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PubMed1997

The cochlear aqueduct in pediatric temporal bones.

The cochlear aqueduct is a bony channel which contains the fibrous periotic duct and connects the perilymphatic space of the basal turn of the cochlea with the subarachnoid space of the posterior cranial cavity. Previous histological studies suggested that patency depended on age, whereas a more recent study showed no statistical correlation between age and patency. To clarify patency in pediatric cochlear aqueducts, we selected 21 temporal bones from 12 infants and children, varying in age from birth to 9 years, in which the cochlear aqueduct was fully visible on one histological section. Photographs were taken for documentation and the length and width of the orifice of the external aperture of the aqueduct at the scala tympani were measured and followed to the internal aperture at the subarachnoid space. The lumen of the duct was examined for mononucleated cells, blood cells and fibrous tissue. Measurements revealed that the mean length of the cochlear aqueduct was 4.6 mm (range, 2.4-10.7 mm), mean width of the external aperture was 484 microm (range, 225-869 microm), and mean width of the internal aperture was 1293 microm (range, 699-2344 microm). The mean diameter of the narrowest part (isthmus) was 151 microm (range, 75-244 microm). In all temporal bones the cochlear aqueduct was patent, with one exception. This latter temporal bone was from a 2-month-old girl with multiple intralabyrinthine anomalies, with the missing cochlear aqueduct believed to be due to an aplasia. Our results support prior measurements of the cochlear aqueduct and demonstrate a short and patent cochlear aqueduct in newborns. With growth, a significant increasing length of the duct was found.

Aging↗
PubMed2005

Tbx1 is required for proper neural crest migration and to stabilize spatial patterns during middle and inner ear development.

Tbx1 belongs to the family of T-box containing transcription factors. In humans, TBX1 is implicated in the etiology of the DiGeorge syndrome. Inactivation of the Tbx1 gene in mice produces a variety of malformations including abnormal branching of the heart outflow tract, deficiencies in the branchial arch derivatives, agenesis of pharyngeal glands and abnormal development of the auditory system. We analyze here the middle and inner ear phenotypes of the Tbx1 null mice. The middle ear is strongly affected. Its skeletal components are malformed to varying degrees, some being slightly hypoplastic and others completely absent. However, a seemingly normal-looking tympanic membrane can still be recognized. Middle ear anomalies are associated with other skeletal deficiencies in the branchial arch-derived skeleton. These phenotypes derive from a combination of the failure of the posterior branchial arches to develop and the misrouting of neural crest cells. The inner ears of Tbx1(-/-) animals are hypoplastic. No vestibular or cochlear structures are detectable, but the endolymphatic duct, the cochleovestibular ganglia and residual sensory patches are still identifiable. Molecular analyses revealed a seemingly normal spatial distribution of a variety of patterning markers in the otic vesicles of Tbx1 null mutants at E9.0. However, 1 day later, several of these markers presented altered domains of expression in the otocysts of these mutant embryos, suggesting that Tbx1 is not required for the establishment of spatial patterns in the otocyst, but rather for their maintenance. The inability of the Tbx1(-/-) embryos to keep properly segregated functional domains in the otocyst is likely the cause of the strong inner ear phenotypes observed in these mutants.

Animals↗
PubMed1988

Morphological changes in the cochlear aqueduct following herpes simplex virus inoculation into the subarachnoid space.

Type 1 herpes simplex virus (HSV-1) was inoculated into the subarachnoid space through the cisterna magna of guinea pigs to study morphological changes of the inner ear and the ability of the cochlear aqueduct to protect the inner ear. Although most of the animals developed clinical manifestations of meningoencephalitis within a few days after inoculation, Preyer's reflex remained intact. Scanning electron microscopy revealed some significant changes in the cochlear aqueduct. Lymphocytes and macrophages were predominant, with narrowing of reticular tissue spaces caused by the swelling of the periotic duct tissue. The cribriform structure of the internal orifice of the cochlear aqueduct appeared to be completely obstructed, whereas it was normal in the presence of bacterial infection as previously reported (1). The morphological changes were confined to the cochlear aqueduct.

Animals↗
PubMed1999

New aspects in the histopathology of the cochlear aqueduct in children.

OBJECTIVE: To study the histoanatomy and pattern of growth of the cochlear aqueduct in children of different ages. BACKGROUND: Since Du Verney described the cochlear aqueduct in 1684, its form, pattern of growth, patency, and function have been controversial. As most of the previous studies of the aqueduct were performed on adults, none had looked at its pattern of growth from the neonate to 9 years of age. In addition, previous histologic studies had suggested an age-dependent patency, but recent investigations had not statistically correlated patency with age. METHOD: Histologic sections of 137 temporal bones from 79 infants and children were studied by light microscopy. From this group, we selected 32 temporal bones from 18 infants, newborn to 9 years (average age 9.1 months, median 0.5 months), in whom the entire length of the cochlear aqueduct was visible on one histologic section. We measured the width of the orifices at the scala tympani (external aperture) and the subarachnoid space (internal aperture) and the length of the aqueduct, and noted the contents of the lumen. RESULTS: The measurements of the cochlear aqueduct were: length 4.19 mm (range 1.7-10.7 mm), width of the external aperture 435 microm (range 225-869 microm), width of the internal aperture 1,323 microm (range 699-2344 microm), mean diameter of the narrowest part (isthmus) 138 microm (range 68-244 microm), intraluminal mononucleated cells 6%, and erythrocytes 15%. CONCLUSIONS: Our findings demonstrate that, in the newborn, the cochlear aqueduct is short and patent. After birth, the duct lengthens significantly primarily by growth of the medial periosteal portion. There was no statistically significant change in the diameter of the external and internal apertures and the isthmus with age. With one exception, the cochlear aqueduct was always present and patent.

Adult↗
PubMed2002

Tympanometric findings in patients with enlarged vestibular aqueducts.

OBJECTIVES: The purpose of this study was to study systematically some relationships between the resonance frequency of the middle-ear transmission system and the volume of the endolymphatic duct and sac in patients with an enlarged vestibular aqueduct (EVA). STUDY DESIGN: Prospective study. METHODS: Thirteen patients (24 ears) with EVA, 17 subjects (29 ears) with normal hearing, and 17 patients (21 ears) with sensorineural hearing loss without EVA served as experimental subjects. Standard pure-tone audiometry, standard clinical tympanometry (using a 226-Hz probe tone), and multifrequency tympanometry were performed on each ear. Magnetic resonance imaging was used to determine the area of the cochlear modiolus and the volume of the endolymphatic duct and sac. RESULTS: The audiometric configurations for most patients sloped downward from the low to the high frequencies. A significant air-bone gap was computed at each of these test frequencies. Multifrequency tympanometry yielded resonance frequencies for the patients with EVA that was significantly lower than those measured for the control subjects. In general, for patients with EVA, the resonance frequency of the middle ear system decreased as the volume of the endolymphatic duct and sac increased. This inverse relation was significant (correlation coefficient = -0.483, P =.0157). However, there was no correlation between resonance frequency and the degree of cochlea modiolar deficiency. CONCLUSIONS: Clinically, our findings suggest that EVA probably should be included in the differential diagnosis for a patient who presents with a moderate to severe mixed hearing loss, a normal tympanogram at 226 Hz, and a resonance frequency that is abnormally low.

Acoustic Impedance Tests↗
PubMed1992

[Human type II collagen induced autoimmune inner ear lesions in guinea pigs].

Guinea pigs were immunized with human type I, type II or type III collagen. Inner ear lesions were induced in some guinea pigs by immunizing them with human type II collagen. Histopathologic changes included endolymphatic hydrops, organ of Corti lesions and endolymphatic duct contained a large number of inflammatory cells. These histologic changes resembled those observed in patient with Meniere's disease. We didn't discover any inner ear lesions in guinea pigs by immunizing them with human type I and type III collagen, although their serum antibody titers were high and antibody presented in perilymph. Immunohistochemical study showed the presence of type II collagen in the cochlea tissues--spiral ligament, basilar membrane, tectorial membrane, spiral limb and Rosenthal's canal. We didn't discover type I and type III collagen in these area.

Animals↗
PubMedDate not supplied

Long-term treatment with chlorthalidone reduces experimental hydrops but does not prevent the hearing loss.

Long-term treatment of guinea pigs with the diuretics chlorthalidone and acetazolamide, following the experimental obstruction of the endolymphatic duct, was assessed using chronically implanted round window cochlear electrodes. The diuretic chlorthalidone appeared to curb the progressive low-frequency sensitivity loss during the first 4 weeks following surgery, as compared with animals receiving the diuretic acetazolamide or no treatment. However, this apparent beneficial effect decreased after 4 weeks and was not apparent at 14 weeks post-induction. On the other hand, morphological control at the end of 14 weeks confirmed a marked reduction in hydrops in the chlorthalidone-treated animals. The data clearly demonstrate a dissociation between hydrops and the development of hearing loss and suggest that the augmenting endolymph volume is only one of several contributing factors to the deteriorating auditory function in experimental hydrops.

Acetazolamide↗
PubMed1988

The effect of cochleostomy on the development of endolymphatic hydrops--morphologic changes in the rabbit cochlea.

The present study was designed to examine the effects of cochleostomy on the development of endolymphatic hydrops in the rabbit. Fistulization of the cochlear partition and simultaneous obstruction of the endolymphatic duct was performed in one group of animals (n = 13). Rabbits in two other groups underwent either cochleostomy (n = 6) or endolymphatic duct obstruction (n = 6) alone. Animals were terminated at 1-, 4-, and 6-week intervals and the cochleas were examined with the light microscope to document the presence or absence of hydrops, or were evaluated with the scanning electron microscope to assess sensory-cell damage. Hydrops was observed in 67% of the animals in the combined duct-obstruction/cochleostomy group, in 100% of the duct-obstruction alone group, and in 0% of the cochleostomy alone group. Widespread sensory-cell degeneration was observed with the scanning electron microscope in the combined and the cochleostomy alone groups.

Animals↗
PubMed1991

The effect of furosemide on the endocochlear potential in ears with experimentally induced endolymphatic hydrops.

The endocochlear potential (EP) was measured in 38 guinea pigs with experimentally induced endolymphatic hydrops at the 3rd, 6th, 12th and 24th postoperative weeks, and the effects of furosemide (FUR, 50 or 80 mg/kg) on the EP were examined. A time-related reduction of the EP from the normal value and increased susceptibility to FUR were disclosed in the hydropic animals. Furthermore, 24-week animals given 80 mg/kg FUR showed a significantly slower recovery rate of the EP than the other groups, indicating impairment of the strial function progressive with post-operative time. The negative component of the EP was considered to be unimpaired until at least 12 weeks after the surgery.

Animals↗
PubMed1995

[High resolution MR imaging of the inner ear apparatus using 3D-Fast spin echo sequence].

To evaluate the efficacy of high resolution MR imaging of the inner ear with 3D-Fast spin echo sequence, one volunteer and 12 patients were imaged with a 1.5 T MR scanner. High resolution T2-weighted images were obtained with a head coil in 13 minutes, and the voxel size was 0.39mm x 0.45mm x 1.2mm in most subjects. Original images and maximum intensity projection (MIP) images of the inner ear were evaluated. On original images, the endolymphatic duct was visualized in 72% of subjects, the cochlear aqueduct in 96%, three branches of the cranial nerves in the internal auditory canal in 100%, and flow void of the vessel in the cerebellopontine angle in 100%. On MIP images, more than two cochlear turns were visualized in 92% of subjects, three semicircular canals in 100%, and the anterior and posterior ampulla in 100%. MR imaging of the inner ear with 3D-Fast Spin Echo sequence provides a variety of useful information regarding the anatomy around the inner ear.

Ear, Inner↗
PubMed1977

Experimental study of sacculotomy in endolymphatic hydrops.

Thirty-nine guinea pigs were used for four groups of experiments: 1. sacculotomy only, 2. sacculotomy and simultaneous obliteration of the endolymphatic duct, 3. sacculotomy followed by obliteration of the endolymphatic duct, and 4. obliteration of the endolymphatic duct followed by sacculotomy. Sacculotomy alone caused only minimal cochlear pathology, whereas sacculotomy on hydropic ears produced severe atrophy of the organ of Corti and cochlear neurons as well as connective cells of the limbus. There was histological evidence that Reissner's membrane in hydropic ears was ruptured by the sacculotomy procedure. The primary cause for the severe atrophic changes is thought to be the toxic effect of intermixing perilymph with a large volume of endolymph. The surgically induced saccular tears appeared to be healed in all ears, and the procedure had no significant effect on the course of endolymphatic hydrops. Although two out of eleven specimens in which sacculotomy was performed on hydropic ears showed tears and collapse of Reissner's membrane, since others with similar tears showed extensive hydrops, the possibility of artifact could not be ruled out. In one specimen with simultaneous sacculotomy and obliteration of the duct, persisting fistulae were noted at the sites of accidental fracture of the osseous spiral lamina; this ear is the only one which failed to develop hydrops following obliteration of the duct. The results of this experiment, namely sacculotomy on hydropic guinea pig ears, suggest that sacculotomy is not a rational procedure for the control of endolymphatic hydrops in Ménière's disease for the following reasons: 1. surgically induced tears in the saccular wall are followed by rapid healing and 2. intermixing of perilymph and a large volume of endolymph causes toxic atrophy of the limbus, organ of Corti and cochlear neurons.

Animals↗
PubMed2003

Claudin 14 knockout mice, a model for autosomal recessive deafness DFNB29, are deaf due to cochlear hair cell degeneration.

Tight junctions (TJs) create ion-selective paracellular permeability barriers between extracellular compartments. In the organ of Corti of the inner ear, TJs of the reticular lamina separate K(+)-rich endolymph and Na(+)-rich perilymph. In humans, mutations of the gene encoding claudin 14 TJ protein cause profound deafness but the underlying pathogenesis is unknown. To explore the role of claudin 14 in the inner ear and in other tissues we created a mouse model by a targeted deletion of Cldn14. In the targeted allele a lacZ cassette is expressed under the Cldn14 promoter. In Cldn14-lacZ heterozygous mice beta-galactosidase activity was detected in cochlear inner and outer hair cells and supporting cells, in the collecting ducts of the kidney, and around the lobules of the liver. Cldn14-null mice have a normal endocochlear potential but are deaf due to rapid degeneration of cochlear outer hair cells, followed by slower degeneration of the inner hair cells, during the first 3 weeks of life. Monolayers of MDCK cells expressing claudin 14 show a 6-fold increase in the transepithelial electrical resistance by decreasing paracellular permeability for cations. In wild type mice, claudin 14 was immunolocalized at hair cell and supporting cell TJs. Our data suggest that the TJ complex at the apex of the reticular lamina requires claudin 14 as a cation-restrictive barrier to maintain the proper ionic composition of the fluid surrounding the basolateral surface of outer hair cells.

Animals↗
PubMed2002

Inner ear pressure changes following square wave intracranial or ear canal pressure manipulation in the same guinea pig.

Inner ear pressure was measured in scala tympani with a micropipette during square wave pressure manipulation of the intracranial compartment and, subsequently, of the external ear canal (EEC) in the same guinea pig. As expected, the combination of the cochlear aqueduct and the inner ear behaves as a low-pass filtering system for intracranial pressure manipulation and as a complementary high-pass system for ear canal pressure manipulation. Time constants for pressure equalization were in the order of seconds and depended on the direction of flow through the cochlear aqueduct. Pressure equalization curves could not be fitted to a single exponential function; more complicated functions were needed for good fits, showing that the pressure equalization process is nonlinear. This means that the flow resistance of the cochlear aqueduct and/or the compliance of the cochlear windows is not constant, which is in accordance with a flow-direction dependent resistance of the cochlear aqueduct. An explanation for this can be found in the special structure of the periotic duct inside the aqueduct.

Animals↗
PubMed1995

Degeneration of vestibular sensory cells caused by ablation of the vestibular aqueduct in the gerbil ear.

The vestibular aqueduct of the gerbil has a unique anatomic feature that makes it possible to selectively obliterate the endolymphatic sac with or without interfering with its venous drainage. In animals in which only the endolymphatic sac was ablated, endolymphatic hydrops was slight in the cochlea and was absent in the vestibular labyrinth. The cochlear and vestibular sensory cells were normal. In animals in which both the endolymphatic duct and the vein were obliterated, hydrops was slight, with the exception of a few cochleas that showed moderate hydrops. The sensory cells of the posterior canal cristae had degenerated in all specimens, while varied pathologic changes in cochlear and vestibular sensory cells were present in some specimens. These results suggest that hydrops is primarily due to blockage of the endolymphatic duct and sac and that degeneration of sensory cells occurs when blood flow in the vestibular aqueduct is impeded. Pathologic changes in the endolymphatic sac, including the vascular plexus at the endolymphatic sac, may play an important role in the production of endolymphatic hydrops and vestibular symptoms in Meniere's disease.

Animals↗
PubMed1987

Glycerol-induced changes in the cochlear responses of the guinea pig hydropic ear.

Pigmented guinea pigs were chronically implanted with bilateral round-window electrodes. Endolymphatic hydrops was induced by obstruction of the endolymphatic duct on one side. At 1-5 months post-surgery, glycerol was orally administered to each animal and the acute effect on cochlear and eighth nerve responses was investigated. Doses from half to four times the clinical dose of glycerol failed to improve the CAP audiogram in operated ears and were often found to raise the thresholds. Glycerol was found to diminish the amplitude of the summating potential as well as that of the compound action potential. Similar effects were observed for the higher doses in the control ears, although no effect was seen when doses used were equal to or less than the clinical dose. Our data suggest that the cochlear conditions in the guinea pig model of hydrops differ notably from those seen in patients with Ménière's disease.

Animals↗
PubMedDate not supplied

[Effect of microphone potential feedback on formation of adjusted curves of the hearing periphery].

The model of the formation of the exiting factor on the neuron endings of the cochlear nerve taking into consideration the feedback mechanisms described in recent experimental investigations is proposed. It is shown that the functioning of the feedback in the model give the possibility to explain the principle of action of the mechanism of enhancement of mechanical duct tuning which produce exquisite tuning, reflected in the tuning properties of cochlear nerve fibers. At the same time the utilisation in the model the mechanism of the lateral inhibition provide it the property similar to the effect of inhibition of the neurone response to a given tone signal when another tone signal arises in a nearby frequency region.

Animals↗
PubMedDate not supplied

The surgical approach to the endolymphatic sac and the cochlear aqueduct in the guinea pig.

The endolymphatic sac and cochlear aqueduct are primary passages of the endolymphatic and perilymphatic fluid compartments in the labyrinth. Closure of the endolymphatic sac and duct in the guinea pig will result in the development of endolymphatic hydrops. Although obstruction of the cochlear aqueduct in this species does not seem to result in any dysfunction, this structure may serve in the dynamics of inner ear fluid physiology. The anatomy of the guinea pig temporal bone is described with special emphasis on the endolymphatic sac and cochlear aqueduct. Surgical techniques to gain access to these structures through both a middle and posterior cranial fossa approach are described.

Animals↗