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Spontaneous otoacoustic emissions in a dog
Hearing Research, 13 (1984) 293-296 Elsevier
HRR
293
00475
Short Communication
Spontaneous otoacoustic emissions in a dog * M.A. Ruggero Deparments
of
I,**, B. Kramek
* and N.C.*Rich
1
’ OtolatyngologV and ’ Veierinaty Clinical Sciences, University of Minnesota, Minneapolis, MN 55455, U.S.A. (Received
1 August
1983; accepted
11 January
1984)
Intense (up to 59 dB SPL) spontaneous otoacoustic emissions are produced by both ears of a young dog. The right ear produces a single, very narrow-band ( -C 4 Hz) emission at about 9100 Hz. Brainstem evoked-response audiometry suggests that this emission is generated near the transition between normal and abnormal regions of the cochlea. spontaneous
acoustic
emission,
brainstem-evoked
response,
cochlea,
Nearly tonal acoustic emissions are detectable in the ear canals of many humans (for a review see [S]). There is general agreement that these spontaneous otoacoustic emissions (SOAEs) originate in the cochlea. While SOAEs appear to be common in humans [12,15], few instances have been reported in other animals: two chinchillas [1,16], one guinea pig [4], one dog [2], and one cat (see p. 133 in discussion following [4]). We report here on the very intense SOAEs produced by both ears of Samson, a young dog. Besides being among the most intense SOAEs ever measured for any species, one of these SOAEs is of interest because of its association with audiometric abnormalities. Samson (an American Eskimo dog, 5 months old when first studied) was brought to the attention of a veterinarian (B. Kramek) after its owners noticed that seemingly continuous tones appeared to emanate from the animal’s ears. In order to obtain quantitative data, the animal was studied under anesthesia on three separate occasions over a period of four months; no further studies were carried out due to the owners’ natural reluctance to submit a pet to possible trauma. After pre-treatPortions of this paper were presented at the 1982 Meeting of the Society for Neuroscience [9]. ** To whom reprint requests should be addressed, at: Department of Otolaryngology, University of Minnesota, Research East, 2630 University Ave. S.E., Minneapolis, MN 55414, U.S.A. l
0378-5955/84/%03.00
0 1984 Elsevier Science Publishers
B.V.
dog
ment with atropine sulfate (0.04 mg/kg), anesthesia was induced with sodium thiamylal (18 mg/kg injected intravenously) and maintained with halothane delivered in oxygen. To record the SOAEs and to present acoustic stimuli an earphone-microphone coupler was inserted into the intact ear canal. The coupler consists of a plastic speculum located in front of a metal-encapsulated Beyer DT-48 earphone. The speculum contains a metal tube with one end terminating at a Knowles EA-1482 miniature microphone and its other end slightly protruding from the speculum tip. The amplified microphone signal was fed to an oscilloscope and to a wave analyzer (Hewlett Packard 3581A) which was swept with selectable frequency spans and bandwidths. Acoustically evoked brainstem electrical responses (BSERs) were measured by means of needle electrodes inserted into the skin overlying the vertex and behind the ear flaps. After suitable amplification these signals were digitized and averaged over 400 repetitions. Acoustic stimuli were digitally generated and computer controlled [lo]. Further details on the sound generation system and other methods may be found in references [lo] and [ll]. Frequency analyses of the sound pressures in the ear canals are shown in the left panels of Fig. 1. The upper left panel (two traces) shows that the right ear produces a single, intense and very narrow-band SOAE centered at 9060 Hz. The half-
294
m
I S.S
t
i 9s
L
1 103
i
11 11.3
1 us
FREQUENCY (KHZ)
4
S
8
FREQUENCY
10
12
14
(KNZ)
Fig. 1. Spontaneous otoacoustic emissions (SOAEs) in the right and left ear canals of a dog (upper and lower panels, respectively). The left panels show acoustic amplitude spectra obtained by passing the microphone output through a wave analyzer, which was swept with a bandwidth of 10 Hz. Two traces are displayed for the right ear, which produces a single emission at 9060 Hz. The left ear (lower left panel) produces multiple emissions, with the most intense at 9450, 10000, 10425 and 10950 I-IL The vertical arrows in the lower right panel indicate the SOAE levels measured at the beginning and at the end of a 3-h recording session. The right panels indicate 3 dB iso-suppression contours (connected open circles): the intensities of externally generated tones, at various frequencies, which reduce the amplitudes of the SOAEs (crosses) by 3 dB. Suppression effects were studied in the left ear (lower right panel) only for the emission at 9450 Hz. In addition to an iso-suppression contour, the upper right panel also displays brainstem evoked response (BSER) pseudo-thresholds: the intensities of 5 ms tone pips required to produce a 2 gV BSER. Note that the SOAE frequency lies in a transition region of the BSER ‘audiogram’, where p~udo-~resholds change from m~erately low at frequencies lower than 8 kHz to quite high above 9 kHz.
power bandwidth, measured from sweeps with the narrowest available setting of the wave analyzer (3 Hz), was at most 4 Hz. The center frequency of this SOAE drifted somewhat within a range of 8915 Hz to 9180 Hz. Its level (re 0.0002 dyne/cm*) averaged 55 dB SPL during the first recording session and 49 dB SPL three months later. The emission produced by the left ear (lower left panel) had a complex spectrum; the four major frequency components were centered at 9450, 10000, 10425 and 10950 Hz. The bandwidths of these components were as narrow as that of the SOAE in the
right ear. Their levels were variable, changing by as much as 33 dB during a single 3-h recording session. The component at 9450 Hz initially measured 52 dB SPL; 2 h later it had grown to 59 dB SPL but it then diminished over the next hour to only 26 dB. We are uncertain whether these changes were spontaneous or resulted from experimental exposure to intense tones (see below). The effects of externally generated tones on the SOAEs were studied as a function of stimulus frequency and level. It has been well documented that some acoustic stimuli are capable of both
295
suppressing and changing the frequencies of SOAEs [4,11,13-161. Taking advantage of the high SOAE levels, we were able to lock the wave analyzer passband (in this case, 30 Hz wide) to the SOAE frequency during suppressor presentations. This allowed recording, independently, the amount of suppression and the frequency changes induced by the external tone. Increases in SOAE frequency as large as 30-45 Hz were common, and only rarely was the SOAE frequency reduced. In the right-hand panels of Fig. 1 suppressive effects are depicted by the connected open circles, which indicate the stimulus frequencies and levels required to reduce the SOAE amplitude by 3 dB. For the right ear (upper right panel), the locus of these symbols is broadly tuned, with the most effective suppressing frequencies being lower than the SOAE frequency. This is an uncommon finding; previously published suppression curves for SOAEs are narrowly tuned and displaced (if at all) toward frequencies higher than that of the SOAE [4,11,13-161. For the left ear, the suppression curve for the SOAE at 9450 Hz (lower right panel, cross) has a maximum in a frequency region just above the frequency region of the SOAE complex; although a complete suppression curve could not be measured, due to time limitations, it would appear that minima probably exist both above and below the SOAE frequencies. Again, this shape contrasts with those of most previously reported SOAE suppression curves, which have a single minimum; however, a widely-tuned two-lobed curve - with two minima more than an octave apart - has been described for a guinea pig [4]. While no further data could be gathered in the left ear, we were able to measure brainstem potentials evoked by tone-pip stimulation of the right ear (filled symbols, upper right panel). An isoresponse criterion of 2 PV was used to estimate relative sensitivity as a function of stimulus frequency. The resulting ‘audiogram’ has a sharp transition (over a span of less than 3 kHz) between frequency regions with moderately low pseudothresholds (below 8 kHz) and regions with high pseudo-thresholds (above 9 kHz). The transition region between moderate and high thresholds encompasses the SOAE frequency. In the absence of BSER audiometric standards for the dog, the fact that behavioral audiometric thresholds [3] are con-
stant (within 10 dB) in the frequency range l-16 kHz appears to indicate that the sharp transition seen in Samson’s right ear is abnormal, and that the thresholds above 8 kHz are substantially elevated, presumably as a result of cochlear pathology. This conclusion is supported by the reasonably good correspondence found between BSER and behavioral thresholds in such species as the chinchilla [6]. It is noteworthy that the minimum in the suppression curve corresponds to a frequency region (6-7 kHz) with relatively low audiometric pseudo-thresholds. The displacement of the suppression curve toward frequencies lower than that of the SOAE might thus be explained as resulting from the spatial distribution of presumed cochlear pathology: high frequency regions (suffering severe hair cell loss or other dysfunction) are deficient in their ability to suppress the SOAE. The unusual shape of the suppression curve for the left ear might similarly result from a non-uniform pattern of hair cell loss consisting of substantial damage in the 11 kHz region with lesser dysfunction elsewhere. In a previous publication [ll] we presented data on the first author’s right ear, in which a SOAE is associated with an audiometric notch. We also noted the occurrence of several other reports in the literature of cases of association of SOAEs with apparent [5,7,13,14] or demonstrated ([16]; see also [l]) cochlear pathology and suggested a causal relationship between localized cochlear damage and the origin of both spontaneous and impulsively-evoked otoacoustic emissions. A similar suggestion has been recently put forth by Clark et al. [l]. According to our hypothesis, SOAEs arise in (or near) relatively normal regions of the organ of Corti immediately adjacent to regions of outer hair cell loss. The data for the right ear of the dog, Samson, are consistent with this hypothesis. Acknowledgements We thank Samson’s owners, Mary and John Morris, for making their pet available for study. Carolyn Reckman typed the manuscript. This work was supported by NINCDS Grant NS12125. References 1 Clark W.W.,Kim, D.O., Bohne, B.A. and Zurek, P.M. (1983): Spontaneous otoacoustic emissions from cKnckl_
2 3
4
5
6
7
8
9
las: I. Comparison of otoacoustic observations with cochlear histopathology. Assoc. Res. Otolaryngol., Abstracts, Midwinter Meeting, 1983, p. 106. Decker, T.N. and Fritsch, J.H. (1982): Objective tinnitus in the dog. J. Am. Vet. Med. Assoc. 180, 74. Dworkin, S., Katzman, J., Hutchinson, G.A. and McCabe, J.R. (1940): Hearing acuity of animals as measured by conditioning methods. J. Exp. Psychol. 26, 281-298. Evans, E.F., Wilson, J.P. and Borerwe, T.A. (1981): Animal models of tinnitus. In: Tinnitus, pp. 108-129 (discussion: pp. 130-138). Editors: D. Evered and G. Lawrenson. Pitman Books Ltd., London (Ciba Found. Symp. 85). Glanville, J.D., Coles, R.R.A. and Sullivan, B.M. (1971): A family with high-tonal objective tinnitus. J. Laryngol. Otol. 85, l-10. Henderson, D., Hamernik, R.P., Woodford, C., Sitler, R.W. and Salvi, R. (1973): Evoked-response audibility curve of the chinchilla. J. Acoust. Sot. Am. 54, 1099-1101. Huizing, E.H. and Spoor, A. (1973): An unusual type of tinnitus. Production of a high tone by the ear. Arch. Otolaryngol. 98, 134-136. McFadden, D. and Wightman, F.L. (1983): Audition: some relations between normal and pathological hearing. Ann. Rev. Psycho]. 34, 95-128. Ruggero, M.A., Kramek, B. and Rich, N.C. (1982):
10
11
12
13
14
15
Otoacoustic emissions in man and dog: association with cochlear pathology. Sot. Neurosci. Abstr. 8, 43. Ruggero, M.A. and Rich, N.C. (1983): Chinchilla auditory nerve responses to low frequency tones. J. Acoust. Sot. Am. 73, 2096-2108. Ruggero, M.A., Rich, N.C. and Freyman, R. (1983): Spontaneous and impulsively-evoked otoacoustic emissions: indicators of cochlear pathology? Hearing Res. 10, 283-300. Tyler, R.S. and Conrad-Armes, D. (1982): Spontaneous acoustic cochlear emissions and sensorineural tinnitus. Br. J. Audio]. 16, 193-194. Wilson, J.P. (1980): Evidence for a cochlear origin for acoustic reemissions, threshold fine-structure and tonal tinnitus. Hearing Res. 2, 233-252. Wilson, J.P. and Sutton, G.J. (1981): Acoustic correlates of tonal tinnitus. In: Tinnitus, pp. 82-107. Editors: D. Evered and G. Lawrenson. Pitman Books Ltd., London (Ciba Found. Symp. 85). Zurek, P.M. (1981): Spontaneous narrowband acoustic signals emitted by human ears. J. Acoust. Sot. Am. 69, 514-523.
16 Zurek, P.M. and Clark, W.W. (1981): Narrow-band acoustic signals emitted by chinchilla ears after noise exposure. J. Acoust. Sot. Am. 70. 446-450.
HRR
293
00475
Short Communication
Spontaneous otoacoustic emissions in a dog * M.A. Ruggero Deparments
of
I,**, B. Kramek
* and N.C.*Rich
1
’ OtolatyngologV and ’ Veierinaty Clinical Sciences, University of Minnesota, Minneapolis, MN 55455, U.S.A. (Received
1 August
1983; accepted
11 January
1984)
Intense (up to 59 dB SPL) spontaneous otoacoustic emissions are produced by both ears of a young dog. The right ear produces a single, very narrow-band ( -C 4 Hz) emission at about 9100 Hz. Brainstem evoked-response audiometry suggests that this emission is generated near the transition between normal and abnormal regions of the cochlea. spontaneous
acoustic
emission,
brainstem-evoked
response,
cochlea,
Nearly tonal acoustic emissions are detectable in the ear canals of many humans (for a review see [S]). There is general agreement that these spontaneous otoacoustic emissions (SOAEs) originate in the cochlea. While SOAEs appear to be common in humans [12,15], few instances have been reported in other animals: two chinchillas [1,16], one guinea pig [4], one dog [2], and one cat (see p. 133 in discussion following [4]). We report here on the very intense SOAEs produced by both ears of Samson, a young dog. Besides being among the most intense SOAEs ever measured for any species, one of these SOAEs is of interest because of its association with audiometric abnormalities. Samson (an American Eskimo dog, 5 months old when first studied) was brought to the attention of a veterinarian (B. Kramek) after its owners noticed that seemingly continuous tones appeared to emanate from the animal’s ears. In order to obtain quantitative data, the animal was studied under anesthesia on three separate occasions over a period of four months; no further studies were carried out due to the owners’ natural reluctance to submit a pet to possible trauma. After pre-treatPortions of this paper were presented at the 1982 Meeting of the Society for Neuroscience [9]. ** To whom reprint requests should be addressed, at: Department of Otolaryngology, University of Minnesota, Research East, 2630 University Ave. S.E., Minneapolis, MN 55414, U.S.A. l
0378-5955/84/%03.00
0 1984 Elsevier Science Publishers
B.V.
dog
ment with atropine sulfate (0.04 mg/kg), anesthesia was induced with sodium thiamylal (18 mg/kg injected intravenously) and maintained with halothane delivered in oxygen. To record the SOAEs and to present acoustic stimuli an earphone-microphone coupler was inserted into the intact ear canal. The coupler consists of a plastic speculum located in front of a metal-encapsulated Beyer DT-48 earphone. The speculum contains a metal tube with one end terminating at a Knowles EA-1482 miniature microphone and its other end slightly protruding from the speculum tip. The amplified microphone signal was fed to an oscilloscope and to a wave analyzer (Hewlett Packard 3581A) which was swept with selectable frequency spans and bandwidths. Acoustically evoked brainstem electrical responses (BSERs) were measured by means of needle electrodes inserted into the skin overlying the vertex and behind the ear flaps. After suitable amplification these signals were digitized and averaged over 400 repetitions. Acoustic stimuli were digitally generated and computer controlled [lo]. Further details on the sound generation system and other methods may be found in references [lo] and [ll]. Frequency analyses of the sound pressures in the ear canals are shown in the left panels of Fig. 1. The upper left panel (two traces) shows that the right ear produces a single, intense and very narrow-band SOAE centered at 9060 Hz. The half-
294
m
I S.S
t
i 9s
L
1 103
i
11 11.3
1 us
FREQUENCY (KHZ)
4
S
8
FREQUENCY
10
12
14
(KNZ)
Fig. 1. Spontaneous otoacoustic emissions (SOAEs) in the right and left ear canals of a dog (upper and lower panels, respectively). The left panels show acoustic amplitude spectra obtained by passing the microphone output through a wave analyzer, which was swept with a bandwidth of 10 Hz. Two traces are displayed for the right ear, which produces a single emission at 9060 Hz. The left ear (lower left panel) produces multiple emissions, with the most intense at 9450, 10000, 10425 and 10950 I-IL The vertical arrows in the lower right panel indicate the SOAE levels measured at the beginning and at the end of a 3-h recording session. The right panels indicate 3 dB iso-suppression contours (connected open circles): the intensities of externally generated tones, at various frequencies, which reduce the amplitudes of the SOAEs (crosses) by 3 dB. Suppression effects were studied in the left ear (lower right panel) only for the emission at 9450 Hz. In addition to an iso-suppression contour, the upper right panel also displays brainstem evoked response (BSER) pseudo-thresholds: the intensities of 5 ms tone pips required to produce a 2 gV BSER. Note that the SOAE frequency lies in a transition region of the BSER ‘audiogram’, where p~udo-~resholds change from m~erately low at frequencies lower than 8 kHz to quite high above 9 kHz.
power bandwidth, measured from sweeps with the narrowest available setting of the wave analyzer (3 Hz), was at most 4 Hz. The center frequency of this SOAE drifted somewhat within a range of 8915 Hz to 9180 Hz. Its level (re 0.0002 dyne/cm*) averaged 55 dB SPL during the first recording session and 49 dB SPL three months later. The emission produced by the left ear (lower left panel) had a complex spectrum; the four major frequency components were centered at 9450, 10000, 10425 and 10950 Hz. The bandwidths of these components were as narrow as that of the SOAE in the
right ear. Their levels were variable, changing by as much as 33 dB during a single 3-h recording session. The component at 9450 Hz initially measured 52 dB SPL; 2 h later it had grown to 59 dB SPL but it then diminished over the next hour to only 26 dB. We are uncertain whether these changes were spontaneous or resulted from experimental exposure to intense tones (see below). The effects of externally generated tones on the SOAEs were studied as a function of stimulus frequency and level. It has been well documented that some acoustic stimuli are capable of both
295
suppressing and changing the frequencies of SOAEs [4,11,13-161. Taking advantage of the high SOAE levels, we were able to lock the wave analyzer passband (in this case, 30 Hz wide) to the SOAE frequency during suppressor presentations. This allowed recording, independently, the amount of suppression and the frequency changes induced by the external tone. Increases in SOAE frequency as large as 30-45 Hz were common, and only rarely was the SOAE frequency reduced. In the right-hand panels of Fig. 1 suppressive effects are depicted by the connected open circles, which indicate the stimulus frequencies and levels required to reduce the SOAE amplitude by 3 dB. For the right ear (upper right panel), the locus of these symbols is broadly tuned, with the most effective suppressing frequencies being lower than the SOAE frequency. This is an uncommon finding; previously published suppression curves for SOAEs are narrowly tuned and displaced (if at all) toward frequencies higher than that of the SOAE [4,11,13-161. For the left ear, the suppression curve for the SOAE at 9450 Hz (lower right panel, cross) has a maximum in a frequency region just above the frequency region of the SOAE complex; although a complete suppression curve could not be measured, due to time limitations, it would appear that minima probably exist both above and below the SOAE frequencies. Again, this shape contrasts with those of most previously reported SOAE suppression curves, which have a single minimum; however, a widely-tuned two-lobed curve - with two minima more than an octave apart - has been described for a guinea pig [4]. While no further data could be gathered in the left ear, we were able to measure brainstem potentials evoked by tone-pip stimulation of the right ear (filled symbols, upper right panel). An isoresponse criterion of 2 PV was used to estimate relative sensitivity as a function of stimulus frequency. The resulting ‘audiogram’ has a sharp transition (over a span of less than 3 kHz) between frequency regions with moderately low pseudothresholds (below 8 kHz) and regions with high pseudo-thresholds (above 9 kHz). The transition region between moderate and high thresholds encompasses the SOAE frequency. In the absence of BSER audiometric standards for the dog, the fact that behavioral audiometric thresholds [3] are con-
stant (within 10 dB) in the frequency range l-16 kHz appears to indicate that the sharp transition seen in Samson’s right ear is abnormal, and that the thresholds above 8 kHz are substantially elevated, presumably as a result of cochlear pathology. This conclusion is supported by the reasonably good correspondence found between BSER and behavioral thresholds in such species as the chinchilla [6]. It is noteworthy that the minimum in the suppression curve corresponds to a frequency region (6-7 kHz) with relatively low audiometric pseudo-thresholds. The displacement of the suppression curve toward frequencies lower than that of the SOAE might thus be explained as resulting from the spatial distribution of presumed cochlear pathology: high frequency regions (suffering severe hair cell loss or other dysfunction) are deficient in their ability to suppress the SOAE. The unusual shape of the suppression curve for the left ear might similarly result from a non-uniform pattern of hair cell loss consisting of substantial damage in the 11 kHz region with lesser dysfunction elsewhere. In a previous publication [ll] we presented data on the first author’s right ear, in which a SOAE is associated with an audiometric notch. We also noted the occurrence of several other reports in the literature of cases of association of SOAEs with apparent [5,7,13,14] or demonstrated ([16]; see also [l]) cochlear pathology and suggested a causal relationship between localized cochlear damage and the origin of both spontaneous and impulsively-evoked otoacoustic emissions. A similar suggestion has been recently put forth by Clark et al. [l]. According to our hypothesis, SOAEs arise in (or near) relatively normal regions of the organ of Corti immediately adjacent to regions of outer hair cell loss. The data for the right ear of the dog, Samson, are consistent with this hypothesis. Acknowledgements We thank Samson’s owners, Mary and John Morris, for making their pet available for study. Carolyn Reckman typed the manuscript. This work was supported by NINCDS Grant NS12125. References 1 Clark W.W.,Kim, D.O., Bohne, B.A. and Zurek, P.M. (1983): Spontaneous otoacoustic emissions from cKnckl_
2 3
4
5
6
7
8
9
las: I. Comparison of otoacoustic observations with cochlear histopathology. Assoc. Res. Otolaryngol., Abstracts, Midwinter Meeting, 1983, p. 106. Decker, T.N. and Fritsch, J.H. (1982): Objective tinnitus in the dog. J. Am. Vet. Med. Assoc. 180, 74. Dworkin, S., Katzman, J., Hutchinson, G.A. and McCabe, J.R. (1940): Hearing acuity of animals as measured by conditioning methods. J. Exp. Psychol. 26, 281-298. Evans, E.F., Wilson, J.P. and Borerwe, T.A. (1981): Animal models of tinnitus. In: Tinnitus, pp. 108-129 (discussion: pp. 130-138). Editors: D. Evered and G. Lawrenson. Pitman Books Ltd., London (Ciba Found. Symp. 85). Glanville, J.D., Coles, R.R.A. and Sullivan, B.M. (1971): A family with high-tonal objective tinnitus. J. Laryngol. Otol. 85, l-10. Henderson, D., Hamernik, R.P., Woodford, C., Sitler, R.W. and Salvi, R. (1973): Evoked-response audibility curve of the chinchilla. J. Acoust. Sot. Am. 54, 1099-1101. Huizing, E.H. and Spoor, A. (1973): An unusual type of tinnitus. Production of a high tone by the ear. Arch. Otolaryngol. 98, 134-136. McFadden, D. and Wightman, F.L. (1983): Audition: some relations between normal and pathological hearing. Ann. Rev. Psycho]. 34, 95-128. Ruggero, M.A., Kramek, B. and Rich, N.C. (1982):
10
11
12
13
14
15
Otoacoustic emissions in man and dog: association with cochlear pathology. Sot. Neurosci. Abstr. 8, 43. Ruggero, M.A. and Rich, N.C. (1983): Chinchilla auditory nerve responses to low frequency tones. J. Acoust. Sot. Am. 73, 2096-2108. Ruggero, M.A., Rich, N.C. and Freyman, R. (1983): Spontaneous and impulsively-evoked otoacoustic emissions: indicators of cochlear pathology? Hearing Res. 10, 283-300. Tyler, R.S. and Conrad-Armes, D. (1982): Spontaneous acoustic cochlear emissions and sensorineural tinnitus. Br. J. Audio]. 16, 193-194. Wilson, J.P. (1980): Evidence for a cochlear origin for acoustic reemissions, threshold fine-structure and tonal tinnitus. Hearing Res. 2, 233-252. Wilson, J.P. and Sutton, G.J. (1981): Acoustic correlates of tonal tinnitus. In: Tinnitus, pp. 82-107. Editors: D. Evered and G. Lawrenson. Pitman Books Ltd., London (Ciba Found. Symp. 85). Zurek, P.M. (1981): Spontaneous narrowband acoustic signals emitted by human ears. J. Acoust. Sot. Am. 69, 514-523.
16 Zurek, P.M. and Clark, W.W. (1981): Narrow-band acoustic signals emitted by chinchilla ears after noise exposure. J. Acoust. Sot. Am. 70. 446-450.