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PubMed2003

Cochlear aqueduct flow resistance is not constant during evoked inner ear pressure change in the guinea pig.

Inner ear fluid pressure was measured during 6.25 mHz square wave middle ear pressure manipulation, with a perforated tympanic membrane. After a negative-going middle ear pressure change the calculated flow resistance of the inner ear pressure release routes (mainly the cochlear aqueduct) was approximately constant, with a value of 12 Pa s/nl (averaged over two ears), when values for the inner ear window compliance are taken from the literature. After a positive-going middle ear pressure change the calculated flow resistance changed with round window position and with the pressure difference across the cochlear aqueduct. It reached an average maximum value of 114 Pa s/nl. The change of flow resistance during inner ear pressure variation can be explained by a permeability change of the cochlear aqueduct, caused by a change of structures filling the aqueduct and its entrance in scala tympani.

Animals↗
PubMed1987

The role of acute and latent virus infections in the pathogenesis of inner ear disturbances.

The possible role of herpesviral infections of the inner ear in suddenly appearing inner ear disturbances was investigated. Experimental pseudorabies virus (PRV, Herpes sui 1) infection of mice and swine was used as a model system. Infected mice represented the productive cycle of PRV infection (acute phase), whereas the latent phase of infection could be tested in swine. From the acutely infected mice the virus could be reisolated from perilymphatic fluid and various parts of the brain. Massive histopathologic alterations and signs of total cell damage to the organ of Corti and the vestibular organ were found. Accordingly, in all of the cells of the inner ear multiple copies of the PRV genome could be demonstrated. We therefore suggest that the disturbances of the inner ear were induced by the acute virus infection. In two latently infected swine (sixty weeks after infection), PRV could not be recovered either from the perilymphatic fluid or from a variety of different neural and extraneural tissues. However, histopathologic changes similar to those found in the acutely infected mice were observed. The presence of viral DNA could be demonstrated by in situ cytohybridization in both sensory and supportive cells of the inner ear and vestibular organ, but not in the corresponding nerve fibers, which is in contrast to the acutely infected mice. The distribution of the viral genome was further analyzed in adjacent areas of the central nervous system. An involvement of acute and latent herpes virus infection in inner ear dysfunction including sudden deafness and vestibular neuronitis in man, might be suggested from the results described. The presented animal model system, PRV-infected swine, should permit further studies on a possible role of herpetic recurrences, particularly with regard to inner ear disturbances.

Acute Disease↗
PubMed1991

Homing of lymphocytes to the inner ear.

The migration of lymphocytes to the inner ear was studied during an immune response in the cochlea. Sensitized lymphocytes from peripheral blood, neck lymph nodes and spleen from strain 13 inbred guinea pigs were labelled with 51Cr and injected intravenously into strain 13 recipients undergoing an inner ear immune response. Eighteen hours later the temporal bones and immune organs of the recipients were assayed for radioactivity to detect the infiltration of labelled cells. In addition autoradiography was performed to localize labelled cells in the inner ear. More lymphocytes from the peripheral blood entered the inner ear during the immune response than spleen or lymph node cells. This indicates that the inner ear comes under the immuno-surveillance of the peripheral circulation in response to antigenic stimulation. Most labelled lymphocytes were observed in the basal turn of the scala tympani and in and around the spiral modiolar vein of the challenged cochlea. A few cells were seen also in the control cochleas but almost all where inside the blood vessels. This pattern suggests that the blood vessels of the spiral modiolar vein are the initial site through which lymphocytes entered the inner ear.

Animals↗
PubMed2004

Localization of endotoxin in the inner ear following inoculation into the middle ear.

Sensorineural hearing loss is known to be a significant sequela of otitis media (OM). The pathophysiology of such hearing loss in OM is thought to be due to transmission of toxins and other bacterial products through the round window membrane, damaging the hair cells of the basal turn of the cochlea. Other routes, such as those involving the oval window, blood vessels and lymphatics, may also be involved. The purpose of this study was to elucidate the routes from the middle ear cavity to the inner ear and also the distribution pattern of endotoxin in the inner ear after injection of fluorescence-labelled endotoxin into the tympanic cavity and detection of fluorescence in the cochleae, vestibular end organs and facial nerves. This fluorescence was far more intense in the lower turns of the cochlea. These findings suggest that endotoxin can reach the inner ear by various routes, e.g. the round window, blood vessels or lymphatics, and/or interscala exchange, resulting in a disturbance not only of the cochlea but also of the vestibular end organs.

Animals↗
PubMed2003

Inner ear extension of vestibular schwannomas.

OBJECTIVE: Inner ear extension of vestibular schwannomas (VSs) is a rare finding but has important clinical implications. This report reviews the treatment options and presents the experience of the Gruppo Otologico, Piacenza, Italy, in this field. STUDY DESIGN: Case report and literature review. METHODS: Five cases of VSs with inner ear extension were surgically removed. In all of them, the cochlea was partially or completely invaded by the lesion. RESULTS: In 4 cases, the inner ear extension was preoperatively identified on magnetic resonance imaging, and the surgical removal was planned through a transotic approach. In the last case, the cochlear invasion was not detected preoperatively, and the lesion was removed during a second surgery performed to seal a cerebrospinal fluid fistula. CONCLUSIONS: VSs with inner ear extension should be distinguished from pure intralabyrinthine schwannomas because of differences in clinical significance. Cochlear involvement is more frequent than vestibular involvement and is often accompanied by a dead ear. Dead ear caused by small VSs should alert the surgeon to the possibility of a cochlear extension. The presence of an intracochlear involvement requires the adoption of an approach that allows control of the cochlear turns, and we found the transotic approach to be the most suitable. Undetected cochlear extensions that are left in place may grow with time.

Adult↗
PubMed2000

Immune response and immunopathology of the inner ear: an update.

Immune-mediated inner-ear disease includes clinical conditions associated with unilateral or bilateral rapidly progressive forms of sensorineural hearing loss. A systemic autoimmune disorder can be present in less than one-third of cases. Because of the lack of well defined detection methods to identify immune-mediated processes within the inner ear, and the fact that the human inner ear is not amenable to diagnostic biopsy, there has been great interest in developing animal models. Experimental models of sterile and virus-induced labyrinthitis support the participation of the immune system in the aetiopathogenesis of inner-ear disorders: interleukin-2 emanates from the endolymphatic sac and assists in changing the spiral modiolar vein, as in the expression of intercellular adhesion molecule 1, which allows the egrees of immune cells from the circulation. The formation of a fibro-osseous matrix ultimately results in degeneration of the inner ear. These investigations have allowed us to alter the immune response for the purpose of regulating its intensity and the subsequent damage to patients.

Animals↗
PubMed1995

Involvement of extracellular matrix in the formation of the inner ear.

Formation of the inner ear from the optic placode differs from invagination of other cup-shaped organ primordia. Activation of the actin cytoskeleton seems to play a limited role because precocious invagination does not occur upon treatment with activators of a contractile event and cannot be prevented by inhibitors. In this study, the possibility that invagination is mediated by changes in the surrounding mesenchyme was tested by treating embryos with agents which interfere with the integrity of extracellular matrix. Enzymes degrading hyaluronate and/or chondroitin sulfate were microinjected into the otic region prior to folding. Synthesis of chondroitin sulfate proteoglycan was inhibited by microinjection of beta-xyloside. All treatments inhibited otic pit formation by interfering with fold formation within the placode. Immunocytochemical procedures showed depletion of the appropriate extracellular matrix components for a short time period after enzyme treatments and for up to 24 hr after beta-xyloside injection. Invagination of the otic primordium is concluded to be controlled in part by anchorage of the epithelium to adjacent structures and possibly by expansion of the mesenchymal extracellular matrix.

Animals↗
PubMed2006

Delivery of drugs to the inner ear.

PURPOSE OF REVIEW: Inner ear delivery of medicines has been a rapidly expanding field in otolaryngology. This technique provides a minimally invasive way of managing a number of otolaryngologic diagnoses and promises to provide a therapeutic option for previously untreatable disorders. The purpose of this review is to examine the literature that has been published recently (since January of 2005) in this field and to explore how this new literature has impacted on current practices. RECENT FINDINGS: While there was a significant volume of work done in this area from 1995 to 2004, publication in this area has slowed considerably. The literature focuses on two areas: the treatment of Ménière's disease with gentamicin and the treatment of sudden sensorineural hearing loss with steroids. The most promising area in this field, which is the development of new medicines to treat a variety of disorders, has not progressed over the last 2 years. SUMMARY: Recent peer-reviewed publications have not had a significant impact on the transtympanic treatment of Ménière's disease or sudden sensorineural hearing loss. We will review the current practices in these two areas, discuss the newest developments and examine how we can progress the field over the next several years.

Drug Delivery Systems↗
PubMedDate not supplied

Glutaraldehyde fixatives for preserving the chick's inner ear.

We preserved the inner ears of chicks in various concentrations of glutaraldehyde (2 to 3.5%) and cacodylate buffers (0.025 to 0.1 M). Buffer concentrations below 0.1 M caused osmotic damage that higher glutaraldehyde concentrations only partially counteracted. The combination of 3.5% glutaraldehyde and 0.1 M cacodylate buffer optimally preserved the different cell types and also eliminated problems of swelling and shrinkage. We further improved cellular preservation by immediately immersing the dissected specimen into chilled (4 degrees C), aerated fixative. The improved fixation greatly increased the retention of cytoplasmic ground substances, particularly in supporting cells and nerve terminals.

Aldehydes↗
PubMed1985

[Technics for postmortem removal of inner ear fluid].

Two methods for sampling inner ear fluid (a mixture of endolymph and perilymph) from corpses are described and compared. Using the classical method, a part of the petrous bone is chiselled out and, subsequently, a needle, attached to a 1-ml-syringe, is inserted through the oval foramen into the region of the utriculus. The inner ear fluid can then be removed. When the method proposed by Trela (1975) is applied, thin layers of the petrous crest are chiselled out until the common crus of the superior and posterior semi-circular becomes apparent. With a needle, attached to a 1-ml-syringe, the inner ear fluid can then be collected. The experiments show Trela's method to be simpler than the classical method. Moreover, only small amounts of inner ear fluid can be obtained by the latter technique. Trela's method is recommended for further studies on this fluid, which may be of forensic interest.

Cadaver↗
PubMed2003

Embolic inner ear decompression illness: correlation with a right-to-left shunt.

OBJECTIVES/HYPOTHESIS: Inner ear decompression illness is thought to be a rare phenomenon in recreational divers, isolated signs and symptoms of inner ear dysfunction usually being attributed to inner ear barotrauma. STUDY DESIGN: We present 11 cases of inner ear dysfunction in nine divers with inner ear decompression illness. RESULTS: All nine divers had significant right-to-left shunt as diagnosed by transcranial Doppler sonography. CONCLUSIONS: The authors thought that mechanism of causation in these cases may have been intravascular bubble emboli and that inner ear decompression illness may be more common among recreational divers than currently recognized. Failure to treat inner ear decompression illness with recompression therapy can result in permanent disability. Because the differential diagnosis between inner ear barotrauma and inner ear decompression illness can be impossible, the authors suggested that divers who present with inner ear symptoms following a dive should have recompression immediately after having undergone bilateral paracentesis.

Decompression Sickness↗
PubMed1996

Standard atlas of the gross anatomy of the developing inner ear of the chicken.

During development, the chicken inner ear undergoes a series of morphological changes which give rise to the various structures found in the adult, including the mature semicircular canals, utricle, saccule, cochlear duct, endolymphatic duct and sac, and neurons of the eighth cranial nerve ganglion. Beginning as a hollow epithelial sphere, the inner ear is sculpted into this complex labyrinth of fluid-filled ducts punctuated by their associated sensory end organs. In this report, the three-dimensional complexity of the developing inner ear of the chicken embryo is documented in the form of a standard atlas. The protocol involved fixation, dehydration, and clearing of embryonic heads harvested at daily intervals, followed by injection of an opaque dye (enamel paint suspension) into the fluid ducts of the inner ear. The position of the ear is shown relative to surface landmarks at seven different stages of development, ranging from embryonic day 5 (E5) to E18. Also shown are higher-power photomicrographs of the inner ear in isolation taken at daily intervals at E3-E17 and viewed from two orthogonal positions. Three orthogonal views are shown at 6-hour intervals during the critical stages of semicircular canal formation (E6-E7). Quantitative measurements of the linear dimensions of the inner ear (dorsoventral, anteroposterior, and mediolateral axes) as a function of time indicate a linear increase in the growth of the ear from E3 through E18. This atlas should prove valuable for evaluating mutant phenotypes in inner ear morphogenesis following gene perturbation experiments in the chicken.

Anatomy, Artistic↗
PubMed2006

Oxidative imbalance in the aging inner ear.

The mammalian inner ear loses its sensory cells with advancing age, accompanied by a functional decrease in balance and hearing. This study investigates oxidant stress in the cochlea of aging male CBA/J mice. Glutathione-conjugated proteins, markers of H2O2-mediated oxidation, began to increase at 12 months of age; 4-hydroxynonenal and 3-nitrotyrosine, products of hydroxyl radical and peroxynitrite action, respectively, were elevated by 18 months. Immunoreactivity to these markers was stronger in the supporting cells (Deiters and pillar cells) than the sensory cells and appeared later (23 months) in spiral ganglion cells and in the stria vascularis and spiral ligament. Conversely, antioxidant proteins (AIF) and enzymes (SOD2) decreased by 18 months in the organ of Corti (including the sensory cells) and spiral ganglion cells but not in the stria vascularis. These results suggest the presence of different reactive oxygen species and differential time courses of oxidative changes in individual tissues of the aging cochlea. An imbalance of redox status may be a component of age-related hearing loss.

Aging↗
PubMed2004

Sustained-release devices in inner ear medical therapy.

Inner ear medical therapy has been gaining increasing popularity during the last 2 decades. Despite the increased use of this therapy,basic questions regarding this type of treatment have not been answered. The authors have used a variety of sustained-release devices in the laboratory to begin to answer some of these basic questions. This article discusses the results of this work and the application and use of sustained-release devices in patients.

Administration, Topical↗
PubMed1996

Acoustically induced vibrations of the Reissner's membrane in the guinea-pig inner ear.

In the inner ear, the Reissner's membrane separates the scala vestibuli from the scala media and is thus of importance for maintaining a positive endocochlear potential. The motion of the membrane is thought to be driven by the vibrations of the underlying hearing organ caused by a hydromechanical coupling between the structures. Since the Reissner's membrane is relatively easily accessible in the cochlea its vibratory response has been used as a measure of the micromechanical behaviour of the hearing organ. To determine whether this indirect measure revealed the true characteristics of the hearing organ, experiments were performed using laser heterodyne interferometry in an in vitro preparation of the guinea-pig temporal bone. Interferometric measurements at the Reissner's membrane and at the surface of the hearing organ directly beneath made it possible to compare the mechanical tuning characteristics of both structures. It was found that the mechanical response characteristics of the Reissner's membrane differed considerably from the hearing organ. The tuning frequency was different and only minor changes in the maximal vibration amplitude were seen when measuring at different radial locations. However, the shape of the response curve changes with location. The Reissner's membrane response appeared to be affected by the mechanical vibrations originating both at the middle ear ossicles and at the hearing organ. It is concluded that the Reissner's membrane response is a poor indicator of cochlear mechanics and that investigations of cochlear micromechanics should be performed directly at the level of the hearing organ.

Acoustic Stimulation↗
PubMed2001

Gene-based therapy for inner ear disease.

Environmental inner ear insults often lead to hair cell injury and loss. Therapeutic measures for the prevention of hair cell loss are currently limited. Several reports have demonstrated the applicability of growth factors for hair cell protection. The goal of the experiments presented here was to assess the protective capability of the human GDNF transgene against noise trauma in the guinea pig cochlea. The left ears of guinea pigs were inoculated with a recombinant adenovirus with a human GDNF insert (Ad.GDNF). Four days later, animals were exposed to noise trauma. One week later, animals were sacrificed and hair cells counted in the left (inoculated) and right (non-inoculated) ears. Auditory brainstem thresholds were measured before the inoculation and just prior to sacrifice. Control groups included inoculation with a reporter gene vector (Ad.lacZ) and Ad.GDNF in normal ears with no noise exposure. The results show that intracochlear inoculation with adenovirus into normal ears does not compromise hair cell counts and ABR thresholds. Both Ad.GDNF and Ad.lacZ vectors can protect the cochlear hair cells and hearing from the noise insult. The difference between the protection afforded by Ad.GDNF and that of the Ad.lacZ vector is not statistically significant. The mechanism of Ad.lacZ protection needs to be elucidated. The data demonstrate the general feasibility of gene therapy for over-expression of neurotrophic factors against noise trauma, and emphasize the complexity of the technique and the problems of variability between subjects.

Journal Article↗
PubMed2003

Aquaporin-mediated fluid regulation in the inner ear.

1. The sensory functions of the inner ear (hearing and balance) critically depend on the precise regulation of two fluid compartments of highly desparate ion composition, i.e., the endolymph and the perilymph. 2. The parameters volume, ion composition, and pH need to be held at homeostasis irrespective of the hydration status of the total organism. 3. Specific cellular water channels, aquaporins, have been shown to be essential for the fluid regulation of several organs, e.g., kidney, lung, and brain. 4. Because of functional similarities of water regulation in the kidney and inner ear this review initially summarizes some aquaporin functions in the kidney and then focuses on 6 out of 11 mammalian aquaporins that are present in the inner ear (AQP1-6). 5. Their potential role in the inner ear fluid control will be discussed on the basis of the respective expression patterns and individual pore properties. 6. Further, a working model is presented of how the endolymphatic sac may contribute to inner ear fluid regulation.

Animals↗
PubMed1979

Endolymphatic sac valve implant surgery. II: The unidirectional inner ear valve implant.

A unidirectional inner ear valve implant was developed to direct excess endolymph out of the inner ear in the hydropic state (Ménière's disease) into the mastoid cavity. A detailed technical description of the valve implant is presented as well as some technical aspects of the valve implant based on the surgical anatomy of the endolymphatic sac.

Ear, Inner↗