of the periotic duct and its adjacent area in the human fetus.

The later stages of development (16-40 weeks in utero) of the periotic duct and its adjacent areas in the human fetus indicate that the critical stages of development occur in four specific time related stages over a six-week period (20-26 weeks). First, the petrous apex ossifies to separate th inferior cochlear vein into the canal of Cotugno and forms the medial wall of the cochlear aqueduct (22 weeks); second, the canalicular otic capsule fuses with the cochlear otic capsule to obliterate Hyrtl fissure and forms of the lateral wall of the cochlear aqueduct (24 weeks); third, progressive bone deposition to the medial surface of the membranous labyrinth and cochlea at the petrous apex elongates the periotic duct and cochlear aqueduct (32 weeks in utero); and fourth, active arachnoid tissue ingrowth into the periotic duct occurs at 20-24 weeks and 34-40 weeks in utero. The terminal event is widening of the CNS opening of the periotic duct at 32 weeks in utero. The periotic duct and cochlear aqueduct length increase with gestation from 25 weeks until term. The periotic duct width remains the same throughout the gestation. The cochlear aqueduct width diminishes with gestational age. The periotic duct remains patent throughout 16-40 weeks in utero.

Cochlea↗