Changes In Cochlear Mechanics Research Articles

Pilot Evaluation of Sheep as In Vivo Model for Cochlear Implantation.

The rise in the use of cochlear implants (CIs) has continued to fuel research aimed at improving surgical approaches and the preservation of residual hearing. Current in vivo models involve small animals not suitable for evaluating full-sized CIs nor are prohibitively expensive nonhuman primates. The objective of this study was to develop and evaluate an in vivo model of cochlear implantation in sheep. Eight adult, female sheep were implanted with full-sized CIs from three manufacturers using a retrofacial approach to the round window. Partial electrode insertions were performed to a depth of 10 to 12 mm before closure. Round window electrocochleography (ECoG) and auditory brainstem responses (ABR) were conducted during and after surgery. Following a 30-day implantation, cochleae were explanted and imaged using both x-ray microscopy and histology. The surgery was well tolerated although limited complications were observed in three of eight sheep. Electrode insertions were up to 12 mm before insertion resistance noted. ECoG and ABR responses were reduced postimplantation, reflecting changes in cochlear mechanics due to the presence of the implant, and/or insertion trauma. Histological and radiological image analysis showed the presence of intracochlear fibrosis as well as one instance of tip fold-over. The use of sheep presents a feasible live-animal model to study cochlear implantations. Full-sized implants as well as surgical techniques can be evaluated on functional outcomes such as ABR and ECoG as well as histological markers for residual hearing including intracochlear fibrosis. Use of this model and surgical approach has potential to evaluate CIs and surgical techniques in both the acute and chronic setting.

Tone-burst auditory brainstem response wave V latencies in normal-hearing and hearing-impaired ears.

The metric used to equate stimulus level [sound pressure level (SPL) or sensation level (SL)] between ears with normal hearing (NH) and ears with hearing loss (HL) in comparisons of auditory function can influence interpretation of results. When stimulus level is equated in dB SL, higher SPLs are presented to ears with HL due to their reduced sensitivity. As a result, it may be difficult to determine if differences between ears with NH and ears with HL are due to cochlear pathology or level-dependent changes in cochlear mechanics. To the extent that level-dependent changes in cochlear mechanics contribute to auditory brainstem response latencies, comparisons between normal and pathologic ears may depend on the stimulus levels at which comparisons are made. To test this hypothesis, wave V latencies were measured in 16 NH ears and 15 ears with mild-to-moderate HL. When stimulus levels were equated in SL, latencies were shorter in HL ears. However, latencies were similar for NH and HL ears when stimulus levels were equated in SPL. These observations demonstrate that the effect of stimulus level on wave V latency is large relative to the effect of HL, at least in cases of mild-to-moderate HL.

Perception of Across-Frequency Asynchrony by Listeners with Cochlear Hearing Loss

Cochlear hearing loss is often associated with broader tuning of the cochlear filters. Cochlear response latencies are dependent on the filter bandwidths, so hearing loss may affect the relationship between latencies across different characteristic frequencies. This prediction was tested by investigating the perception of synchrony between two tones exciting different regions of the cochlea in listeners with hearing loss. Subjective judgments of synchrony were compared with thresholds for asynchrony discrimination in a three-alternative forced-choice task. In contrast to earlier data from normal-hearing (NH) listeners, the synchronous-response functions obtained from the hearing-impaired (HI) listeners differed in patterns of symmetry and often had a very low peak (i.e., maximum proportion of "synchronous" responses). Also in contrast to data from NH listeners, the quantitative and qualitative correspondence between the data from the subjective and the forced-choice tasks was often poor. The results do not provide strong evidence for the influence of changes in cochlear mechanics on the perception of synchrony in HI listeners, and it remains possible that age, independent of hearing loss, plays an important role in temporal synchrony and asynchrony perception.

The Influence of a Cochlear Implant Electrode on the Mechanical Function of the Inner Ear

With the use of standard electrodes in cochlear implantation, residual acoustic hearing is markedly reduced or even lost. Possible reasons for this loss are direct implantation trauma to the inner ear, reaction of the cochlea triggered by the implantation, and change of cochlear mechanics due to the electrode. The introduction of a cochlear implant electrode does not alter the global mechanical behavior of the cochlear fluid as recorded at the stapes and the round window (RW) to the point of clinical relevance. 1) To assess RW motion in response to acoustic stimulation in live human subjects for the first time and to compare findings with the published data on similar measurements in human temporal bones; 2) to test the hypothesis by comparing intraoperative measurements of the stapes with the RW before and after cochlear implant. The study included 18 adult patients with profound bilateral hearing loss. A scanning laser Doppler interferometer system measuring through the facial recess and a calibrated multi-sinewave acoustic stimulation tone in the ear canal were used. Changes in cochlear mechanics were assessed by comparing intraoperative measurements of stapes with RW membrane responses to acoustic signals before and after cochlear implantation. Vibration amplitudes and phase at the stapes and RW were not different in our patient group from published results from temporal bones. No significant changes in amplitude and phase were seen at the stapes and RW after cochlear implantation. It was possible to assess RW motion in live human subjects. Our results provide evidence that even a standard electrode does not alter cochlear mechanics to the point of clinical relevance.

Contextual modulation of cochlear hearing desensitization depends on the type of loud sound trauma

In ears in which cochlear efferent pathways were cut and with testing done under anaesthetic conditions that preclude middle ear muscle activity (so as to examine the “intrinsic” effects of loud sound on the cochlea without any confounding effect of efferent pathways to the auditory periphery), atraumatic background white noise (WN) increases cochlear hearing loss (temporary threshold shifts, TTSs) induced by a traumatic pure tone but reduces TTSs caused by traumatic 5-kHz wide narrow band (NB) sound. The short-duration moderately intense traumata used in these studies most likely cause TTSs by affecting cochlear mechanics and these WN modulatory effects, exerted directly on the cochlea’s intrinsic susceptibility to TTSs, are not predicted by any current description of cochlear mechanics. Here it is demonstrated that background WN reduces trauma-induced TTSs with even a relatively small increase in trauma bandwidth beyond that of a pure tone, discounting the alternative that contextual modulatory effects transition systematically along a continuum as trauma bandwidth increases from a pure tone to a broader bandwidth (albeit 2 kHz-wide NB) trauma. These results have implications for cochlear mechanics as the TTSs due to the traumatic sound of this study are most likely due to changes in cochlear mechanics but are not easily explained by what is currently known of cochlear mechanics.

Transient evoked otoacoustic emissions after vestibular nerve section in chinchillas

Problem: The most well-known function of the medial efferent system is that of cochlear response inhibition, achieved through electric stimulation of the floor of the fourth ventricle. However, studies investigating the effects of lesion-related de-efferentation have obtained contradictory results. In fact, there is evidence that de-efferentation causes the relationship between transient evoked otoacoustic emissions and distortion product otoacoustic emissions to become unbalanced. To determine the role that the medial efferent system plays in outer hair cell function, transient evoked otoacoustic emissions were recorded before and after vestibular nerve section in chinchillas. Methods: Twenty-two adult male chinchillas, weighing between 500 and 750 g, were divided into 2 groups: (1) experimental group (n = 17), which underwent surgery for right vestibular nerve section; and (2) control group (n = 5), which underwent the same operation but without the right vestibular nerve section. Transient evoked otoacoustic emissions were recorded before and immediately after the surgery in both groups. Responses at frequencies of 0.8, 1.6, 2.4, 3.2, and 4.0 kHz, as well as total emission responses, were analyzed. Results: After the vestibular nerve section, there were significant increases in the amplitudes of the 2.4 and 4.0 kHz responses ( P = 0.004 and P = 0.047) and of the total response ( P = 0.0003). Conclusion: Transient evoked otoacoustic emissions were sensitive in detecting changes of the cochlear mechanics after vestibular nerve section in chinchillas. Significance: These results indicate that changes in cochlear mechanics directly affect transient evoked otoacoustic emissions. Therefore we support the hypothesis that the medial efferent system is involved in the control or modulation of outer hair cell activity. Support: None reported.

Loud sound-induced changes in cochlear mechanics.

To investigate the inner ear response to intense sound and the mechanisms behind temporary threshold shifts, anesthetized guinea pigs were exposed to tones at 100-112 dB SPL. Basilar membrane vibration was measured using laser velocimetry, and the cochlear microphonic potential, compound action potential of the auditory nerve, and local electric AC potentials in the organ of Corti were used as additional indicators of cochlear function. After exposure to a 12-kHz intense tone, basilar membrane vibrations in response to probe tones at the characteristic frequency of the recording location (17 kHz) were transiently reduced. This reduction recovered over the course of 50 ms in most cases. Organ of Corti AC potentials were also reduced and recovered with a time course similar to the basilar membrane. When using a probe tone at either 1 or 4 kHz, organ of Corti AC potentials were unaffected by loud sound, indicating that transducer channels remained intact. In most experiments, both the basilar membrane and the cochlear microphonic response to the 12-kHz overstimulation was constant throughout the duration of the intense stimulus, despite a large loss of cochlear sensitivity. It is concluded that the reduction of basilar membrane velocity that followed loud sound was caused by changes in cochlear amplification and that the cochlear response to intense stimulation is determined by the passive mechanical properties of the inner ear structures.

PPADS, an ATP antagonist, attenuates the effects of a moderately intense sound on cochlear mechanics

Increasing attention is being given to the role of neurotransmitters and other signaling substances in the damage induced by intense sound to the cochlea. Adenosine triphosphate (ATP) is one example of a putative neurotransmitter that may alter cochlear mechanics during sound exposure. The purpose of the present study was to test the hypothesis that endogenous extracellular ATP has a role in the generation of the changes in cochlear mechanics induced by moderate intense sound exposure. Guinea pigs were exposed to either: (1) a perilymphatic administration of pyridoxal-phosphate-6-azophenyl-2′,4′-disulphonic acid (PPADS, 1 mM), an ATP antagonist; (2) a moderately intense sound (6 kHz tone, 95 dB SPL, 15 min); or (3) a combination of the PPADS and the sound. The effects on the cubic distortion product otoacoustic emissions (DPOAEs; 2 f 1− f 2) were monitored using three sets of equal level primaries ( f 1=9.25 kHz, f 2=10.8 kHz, 2 f 1− f 2=7.7 kHz; f 1=7.2 kHz, f 2=8.4 kHz, 2 f 1− f 2=6 kHz; f 1=5.55 kHz, f 2=6.5 kHz, 2 f 1− f 2=4.6 kHz). PPADS alone had no effect on the cubic DPOAEs monitored. The intense sound alone suppressed all three cubic DPOAEs. The combination of PPADS with the intense sound induced a suppression of the cubic DPOAEs that was equal to or greater than induced by the intense sound alone at f 2=10.8 kHz but was equal to or less than induced by the intense sound at f 2=8.4 and 6.5 kHz. After washing the PPADS out of the cochlea with artificial perilymph, all three cubic DPOAEs were suppressed less in the PPADS with intense sound treatment group than in the intense sound alone group. The PPADS appeared to provide protection from the intense sound. Results are consistent with the hypothesis that extracellular ATP is involved in the changes in cochlear mechanics induced by moderately intense sound exposure.

Changes in cochlear mechanics during vocalization: evidence for a phasic medial efferent effect

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.

The influence of evoking stimulus level on the neural suppression of transient evoked otoacoustic emissions

This study concerns the suppression of transient evoked otoacoustic emissions (TEOAEs) by contralateral noise. The suppression is interpreted as neurally induced changes in cochlear mechanics. The magnitude of TEOAE suppression is explored in response to a single level of contralateral noise, in 20 normal subjects, and as a function of TEOAE evoking stimulus power in 6 subjects. TEOAE were found to be relatively more susceptible to contralateral suppression when the TEOAE evoking stimulus was low. This suggests that saturation of the TEOAE generator by the evoking stimulus reduces the susceptibility of the generator to neural suppression. However, this relation did not hold between ears. Those ears in which the TEOAE seemed easier to saturate were easier to suppress by contralateral noise. We have concluded that TEOAE generators can differ in their susceptibility to neural suppression. Ears in which the TEOAE generating mechanism is less dependant on the ipsilateral evoking stimuli power level, are also naturally more susceptible to efferent suppression.

Evoked Ofoacoustic Emissions in Normal Hearing Infants and Children

Evoked otoacoustic emissions (EOAEs) are a promising tool for evaluating cochlear status in children. Preliminary data from normal-hearing subjects ranging from birth to 29.9 years old are discussed. EOAEs are present and robust in infant ears. However, there is a statistically significant decrease in EOAE amplitude for a fixed stimulus level with increasing age even in a carefully screened sample. At the present time it is unclear if these age-associated changes are due to normal developmental changes in the external and/or middle ear acoustics, normal developmental changes in cochlear mechanics and/or everyday cochlear wear and tear. Issues related to further application of evoked emissions to pediatric populations are discussed.

Short-term effects of sound exposure on the 2f1-f2 acoustic emission.

The 2f1-f2 acoustic emission (AE) was recorded in the ear canals of cats following exposure to tone bursts of 200-ms duration. Exposures known to result in short-term adaptation (i.e., adaptation lasting under 1 s) at the level of the auditory nerve failed to produce significant post-exposure changes in AE amplitude. Given the apparent cochlear origin of the 2f1-f2 AE, this result is consistent with the view that short-term adaptation in the auditory periphery does not involve substantial changes in cochlear mechanics.

Adaptation of the acoustically emitted 2f1−f2 combination tone

Recent studies suggest that the 2f1−f2 ear‐canal distortion product is produced by nonlinearities in the motion of the cochlear partition. Given its cochlear origin, we attempted to use the acoustically emitted combination tone (ACT) to indirectly examine changes in cochlear mechanics that may be associated with long‐term adaptation (i.e., adaptation lasting several seconds) of eighth‐nerve responses. We examined the effects of 1‐min tonal exposures the amplitude of the 2f1−f2 ACT in the ear canals of cats. These effects were compared with post‐exposure changes in the whole‐nerve action potential (AP) responses to tone bursts that resulted from similar exposures. Both the distortion product and N1 amplitudes were reduced for several seconds following exposure. The reduction in ACT amplitude suggests that 1‐min exposures can alter cochlear mechanics. The fact that the same exposure tones cause reductions in N1 amplitude further suggests that neurally measured long‐term adaptation is linked to changes in th...

Intense sounds may alter the mechanical properties of the cochlear partition

Morphological and structural changes have been observed in various cochlear elements following exposure to intense sounds. Whether these changes are sufficient to locally alter the mechanical properties of the cochlear partition is unknown. Here a psychophysical test for mechanical changes in the partition is developed and applied. Monaural exposures to an intense 1700-Hz tone were preceded and followed by a binaural task in which the subject adjusted the interaural time difference of a 250-Hz tone in order to perceive it as centered inside his head. If the local gradients of mass, stiffness, and/or coupling were altered by the exposure, then the post-exposure settings should contain a time lead toward one ear or the other, depending upon the direction of the mechanical changes. Following exposure to an intense tone, the maximum temporary threshold shift (TTS) is often displaced upward in frequency from the exposure stimulus--an effect widely known as the half-octave shift in TTS. Time leads toward the nonexposed ear in the post-exposure centering task would be in accord with a mechanical-change explanation of the half-octave shift. Settings in this direction were observed with the most intense and longest durations of exposure used, but with less intense or shorter exposures, the post-exposure settings were initially toward the exposed ear. Thus, the psychophysical evidence reported here supports the idea that exposure to intense sounds does produce temporary, local changes in cochlear mechanics, but it fails to provide a simple confirmation of the possibility that these mechanical changes underlie the half-octave shift in TTS.