Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Ear, Inner”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 523 records · Page 29Linked to original sources
PubMed2004

[Acute diseases of the inner ear--are cardiovascular treatment strategies lacking?].

The underlying cause of acute functional disorders of the inner ear (sudden hearing loss) is usually not detectable with clinical diagnostic measures. It is assumed that functional disorders of the inner ear are merely symptoms and not a disease entity in itself. In particular regional perfusion disturbances, but also autoimmune phenomena, viral infections and micromechanical disorders of the cochlea are seen as pathogenetic principles in inner ear disturbances. Although numerous effective therapeutic options and prophylactic measures for such diseases as myocardial infarction and stroke are available to cardiovascular medicine, they have so far not been applied to the treatment of inner ear problems. Here there is a promising and wide field of options for such diseases that can be traced back to regional perfusion disorders.

Blood Component Removal↗
PubMed2000

Cell proliferation and cell death in the developing chick inner ear: spatial and temporal patterns.

Morphogenesis of the inner ear is a complex process in which the balance of cell division and death is presumed to play an important role. Surprisingly, there are no reports of a systematic comparison of these two processes in individual ears at different stages of development. This study presents such an analysis for the chicken otocyst at stages 13-29 (embryonic days 2.5-6). To detect proliferating cells, we used exposure to bromodeoxyuridine. To detect apoptotic cells, we used nuclear condensation and fragmentation or terminal dUTP nick-end labeling (TUNEL). The spatial and temporal locations of proliferating and dying cells were mapped across serial sections, revealing regional differences in proliferation within the otocyst epithelium that are more complex than previously reported. In addition, almost all of the previously identified "hot spots" of cell death correspond spatially to regions of reduced cell proliferation. An exception is the ventromedial hot spot of cell death, which is intermingled with proliferating cells when it first appears at stages 19-23 before becoming a cold spot of proliferation. The results further show that the inferior part of the otocyst has a high level of proliferation, whereas the superior part does not. Since the superior part of the otocyst demonstrates outward expansion that is comparable to the inferior part, it appears that regional outgrowth of the otic vesicle is not necessarily coupled to cell proliferation. This study provides a basis for exploring the regulation and function of cell proliferation and cell death during inner ear morphogenesis.

Animals↗
PubMedDate not supplied

The pathway enabling external sounds to reach and excite the fetal inner ear.

The human fetus in utero is able to respond to sounds in the amniotic fluid enveloping the fetus after about 20 weeks gestation. The pathway by which sound reaches and activates the fetal inner ear is not entirely known. It has been suggested that in this total fluid environment, the tympanic membrane and the round window membrane become 'transparent' to the sound field, enabling the sounds to reach the inner ear directly through the tympanic membrane and the round window membrane. It is also possible that sounds reach the inner ear by means of tympanic membrane--ossicular chain--stapes footplate conduction (as in normal air conduction). There is also evidence that sounds reach the fetal inner ear by bone conduction. Several animal and human models of the fetus in utero were studied here in order to investigate the pathway enabling sounds to reach and activate the fetal inner ear. This included studying the auditory responses to sound stimuli of animals and humans under water. It was clearly shown in all the models that the dominant mechanism was bone conduction, with little if any contribution from the external and middle ears. Based on earlier experiments on the mechanism and pathway of bone conduction, the results of this study lead to the suggestion that the skull bone vibrations induced by the sound field in the amniotic fluid enveloping the fetus probably give rise to a sound field within the fetal cranial cavity (brain and CSF) which reaches the fetal inner ear through fluid communication channels connecting the cranial cavity and the inner ear.

Animals↗
PubMedDate not supplied

Congenital anomalies of the inner ear: introducing a new classification of labyrinthine anomalies.

In a literature review of 108 articles a special effort was made to find and classify inner ear anomalies and diseases associated with inner ear anomalies. This study showed the following. Most of the diseases associated with inner ear anomalies are also associated with anomalies in other parts of the body. Hereditary characteristics comprise the most common etiological factor among the diseases associated with inner ear anomalies. Among anomalies observed in the cochlea, the vestibule, and the semicircular canals, anomalies in the cochlea are most frequently associated with various diseases and were observed in 30 of 40 diseases. Anomalies of the vestibule were observed in 25 diseases, and those of the semicircular canals in 18 diseases. Anomalies in both the osseous and the membranous labyrinth were most frequently associated with the diseases studied, as they were observed to occur with 10 of the 43 diseases. In this paper a new classification system for labyrinthine anomalies is introduced, based on this study of the literature.

Ear, Inner↗
PubMed2001

A specific promoter of the sensory cells of the inner ear defined by transgenesis.

To date, no promoter sequence specific to the inner ear sensory cells (hair cells) has been reported. In an effort to understand the molecular mechanisms that determine hair cell fate in the inner ear, and with the goal of developing a valuable tool for gene therapy and for the generation of conditional knockouts, we initiated a search for cis-acting DNA sequences that regulate the expression of the murine Myo7a and human MYO7A genes. These genes encode the unconventional myosin VIIA which is expressed in hair cells and in some other epithelial cells. We generated lines of transgenic mice expressing the green fluorescent protein (GFP ) reporter gene under the control of several 5'-truncated versions of the Myo7a/MYO7A promoter region and intron 1. We obtained transgenic mice with a GFP expression restricted to the hair cells of the inner ear, cochlea and vestibule. Successive deletions of the promoter allowed us to define a minimal sequence of 118 bp that is sufficient, in the presence of intron 1, to target the transgene expression to hair cells. In addition, the deletion of intron 1 from the transgenes abolished hair cell expression, thus indicating the presence of a strong enhancer in the intron. This is the first report of regulatory sequences sufficient to target the expression of a gene exclusively in sensory cells of the inner ear. It also opens up the possibility for the analysis of the hair cell transcriptome.

Animals↗
PubMed1979

Extracorporeal preservation. Organ culture of the post-natal mammalian inner ear.

Postnatal (newborn and mature) inner ear organs from CBA/CBA mouse and guinea pig were analysed concerning hair cell survival in an in vitro system. After only a few days in the artificial surroundings a transformation of hair cell characteristics occurred, in the form of either loss of sensory hairs (cochlear hair cells) or hair fusion (vestibular hair cells), although the hair cell itselt survived for a considerably longer time. Intracellular myelin figures became evident after 2--3 days in culture. However, a considerable individual variation among hair cells was observed concerning the ultrastructure of the cell at this stag in vitro. Completely normal hair cells could in rare cases be recognised after 1 week in organ culture (cochlear inner hair cells of the CBA/CBA mouse). Loss of the surface structures of the hair cells is likely to constitute an irreversible transformation not in agreement with the true hair cell characteristics.

Adaptation, Physiological↗
PubMed1988

The effects of cetrimide and potassium bromate on the potassium ion concentration in the inner ear fluid of the guinea-pig.

The mammalian inner ear is located deep within the temporal bone. The organ of Corti, the delicate sensory system for sound, is surrounded by two fluid systems; the potassium-rich endolymph and the sodium-rich perilymph. The pathogenesis of inner ear deafness is thought to be largely due to an imbalance of potassium and sodium ions in the inner ear fluids. Dynamic changes in K+ in the endolymph and perilymph were studied in the guinea-pig following cetrimide (cetrimonium bromide, a powerful cationic detergent which shows ototoxicity) applications on the round window membrane, intramuscular injection of potassium bromate (bread whitener, known to cause renal damage and permanent deafness in animals and man). Maximum fall in K+ concentration in the endolymoh (mM/min) and maximum K+ conductance (mM/min/mV) were 3.54 +/- 1.65 and 0.036 +/- 0.02 in cetrimide, and 1.85 +/- 0.35 and 0.021 +/- 0.009 in potassium bromate, respectively. In view of these findings, the influence of the active transport mechanism to K+ concentrations are discussed in comparison with dynamic changes in endolymph K+ induced by asphyxia and ethacrynic acid.

Animals↗
PubMed1999

Localization of nontypeable Haemophilus influenzae endotoxin in the middle and inner ear during experimental otitis media.

Nontypeable Haemophilus influenzae (NTHi) lipooligosaccharide, the major component of H. influenzae endotoxin, was localized in the middle and inner ear subsequent to the resolution of experimental otitis media induced by this pathogen. A monoclonal antibody specific for the lipooligosaccharide of this strain was used to probe sections of middle and inner ear tissue and visualized by means of the avidin-biotin peroxidase complex technique. Sixteen to seventeen days post inoculation with either viable or formalin-inactivated NTHi, endotoxin could be localized in both the middle and inner ear at a time when the middle ear was culture negative. Our data demonstrate that endotoxin shed by NTHi during otitis media penetrates the inner ear and binds to both tissue components and inflammatory cells in both the middle and inner ear.

Animals↗
PubMed2002

A review of inner ear fate maps and cell lineage studies.

A renewed interest in the development of the inner ear has provided more data on the fate and cell lineage relationships of the tissues making up this complex structure. The inner ear develops from a simple ectodermal thickening of the head called the otic placode, which undergoes a great deal of growth and differentiation to form a multichambered nonsensory epithelium that houses the six to nine sensory organs of the inner ear. Despite a large number of studies examining otic development, there have been surprisingly few fate maps generated. The published fate maps encompass four species and range from preotic to otocyst stages. Although some of these studies were consistent with a compartment and boundary model, other studies reveal extensive cell mixing during development. Cell lineage studies have been done in fewer species. At the single cell level the resulting clones in both chicks and frogs appear somewhat restricted in terms of distribution. We conclude that up until late placode stages there are no clear lineage restriction boundaries, meaning that cells seem to mix extensively at these early stages. At late placode stages, when the otic cup has formed, there are at least two boundaries located dorsally in the forming otocyst but none ventrally. These conclusions are consistent with all the fate maps and reconciles the chick and frog data. These results suggest that genes involved in patterning the inner ear may have dynamic and complex expression patterns.

Animals↗
PubMed2005

EYA1 expression in the developing inner ear.

OBJECTIVES: We sought to determine the developmental anatomy and EYA1 protein distribution in the inner ear of Xenopus laevis. METHODS: Xenopus laevis embryos were stained with monoclonal antibodies and imaged with confocal microscopy. RESULTS: At stage 27, the otocyst fully forms, with strong tubulin staining of early sensory cells at its ventromedial aspect. Neuronal ingrowth follows at stage 33/34. At stage 50, the semicircular canals are complete. EYA1 localizes to the anterior aspect of the otocyst from stages 37 to 44. By stage 50, EYA1 distribution is localized primarily to the sensory maculae and the endolymphatic duct of the developing inner ear. CONCLUSIONS: Whole mount confocal imaging of the developing Xenopus inner ear delineates the exact timing of otic development, sensory cell differentiation, and innervation. EYA1 protein expression has a distinct distribution pattern at the anterior aspect of the developing otocyst in stages 41 and 44. Later stages have a more localized pattern, in which EYA1 is detected only in the sensory epithelium and endolymphatic duct. This specific pattern of expression indicates a possible role in the determination of the anterior-posterior orientation of the inner ear, as well as a later role in sensory cell differentiation.

Animals↗
PubMed1992

Localization of type IV collagen and laminin in the guinea pig inner ear.

The distribution of type IV collagen (C-IV) and laminin, which are important components of the basement membrane (BM), was studied immunohistochemically in the inner ear of healthy Hartley guinea pigs. Antibodies against C-IV and laminin were used in this study. The distribution of C-IV in the inner ear was almost the same as that of laminin, but the extent of staining for laminin was less than that for C-IV in some sites. The sites of the inner ear in which these components were most densely localized were the areas surrounding the spiral ganglion cells and nerve fibers, the capillary vessels in the stria vascularis and the spiral prominence, and an area directly beneath the epithelium of the endolymphatic sac. Type IV collagen and laminin were also localized around the other vascular BM and the epithelial BM in the inner ear, but the tectorial membrane, the cupula of the crista ampulla, and the sensory epithelium did not take up stain. These results suggest that the vascular BM of the stria vascularis and spiral prominence, as well as the epithelial BM of the endolymphatic sac, may play an important role in fluid transport, and that the perineural BM of the inner ear might play an important role in the functional maintenance of the optimal environment of the inner ear nervous system.

Animals↗
PubMed2002

Sequence similarity between stereocilin and otoancorin points to a unified mechanism for mechanotransduction in the mammalian inner ear.

BACKGROUND: Interaction between hair cells and acellular gels of the mammalian inner ear, the tectorial and otoconial membranes, is crucial for mechanoreception. Recently, otoancorin was suggested to be a mediator of gel attachment to nonsensory cells, but the molecular components of the interface between gels and sensory cells remain to be identified. HYPOTHESIS: We report that the inner ear protein stereocilin is related in sequence to otoancorin and, based on its localisation and predicted GPI-anchoring, may mediate attachment of the tectorial and otoconial membranes to sensory hair bundles. TESTING: It is expected that antibodies directed against stereocilin would specifically label sites of contact between sensory hair cells and tectorial/otoconial membranes of the inner ear. IMPLICATIONS: Our findings support a unified molecular mechanism for mechanotransduction, with stereocilin and otoancorin defining a new protein family responsible for the attachment of acellular gels to both sensory and nonsensory cells of the inner ear.

Amino Acid Sequence↗
PubMed1993

Inner ear barotrauma in scuba divers. A long-term follow-up after continued diving.

Divers who suffer inner ear barotrauma are usually counseled to permanently avoid diving, reasoning that the injured inner ear is at increased risk of further damage. Twenty patients who suffered inner ear barotrauma while diving, but continued to dive against medical advice, were assessed on an interim basis for 1 to 12 years. As difficulty equalizing the ears during the barotraumatic event was a universal finding, prior to resuming diving, all patients were reinstructed on methods of maximizing eustachian tube function. No further deterioration of cochleovestibular function was noted. Based on these preliminary results, we conclude that recommending no further diving after inner ear barotrauma may be unnecessarily restrictive.

Adult↗
PubMed1990

[The histologic study of the inner ear in guinea pigs on anaphylatoxin].

Complement is known to relate to many inflammatory reactions. C4a, C3a and C5a, known as anaphylatoxins, are known to cause strong inflammatory reactions. In this study, the role of anaphylatoxins on the pathogenesis in the cochlea was examined. On hundred forty six male Harley guinea pigs, weighing about 350 grs, all susceptible to preyer's reflex, were used in this study. Anaphylatoxins were made from guinea pig serum treated with zymosan, and inoculated into the carotid artery of the guinea pigs. Parts of these animals were sacrificed and examined at ten minutes, one day, two days, three days, seven days, ten days and fifteen days after injection of anaphylatoxins. Pathological changes in inner ears were observed by light microscopy. After 10 minutes, inner ears were found morphologically normal. After one day, inner ears were found to be almost morphologically normal but the stria vascularis was observed with cystic formation. After two days, cystic formations in the stria vascularis were enlarged and Reissner's membranes were collapsed in some other animals. After three days, the stria vascularis in the various cochlear turns except in the basal turn, were extremely atrophied, some cochlear nerves showed degeneration and some cochlea showed endolymphatic hydrops. After seven days, ten days and fifteen days, the morphological changes showed atrophy in the stria vascularis similar to the results observed on the third days. Atrophy in the stria vascularis was improved gradually with time, but the degeneration of the cochlear nerve was not improved. Opinions have been divided on the cause of inner ear disease including Meniere's disease. Many authors have reported that infectious diseases, for example mumps, measles and cytomegalovirus infection, have caused human sensorineural hearing loss. These diseases have been reported to result in atrophy in the stria vascularis, degeneration of the cochlear nerve and some other pathological changes. In this study, it was clearly observed that the atrophy of the stria vascularis, the endolymphatic hydrops and other morphological changes were caused by introduction of anaphylatoxins. These results were similar to the pathological changes observed in inner ear diseases in human beings. Therefore, inflammatory substances, including anaphylatoxins, were closely related to the cause of inner ear diseases. The animal model used in this report is considered to be important for elucidating the pathogenesis of inner ear diseases.

Anaphylatoxins↗
PubMed2002

Magnetic resonance imaging-based virtual endoscopy of inner ear pathology.

OBJECTIVE: To study the feasibility of high-resolution magnetic resonance imaging (MRI)-based virtual endoscopy of the labyrinth to assess subtle inner ear pathology. STUDY DESIGN: A retrospective case review of patient with known inner ear pathology to determine the feasibility and clinical value of MRI-based virtual labyrinthoscopy. SETTING: Tertiary referral center. PATIENTS: Ten patients with symptoms of sensorineural hearing loss or vertigo who underwent high-resolution MRI between 1996 and 1999. INTERVENTION: Diagnostic image modality with three-dimensional (3-D) postprocessing to assess inner ear pathology. MAIN OUTCOME MEASURES: To evaluate how 3-D rendering with virtual labyrinthoscopy can depict subtle labyrinthine pathology. RESULTS: Cases with typical 3-D models and virtual labyrinthoscopic views are presented to illustrate this new image processing approach. CONCLUSION: The virtual endoscopic view of the labyrinth revealed subtle inner ear pathology. This 3-D postprocessing technique is able to render inner surface changes of tiny structures within the inner ear. It can be performed within a very short time using dedicated hybrid rendering techniques. It allows visualization of pathology in a comprehensive way for clinicians and is able to add 3-D information for troubleshooting in doubtful two-dimensional findings. We suggest the term virtual labyrinthoscopy for virtual intraluminal visualization of the labyrinth.

Adolescent↗
PubMedDate not supplied

Constructive interference in steady state-3DFT MR imaging of the inner ear and cerebellopontine angle.

PURPOSE: To assess the value of a three-dimensional Fourier transformation MR technique "CISS" (constructive interference in steady state) in imaging the inner ear. SUBJECTS: We studied 50 normal inner ears (40 axial, 10 coronal) and 10 pathologic inner ears in 60 patients. RESULTS: The cochlea, semicircular canals, and vestibulum were visualized in detail. Cranial nerve VII and the cochlear, superior vestibular, and inferior vestibular branch of cranial nerve VIII were identified in 90%, 94%, 80%, and 88% of the cases, respectively. A vascular loop was recognized inside the internal auditory canal in 6%, and in the porus in 30%, of the cases. The high signal of the cerebrospinal fluid and labyrinthine fluids (perilymph and endolymph) on the CISS images made excellent delineation of tumors in the cerebellopontine angle and internal canal possible and allowed detection of tumoral labyrinth involvement. The thin sections, high resolution of the images, and capability of producing multiplanar and three-dimensional reconstructions often offered additional information. CONCLUSIONS: The CISS sequence allows detailed study of the normal and pathologic inner ear and promises to be highly valuable in the demonstration of the vascular loop.

Adolescent↗
PubMed1980

[Causes of inner ear deafness; a critique of therapy (author's transl)].

In spite of recent criticisms, the diagnosis of inner ear hearing impairment is based on both pure tone thresholds and suprathreshold tests. The acoustico-facial reflex is useful only when used in conjunction with the suprathreshold tests.--Noise-induced deafness is generally confined to the higher frequencies of sound, and only exceptionally involve the middle frequencies as well. Low-tone hearing impairment may represent a partial symptom of Meniere's Disease as well as functional hearing loss. Zoster oticus produces a sensory hearing impairment but not a neural one, as might be expected from the neurotropy of the Herpes virus. Patients with socalled presbyacusis exhibit criteria of inner ear pathology which may represent a summation of different noxious agents damaging the inner ear throughout life rather than result from the physiologic process of aging. Traumatic hearing impairment seldom progresses, and usually involves central parts of the auditory pathways following blunt trauma.--We believe that uncritical therapy with vasodilating drugs is not useful in sensory hearing loss, especially if it is continued for months and if several drugs are employed at the same time. The danger of an unintended decrease in blood pressure is greater in these patients since many also suffer from hypotension which can then cause vascular insufficiency to the inner ear, similar to the "steal" effect. Therapy for inner ear hearing loss remains the responsibility of the otolaryngologist, and should still be based on proper diagnosis.

Audiometry↗