Is COVID-19 to Blame for Sensorineural Hearing Deterioration? A Pre/Post COVID-19 Hearing Evaluation Study.

OBJECTIVES: Here, we aimed to (a) determine whether a clinically significant sensorineural hearing loss (SNHL) change could be detected in post-coronavirus disease (COVID-19) hearing levels on comparing them with pre-infection hearing levels after controlling for the effect of age and (b) to identify risk factors, such as hypertension, diabetes, and smoking, which increase the likelihood of hearing loss in COVID-19 patients. METHODS: We retrospectively analyzed hearing thresholds in unvaccinated patient's pre- and post-COVID-19 infection. Thresholds were controlled for age and the duration between the pre- and post-COVID-19 hearing evaluations. Correlations between additional COVID-19-related symptoms, hypertension, diabetes, and smoking and hearing threshold changes were analyzed. RESULTS: A significant (but not clinical) threshold elevation was found post-COVID-19 infection. However, on controlling for age and the duration between the pre- and post-COVID-19 hearing evaluations, no significant threshold elevation was found. No significant correlation was found between hearing threshold changes and additional COVID-19-related symptoms, hypertension, diabetes, or smoking. CONCLUSION: COVID-19 did not lead to a significant hearing threshold elevation in our cohort, even among patients with additional COVID-19 symptoms, hypertension, or diabetes mellitus or among those who smoked. LEVEL OF EVIDENCE: 3: nonrandomized controlled cohort, follow-up study Laryngoscope, 133:1976-1981, 2023.

Auditory Performance in Recovered SARS-COV-2 Patients.

OBJECTIVE: While COVID-19 symptoms impact rhinology (anosmia) and laryngology (airways), two major disciplines of the otolaryngology armamentarium, the virus has seemed to spare the auditory system. A recent study, however, reported changes in otoacoustic emission (OAE) signals measured in SARS-COV-2 positive patients. We sought to assess the effect of COVID-19 infection on auditory performance in a cohort of recovered SARS-COV-2 patients and controls. To avoid a potential bias of previous audiological dysfunction not related to SARS-COV-2 infection, the study encompasses patients with normal auditory history. We hypothesized that if SARS-COV-2 infection predisposes to hearing loss, we would observe subtle and early audiometric deficits in our cohort in the form of subclinical auditory changes. STUDY DESIGN: Cross-sectional study. SETTING: Tertiary referral center. PATIENTS: The Institutional Review Board approved the study and we recruited participants who had been positive for SARS-COV-2 infection, according to an Reverse Transcription Polymerase Chain Reaction (RT-PCR) test on two nasopharyngeal swabs. The patients included in this study were asymptomatic for the SARS-COV-2 infection and were evaluated following recovery, confirmed by repeated swab testing. The control group comprised healthy individuals matched for age and sex, and with a normal auditory and otologic history. INTERVENTIONS: The eligibility to participate in this study included a normal audiogram, no previous auditory symptoms, normal otoscopy examination with an intact tympanic membrane, and bilateral tympanometry type A. None of our volunteers reported any new auditory symptoms following SARS-COV-2 infection. Ototacoustic emissions (OAE) and auditory brainstem response (ABR) measurements were used to evaluate the auditory function. MAIN OUTCOME MEASURES: OAE and ABR measurements. RESULTS: We have found no significant differences between recovered asymptomatic SARS-COV-2 patients and controls in any of transitory evoked otoacoustic emission (TEOAE), distortion product otoacoustic emissions (DPOAE), or ABR responses. CONCLUSIONS: There is no cochlear dysfunction represented by ABR, TEOAE, and DPOAE responses in recovered COVID-19 asymptomatic patients. Retrocochlear function was also preserved as evident by the ABR responses. A long-term evaluation of a larger cohort of SARS-COV-2 patients will help to identify a possible contribution of SARS-COV-2 infection to recently published anecdotal auditory symptoms associated with COVID-19.

The Effect of Soft Tissue Stimulation on Skull Vibrations and Hearing Thresholds in Humans.

HYPOTHESIS: Hearing via soft tissue stimulation involves an osseous pathway. BACKGROUND: A recent study that measured both hearing thresholds and skull vibrations found that vibratory stimulation of soft tissue led to hearing sensation that correlated with skull vibrations, supporting the hypothesis of an osseous pathway. It is possible, however, that a lower application force of the vibrator on the stimulated soft tissue would not be sufficient to elicit skull vibration suggesting hearing via a nonosseous pathway. The purpose of the present study was to confirm the osseous pathway by measuring skull vibrations and behavioral thresholds using a low application force on a layer of ultrasound gel. Gel was used to mimic soft tissue because of its similar acoustic impedance and to control for variability between participants. METHODS: Hearing thresholds and the skull vibrations of five patients who were implanted with bone-anchored implants were assessed in two conditions when the bone vibrator was applied on the forehead: 1) direct application with 5N force; 2) through a layer of ultrasound gel with minimal application force. Skull vibrations were measured in both conditions by a laser Doppler vibrometer focused on the bone-anchored implant. RESULTS: Skull vibrations were present even when minimal application force was applied on soft tissue. The difference in skull vibrations when the vibrator was directly on the forehead compared with the gel condition was consistent with the variability in hearing thresholds between the two conditions. CONCLUSION: These results reinforce the hypothesis that skull vibrations are involved in hearing when sound is transmitted via either soft tissue or bone.

Occlusion Effect in Response to Stimulation by Soft Tissue Conduction-Implications.

To gain insight into the broader implications of the occlusion effect (OE-difference between unoccluded and occluded external canal thresholds), the OE in response to pure tones at 0.5, 1.0, 2.0 and 4.0 kHz to two bone conduction sites (mastoid and forehead) and two soft tissue conduction (STC) sites (under the chin and at the neck) were assessed. The OE was present at the soft tissue sites and at the bone conduction sites, with no statistical difference between them. The OE was significantly greater at lower frequencies, and negligible at higher frequencies. It seems that the vibrations induced in the soft tissues (STC) during stimulation at the soft tissue sites are conducted not only to the inner ear and elicit hearing, but also reach the walls of the external canal and initiate air pressures in the occluded canal which drive the tympanic membrane and excite the inner ear, leading to hearing. Use of a stethoscope by the internist to hear intrinsic body sounds (heartbeat, blood flow) serves as a clear demonstration of STC and its relation to hearing.

Audiogram in Response to Stimulation Delivered to Fluid Applied to the External Meatus.

BACKGROUND AND OBJECTIVES: Hearing can be elicited in response to vibratory stimuli delivered to fluid in the external auditory meatus. To obtain a complete audiogram in subjects with normal hearing in response to pure tone vibratory stimuli delivered to fluid applied to the external meatus. Subjects and. METHODS: Pure tone vibratory stimuli in the audiometric range from 0.25 to 6.0 kHz were delivered to fluid applied to the external meatus of eight participants with normal hearing (15 dB or better) using a rod attached to a standard clinical bone vibrator. The fluid thresholds obtained were compared to the air conduction (AC), bone conduction (BC; mastoid), and soft tissue conduction (STC; neck) thresholds in the same subjects. RESULTS: Fluid stimulation thresholds were obtained at every frequency in each subject. The fluid and STC (neck) audiograms sloped down at higher frequencies, while the AC and BC audiograms were flat. It is likely that the fluid stimulation audiograms did not involve AC mechanisms or even, possibly, osseous BC mechanisms. CONCLUSIONS: The thresholds elicited in response to the fluid in the meatus likely reflect a form of STC and may result from excitation of the inner ear by the vibrations induced in the fluid. The sloping fluid audiograms may reflect transmission pathways that are less effective at higher frequencies.

Implications for Bone Conduction Mechanisms from Thresholds of Post Radical Mastoidectomy and Subtotal Petrosectomy Patients.

OBJECTIVES: To assess bone conduction (BC) thresholds following radical mastoidectomy and subtotal petrosectomy, in which the tympanic membrane and the ossicular chain, responsible for osseous BC mechanisms, are surgically removed. The removal of the tympanic membrane and the ossicular chain would reduce the contributions to BC threshold of the following four osseous BC mechanisms: the occlusion effect of the external ear, middle ear ossicular chain inertia, inner ear fluid inertia, and distortion (compression-expansion) of the walls of the inner ear. MATERIALS AND METHODS: BC thresholds were determined in 64 patients who underwent radical mastoidectomy and in 248 patients who underwent subtotal petrosectomy. RESULTS: BC thresholds were normal (≤15 dB HL, i.e., better) in 19 (30%) radical mastoidectomy patients and in 19 (8%) subtotal petrosectomy patients at each of the frequencies assessed (0.5, 1.0, 2.0, and 4.0 kHz). CONCLUSION: Normal BC thresholds seen in many patients following mastoidectomy and petrosectomy may be induced by a non-osseous mechanism, and the onset ("threshold") of the classical osseous BC mechanisms may be somewhat higher.

Does hearing in response to soft-tissue stimulation involve skull vibrations? A within-subject comparison between skull vibration magnitudes and hearing thresholds.

Hearing can be elicited in response to bone as well as soft-tissue stimulation. However, the underlying mechanism of soft-tissue stimulation is under debate. It has been hypothesized that if skull vibrations were the underlying mechanism of hearing in response to soft-tissue stimulation, then skull vibrations would be associated with hearing thresholds. However, if skull vibrations were not associated with hearing thresholds, an alternative mechanism is involved. In the present study, both skull vibrations and hearing thresholds were assessed in the same participants in response to bone (mastoid) and soft-tissue (neck) stimulation. The experimental group included five hearing-impaired adults in whom a bone-anchored hearing aid was implanted due to conductive or mixed hearing loss. Because the implant is exposed above the skin and has become an integral part of the temporal bone, vibration of the implant represented skull vibrations. To ensure that middle-ear pathologies of the experimental group did not affect overall results, hearing thresholds were also obtained in 10 participants with normal hearing in response to stimulation at the same sites. We found that the magnitude of the bone vibrations initiated by the stimulation at the two sites (neck and mastoid) detected by the laser Doppler vibrometer on the bone-anchored implant were linearly related to stimulus intensity. It was therefore possible to extrapolate the vibration magnitudes at low-intensity stimulation, where poor signal-to-noise ratio limited actual recordings. It was found that the vibration magnitude differences (between soft-tissue and bone stimulation) were not different than the hearing threshold differences at the tested frequencies. Results of the present study suggest that bone vibration magnitude differences can adequately explain hearing threshold differences and are likely to be responsible for the hearing sensation. Thus, the present results support the idea that bone and soft-tissue conduction could share the same underlying mechanism, namely the induction of bone vibrations. Studies with the present methodology should be continued in future work in order to obtain further insight into the underlying mechanism of activation of the hearing system.

Inner Ear Excitation in Normal and Postmastoidectomy Participants by Fluid Stimulation in the Absence of Air- and Bone-Conduction Mechanisms.

BACKGROUND: Hearing can be induced not only by airborne sounds (air conduction [AC]) and by the induction of skull vibrations by a bone vibrator (osseous bone conduction [BC]), but also by inducing vibrations of the soft tissues of the head, neck, and thorax. This hearing mode is called soft tissue conduction (STC) or nonosseous BC. PURPOSE: This study was designed to gain insight into the mechanism of STC auditory stimulation. RESEARCH DESIGN: Fluid was applied to the external auditory canal in normal participants and to the mastoidectomy common cavity in post-radical mastoidectomy patients. A rod coupled to a clinical bone vibrator, immersed in the fluid, delivered auditory frequency vibratory stimuli to the fluid. The stimulating rod was in contact with the fluid only. Thresholds were assessed in response to the fluid stimulation. STUDY SAMPLE: Eight ears in eight normal participants and eight ears in seven post-radical mastoidectomy patients were studied. DATA COLLECTION AND ANALYSIS: Thresholds to AC, BC, and fluid stimulation were assessed. The postmastoidectomy patients were older than the normal participants, with underlying sensorineural hearing loss (SNHL). Therefore, the thresholds to the fluid stimulation in each participant were corrected by subtracting his BC threshold, which expresses any underlying SNHL. RESULTS: Hearing thresholds were obtained in each participant, in both groups in response to the fluid stimulation at 1.0 and 2.0 kHz. The fluid thresholds, corrected by subtracting the BC thresholds, did not differ between the groups at 1.0 kHz. However, at 2.0 kHz the corrected fluid thresholds in the mastoidectomy patients were 10 dB lower (better) than in the normal participants. CONCLUSIONS: Since the corrected fluid thresholds at 1.0 kHz did not differ between the groups, the response to fluid stimulation in the normal participants at least at 1.0 kHz was probably not due to vibrations of the tympanic membrane and of the ossicular chain induced by the fluid stimulation, since these structures were absent in the mastoidectomy patients. In addition, the fluid in the external canal (normal participants) and the absence of the tympanic membrane and the ossicular chain (mastoidectomy patients) induced a conductive hearing loss (threshold elevation to air-conducted sounds coming from the bone vibrator), so that AC mechanisms were probably not involved in the thresholds to the fluid stimulation. In addition, as a result of the acoustic impedance mismatch between the fluid and skull bone, the audio-frequency vibrations induced in the fluid at threshold would probably not lead to vibrations of the bony wall of the meatus, so that hearing by osseous BC is not likely. Therefore, it seems that the thresholds to the fluid stimulation, in the absence of AC and of osseous BC, represent an example of STC, which is an additional mode of auditory stimulation in which the cochlea is activated by fluid pressures transmitted along a series of soft tissues, reaching and exciting the inner ear directly. STC can explain the mechanism of several auditory phenomena.

Soft tissue conduction as a possible contributor to the limited attenuation provided by hearing protection devices.

CONTEXT: Damage to the auditory system by loud sounds can be avoided by hearing protection devices (HPDs) such as earmuffs, earplugs, or both for maximum attenuation. However, the attenuation can be limited by air conduction (AC) leakage around the earplugs and earmuffs by the occlusion effect (OE) and by skull vibrations initiating bone conduction (BC). AIMS: To assess maximum attenuation by HPDs and possible flanking pathways to the inner ear. SUBJECTS AND METHODS: AC attenuation and resulting thresholds were assessed using the real ear attenuation at threshold (REAT) procedure on 15 normal-hearing participants in four free-field conditions: (a) unprotected ears, (b) ears covered with earmuffs, (c) ears blocked with deeply inserted customized earplugs, and (d) ears blocked with both earplugs and earmuffs. BC thresholds were assessed with and without earplugs to assess the OE. RESULTS: Addition of earmuffs to earplugs did not cause significantly greater attenuation than earplugs alone, confirming minimal AC leakage through the external meatus and the absence of the OE. Maximum REATs ranged between 40 and 46 dB, leading to thresholds of 46-54 dB HL. Furthermore, calculation of the acoustic impedance mismatch between air and bone predicted at least 60 dB attenuation of BC. CONCLUSION: Results do not support the notion that skull vibrations (BC) contributed to the limited attenuation provided by traditional HPDs. An alternative explanation, supported by experimental evidence, suggests transmission of sound to inner ear via non-osseous pathways such as skin, soft tissues, and fluid. Because the acoustic impedance mismatch between air and soft tissues is smaller than that between air and bone, air-borne sounds would be transmitted to soft tissues more effectively than to bone, and therefore less attenuation is expected through soft tissue sound conduction. This can contribute to the limited attenuation provided by traditional HPDs. The present study has practical implications for hearing conservation protocols.

Bone Conduction Thresholds without Bone Vibrator Application Force.

BACKGROUND: Osseous bone conduction (BC) stimulation involves applying the clinical bone vibrator with an application force of about 5 Newton (N) to the skin over the cranial vault of skull bone (e.g., mastoid, forehead). In nonosseous BC (also called soft tissue conduction), the bone vibrator elicits hearing when it is applied to skin sites not over the cranial vault of skull bone, such as the neck. PURPOSE: To gain insight into the mechanisms of osseous and nonosseous BC. RESEARCH DESIGN: In general, thresholds were determined with the bone vibrator applied with about 5 N force directly to osseous sites (mastoid, forehead) on the head of the participants, as classically conducted in the clinic, and again without direct physical contact (i.e., 0 N force) achieved by coupling the bone vibrator to gel as in ultrasound diagnostic imaging, on the same or nearby skin sites (nonosseous BC). The participants were equipped with earplugs to minimize air-conducted stimulation. STUDY SAMPLE: In the first experiment, 10 normal-hearing participants were tested with stimulation (5 and 0 N) at the forehead; in the second experiment, 10 additional normal-hearing participants were tested with stimulation at the mastoid (about 5 N) and at the nearby tragus and cavum concha of the external ear (0 N). RESULTS: The mean thresholds with 0 N were much better than might be expected from classical theories in response to stimulation by a bone vibrator, in the absence of any application force. The differences between the mean thresholds with the 0 N and the 5 N forces depended on condition, site, and stimulus frequency of the comparisons. The difference was 1.5 dB at 1.0 kHz on the forehead; ranged between 10 and 12.5 dB at 1.0 kHz on the cavum and tragus (versus on the mastoid) and at 2.0 and 4.0 kHz on the forehead; 17 and 19 dB at 2.0 kHz on the cavum and tragus (versus on the mastoid); reaching 32 dB only in a single condition (forehead at 0.5 kHz). CONCLUSIONS: As it is unlikely that threshold intensity stimulation delivered with 0 N application force could have induced vibrations of the underlying or nearby bone, inducing osseous BC, the relatively low thresholds in the absence of any application force, together with the small differences between the thresholds with 0 N (gel/soft tissue, nonosseous) and 5 N force (osseous BC) lead to the suggestion that in most situations, the BC thresholds actually represent the nonosseous (soft tissue conduction) thresholds at the stimulation site.

Relation between Body Structure and Hearing during Soft Tissue Auditory Stimulation.

Hearing is elicited by applying the clinical bone vibrator to soft tissue sites on the head, neck, and thorax. Two mapping experiments were conducted in normal hearing subjects differing in body build: determination of the lowest soft tissue stimulation site at which a 60 dB SL tone at 2.0 kHz was effective in eliciting auditory sensation and assessment of actual thresholds along the midline of the head, neck, and back. In males, a lower site for hearing on the back was strongly correlated with a leaner body build. A correlation was not found in females. In both groups, thresholds on the head were lower, and they were higher on the back, with a transition along the neck. This relation between the soft tissue stimulation site and hearing sensation is likely due to the different distribution of soft tissues in various parts of the body.

Air conduction, bone conduction, and soft tissue conduction audiograms in normal hearing and simulated hearing losses.

BACKGROUND: In order to differentiate between a conductive hearing loss (CHL) and a sensorineural hearing loss (SNHL) in the hearing-impaired individual, we compared thresholds to air conduction (AC) and bone conduction (BC) auditory stimulation. The presence of a gap between these thresholds (an air-bone gap) is taken as a sign of a CHL, whereas similar threshold elevations reflect an SNHL. This is based on the assumption that BC stimulation directly excites the inner ear, bypassing the middle ear. However, several of the classic mechanisms of BC stimulation such as ossicular chain inertia and the occlusion effect involve middle ear structures. An additional mode of auditory stimulation, called soft tissue conduction (STC; also called nonosseous BC) has been demonstrated, in which the clinical bone vibrator elicits hearing when it is applied to soft tissue sites on the head, neck, and thorax. PURPOSE: The purpose of this study was to assess the relative contributions of threshold determinations to stimulation by STC, in addition to AC and osseous BC, to the differential diagnosis between a CHL and an SNHL. RESEARCH DESIGN: Baseline auditory thresholds were determined in normal participants to AC (supra-aural earphones), BC (B71 bone vibrator at the mastoid, with 5 N application force), and STC (B71 bone vibrator) to the submental area and to the submandibular triangle with 5 N application force) stimulation in response to 0.5, 1.0, 2.0, and 4.0 kHz tones. A CHL was then simulated in the participants by means of an ear plug. Separately, an SNHL was simulated in these participants with 30 dB effective masking. STUDY SAMPLE: STUDY SAMPLE consisted of 10 normal-hearing participants (4 males; 6 females, aged 20-30 yr). DATA COLLECTION AND ANALYSIS: AC, BC, and STC thresholds were determined in the initial normal state and in the presence of each of the simulations. RESULTS: The earplug-induced CHL simulation led to a mean AC threshold elevation of 21-37 dB (depending on frequency), but not of BC and STC thresholds. The masking-induced SNHL led to a mean elevation of AC, BC, and STC thresholds (23-36 dB, depending on frequency). In each type of simulation, the BC threshold shift was similar to that of the STC threshold shift. CONCLUSIONS: These results, which show a similar threshold shift for STC and for BC as a result of these simulations, together with additional clinical and laboratory findings, provide evidence that BC thresholds likely represent the threshold of the nonosseous BC (STC) component of multicomponent BC at the BC stimulation site, and thereby succeed in clinical practice to contribute to the differential diagnosis. This also provides evidence that STC (nonosseous BC) stimulation at low intensities probably does not involve components of the middle ear, represents true cochlear function, and therefore can also contribute to a differential diagnosis (e.g., in situations where the clinical bone vibrator cannot be applied to the mastoid or forehead with a 5 N force, such as in severe skull fracture).

Experimental Analysis of the Mechanism of Hearing under Water.

The mechanism of human hearing under water is debated. Some suggest it is by air conduction (AC), others by bone conduction (BC), and others by a combination of AC and BC. A clinical bone vibrator applied to soft tissue sites on the head, neck, and thorax also elicits hearing by a mechanism called soft tissue conduction (STC) or nonosseous BC. The present study was designed to test whether underwater hearing at low intensities is by AC or by osseous BC based on bone vibrations or by nonosseous BC (STC). Thresholds of normal hearing participants to bone vibrator stimulation with their forehead in air were recorded and again when forehead and bone vibrator were under water. A vibrometer detected vibrations of a dry human skull in all similar conditions (in air and under water) but not when water was the intermediary between the sound source and the skull forehead. Therefore, the intensities required to induce vibrations of the dry skull in water were significantly higher than the underwater hearing thresholds of the participants, under conditions when hearing by AC and osseous BC is not likely. The results support the hypothesis that hearing under water at low sound intensities may be attributed to nonosseous BC (STC).

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.

Investigation of the mechanism of soft tissue conduction explains several perplexing auditory phenomena.

Soft tissue conduction (STC) is a recently expounded mode of auditory stimulation in which the clinical bone vibrator delivers auditory frequency vibratory stimuli to skin sites on the head, neck, and thorax. Investigation of the mechanism of STC stimulation has served as a platform for the elucidation of the mechanics of cochlear activation, in general, and to a better understanding of several perplexing auditory phenomena. This review demonstrates that it is likely that the cochlear hair cells can be directly activated at low sound intensities by the fluid pressures initiated in the cochlea; that the fetus in utero, completely enveloped in amniotic fluid, hears by STC; that a speaker hears his/her own voice by air conduction and by STC; and that pulsatile tinnitus is likely due to pulsatile turbulent blood flow producing fluid pressures that reach the cochlea through the soft tissues.

The mechanism of direct stimulation of the cochlea by vibrating the round window.

BACKGROUND: Active middle ear implants such as the vibrant sound bridge (VSB) have been placed on the round window (RW) in patients with conductive or mixed hearing loss, with satisfactory hearing results. Several observations show that the mechanism of RW stimulation is not completely understood. The purpose of the present study was to compare different coupling procedures between the transducer and the RW in order to contribute to an understanding of the mechanism of RW stimulation. METHODS: Five fat sand rats underwent ablation of the left ear and opening of the right bulla, followed by baseline measurements of thresholds of auditory nerve brainstem evoked responses (ABR) to air and bone conduction click stimuli. Subsequently the malleus and incus were removed from the right middle ear, modeling a conductive hearing loss in which the VSB on the RW is indicated. In the next stage of the experiment, a rod attached to the bone vibrator was placed gently on the RW membrane and then on saline fluid applied to the RW niche. ABR thresholds were recorded following both placements. RESULTS: Mean baseline ABR threshold in response to air conduction stimuli was 48 ± 4 dB; mean ABR threshold when the rod was placed on the dry RW membrane was 99 ± 12 dB; mean ABR threshold when the rod was in the saline on RW niche was 79 ± 7 dB. CONCLUSIONS: ABR thresholds were better (lower) with stimulation of fluid on the RW membrane compared to direct stimulation of the RW, providing further evidence of a direct fluid pathway.

Assessment of inner ear bone vibrations during auditory stimulation by bone conduction and by soft tissue conduction.

BACKGROUND: Soft tissue conduction (STC), a recently described mode of auditory stimulation elicited when the clinical bone vibrator is applied to skin sites over the head, neck, and thorax, complements air conduction (AC) and bone conduction (BC), elicited by the same vibrator. The study assessed skull bone vibrations induced during STC and BC stimulation. METHODS: The experiments were conducted on fat sand rats. Thresholds of auditory nerve brainstem evoked responses (ABRs) were recorded and compared to the lowest-intensity sound stimuli that elicited vibrations at the bony vestibule of the inner ear detected by a laser Doppler vibrometer. RESULTS: Vibrations were detected during BC but not during STC stimulation. ABR was recorded to both STC and to BC stimulation. CONCLUSIONS: Low-intensity STC stimulation does not induce vibrations of the inner ear, showing that STC apparently does not involve mechanisms based on vibrations of bone.

Mutual cancellation between tones presented by air conduction, by bone conduction and by non-osseous (soft tissue) bone conduction.

Auditory sensation can be elicited not only by air conducted (AC) sound or bone conducted (BC) sound, but also by stimulation of soft tissue (STC) sites on the head and neck relatively distant from deeply underlying bone. Tone stimulation by paired combinations of AC with BC (mastoid) and/or with soft tissue conduction produce the same pitch sensation, mutual masking and beats. The present study was designed to determine whether they can also cancel each other. The study was conducted on ten normal hearing subjects. Tones at 2 kHz were presented in paired combinations by AC (insert earphone), by BC (bone vibrator) at the mastoid, and by the same bone vibrator to several STC sites; e.g. the neck, the sterno-cleido-mastoid muscle, the eye, and under the chin, shifting the phases between the pairs. Subjects reported changes in loudness and cancellation. The phase for cancellation differed across subjects. Neck muscle manipulations (changes in head position) led to alterations in the phase at which cancellation was reported. Cancellation was also achieved between pairs of tones to two STC sites. The differing phases for cancellation across subjects and the change in phase accompanying different head positions may be due to the different acoustic impedances of the several tissues in the head and neck. A major component of auditory stimulation by STC may not induce actual skull bone vibrations and may not involve bulk fluid volume displacements.

Experimental confirmation that vibrations at soft tissue conduction sites induce hearing by way of a new mode of auditory stimulation.

BACKGROUND: A new mode of auditory stimulation has been demonstrated which is through soft tissue conduction (STC). It involves evoking auditory sensations by applying the clinical bone vibrator to the skin over soft tissue (not over bone) sites on the head and neck. METHODS: This study was designed to show that stimulation by STC excites the cochlea in a way similar to that of air conduction (AC) and bone conduction (BC). RESULTS: It is shown here that auditory nerve brainstem evoked response (ABR) thresholds in mice and in the fat sand rat to AC, to BC and to STC stimulation are all elevated following administration of drugs (salicylic acid and furosemide) which depress the cochlear amplifier. In addition, the present study brings evidence that STC stimulation is not a variant of BC since the sound pressures recorded in the occluded external auditory canal (the occlusion effect) in response to STC are significantly smaller than that to BC stimulation, though both are of equal loudness. CONCLUSIONS: This new mode, STC, therefore appears to bypass the middle ear mechanisms and consequently may contribute to auditory diagnosis.