Soft Tissue Conduction Activates the Auditory Pathway in the Brain.

Soft tissue conduction is a mode of hearing which differs from air and bone conduction since the soft tissues of the body convey the audio-frequency vibrations to the ear. It is elicited by inducing soft tissue vibrations with an external vibrator applied to sites on the body or by intrinsic vibrations resulting from vocalization or the heartbeat. However, the same external vibrator applied to the skin sites also excites cutaneous mechanoreceptors, and attempts have been made to assist patients with hearing loss by audio-tactile substitution. The present study was conducted to assess the contribution of the auditory nerve and brainstem pathways to soft tissue conduction hearing. The study involved 20 normal hearing students, equipped with ear plugs to reduce the possibility of their response to air-conducted sounds produced by the external vibrator. Pure tone audiograms and speech reception (recognition) thresholds were determined in response to the delivery of the stimuli by a clinical bone vibrator applied to the cheek, neck and shoulder. Pure tone and speech recognition thresholds were obtained; the participants were able to repeat the words they heard by soft tissue conduction, confirming that the auditory pathways in the brain had been stimulated, with minimal involvement of the somatosensory pathways.

How Is the Cochlea Activated in Response to Soft Tissue Auditory Stimulation in the Occluded Ear?

Soft tissue conduction is an additional mode of auditory stimulation which can be initiated either by applying an external vibrator to skin sites not overlying skull bone such as the neck (so it is not bone conduction) or by intrinsic body vibrations resulting, for example, from the heartbeat and vocalization. The soft tissue vibrations thereby induced are conducted by the soft tissues to all parts of the body, including the walls of the external auditory canal. In order for soft tissue conduction to elicit hearing, the soft tissue vibrations which are induced must penetrate into the cochlea in order to excite the inner ear hair cells and auditory nerve fibers. This final stage can be achieved either by an osseous bone conduction mechanism, or, more likely, by the occlusion effect: the vibrations of the walls of the occluded canal induce air pressures in the canal which drive the tympanic membrane and middle ear ossicles and activate the inner ear, acting by means of a more air conduction-like mechanism. In fact, when the clinician applies his stethoscope to the body surface of his patient in order to detect heart sounds or pulmonary air flow, he is detecting soft tissue vibrations.

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.

Hearing at threshold intensities: by slow mechanical traveling waves or by fast cochlear fluid pressure waves.

The three modes of auditory stimulation (air, bone and soft tissue conduction) at threshold intensities are thought to share a common excitation mechanism: the stimuli induce passive displacements of the basilar membrane propagating from the base to the apex (slow mechanical traveling wave), which activate the outer hair cells, producing active displacements, which sum with the passive displacements. However, theoretical analyses and modeling of cochlear mechanics provide indications that the slow mechanical basilar membrane traveling wave may not be able to excite the cochlea at threshold intensities with the frequency discrimination observed. These analyses are complemented by several independent lines of research results supporting the notion that cochlear excitation at threshold may not involve a passive traveling wave, and the fast cochlear fluid pressures may directly activate the outer hair cells: opening of the sealed inner ear in patients undergoing cochlear implantation is not accompanied by threshold elevations to low frequency stimulation which would be expected to result from opening the cochlea, reducing cochlear impedance, altering hydrodynamics. The magnitude of the passive displacements at threshold is negligible. Isolated outer hair cells in fluid display tuned mechanical motility to fluid pressures which likely act on stretch sensitive ion channels in the walls of the cells. Vibrations delivered to soft tissue body sites elicit hearing. Thus, based on theoretical and experimental evidence, the common mechanism eliciting hearing during threshold stimulation by air, bone and soft tissue conduction may involve the fast-cochlear fluid pressures which directly activate the outer hair cells.

Implications from cochlear implant insertion for cochlear mechanics.

It is usually thought that the displacements of the two inner ear windows induced by sound stimuli lead to pressure differences across the basilar membrane and to a passive mechanical traveling wave progressing along the membrane. However, opening a hole in the sealed inner ear wall in experimental animals is surprisingly not accompanied by auditory threshold elevations. It has also been shown that even in patients undergoing cochlear implantation, elevation of threshold to low-frequency acoustic stimulation is often not seen accompanying the making of a hole in the wall of the cochlea for insertion of the implant. Such threshold elevations would be expected to result from opening the cochlea, reducing cochlear impedance, altering hydrodynamics. These considerations can be taken as additional evidence that it may not be the passive basilar membrane traveling wave which elicits hearing at low sound intensities, but rather factors connected with cochlear fluid pressures and fluid mechanics.

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.

Soft Tissue Conduction: Review, Mechanisms, and Implications.

Soft tissue conduction (STC) is a recently explored mode of auditory stimulation, complementing air (AC) and bone (BC) conduction stimulation. STC can be defined as the hearing induced when vibratory stimuli reach skin and soft tissue sites not directly overlying skull bone such as the head, neck, thorax, and body. Examples of STC include the delivery of vibrations to the skin of parts of the body by a clinical bone vibrator, hearing underwater sounds and free field air sounds, while AC hearing is attenuated by earplugs. The vibrations induced in the soft tissues are apparently transmitted along soft tissues, reaching, and exciting the ear. Further research is required to determine whether the mechanism of the final stage of STC hearing involves the excitation of the ear by eliciting inner ear fluid pressures that activate the hair cells directly, by the induction of skull bone vibrations, or by a combination of both mechanisms, depending on the magnitude of each mechanism.

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.

Fluid stimulation elicits hearing in the absence of air and bone conduction--An animal study.

Conclusion Cochlea can be directly excited by fluid (soft-tissue) stimulation. Objective To determine whether there is no difference in auditory-nerve-brainstem evoked response (ABR) thresholds to fluid stimulation between normal and animal models of post radical-mastoidectomy, as seen in a previous human study. Background It has been shown in humans that hearing can be elicited with stimulation to fluid in the external auditory meatus (EAM), and radical-mastoidectomy cavity. These groups differed in age, initial hearing, and drilling exposure. To overcome this difference, experiments were conducted in sand-rats, first intact, and after inducing a radical-mastoidectomy. Methods The EAM of five sand-rats was filled with 0.3 ml saline. ABR thresholds were determined in response to vibratory stimulation by a clinical bone-vibrator with a plastic rod, applied to the saline in the EAM. Then the tympanic membrane was removed, and malleus dislocated (radical-mastoidectomy model). The cavity was filled with 0.45 ml saline and the ABR threshold was determined in response to vibratory stimulation to the cavity fluid. Results There was no difference in ABR fluid thresholds to EAM and mastoidectomy cavity stimulation. Air-conduction stimulation from the bone-vibrator was not involved (conductive loss due to fluid). Bone-conduction stimulation was not involved (large difference in acoustic impedance between fluid and bone).

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.

Reflections on the role of a traveling wave along the basilar membrane in view of clinical and experimental findings.

Air conduction (AC) is accompanied by displacements of the two cochlear windows, bulk fluid flow between them, a pressure difference across the basilar membrane, leading to a passive traveling wave along the membrane, which activates the cochlear amplifier and enhances the displacements. AC interacts with bone conduction (BC) stimulation, so that it has been assumed that BC stimulation also involves a passive traveling wave. However, several clinical conditions and experimental manipulations provide evidence that a passive traveling wave may not be involved in BC stimulation at low intensities. Soft tissue conduction (STC) (also called non-osseous bone conduction) involves applying the bone vibrator to soft tissues on the head, neck and thorax, eliciting auditory sensation. STC stimulation probably does not involve a passive traveling wave. This review presents clinical conditions and experimental manipulations which assess the contributions of AC, BC and STC stimulation to the passive traveling wave. Evidence from the clinic (otosclerosis, round window atresia) and from the laboratory (holes in the wall of the inner ear, immobilization of the ossicular chain and the windows, discontinuity of the chain, measurement of basilar membrane displacements in the absence of the cochlear amplifier) lead to the conclusion that a passive basilar membrane traveling wave may not be involved in stimulation at low sound intensities. It is suggested that at low sound levels, the outer hair cell cochlear amplifier may not be activated by a passive traveling wave, but may be directly activated by the fast cochlear fluid pressures induced by AC, BC and STC stimulation. On the other hand, at high intensities, the cochlea is activated by the slow passive traveling wave.