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At least 199 records · Page 11Linked to original sources
PubMed1992

Positional audiometry in the diagnosis of perilymphatic fistula.

Fifty-eight cases with a presumptive clinical diagnosis of perilymphatic fistula (PLF) are described with the results of a positional audiometric test designed to detect the presence of air in the cochlea. All patients underwent tympanotomy and observations of the middle ear are recorded together with the results of treatment. A definite leak was found in 33 cases and none in 25, but grafting of the round and oval window was performed in all but 10 cases. Pure-tone audiometry was performed before and after a 30-minute period of positioning the patient horizontally with the affected ear uppermost. A change in audiometric thresholds was noted in the group where a presumptive diagnosis of PLF was made, including some of those not found to have leaks at operation. However these changes were not observed in the positional tests of a group of 22 patients with hearing losses attributable to other causes. Also, an abnormal air-bone gap was noted in the PLF group compared with the other group. Although the original two-frequency criteria of earlier studies applied to the positional test did not predict the operative findings (leak or no leak), new data on frequency specific changes are presented. It is possible that fistulas at the oval window may be associated with positional threshold change at 500 Hz, and those at the round window with changes at 8 kHz.

Audiometry, Pure-Tone↗
PubMed1984

Blast injury to sensory hairs: a study in the guinea pig using scanning electron microscopy.

Guinea pigs were exposed to a blast (maximum 1.0 kg/cm2) of nitrous gas for 0.2 s through the external auditory canal. Then, they were either killed immediately, 1 day, 3 days, 1 week, 2 weeks, or 4 weeks after exposure to the blast. The morphological changes of the cochlear sensory hairs were examined by means of a scanning electron microscope. Changes in the sensory hairs of the animals exposed to the blast for 1 s were examined in the same manner. The results of these experiments show that sensory hairs of the basal and the second turns were damaged more markedly than those of the third and subsequent turns. Outer sensory hairs were damaged more than inner ones.

Animals↗
PubMed1990

Otopathologic correlates of the continuum of otitis media.

It has been our hypothesis that different types of middle ear effusions and the clinical manifestations with which they are associated represent the typical inflammatory response. Employing an animal model under controlled conditions, we present statistical evidence that change in the mucosa of the middle ear in otitis media can occur along a continuum, with early forms regressing to more chronic stages of the disease. We also demonstrate an increase in the thickness and a decrease in the permeability of the round window membrane in a longitudinal study of otitis media in the same animal model. Histopathologic changes in human temporal bones with otitis media with effusion or chronic otitis media are similar to the changes in the animal models. These results support a concept that all categories of otitis media (serous, purulent, mucoid, and chronic) represent different stages in a continuum of events.

Adolescent↗
PubMed1986

Role of air bubbles in the perilymph as a cause of sudden deafness.

In the course of exploratory tympanotomies we have several times come across air bubbles leaking with perilymph. The fact prompted the hypothesis that in some cases of perilymphatic fistulas, air bubbles could enter the perilymphatic space from the fistula of the inner ear membrane and cause acute, reversible, profound sensory hearing loss. The experimental study described here was designed to test this hypothesis on guinea pigs. Experiments showed that sudden elevation of middle ear pressure by artificial means caused air bubbles to appear in the scala tympani even at a pressure level of 400 mm H2O. It also proved that air bubbles entered the perilymphatic space through the ruptured round window membrane without damaging Corti's organ or the membranous structure of the cochlea. Sequential recording of the action potential revealed that air bubbles induced acute, reversible, and profound hearing loss of cochlear origin, probably by disturbing the propagation of traveling waves of the perilymph.

Animals↗
PubMed2002

Chemical perfusion of the inner ear.

In general, chemical perfusion therapy of inner ear disease is safe, inexpensive, and easy to perform. High inner ear medication concentrations can be achieved while minimizing systemic side effects. Most delivery methods are minimally invasive and can be performed in the office. The treatment is usually well accepted by patients. Vertigo control rates for Meniere's disease have been excellent--rivaling other prominent surgical treatments--allowing intratympanic therapy to become the most prominent first-line treatment for Meniere's disease. Side effects of ototoxicity occurring in approximately 30% of patients remain as one of the primary hurdles to overcome. Most patients who experience hearing loss, however, do not complain of the loss and are simply happy to be free of their vertigo attacks. The use of oral steroids to rescue and preserve hearing during gentamicin perfusion remain promising, and complete recovery and even hearing improvement have been observed [30]. Steroid perfusion of the inner ear also is variably effective for the treatment of SSHL, and is particularly indicated when oral steroids fail or are contraindicated due to other health reasons. Many inner ear perfusion methods and philosophies of treatment exist. Each technique has its associated advantages and disadvantages, and the individual surgeon must decide which technique to use in concordance with the patient's disease and expectations. In the future, new medications likely will be developed to treat certain types of inner ear disease, including SSHL, tinnitus, and various forms of vertigo. These medications can be administered by direct chemical perfusion of the inner ear.

Adrenal Cortex Hormones↗
PubMed2006

Cochlear transducer operating point adaptation.

The operating point (OP) of outer hair cell (OHC) mechanotransduction can be defined as any shift away from the center position on the transduction function. It is a dc offset that can be described by percentage of the maximum transduction current or as an equivalent dc pressure in the ear canal. The change of OP can be determined from the changes of the second and third harmonics of the cochlear microphonic (CM) following a calibration of its initial value. We found that the initial OP was dependent on sound level and cochlear sensitivity. From CM generated by a lower sound level at 74 dB SPL to avoid saturation and suppression of basal turn cochlear amplification, the OHC OP was at constant 57% of the maximum transduction current (an ear canal pressure of -0.1 Pa). To perturb the OP, a constant force was applied to the bony shell of the cochlea at the 18 kHz best frequency location using a blunt probe. The force applied over the scala tympani induced an OP change as if the organ of Corti moved toward the scala vestibuli (SV) direction. During an application of the constant force, the second harmonic of the CM partially recovered toward the initial level, which could be described by two time constants. Removing the force induced recovery of the second harmonic to its normal level described by a single time constant. The force applied over the SV caused an opposite result. These data indicate an active mechanism for OHC transduction OP.

Acoustic Stimulation↗
PubMed2003

Candidate's thesis: Platelet-activating factor-induced hearing loss: mediated by nitric oxide?

OBJECTIVES/HYPOTHESIS: Platelet-activating factor (PAF)in middle ear effusion is thought to induce hearing loss. The purpose of this study is to investigate the role of nitric oxide (NO) in the mechanism of PAF-induced hearing loss by studying the effects of PAF application on the round window membrane (RWM) with and without PAF-antagonist NO-blocker. STUDY DESIGN: Longitudinal study on randomized guinea pigs using PAF to induce hearing loss. METHODS Guinea pigs were divided into four groups: PBS, PAF, PAF-antagonist, and L-NAME. The PBS group received phosphate buffered saline (PBS) and the PAF groups received 10, 20, and 40 microg of PAF soaked into gelfoam and placed on the RWM. PAF-antagonist (WEB 2170) and NOS inhibitor NG-nitro-l-arginine-methylester (L-NAME) were injected intraperitoneally prior to PAF 20 microg application on the RWM. The following three tests were performed on each animal group: Hearing was tested with an auditory brainstem response (ABR) test over 24 hours. At the end of 24 hours, cochlear hair cells were examined by scanning electron microscopy (SEM) and immunohistochemistry was carried out on the cochlea to test the expression of inducible nitric oxide synthase (iNOS). RESULTS: The PAF group developed significant elevation of ABR threshold and cochlear hair cell damage in the SEM group as compared with the PBS control group. The PAF-antagonist (WEB 2170) and the L-NAME groups did not show significant elevation of ABR threshold and cochlear hair cell damage compared with the group administered PAF 20 microg, but in the PAF-antagonist group, the elevation of ABR threshold was significant compared with that of the PBS control group, whereas it was not significant compared with the PBS group in the L-NAME group. Strong expression of iNOS on cochlea was observed in the PAF group and lighter expression was seen in PBS, WEB 2170, and L-NAME groups. CONCLUSIONS: This study demonstrated that PAF placed on the RWM induced hearing loss and cochlear hair cell damage. The PAF-antagonists and L-NAME prevented the PAF-induced hearing loss and inhibited iNOS expression in the cochlea. These findings suggest that the PAF-induced hearing loss caused by cochlear hair cell damage may have been mediated by NO. PAF-antagonists and L-NAME may have future therapeutic implications in preventing sensorineural hearing loss associated with chronic otitis media. The results of this study have significant potential clinical application.

Animals↗
PubMed1977

A new hypothesis on the plurifactorial etiology of Meniere's disease.

Meniere's disease is characterized by an extremely long trend: this fact, as in other diseases of very wide chronicity, permits one to formulate a special type of hypothesis regarding the aetiology and the pathogenesis of the disease; it is comprised of many individual factors, of differing chronology and which are connected to each other with successive causality. This hypothesis was founded on a large body of data concerning the multiple histopathological effects on the inner ear of an initially inflammatory disease of the middle ear.

Acute Disease↗
PubMed2006

Inner ear therapy for neural preservation.

A gradual loss of auditory neurons often occurs following sensorineural hearing loss. Since the cochlear implant must stimulate the remaining auditory neuron population, it would be beneficial to preserve as many auditory neurons as possible. Neurotrophic factors protect auditory neurons from degradation after sensorineural hearing loss in experimental animals, but have not yet been translated into the clinical setting. Current experimental and clinical techniques for drug delivery to the inner ear are examined in this review, covering the routes for drug delivery to the cochlea and the delivery systems used to introduce them. Duration of treatment, drug diffusion, effectiveness and safety are discussed with references to how they may be translated to the implementation of neurotrophic factor treatment for neural preservation.

Animals↗
PubMedDate not supplied

No change detected on distortion products in awake or anesthetized guinea pigs.

Two pure tones presented simultaneously to one ear can produce physiologically and perceptively other tones called distortion products which originate in the inner ear. Notable differences exist between their physiological and perceptive features. In physiological experiments the anesthesia may alter the functioning of the cochlea, especially its efferent system. Physiological measurements made of distortion products taken from the same animals under anesthesia or in the awake state were compared using round window cochlear microphonic responses and evoked potentials from the eighth nerve and the auditory cortex. The physiological measures appeared unaltered by anesthesia, but in both the awake and anesthetized states, repeated measuring at intervals of several minutes could show apparently random variations of a few decibels.

Acoustic Stimulation↗
PubMed1997

Recovery of structure and function of inner ear afferent synapses following kainic acid excitotoxicity.

The present study was conducted to examine the re-establishment of IHC/VIII nerve synapses following kainic acid (KA) excitotoxicity and to discern if the re-organized afferent could render not only a normal auditory threshold but also a normal supra-threshold function. KA (60 mM) applied to the intact round window membrane in chinchilla destroyed postsynaptic endings of the auditory nerve, depressed the input-output (I/O) functions of auditory evoked potentials (EVP) and produced an average loss of sensitivity of over 80 dB at 4, 8, and 16 kHz, with less substantial losses (40-60 dB) at lower frequencies. However, there was no significant difference in 2f1-f2 distortion-product otoacoustic emissions (DPOAE) before and after the application of KA. The nerve endings went through a sequence of swelling, degeneration and recovery over a 3-5 day period at higher frequency. Auditory sensitivity and supra-threshold response returned accordingly. In contrast, complete recovery at lower frequencies (1 and 2 kHz) required more than 5 days. The results provide strong evidence that (1) excitotoxically damaged cochlear afferent neurons can recover and render both a normal EVP threshold and EVP I/O function and (2) afferent innervation to IHCs is not necessary for DPOAE generation.

Animals↗