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.
Keywords: Air conduction, bone conduction, free field, hearing protection devices, non-osseous BC, occlusion effect, real ear attenuation at threshold, soft tissue conduction
|How to cite this article:|
Chordekar S, Adelman C, Sohmer H, Kishon-Rabin L. Soft tissue conduction as a possible contributor to the limited attenuation provided by hearing protection devices. Noise Health 2016;18:274-9
|How to cite this URL:|
Chordekar S, Adelman C, Sohmer H, Kishon-Rabin L. Soft tissue conduction as a possible contributor to the limited attenuation provided by hearing protection devices. Noise Health [serial online] 2016 [cited 2020 Oct 31];18:274-9. Available from: https://www.noiseandhealth.org/text.asp?2016/18/84/274/192476
| Introduction|| |
It is generally thought that exposure to sounds with an intensity of over 85 dBA, for a duration exceeding 8 h, can cause damage to the auditory system if no protection is provided, with a trade-off between duration of unprotected exposure and intensity. The increased awareness of the need for conserving hearing in work places and public domains has led to the use and enforcement (by law in some countries) of hearing protection devices (HPDs). These HPDs usually come in the form of earmuffs, earplugs, helmets, and face shields, each differing in the amount of sound attenuation provided, depending on the type of the HPD, their properties as well as on the experience of the user with the HPD. However, studies have shown that regardless of the HPD used, and even if more than one type is used simultaneously, the maximum achievable attenuation is limited and does not sum linearly.,, This finding has led to the assumption that the effectiveness of HPDs does not depend only on the noise reduction rating (NRR) specified by the manufacturer. Actually, there may be additional physiological flanking mechanisms of hearing which would limit the attenuation provided by HPDs in the external auditory meatus (EAM). The present study was designed to provide further insight into the factors that limit the sound attenuation provided by HPDs and to suggest possible alternative sound pathways to the inner ear which have not been sufficiently studied.
Several explanations related to the hearing mechanism have been offered for the limited effectiveness of HPDs. The first mechanism is the possibility that the HPD did not completely seal the EAM, thus allowing sound pressure to flank or bypass the HPD in the EAM, and reach the tympanic membrane. Evidence for this comes from studies showing that hearing thresholds of participants with earplugs were further elevated when adding earmuffs, suggesting that combined HPDs provided additional blockage of the EAM compared to earplugs alone.,, However, in an earlier study on six adults, deep insertion of earplugs into the EAM (up to the bony part of the EAM) resulted in an air conduction (AC) attenuation which was not further elevated by the addition of earmuffs.
A second explanation for the limited protection provided by HPDs is the possibility that loud sounds may induce skull vibrations. These vibrations could lead to hearing via bone conduction (BC), in which actual bone vibrations are involved. BC hearing is a complex phenomenon, in which the vibrations of skull bone are transmitted along bone to the temporal − petrous bone, where they lead to vibrations of the walls of the outer, middle, and inner ears. These, in turn, induce inertia of the middle ear ossicles, inertia of the cochlear fluids, compression of the cochlear walls, and the occlusion effect (OE)., Previous studies suggested that the OE may contribute to the underestimation of the attenuation provided by the HPDs. It is thought that the OE is elicited by sound pressure which is induced in the EAM by the vibrations of the bony or soft tissue (cartilaginous) walls of the occluded EAM. This sound pressure vibrates the tympanic membrane and induces hearing by an “AC-like” mechanism, via the middle ear into the inner ear.,, The OE is also described as an improvement of BC hearing thresholds at low frequencies when the EAM is occluded. Thus, the use of the earplugs or earmuffs can lead to an inherent improvement in threshold at low frequencies, contributing by themselves to a limitation of the effectiveness of these HPDs. However, it has been shown that when deeply inserted earplugs are used, the OE can be avoided because the occluded volume of air in the cavity is minimal and the deep insertion limits the vibrations of the walls of the cavity, minimizing the creation of sound pressure in the EAM.,,, Each of these BC mechanisms, initiated by skull vibration due to loud sound, induces mechanical waves (a passive traveling wave along the basilar membrane) in the inner ear which activates the outer hair cells resulting in auditory sensation.
After excluding the effects of AC leakage and the OE, one should also attempt to quantitatively evaluate the acoustic impedance mismatch between air and bone to determine whether a sound field in air is capable of inducing skull bone vibrations and lead to BC hearing. If the maximum attenuation provided by the HPDs would be similar to the calculated attenuation due to the air-bone mismatch at the interface, BC is probably the mechanism responsible for the limitation. On the other hand, any difference between the calculated and measured attenuation would suggest different flanking hearing mechanism.
Therefore, the aims of this study were twofold: (1) to confirm the maximum attenuation that can be provided by HPDs while controlling for AC leakage and OE and (2) to consider alternative paths, particularly forms of BC, to explain the difference between the actually measured thresholds and the calculated attenuation level of HPDs.
| Subjects and Methods|| |
Fifteen healthy young adults (7 males; 8 females) participated in the present study with age ranging between 22 and 33 years (M = 28.87, SD = 3.02). All participants had normal hearing, that is, hearing thresholds of 15 dB HL or better at frequencies 0.5 kHz, 1.0 kHz, 2.0 kHz, and 4.0 kHz.
The entire experiment was conducted in a sound-treated room. Warble tone stimuli of 0.5, 1.0, 2.0, and 4.0 kHz were generated by a clinical audiometer (GSI-61, Grason-Stadler, USA). Warble tones were used to avoid standing waves. AC hearing thresholds were obtained in response to sound stimuli delivered through one speaker at 0° in the free-field mode. BC hearing thresholds were obtained using the standard bone vibrator (B-71) with the standard headband (Radioear P-3333) applied to the forehead with the standard application force of 5 Newton (5 N).
Two types of HPDs were assessed in this experiment. The first was circum-aural earmuffs (Pyramex PM5010, NRR = 31 dB, USA), and the second was customized earplugs which were molded individually for each participant using an impression material (Dreve Otoform Ak, Germany) in both ears. Before pressing the impression material into the EAM, a foam canal block (Foam Oto-Blocks, Precision Laboratories Inc., United Kingdom) was prepared, and the earplug carefully inserted by a certified clinician who has experience in preparing ear-mould impressions, up to the bony part of the EAM beyond the second bend, close to the tympanic membrane.
Hearing threshold measurements
Hearing thresholds were determined using an adaptive threshold-seeking procedure following the 5 dB-up 10 dB-down rule similar to that used in clinical audiometry.,
The usual method for assessing the attenuation provided by the HPDs is to measure the sound-field real ear attenuation at threshold (REAT). REAT is evaluated by obtaining hearing thresholds of normal-hearing participants in a free field with open EAM, and then again while using HPDs. Common HPDs for REAT evaluation are earplugs, earmuffs, or a combination of both.
Participants sat on a chair one meter in front of the free-field speaker (azimuth 0°). Each participant was instructed to focus his gaze on the center of the speaker, marked with a small red sticker. AC hearing thresholds were obtained in four conditions: (a) unprotected ears while EAMs were open (with no HPDs); (b) external ears were covered by the earmuffs; (c) EAMs were blocked by individually molded, customized earplugs; and (d) earmuffs were worn on top of the inserted customized earplugs. After determining hearing thresholds in each condition, the REAT for each HPD combination was calculated.
To assess the possible contribution of the OE, BC thresholds were obtained while the bone vibrator was applied to the forehead with a 5 N application force using the standard headband in two conditions: (a) while ears were unprotected and (b) while the customized earplugs blocked the EAM. If there is no change in threshold between the unprotected condition and that in the presence of the deeply inserted earplugs, then it can be assumed that an OE was not present. This is based on the findings that OE was negligible when the position of the earplugs was deep enough in the EAM.
The study was assessed and approved by the Shaarei-Zedek Medical Center Helsinki Ethics Committee and the Research Ethics Committee of Tel-Aviv University.
| Results|| |
Means and standard deviations of the AC hearing thresholds at the different conditions with and without the HPDs are shown in [Figure 1]. It can be seen that hearing threshold without the HPDs was within normal limits as expected. Wearing earmuffs alone resulted in a mean threshold elevation of 19.6–36.3 dB, depending on the frequency. Using only the customized earplugs increased thresholds by 39.6–45.8 dB, resulting in mean thresholds between 43.8 dB HL at 1.0 kHz and 54.6 dB HL at 4.0 kHz. Finally, applying the earmuffs over the earplugs leads to an additional small increase of 0.8 and 2.1 dB at 4.0 kHz and 0.5 kHz, respectively, so that the attenuation provided by the use of both types of HPDs together was 40–46 dB, that is, thresholds of 46–54 dB HL.
|Figure 1: Mean and standard deviation AC thresholds at the four tested frequencies at all tested conditions|
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A two-way repeated measure ANOVA was conducted with main effects of condition (DF = 3) and frequency (DF = 3). The results indicated a main effect of condition [F(3,239) = 1157.8, P < 0.001]. Contrast analysis (Holm-Sidak) found that with one exception (earplugs vs earplugs plus earmuffs), all other conditions (unprotected, earmuffs, earplugs, and combination of earplugs with earmuffs) were significantly different from each other (M = 6.7 dB HL, M = 36.2 dB HL, M = 47.6 dB HL, and M = 49.1 dB HL, respectively) (P < 0.05). The ANOVA analysis also found a significant frequency effect [F(3,239) = 8.5, P < 0.001]. Contrast analysis revealed less attenuation (P < 0.05) at 0.5 kHz (M = 31.6 dB HL) and 1.0 kHz (M = 32.7 dB HL) compared to 4.0 kHz (M = 39.9 dB HL). Also found was a significant interaction between tested condition and frequency [F(9,239) = 11.3, P < 0.001]. Contrast analysis (Holm-Sidak) revealed that there was less attenuation provided by the earmuffs at 0.5 kHz (P < 0.05). Overall, the results here suggest that adding the earmuff protection to the customized earplugs did not have an additional protective value.
As shown in [Figure 1], maximal achievable attenuation (REATs) was reached when earplugs and earmuffs were used together (with no statistical difference compared to earplugs only). The distribution of these values (in dB) for each frequency is shown in box and whiskers plot in [Figure 2].
|Figure 2: Box and whiskers plot for the maximum achievable REATs (in dB) (participant equipped with both earplugs and ear muffs) at each frequency. Box limits include the 25th–75th percentile data. The horizontal line within the box represents the median. Horizontal lines in the bars represent the outliers|
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With respect to the OE, the BC thresholds in the absence of any occlusion (open canal) compared to those in the presence of the deeply inserted earplug occluded state ranged from −0.7 at 2.0 kHz to a maximum 1.3 dB at 0.5 kHz. A two-way ANOVA revealed no main effect of tested condition [(F(1,119) = 3.0, P = 0.1] and no significant interaction between condition and frequency [F(3,119) = 0.9, P = 0.4], thus confirming the absence of any significant OE in the presence of the deeply inserted earplugs.
| Discussion|| |
The first purpose of the present study was to assess the maximum degree of attenuation that can be provided by HPDs designed to prevent sound from reaching the tympanic membrane, to reduce AC hearing in the sound field. Our results show that when the customized individually molded earplugs were inserted deep into the EAM, AC threshold was elevated by 38.3–45.7 dB. The addition of earmuffs over the earplugs leads to 40–46 dB attenuation. This, however, was not a statistically significant threshold elevation compared to the thresholds with earplugs alone. This finding serves as evidence that the deeply inserted customized earplugs probably provided close to the maximum attenuation of sound to the tympanic membrane, with minimal flanking around the earplug. It is likely that those studies, which reported that adding an additional type of HPD to the earplug led to further attenuation, had not inserted the earplug deep enough in the EAM, allowing leakage to the tympanic membrane.
An additional purpose of this study was to consider the possible influence of the OE, which was usually not controlled for in previous studies. In the present study, it was expected that OE would be reduced or even eliminated because of the customized and deeply inserted earplugs. These are known to reduce the volume of air in occluded cavity and prevent vibrations of walls of the meatus. Our findings showed that the BC hearing threshold in the unoccluded ear was not statistically different from that in the ear with deeply inserted ear plugs. This result supports the notion that the customized and deeply inserted earplugs prevented an OE, so that the special earplugs do not contribute, by their very presence, to a limitation on the effectiveness of the HPDs.
After confirming that close to a maximal degree of attenuation of free-field sound along the direct path to the tympanic membrane (EAM) had been achieved, and that an OE was also minimal, AC hearing was then attenuated by 40–46 dB. In other words, if the intensity of the sound field exceeded this level, it would be heard, probably via a flanking mechanism other than AC to the tympanic membrane.
It has therefore been suggested that when maximum attenuation of AC has been achieved, some form of BC hearing may be effective.,,, This is based on the fact that an effective BC mechanism could be initiated when the intensity of the sound in air is greater than 60 dB HL. With respect to the possibility that BC is contributing, one can estimate the ability of sound field in air to induce the prerequisite vibrations of skull bone required for BC mechanisms by calculating the acoustic impedance mismatch between air and bone. This estimation can be achieved by calculating the magnitude of the transmission and reflection of sound pressure from air (acoustic impedance 0.0004 kg/(s m2) × 106) to skull bone (acoustic impedance 7.8 kg/(s m2) × 106), using equation (1−(Z1−Z2)2/(Z1 + Z2)2) (where Z1 is the acoustic impedance of air, and Z2 is the acoustic impedance of bone). The calculation shows that the sound pressure at the boundary between air and bone would be attenuated by approximately 70 dB. One may argue that when hearing in a sound field, sound reaches the skin and other soft tissues before the underlying bone. Therefore, impedance mismatch calculations should include air to soft tissue attenuation and then soft tissue to bone attenuation. Since the acoustic impedance of soft tissue range is 1.38–1.99 kg/(s m2) × 106, an attenuation of around 55 dB is expected from air. Soft tissue to bone mismatch adds an additional 10–20 dB of attenuation. Thus, sound propagating from air to skin to bone is expected to lose approximately 65–75 dB of its original intensity. These attenuations are in keeping with the expected hearing loss in severe middle ear pathologies, where there is interference with the impedance matching mechanisms of the middle ear., The maximum air-bone gap then seen is 60 dB. Thus, the maximum expected attenuation if BC were effective ranges between 60 dB (middle ear pathologies) and 70 dB (acoustic impedance mismatch between air and bone). However, in the present study in which maximal possible AC attenuation was achieved, the thresholds of the subjects were 46–54 dB HL, and not 60–70 dB HL. This estimation of 60–70 dB is also supported by an unpublished study in our laboratory. In that study, vibrations of dry human skulls and sheep inner ear bone (promontorium) in the free field were assessed by vibrometers. Vibrations could be elicited only when stimuli in the sound field in air were at least 65–70 dB HL, similar to the test conditions in the present study. The result of maximum attenuation of 40–46 dB and not 60–70 dB as predicted does not support the assumption that hearing was initiated by a BC mechanism, especially not at threshold-intensity level. Thus, it is possible that an alternative hearing mechanism (other than AC and BC) was involved in eliciting hearing at intermediate intensity levels of 46–54 dB HL (hearing thresholds with the HPDs).
A possible hearing mechanism that does not involve AC and BC hearing, as the latter has been classically understood (i.e., all pathways to the inner ear except air-conduction), is the mechanism of “soft tissue conduction” (STC). STC has also been referred to as non-osseous BC. This pathway is supported by experimental evidence from animal models and humans showing that hearing could be elicited in the absence of actual skull bone vibration.,,, For example, auditory brainstem responses were recorded in animals when vibratory stimuli were applied directly to the brain tissue (dura) with no measurable vibration of the skull, or the bony shell of the inner ear. In human participants, hearing could be elicited when vibratory stimuli were applied to soft tissues such as the eye, neck, back, and thorax.,, These findings, as well as clinical observations showing preserved BC thresholds in the absence of two mobile windows in the inner ear,, support the existence of a mechanism that is different from AC and osseous BC.
Thus, a soft tissue sound path to the inner ear may serve as an additional bypassing mechanism which can also explain the limited attenuation provided by the traditional HPDs (earplugs and earmuffs) in a sound field. Moreover, the acoustic impedance mismatch between air (impedance in air: 0.0004 kg/(s m2) × 106) and soft tissues (1.38–1.99 kg/(s m2) × 106) is smaller than the impedance mismatch between air (0.0004 kg/(s m2) × 106) and bone (7.8 kg/(s m2) × 106). Thus, air-borne sounds would be transmitted to soft tissues more effectively than to bone, and therefore less attenuation is expected from air in the free field to both soft tissue and fluid during such non-osseous sound transmission. Thus, from air, the sound pressure would be preferentially/more effectively transmitted to a series of soft tissues, and from there to the inner ear fluids, rather than to bone. This is further supported by recent findings of Sim et al. who reported that stimulation to the dura (a non-osseous site) does not affect bone vibrations at the promontory (an osseous site).
Hearing by STC mechanisms can also be induced without any actual bone vibrations.,,,, Nevertheless, the term “BC hearing” has been used as a general term for any type of hearing sensation in which an AC mechanism was not involved. In fact, it was shown that when AC hearing is eliminated, several non-osseous (soft tissue) components can be responsible for the activation of hearing in a sound field, including the head (head conduction) and body (body conduction) when they are exposed to the sound-field.,, Nixon and von Gierke very early on suggested a contribution of the chest to hearing in the sound-field, as part of “body conduction.” Recently, Sim et al. also mentioned that soft tissue stimulation may be elicited by loud sounds. It is therefore possible that other parts of the body may also play a role in hearing in a sound-field. However, because there is no direct or continuous bony path from the body to the inner ear, it is not likely that the vibrations initiated at various sites on the body would lead to direct vibrations of the skull or the bony shell of the inner ear, as required for the initiation of osseous BC., Thus, STC is then the likely final, common mechanism of the flanking path from the several sites on the head and body to the inner ear.The findings of the present study have practical implications for the protection of the inner ears from the damaging effects of loud sounds. The notion that the sound can be delivered via soft tissue implies that protection should be provided not only to the ears but also to the head and body that are exposed to the sound.,,, The general idea that humans exposed to loud sounds should wear body protectors from sound is not novel. However, these studies assumed that the protection was from loud sounds that induce BC mechanisms due to skull vibrations. We propose here that STC can initiate hearing at considerably lower intensity sounds (45–55 dB HL), and this limits the maximum attenuation in which traditional HPDs can provide. This explanation provides a revised theoretical framework showing the need for body protectors from sounds that exceed 45–55 dB HL. However, if the sound exceeds 60–70 dB HL, sound from soft tissues will probably be transmitted to the underling bone, thus leading to osseous BC hearing.
In conclusion, the results of the present study provide evidence that there is an additional mechanism which can substantially contribute to the limited maximum possible attenuation by HPDs applied to the EAM. It is in keeping with other emerging evidence for the existence of a STC mechanism and leads to a different perspective on HPDs. That is, in the presence of deeply inserted earplugs which eliminate AC hearing and the OE, a STC mechanism can become effective. This should be considered in hearing conservation protocols.
This work was performed in partial fulfillment of the requirements for a Ph.D. degree of Shai Chordekar, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
The authors wish to acknowledge the contribution of acoustic engineer Leonid Kriksunov, M.Sc. for clarifying the energy interactions at the interface between air, bone and soft tissue.
Financial support and sponsorship
We would also like to acknowledge the financial support Shai Chordekar received from the School of Health Professions via Steyer Foundation and from the Communication Disorders Department via the Yairi Foundation.
Conflicts of interest
There are no conflicts of interest.
| References|| |
Occupational Noise Exposure Revised Criteria 1998. Cincinnati: National Institute for Occupational Safety and Health; 1998.
Fligor B, Chasin M, Neitzel R. Noise exposure. In: Katz J, Chasin M, English K, Hood LJ, Tillery KL, editors. Handbook of Clinical Audiology. 7th ed. Philadelphia, USA: Lippincott, Williams & Wilkins; 2015. p. 595-615.
Verbeek JH, Kateman E, Morata TC, Dreschler WA, Mischke C. Interventions to prevent occupational noise-induced hearing loss. Cochrane Database Syst Rev 2012;10:CD006396. doi: 10.1002/14651858. CD006396.pub3
Berger EH, Kieper RW, Gauger D. Hearing protection: Surpassing the limits to attenuation imposed by the bone-conduction pathways. J Acoust Soc Am 2003;114:1955-67.
Ravicz ME, Melcher JR. Isolating the auditory system from acoustic noise during functional magnetic resonance imaging: Examination of noise conduction through the ear canal, head, and body. J Acoust Soc Am 2001;109:216-31.
Reinfeldt S, Stenfelt S, Good T, Håkansson B. Examination of bone-conducted transmission from sound field excitation measured by thresholds, ear-canal sound pressure, and skull vibrations. J Acoust Soc Am 2007;121:1576-87.
Zwislocki J. In search of bone-conduction threshold in a free sound field. J Acoust Soc Am 1957;29:795-804.
Dietz AJ, May BS, Knaus DA, Greeley HP. Hearing protection for bone-conduction sound. NATO Human Factors & Medicine Panel Symposium on New Direction for Improving Audio Effectiveness, Amsterdam, 2005.
Stenfelt S. Acoustic and physiologic aspects of bone conduction hearing. Adv Otorhinolaryngol 2011;71:10–21.
Röösli C, Chhan D, Halpin C, Rosowski JJ. Comparison of umbo velocity in air- and bone-conduction. Hear Res 2012;290:83-90.
Stenfelt S, Reinfeldt S. A model of the occlusion effect with bone-conducted stimulation. Int J Audiol 2007;46:595-608.
Reinfeldt S, Stenfelt S, Håkansson B. Estimation of bone conduction skull transmission by hearing thresholds and ear-canal sound pressure. Hear Res 2013;299:19-28.
Dean MS, Martin FN. Insert earphone depth and the occlusion effect. Am J Audiol 2000;9:131-4.
Tsai V, Ostroff J, Korman M, Chen JM. Bone-conduction hearing and the occlusion effect in otosclerosis and normal controls. Otol Neurotol 2005;26:1138-42.
Stenfelt S, Wild T, Hato N, Goode RL. Factors contributing to bone conduction: The outer ear. J Acoust Soc Am 2003;113:902-13.
Stenfelt S, Goode RL. Bone-conducted sound: Physiological and clinical aspects. Otol Neurotol 2005;26:1245-61.
ANSI. Method of Manual Pure-tone Threshold Audiometry. New York: American National Standards Institute; 2004. S3.21-2004.
Schlauch RS, Nelson R. Puretone evaluation. In: Katz J, English K, Hood L, Tillery KL, editors. Handbook of Clinical Audiology. 7th ed. Baltimore: Lippincott, Williams & Wilkins; 2015. p. 29-46.
Steiger JR. Bone conduction evaluation. In: Katz J, Chasin M, English K, Hood L, Tillery KL, editors. Handbook of Clinical Audiology. 7th ed. Philadelphia: Lippincott, Williams & Wilkins; 2015. p. 53.
Baun J. Interaction with soft tissue. Physical Principles of General and Vascular Sonography. San Francisco: ProSono Publishing; 2004. p. 28-41.
Tjellström A, Håkansson B, Lindström J, Brånemark PI, Hallén O, Rosenhall U et al.
Analysis of the mechanical impedance of bone-anchored hearing aids. Acta Otolaryngol 1980;89:85-92.
Backous D, Niparko J. Evaluation and surgical management of conductive hearing loss. In: Cummings CW, Fredrickson JM, Harker LA, Krause CJ, Schuller DE, Richardson A, editors. Otolaryngology Head and Neck Surgery. 3rd ed. St. Louis, MO: Mosby; 1998. p. 2894-907.
Chordekar S, Kriksunov L, Kishon-Rabin L, Adelman C, Sohmer H. Mutual cancellation between tones presented by air conduction, by bone conduction and by non-osseous (soft tissue) bone conduction. Hear Res 2012;283:180-4.
Vento BA, Durrant JD. Assessing bone conduction thresholds in clinical practice. In: Katz J, Burkard R, Hood L, Medwetsky L, editors. Handbook of Clinical Audiology. 6th ed. Baltimore: Lippincott, Williams & Wilkins; 2009. p. 52.
Ito T, Röösli C, Kim CJ, Sim JH, Huber AM, Probst R. Bone conduction thresholds and skull vibration measured on the teeth during stimulation at different sites on the human head. Audiol Neurootol 2011;16:12-22.
Adelman C, Fraenkel R, Kriksunov L, Sohmer H. Interactions in the cochlea between air conduction and osseous and non-osseous bone conduction stimulation. Eur Arch Otorhinolaryngol 2012;269:425-9.
Chordekar S, Perez R, Adelman C, Sohmer H. Assessment of inner ear bone vibrations during auditory stimulation by bone conduction and by soft tissue conduction. J Basic Clin Physiol Pharmacol 2013;24:201-4.
Sim JH, Dobrev I, Gerig R, Pfiffner F, Stenfelt S, Huber AM et al.
Interaction between osseous and non-osseous vibratory stimulation of the human cadaveric head. Hear Res 2016. doi: 10.1016/j.heares.2016.01.013
Freeman S, Sichel JY, Sohmer H. Bone conduction experiments in animals − Evidence for a non-osseous mechanism. Hear Res 2000;146:72-80.
Seaman RL. Non-osseous sound transmission to the inner ear. Hear Res 2002;166:214-5.
Sohmer H, Freeman S, Geal-Dor M, Adelman C, Savion I. Bone conduction experiments in humans − A fluid pathway from bone to ear. Hear Res 2000;146:81-8.
Watanabe T, Bertoli S, Probst R. Transmission pathways of vibratory stimulation as measured by subjective thresholds and distortion-product otoacoustic emissions. Ear Hear 2008;29:667-73.
Borrmann A, Arnold W. Non-syndromal round window atresia: An autosomal dominant genetic disorder with variable penetrance? Eur Arch Otorhinolaryngol 2007;264:1103-8.
Vincent R, Sperling NM, Oates J, Jindal M. Surgical findings and long-term hearing results in 3,050 stapedotomies for primary otosclerosis: A prospective study with the otology-neurotology database. Otol Neurotol 2006;27:25-47.
Sohmer H. Reflections on the role of a traveling wave along the basilar membrane in view of clinical and experimental findings. Eur Arch Otorhinolaryngol 2015;272:531-5.
Lenhardt ML. Eyes as fenestrations to the ears: A novel mechanism for high-frequency and ultrasonic hearing. Int Tinnitus J 2007;13:3-10.
Nixon CW, von Gierke HE. Experiments on the bone conduction threshold in a free sound field. J Acoust Soc Am 1959;31:1121-5.
Kaufmann M, Adelman C, Sohmer H. Mapping sites on bone and soft tissue of the head, neck and thorax at which a bone vibrator elicits auditory sensation. Audiol Neurotol Extra 2012;2:9-15.
Department of Communication Disorders, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 52621
Source of Support: None, Conflict of Interest: None
[Figure 1], [Figure 2]