Stimulated acoustic emissions from within the human ... · Stimulated acoustic emissions from within the human auditory system D. T. Kemp Auditory Perception Research Laboratory,

Stimulated acoustic emissions from within the human

auditory system D. T. Kemp

Auditory Perception Research Laboratory, The Royal National Throat, Nose and Ear Hospital, Gray's Inn Road, London, England WCIX 8DA (Received 5 April 1978; revised 10 July 1978)

A new auditory phenomenon has been idenQfied in the acoustic impulse response of the human ear. Using a signal averaging technique, a study has been made of the response of the closed external acoustic meatus to acoustic impulses near to the threshold of audibility. Particular attention has been paid to the waveform of the response at post excitation times in excess of 5 ms. No previous worker appears to have extended observations into this region. The response observed after about 5 ms is not a simple extension of the initial response attributable to the middle ear. The oscillatory response decay time constant was found to change from approximately 1 ms to over 12 ms at about this time. The slowly decaying response conponent was present in all normal ears tested, but was not present in ears with cochlear deafness. This component of the response appears to have its origin in some nonlinear mechanism probably located in the cochlea, responding mechanically to auditory stimulation, and dependent upon the normal functioning of the cochlea transduction process. A cochlear reflection hypothesis received some support from these results.

PACS numbers: 43.66.Ba, 43.63.Kz, 43.63.Rf

INTRODUCTION

Cochlea wave propagation characteristics at moderate and high levels of stimulation are well known from the many direct physical measurements of basilar membrane movement that have been made on live animals

and post mortem specimens, e.g., Rhode (1971), Kohl- liJffel (1972), Wilson and Johnstone (1975). Unfortunate- ly the most sensitive direct techniques fail to give data at stimulus levels within 50 dB of hearing threshold. More sensitive techniques are needed to explore this important region, particularly as some evidence sug- gests that the living and intact cochlea exhibits nonlinear vibration characteristics which persist down to the lowest levels of stimulation so far observed (Rhode and Robles, 1974). Until the nature of this mechanical nonlinearity is understood, its true impact on cochlea behavior at low stimulus levels is open to conjecture (Kim and Molnar, 1975). It was the examination of one some- what unconventional but experimentally exciting possibility, which prompted the experimental investigation reported here.

When an acoustic impulse strikes the ear drum, a well-damped oscillatory motion of the whole middle ear structure is initiated, as observed by Bekesy (1936), Blauert et al. (1974) and others. A significant proportion of the middle ear damping (time constant, T-1 ms) is attributable to absorption of acoustic energy by the cochlea in the launching of a traveling disturbance along the basilar membrane (Zwislocki, 1962). Within the conventional cochlea this energy is totally dissipated over a period of about 5 ms as the disturbance propa- gates from base to apex (Anderson et al., 1971). Sup- pose however that localized mechanical impedance discontinuities existed to any degree on the basilar membrane. Partial reflection of the cochlea wave would

necessarily occur, back towards the basal end. Differ- ential hydrodynamic forces at the oval and round windows would result in movement of the middle ear system giv- ing rise to a secondary disturbance of the ear drum.

Retrograde energy transfer in the cochlea can occur only in special circumstances, as observed by Bekesy in model studies (Bekesy, 1960) viz., the source of excitation must be on the basilar membrane and extend over

a region of mechanical impedance gradient. It is hypothesized here that impedance discontinuities arise in the cochlea because of a MECHANICAL response of the transduction mechanism to stimulation leading to traveling wave reflection. Some "place" linked frequency specificity is envisaged such that lower frequencies would be reflected more apecally and therefore later than higher frequencies. The resultant frequency dispersion plus the likelihood of multiple internal reflections lead to the prediction of a prolonged complex and oscillatory "echo" of an impulse stimulus appearing in the acoustic meatus, and lasting for several milliseconds.

Further elaboration of this hypothesis would be pre- mature. Of importance here is the ease with which this hypothesis can be tested experimentally. The expected temporal separation of the middle ear transient response and the hypothetical echo, permits'the application of signal averaging techniques to the detection of the sound field in the meatus. The detection of "e.choes" of very low intensity is therefore practicable. An attempt to detect cochlear echoes by this technique is described in this paper.

I. EXPERIMENTAL TECHNIQUE

An acoustic probe was constructed, consisting of a miniature microphone and a sound source, encapsulated in plastic. The assembly was 1.5 cm long and 1 cm diameter. Both transducers opened onto one end of the probe. The external auditory meatus of the ear to be tested was closed by fixing and sealing (with malleable silicon rubber) the transducer end of the probe over the entrance to the meatus. Optimum transient responses were obtained from the transducers by this arrangement. Closure of the meatus served the purposes of this investigation by greatly intensifying the sound pressure

1386 J. Acoust Soc Am. 64(5), Nov. 1978 0001-4966/78/640•1386500.80 (D 1978 Acoustical Society of America 1386

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1387 D.T. Kemp' Acoustic emissions from the human ear 1387

fluctuations created by movement of the ear drum. This cavity introduces an additional capacitive loading on the drum which would be expected to modify, to a small ex- tent, the transient response of the middle ear.

Transient acoustic excitation of the meatal cavity was achieved by the application of a 200-/•s rectangular voltage pulse to the source transducer. The excitation repetition rate was 16/s. The magnitude of the transient sound field generated was measured via the integral cali- brated microphone. This magnitude is expressed below as a spectral density, i.e., dB SPL (re 2x 10 '5 N/m •') per Hz bandwidth. Constancy with frequency to within ñ6 dB, from 100 to 3500 Hz was typically obtained. In- tensity fell rapidly above this range and was minimal at the fundamental longitudinal resonant frequency of the typical closed metal cavity of approximately 5 kHz. Excitation levels used varied from just below the mean normal threshold of pulse audibility (found experimentally to be -38 ñ 3 dB SPL/Hz) up to 60 dB above this level. Due to the short duration and wide bandwidth of

the stimulus the peak pressure excursion in the typical normal ear canal of a just audible acoustic impulse was 40 dB SPL. Voltage to sound field conversion linearity was confirmed for the source at peak levels of up to 120 dBS

The sound pressure fluctuations in the meatal cavity were recorded during and after excitation. The sensitivity of the integral microphone was constant with frequency to within ñ 3 dB over and beyond the range of excitation. After the preliminary amplification the microphone signal was processed electronically to recover the small response present after 5 ms post stimulus time (pst). Low frequency noise, largely due to blood flow and muscular activity, was rejected below 400 Hz at the rate of 12 dB/octave. Symmetrical peak clipping of the signal eliminated most of the initial large response per- mitting further signal amplification prior to the averaging of consecutive responses using a 1024 word, 8 bit digital averager. The minimum system noise was set by the electret microphone with its built-in amplifier, this noise being equivalent to 32 dB SPL in the ear canal. The synchronous averaging of the nearly 2000 consecutive 62-ms sections of signal during the 2-min test interval reduced the effective system noise level to 0 dB SPL.

All observations were made with the subject comfort- ably seated in an acoustically damped sound-proofed room. To minimize interfering noises, the subject was asked not to move or swallow during the recording period. The impulse response waveform was obtained at several levels of excitation for each ear tested. The

initial response (0-5 ms pst) and the much smaller sub- sequent response (5-62 ms pst) were recorded separately with appropriate system gains.

,

II. RESULTS

Figure I shows two contrasting sets of impulse response waveforms- a,b,c and d, e, f, respectively. The upper traces of both sets [l(a) and 1 (d)] are uriclipped re-. sponse waveforms showing the initial response in full. The traces below each of these show responses for the

J. Acoust. Sec. Am., Vol. 64, No. 5, November 1978

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FIG. 1. The acoustic impulse response waveform from a 1.5- cc test cavity (left) is compared to that of a healthy human ear (right), under identical excitation and signal amplification conditions. An ear with a stronger than average emission was selected for this example to ensure its visibility in presentation (d). Another feature of this particular ear was the slower than average decay of the emission. The acoustic acativity apparently preceding the stimulus in (c) is in fact the continuing response from the previous stimulus 62 ms earlier. Multiple internal reflection is proposed as the mechanism for this. Stimulation at slower rates showed the acitivity to eventually fall to zero.

same conditions but with 30 dB greater amplification. The initial clipped portions have been erased, for clarity. Transient acoustic excitation of spectral density, -15 dB S PL/Hz (23 dB above mean threshold level) was ap- plied in all cases. Waveforms (a), (b), and (c) were obtained with the probe fitted to a simple damped cavity having an acoustic impedance similar to that of the human ear. The impulse response is seen to decay rapidly and is not discernible after about 6 ms pst even with increased amplification, [Figs. l(b) and 1(c)]. A human ear response is presented in Figs. l(d)-l(f). The initial response also decays to near zero at 6 ms pst. There are quantitative differences in the precise form of this initial response compared to that of the test cavity but of greater importance is the qualitative difference; the reappearance of a small but significant response after 6 ms pst. This is the small ripple just visible in Fig. l(d), and amplified in Fig. l(f). This secondary response reaches a maximum at approximately 10 ms pst and has a peak pressure deviation of 20 dB SPL re 2x10 '5 N/m •'. The dominant period of oscillation can be seen to increase with time over the first 10 ms of this

secondary response, i.e., frequency dispersion is present.

A similar phenomenon was observed in all responses collected from normal ears. The detailed structure of

the secondary response differed markedly from ear to ear, as did the rate of decay of response after the first 10-15 ms [Figs. 2(a)-2(d)]. Frequency dispersion was evident in most responses and is further demonstrated by Figs. 2(e)-2(g).

In Fig. 3, impulse response waveforms are shown for another ear, for several levels of excitation. (Clipping


1388 D.T. Kemp: Acoustic emissions form the human ear ß

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FIG. 2. Typical emission waveforms from four healthy young ears. Individual differences in the presence and strength of specific periodicities are apparent. Frequency dispersion is clearly present in (a) and (b). The level of stimulation for (a)- (d) was -15 dB SPL/Hz. Frequency dispersion is further demonstrated (for the ear used in Fig. 1) in sections (e), (f), and (g) of this figure• Exceptionally in this study, a tone burst of four cycles was used to stimulate the ear. Frequencies of 800, 1100, and 1800 Hz were used, respectively. Echoes re- lated to the three stimuli emerge at different times. The rate of excitation was 4/s to avoid interference from previous emissions. For (e), (f), and (g) the level was equal to that of a continuous tone 20 dB above subjective threshold. Stimuli are shown schematically.

of the initial large response is visible. ) To demonstrate the high degree of waveform reproducibility character- istically obtained for one ear, two entirely separate observations have been superimposed in the top trace. The response waveform changes significantly with excitation level but prominent waveform features between 5 and 15 ms pst are identifiable from the highest to the lowest levels used (which are 40 dB apart). The magnitude of the responses between 5 and 15 ms are seen to decrease with that of the acoustic excitation but, very significantly, not in a proportional manner. This nonlinearity was not of instrumental origin. The linearity of the instrumentation was confirmed by tests with syn- thesized response signals. All secondary responses exhibited this nonlinearity.

In the pilot experiment reported below, responses from 15 subjects were collected at various levels of acoustic excitation. Three of these subjects had moderate to severe cochlea hearing loss, the remainder had otologically normal ears. A total of 15 normal and five deaf ears were tested. Figure 4 summarizes the results of the waveform analysis conducted.

In Fig. 4(a) the temporal pattern of the mean peak sound pressure excursion is shown for the 15 normal ears, together with that for the test cavity. The acoustic excitation transient was of spectral density -15 dB S PL/Hz. In both the test cavity and the averaged human ear data, the initial oscillatory response magnitude decays at approximately 13 dB/ms (time constant 0.7 ms). In the cavity case, this decay continues, reaching the system noise level of 2 dB SPL peak pressure excursion, at 6 ms pst. In contrast, for the average normal human

1388

ear the response level stabilizes at about 19 dB SPL from 5 to 10 ms pst thereafter falling relatively slowly on average by 1 dB/ms (time constant 12 ms) and in a few ears by as little as 0.25 dB/ms. All normal ears had response waveforms between 5 and 10 ms which were above the system noise and which either increased or remained constant with time. The standard deviation

shown in Fig. 4(a) demonstrates the high intersubject similarity.

The mean instantaneous frequency taking all responses, from 5 to 20 ms pst is shown in Fig. 4(b). It falls from 1700 to 900 Hz at 50 Hz/ms. This represents the dominant, not the entire frequency content, but demonstrates the complex character of the prolonged response.

Figure 4(c) is particularly important. It demonstrates the cochlea linked, nonlinear nature of the mechanism which prolongs the impulse response, thereby distinguishing it from the initial, middle ear response. First- ly the figure shows the mean sound pressure level sampled in the 2« ms pst time window from 10 to 12.5 ms pst, for all subjects and at various excitation levels. (Time windows from 7.5 to 15 ms give similar results. ) Data for normal and deaf ears are shown separately. The level for all the 15 normal ears rises approximately as the cube root of the input excitation level. No linear system (as is the middle ear at low stimulus levels) can behave in this way.

The total energy contained in the average slowly decaying response tail from 6 ms pst is readily assessed from the temporal characteristics [ Fig. 4(a)] and the mean, sampled intensity data [Fig. 4(c)]. Expressed as a proportion of the input energy in the bandwidth 100- 3500 Hz the energy arriving after 6 ms drops smoothly with increasing stimulation from -12 dB re input at an

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FIG. 3. The impulse response waveform for one ear at several stimulus levels, the lowest of which was just below subjective threshbid. Clipping of the large initial response is visible. Presentation scale is the same for each waveform. This ear

has relatively strong emissions with slow decay. Frequency dispersion is not clearly evident in these responses. However, sections of dominant frequency 1800 Hz can be seen at about 8, 16, and 26 ms and a section of approximately 1200 Hz can be seen at approximately 11, 20, and 32 ms. This could represent multiple reflections of these two components of the response.

J. Acoust. Soc. Am., Vol. 64, No. 5, November 1978


1389 D.T. Kemp: Acoustic emissions from the human ear 1389

• 30

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FIG. 4. Summary of data from all ears in the pilot study. (a) Average temporal characteristics of the response intensity. ß Normal ears, o: cavity. (b) Waveform periodicity. Temporal characteristics of the dominant frequency content obtained from zero crossing rate measurements. (c) Response intensity de- pendence on stimulus level in the time window 10-12.5 ms pst. The upper line is a linear fit to data from normal ears. The lower line follows the effective system noise level. (This rises for data taken with high stimulus levels due to the limited available dynamic range. ) ©: Mean normal stimulus audibility levelo gk: Data from ears with cochlea deafness., Audiological details of the five cochlea deaf ears tested. Hearing losses quoted for frequencies 250, 500, 1000, 2000, 4000, and 8000 Hz, respectively. Subject TB: Age 21; right ear loss 35, 40, 65, 65, 60, 65 dB, respectively; left ear loss 25, 40, 55, 55, 60, 60 dB, respectively. No conductive element ofloss revealed by bone conduction audiograms. Middle ears healthy and normal. Loudness recruitment, a distinguishing characteristic of cochlear deafness, was present in both ears. Speech discrimination was fairly good. Diagnosis; bilateral sensorineural deafness due to congenital cochlea lesions. Subject SE: Age 20; right ear loss 90, 100, 105, 115, 110, above 100 dB, respectively; left ear loss 80, 95, 95, 120, 120, above 100 dB, respectively. No conductive element of loss detectable within limits of audiometer. Acoustic tympanometry showed normal healthy midlde ears. Loudness recruitment present in both ears. Speech discrimination was very poor. Diagnosis, bilateral sensorineural deafness due to congenital cochlea lesions. Subject SN: Age 21; right ear loss 90, 95, 85, 85, 80, 70 dB, respectively. No significant conductive element of loss detected. Middle ears apparently normal. Loudness recruit- merit present in both ears. Speech discrimination was poor. Diagnosis, bilateral sensorineural deafness due to cochlea lesions of unknown cause.

excitation level equaling the mean pulse audibility threshold, to -52 dB re input at 60 dB above threshold excita-

•' dB/dB) tion, (i.e., -• .

The second important result shown in Fig. 4(c) con- cerns the five ears with cochlea deafness, details of which are given in the legend. In each ear the impulse response became insignificant soon after 5-mspst, as in the nonbiological example. Figure 4(c) shows the level

in the 10-12.5-mspsttime window to be coincident with the system noise level for these ears. Following the pilot study reported above, a further series of ears were tested. Four subjects with immobile middle ears due to disease were tested and found not to exhibit the phenomenon. A further 22 ears with various degrees of sensory neural deafness but normal middle ears were screened.

The phenomenon was generally not present in those ears with hearing losses exceeding 30 dB and was frequently reduced in the remaining cases. The normal occurrence of the phenomenon was confirmed in a further 20 otologically normal ears.

III. ORIGIN

A change in the rate of decay of the normal ear's acoustic impulse response has been observed at about 6 ms pst, resulting in detectable sound persisting and occasionally increasing, in the closed ear canal for tens of milliseconds after stimulation. No previous reports of the phenomenon have been found and an interpretation in terms of present knowledge has proved difficult. The slowly decaying component will be referred to as the response "tail." Many plausible artefactual origins (e.g., a complex impulse response of the probe itself, or of the signal retrieval system), can be discounted on the basis of the nonappearance of the phenomenon with the dummy ear cavity. Nevertheless a thorough examination of the experimental system and environment was undertaken. The possibility of the reception of sonar type echoes of the stimulus from objects within 4 m of the probe was rejected. These echoes were found to be 45 dB below the signals in question. No defect in or spurious behavior of the instrumentation has been found which in any way mimics phenomenon seen in the normal human ears. Identical results have since been obtained

in entirely different sets of apparatus. It is therefore concluded that the "tail" is present because of some physical property peculiar to the human ear.

It has not been possible to formulate a purely acoustic explanation. The undetectability of the slowly decaying component in the impulse responses from the four subjects with immobile middle ears shows that this part of the response either orignates in the middle ear, or is conducted through it. An origin in the middle ear itself is strongly counterindicated by the acoustic analyses per- formed by Zwislocki and others, which show too great a degree of damping. The decay time constant, T of the tail is typically 12 ms indicating a damping ratio: (2•fT) 't of 0.013 for a mean response frequency of 1200 Hz. No branch of Zwislocki's analogue model with or without the closed meatus loading, has a damping ratio less than 0.12 at this frequency. The intensity of the response tail is however very small in relation to the initial middle ear response and so might be attributable to the response of some highly resonant cavity in the head, very lightly coupled to the external meatus through the middle ear. The observed decay time constant of the average tail allows the bandwidth B of this hypothetical resonator to be estimated as 27 Hz, from B =.(•T) 't. This is too narrow a bandwidth to be consistent with the

data. The observed waveforms are not characteristic

of a single resonator. They are complex and change




periodicity rapidly. Figures 1, 2, 3, and 4(b) together imply an overall bandwidth typically of the order of 1000 Hz. The acoustic resonator model could be rescued by proposing a set of several such resonant cavities each having different frequencies. Suitable anatomical cor- relates are not readily found and this purely acoustic model becomes unacceptably elaborate when the nonlinear dependance of the amplitude of the response, on excitation level [Fig. 4(c)] is considered. Either the damping of, or the coupling to the hypothesized resonators would need to be intensity dependent to accommodate the observed behavior. Nonlinear behavior in an essentially low-level phenomenon, strongly indicates active physiological involvement. It is concluded that sound generated by some physiological activity is being conducted through the middle ear to the acoustic meatus.

Various physiological possibilities have been examined Sound generation during auditory reflex contractions of either the stapedius (Borg, 1976) or post auricular (Douek el al, 1973) muscles, cannot, for several rea- sons account for the phenomenon. Both these reflexes occur binaurally for monaural stimulation; the acoustic response reported here could be detected only ipsilater- ally. Furthermore, reflexes are independent of stimulus polarity. In contrast the entire acoustic impulse response waveform is found to invert unchanged with excitation polarity change. The waveform of the acoustic impulse responses remain unchanged for stimulus rates from 1 to 80 Hz (apart from the overlapping effect of the tail of the previous response). This invariance would not be expected for signals of muscular origin. Finally the stapedial reflex in particular has a high activation threshold and a response latency which places it outside the range of measurements made.

The possibility that electrophysiological signals of cochlea microphonic, neurogenic, or myogenic origin, where received and mistaken for acoustic signal was also rejected. The microphone unit was fully screened electrically and was highly insulated from the body. The system was demonstrably not sensitive to the very small electrophysiological signals present at the ear. The acoustic signals have quite different characteristics from any electrophysiological signals.

A third physiological possibility to be considered is that the response tail is conducted through the middle ear from the cochlea• The Undetectability of the phenomenon. in subjects with healthy middle ears but suffer- ing cochlear deafness clearly supports this especially in the absence of viable auditory reflex and electrophysiological hypotheses. If this were the case the attenuation suffered in the transfer of the response tail signal from the oval window to the closed meatal cavity would have considerably distorted the observed input-to-tail energy ratio. Using Zwislocki's analog middle ear model and taking the closed meatal cavity volume to be icc, the mean attenuation between 900 and 1700 Hz was calculated

to be approximately 20 dB. Recomputation (from Fig. 4 data) of the energy ratio referred now to the cochlea end of the middle ear reveals that for near-threshold stimu-

lation levels, incident and returned signals are of the same order, within experimental limits. If internal

cochlea reflection is the mechanism causing the re- emergence of energy (see the Introduction) then 100% internal reflection is implied. This strange situation is however confined to very near threshold levels due to the slow, nonlinear growth of the response with increasing stimulation. The reflection coefficient implied with stimuli 60 dB above threshold is only 2.5% (-32 dB). By extrapolation, for stimuli 90 dB above threshold the reflection would be only 0.25% (-52 dB).

Superficially the cochlea reflection hypothesis appears to be at variance with a great body of experimental knowledge, but this is not so. The hypothesis describes an aspect of cochlea behavior which would be significant only at very low levels of stimulation. The predicted retrograde cochlea wave would have been too small to have been detected by any of the invasive direct physical measurement techniques used to date which have re-

quir.ed moderate to high levels of stimulation. Previous- ly observable psychophysically effects are however in- dicated since at very low levels of stimulation compar- able incident and reflected waves are predicted. Promi- nent maxima and minima in the sensitivity of the audi- to•y system as a function of frequency, would necessarily arise because of interference between incident and mul-

tiply reflected waves, i.e., audio frequency cochlear resonances would occur. Significantly, the existence of sharp maxima and minirna in the sensitivity of normal hearing, as a function of frequency has been known for some time from psychophysical measurements by Elliot (1958), Van den Brink (1970), Thomas (1975) and Kemp (1976), but this phenomenon has never been adequately explained. The peak to valley sensitivity differences found commonly exceed 6 dB. The frequency spacing of these maxima which occur most commonly between 500 Hz and 3 kHz is of the order of 100 Hz. This frequency interval is consistent with reflection latency of around 10 ms; the same order as the latency of the tail maxima found in acoustic emissions. Correspondence between frequency specific emission latencies [see Figs. 2(e)-2(g)] and psychoacoustical sensitivity.maxima frequencies is good for the individual subjects so far studied. (This work is being reported separately. )

The frequency dispersion apparent in most emission waveforms is in qualitative agreement with the cochlea reflection hypothesis although the magnitude of the latencies observed (e.g., 12 ms at 1 kHz) are up to five times greater than the simplistic model predicts from the known travel times to the "place" of reception. In a developed model, to be reported, proper consideration of the group latency of energy reflected from portions of the basilar membrane with enhanced tuning, allows these latencies to be accommodated.

To summarize, the cochlear reflection hypothesis receives support from the new evidence here and from existing psychoacoustical evidence. Furthermore it cannot be discounted on the grounds of contrary evidence from other direct sources of data.

As to the mechanism which might cause a cochlea "reflection" it is conceivable that the stimulated release of

coherent mechanical energy by the transduction mechanism onto the basilar membrane (Gold, 1048) may serve




to locally modify wave propagation parameters. En- hancement of low level signal acquisition could be the function of this activity. At high levels of stimulation the saturated response of such a bioacoustic mechanism would probably be inconsequential. At very low levels the critically set mechanism might over-react at some frequencies, with the recoil resulting in the creation of a retrograde wave on the basilar membrane eventually appearing in the external auditory meatus, as a "cochlea echo." Between these extremes useful wave amplification by stimulated mechanical energy release might occur, perhaps contributing to the enhancement of cochlear mechanical tuning.

In the absence of a complete understanding of the mode of operation of the sensory cells in the cochlea, it is tempting to suggest that one of the functions of the outer hair cell population is the generation of this mechanical energy. At least, the recent discovery of actinlike pro- teins in the sensory cell hairs (Flock, 1077) supports the contention that the mechanical properties of the cochlea may be partially under physiological control.

IV. CONCLUSIONS

Sound energy appears to be emitted by the auditory system, into the external ear canal, for some tens of milliseconds after impulsive acoustic excitation. The origin of this newly discovered phenomenon remains essentially unknown but a physiologically active mechanism in the cochlea is supported by the evidence that these acoustic emissions have nonlinear characteristics

and are inhibited by damage to the sensory system such as occurs in cochlea deafness. Much more detailed

study is both possible and desirable. If a cochlea origin is confirmed by experiments currently in progress, the technique developed in this study will provide a new avenue for investigation of the auditory system, with ap- plications in both research and audiological medicine (Kemp, 1078).

The motivating hypothesis of this investigation--that partiM reflection of the cochlea wave might be a by- product of the transduction process at low levels--has received support from the experimental results and is therefore worthy of further consideration. If proven it would provide a new insight into the microscopic behavior of the cochlear transduction mechanism which is

not yet adequately understood.

ACKNOWLEDGMENTS

This work was jointly supported by the Department of Health, the Medical Research Council, and the Hospi- tal Board of Governors. The author wishes to acknowl-

edge the valuable contribution made by J. A. Martin, F. R. C. S., D. L. O., and also the many other colleagues involved in this work. Additional thanks are due the

NRDC.

ADDENDUM

Since the submission of this paper, other important results have become available which support the primary finding of evoked acoustic emissions from the normal auditory system.

(i) In joint work with S. D. Anderson of the Institute of Laryngology and Otology (London), stimulated acoustic emissions have been observed in anaesthetized Cyno- molgus monkeys (Macaca irus). Emissions were of similar magnitude to the human response and exhibited similar nonlinearity. Frequency dispersion was significantly less. The response was suppressed by loop diuretic drugs and by noise trauma.

(ii) The emissions evoked by tonal stimuli can be suppressed by a second steady tone. Derived tuning curves show high selectivity such that a eochlear origin at the second filter level is certain.

(iii) Using techniques based on the author's, J.P. Wilson of the Department of Communication, Keele Uni- versity, has been able to confirm the existence of evoked acoustic emissions from human ears (private communication).

Anderson, D. J., Rose, J. E., Hind, J. E., and Brugge, J. F. (1971). "Temporal position of discharges in single auditory nerve fibers within the cycle of a sinewave stimulus," J. Acoust. Soc. Am. 49, 1131-1339.

Bekesy, G. von (1936). "Zur Physik des Mittelobres und iiber das Hf•ren bei fehlerhaftem Trommelfell," Akust. Zh. 1, 13.

Bekesy, G. von (1960). Experiments in Hearing (McGraw- Hill, New York), pp. 510-524.

Blauert, J. von, Laws, P., and Platte, H. J. (1974). "Impuls- verfahren zur Messung von Assenohriibertragungsfunktionen," Acustica 31, 35-41.

Borg, E. (1976). Acoustic admittance and impedance (Williams & Wilkins, Baltimore), pp. 236-299.

Brink, G. van den (1970). Frequency Analysis and Periodicity Detection in Hearing (S•rthoff, Leiden), pp. 362-374.

Douek, E., Gibson, W., and Humphries, K. (1973). "The crossed acoustic response," J. Laryngol. Otol. 87, 711-726.

Elliot, E. (1958). "A Ripple Effect in the Audiogram," Nature 181, 1076.

Flock, A. (1977). Psychophysics and Physiology of Hearing (Academic, London), pp. 15-25.

Gold, T. (1948). "Hearing. II. The physical basis of the ac- tion of the cochlea," Proc. Roy. Soc. B 135, 492-498.

Hall, J. L. (1975). "Nonmonotomic behavior of distortion product 2fl-f2; Psychophysical observations," J. Acoust. Soc. Am. 58, 1046-1050.

Kemp, D. T. (1976). "Active Resonance Systems in Audition," 13th International Congress of Audiology, Abstracts, 64-65.

Kemp, D. T. (1978). U.K. provisional patent No. 5467/78. Kim, D. O., and Molnar, C. E. (1975).' The Nervous System.

Vol. 3. Human Communication and its Disorders (Raven, New York), pp. 57-67.

Kohll;Sffel, L. U. E. (1972). "A study of basilar membrane mechanics I, II, III," Acustica 27, 49-89.

Rhode, W. S. (1971). "Observations of the vibration of the basilar membrane in squirrel monkeys using the Mossbauer technique," J. Acoust. Soc. Am. 49, 1218-1321.

Rhode, W. S., and Robles, L. (1974). "Evidence from Moss- bauer experiments for nonlinear vibration in the cochlea," J. Acoust. Soc. Am. 55, 558-596.

Thomas, I. B. (1975). "Microstructure of the pure-tone threshold," J. Acoust. Soc. Am. 57, 26-27.

Wilson, J.P. (1978). Private communications. Wilson, J.P., and Johnstone, J. R. (1975). "Basilar mem-

brane and middle ear vibration in guinea pig measured by capacitive probe," J. Acoust. Soc. Am. 57, 705-723.

Zwislocki, J. (1952). "Analysis of Middie-Ear Function. Part I: Input Impedance," J. Acoust. Soc. Am. 34, 1514- 1523.



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Stimulated acoustic emissions from within the human ... · Stimulated acoustic emissions from within the human auditory system D. T. Kemp Auditory Perception Research Laboratory,