Nanomechanical mapping reveals localized stiffening of the basilar membrane after cochlear implantation.

Cochlear implantation leads to many structural changes within the cochlea which can impair residual hearing. In patients with preserved low-frequency hearing, a delayed hearing loss can occur weeks-to-years post-implantation. We explore whether stiffening of the basilar membrane (BM) may be a contributory factor in an animal model. Our objective is to map changes in morphology and Young's modulus of basal and apical areas of the BM after cochlear implantation, using quantitative nanomechanical atomic force microscopy (QNM-AFM) after cochlear implant surgery. Cochlear implantation was undertaken in the guinea pig, and the BM was harvested at four time-points: 1 day, 14 days, 28 days and 84 days post-implantation for QNM-AFM analysis. Auditory brainstem response thresholds were determined prior to implantation and termination. BM tissue showed altered morphology and a progressive increase in Young's modulus, mainly in the apex, over time after implantation. BM tissue from the cochlear base demonstrated areas of extreme stiffness which are likely due to micro-calcification on the BM. In conclusion, stiffening of the BM after cochlear implantation occurs over time, even at sites far apical to a cochlear implant.

Lateralization of virtual sound sources with a binaural cochlear-implant sound coding strategy inspired by the medial olivocochlear reflex.

Many users of bilateral cochlear implants (BiCIs) localize sound sources less accurately than do people with normal hearing. This may be partly due to using two independently functioning CIs with fixed compression, which distorts and/or reduces interaural level differences (ILDs). Here, we investigate the potential benefits of using binaurally coupled, dynamic compression inspired by the medial olivocochlear reflex; an approach termed "the MOC strategy" (Lopez-Poveda et al., 2016, Ear Hear 37:e138-e148). Twelve BiCI users were asked to localize wideband (125-6000 Hz) noise tokens in a virtual horizontal plane. Stimuli were processed through a standard (STD) sound processing strategy (i.e., involving two independently functioning sound processors with fixed compression) and three different implementations of the MOC strategy: one with fast (MOC1) and two with slower contralateral control of compression (MOC2 and MOC3). The MOC1 and MOC2 strategies had effectively greater inhibition in the higher than in the lower frequency channels, while the MOC3 strategy had slightly greater inhibition in the lower than in the higher frequency channels. Localization was most accurate with the MOC1 strategy, presumably because it provided the largest and less ambiguous ILDs. The angle error improved slightly from 25.3° with the STD strategy to 22.7° with the MOC1 strategy. The improvement in localization ability over the STD strategy disappeared when the contralateral control of compression was made slower, presumably because stimuli were too short (200 ms) for the slower contralateral inhibition to enhance ILDs. Results suggest that some MOC implementations hold promise for improving not only speech-in-noise intelligibility, as shown elsewhere, but also sound source lateralization.

Mechanical Effects of Cochlear Implant on Acoustic Hearing.

Residual hearing loss in cochlear implant users is investigated using the mechanical-human-cochlear model. Hearing loss due to stiffening of the round window increases significantly as input frequencies decrease from 3 kHz to 1 kHz but remains constant at lower frequencies, whereas loss due to the presence of an electrode insert becomes significantly higher at lower frequencies ([Formula: see text] kHz). The latter also shifts the characteristic frequency map toward the basal end of the cochlea. In the region away from the end of the electrode insert, cochlear function recovers, but the user still suffers from hearing loss caused by round window stiffening.

Numerical analysis of intracochlear mechanical auditory stimulation using piezoelectric bending actuators.

Cochlear implantation can restore a certain degree of auditory impression of patients suffering from profound hearing loss or deafness. Furthermore, studies have shown that in case of residual hearing, patients benefit from the use of a hearing aid in addition to the cochlear implant. The presented studies aim at the improvement of this electromechanical stimulation (EMS) approach by substituting the external hearing aid by an internal stimulus provided by miniaturized piezoelectric actuators. Finite element analyses are performed in order to derive fundamental guidelines for the actuator layout aiming at maximal mechanical stimuli. Further analyses aim at investigating how the actuator position inside the cochlea influences the basilar membrane oscillation profile. While actuator layout guidelines leading to maximized acoustic stimuli could be derived, some of these guidelines are of complementary nature suggesting that further studies under realistic boundary conditions must be performed. Actuator positioning inside the cochlea is shown to have a significant influence on the resulting auditory impression of the patient. Based on the results, the main differences of external and internal stimulation of the cochlea mechanism are identified. It is shown that if the cochlea tonotopy is considered, the frequency selectivity resulting from the mechanical cochlea stimulus may be improved.

Investigating time-efficiency of forward masking paradigms for estimating basilar membrane input-output characteristics.

It is well known that pure-tone audiometry does not sufficiently describe individual hearing loss (HL) and that additional measures beyond pure-tone sensitivity might improve the diagnostics of hearing deficits. Specifically, forward masking experiments to estimate basilar-membrane (BM) input-output (I/O) function have been proposed. However, such measures are very time consuming. The present study investigated possible modifications of the temporal masking curve (TMC) paradigm to improve time and measurement efficiency. In experiment 1, estimates of knee point (KP) and compression ratio (CR) of individual BM I/Os were derived without considering the corresponding individual "off-frequency" TMC. While accurate estimation of KPs was possible, it is difficult to ensure that the tested dynamic range is sufficient. Therefore, in experiment 2, a TMC-based paradigm, referred to as the "gap method", was tested. In contrast to the standard TMC paradigm, the maker level was kept fixed and the "gap threshold" was obtained, such that the masker just masks a low-level (12 dB sensation level) signal. It is argued that this modification allows for better control of the tested stimulus level range, which appears to be the main drawback of the conventional TMC method. The results from the present study were consistent with the literature when estimating KP levels, but showed some limitations regarding the estimation of the CR values. Perspectives and limitations of both approaches are discussed.

Intracochlear Pressure Transients During Cochlear Implant Electrode Insertion.

HYPOTHESIS: Cochlear implant (CI) electrode insertion into the round window induces pressure transients in the cochlear fluid comparable to high-intensity sound transients. BACKGROUND: Many patients receiving a CI have some remaining functional hearing at low frequencies; thus, devices and surgical techniques have been developed to use this residual hearing. To maintain functional acoustic hearing, it is important to retain function of any hair cells and auditory nerve fibers innervating the basilar membrane; however, in a subset of patients, residual low-frequency hearing is lost after CI insertion. Here, we test the hypothesis that transient intracochlear pressure spikes are generated during CI electrode insertion, which could cause damage and compromise residual hearing. METHODS: Human cadaveric temporal bones were prepared with an extended facial recess. Pressures in the scala vestibuli and tympani were measured with fiber-optic pressure sensors inserted into the cochlea near the oval and round windows, whereas CI electrodes (five styles from two manufacturers) were inserted into the cochlea via a round window approach. RESULTS: Pressures in the scala tympani tended to be larger in magnitude than pressures in the scala vestibuli, consistent with electrode insertion into the scala tympani. CI electrode insertion produced a range of pressure transients in the cochlea that could occur alone or as part of a train of spikes with equivalent peak sound pressure levels in excess of 170 dB sound pressure level. Instances of pressure transients varied with electrode styles. CONCLUSION: Results suggest electrode design, insertion mechanism, and surgical technique affect the magnitude and rate of intracochlear pressure transients during CI electrode insertion. Pressure transients showed intensities similar to those elicited by high-level sounds and thus could cause damage to the basilar membrane and/or hair cells.

A Triboelectric-Based Artificial Basilar Membrane to Mimic Cochlear Tonotopy.

A triboelectric-based artificial basilar membrane (TEABM) can mimic cochlear tonotopy by triboelectrification between Kapton film and aluminum foil. The two films are stacked and clamped to form a beam structure. The TEABM tonotopy is tested using an animal model to verify the feasibility of a self-powered acoustic sensor for a prototype cochlear implant.

Fatigue Modeling via Mammalian Auditory System for Prediction of Noise Induced Hearing Loss.

Noise induced hearing loss (NIHL) remains as a severe health problem worldwide. Existing noise metrics and modeling for evaluation of NIHL are limited on prediction of gradually developing NIHL (GDHL) caused by high-level occupational noise. In this study, we proposed two auditory fatigue based models, including equal velocity level (EVL) and complex velocity level (CVL), which combine the high-cycle fatigue theory with the mammalian auditory model, to predict GDHL. The mammalian auditory model is introduced by combining the transfer function of the external-middle ear and the triple-path nonlinear (TRNL) filter to obtain velocities of basilar membrane (BM) in cochlea. The high-cycle fatigue theory is based on the assumption that GDHL can be considered as a process of long-cycle mechanical fatigue failure of organ of Corti. Furthermore, a series of chinchilla experimental data are used to validate the effectiveness of the proposed fatigue models. The regression analysis results show that both proposed fatigue models have high corrections with four hearing loss indices. It indicates that the proposed models can accurately predict hearing loss in chinchilla. Results suggest that the CVL model is more accurate compared to the EVL model on prediction of the auditory risk of exposure to hazardous occupational noise.

Comparing auditory filter bandwidths, spectral ripple modulation detection, spectral ripple discrimination, and speech recognition: Normal and impaired hearing.

Some listeners with hearing loss show poor speech recognition scores in spite of using amplification that optimizes audibility. Beyond audibility, studies have suggested that suprathreshold abilities such as spectral and temporal processing may explain differences in amplified speech recognition scores. A variety of different methods has been used to measure spectral processing. However, the relationship between spectral processing and speech recognition is still inconclusive. This study evaluated the relationship between spectral processing and speech recognition in listeners with normal hearing and with hearing loss. Narrowband spectral resolution was assessed using auditory filter bandwidths estimated from simultaneous notched-noise masking. Broadband spectral processing was measured using the spectral ripple discrimination (SRD) task and the spectral ripple depth detection (SMD) task. Three different measures were used to assess unamplified and amplified speech recognition in quiet and noise. Stepwise multiple linear regression revealed that SMD at 2.0 cycles per octave (cpo) significantly predicted speech scores for amplified and unamplified speech in quiet and noise. Commonality analyses revealed that SMD at 2.0 cpo combined with SRD and equivalent rectangular bandwidth measures to explain most of the variance captured by the regression model. Results suggest that SMD and SRD may be promising clinical tools for diagnostic evaluation and predicting amplification outcomes.

All Three Rows of Outer Hair Cells Are Required for Cochlear Amplification.

In the mammalian auditory system, the three rows of outer hair cells (OHCs) located in the cochlea are thought to increase the displacement amplitude of the organ of Corti. This cochlear amplification is thought to contribute to the high sensitivity, wide dynamic range, and sharp frequency selectivity of the hearing system. Recent studies have shown that traumatic stimuli, such as noise exposure and ototoxic acid, cause functional loss of OHCs in one, two, or all three rows. However, the degree of decrease in cochlear amplification caused by such functional losses remains unclear. In the present study, a finite element model of a cross section of the gerbil cochlea was constructed. Then, to determine effects of the functional losses of OHCs on the cochlear amplification, changes in the displacement amplitude of the basilar membrane (BM) due to the functional losses of OHCs were calculated. Results showed that the displacement amplitude of the BM decreases significantly when a single row of OHCs lost its function, suggesting that all three rows of OHCs are required for cochlear amplification.

Further tests of the local nonlinear interaction-based mechanism for simultaneous suppression of tone burst-evoked otoacoustic emissions.

Tone burst-evoked otoacoustic emission (TBOAE) components measured in response to a 1 kHz tone burst (TB1) are suppressed by the simultaneous presence of an additional tone burst (TB2). This "simultaneous suppression of TBOAEs" has been explained in terms of a mechanism based on local nonlinear interactions between the basilar membrane (BM) travelling waves caused by TB1 and TB2. A test of this local nonlinear interaction (LNI)-based mechanism, as a function of the frequency separation (Δf, expressed in kHz) between TB1 and TB2, has previously been reported by Killan et al. (2012) using a simple mathematical model [Killan et al., Hear. Res. 285, 58-64 (2012)]. The two experiments described in this paper add additional data on the extent to which the LNI-based mechanism can account for simultaneous suppression, by testing two further hypotheses derived from the model predictions. Experiment I tested the hypothesis that TBOAE suppression is directly linked to TBOAE amplitude nonlinearity where ears that exhibit a higher degree of amplitude nonlinearity yield greater suppression than more linear ears, and this relationship varies systematically as a function of Δf. In order to test this hypothesis simultaneous suppression at a range of values of Δf at 60 dB peak-equivalent sound pressure level (p.e. SPL) and TBOAE amplitude nonlinearity from normal human ears was measured. In Experiment II the hypothesis that suppression will also increase progressively as a function of increasing tone burst level was tested by measuring suppression for a range of Δf and tone burst levels at 40, 50, 60 and 70 dB p.e. SPL. The majority of the findings from both experiments provide support for the LNI-based mechanism being primarily responsible for simultaneous suppression. However, some data were inconsistent with this view. Specifically, a breakdown in the relationship between suppression and TBOAE amplitude nonlinearity at Δf = 1 (i.e. when TB2 was reasonably well separated from, and had a higher frequency than TB1) and unexpected level-dependence, most notably at Δf = 1, but also where Δf = -0.5, was observed. Either the LNI model is too simple or an alternative explanation, involving response components generated at basal regions of the basilar membrane, is required to account for these findings.

Air, bone and soft tissue excitation of the cochlea in the presence of severe impediments to ossicle and window mobility.

Clinical conditions have been described in which one of the two cochlear windows is immobile (otosclerosis) or absent (round window atresia), but nevertheless bone conduction (BC) thresholds are relatively unaffected. To clarify this apparent paradox, experimental manipulations which would severely impede several of the classical osseous mechanisms of BC were induced in fat sand rats, including discontinuity or immobilization of the ossicular chain, coupled with window fixation. Effects of these manipulations were assessed by recording auditory nerve brainstem evoked response (ABR) thresholds to stimulation by air conduction (AC), by osseous BC and by non-osseous BC (also called soft tissue conduction-STC) in which the BC bone vibrator is applied to skin sites. Following the immobilization, discontinuity and window fixation, auditory stimulation was also delivered to cerebro-spinal fluid (CSF) and to saline applied to the middle ear cavity. While the manipulations (immobilization, discontinuity, window fixation) led to an elevation of AC thresholds, nevertheless, there was no change in osseous and non-osseous BC thresholds. On the other hand, ABR could be elicited in response to fluid pressure stimulation to CSF and middle ear saline, even in the presence of the severe restriction of ossicular chain and window mobility. The results of these experiments in which osseous and non-osseous BC thresholds remained unchanged in the presence of severe restriction of the classical middle ear mechanisms and in the absence of an efficient release window, while ABR could be recorded in response to fluid pressure auditory stimulation to fluid sites, indicate that it is possible that the inner ear may be activated at low sound intensities by fast fluid pressure stimulation. At higher sound intensities, a slower passive basilar membrane traveling wave may serve to excite the inner ear.

Low power adder based auditory filter architecture.

Cochlea devices are powered up with the help of batteries and they should possess long working life to avoid replacing of devices at regular interval of years. Hence the devices with low power consumptions are required. In cochlea devices there are numerous filters, each responsible for frequency variant signals, which helps in identifying speech signals of different audible range. In this paper, multiplierless lookup table (LUT) based auditory filter is implemented. Power aware adder architectures are utilized to add the output samples of the LUT, available at every clock cycle. The design is developed and modeled using Verilog HDL, simulated using Mentor Graphics Model-Sim Simulator, and synthesized using Synopsys Design Compiler tool. The design was mapped to TSMC 65 nm technological node. The standard ASIC design methodology has been adapted to carry out the power analysis. The proposed FIR filter architecture has reduced the leakage power by 15% and increased its performance by 2.76%.

A mouse model for human deafness DFNB22 reveals that hearing impairment is due to a loss of inner hair cell stimulation.

The gene causative for the human nonsyndromic recessive form of deafness DFNB22 encodes otoancorin, a 120-kDa inner ear-specific protein that is expressed on the surface of the spiral limbus in the cochlea. Gene targeting in ES cells was used to create an EGFP knock-in, otoancorin KO (Otoa(EGFP/EGFP)) mouse. In the Otoa(EGFP/EGFP) mouse, the tectorial membrane (TM), a ribbon-like strip of ECM that is normally anchored by one edge to the spiral limbus and lies over the organ of Corti, retains its general form, and remains in close proximity to the organ of Corti, but is detached from the limbal surface. Measurements of cochlear microphonic potentials, distortion product otoacoustic emissions, and basilar membrane motion indicate that the TM remains functionally attached to the electromotile, sensorimotor outer hair cells of the organ of Corti, and that the amplification and frequency tuning of the basilar membrane responses to sounds are almost normal. The compound action potential masker tuning curves, a measure of the tuning of the sensory inner hair cells, are also sharply tuned, but the thresholds of the compound action potentials, a measure of inner hair cell sensitivity, are significantly elevated. These results indicate that the hearing loss in patients with Otoa mutations is caused by a defect in inner hair cell stimulation, and reveal the limbal attachment of the TM plays a critical role in this process.

Cell-cell junctions: a target of acoustic overstimulation in the sensory epithelium of the cochlea.

BACKGROUND: Exposure to intense noise causes the excessive movement of the organ of Corti, stretching the organ and compromising sensory cell functions. We recently revealed changes in the transcriptional expression of multiple adhesion-related genes during the acute phases of cochlear damage, suggesting that the disruption of cell-cell junctions is an early event in the process of cochlear pathogenesis. However, the functional state of cell junctions in the sensory epithelium is not clear. Here, we employed graded dextran-FITC, a macromolecule tracer that is impermeable to the organ of Corti under physiological conditions, to evaluate the barrier function of cell junctions in normal and noise-traumatized cochlear sensory epithelia. RESULTS: Exposure to an impulse noise of 155 dB (peak sound pressure level) caused a site-specific disruption in the intercellular junctions within the sensory epithelium of the chinchilla cochlea. The most vulnerable sites were the junctions among the Hensen cells and between the Hensen and Deiters cells within the outer zone of the sensory epithelium. The junction clefts that formed in the reticular lamina were permeable to 40 and 500 but not 2,000 kDa dextran-FITC macromolecules. Moreover, this study showed that the interruption of junction integrity occurred in the reticular lamina and also in the basilar membrane, a site that had been considered to be resistant to acoustic injury. Finally, our study revealed a general spatial correlation between the site of sensory cell damage and the site of junction disruption. However, the two events lacked a strict one-to-one correlation, suggesting that the disruption of cell-cell junctions is a contributing, but not the sole, factor for initiating acute sensory cell death. CONCLUSIONS: Impulse noise causes the functional disruption of intercellular junctions in the sensory epithelium of the chinchilla cochlea. This disruption occurs at an early phase of cochlear damage. Understanding the role of this disruption in cochlear pathogenesis will require future study.

Effects of a perilymphatic fistula on the passive vibration response of the basilar membrane.

In this study, a three-dimensional finite-element model of the passive human cochlea was created. Dynamic behavior of the basilar membrane caused by the vibration of the stapes footplate was analyzed considering a fluid-structure interaction with the cochlear fluid. Next, the effects of a perilymphatic fistula (PLF) on the vibration of the cochlea were examined by making a small hole on the wall of the cochlea model. Even if a PLF existed in the scala vestibuli, a traveling wave was generated on the basilar membrane. When a PLF existed at the basal end of the cochlea, the shape of the traveling wave envelope showed no remarkable change, but the maximum amplitude became smaller at the entire frequency range from 0.5 to 5kHz and decreased with decreasing frequency. In contrast, when a PLF existed at the second turn of the cochlea, the traveling wave envelope showed a notch at the position of the PLF and the maximum amplitude also became smaller. This model assists in elucidating the mechanisms of hearing loss due to a PLF from the view of dynamics.

Post-processing analysis of transient-evoked otoacoustic emissions to detect 4 kHz-notch hearing impairment--a pilot study.

BACKGROUND: To identify a parameter to distinguish normal hearing from hearing impairment in the early stages. The parameter was obtained from transient-evoked otoacoustic emissions (TEOAEs), overcoming the limitations of the usually adopted waveform descriptive parameters which may fail in standard clinical screenings. MATERIAL/METHODS: Audiometric examinations and TEOAE analysis were conducted on 15 normal ears and on 14 hearing-impaired ears that exhibited an audiometric notch around 4 kHz. TEOAE signals were analyzed through a multivariate technique to filter out the individual variability and to highlight the dynamic structure of the signals. The new parameter (named radius 2-dimension--RAD2D) was defined and evaluated for simulated TEOAE signals modeling a different amount of hearing impairment. RESULTS: Audiometric examinations indicated 14 ears as impaired-hearing (IH), while the TEOAE ILO92 whole reproducibility parameter (WWR) indicated as IH 7 signals out of 14 (50%). The proposed new parameter indicated as IH 9 signals out of 14 (64%), reducing the number of false negative cases of WWR. CONCLUSIONS: In this preliminary study there is evidence that the new parameter RAD2D defines the topology and the quantification of the damage in the inner ear. The proposed protocol can be useful in hearing screenings to identify hearing impairments much earlier than conventional pure tone audiometry and TEOAE pass/fail test.

Comparison of distortion-product otoacoustic emission growth rates and slopes of forward-masked psychometric functions.

Slopes of forward-masked psychometric functions (FM PFs) were compared with distortion-product otoacoustic emission (DPOAE) input/output (I/O) parameters at 1 and 6 kHz to test the hypothesis that these measures provide similar estimates of cochlear compression. Implicit in this hypothesis is the assumption that both DPOAE I/O and FM PF slopes are functionally related to basilar-membrane (BM) response growth. FM PF-slope decreased with signal level, but this effect was reduced or reversed with increasing hearing loss; there was a trend of decreasing psychometric function (PF) slope with increasing frequency, consistent with greater compression at higher frequencies. DPOAE I/O functions at 6 kHz exhibited an increase in the breakpoint of a two-segment slope as a function of hearing loss with a concomitant decrease in the level of the distortion product (L(d)). Results of the comparison between FM PF and DPOAE I/O parameters revealed only a weak correlation, suggesting that one or both of these measures may provide unreliable information about BM compression.

Basilar membrane velocity in a cochlea with a modified organ of Corti.

Many cochlear models assign zero longitudinal coupling in the cochlea. Although this is consistent with the transverse basilar membrane (BM) fibers, the cochlear partition contains cellular longitudinal coupling. In cochlear models, longitudinal coupling diminishes passive BM tuning; however, it has recently been employed in theories of active mechanics to enhance tuning. Our goal in this study was to probe passive longitudinal coupling by comparing BM responses in damaged cochleae with passive responses in normal cochleae. The cochleae of gerbils were damaged with intratympanic neomycin followed by a waiting period to ensure that all of the cells of the partition were missing or severely disrupted. We then measured BM motion and examined the cochleae histologically. In comparison with passive responses in normal cochleae, we observed a downward shift in characteristic frequency, an expected consequence of reduced stiffness from cellular damage. However, we did not observe enhanced passive tuning in the damaged cochleae, as would be expected if longitudinal coupling were substantially greater in the normal cochleae. Thus, we conclude that cell-based longitudinal coupling is not large enough to influence passive cochlear mechanics. This finding constrains theories of active mechanics.

The clinical value of extratympanic electrocochleography in the diagnosis of Ménière's disease.

OBJECTIVE: To evaluate the clinical conditions causing an elevation in the click-evoked summation potential (SP)/action potential (AP) amplitude ratio (SP/AP ratio), the cause of the SP enhancement in Ménière's disease (MD) and the diagnostic efficacy of electrocochleography (ECoG) were discussed. STUDY DESIGN: Retrospective case review. SETTING: An outpatient clinic of the Otolaryngology Department of Kochi Medical School. PATIENTS: ECoG testing was performed in 632 patients (727 ears) with vertigo/dizziness and/or deafness over a 10-year period (1995-2005). Among them, 334 patients had diagnoses of definite MD, including 95 cases of bilateral involvement. MAIN OUTCOME MEASURES: Audiological thresholds and SP/AP ratio. RESULTS: An enhanced SP was observed in 56.3% of patients with MD. The incidence of an enhanced SP was low in patients for whom the disease duration was 2 years or less and the frequency of attacks was once a year or less, but was significantly higher in cases where the disease duration was 2 years or longer and/or the frequency of attacks was several times a year (Games-Howell test, p < 0.05). The incidence of an enhanced SP was significantly elevated in cases with pure-tone average exceeding 31 dB (Kendall's rank correlation test, p < 0.001). However, the enhanced SP, once it appeared, did not always disappear in spite of hearing improvement. Hearing improvement induced by the glycerol test also produced no alteration in an SP/AP ratio, and there was no significant difference between the glycerol test results and the incidence of an enhanced SP (chi2 goodness-of-fit test). CONCLUSIONS: The longer the patients were symptomatic or the severer the ear symptoms, the more likely the ECoG was to be positive. The abnormally elevated SP, once it had appeared, persisted for long periods. Spontaneous and glycerol-induced hearing gains did not result in a decrease in SP/AP ratio. These clinical characteristics of ECoG seem to indicate that the enhanced SP in MD might be caused by the malfunction of hair cells, not by the displacement of the basilar membrane toward the scala tympani.