Cartilage conduction hearing Ryota Shimokura,a) Hiroshi Hosoi, Tadashi Nishimura, and Toshiaki Yamanaka Department of Otorhinolaryngology, Head and Neck Surgery, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8522, Japan
Harry Levitt Advanced Hearing Concepts Incorporated, 998 Sea Eagle Loop, Bodega Bay, California 94923
(Received 12 November 2013; revised 10 February 2014; accepted 19 February 2014) Sound information is known to travel to the cochlea via either air or bone conduction. However, a vibration signal, delivered to the aural cartilage via a transducer, can also produce a clearly audible sound. This type of conduction has been termed “cartilage conduction.” The aural cartilage forms the outer ear and is distributed around the exterior half of the external auditory canal. In cartilage conduction, the cartilage and transducer play the roles of a diaphragm and voice coil of a loudspeaker, respectively. There is a large gap between the impedances of cartilage and skull bone, such that cartilage vibrations are not easily transmitted through bone. Thus, these methods of conduction are distinct. In this study, force was used to apply a transducer to aural cartilage, and it was found that the sound in the auditory canal was amplified, especially for frequencies below 2 kHz. This effect was most pronounced at an application force of 1 N, which is low enough to ensure comfort in the design of hearing aids. The possibility of using force adjustments to vary amplificaC 2014 Acoustical Society of America. tion may also have applications for cell phone design. V [http://dx.doi.org/10.1121/1.4868372] PACS number(s): 43.66.Ba, 43.66.Lj, 43.66.Yw, 43.20.Mv [MRB]
I. INTRODUCTION
Sound is known to reach the cochlea through two distinct pathways; i.e., air and bone conductions. In air conduction, externally generated dilatational air waves arrive at the external auditory canal, and are transmitted to the inner ear through the eardrum and middle ear. In bone conduction, a transducer vibrates the skull bone, and the vibrational information travels directly to the inner ear. Air and bone conduction thresholds can be distinguished in an audiogram according to the different transmission routes; however, there is some crossover in the signals. In 2004, Hosoi found that a specific type of transducer, gently placed on the aural cartilage, could be used to create clear audible sound.1,2 Thus he proposed the concept of “cartilage conduction,” which is difficult to categorize within the two previously known types of conduction. The aural cartilage comprises the outer ear and is distributed around the exterior half of the external auditory canal. The cartilage and transducer play the roles of a diaphragm and voice coil of a loudspeaker, respectively. In contrast to the auditory properties of dilatational waves that are externally generated in the air, cartilage conduction produces sound directly in the external auditory canal. Distinct from that of the heavy skull bone, conduction through the light and discrete aural cartilage requires minimal force, and thus is likely to be driven by a powerless transducer. A prototype of a transducer that can effectively vibrate aural cartilage has been developed to facilitate cartilage conduction research [Fig. 1(a)].3–12 The transducer is composed a)
Author to whom correspondence should be addressed. Electronic mail: [email protected]
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of a piezoelectric bimorph covered in elastic material. The elastic covering broadens the spectral range of the vibration output. The shape of the earpiece can be selected according to individual requirements. For example, a ring-shaped transducer permits the user to hear without occluding the external auditory canal, eliminating occlusion and enabling researchers to observe unmodified cartilage conduction sound. Aside from acoustic research, the ring-shaped transducer has several advantages for hearing aid design, including reducing stress related to a feeling of “ear fullness” reported by some users.3,5,10 The cartilage conduction hearing aid also has potential for patients who are unable to wear the earplug component of a conventional hearing aid because of disorders of the outer ear.9,11 Conversely, when the outer ear is vibrated regionally in a point, the closed earpiece is more useful because of the smaller head. Although there is some variation according to the different components, the transducer is especially effective for vibrations and sounds greater than 500 Hz and 1 kHz, respectively [Fig. 1(b)]. There are three possible transmission pathways for acoustic energy traveling from a cartilage conduction transducer to the cochlea (Fig. 2). The first is the air conduction pathway from the transducer to the eardrum, which includes the resonance effect in the canal (air pathway) because the transducer also generates a low level air-born signal. The second pathway involves both air conduction and cartilage conduction. Vibrations of the aural cartilage and tissue surrounding the external auditory canal generate sound in the ear canal that reaches the eardrum by air conduction (cartilage-air pathway). The third pathway involves cartilage and bone conduction via the skull from the transducer to the cochlea (cartilage-bone pathway). The air and cartilage-bone pathways are common routes that operate based on the same
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C 2014 Acoustical Society of America V
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bone (i.e., mastoid). For the psycho-acoustic measurement, participants adjusted the SPL of an earbud in the ear opposite that of the simulation to match the perceived loudness of the cartilage and bone conduction (loudness matching test). We assumed that the difference between the measured and adjusted SPL would be a measure of how much acoustic energy was transmitted via the bone and/or cartilage-bone pathways (Fig. 2). Third, to explore the mechanisms of cartilage conduction, we simultaneously measured the SPL in the canal and the mechanical pressure of the transducer at the ear tragus. The bone conduction transducer component of a hearing aid must be strongly compressed at the mastoid (5.4 N) to produce a clear vibrational transmission to the skull bone.13 As a result, implant hearing aids (e.g., bone anchored hearing aids) are often used because they cause less overall discomfort.14–16 However, it is unclear whether cartilage conduction also requires strong compression against the aural cartilage to achieve effective sound transmission. II. METHODS FIG. 1. Cartilage conduction transducers. (a) Front and side surfaces of cartilage conduction transducer (open and closed types). (b) Vibration acceleration level (VAL) and sound pressure level (SPL) of the transducer. The VAL (—) and SPL (- - -) were measured by a subminiature charge accelerometer (type 4374; Br€ uel & Kjaer, Naerum, Denmark) and a probe microphone (type 4182; Br€uel & Kjaer), respectively.
principles that pertain to regular air and bone conduction hearing, respectively. In contrast, the cartilage-air pathway is not a common sound conduction route. The aim of this study was to clarify the mechanisms of cartilage conduction by contrasting this pathway with the air and bone conduction routes. We first compared cartilage conduction with air conduction by measuring the sound pressure level (SPL) in the auditory external canal under two conditions: (1) with the transducer placed such that it touched the aural cartilage (touching condition) and (2) with the transducer placed in essentially the same position but not touching the aural cartilage (non-touching condition). Because the transducer generated a collateral air-borne signal, the difference in the SPL between the two conditions allowed us to specify the amount of signal transmitted through the cartilage-air pathway alone (Fig. 2). Second, we compared cartilage conduction with bone conduction by collecting both physio- and psycho-acoustic data. For the physio-acoustic measurement, we recorded the SPL in the canal while stimulating either the aural cartilage or the skull
A. Sound measurement in the external auditory canal
The input signal for the transducer was a pure-tone train ranging from 125 Hz to 16 kHz in 1/12 octave steps. The tones were 1 s in duration and were each followed by a silent interval of 0.5 s. The signal levels were used to drive the cartilage-conduction transducer in 0.5, 1.0, and 2.0 V. In this experiment, we used a ring-shaped transducer (Fig. 3). The resulting sound in the auditory canal was measured using a calibrated probe microphone (type 4182; Br€uel & Kjaer, Naerum, Denmark), which had a metallic probe tube (length: 100 mm, diameter: 1.24 mm) that allowed sound pressure to be measured in a closed or narrow space. A rubber tube was placed on the distal end of the probe for safety, and the probe was inserted 15 mm from the entrance of the external auditory canal. The measured signals were pre-amplified by a conditioning amplifier (NEXUS, Br€uel & Kjaer) and then digitized for subsequent analysis with a sampling rate of 44.1 kHz and a 16-bit resolution (UA-101 analog-to-digital converter, Roland, Hamamatsu, Japan). For the touching condition, the transducer was fitted at the entrance of the ear canal [Figs. 3(a) and 3(c)] and the participants were asked to lie horizontally. The probe was inserted into the external auditory canal through the hole in the ringshaped component, without touching the transducer. For the non-touching condition, the transducer was placed very close to the entrance of the external auditory canal (7–10 mm),
FIG. 2. (a) Wearing the transducer on the entrance of the ear canal and (b) possible transmission pathways from the transducer.
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FIG. 3. (Color online) Setup schematics of sound measurement in the external auditory canal for (a) the touching condition and (b) the nontouching condition, and transmission pathways for (c) the touching and (d) the non-touching condition.
where it was attached to a stand [Figs. 3(b) and 3(d)]. The probe was inserted through the gap between the transducer and the aural cartilage. The transducer did not touch the ear or the probe. We repeated the above methods three times for three participants (one male and two females, age: 31–40) who did not have diseases of the outer or middle ear. Measurements were conducted in an ordinary soundinsulated test room, and all participants took part in this study after providing informed consent. These procedures were approved by the ethics committee of Nara Medical University. B. Loudness matching test
In the aural cartilage stimulation condition, the ringshaped transducer was placed at the entrance of the canal [Fig. 4(a)]. In the skull bone stimulation condition, a bone conduction transducer (BR41, Rion CO., Ltd., Kokubunji, Japan) was attached over the mastoid using a headband (application force: 5.4 N). The signal consisted of a puretone train ranging from 250 Hz to 8 kHz in 1/3 octave steps (level: 1.0 V). Five participants (three males and two females, age: 31–35) without hearing disorders compared the perceived loudness of sounds produced by each type of transducer with sounds of the same frequency produced by an earbud (Eartone 3A, 3M Company E-A-R, Two Harbors, MN), which they wore in the opposite ear. We used an ear simulator to smooth the amplitude of the earbud input
according to the resonance in the external auditory canal for all frequencies (HATS4128, Br€uel & Kjaer). The participants could switch between the input from the transducer and earbud at any time, and were asked to adjust the volume of the earbud to match the perceived loudness of the transducer input [Fig. 4(b)]. A programmable attenuator (PA5, Tucker-Davis Technology, Gainesville, FL) was added to the acoustic output circuit to serve as the volume control. The participant audiograms showed that the difference in hearing level between the left and right ear was within 5 dB. We used the same stimuli, equipment, and procedure to measure the SPL in the external auditory canal in the touchingcondition [Fig. 3(a)]. The physio-acoustic data was obtained on a separate day. C. Application force measurement
To examine the relationship between the application force of the transducer and the SPL in the external auditory canal, we measured the SPL while maintaining a constant application force. For this measurement, we used a closed type of transducer for stimulus presentation because this transducer type was more appropriate for the application of force onto the ear tragus, i.e., the surface area had a smaller diameter of 10 cm [Fig. 1(a)]. The signal consisted of a puretone train ranging from 125 Hz to 16 kHz in 1/3 octave steps (level: 2.0 V). The pressure sensor (FSR400, Interlink Electronics Inc., Camarillo, CA), which was composed of
FIG. 4. (Color online) (a) Setup schematic for the loudness matching test with cartilage stimulation and (b) dialog box.
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FIG. 5. (Color online) (a) Setup schematic for the application force measurement, (b) transaxial plane of the external auditory canal, and (c) pressure sensor placed on the transducer.
thick polymer film, measured the change in resistance as a function of the force applied to the activation area (diameter: 7.6 mm) of the device [Fig. 5(c)]. We developed a preamplifier circuit for the device so that we could read the output voltage corresponding to the resistance. The output voltage was read through a 2/1-channel input/output module (type 3110, Br€ uel & Kjaer), as shown in Fig. 5(a). For measuring SPL in the external auditory canal, we inserted a small microphone (diameter: 2.6 mm, height: 2.5 mm) of the type that are commonly used in hearing aids (FC-23453-C05, Knowles Electronics, Itasca, IL) 15 mm from the entrance of the canal [Fig. 5(b)]. Nine participants (seven male and two females, age: 23–36), who had no disorders of the outer ear, participated in this experiment, in which the closed type of transducer with attached pressure sensor was pressed onto the ear tragus. The intended application forces were 1.00, 0.75, 0.50, 0.25, and 0.10 V, which corresponded to 3.12, 2.12, 1.43, 0.97, 0.77 N, respectively (see the Appendix). The participants maintained the force by directly monitoring the value during the signal presentation (approximately 2 min), and were asked not to exceed 10% error. If the error exceeded 10%, the participant was asked to try again. III. RESULTS
Figure 6 compares the SPLs in the external auditory canal between the touching and non-touching conditions. Although we observed some individual differences, we generally found that in the non-touching condition, there was a resonance in the canal around 2.5 kHz, and sound in the lower frequency range decayed rapidly. In the touching condition, the SPL in the canal was an average of 25.5 dB higher than in the non-touching condition. Moreover, we observed remarkable increase in the low frequency range, i.e., below 1 kHz. The average gain below 1 kHz was 35.1 dB, while the maximum gain was approximately 45 dB, at around 500 Hz. The linearity of the output was generally maintained. The averaged differences between the input voltages were 1962
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6.5 dB (0.5 vs 1.0 V) and 6.2 dB (1.0 vs 2.0 V) in the touching condition (6 20log102) and 4.6 dB (0.5 vs 1.0 V) and 5.5 dB (1.0 vs 2.0 V) in the non-touching condition. Figure 7 compares the measured SPL and adjusted SPL according to the difference in loudness between the aural cartilage and skull bone stimulation. The SPL in the canal was measured using the same methods as in the touching condition. We found that the loudness of the sound induced by cartilage conduction was predominantly determined by the SPL in the canal. Although we observed a slight increase in the adjusted SPL for sounds 4 kHz and higher produced by cartilage conduction, the adjusted SPL was an approximate fit to the standard deviation of the measured SPL in the canal. The averaged difference between the measured and adjusted SPL was 0.6 dB, while the sound induced by bone conduction was rated as being much larger than the SPL in the canal. Although the spectral shapes were similar, the adjusted SPL was 17.5 dB higher than the measured SPL. Figure 8 shows the SPL in the external auditory canal in response to six different amounts of force applied onto the transducer and the ear tragus. The amplitude peaks around 2.5 and 8 kHz in the non-touching condition appear to be due to the resonance of the external auditory canal. However, in the touching condition, the sound in the canal increased for frequencies ranging from 200 Hz to 2 kHz. We found an especially large increase around 1 kHz when the applied force approached 1 N. Above a force of 1 N, the increase continued to rise gradually. We calculated the SPL gradient as a function of force, and obtained values of 34 dB/N below 1 N of force and 2.5 dB/N above 1 N of force. IV. DISCUSSION A. Comparison with air conduction
In the touching condition in our study, sound reached the eardrum through both the air and cartilage-air pathways [Fig. 3(c)]. In the non-touching condition, sound reached the eardrum through the air pathway only [Fig. 3(d)]. The Shimokura et al.: Cartilage conduction hearing
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FIG. 6. SPL in the canal in the touching (—) and non-touching (- - -) conditions. The black, dark gray, and gray lines indicate input voltages of 2.0, 1.0, 0.5 V, respectively.
difference in SPL between the touching and non-touching conditions is thus likely a result of additional sound reaching the eardrum by means of cartilage-air conduction. Stenfelt et al. reported that stimulation at the mastoid produced a SPL increase in the external auditory canal that was 10 dB greater in an intact ear than when the cartilage part had been removed, for frequencies below 3 kHz.17 This 10 dB increase may correspond to the sound transmitted through the cartilage-air pathway from the skull bone vibration. When the aural cartilage was stimulated directly in the present study, the increase in SPL for frequencies lower than 1 kHz reached 35 dB. However, unlike the heavy skull bone, aural cartilage can be driven by a powerless transducer.12 Whether the vibrations of the aural cartilage produced the amplification in the canal is unclear. After conducting the experiments described in our methods section, we measured the vibration acceleration level (VAL) of the aural cartilage by replacing the probe microphone with a subminiature charge accelerometer (type 4374; Br€uel & Kjaer). The
experimental design was the same as in the current study with respect to measuring sound in the external auditory canal. The accelerometer (diameter 5 mm, height 6.7 mm, weight 0.65 g) was attached to the participant’s ear tragus with double-sided adhesive tape. Figure 9 shows the VAL at the tragus for each participant. As reported in our previous study,10 the aural cartilage vibrated more strongly for frequencies below 2 kHz. Thus, it appears that the vibrations of the aural cartilage generated sound in the canal, especially in the low frequency range. In the non-touching condition, the earpiece component of the cartilage-conduction transducer was located 7–10 mm from the entrance of the external auditory canal, while the distance between the earpiece and the entrance to the canal was about 3 mm in the touching condition. Therefore, the distance-decay effect may have contributed to the difference in the SPL between the touching and non-touching conditions. To address this issue, we conducted an additional experiment in which we simulated the sound in the external
FIG. 7. Measured SPL in the canal (line) and adjusted SPL according to loudness (marker) for the two presentation conditions: (a) cartilage and (b) bone conduction. The averaged values among five participants and three trials (total 15 trials) are shown. The hatching and error bars indicate the standard deviations for the line and markers, respectively.
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earpiece were moved closer to the entrance of the external auditory canal (without touching). Although we observed some differences at particular frequencies, the two sets of SPL curves were similar. Therefore, it appears that the distance-decay effect had a minimal contribution to the amplification of sound in the external auditory canal. B. Comparison with bone conduction
FIG. 8. SPL in the canal in response to six different force levels. In the nontouching condition, the transducer was held in front of the entrance to the aural canal without touching the ear. In the touching condition, the transducer was gently placed on the tragus without pushing. The averaged values among the nine participants and three trials (total 27 trials) are shown. The standard deviations are distributed from 10 to 22 dB in an irregular fashion.
auditory canal. We simulated the sound traveling via the air pathway using a free-field-to-eardrum transfer function.18 Figure 10 shows the average SPLs for three participants in the non-touching condition (dashed lines) and the SPLs of the transducer [dashed lines in Fig. 1(b)], which were frequency-weighted using the transfer function (rigid lines). We used the same probe microphone that had been used to measure the airborne sound produced by the transducer at a distance of 3 mm from the transducer earpiece. Thus, we considered the simulated sound level to provide an estimate of the SPL that would be present in the ear canal if the
The cartilage conduction hearing aid has often been assumed to be a type of bone conduction hearing aid because both devices use vibrational transducers. However, our comparison between the measured SPL in the canal and the adjusted SPL (according to loudness) indicated that the contribution of bone conduction to hearing is negligible in the case of excitation of the aural cartilage. The acoustic impedance (kg/m2 s 106) of soft tissue and bone are approximately 1.5 and 7.8, respectively.19,20 This gap in impedance prevents acoustic signals from being transmitted from the aural cartilage to the skull bone. Instead, the impedance gap causes compression and expansion of the air in the auditory external canal, which increases the size of the signal transmitted via cartilage conduction. Although several pathways implicating bone conduction hearing (e.g., non-osseous bone conduction21–24 and distortional vibrations causing compression of bone conducted signal25) have been proposed, the contribution of these additional pathways to hearing via cartilage conduction appears to be minimal. We found the adjusted SPL to be much larger than the measured SPL for the skull bone stimulation. This is likely due to the contribution of sounds produced by bone conduction, as they travel to the inner ear. Although some air borne sound generated by the bone conduction transducer reaches
FIG. 9. VAL at the ear tragus. The black, dark gray, and gray lines indicate input voltages of 2.0, 1.0, 0.5 V, respectively.
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(15 mm), the obtained SPL shown in Figs. 4, 6, and 8 may fluctuate within 62 dB, depending on the location in the canal. In future research, we plan to map out the spatial distribution of sounds transmitted via cartilage conduction. D. General discussion and applications
FIG. 10. Measured (- - -) and simulated (—) sound coming through the air pathway. The black, dark gray, and gray lines indicate input voltages of 2.0, 1.0, 0.5 V, respectively.
the auditory external canal,26,27 the contribution of this type of sound to hearing is minimal.17 The SPL in the canal for bone stimulation was smaller than that for cartilage stimulation even though the application force of the bone transducer13 (5.4 N) was much larger than that for the cartilage transducer. C. Amplifying sound by increasing application force
Aural cartilage can be driven by a small application force. However, whether the amplification of the sound increases with the force of compression applied to the transducer is unclear. We found that during simultaneous measurements, the SPL in the canal increased with the application force at the ear tragus. This increase took place rapidly below an application force of 1 N and gradually above 1 N. The ear tragus remained in the initial position below a force of 1 N, and moved towards the eardrum at forces higher than 1 N. At applied forces of 2.12 and 3.12 N, the ear tragus obscured the external auditory canal. Therefore, applying force to the transducer appeared to facilitate vibrational transmission to the cartilage, but only up to a force of 1 N. In this force range, we found an especially large increase in the amplitude of sounds below 2 kHz. This is expected, as the aural cartilage appears to vibrate most effectively in this frequency range (Fig. 9). Above 1 N, the surface of the tragus occluded the canal, which caused the sound in the canal to be amplified for frequencies lower than 1 kHz. Frequencies in this range are also amplified by occluding the canal in bone stimulation.17 In all of the above experiments, the microphone was inserted at a depth of approximately 15 mm, and was located at a middle position in the external auditory canal. However, the recorded SPL in the canal can vary according the insertion depth. Shaw and Teranishi described the spatial distribution of the canal in terms of the resonance along the canal.28 In that study, they found a large gap in the sound pressure around 3 kHz, and the difference in SPL at a position near the canal entrance vs the eardrum was 4 dB. Because the microphone in this study was inserted halfway into the canal J. Acoust. Soc. Am., Vol. 135, No. 4, April 2014
In contrast to the mechanisms of general air conduction, aural cartilage acts as a sound source, generated directly in the external auditory canal. The transmission pathway of the cartilage conduction signal appears to be different than that of bone conduction because aural cartilage vibrations are not transmitted to the skull bone. Because aural cartilage is lighter than the skull bone, the vibrational power required to drive the cartilage is less than that for the skull bone. Therefore, aural cartilage is a high performance converter, and this mode of sound transmission has potential in the development of new types of audio equipment. For example, cartilage conduction hearing aids with a ring-shaped transducer have been found to provide comfort because they do not obstruct the ear canal.3,5,7 They can also be prescribed for patients who are unable to wear the earpiece of a conventional hearing aid because of disorders of the outer ear (e.g., atresia of the external auditory canal and severe otorrhea).9,11 The sound produced via cartilage stimulation had minimal leakage from the canal, despite the ring-shaped transducer, and so we suggest that this method would also be suitable for a behind-the-ear type of hearing aid. This would reduce the potential for acoustic feedback caused by the short distance between the speaker and microphone.10 The ability to adjust the amplification of a sound by changing the application force could be applied to the design of smartphones. For instance, a user could press a transducer embedded in the phone to his/her aural cartilage to modulate the volume. With conventional smartphones and cellphones, volume has to be adjusted by changing the setting on a volume control. This operation is often necessary when the device is being used in a noisy environment (e.g., a station or busy street). However, the necessary sequence of actions (i.e., looking for and operating the volume button) often inhibits conversation. In the case of a cartilage conduction smartphone, however, the output volume could be easily controlled with one hand by adjusting the contact pressure. In loud environments, sufficient pressure may be required to occlude the canal with the ear tragus, producing insulation against external noise. V. CONCLUSION
Cartilage conduction has three possible sound transmission routes; air, cartilage-air, and cartilage-bone pathways (Fig. 2). By measuring the SPL in the external auditory canal, we found that aural cartilage vibrations generated sound in a range of frequencies. Notably, cartilage conduction produced sounds at frequencies lower than 1 kHz, and also produced sounds that were 35 dB louder than sounds transmitted via the air pathway. The sound generated by cartilage conduction had an SPL that was very close to the adjusted SPL of an earbud that had been set to match the perceived loudness induced by the cartilage conduction. Shimokura et al.: Cartilage conduction hearing
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Therefore, sound produced by a cartilage conduction transducer appears to be effectively transmitted via the cartilageair pathway (i.e., cartilage conduction sound). The amplitude of the sound produced by the cartilage conduction transducer increased with the application force at the contact surface (the ear tragus). We found the increase in SPL to be rapid below an application force of 1 N (34 dB/N), and gradual above 1 N (2.5 dB/N). This rapid increase may be due to the contribution of vibrational transmission, and the gradual increase may be due to the occlusion of the external auditory canal by folding of the ear tragus. ACKNOWLEDGMENTS
We would like to thank the participants for their cooperation in our study. We would also like to thank Dr. Yuya Takaki (International Pacific University) and Dr. Toshie Matsui (University of Tsukuba) for providing useful advice; Takaaki Nagura, Masahide Tanaka, and Masashi Morimoto (ROHM Co., Ltd.) for prototyping cartilage-conduction smartphones; and Takashi Iwakura and Kyoji Yoshikawa (Rion Co., Ltd.) for prototyping cartilage-conduction hearing aids. This research was supported by a Health and Labor Science Research Grant for Sensory and Communicative Disorders from the Ministry of Health, Labor and Welfare of Japan. APPENDIX: DEFINITION OF APPLICATION FORCE
To examine the relationship between the voltage and application force, we placed the pressure sensor on the surface of the fitted component of the transducer (closed type), and pushed them together with the activation area face down on an approved digital weight scale (SJ-1000, A&D Co., Ltd., Tokyo, Japan). The voltage value was recorded while the application force was maintained manually (error within 10%) at the desired value on the weight scale (100–800 g in 100 g steps). A sheet of molded polyurethane resin (Human skin gel with consistency degree 0, Exseal Co., Ltd., Minou, Japan) was also placed on the scale to simulate the touch of the device on skin, and the pressure sensor was wedged between the transducer and the resin sheet. We obtained an exponential relationship with a high correlation (r ¼ 0.99, p < 0.01), as follows: M ¼ 67:4expð1:55EÞ;
(A1)
where M is the load on the transducer [g] and E is the output voltage [V]. The application force used in this study [N] is expressed in terms of the load value obtained by this equation (F ¼ 9.8M [N]). 1
H. Hosoi, “Receiver,” Japanese Patent Application Number 166644 (June 4, 2004). 2 H. Hosoi, “Approach in the use of cartilage conduction speaker,” Japanese Patent Number 4541111 (November 17, 2004). 3 T. Sakaguchi, O. Saito, and H. Hosoi, “Hearing aid using cartilage conduction,” Proceedings of the Midwinter Research Meeting of Association for Research in Otolaryngology, No. 545, Phoenix (February 2008) 4 T. Sakaguchi, O. Saito, and H. Hosoi, “Cartilage conduction hearing aid for the patient with atresia auris,” J. Acoust. Soc. Am. 123, 3305 (2008).
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H. Hosoi, S. Yanai, T. Nishimura, T. Sakaguchi, T. Iwakura, and K. Yoshino, “Development of cartilage conduction hearing aid,” Arch. Mater. Sci. Eng. 42, 104–110 (2010). 6 H. Hosoi, “Hearing aids—Recent advance and our studies for outstanding issue,” Proceedings of the 13th Korea-Japan Joint Meeting Otorhinolaryngology-Head and Neck Surgery, Seoul (September 2010), p. 23. 7 R. Shimokura, Y. Takaki, T. Nishimura, and H. Hosoi, “Development of cartilage conduction hearing aid—Loudness given by cartilage conduction transducer,” Proceedings of the Midwinter Research Meeting of Association for Research in Otolaryngology, No. 194, Baltimore (February 2011). 8 R. Shimokura, T. Matsui, T. Nishimura, and H. Hosoi, “Advantages of cartilage sound conduction in hearing aids,” Proceedings of the 2012 ICME International Conference on Complex Medical Engineering, Kobe (July 2012), pp. 134–141. 9 T. Nishimura, H. Hosoi, O. Saito, R. Miyamae, R. Shimokura, T. Matsui, and T. Iwagami, “Benefit of a new hearing device utilizing cartilage conduction,” Auris Nasus Larynx 40, 440–446 (2013). 10 R. Shimokura, H. Hosoi, T. Iwakura, T. Nishimura, and T. Matsui, “Development of monaural and binaural behind-the-ear cartilage conduction hearing aids,” Appl. Acoust. 74, 1234–1240 (2013). 11 C. Morimoto, T. Nishimura, H. Hosoi, O. Saito, F. Fukuda, R. Shimokura, and T. Yamanaka, “Sound transmission of cartilage conduction in the ear with fibrotic aural atresia,” J. Rehab. Res. Dev., in press (2014). 12 T. Nishimura, H. Hosoi, O. Saito, R. Miyamae, R. Shimokura, T. Matsui, T. Yamanaka, and H. Levitt, “Is cartilage conduction classified into air or bone conduction?,” Laryngoscope, http://onlinelibrary.wiley.com/doi/ 10.1002/lary.24485/full (Last viewed March 11, 2014). 13 ISO 389-3: Acoustics—Reference Zero for the Calibration of Audiometric Equipment—Part 1: Reference Equivalent Threshold Force Levels for Pure Tones and Bone Vibrators (International Organization for Standardization, Geneva, 1994). 14 P. I. Bra˚nemark and T. Albrektsson, “Titanium implants permanently penetrating human skin,” Scand. J. Plast. Reconstr. Surg. 16, 17–21 (1982). 15 B. Ha˚kkansson, A. Tjellstr€ om, U. Rosenhall, and P. Carlsson, “The boneanchored hearing aid: Principle design and a psychoacoustical evaluation,” Acta Otolaryngol. 100, 229–239 (1985). 16 J. Hough, B. Johnson, and T. Himelick, “Implantable bone conduction hearing device,” Ann. Otol. Rhinol. Laryngol. 95, 498–504 (1986). 17 S. Stenfelt, T. Wild, N. Hato, and R. Goode, “Factor contributing to bone conduction: The outer ear,” J. Acoust. Soc. Am. 113, 902–913 (2003). 18 R. A. Bentler and C. V. Pavlovic, “Transfer functions and correction factors used in hearing aid evaluation and research,” Ear Hear. 10, 58–63 (1989). 19 F. A. Duck, Physical Properties of Tissue (Academic Press, London, 1990). 20 F. A. Duck, “Propagation of sound through tissue,” in The Safe Use of Ultrasound in Medical Diagnosis, edited by G. Haar and F. A. Duck (British Institute of Radiology, London, 2000), pp. 4–15. 21 T. Watanabe, S. Bertoli, and R. Probst, “Transmission pathways of vibratory stimulation as measured by subjective thresholds and distortionproduct otoacoustic emissions,” Ear Hear. 29, 667–673 (2008). 22 S. Freeman, J. Y. Sichel, and H. Sohmer, “Bone conduction experiments in animals—Evidence for a non-osseous mechanism,” Hear. Res. 146, 72–80 (2000). 23 H. Sohmer, S. Freeman, M. Geal-Dor, C. Adelman, and I. Savion, “Bone conduction experiments in humans—A fluid pathway from bone to ear,” Hear. Res. 146, 81–88 (2000). 24 T. Ito, C. R€ o€ osli, C. J. Kim, J. H. Sim, A. M. Huber, and R. Probst, “Bone conduction thresholds and skull vibration measured on the teeth during stimulation at different sites on the human head,” Audiol. Neurootol. 16, 12–22 (2010). 25 J. Tonndorf, “Compression bone conduction in cochlear models,” J. Acoust. Soc. Am. 34, 1127–1131 (1962). 26 G. R. Lightfoot, “Air-borne radiation from bone conduction transducers,” Brit. J. Audiol. 13, 53–56 (1979). 27 S. Stenfelf and R. L. Goode, “Bone-conducted sound: Physiological and clinical aspects,” Otol. Neurotol. 26, 1245–1261 (2005). 28 E. A. G. Shaw and R. Teranishi, “Sound pressure generated in an externalear replica and real human ears by a nearby point source,” J. Acoust. Soc. Am. 44, 240–249 (1968).
Shimokura et al.: Cartilage conduction hearing
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Harry Levitt Advanced Hearing Concepts Incorporated, 998 Sea Eagle Loop, Bodega Bay, California 94923
(Received 12 November 2013; revised 10 February 2014; accepted 19 February 2014) Sound information is known to travel to the cochlea via either air or bone conduction. However, a vibration signal, delivered to the aural cartilage via a transducer, can also produce a clearly audible sound. This type of conduction has been termed “cartilage conduction.” The aural cartilage forms the outer ear and is distributed around the exterior half of the external auditory canal. In cartilage conduction, the cartilage and transducer play the roles of a diaphragm and voice coil of a loudspeaker, respectively. There is a large gap between the impedances of cartilage and skull bone, such that cartilage vibrations are not easily transmitted through bone. Thus, these methods of conduction are distinct. In this study, force was used to apply a transducer to aural cartilage, and it was found that the sound in the auditory canal was amplified, especially for frequencies below 2 kHz. This effect was most pronounced at an application force of 1 N, which is low enough to ensure comfort in the design of hearing aids. The possibility of using force adjustments to vary amplificaC 2014 Acoustical Society of America. tion may also have applications for cell phone design. V [http://dx.doi.org/10.1121/1.4868372] PACS number(s): 43.66.Ba, 43.66.Lj, 43.66.Yw, 43.20.Mv [MRB]
I. INTRODUCTION
Sound is known to reach the cochlea through two distinct pathways; i.e., air and bone conductions. In air conduction, externally generated dilatational air waves arrive at the external auditory canal, and are transmitted to the inner ear through the eardrum and middle ear. In bone conduction, a transducer vibrates the skull bone, and the vibrational information travels directly to the inner ear. Air and bone conduction thresholds can be distinguished in an audiogram according to the different transmission routes; however, there is some crossover in the signals. In 2004, Hosoi found that a specific type of transducer, gently placed on the aural cartilage, could be used to create clear audible sound.1,2 Thus he proposed the concept of “cartilage conduction,” which is difficult to categorize within the two previously known types of conduction. The aural cartilage comprises the outer ear and is distributed around the exterior half of the external auditory canal. The cartilage and transducer play the roles of a diaphragm and voice coil of a loudspeaker, respectively. In contrast to the auditory properties of dilatational waves that are externally generated in the air, cartilage conduction produces sound directly in the external auditory canal. Distinct from that of the heavy skull bone, conduction through the light and discrete aural cartilage requires minimal force, and thus is likely to be driven by a powerless transducer. A prototype of a transducer that can effectively vibrate aural cartilage has been developed to facilitate cartilage conduction research [Fig. 1(a)].3–12 The transducer is composed a)
Author to whom correspondence should be addressed. Electronic mail: [email protected]
J. Acoust. Soc. Am. 135 (4), April 2014
Pages: 1959–1966
of a piezoelectric bimorph covered in elastic material. The elastic covering broadens the spectral range of the vibration output. The shape of the earpiece can be selected according to individual requirements. For example, a ring-shaped transducer permits the user to hear without occluding the external auditory canal, eliminating occlusion and enabling researchers to observe unmodified cartilage conduction sound. Aside from acoustic research, the ring-shaped transducer has several advantages for hearing aid design, including reducing stress related to a feeling of “ear fullness” reported by some users.3,5,10 The cartilage conduction hearing aid also has potential for patients who are unable to wear the earplug component of a conventional hearing aid because of disorders of the outer ear.9,11 Conversely, when the outer ear is vibrated regionally in a point, the closed earpiece is more useful because of the smaller head. Although there is some variation according to the different components, the transducer is especially effective for vibrations and sounds greater than 500 Hz and 1 kHz, respectively [Fig. 1(b)]. There are three possible transmission pathways for acoustic energy traveling from a cartilage conduction transducer to the cochlea (Fig. 2). The first is the air conduction pathway from the transducer to the eardrum, which includes the resonance effect in the canal (air pathway) because the transducer also generates a low level air-born signal. The second pathway involves both air conduction and cartilage conduction. Vibrations of the aural cartilage and tissue surrounding the external auditory canal generate sound in the ear canal that reaches the eardrum by air conduction (cartilage-air pathway). The third pathway involves cartilage and bone conduction via the skull from the transducer to the cochlea (cartilage-bone pathway). The air and cartilage-bone pathways are common routes that operate based on the same
0001-4966/2014/135(4)/1959/8/$30.00
C 2014 Acoustical Society of America V
1959
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bone (i.e., mastoid). For the psycho-acoustic measurement, participants adjusted the SPL of an earbud in the ear opposite that of the simulation to match the perceived loudness of the cartilage and bone conduction (loudness matching test). We assumed that the difference between the measured and adjusted SPL would be a measure of how much acoustic energy was transmitted via the bone and/or cartilage-bone pathways (Fig. 2). Third, to explore the mechanisms of cartilage conduction, we simultaneously measured the SPL in the canal and the mechanical pressure of the transducer at the ear tragus. The bone conduction transducer component of a hearing aid must be strongly compressed at the mastoid (5.4 N) to produce a clear vibrational transmission to the skull bone.13 As a result, implant hearing aids (e.g., bone anchored hearing aids) are often used because they cause less overall discomfort.14–16 However, it is unclear whether cartilage conduction also requires strong compression against the aural cartilage to achieve effective sound transmission. II. METHODS FIG. 1. Cartilage conduction transducers. (a) Front and side surfaces of cartilage conduction transducer (open and closed types). (b) Vibration acceleration level (VAL) and sound pressure level (SPL) of the transducer. The VAL (—) and SPL (- - -) were measured by a subminiature charge accelerometer (type 4374; Br€ uel & Kjaer, Naerum, Denmark) and a probe microphone (type 4182; Br€uel & Kjaer), respectively.
principles that pertain to regular air and bone conduction hearing, respectively. In contrast, the cartilage-air pathway is not a common sound conduction route. The aim of this study was to clarify the mechanisms of cartilage conduction by contrasting this pathway with the air and bone conduction routes. We first compared cartilage conduction with air conduction by measuring the sound pressure level (SPL) in the auditory external canal under two conditions: (1) with the transducer placed such that it touched the aural cartilage (touching condition) and (2) with the transducer placed in essentially the same position but not touching the aural cartilage (non-touching condition). Because the transducer generated a collateral air-borne signal, the difference in the SPL between the two conditions allowed us to specify the amount of signal transmitted through the cartilage-air pathway alone (Fig. 2). Second, we compared cartilage conduction with bone conduction by collecting both physio- and psycho-acoustic data. For the physio-acoustic measurement, we recorded the SPL in the canal while stimulating either the aural cartilage or the skull
A. Sound measurement in the external auditory canal
The input signal for the transducer was a pure-tone train ranging from 125 Hz to 16 kHz in 1/12 octave steps. The tones were 1 s in duration and were each followed by a silent interval of 0.5 s. The signal levels were used to drive the cartilage-conduction transducer in 0.5, 1.0, and 2.0 V. In this experiment, we used a ring-shaped transducer (Fig. 3). The resulting sound in the auditory canal was measured using a calibrated probe microphone (type 4182; Br€uel & Kjaer, Naerum, Denmark), which had a metallic probe tube (length: 100 mm, diameter: 1.24 mm) that allowed sound pressure to be measured in a closed or narrow space. A rubber tube was placed on the distal end of the probe for safety, and the probe was inserted 15 mm from the entrance of the external auditory canal. The measured signals were pre-amplified by a conditioning amplifier (NEXUS, Br€uel & Kjaer) and then digitized for subsequent analysis with a sampling rate of 44.1 kHz and a 16-bit resolution (UA-101 analog-to-digital converter, Roland, Hamamatsu, Japan). For the touching condition, the transducer was fitted at the entrance of the ear canal [Figs. 3(a) and 3(c)] and the participants were asked to lie horizontally. The probe was inserted into the external auditory canal through the hole in the ringshaped component, without touching the transducer. For the non-touching condition, the transducer was placed very close to the entrance of the external auditory canal (7–10 mm),
FIG. 2. (a) Wearing the transducer on the entrance of the ear canal and (b) possible transmission pathways from the transducer.
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J. Acoust. Soc. Am., Vol. 135, No. 4, April 2014
Shimokura et al.: Cartilage conduction hearing
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FIG. 3. (Color online) Setup schematics of sound measurement in the external auditory canal for (a) the touching condition and (b) the nontouching condition, and transmission pathways for (c) the touching and (d) the non-touching condition.
where it was attached to a stand [Figs. 3(b) and 3(d)]. The probe was inserted through the gap between the transducer and the aural cartilage. The transducer did not touch the ear or the probe. We repeated the above methods three times for three participants (one male and two females, age: 31–40) who did not have diseases of the outer or middle ear. Measurements were conducted in an ordinary soundinsulated test room, and all participants took part in this study after providing informed consent. These procedures were approved by the ethics committee of Nara Medical University. B. Loudness matching test
In the aural cartilage stimulation condition, the ringshaped transducer was placed at the entrance of the canal [Fig. 4(a)]. In the skull bone stimulation condition, a bone conduction transducer (BR41, Rion CO., Ltd., Kokubunji, Japan) was attached over the mastoid using a headband (application force: 5.4 N). The signal consisted of a puretone train ranging from 250 Hz to 8 kHz in 1/3 octave steps (level: 1.0 V). Five participants (three males and two females, age: 31–35) without hearing disorders compared the perceived loudness of sounds produced by each type of transducer with sounds of the same frequency produced by an earbud (Eartone 3A, 3M Company E-A-R, Two Harbors, MN), which they wore in the opposite ear. We used an ear simulator to smooth the amplitude of the earbud input
according to the resonance in the external auditory canal for all frequencies (HATS4128, Br€uel & Kjaer). The participants could switch between the input from the transducer and earbud at any time, and were asked to adjust the volume of the earbud to match the perceived loudness of the transducer input [Fig. 4(b)]. A programmable attenuator (PA5, Tucker-Davis Technology, Gainesville, FL) was added to the acoustic output circuit to serve as the volume control. The participant audiograms showed that the difference in hearing level between the left and right ear was within 5 dB. We used the same stimuli, equipment, and procedure to measure the SPL in the external auditory canal in the touchingcondition [Fig. 3(a)]. The physio-acoustic data was obtained on a separate day. C. Application force measurement
To examine the relationship between the application force of the transducer and the SPL in the external auditory canal, we measured the SPL while maintaining a constant application force. For this measurement, we used a closed type of transducer for stimulus presentation because this transducer type was more appropriate for the application of force onto the ear tragus, i.e., the surface area had a smaller diameter of 10 cm [Fig. 1(a)]. The signal consisted of a puretone train ranging from 125 Hz to 16 kHz in 1/3 octave steps (level: 2.0 V). The pressure sensor (FSR400, Interlink Electronics Inc., Camarillo, CA), which was composed of
FIG. 4. (Color online) (a) Setup schematic for the loudness matching test with cartilage stimulation and (b) dialog box.
J. Acoust. Soc. Am., Vol. 135, No. 4, April 2014
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FIG. 5. (Color online) (a) Setup schematic for the application force measurement, (b) transaxial plane of the external auditory canal, and (c) pressure sensor placed on the transducer.
thick polymer film, measured the change in resistance as a function of the force applied to the activation area (diameter: 7.6 mm) of the device [Fig. 5(c)]. We developed a preamplifier circuit for the device so that we could read the output voltage corresponding to the resistance. The output voltage was read through a 2/1-channel input/output module (type 3110, Br€ uel & Kjaer), as shown in Fig. 5(a). For measuring SPL in the external auditory canal, we inserted a small microphone (diameter: 2.6 mm, height: 2.5 mm) of the type that are commonly used in hearing aids (FC-23453-C05, Knowles Electronics, Itasca, IL) 15 mm from the entrance of the canal [Fig. 5(b)]. Nine participants (seven male and two females, age: 23–36), who had no disorders of the outer ear, participated in this experiment, in which the closed type of transducer with attached pressure sensor was pressed onto the ear tragus. The intended application forces were 1.00, 0.75, 0.50, 0.25, and 0.10 V, which corresponded to 3.12, 2.12, 1.43, 0.97, 0.77 N, respectively (see the Appendix). The participants maintained the force by directly monitoring the value during the signal presentation (approximately 2 min), and were asked not to exceed 10% error. If the error exceeded 10%, the participant was asked to try again. III. RESULTS
Figure 6 compares the SPLs in the external auditory canal between the touching and non-touching conditions. Although we observed some individual differences, we generally found that in the non-touching condition, there was a resonance in the canal around 2.5 kHz, and sound in the lower frequency range decayed rapidly. In the touching condition, the SPL in the canal was an average of 25.5 dB higher than in the non-touching condition. Moreover, we observed remarkable increase in the low frequency range, i.e., below 1 kHz. The average gain below 1 kHz was 35.1 dB, while the maximum gain was approximately 45 dB, at around 500 Hz. The linearity of the output was generally maintained. The averaged differences between the input voltages were 1962
J. Acoust. Soc. Am., Vol. 135, No. 4, April 2014
6.5 dB (0.5 vs 1.0 V) and 6.2 dB (1.0 vs 2.0 V) in the touching condition (6 20log102) and 4.6 dB (0.5 vs 1.0 V) and 5.5 dB (1.0 vs 2.0 V) in the non-touching condition. Figure 7 compares the measured SPL and adjusted SPL according to the difference in loudness between the aural cartilage and skull bone stimulation. The SPL in the canal was measured using the same methods as in the touching condition. We found that the loudness of the sound induced by cartilage conduction was predominantly determined by the SPL in the canal. Although we observed a slight increase in the adjusted SPL for sounds 4 kHz and higher produced by cartilage conduction, the adjusted SPL was an approximate fit to the standard deviation of the measured SPL in the canal. The averaged difference between the measured and adjusted SPL was 0.6 dB, while the sound induced by bone conduction was rated as being much larger than the SPL in the canal. Although the spectral shapes were similar, the adjusted SPL was 17.5 dB higher than the measured SPL. Figure 8 shows the SPL in the external auditory canal in response to six different amounts of force applied onto the transducer and the ear tragus. The amplitude peaks around 2.5 and 8 kHz in the non-touching condition appear to be due to the resonance of the external auditory canal. However, in the touching condition, the sound in the canal increased for frequencies ranging from 200 Hz to 2 kHz. We found an especially large increase around 1 kHz when the applied force approached 1 N. Above a force of 1 N, the increase continued to rise gradually. We calculated the SPL gradient as a function of force, and obtained values of 34 dB/N below 1 N of force and 2.5 dB/N above 1 N of force. IV. DISCUSSION A. Comparison with air conduction
In the touching condition in our study, sound reached the eardrum through both the air and cartilage-air pathways [Fig. 3(c)]. In the non-touching condition, sound reached the eardrum through the air pathway only [Fig. 3(d)]. The Shimokura et al.: Cartilage conduction hearing
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FIG. 6. SPL in the canal in the touching (—) and non-touching (- - -) conditions. The black, dark gray, and gray lines indicate input voltages of 2.0, 1.0, 0.5 V, respectively.
difference in SPL between the touching and non-touching conditions is thus likely a result of additional sound reaching the eardrum by means of cartilage-air conduction. Stenfelt et al. reported that stimulation at the mastoid produced a SPL increase in the external auditory canal that was 10 dB greater in an intact ear than when the cartilage part had been removed, for frequencies below 3 kHz.17 This 10 dB increase may correspond to the sound transmitted through the cartilage-air pathway from the skull bone vibration. When the aural cartilage was stimulated directly in the present study, the increase in SPL for frequencies lower than 1 kHz reached 35 dB. However, unlike the heavy skull bone, aural cartilage can be driven by a powerless transducer.12 Whether the vibrations of the aural cartilage produced the amplification in the canal is unclear. After conducting the experiments described in our methods section, we measured the vibration acceleration level (VAL) of the aural cartilage by replacing the probe microphone with a subminiature charge accelerometer (type 4374; Br€uel & Kjaer). The
experimental design was the same as in the current study with respect to measuring sound in the external auditory canal. The accelerometer (diameter 5 mm, height 6.7 mm, weight 0.65 g) was attached to the participant’s ear tragus with double-sided adhesive tape. Figure 9 shows the VAL at the tragus for each participant. As reported in our previous study,10 the aural cartilage vibrated more strongly for frequencies below 2 kHz. Thus, it appears that the vibrations of the aural cartilage generated sound in the canal, especially in the low frequency range. In the non-touching condition, the earpiece component of the cartilage-conduction transducer was located 7–10 mm from the entrance of the external auditory canal, while the distance between the earpiece and the entrance to the canal was about 3 mm in the touching condition. Therefore, the distance-decay effect may have contributed to the difference in the SPL between the touching and non-touching conditions. To address this issue, we conducted an additional experiment in which we simulated the sound in the external
FIG. 7. Measured SPL in the canal (line) and adjusted SPL according to loudness (marker) for the two presentation conditions: (a) cartilage and (b) bone conduction. The averaged values among five participants and three trials (total 15 trials) are shown. The hatching and error bars indicate the standard deviations for the line and markers, respectively.
J. Acoust. Soc. Am., Vol. 135, No. 4, April 2014
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earpiece were moved closer to the entrance of the external auditory canal (without touching). Although we observed some differences at particular frequencies, the two sets of SPL curves were similar. Therefore, it appears that the distance-decay effect had a minimal contribution to the amplification of sound in the external auditory canal. B. Comparison with bone conduction
FIG. 8. SPL in the canal in response to six different force levels. In the nontouching condition, the transducer was held in front of the entrance to the aural canal without touching the ear. In the touching condition, the transducer was gently placed on the tragus without pushing. The averaged values among the nine participants and three trials (total 27 trials) are shown. The standard deviations are distributed from 10 to 22 dB in an irregular fashion.
auditory canal. We simulated the sound traveling via the air pathway using a free-field-to-eardrum transfer function.18 Figure 10 shows the average SPLs for three participants in the non-touching condition (dashed lines) and the SPLs of the transducer [dashed lines in Fig. 1(b)], which were frequency-weighted using the transfer function (rigid lines). We used the same probe microphone that had been used to measure the airborne sound produced by the transducer at a distance of 3 mm from the transducer earpiece. Thus, we considered the simulated sound level to provide an estimate of the SPL that would be present in the ear canal if the
The cartilage conduction hearing aid has often been assumed to be a type of bone conduction hearing aid because both devices use vibrational transducers. However, our comparison between the measured SPL in the canal and the adjusted SPL (according to loudness) indicated that the contribution of bone conduction to hearing is negligible in the case of excitation of the aural cartilage. The acoustic impedance (kg/m2 s 106) of soft tissue and bone are approximately 1.5 and 7.8, respectively.19,20 This gap in impedance prevents acoustic signals from being transmitted from the aural cartilage to the skull bone. Instead, the impedance gap causes compression and expansion of the air in the auditory external canal, which increases the size of the signal transmitted via cartilage conduction. Although several pathways implicating bone conduction hearing (e.g., non-osseous bone conduction21–24 and distortional vibrations causing compression of bone conducted signal25) have been proposed, the contribution of these additional pathways to hearing via cartilage conduction appears to be minimal. We found the adjusted SPL to be much larger than the measured SPL for the skull bone stimulation. This is likely due to the contribution of sounds produced by bone conduction, as they travel to the inner ear. Although some air borne sound generated by the bone conduction transducer reaches
FIG. 9. VAL at the ear tragus. The black, dark gray, and gray lines indicate input voltages of 2.0, 1.0, 0.5 V, respectively.
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(15 mm), the obtained SPL shown in Figs. 4, 6, and 8 may fluctuate within 62 dB, depending on the location in the canal. In future research, we plan to map out the spatial distribution of sounds transmitted via cartilage conduction. D. General discussion and applications
FIG. 10. Measured (- - -) and simulated (—) sound coming through the air pathway. The black, dark gray, and gray lines indicate input voltages of 2.0, 1.0, 0.5 V, respectively.
the auditory external canal,26,27 the contribution of this type of sound to hearing is minimal.17 The SPL in the canal for bone stimulation was smaller than that for cartilage stimulation even though the application force of the bone transducer13 (5.4 N) was much larger than that for the cartilage transducer. C. Amplifying sound by increasing application force
Aural cartilage can be driven by a small application force. However, whether the amplification of the sound increases with the force of compression applied to the transducer is unclear. We found that during simultaneous measurements, the SPL in the canal increased with the application force at the ear tragus. This increase took place rapidly below an application force of 1 N and gradually above 1 N. The ear tragus remained in the initial position below a force of 1 N, and moved towards the eardrum at forces higher than 1 N. At applied forces of 2.12 and 3.12 N, the ear tragus obscured the external auditory canal. Therefore, applying force to the transducer appeared to facilitate vibrational transmission to the cartilage, but only up to a force of 1 N. In this force range, we found an especially large increase in the amplitude of sounds below 2 kHz. This is expected, as the aural cartilage appears to vibrate most effectively in this frequency range (Fig. 9). Above 1 N, the surface of the tragus occluded the canal, which caused the sound in the canal to be amplified for frequencies lower than 1 kHz. Frequencies in this range are also amplified by occluding the canal in bone stimulation.17 In all of the above experiments, the microphone was inserted at a depth of approximately 15 mm, and was located at a middle position in the external auditory canal. However, the recorded SPL in the canal can vary according the insertion depth. Shaw and Teranishi described the spatial distribution of the canal in terms of the resonance along the canal.28 In that study, they found a large gap in the sound pressure around 3 kHz, and the difference in SPL at a position near the canal entrance vs the eardrum was 4 dB. Because the microphone in this study was inserted halfway into the canal J. Acoust. Soc. Am., Vol. 135, No. 4, April 2014
In contrast to the mechanisms of general air conduction, aural cartilage acts as a sound source, generated directly in the external auditory canal. The transmission pathway of the cartilage conduction signal appears to be different than that of bone conduction because aural cartilage vibrations are not transmitted to the skull bone. Because aural cartilage is lighter than the skull bone, the vibrational power required to drive the cartilage is less than that for the skull bone. Therefore, aural cartilage is a high performance converter, and this mode of sound transmission has potential in the development of new types of audio equipment. For example, cartilage conduction hearing aids with a ring-shaped transducer have been found to provide comfort because they do not obstruct the ear canal.3,5,7 They can also be prescribed for patients who are unable to wear the earpiece of a conventional hearing aid because of disorders of the outer ear (e.g., atresia of the external auditory canal and severe otorrhea).9,11 The sound produced via cartilage stimulation had minimal leakage from the canal, despite the ring-shaped transducer, and so we suggest that this method would also be suitable for a behind-the-ear type of hearing aid. This would reduce the potential for acoustic feedback caused by the short distance between the speaker and microphone.10 The ability to adjust the amplification of a sound by changing the application force could be applied to the design of smartphones. For instance, a user could press a transducer embedded in the phone to his/her aural cartilage to modulate the volume. With conventional smartphones and cellphones, volume has to be adjusted by changing the setting on a volume control. This operation is often necessary when the device is being used in a noisy environment (e.g., a station or busy street). However, the necessary sequence of actions (i.e., looking for and operating the volume button) often inhibits conversation. In the case of a cartilage conduction smartphone, however, the output volume could be easily controlled with one hand by adjusting the contact pressure. In loud environments, sufficient pressure may be required to occlude the canal with the ear tragus, producing insulation against external noise. V. CONCLUSION
Cartilage conduction has three possible sound transmission routes; air, cartilage-air, and cartilage-bone pathways (Fig. 2). By measuring the SPL in the external auditory canal, we found that aural cartilage vibrations generated sound in a range of frequencies. Notably, cartilage conduction produced sounds at frequencies lower than 1 kHz, and also produced sounds that were 35 dB louder than sounds transmitted via the air pathway. The sound generated by cartilage conduction had an SPL that was very close to the adjusted SPL of an earbud that had been set to match the perceived loudness induced by the cartilage conduction. Shimokura et al.: Cartilage conduction hearing
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Therefore, sound produced by a cartilage conduction transducer appears to be effectively transmitted via the cartilageair pathway (i.e., cartilage conduction sound). The amplitude of the sound produced by the cartilage conduction transducer increased with the application force at the contact surface (the ear tragus). We found the increase in SPL to be rapid below an application force of 1 N (34 dB/N), and gradual above 1 N (2.5 dB/N). This rapid increase may be due to the contribution of vibrational transmission, and the gradual increase may be due to the occlusion of the external auditory canal by folding of the ear tragus. ACKNOWLEDGMENTS
We would like to thank the participants for their cooperation in our study. We would also like to thank Dr. Yuya Takaki (International Pacific University) and Dr. Toshie Matsui (University of Tsukuba) for providing useful advice; Takaaki Nagura, Masahide Tanaka, and Masashi Morimoto (ROHM Co., Ltd.) for prototyping cartilage-conduction smartphones; and Takashi Iwakura and Kyoji Yoshikawa (Rion Co., Ltd.) for prototyping cartilage-conduction hearing aids. This research was supported by a Health and Labor Science Research Grant for Sensory and Communicative Disorders from the Ministry of Health, Labor and Welfare of Japan. APPENDIX: DEFINITION OF APPLICATION FORCE
To examine the relationship between the voltage and application force, we placed the pressure sensor on the surface of the fitted component of the transducer (closed type), and pushed them together with the activation area face down on an approved digital weight scale (SJ-1000, A&D Co., Ltd., Tokyo, Japan). The voltage value was recorded while the application force was maintained manually (error within 10%) at the desired value on the weight scale (100–800 g in 100 g steps). A sheet of molded polyurethane resin (Human skin gel with consistency degree 0, Exseal Co., Ltd., Minou, Japan) was also placed on the scale to simulate the touch of the device on skin, and the pressure sensor was wedged between the transducer and the resin sheet. We obtained an exponential relationship with a high correlation (r ¼ 0.99, p < 0.01), as follows: M ¼ 67:4expð1:55EÞ;
(A1)
where M is the load on the transducer [g] and E is the output voltage [V]. The application force used in this study [N] is expressed in terms of the load value obtained by this equation (F ¼ 9.8M [N]). 1
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Shimokura et al.: Cartilage conduction hearing
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