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At least 19 recordsLinked to original sources
PubMed1996

Effect of increased middle ear pressure on blood flow to the middle ear, inner ear and facial nerve in guinea pigs.

We investigated the effect of increased middle ear pressure on blood flow to the inner ear, middle ear, and facial nerve in guinea pigs using a nonradioactive microsphere technique. The elevation of middle ear pressure significantly reduced blood flow to the middle ear. Blood flow to the facial nerve also decreased due to the elevation of the middle ear pressure but the reduction was not significant. Blood flow to the inner ear did not change even after the middle ear pressure was increased. Findings are discussed in relationship to aural barotrauma, alternobaric vertigo and facial baroparesis.

Animals↗
PubMed2005

A new method for drug application to the inner ear.

Inner ear sensory cells are very susceptible to injuries and recovery after damage is very difficult. Recently several drugs including neurotrophic factors have been reported to protect against inner ear injury. The purpose of this experimental study is to find new methods for applying drugs to the inner ear that effectively protect against inner ear damage. Biodegradable hydrogel was used as a carrier for application of brain-derived neurotrophic factor (BDNF) into the inner ear of guinea pigs through the round window membrane. After application of BDNF the number of surviving spiral ganglion neurons increased following injury of inner ear hair cells and spiral ganglion neurons by ototoxic treatment. This result indicates that BDNF provides effective protection against inner ear damage and that biodegradable hydrogel is useful for application of drugs to the inner ear.

Animals↗
PubMedDate not supplied

Inner ear disturbances following inoculation of endotoxin into the middle ear.

Inner ear function was assessed by a frequency-specific (+/-100 Hz) auditory brainstem response (ABR) technique after a single instillation of a suspension of purified E. coli lipopolysaccharide in sterile water into the round window (RW) niche in rats. Instillation of endotoxin caused a transient concentration and tonotopically dependent dysfunction of the inner ear. The largest threshold impairment occurred in the high-frequency region anatomically located close to the RW. At 31.5 kHz the threshold impairment persisted throughout the study. Morphologic damage to the inner ear was not detected at the light microscopic level when using serial sections from decalcified specimens. Our study supports the clinical hypothesis that remnants of non-viable bacteria such as endotoxins, when trapped in the middle ear, can promote middle ear effusion and dysfunction of the inner ear.

Animals↗
PubMed2002

Determination of the embryonic inner ear.

Inner ear induction, like induction of other tissues examined in recent years, is likely to be comprised of several stages. The process begins during gastrulation when the ectoderm is competent to respond to induction. It appears that a signal from the endomesoderm underlying the otic area during gastrulation initiates induction complemented by a signal from presumptive neural tissue. By the neural plate stage, a region of ectoderm outside the neural plate is "biased" toward ear formation; this process may be part of a more general "placodal" bias shared by several sensory tissues. Induction continues during neurulation when a signal from neural tissue (possibly augmented by mesoderm underlying the otic area) results in ectoderm committed to otic vesicle formation at the time of neural tube closure. Studies on several gene families implicate them in the ear determination process. Fibroblast Growth Factor (FGF) family members are clearly involved in induction: FGFs are appropriately expressed for such a role, and have been shown to be essential for inner ear development. FGFs also have inductive activity, although it is not clear if they are sufficient for ear induction. Activation of transcription factors in the otic ectoderm, for example, by Pax gene family members, provides evidence for important changes in the responding ectoderm beginning during gastrulation and continuing through specification at the end of neurulation, although few functional tests have defined the role of these genes in determination. The challenge remains to merge embryologic data with gene function studies to develop a clear model for the molecular basis of inner ear induction.

Animals↗
PubMed1992

Characteristic ionic composition of endolymph is maintained in cultured inner ear.

Inner ear anlagen from mouse were explanted on the 16th gestational day (gd) and cultured for 5 days, i.e. corresponding to the time of birth. By using energy dispersive X-ray technique an elemental composition characteristic for endolymph was found within the membranous labyrinth of the explants. The sodium to potassium ratio in the endolymphatic space of the cultured inner ears corresponded to endolymph of the 16th gd fetus in vivo. There was no difference in the endolymph compartment between the cochlear and vestibular halves of the in vitro specimens. Differences in Na to K ratio between endolymph of the inner ears and the surrounding medium were statistically significant. Thus, endolymph-regulating mechanisms are active also under organ culture conditions, although not fully optimal.

Animals↗
PubMed2004

Molecular characterization of conditionally immortalized cell lines derived from mouse early embryonic inner ear.

Inner ear sensory hair cells (HCs), supporting cells (SCs), and sensory neurons (SNs) are hypothesized to develop from common progenitors in the early embryonic otocyst. Because little is known about the molecular signals that control this lineage specification, we derived a model system of early otic development: conditionally immortalized otocyst (IMO) cell lines from the embryonic day 9.5 Immortomouse. This age is the earliest stage at which the otocyst can easily be separated from surrounding mesenchymal, nervous system, and epithelial cells. At 9.5 days post coitum, there are still pluripotent cells in the otocyst, allowing for the eventual identification of both SN and HC precursors--and possibly an elusive inner ear stem cell. Cell lines derived from primitive precursor cells can also be used as blank canvases for transfections of genes that can affect lineage decisions as the cells differentiate. It is important, therefore, to characterize the "baseline state" of these cell lines in as much detail as possible. We characterized seven representative "precursor-like" IMO cell populations and the uncloned IMO cells, before cell sorting, at the molecular level by polymerase chain reaction (PCR) and immunocytochemistry (IHC), and one line (IMO-2B1) in detail by real-time quantitative PCR and IHC. Many of the phenotypic markers characteristic of differentiated HCs or SCs were detected in IMO-2B1 proliferating cells, as well as during differentiation for up to 30 days in culture. These IMO cell lines represent a unique model system for studying early stages of inner ear development and determining the consequences of affecting key molecular events in their differentiation.

Animals↗
PubMed1994

Congenital perilymphatic fistula: computed tomography appearance of middle ear and inner ear anomalies.

Congenital perilymphatic fistula is an abnormal communication between the inner ear and middle ear. Inner ear anomalies have been described on computed tomography scans. Middle ear anomalies have been found at surgery; the most frequent are anomalies of the stapes and round window. This retrospective study describes the appearance of the inner and middle ear on computed tomography scans, and of the middle ear at surgery, in 10 patients (15 ears) in whom perilymphatic fistula was found at surgery. Twelve of 15 stapes were abnormal at surgery; 4 of these 12 (33%) could be seen on computed tomography scans. Two stapes normal at surgery were normal on computed tomography. Three round windows were abnormal at surgery; none of these was seen on computed tomography scans. There were also four dysplastic cochleas, four dysplastic vestibules, and three dilated vestibular aqueducts. Computed tomography scans identified an abnormal inner ear, middle ear, or both in 8 (53%) of the 15 ears with perilymphatic fistula. An inner ear or middle ear anomaly on computed tomography may heighten clinical suspicion of congenital perilymphatic fistula.

Adolescent↗
PubMedDate not supplied

Single gene influences on radiologically-detectable malformations of the inner ear.

Inner ear malformations associated with hearing loss or vestibular dysfunction are discussed from the viewpoint of the etiologies of the malformation. Symptoms of classification of inner ear malformations are discussed. The significance of malformations of the cochlea and vestibular aqueduct to auditory function are discussed. Genetics features and characteristics of Branchio-oto-renal, Waardenburg's, Pendred's, DiGeorge's, Wildervanck, Fountain, and Treacher Collins syndromes are discussed in relation to ear abnormalities and hearing. Similar attention is given to genetic studies of nonsyndromic hearing loss.

Deafness↗
PubMed1980

[Cellular detection of the in vivo incorporation of tritiated 2-deoxyglucose. Radioautographic study in the inner ear].

Inner ear injection of (3H) deoxyglucose was followed by in situ glutaraldehyde fixation and, after removal, by traditional preparation of the tissue for electron microscopy. Radioautography of semi-thin sections revealed preferential tracer accumulation in metabolically active structures such as the cochlear stria vascularis and the dark cells surrounding the basis of the vestibular cristae. Furthermore, in the vestibule, the perikaryon of some sensory cells was intensely labelled. These results show that an in vivo injection of deoxyglucose, followed by conventional histological processing can be used to mark active cells at both cellular and subcellular levels.

Animals↗
PubMed1999

Tympanoplasty: prudent considerations of silent otitis media and interactions of middle ear and inner ear.

Otitis media is a common problem, often with simple, minimally invasive solutions; however, a small subset of patients progress to chronic disease despite provision of standard therapies. The flexible approach to tympanoplasty is a prudent consideration for patients with chronic otitis media, especially children. This article discusses the findings and implications of silent otitis media, interactions of the middle ear and inner ear, and obstructive sites in the middle ear cleft. Tympanoplasty by the flexible approach is described in the context of these findings.

Acute Disease↗
PubMed1989

Survey of interactions between middle ear and inner ear.

Diseases with interaction between the middle ear and inner ear include 1) congenital anomalies, 2) trauma, 3) infection/inflammation, 4) tumors, 5) granulomas, 6) ototoxic eardrops, 7) cochlear implants, 8) otosclerosis, 9) Meniere's disease-decompensated, and Meniere's disease with perilymphatic fistula, and 10) perilymphatic hypertension. Clinical and pathological characteristics are briefly categorized in this survey. The clinical utility of exploratory tympanotomy in diagnosis and treatment of middle ear pathology and middle ear/inner ear interactions is commented upon.

Ear↗
PubMed1995

Middle ear and inner ear effects on clinical bone-conduction threshold.

The measurement of bone-conduction thresholds is an integral part of audiologic evaluation. The relationship between bone-conduction and air-conduction thresholds is the differentiating diagnostic indicator between conductive and sensorineural hearing loss. At the same time, the influence of middle ear and inner ear structures upon the bone-conduction response has been well documented. We present two cases illustrating this influence and attempt to explain the clinical bone-conduction thresholds with operative findings.

Acoustic Impedance Tests↗
PubMed1987

[Binding of serum immunoglobulins to human inner ear tissue in inner ear hearing loss: methodologic limits].

The immunopathological processes possibly involved in cryptogenic sensorineural hearing loss were investigated. In a pilot study the sera from 66 patients were tested by the indirect immunofluorescence technique for immunoglobulins which bind to normal human inner ear tissue. The reaction was positive in two thirds of all patients with sudden hearing loss, especially bilateral. This was mostly for IgG, and to the organ of Corti. Others have found that Corti's organ showed marked degenerative changes in cases of sudden hearing loss, examined by histology. The reaction was positive in half of the patients with progressive sensorineural hearing loss. It was noticeable that positive reactions for IgA were twice as frequent in sera of patients with progressive hearing loss than in those with sudden deafness. In a control study, the sera of ten patients were tested in parallel by the same method on histological sections of inner ears taken from four individuals. Similar results were found for the sera of two patients only. The sera of the remaining eight patients revealed very inconsistent reaction patterns. These preliminary results may indicate that temporary or permanent humoral (auto) immune mechanisms could have occurred in certain inner ear diseases. So far however reliable diagnostic methods have not been established, and not enough patients have been followed up.

Adolescent↗
PubMed2001

[Relationship between three inner ear antigens and autoimmune inner ear disease].

OBJECTIVE: To investigate the relationship between three purified inner ear antigens and autoimmune inner ear disease (AIED), and to determine their expressions in normal guinea pig cochleas. METHODS: Guinea pigs were divided into group B, group C and group D and immunized respectively with three subcomponents of crude inner ear antigens (31,000, 42,000-45,000 and 60,000 proteins). Hearing thresholds, serum IgG levels and morphological changes of inner ear were observed. The protein expressions of these antigens were examined by immunohistochemistry. In the control group, antigens were replaced by gel homogenate of polyacrylamide. RESULTS: There were no significant differences of hearing threshold among groups before immunization with inner ear antigens (F = 0.07, P > 0.05). There were no significant changes of hearing thresholds and inner ear morphology in group C and control group. Hearing thresholds dropped in part of animals immunized with 31,000 or 60,000 protein. Hearing threshold of group B and D changed significantly after immunization, as compared with the control group(F = 9.12, P < 0.01). Serum IgG levels increased significantly in all experimental groups compared with the control group(F = 7.46, P < 0.01). The 31,000 protein distributed strictly in cochlear nerve, and 42,000-45,000 or 60,000 protein distributed widely, including the spiral ganglion, Corti's organ, stria vascularis and spiral ligament. CONCLUSIONS: Two subcomponents of 31,000 and 60,000 in crude inner ear antigen could induce autoimmune inner ear disease. The distribution of 31,000 protein was more tissue specific and might be used as a marker protein for clinical diagnosis of autoimmune inner ear disease.

Animals↗