Contralateral auditory stimulation alters acoustic distortion products in humans

It is now generally accepted that otoacoustic emissions (OAE) represent the only objective and non-intrusive means of functional exploration of the active micromechanical characteristics of the outer hair cells of the organ of Corti. Previous studies showed a decrease of the transiently evoked otoacoustic emissions and spontaneous otoacoustic emissions in humans, during acoustic stimulation of the contralateral ear, and attributed this effect to the medial efferent system. Such an effect has been shown on acoustic distortion product otoacoustic distortion emissions (DPOAE) in guinea pigs, but has not been investigated for DPOAEs recorded in humans, although DPOAEs represent the easiest means of exploring active micromechanical cochlear properties both in humans and in laboratory animals. The present study sought to investigate the existence and characteristics of a contralateral auditory stimulation effect on DPOAEs recorded in humans. This study shows that contralateral broad-band noise (BBN) has a suppressive effect on DPOAEs recorded from 0.5 kHz to 5 kHz. This effect is not due to air conduction, as no change in the noise floor occurred under increasing contralateral stimulation, and as no reduction in DPOAE amplitude was obtained in subjects whose contralateral ear was sealed with a plastic ear plug. Moreover, cross-over attenuation by bone transmission has been ruled out, as no change in DPOAE amplitude was recorded in the healthy ear of total unilaterally deaf patients during acoustic stimulation of the deaf ear. The effect seen was not entirely due to the acoustic reflex, as it was found and could indeed be even greater in subjects with no acoustic reflex. Results presented here show that the contralateral BBN effect is greater at low levels of ipsilateral stimulation, which leads us to discuss the involvement of both passive and active mechanisms in DPOAE generation at high stimulation levels. The contralateral BBN effect seems to be greater in mid frequency cochlear regions. There is strong evidence that the medial efferent system is involved and that afferent and efferent inputs are, at least partly, integrated at a brainstem level in order to ensure cochlear interaction. DPOAEs provide an interesting model for functional exploration of the efferent system, since they seem to be the only type of otoacoustic emission that can be recorded in both humans and in the majority of animals, and since results are obtained in the same way from both animals and humans, which allows experimental animal models very close to the human model.     

Implantation of multiple intracochlear electrodes for rehabilitation of total deafness: preliminary report

Many instances of total deafness are due to destruction of the organ of Corti but with partial or complete preservation of the function of the cochlear nerve. In such cases, it is possible to restore some hearing by electrically stimulating the fibers of the cochlear nerve with the help of implanted electrodes. Preoperative testing with electric shocks applied to the round window have aroused sensations of noise in 45 cases of total bilateral deafness with a great variety of etiologies. The only negative results were in two cases of operated acoustic neuromas. Our operation places up to eight intracochlear electrodes, each with a separate fenestration opening into an electrically isolated compartment of the scala tympani. Stimulation of each electrode yields a different sound sensation of a pitch that depends on its location along the cochlea. Electric filters direct different frequency bands to the appropriate electrodes, with the necessary compression of dynamic range. In three experimental cases of unilateral deafness, pitch matches to the normal ear were made. In seven therapeutic operations on adult cases of acquired total bilateral deafness, speech recognition was usually relearned within a month or two. Improvement of voice quality was also dramatic. The intracochlear electrodes have been well tolerated for months, but the method of connection to the external equipment still presents difficulties.     

Energy reflectance in the ear canal can exceed unity near spontaneous otoacoustic emission frequencies

There is some controversy in the literature over whether the so-called "active mechanism" or "cochlear amplifier" is actually a power amplifier that can produce an output signal with more power than its input, or whether it simply minimizes dissipative losses within the cochlea without providing an actual power gain greater than unity. A corollary of this controversy is whether spontaneous otoacoustic emissions (SOAEs) represent the output of a nonlinear oscillator mechanism, i.e., a power amplifier which can produce an oscillatory output signal in the absence of an input oscillatory signal, or whether they represent the output of a noise-driven, passive, nonlinear system. This paper describes measurements of energy reflectance, and acoustic impedance in the ear canals of human subjects with strong SOAEs. The reflectance, and the resistive and reactive parts of the acoustic impedance, all show a frequency fine structure which correlates with SOAE frequencies, and which becomes more pronounced at low stimulus levels. In some ears at some SOAE frequencies, energy reflectance exceeds unity, and correspondingly, acoustic resistance is negative. This result demonstrates that there is a power gain at these frequencies: The power reflected from the cochlea to the ear canal exceeds the power incident. It is also consistent with the theory that these SOAEs are produced by a nonlinear oscillator mechanism in the cochlea.     

New growth of axons in the cochlear nucleus of adult chinchillas after acoustic trauma

This study determined the effect of acoustic overstimulation of the adult cochlea on axons in the cochlear nucleus. Chinchillas were exposed to an octave-band noise centered at 4 kHz at 108 dB sound pressure level for 1.75 h. One chinchilla was never exposed to the noise, and several others had one ear protected by an ear plug or prior removal of the malleus and incus. Exposure of unprotected ears caused loss of inner and outer hair cells and myelinated nerve fibers, mostly in the basal half of the cochlea. Cochlear nerve fiber degeneration, ipsilateral to the exposed ears, was traced to regions of the cochlear nucleus representing the damaged parts of the cochlea. In silver impregnations of a deafferented zone in the posteroventral cochlear nucleus, the concentration of axons decreased by 43% after 1 month and by 54% after 2 months. However, by 8 months, the concentration of thinner axons, with diameters of less than 0.46 microm, increased by 46-90% over that at 2 months. The concentration of axons with larger diameters did not change. Between 2 and 8 months small axonal endings appeared next to neuronal cell bodies. This later increase of thinner axons and endings is consistent with a reactive growth of new axons of relatively small diameter. The emergence of small perisomatic boutons suggests that the new axons formed synaptic endings, which might contribute to an abnormal reorganization of the central auditory system and to the pathological changes that accompany acoustic overstimulation.     

Distortion-product otoacoustic emissions in kanamycin-treated guinea pig cochlea

Measurement of distortion-product otoacoustic emissions (DPOAE) is widely accepted as one of the most valuable tools for evaluating the frequency of specific cochlear pathology. Previous studies have revealed that distortion-product levels in the ear canal are definitely correlated with degree of damage in the cochlea. However, there seem to be no clear data of help in predicting the distribution and grade of damage in the cochlea quantitatively on the basis of the results of this non-invasive test. The present study is designed to assess correlations between degree of outer hair cell (OHC) damage by a potent ototoxic antibiotic, kanamycin, and DPOAE levels at the characteristic frequency at the site. Guinea pigs were used after daily intramuscular administration of kanamycin for 7 or 10 days. DPOAE levels were measured using a system (CUBDIS: Etymotic Research) with 78 frequency combinations of iso-intensity primaries from 0.5kHz to 16kHz of f2. The frequency ratio (f2/f1) was set at 1.2. Distortion-product level plots versus f2 (DP-grams) were constructed. The integrity of the OHC system was evaluated histologically by the succinic dehydrogenase (SDH) method under a light microscope. Cochleograms were constructed by calculating percentages of intact OHCs along the basilar membrane in 1-mm blocks. The DP-grams and the histopathological cochleograms showed essentially identical patterns in the kanamycin-damaged guinea pig cochlea. The results suggest that: 1) The generation of DPOAE requires functioning OHCs. 2) DPOAE measurement provides information allowing prediction of OHC damage distribution in the cochlea without histological investigations. 3) Careful setting of primary levels and other parameters is necessary to reliably predict the pathology. 4) Attempts to detect of minimal OHC damage could fail. 5) DPOAE seem very useful for monitoring cochlear function in clinically.     

Degeneration of axons in the brainstem of the chinchilla after auditory overstimulation

The patterns of axonal degeneration following acoustic overstimulation of the cochlea were traced in the brainstem of adult chinchillas. The Nauta-Rasmussen method for axonal degeneration was used following survivals of 1-32 days after a 105 min exposure to an octave-band noise with a center frequency of 4 kHz and a sound pressure level of 108 dB. Hair-cell and myelinated nerve-fiber loss were assessed in the cochlea. The cochleotopic pattern of terminal degeneration in the ventral cochlear nucleus correlated with the sites of myelinated fiber and inner-hair-cell loss: this correlation was less rigorous with outer-hair-cell loss, especially in the dorsal cochlear nucleus. These results are consistent with a dystrophic process with a slow time course depending on hair-cell loss and/or direct cochlear nerve-fiber damage. However, in a number of cases with no damage in the apical cochlea, fine fiber degeneration occurred with a faster course in low-frequency regions in the dorsal cochlear nucleus and, transynaptically, in a non-cochleotopic pattern in the superior olive and inferior colliculus. These findings suggest that neuronal hyperactivity plays a role in the central degeneration following acoustic overstimulation, possibly by an excitotoxic process.     

Ear canal reflectance in the presence of spontaneous otoacoustic emissions. I. Limit-cycle oscillator model

Allen et al. [Abstract in Eighteenth Midwinter Research Meeting of the Association for Research in Otolaryngology, Des Moines, IA (1995)] have found that the ear canal reflectance passes through a minimum around the frequency of a spontaneous otoacoustic emission (SOAE). They considered this result to constitute evidence against active nonlinear cochlear function as the basis for SOAEs. In order to investigate theoretically the expected behavior of ear canal reflectance in the neighborhood of a SOAE associated with an active-nonlinear cochlea, we use a simplified model in which the ear drum end of the ear canal is effectively terminated by a nonlinear-active element. Under the influence of a sinusoidal driver at the entrance of the ear canal, this element will, to a good approximation, either (1) oscillate at both the frequency of the driver (at which the reflectance is determined) and the SOAE (at a suppressed level, corresponding to nonentrainment), or (2) be entrained and only oscillate at the driving frequency. The magnitude of the nonlinear ear canal reflectance is found to exceed unity only at sufficiently low stimulus levels, and occurs under conditions of entrainment and nonentrainment of the spontaneous emission. Otherwise, the reflectance is less than unity and, as a function of frequency, has a minimum around the SOAE frequency.     

Basilar membrane nonlinearity and loudness

Loudness matching functions for tones for persons with one shifted-threshold ear (hearing loss and noise-shifted thresholds) and one ear within normal limits were used to derive the presumed basilar membrane (BM) input-output (I/O) function in a normal ear. The comparison was made by assuming that the BM I/O function for the ear with the cochlear threshold shift has a slope of one (a linearized cochlea). The function for the normal ear was derived from the loudness matching function based on this assumption. Comparisons were made for archival basilar membrane data [M. A. Ruggero, N. C. Rich, A. Recio, S. S. Narayan, and L. Robles, J. Acoust. Soc. Am. 101, 2151-2163 (1997)] for chinchilla and archival loudness matches for long-duration tones for persons with various degrees of cochlear hearing loss [F. Miskolczy-Fodor, J. Acoust Soc. Am. 32, 486-492 (1960)]. Comparisons were made also between BM I/O functions and ones derived from loudness matches for persons with unilateral hearing loss simulated by broadband noise. The results show a close resemblance between the basilar membrane I/O function and the function derived from loudness matches for long-duration tones, even though the comparison was between human and chinchilla data. As the degree of threshold shift increases from 40 to 80 dB, the derived BM I/O functions become shallower, with slopes for losses of 60 dB or more falling in the range of values reported for physiological data. Additional measures with short-duration tones in noise show that the slope of the loudness function and the slope of the derived basilar membrane I/O function are associated with the behavioral threshold for the tone. The results for long-duration tones suggest a correspondence between BM displacement and loudness perception in cases of recruitment, but the relation between the degree of loss and the amount of BM compression and the relation between signal duration and compression suggests that other factors, such as the neural population response, may play a role.     

Labyrinthine anomalies in trisomy 13 mosaicism

The temporal bone histopathology of a 2-month-old male with a bilateral cleft palate, cleft lip and polydactylia due to trisomy 13 mosaicism was studied. Anomalies in the ear involved a partial absence of the superior semicircular canal, an abnormally wide lateral semicircular canal, underdeveloped cochlear coils, an abnormally broad modiolus, an undeveloped organ of Corti and an underdeveloped basilar membrane in the basal turn of the cochlea, an unusually wide cochlear aqueduct, and deformed stapedial crura.     

An animal model for cochlear microcirculatory disorders by photochemically initiated thrombosis

Making an ideal animal model of cochlear microcirculatory disorders is an important method in studying inner ear microcirculation. After intravenous injection of Rose bengal (30 mg/kg), the lateral wall of the cochlea of guinea pigs was illuminated with green light (wavelength: 550 +/- 20 nm). The Rose bengal photoactivatedly produces oxygen radicals and oxygen singlets, which subsequently damage the endotheliocytes to cause adhesion and aggregation of platelets in the small vessels. After the photo-illumination, cochlea blood flow reduced sharply, and CAP amplitude decreased in 10 min and disappeared completely in about 20-40 min. With prolongation of time, stria vascularis, Corti's organ and spiral ganglion cells showed further disintegration due to ischemia, which resembled the histopathological changes of the cochlea with microcirculatory disorders. Therefore, this animal model may be considered an ideal one for studying the mechanisms of hearing loss that was caused by microcirculatory disorders and also for evaluating the effects of drugs on microcirculation of damaged cochlea.     

Observing middle and inner ear mechanics with novel intracochlear pressure sensors

Intracochlear pressure was measured in vivo in the base of the gerbil cochlea. The measurements were made over a wide range of frequencies simultaneously in scalae vestibuli and tympani. Pressure was measured just adjacent to the stapes in scala vestibuli and at a number of positions spaced by tens of micrometers, including a position within several micrometers of the basilar membrane, in scala tympani. Two findings emerged from the basic results. First, the spatial variation in scala tympani pressure indicated that the pressure is composed of two modes, which can be identified with fast and slow waves. Second, at frequencies between 2 and 46 kHz (the upper frequency limit of the measurements) the scala vestibuli pressure adjacent to the stapes had a gain of approximately 30 dB with respect to the pressure in the ear canal, and a phase which decreased linearly with frequency. Thus, over these frequencies the middle ear and its termination in the cochlea operate as a frequency independent transmission line. A subset of the data was analyzed further to derive the velocity of the basilar membrane, the pressure difference across the organ of Corti complex (defined to include the tectorial and basilar membranes) and the specific acoustic impedance of the organ of Corti complex. The impedance was found to be tuned in frequency.     

Analysis of c-Fos and glial fibrillary acidic protein (GFAP) expression following topical application of potassium chloride (KCl) to the brain surface

The mustached bat, Pteronotus p. parnellii, has a finely tuned cochlea that rings at its resonant frequency in response to an acoustic tone pip. The decay time (DT) and frequency of these damped oscillations can be measured from the cochlear microphonic potential (CM) to study changes in cochlear mechanics. In this report, we describe phasic changes that occur in synchrony with communication sound vocalizations of the bat. Three animals with chronically implanted electrodes were studied. During the experiments, 1-2 ms tone pips were emitted from a speaker every 200 ms. This triggered a computer analysis of the resulting CM to determine the DT and cochlear resonance frequency (CRF) of the ringing. The time relative to vocalizations was determined by monitoring the output of a microphone placed near a bat's mouth. Similar results were obtained from all three bats tested. In a representative case, the average DT was 2.33 +/- 0.25 ms while the bat was quiet, but it decreased by 46% to 1.26 +/- 0.75 during vocalizations, which indicates a greater damping of the cochlear partition. Sometimes, DT started decreasing immediately before the bat vocalized. After the end of a vocalization, the return to baseline values varied from rapid (milliseconds) to gradual (1-2 seconds). The CRF also changed from baseline values during vocalization, although the amount and direction of change were not predictable. When gentamicin was administered to block the action of medial olivocochlear (MOC) efferents, DT reduction was still evident during vocalization but less pronounced. We conclude that phasic changes in damping occur in synchrony with vocalization, and that the MOC system plays a role in causing suppression. Since suppression can begin prior to vocalization, this may be a synkinetic effect, mediated by neural outflow to the ear in synchrony with neural outflow to the middle ear muscles and the muscles used for vocalization.     

Noise and the young mouse: Genotype modifies the sensitive period for effects on cochlear physiology and audiogenic seizures.

Examined the correspondence between the critical period, during which acoustic trauma will profoundly alter subsequent auditory behavior, and the broader sensitive period, during which acoustic trauma is most damaging to cochlear functions in the young ear, using 133 C57BL/6 and 183 CBA mice (aged 12–54 days) as Ss. Ss were exposed to 2 min of 124-db octave band noise (8–26 kHz). A noninvasive electrocochleographic technique was used to assess cochlear microphonic (CM) and action potential (AP) thresholds in exposed Ss and nonexposed littermate controls. Noise had no effect on 12-day-old CBA Ss but produced a maximal threshold elevation at 30–36 days in 54-day-old Ss. Susceptibility to audiogenic seizures in exposed CBA Ss was greatest at the peak of the sensitive period for cochlear damage. 12-day-old C57BL/6 Ss were also unaffected by noise exposure; 36-day-old C57BL/6 Ss had maximal AP (23 db) and CM (17 db) threshold; elevations and 54-day-old C57BL/6 Ss had an 18-db elevation of the AP; and their CM was no longer affected. It is concluded that both genotypes have a sensitive period for the effects of noise trauma on CM and AP thresholds: CBA has a sensitive period for acoustic priming for audiogenic seizures, and C57BL/6 has a critical period for acoustic priming. (48 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Attenuation of cochlear damage from noise trauma by an iron chelator, a free radical scavenger and glial cell line-derived neurotrophic factor in vivo

Tissue injury by reactive oxygen species (ROS) may play a role in noise-induced hearing loss (NIHL). Since iron is involved in ROS generation, we studied if an iron chelator, deferoxamine mesylate (DFO), alone or in combination with mannitol, a hydroxyl scavenger and weak iron chelator, attenuates NIHL. Further, we investigated if glial cell line-derived neurotrophic factor (GDNF) provides additive or synergistic protection of the cochlea from acoustic trauma when given together with DFO and mannitol. Pigmented female guinea pigs were exposed to noise (4 kHz octave band, 115 dB SPL, 5 h). One hour before, immediately after, and 5 h after noise exposure, subjects received an injection of 5 ml saline/kg (control, group I), 100 mg DFO/kg (group II), 15 mg mannitol/kg (group III), or both DFO and mannitol (group IV and V). Animals in group V underwent implantation of an osmotic pump filled with GDNF (100 ng/ml) in the left ear 4 days before noise. Each treatment afforded some protection from noise damage. Group I showed significantly greater outer hair cell loss and threshold shifts at two or more frequencies compared to groups II through V. GDNF provided an additive functional, but not morphological, protection with DFO and mannitol. These findings indicate that iron chelators can attenuate NIHL, as do ROS scavengers, supporting the notion that ROS generation plays a role in NIHL. Additional functional protection provided with GDNF suggests that GDNF may attenuate noise-induced cochlear damage through a mechanism that is additive with antioxidants.     

Active electronic cochlear implants for middle and inner ear hearing loss--a new era in ear surgery. I: Basic principles and recommendations on nomenclature

Hearing aids have fundamental disadvantages: (1) stigmatization of the patient; (2) the sound is often found to be unsatisfactory due to the limited frequency range and undesired distortion; (3) in many patients, the ear canal fitting device generally necessary leads to an occlusion effect; (4) acoustic feedback when amplification is high. Conventional hearing aids transmit sound into the ear canal via a small microphone. Sound has the disadvantage of requiring high output sound pressure levels for its transmission. This along with the necessary miniaturization of the loudspeaker as well as the resonances and reflections in the closed ear canal contribute to the disadvantages mentioned. In contrast, implantable hearing aids do not make sound signals but micromechanical vibrations. An implantable hearing aid has an electromechanical transducer instead of the loudspeaker of a conventional hearing aid. The hearing signal does not leave the transducer as sound but as a mechanical vibration which is directly coupled to the auditory system bypassing the air. This implantable hearing aid is either coupled to the tympanic membrane, the ossicular chain, the perilymph of the inner ear, or the skull. An implantable hearing aid is expected to have: 1 Better sound fidelity than a hearing aid 2 No ear canal fitting device, free ear canal 3 No feedback 4 Invisibility Requirements on electronic hearing implants designed for patients with conductive hearing loss differ from those on implants for sensorineural hearing loss. Conductive hearing loss requires the implant to replace the impedance transformation, thus being an impedance transformation implant (ITI). In various respects, the demands on an ITI are lower than the demands on an electronic hearing aid for patients with sensorineural hearing loss. The latter are mostly patients with a failure of the cochlea amplifier (CA). A damage to the CA is clinically discernible by a positive recruitment and loss of otoacoustic emissions (OAE). Since these patients form the majority of cases with sensorineural hearing loss, an active hearing implant for such patients should partially replace the function of the CA. Therefore, the suggestion is to refer to a CAI (cochlea amplifier implant). The implant expressions ITI (for patients with conductive hearing loss) and CAI (for patients with sensorineural hearing loss) used in this context allow nomenclatural association with the CI (cochlear implant) for complete inner ear failure as well as with the BSI (brainstem implant) in the case of hearing nerve failure.     

Neuregulins and erbB receptors at neuromuscular junctions and at agrin-induced postsynaptic-like apparatus in skeletal muscle

This study has characterized the repertoire of the anion exchanger (AE) family members expressed within the guinea pig organ of Corti, the auditory neuroepithelia. Both AE2 and AE3 cDNAs were present, but AE1 cDNA was not detected. The more abundant AE2 was sequenced and its expression characterized in the cochlea. The 3888 base pairs (bp) AE2 sequence, compiled from multiple clones, includes 150 bp of upstream non-coding sequence and 3717 bp of open reading frame encoding a protein of 1238 amino acids. Immunoblot of cochlear homogenate revealed a single AE2-immunoreactive band of Mr 180 kDa. In situ hybridization and immunohistochemical analysis localized AE2 expression to several tissues and cell types within the guinea pig inner ear, including superior half of the spiral ligament and within the interdental cells lining the spiral limbus. However, AE2 was not clearly detected in the outer hair cells (OHC) of the organ of Corti by either immunohistochemistry or in situ hybridization. The results of these studies imply a physiologic role of AE2 in the cochlear homeostasis, but do not support its role as a potential 'motor protein' in mediating the in vitro-observed voltage-gated, ATP-independent OHC motility.     

Favourite objects of autistic children

This paper presents a lumped-parameter model that stimulates the in vivo electrical properties of a guinea pig cochlea implanted with a multielectrode stimulating array. A basic model of the low-frequency electroanatomy in a normally functioning guinea pig cochlea is developed by adding critical membrane capacitances to Strelioff's resistive network model [1]. The basic model of normal cochlear tissues is modified to account for anatomical and physiological differences between a normal and implanted cochlea, which results in an impedance model of an implanted cochlea. Simulating the results of in vivo cochlear stimulation verifies the accuracy with which the modified cochlear model represents electrical properties within an electrically stimulated cochlea. Generalized simulations using this model suggest a straightforward phasing scheme capable of achieving sharply focused, channel-independent multielectrode cochlear stimulation.     

The effects of attenuation of frequency segments on binaural localization of sound

Perceived location of tonal stimuli d and narrow noise bands presented in two-dimensional space varies in an orderly manner with changes in stimulus frequency. Hence, frequency has a referent in space that is most apparent during monaural listening. The assumption underlying the present study is that maximum sound pressure level measured at the ear canal entrance for the various frequencies serves as a prominent spectral cue for their spatial referents. Even in binaural localization, location judgments in the vertical plane are strongly influenced by spatial referents. We measured sound pressure levels at the left ear canal entrance for 1.0-kHz-wide noise bands, centered from 4.0 kHz through 10.0 kHz, presented at locations from 60 degrees through -45 degrees in the vertical plane; the horizontal plane coordinate was fixed at -90 degrees. On the basis of these measurements, we fabricated three different bandstop stimuli in which differently centered 2.0-kHz-wide frequency segments were filtered from a broadband noise. Unfiltered broadband noise served as the remaining stimulus. Localization accuracy differed significantly among stimulus conditions (p < .01). Where in the vertical plane most errors were made depended on which frequency segment was filtered from the broadband noise.     

Otoacoustic emissions evoked by electrical stimulation

Otoacoustic emissions evoked by electrical stimulation of the cochlea were measured in guinea pigs. Alternating current with acoustic frequencies was delivered directly to the scala tympani and the vestibuli of the basal turn by using a constant current stimulator made in our laboratory. The amplitude of the electrically evoked otoacoustic emmisson (EEOAE), which was 21.0 dB SPL in response to 2 kHz electrical stimuli of 120 microArms, was decreased gradually with anoxia of the animal and was reduced to below the noise level by extirpation of the ossiculum. The EEOAEs rose with a delay of 100 microseconds from the beginning of the stimulus, and reached maximum amplitude within three cycles. The output of EEOAE was magnified in a linear manner as the stimulus current increased from 10 to 200 microArms. The averages and standard deviations of the EEOAE output at the stimulus level of 170 microArms in six animals were 20.5 +/- 4.1 dB SPL for 1 kHz, 23.3 +/- 4.8 dB SPL for 2 kHz, 10.5 +/- 6.0 dB SPL for 3 kHz, 17.1 +/- 4.7 dB SPL for 4 kHz, 13.6 +/- 4.4 dB for 5 kHz and 18.3 +/- 4.8 dB SPL for 6 kHz. Measurement of EEOAE, in which stable responses could be obtained with simple and easy preparation, was considered a potential procedure for assessing the electromotility of the cochlear outer hair cells in vivo.     

Indications for middle ear obliteration within the scope of cochlear implant management

BACKGROUND: Cochlear implants have gained worldwide acceptance as a reliable method of rehabilitation of profoundly hearing-impaired patients. Due to thorough patient selection major postoperative complications rarely occur and are flap related in most cases. Deafness can develop during chronic suppurative otitis media, either coincidentally or secondary to the medical treatment; normally this condition is regarded as a contraindication for cochlear implantation. In cases with a mastoid cavity after surgical treatment for cholesteatoma, the electrode covered only by the epithelial lining will likely become exposed or extruded. Therefore we suggest the obliteration of the middle ear cleft with abdominal fat and the blindsac closure of the external ear canal before cochlear implantation in these conditions. PATIENTS: The average age of our 12 patients was 48 years, whereas the youngest was 2 1/2 years of age. Due to chronic inflammatory ear disease. 11 patients had a mastoid cavity on both ears. Eight patients had a cholesteatoma, the chronic bone destroying process in the temporal bone of two female patients was considered as a fibroinflammatory pseudotumor. The child had a congenital deafness in both ears with a Mondini dysplasia in CT scan. She had already developed two episodes of pneumococcal meningitis which was caused by a defect in the stapes footplate through which a liquor-filled cystic sac herniated in the middle ear. Because of a massive liquorrhoea after opening of the sac, we decided to obliterate the middle ear cleft after successful insertion of the electrode array. RESULTS: All active electrodes of 10 Nucleus implants (Cochlear) and two Clarion devices (Advanced Bionics Corp.) were successfully inserted in the cochlea of the 12 patients. After an average follow-up of 15 months, a temporary facial palsy in one patient and an insufficient closure of a retroauricular fistula over the mastoid cavity in two cases were observed as postoperative complications. One patient with a fibroinflammatory pseudotumor developed a massive inflammatory reaction in the implanted ear two months after cochlear implantation, which could not be controlled by conservative treatment. The implant had to be removed and local conditions settled after administration of immunosuppressive treatment with cyclophosphamide. The patient received a new implant seven months ago. CONCLUSIONS: Implantation of a foreign body in a potentially infected space which communicates intracranially means a surgical challenge which can be managed by obliteration of the middle ear after subtotal petrosectomy with abdominal wall fat combined with a reliable closure of the external ear canal. In case of massive inflammation we would prefer a two-stage procedure.