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.

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).

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.

Effect on auditory threshold of air and water pockets bordering the pathway between soft tissue stimulation sites and the cochlea.

OBJECTIVES: Auditory sensation can be elicited by applying a bone conduction vibrator to skin sites on the head, neck, and thorax over soft tissues. This is called soft tissue conduction (STC). We hypothesized that introducing substances with acoustic impedances that sharply deviate from those of soft tissues, such as air pockets, into the soft tissues beneath soft tissue stimulation sites would have an effect on the auditory threshold to stimulation at skin sites over soft tissue. METHODS: In human subjects, we assessed the auditory threshold with a bone vibrator applied to several STC sites, especially the cheek, and to several bone conduction sites on the skull. The subjects were equipped with bilateral earplugs. The subject then filled his or her cheek with either air or water, and the auditory threshold was again determined. We also recorded the auditory brain stem response to STC stimulation under the chin in fat sand rats in the absence and presence of subcutaneous air or saline solution pockets (0.4 mL) under the chin. RESULTS: In humans, the threshold to stimulation on the cheek was elevated (13 to 18 dB) in the presence of an air-inflated cheek, but not with a water-filled cheek. In animals, in the presence of an air pocket, the auditory brain stem response threshold was elevated by 10 to 20 dB; no threshold change occurred with a saline solution pocket. CONCLUSIONS: The introduction of air (but not water) into the soft tissues beneath the soft tissue stimulation sites led to a threshold elevation in both humans and animals. This was not the case when an identical volume of water was introduced, which would also have interrupted a possible parallel bone conduction pathway. These results provide evidence that soft tissue stimulation at low intensities induces tissue vibrations that are transmitted to the cochlea along a series of soft tissues with similar acoustic impedances.

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.

Cochlear activation at low sound intensities by a fluid pathway.

In order to assess the mechanisms responsible for cochlear activation at low sound intensities, a semi-circular canal was fenestrated in fat sand rats, and in other experiments a hole was made in the bone over the scala vestibuli of the first turn of the guinea-pig cochlea. Such holes, which expose the cochlear fluids to air, provide a sound pathway out of the cochlea which is of lower impedance than that through the round window. This should attenuate the pressure difference across the cochlear partition and thereby reduce the driving force for the base-to-apex traveling wave along the basilar membrane. The thresholds of the auditory nerve brainstem evoked responses (ABR) and of the cochlear microphonic potentials were not affected in the fenestration experiments. In addition, holes in the scala vestibuli of the first turn did not cause ABR threshold elevations. These results contribute further evidence that at low sound intensities the outer hair cells are probably not activated by a base-to-apex traveling wave along the basilar membrane. Instead it is possible that they are excited directly by the alternating condensation/rarefaction fluid pressures induced by the vibrations of the stapes footplate. The activated outer hair cells would then cause the localized basilar membrane movement.

Use of ABR threshold and OAEs in detection of noise induced hearing loss.

OBJECTIVE: To determine which measure is the most sensitive to noise induced hearing loss (NIHL): auditory nerve brainstem response (ABR), distortion product otoacoustic emission (DPOAE) or transient evoked otoacoustic emission (TEOAE), and how to assess possible changes in these responses. SUBJECTS & METHODS: Four groups of rats were exposed to various durations of 113 dB SPL broadband noise: 5 or 10 minutes (temporary changes in cochlear function), and 3 or 4 hours (permanent changes). Group means and data from individual animals were compared before and after exposure. RESULTS: Mean group DPOAE amplitude reduction showed no clear advantage over mean ABR threshold elevation in detection of temporary and permanent NIHL. Data from individual rats, however, indicated a clinical advantage for DPOAEs in detecting slight temporary, but not permanent, changes. TEOAEs were more sensitive in detecting changes in individual rats than as a group measure. CONCLUSIONS: TEOAE and DPOAE monitoring may improve detection of NIHL, though it should be used in conjunction with audiometric threshold monitoring.

Lateralization during the Weber test: animal experiments.

OBJECTIVES/HYPOTHESIS: The objective of this study were to present an assessment of a new theory to explain lateralization during the Weber test using an animal model. This theory is based on the discovery that a major pathway in bone conduction stimulation to the inner ear is through the skull contents (probably the cerebrospinal fluid [CSF]). The placement of a bone vibrator or tuning fork on the skull excites the inner ear by the classic osseous pathway and by the suggested CSF pathway. We assume that there is a phase difference between the stimulation mediated by the ossicular chain (inertial and occlusion mechanisms) and the one mediated by the CSF. The presence of a conductive pathology will decrease the magnitude of the sound energy mediated by the ossicular chain. Thus, the out-of-phase signal arriving through the bony pathways will be decreased, hence increasing the resultant sound intensity stimulating the cochlea. STUDY DESIGN: Prospective animal study. METHODS: The experiment was performed on 10 fat sand rats, which had undergone unilateral cochleostomy and a small craniotomy. The auditory nerve brainstem response (ABR) thresholds were measured to air-conducted stimulation, to stimulation with the bone vibrator applied to the skull, and to stimulation with the bone vibrator applied directly to the brain through the craniotomy. The ossicular chain of the second ear was then fixed to the middle ear walls with cyanoacrylate glue to induce a conductive hearing loss. The ABR thresholds to the same three stimuli were then measured again. RESULTS: After ossicular chain fixation, the ABR threshold to air-conducted stimulation increased, to bone vibrator stimulation on the bone decreased (hearing improvement), and to bone vibrator stimulation directly on the brain remained unchanged. CONCLUSIONS: This experiment confirms the proposed theory. During clinical bone conduction stimulation, there is a phase difference between sound energy reaching the inner ear through the middle ear ossicles and from the CSF. A middle ear conductive pathology removes one of these components, thus increasing the effective sound intensity in the affected ear. On the other hand, when the bone vibrator is applied on the brain, the inner ear is stimulated only through the CSF, so ossicular chain fixation does not change the ABR threshold. Moreover, this study proves that lateralization during the Weber phenomenon is the result, at least in part, of an intensity difference between sound energy reaching the two cochleae.

Bone conduction hearing on the teeth of the lower jaw.

Bone conduction stimulation of the teeth of the lower jaw initiates auditory sensations. However the lower jaw is only loosely coupled to the skull by the temporo-mandibular joint. Therefore the 'classical' bone conduction pathway involving skull vibration transmission entirely along bone to the temporal-petrous bone requires further consideration. Bone conduction hearing thresholds to stimulation at the forehead and at the teeth of the upper and lower jaw were determined in human subjects. Thresholds on the teeth were better than those on the forehead and there was no difference between the thresholds measured following stimulation of the upper and lower teeth. Experiments in guinea-pigs provided evidence that vibration of the teeth leads to transmission of the audio-frequency vibrations by means of soft tissue, through skull foramina, into the skull cavity (brain and CSF) and from there by fluid channels directly into inner ear fluids, exciting the cochlea.