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PubMed1985

Applications of scanning electron microscopy and X-ray microanalysis in inner ear pathology.

Surface pathology of inner ear structures so far described in detail concern cochlear and vestibular hair cells and the stria vascularis. In man, surgical intervention into the inner ear is very uncommon and when performed is in general with the primary objective of destroying the diseased peripheral end organs. The vast majority of inner ear tissue available for use with scanning electron microscopy (SEM) is therefore obtained from animals. The present paper reviews the progression of surface pathology caused by aminoglycoside antibiotics, acoustic overstimulation and in a guinea pig strain with genetic inner ear disease. The primary site of onset of surface pathology differs, depending on the underlying cause. Advanced surface pathology shows a similar type of morphological degeneration independent of cause. The combination of SEM and energy dispersive X-ray microanalysis (XRMA) of inner ear pathology has as yet been reported in only three studies, all concerning inner ear fluids or otoconia.

Aminoglycosides↗
PubMedDate not supplied

Congenital anomalies of the inner ear.

This study investigated congenital anomalies occurring in the inner ear, with particular attention to their features, localizations, and frequencies. Seventy-seven human temporal bones obtained from 53 individuals, aged one day to 39 years, each of whom had anomalies of the external ear, middle ear, and/or inner ear, were used for this study. The temporal bones had been removed at autopsy, fixed, dehydrated, embedded in celloidin, and sectioned horizontally or vertically at 20 microns. Every tenth horizontal section or every 20th vertical section was stained with hematoxylin and eosin, mounted, and studied under a light microscope. There were 206 inner ear anomalies (117 in the vestibular system, 79 in the cochlea, 10 in the internal auditory meatus) in the 51 bones studied. Fifty-four different features of anomalies were present at 33 different locations in the inner ear. The most frequent anomalies observed were shortened cochlea (23 bones), enlarged vestibule (17 bones), wide cochlear aqueduct (16 bones), absence of lateral semicircular canal (14 bones), and large osseous lateral semicircular canal (10 bones). The most common site of inner ear anomalies was thus the lateral semicircular canal, which was involved in 46 of the 206 anomalies observed; the anomalies in this organ were variable in type. The implications of inner ear anomalies are discussed as they relate to fetal development, inner ear dysfunction, and clinical interpretation of polytomographic studies.

Abnormalities, Multiple↗
PubMed1991

Pathophysiology of inner ear fluid imbalance.

Maintenance of homeostasis of inner ear fluids and biochemical integrity of inner ear tissue are essential for proper functioning of the auditory and vestibular end organs. Although various regulatory mechanisms exist in a different portion of the labyrinth, the inner ear is known to respond to systemic challenges. The association of Meniere's syndrome with an imbalance of inner ear fluid homeostasis has been hypothesized for the past century. Among many factors, the effects of hormonal imbalance on inner ear fluid composition and inner ear function have however scarcely been studied. The purpose of this study was to explore the relationship between the autonomic nervous system and inner ear function and possible mechanisms of functional disturbances in an experimental condition. An infusion of supraphysiologic amounts of epinephrine, a stress related hormone, resulted in an elevation of osmolality in serum and perilymph. Furthermore, the infusion of epinephrine resulted in elevation of threshold, prolongation of latency, and depression of amplitude in the compound action potential of the auditory nerve. These findings were most marked at high frequencies. We hypothesized that the epinephrine-induced hearing loss was brought about by an increase in perilymphatic osmolality, as well as by the ionic imbalance caused by the osmotic gradient. Since emotional stress has been implicated as a mechanism of inducing a Meniere's attack, evaluation of the relationship between the autonomic system and cochlear function may contribute to the understanding of possible mechanisms of inner ear dysfunction caused by hormonal imbalances.

Animals↗
PubMed1991

Diving-related inner ear injuries.

Diving-related inner ear barotrauma (IEB) and inner ear decompression sickness (IEDS) most often result in permanent severe cochleovestibular deficits, unless immediate diagnosis is reached and the correct treatment is commenced early. Nine cases of sport-diving-induced inner ear injuries that were referred to the Israeli Naval Hyperbaric Institute between October 1987 and September 1989 are presented with regard to evaluation, treatment, and follow-up. The diagnosis was IEB in five divers and IEDS in four. Explorative tympanotomy was carried out with remarkable results in two patients with IEB, while the remaining three were relieved by bed rest alone. Three of the four IEDS patients were recompressed according to the extended US Navy Table 6 with good short-term results. The role of complete otoneurological evaluation in the decision-making process leading to the correct diagnosis and treatment is emphasized.

Adolescent↗
PubMed1982

DNA content, mitotic activity, and incorporation of tritiated thymidine in the developing inner ear of the rat.

The rat inner ear is ectodermally derived from a region adjacent to the developing hindbrain. Beginning on day 8 of a 22-day gestational period, This zone of ectoderm first forms the otic placode, then the otocyst, and ultimately the definitive membranous labyrinth. This report provides an estimation of total DNA content of the developing inner ear, and hence an estimation of the total number of cells that comprise the inner ear at each developmental stage. The incorporation of 3H-thymidine indicates that most cells of the inner ear undergo DNA synthetic activity during gestational days 13 to 15. Radioautographic observations indicate a zone of DNA synthetic activity at the base of the outpocketing cochlear duct during early development. At the later stages of development, DNA synthesis is restricted to the cristae ampullares of the semicircular canals and the maculae of the utricle and the saccule. In contradistinction to the findings of other investigators, the statoacoustic ganglion complex undergoes terminal mitosis during gestational days 17 and 18. The gestational period between days 13 and 15 may prove to be a critical stage in normal otic development. The normal values of total DNA content and the number of cells that comprise the inner ear during development, established by these methods, can be compared with pathologic inner ears to provide quantitative means of assessing the damage in malformed inner ears. These values also form the baseline for future experimental studies of inner ear development.

Animals↗
PubMed2004

Apaf1-dependent programmed cell death is required for inner ear morphogenesis and growth.

During inner ear development programmed cell death occurs in specific areas of the otic epithelium but the significance of it and the molecules involved have remained unclear. We undertook an analysis of mouse mutants in which genes encoding apoptosis-associated molecules have been inactivated. Disruption of the Apaf1 gene led to a dramatic decrease in apoptosis in the inner ear epithelium, severe morphogenetic defects and a significant size reduction of the membranous labyrinth, demonstrating that an Apaf1-dependent apoptotic pathway is necessary for normal inner ear development. This pathway most probably operates through the apoptosome complex because caspase 9 mutant mice suffered similar defects. Inactivation of the Bcl2-like (Bcl2l) gene led to an overall increase in the number of cells undergoing apoptosis but did not cause any major morphogenetic defects. In contrast, decreased apoptosis was observed in specific locations that suffered from developmental deficits, indicating that proapoptotic isoform(s) produced from Bcl2l might have roles in inner ear development. In Apaf1(-/-)/Bcl2l(-/-) double mutant embryos, no cell death could be detected in the otic epithelium, demonstrating that the cell death regulated by the anti-apoptotic Bcl2l isoform, Bcl-X(L) in the otic epithelium is Apaf1-dependent. Furthermore, the otic vesicle failed to close completely in all double mutant embryos analyzed. These results indicate important roles for both Apaf1 and Bcl2l in inner ear development.

Animals↗
PubMed1978

[The vessels of the inner ear (author's transl)].

The inner ear as an example of a highly specialized sensory organ also possesses a highly specialized vascularisation. This represents an impressive example for a reasonable adaption of the terminal blood vessels to a specific function of the organ fulfilling more than only the nutrition. In this paper the microvascular bed of the cochlea is examined using both the injection method of the vessels and the biomicroscopic observation in vivo. The combination of these technics supported by histologic and stereoscan microscopic examinations has made it possible to give an account of the functional morphology of the inner ear vessels. As a detailed structural analysis of the vessels morphology with the help of dyes that fill the whole of the vessels space (i.e. Berlin blue) is not possible, perfusion experiments with silver nitrate were performed on the inner ear. After the perfusion the vessels are cleaned again, the silver however imbibes the intercellular reticular substances and after exposure produces a continous and sharp framework of the endothelium and--when present--muscular cells, thus showing the angioarchitectural contours. There is a very clear division of the cochlear vessels in a three dimensional space: The arterial and venous vessels are vividly separated from one another, forming two systems of microvascular units in the lateral wall and the spiral lamina. Each unit begins with special blood vessel convoluts in the modiolus, consisting of loops of arterioles. They are weakly muscularized whereas no muscle structures are seen elsewhere in the other parts of the inner ear vessels. There are no a.-v. anastomoses or sphinkters at all. The function of the vessel loops in the modiolus is to flatten the pulse wave as well as to regulate the blood flow in the microvascular bed by vasomotion. This was proved by statistical examinations of 1200 measurements of the widths of the vessels at several points of the cochlea in a blind study with and without vasoactive drugs. The terminology of the vessels is not standardized. The nomenclature in this paper has regard to the classification of the vessels, the course and the topographic localisation. Silver staining reveals changes in the form of the endothelium cells from the arterial towards the venous end. While the arteries show a long stretched spinle or lancet like form they change over blunt, oval, triangular or rhomboid forms into polygonal cells with spiked border lines at the venules. All experiments together give an account that the blood supply of the inner ear is in close correlation with the blood supply of the brain and too possesses autoregulative mechanisms, which must be localized in the convoluts at the beginning of every microvascular unit of the cochlear vessels.

Arterioles↗
PubMed1997

A totally implantable drug delivery system for local therapy of the middle and inner ear.

Local therapy of middle and inner ear diseases is being used, but is restricted to cases of ear drum perforation or to repeated invasive intratympanic drug application by the physician. In accordance with the Medical Device Directive (class III), a bone-anchored, totally implantable drug delivery system (TI-DDS) has been developed. It includes a micropump for subcutaneous, patient-controlled activation, a drug reservoir and a septum port. A thin guide-wired catheter leads from the pump outlet to the point of application in the mastoid or middle ear cavities. Local inner ear therapy with suitable drugs is possible by positioning the catheter's end near the round window membrane. The system requires no battery and will offer a wide range of patient-controlled bolus applications (25 microliters per activation). We first analyzed the three-dimensional implantation geometry of the mastoid cavity. Basic micromechanical problems have been solved in order to create several prototypes. The TI-DDS has already undergone extensive in vitro testing. Recent results of pump rate precision and digital pressure force testing are promising. Local drug treatment for conditions such as lidocaine-sensitive tinnitus, secretory otitis media, Meniere's disease, localized pain and intralesional cancer is under discussion. Furthermore, local application of future biotechnological trophic factors for inner ear treatment is anticipated. The basic engineering is completed and initial animal tests are in preparation.

Animals↗
PubMedDate not supplied

The effects of calcitonin gene-related peptide on the blood flow of the upper respiratory tract and the middle and inner ear.

The effects of intravenously infused CGRP on regional blood flows and vascular resistance in the upper respiratory tract, the middle ear, and the inner ear were studied in cats. CGRP caused a pronounced vasodilation and an increase in blood flow of the respiratory mucosa and structures of the middle ear. The substance did not affect the blood flows of the cochlea and the vestibular organ in the inner ear.

Animals↗
PubMed1994

Diffusible factors regulate hair cell regeneration in the avian inner ear.

Damage to the avian inner ear results in up-regulation of mitotic activity resulting in regeneration of hair cells. The objective of this investigation was to determine whether the damaged inner ear epithelium releases a soluble mitogen that is responsible for the up-regulation of proliferation. The sensory epithelium from normal and drug-damaged avian inner ears was cultured alone or in the presence of other cultures. As previously shown in vivo and in vitro, damaged organs displayed increased supporting cell proliferation compared with undamaged organs, leading to eventual morphologic and functional recovery. When damaged organs were cocultured with an undamaged organ, proliferation was increased in the undamaged tissue. When undamaged organs were cultured together, proliferation was decreased. These results indicate that a soluble factor released from the damaged inner ear epithelium stimulates proliferation and suggest the release of a factor from normal tissue that suppressed mitotic activity. Thus, reparative hair cell regeneration in the inner ear appears to be regulated by a balance between proliferative and antiproliferative paracrine factors.

Animals↗
PubMed1999

Inner ear barotrauma from scuba diving.

Inner ear barotrauma among scuba divers is believed to be caused by any of three conditions: a hemorrhage in the inner ear, a tear of the labyrinthine membrane, or a perilymphatic fistula. These injuries may occur concurrently or separately. Hemorrhage and membrane rupture are managed conservatively, while fistula requires surgical repair. In this report, we describe three cases of inner ear barotrauma in scuba divers. We also discuss the proposed etiologies of this injury and the controversy over whether or not divers who have suffered an inner ear trauma can safely resume scuba diving. Although the older literature clearly suggests otherwise, we believe that scuba divers who completely recover from inner (or middle) ear barotrauma may return to diving as long as they exercise caution and care.

Adult↗
PubMed1989

[Acute low tone sensorineural hearing loss caused by inner ear barotrauma].

Three cases of inner ear barotrauma with subjective symptoms and hearing impairment which were similar to the low tone sudden deafness were reported. Case 1 was a 34-year-old man who developed a hearing loss in the next morning of taking an airplane and recovered four days after. Case 2 was a 42-year-old man who developed a hearing loss 2 days after flying in an airplane and hearing loss have recurred 4 times in his right ear for 3 months. Eight months after recovery of previous recurrent attack, a hearing loss occurred in his left ear without flying and recurred twice for 3 weeks. Case 3 was a 25-year-old woman who developed a hearing loss in the right ear after 24 meter depth scuba diving and recurred 4 times for 40 days. Those three patients complained of no vertigo at any attacks and were treated conservatively. From previous reports and the onset and the course of hearing disturbance, acute low tone sensorineural hearing loss in case 1 and case 2 was thought to be caused by circulatory disturbance of the inner ear and in case 3 thought to be caused by inner ear window rupture. But, endolymphatic hydrops was also needed to be take into account in those three cases as a common possible cause. Inner ear barotrauma and so called labyrinthine window rupture were considered to be one of the diseases needed to differentiate from low tone sudden deafness without reference to mono-attack type or recurrent type.

Acute Disease↗
PubMed1997

Autoantibodies in inner ear disease.

The etiopathogenesis of many inner ear disorders still remains idiopathic. Immunological mechanisms are attracting attention in relation to a number of these diseases. Some cases are believed to be autoimmune in origin. The present study was conducted to determine whether patients with inner ear disorders produce antibodies that may be pathologic to the inner car or result from its damage. Sera from 100 patients with various inner ear disorders were tested for autoantibodies using the indirect immunofluorescence test. Inner ear tissue preparations from healthy guinea pigs were used as antigen substrates. Adequate tissue and serological controls were applied. Two groups of antibodies were detected; antibodies directed against the inner ear tissues (18%) and antibodies directed against different tissue/cellular elements (41%). A wide variety of inner ear antibodies were found, though no common type manifested itself. Meniere's disease was the most common clinical diagnosis in the antibody-positive group.

Antibody Formation↗
PubMed1989

[Neuronotrophic interactions in the developing inner ear].

In the developing inner ear, the existence of a neuronal death and of a peripheral target-derived trophic effect on the embryonic cochleovestibular neurons is described. We investigate the molecular vector(s) of such neuronotrophic influences on the cochleovestibular neurons, particularly the nerve growth factor (NGF) which is a good candidate since receptors for this trophic factor are described in the embryonic inner ear. In 12 day-old rat embryos, we demonstrate the release of an NGF-like activity by the otic vesicle and the effect of this trophic factor on the survival and the neuritogenesis of the cochleovestibular neurons. We suggest an important role for NGF in the neuronal stabilisation of the cochleovestibular ganglion and the invasion of the otic vesicle by the neurites. The study of the neuronotrophic interactions in the inner ear is then applied on more mature auditory neurons. In the 5 day-old rat cochlea, we also show the release by the central and the peripheral targets of a trophic activity allowing the survival of the afferent auditory neurons. These neuronotrophic factors may play an important role in the secondary degeneration of the auditory neurons following an injury of the Corti's organ or of the central target. The effect of NGF is also investigated on these neurons and we demonstrate that NGF has a neuritogenic but not a survival promoting effect on the 5 day-old rat afferent auditory neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Change of guinea pig inner ear pressure by square wave middle ear cavity pressure variation.

The inner ear fluid pressure of guinea pigs was measured during square wave middle ear cavity pressure variation. Time constants were derived for the slopes of the inner ear pressure recovery curves after middle ear pressure change. A "single exponential" function did not fit well and therefore more complicated functions were used for this purpose. For middle ear pressure increasing from zero to a few centimetres of water, returning to zero again, decreasing from zero to minus a few centimetres of water and then returning to zero again, time constants for the inner ear pressure recovery curves were on average 15.0, 8.6, 2.5 and 2.5 s, respectively. The results could not be described using a linear model with constant window membrane compliance and cochlear aqueduct flow resistance. A possible explanation for the large difference in time constants for positive or negative middle ear pressure changes is a dependence on aqueduct flow resistance or round window membrane position.

Animals↗
PubMed2001

Vascular variations of the inner ear.

Vascular anomalies of the inner ear have been documented in only a few isolated case reports. The goal of our study was to describe, qualify and quantify vascular variations of the inner ear in 122 temporal bones from 64 pediatric subjects aged between 0 and 10 years. The average age was 11.6 months. Horizontal sections of the temporal bone, examined by light microscopy, revealed vessels coursing freely through the perilymphatic space of the cochlea, especially in the apical turn. Other findings included abnormally wide vessels in the stria vascularis as well as a vascular malformation of the internal auditory canal. Our study demonstrated more atypical vessels in the cochlea than in the vestibular labyrinth. We found a statistically significant positive correlation between vascular variations of the inner ear and concomitant cardiac anomalies or endolymphatic hydrops. We also discuss the possible etiology and potential significance of these findings in terms of disturbances of the function of the inner ear.

Child↗
PubMed1999

Immunolocalization of tenascin in the chinchilla inner ear.

Tenascin was immunolocalized in the chinchilla cochlea and vestibular system to better understand the functional morphology of the inner ear. Inner ear tissues were fixed with acetone, decalcified and cryosectioned. Indirect immunofluorescence, using antibodies directed against human tenascin epitopes, were used to detect tenascin. As a positive control, tenascin immunoreactivity was found in kidney, cortical mesangial cells and the extracellular matrix of glomeruli and medullary tubule interstitial spaces, concurring with previously reported results. In the cochlea, tenascin immunoreactivity was present in osteocytes, the mesothelial cells underlying the basilar membrane (BM) and within the fibrous matrix of the BM. Greater reactivity was observed in the mesothelial cells than in the fibrous matrix of the BM. In the vestibular system, tenascin immunoreactivity formed a diffuse band directly beneath the basal lamina of the ampullary and otoconial organs. Tenascin immunoreactivity was also observed in cup-shaped regions between the type I vestibular hair cells and their surrounding VIII nerve calyces in the ampullary and otoconial organs. This is the first report of the anatomical distribution of tenascin in the adult, mammalian inner ear, other than our previously published abstract P.A. Santi and D. Swartz, Soc. Neurosci. Abstr. 23 (1997) 731.

Animals↗
PubMed1994

Immune-mediated inner ear disorders.

Immune-mediated inner ear disease is characterized by sensorineural hearing loss which is most often rapidly progressive and bilateral, may be accompanied by vestibular symptoms, and for which no cause can otherwise be identified. The problem may occur alone or in combination with other systemic autoimmune disorders. Recognition of this entity is important as a substantial number of such patients experience improvement in hearing following treatment with corticosteroids with or without other immunosuppressive agents. Immune response to inner ear antigens can be helpful in establishing the diagnosis. The lymphocyte transformation assay has been used in identifying such responses but is limited by sensitivity and inhibited by immunosuppression. Western blot identification of serum antibodies to a 68-kD antigen of the inner ear appears to be a promising means of identifying patients with immune-mediated inner ear disease. The antibody is present in the majority of patients with clinical features consistent with the disorder; it correlates with disease activity and is predictive of response to treatment. Nevertheless, response to corticosteroid therapy remains the most convincing evidence of the disease.

Antibody Formation↗