With Sentiero you get the best diagnostic OAE functions in a simple to use handheld device.

Having the experience in house is a major advantage when designing new algorithms. PATH medical’s long term experience derives from the same core development team who brought to you the first EchoScreen and also the new AccuScreen for neonatal hearing screening.
Using this experience in designing robust algorithms and easy to use test modules, we were able to use the processing power of the next generation digital signal processors to implement reliable diagnostic solutions in a unique handheld device. 


To provide a short overview over OAE measurements you can download our How-To Manual HERE.

Types of OAEs

The discovery of otoacoustic emissions (OAEs) (Kemp, 1978) has produced a totally new tool for diagnosing cochlear function. OAEs are the by-product of the non-linear sound amplification process in the cochlea (Davis, 1983, Dallos, 1992). In sound-conductive hearing-loss, where both the stimulus and the response amplitude are reduced, OAEs are difficult to measure, even with a mild sound-conductive hearing-loss (Margolis, 2002). Along with tympanometry and auditory brain stem responses, OAEs can differentiate between middle-ear, cochlear, and neural disorders. OHCs are reported to be impaired by sound overexposure, ototoxic drugs (e.g., therapeutic antibiotics), infections (e.g., meningitis, mumps, materno-fetal infection), and anoxia (e.g., birth trauma), or to be partly missing in genetic hearing-loss. OHC impairment results in a loss of sensitivity and frequency selectivity of the hearing organ (Liberman and Dodds, 1984). OAEs, as a by-product of cochlear non-linear sound amplification, then appear with reduced amplitude or disappear (Mills and Rubel, 1994).


Spontaneous OAEs (SOAEs) appear without any sound stimulation at a few frequencies in a healthy cochlea and seem to be a direct consequence of the cellular force generation of outer hair cells (OHCs) (Zwicker and Schloth, 1984, Burns et al., 1998, Jülicher et al., 2003). SOAEs do not appear in each normally hearing subject and are present in about a half of the normally hearing population, with a distinctly higher prevalence in women than in men (Bilger et al., 1990, Penner et al., 1993, Penner and Zhang, 1997). SOAEs are therefore not suited for audiological diagnostics.

Evoked OAEs are generated by external sounds, either by transient (clicks and tone bursts) or stationary stimuli (tones). Transiently evoked OAEs (TEOAEs), elicited by clicks or tone-bursts, represent the sum of the pulse responses of OHCs along the cochlea. TEOAEs already disappear at mild hearing losses and are therefore a suitable tool for newborn hearing screening which is a selection procedure for deciding whether further diagnostics are advised or not (Robinette and Glattke, 2002). Distortion product OAEs (DPOAEs) represent cubic distortions of OHCs when stimulated simultaneously by two tones f1 (lower frequency) and f2 (higher frequency). DPOAEs arise directly from the frequency-selective compressive non-linearity of OHCs (Brownell et al., 1985, Kemp et al., 1986). The two tones interact in the cochlea close to the characteristic place of f2. Thus, DPOAEs can be applied as a probe for frequency-specific assessment of cochlear dysfunction at the f2 place. In humans the 2f1-f2 distortion component yields the highest amplitude and is therefore primarily used in audiological diagnostics (Gorga et al., 2000a). DPOAEs are reported to be measurable at a cochlear hearing-loss of up to 40-50 dB HL, representing approximately the range of the cochlear amplifier (Davis, 1983, Ruggero et al., 1997). TEOAEs and DPOAEs are present in essentially every normally hearing subject.

Stimulus frequency OAEs (SFOAEs) are elicited by one continuous, low-level sinusoidal signal. Recording of SFOAEs is difficult because stimulus and response superimpose.


Where as TEOAEs more qualitatively assess cochlear function, DPOAEs provide quantitative information about the range and operational characteristics of the cochlear amplifier (CA), i.e. sensitivity, compression, and frequency selectivity. There are several DPOAE measures which are used for assessing the functioning of the CA:


DPOAE-grams plot the DPOAE level Ldp as a function of f2 (the main DPOAE generation site) for a selected combination of the primary-tone levels L1 and L2. It should be emphasized that DPOAE-grams reflect CA sensitivity best when recorded at close-to threshold stimulus levels (Janssen et al., 1998, Kummer et al., 1998, Dorn et al., 2001). DPOAE-grams when recorded with narrow frequency spacing of f2 (DPOAE fine-structure) may give information about the fine-structure of the behavioral pure-tone threshold. However, due to the superposition of the second DPOAE source (He and Schmiedt, 1993, He and Schmiedt, 1996, He and Schmiedt, 1997, Shera and Guinan, 1999) the correlation between the two measures is not clear. In normal hearing (normal CA), DPOAE-grams are close to each other at high and more separated at low stimulus levels reflecting cochlear non-linear sound processing. In cochlear hearing-loss ears (impaired CA), DPOAE-grams are more separated even at high stimulus levels, revealing loss of CA compression (Janssen et al., 1998, Kummer et al., 1998, Neely et al., 2003).


DPOAE level I/O-functions plot the DPOAE level Ldp as a function of primary-tone level L2 for a selected f2 and thus reflect CA dynamics at the f2 place in the cochlea (Dorn et al., 2001). In normal hearing, in response to low-level stimuli, DPOAE level I/O-functions exhibit steep slopes, while at high stimulus levels slopes decrease, thus mirroring the strong amplification at low and decreasing amplification (saturation) at moderate sound levels. However, this is only true when a stimulus setting (e.g. the “scissor” paradigm) is used which accounts for the different compression of the primary-tones at the f2 place (Kummer et al., 2000).


DPOAE pressure I/O-functions plot the DPOAE pressure pdp (instead of the DPOAE level Ldp) as a function of the primary-tone level L2. Due to the logarithmic dependency of the DPOAE level on the primary-tone level there is a linear dependency between DPOAE pressure pdp and primary-tone level L2 (Boege and Janssen, 2002). Thus, DPOAE data can easily be fitted by linear regression analysis. The intersection point of the linear regression line with the L2-axis at pdp = 0 Pa can then serve as an estimate of the stimulus level at the DPOAE threshold, i.e., Ldpth (Boege and Janssen, 2002, Gorga et al., 2003).

Estimated threshold level Ldpth when plotted across frequency f2 provides a measure for estimating CA threshold at the f2-place.


DPOAE slope, calculated from DPOAE level I/O-functions (e.g., between stimulus levels L2 of 40 and 60 dB SPL), indicates CA compression. When plotted across frequency, a slope profile can be established. In ears with cochlear hearing-loss, the slope s of the DPOAE level I/O-function increases with increasing hearing-loss indicating loss of CA compression (Janssen et al., 1998, Kummer et al., 1998, Müller and Janssen, 2004, Neely et al., 2003).

There are some limitations when using DPOAE measures for assessing peripheral sound processing. First, electric microphone noise, physiological noise (breathing, blood flow) and external acoustic noise do not allow OAE measurements at very low stimulus levels. Especially below 0.5 kHz, reliable OAE measurements are not possible even at high stimulus levels. Second, because of the limited frequency range of the sound probe’s electro-acoustic transducers, high-frequency OAE measurements are difficult without using specialized devices. Third, standing waves in the outer ear canal make a defined stimulus setting difficult to obtain. Fourth, beside the main DPOAE source at f2, a secondary DPOAE source is present at the 2f1-f2 place, which interacts with the main source constructively or destructively at the f2 place (Whitehead et al., 1992, Brown et al., 1996, Shera and Guinan, 1999). Therefore, the DPOAE does not exactly reflect OHC function at the f2 place. When all these factors are considered, it is easy to see how OAE measures can be misinterpreted.


Clinical applications of TEOAEs/DPOAEs

30 years after the discovery of OAEs, OAE measurements are a standard part of the audiometric diagnostic test battery. OAEs are a means of acquiring non-invasive information about disorders of an essential element of sound processing, i.e., the cochlear amplifier (CA), and hence allow assessment of loss of sensitivity, compression, and frequency-selectivity of the hearing organ. Like tympanometry, which examines the status of the middle-ear, OAEs are a fast and easy-to-handle method for examining cochlear function objectively. OAEs extend the objective audiometric test battery. They allow a direct examination of cochlear function. Subjective tests are only able to assess disorders of sound processing as a whole. Tympanometry, OAEs, and auditory brain stem responses (ABRs, ASSRs), in combination, allow for a differentiation between sound-conductive, cochlear, and neural hearing-loss. Minute changes in hearing capability are detectable by OAEs.

There are four main OAE applications in clinical diagnostics:

  • Newborn hearing screening
  • Confirmation of a cochlear hearing-loss along with tympanometry and auditory brain stem responses
  • Quantitative evaluation of hearing-loss and recruitment for providing hearing aid fitting parameters
  • Detecting beginning cochlear impairment during noise exposure or ototoxic drug administration


Newborn Hearing Screening is a selection procedure used to decide whether further diagnostics are advised or not (Wilson and Jungner, 1968). Consequently, a screening decision is binary: “pass” (negative finding, no diagnostics necessary), or “refer” (positive finding, follow-up diagnostics advised). The requirements for screening are different from those for diagnostics. Because screening is performed in large populations, the devices used typically provide automatic evaluation rather than rely on an expert’s judgement.

A screening test should be performed as quickly as possible. Therefore, the respective methods must avoid long preparation times and the test should stop automatically if the desired quality of the result is achieved. TEOAE and DPOAE are widely regarded as being suitable for screening in newborns and infants, as they are not present in the case of outer hair cell (OHC) dysfunction (e.g. Kemp and Ryan, 1991, Gorga et al., 2000b, Norton et al., 2000b, Norton et al., 2000a). The premise for this approach is that inner ear hearing-loss always includes OHC damage or malfunction. Additionally, significant conductive losses due to Eustachian tube dysfunction and/or amniotic fluid in the tympanic cavity also cause “refer” results under screening conditions.

DPOAE newborn hearing screening is usually performed in the mid-frequency region (e.g. between 1.5 and 4 kHz). High-frequency testing is less reliable, due to the standing-wave problem and the limitation of the electro-acoustic transducer. Below 1 kHz, the SNR is insufficient, so that also low-frequency testing is inadvised. DPOAEs are elicited at different primary-tone levels, so that a multi-frequency and multi-level test procedure is provided. Extrapolated DPOAE I/O-functions are used to estimate hearing thresholds (Boege and Janssen, 2002, Gorga et al., 2003).

A therapy for hearing disorder can be developed only after knowing which stage of the auditory pathway is impaired. Psychoacoustic tests are able to differentiate between sound-conductive and sensorineural hearing-loss by evaluating the difference between sound and bone-conductive pure-tone thresholds. The discrimination of a sensorineural hearing-loss, i.e., the differentiation between a sensory (cochlear) and a neural disorder with subjective testing is unreliable, because the validity of these tests (Short Increment Sensitivity Index (SISI), Fowler, Carhart) is limited. Moreover, in non-cooperative patients or infants, psychoacoustic tests can not be performed. In such cases, only objective tests help in achieving the goal of determining end organ integrity. Using tympanometry, OAEs, and ABRs/ASSRs, the site of the impairment in the auditory pathway can be ascertained with high reliability.

OAEs are used primarily as function detectors in clinical practice. As a general rule, if there is a suspicion of a hearing disorder, the measurement of OAEs should be used as the first audiological test. It is fast and helps to confirm normal middle-ear and cochlear function. This is the case if OAEs are present over a wide frequency range. If OAEs are absent, then middle-ear or cochlear (OHC) pathology is likely. OAEs then should be followed by tympanometry. If the tympanogram is normal and OAEs are absent, then a cochlear disorder is likely. If the tympanogram is abnormal, a sound-conductive hearing-loss is likely. If both the tympanogram and OAEs are normal, ABRs/ASSRs are needed to reveal whether there is a cochlear (inner hair cell) or neural pathology. For example, in auditory neuropathy, where synchronization of neural activity is malfunctioning (either due to inner hair cell synaptic or neural dysfunction), normal OAEs and abnormal ABRs occur (Doyle et al., 1998, Starr et al., 1996). OAEs are, of course, also a suitable means for testing individuals, who are only simulating a hearing-loss.

Especially for hearing-aid adjustment in infants, a quantitative evaluation of the hearing-loss and recruitment is necessary. When elicited by high stimulus levels (which is common in clinical practice), TEOAEs are absent at a cochlear hearing-loss exceeding 20 dB HL, whereas DPOAEs are absent only at a cochlear hearing-loss exceeding 40-50 dB HL. Thus, when using TEOAEs and DPOAEs elicited at high stimulus levels only, a rough estimate of the hearing-loss is possible. For example, when TEOAEs are absent and DPOAEs are present, then the hearing-loss is suggested to be not more than 30 dB HL.

In principle, both DPOAEs and TEOAEs allow acquisition of frequency-specific information about a hearing-loss problem. When stimulating the ear with a click or a tone-burst, almost all OHCs along the cochlear partition, or a part of them (the site in the cochlea depending on the carrier frequency of the tone-burst), are excited. Due to frequency dispersion in the cochlea, a specific component of the TEOAE response can be directly traced to a specific frequency component of the transient signal. As the basilar membrane at basal sites moves faster than at more apical sites, high-frequency TEOAE components stem from basal cochlear sites, whereas low-frequency TEOAE components come from more apical ones. However, due to the fact that the stimulus and the high-frequency TEOAE components superimpose (and therefore have to be canceled during TEOAE recording), TEOAEs fail to measure cochlear function above 4 kHz. In contrast, DPOAEs have the advantage of being capable of superior detection of a high-frequency hearing-loss. This is due to the fact that stimulus (primary-tones at f2 and f1) and response (2f1-f2) do not superimpose. However, calibration errors due to standing waves in the outer-ear canal, can lead to misinterpretation of DPOAE results above 6 kHz.


The relation between OAE level and auditory threshold – or rather the lack of it – is strongly debated. Earlier, it was common to define confidence limits to determine the degree of certainty with which any measured response could be assigned to either normal or impaired hearing (Gorga et al., 1996, Gorga et al., 2000a), or to define a ‘DPOAE detection threshold’ as the stimulus level at which the response equalled the noise present in the instrument (Dorn et al., 2001). However, since the noise is of technical origin (e.g., microphone noise) the threshold evaluated in this way does not match the behavioural threshold. A more relevant measure is the intersection point between the extrapolated DPOAE I/O-function and the primary-tone level axis at which the response’s sound pressure is zero and hence at which OHCs are inactive (Boege and Janssen, 2002, Gorga et al., 2003). A linear dependency between the DPOAE sound pressure and the primary-tone sound pressure level is present (Boege and Janssen, 2002) when using the “scissor” paradigm for eliciting DPOAEs (Kummer et al., 2000). Because of the linear dependency, DPOAE data can be easily fitted by linear regression analysis in a semi-logarithmic plot, where the intersection point of the regression line with the L2 primary-tone level axis at pdp = 0 Pa can thus serve as an estimate of the DPOAE threshold. The estimated DPOAE threshold Ldpth is independent of noise and seems to be more closely related to behavioural threshold than the DPOAE detection threshold (Boege and Janssen, 2002, Gorga et al., 2003).

When converting DPOAE sound pressure level (SPL) to hearing level (HL), the estimated DPOAE thresholds can be plotted in an audiogram form (DPOAE-audiogram). DPOAE-audiograms can be applied in babies with a refer result in newborn hearing screening to reveal a transitory sound-conductive hearing loss due to Eustachian tube dysfunction and/or amniotic fluid in the tympanic cavity or to confirm a persisting cochlear hearing loss in follow-up diagnostics. Test time for establishing a DPOAE-audiogram takes a couple of minutes. DPOAE-audiograms are an alternative method to behavioural audiometry or frequency-specific evoked response audiometry (tone burst auditory brain-stem responses (ABRs), auditory steady state responses (ASSRs) in case of mild and moderate hearing loss. In contrast to TEOAE, common DPOAE elicited at high primary tone levels, and click-evoked ABR, which only qualitatively describe the hearing loss, DPOAE-audiograms are able to quantitatively assess the hearing loss at distinct frequencies. This is an essential advantage over tone burst ABR or ASSR. Predicting hearing loss at five frequencies by tone burst ABR or ASSR takes more than half an hour. Thus, DPOAE audiograms can serve as an advanced tool for bridging the gap between screening and audiological testing in pediatric audiology.

The objective of hearing screening in childhood is to identify hearing impairment which are not obvious or apparent and will cause significant disability or handicap for the child concerned. Late identification may compound problems in communication, language acquisition and affect other areas of development. Contrary to newborn hearing screening, preschool hearing screening tests should provide more frequency-specific and quantitative information on the hearing loss. Extrapolated DPOAE I/O-functions provide a frequency-specific and quantitative assessment of the hearing loss.


The DPOAE growth rate steepens when the auditory threshold is elevated (Janssen et al., 1998, Kummer et al., 1998, Boege and Janssen, 2002, Gorga et al., 2003, Neely et al., 2003) and differs significantly between hearing-loss classes (their width being 10 dB) (Janssen et al., 2005b). The slope of DPOAE I/O-functions is reported to be related to the slope of the loudness functions (Neely et al., 2003, Müller and Janssen, 2004). Thus, the slope of DPOAE I/O-functions is suggested to allow a quantitative assessment of CA compression and hence provide an objective recruitment test. Especially for hearing aid adjustment in children, a quantitative evaluation of the hearing loss and recruitment is necessary. With the help of the DPOAE audiogram and the DPOAE growth characteristic quantities of the cochlear impaired ear and hence additional parameters for a non-cooperative hearing aid adjustment can be provided (Müller and Janssen, 2004).

OAE measures are stable through time in any particular individual and hence are capable of monitoring recovery from OHC impairment. Therapeutic drugs such as antibiotic (e.g., aminoglycosides) and anti-tumor chemotherapeutic (e.g., cisplatin) agents are reported to induce an irreversible hearing-loss, that typically affects the highest frequencies first, with hearing-loss systematically progressing to the lower frequencies (e.g. Kopelman et al., 1988, Fausti et al., 1994, Berg et al., 1999, Stavroulaki et al., 2001). Early detection of ototoxicity is important for providing effective management options such as substitution of medications, change of dosage, and mode of administration (Lonsbury-Martin and Martin, 2001). Because TEOAEs are less effective above 4 kHz, DPOAEs are the test of first choice for detecting and monitoring OHC dysfunction due to ototoxic drugs. Moreover, DPOAEs have an additional advantage over TEOAEs, in that they can give information about compression of the OHC amplifiers. If OHC function is disturbed during the toxic process then not only DPOAE level, but also DPOAE growth should be altered. Like anitibiotic and chemotherapeutic drugs, salicylate is also known to affect hearing sensitivity and to induce tinnitus. (Myers and Bernstein, 1965, McFadden and Plattsmier, 1984, Wier et al., 1988, Long and Tubis, 1988, Boettcher and Salvi, 1991, Brown et al., 1993, McFadden and Pasanen, 1994). However, most importantly, impairment due to salicylate toxicity is reversible. Assuming that a loss of OHC stiffness is responsible for distortions within cochlear micromechanics, the corresponding tonic change at the inner hair cell activity may be one potential correlate of tinnitus (Janssen et al., 2000).

Since OAEs directly reflect OHC dysfunction, they are therefore the method of choice in occupational medicine where the indisputable proof of a cochlear hearing-loss is required.

TEOAE/DPOAE recording

OAEs are low-level sound emissions that occur with sound pressure levels from a maximum amounting to about 20 dB SPL down to the limiting noise-floor level. Therefore, the recording of OAEs requires the use of a highly sensitive low-noise microphone. For DPOAE recording, separate loudspeakers are commonly used for each primary-tone in order to exclude technically generated distortion components. Both the microphone and the loudspeakers of the ear probe need to be miniaturized so that the ear probe is small enough to be placed inside the ear canal (Fig. 1). A tight fit of the probe is essential for OAE recording. If there is leakage between the ear-tip and ear canal, low frequency sound components cannot be recorded properly. Furthermore, the closure of the ear canal by the ear-tip excludes external sounds. In addition, it is essential to make sure that the ear canal is clean and that the ear probe ports are not blocked with ear canal wax. For clinical practice, it is important that ear probes are designed to offer easy access for cleaning ports or replacing clogged ear-tips.

To achieve low noise-floor levels, OAE measurements are conducted in a sound-attenuating booth or any other quiet environment. For bedside use portable measuring devices are used. Automated measuring and evaluation procedures guarantee test consistency and simplify the interpretation of OAE recordings.


Fourier transform (FFT) computations from the time-domain signal allows for automatic evaluation of OAE signals. To minimize the influence of unwanted external signals, algorithms for noise reduction and artefact rejection are applied. In addition, the noise-floor level is reduced by time domain averaging of the recorded signal. TEOAE response ‘sees’ almost the whole cochlea, whereas the DPOAE response reflects only a limited region of the cochlea. Therefore, TEOAEs give a rapid overview of cochlear function, whereas DPOAEs provide more quantitative information about sound processing at distinct cochlear places.

The noise-floor level is usually higher at low frequencies due to microphone properties and low-frequency body sounds such as breathing. Artefact rejection can be performed by elimination of high noise level buffers sensitive to, e.g., breathing, swallowing, or head movements of the subject. Furthermore, when recording TEOAEs, stimulus artefacts may generate signals being in phase in two averaging buffers resulting in a pseudo response of high reproducibility. By means of windowing functions, the stimulus artefact can be excluded so that the reproducibility of the overall signal is restricted to the signal section of interest (Kemp et al., 1990a, Kemp et al., 1990b). It should be emphasized that since the stimulus artefact always appears in the early recording period the high frequency TEOAE components get lost as a result of the windowing procedure.


There are several objective methods for separating the emission signal from the background noise and for automatically evaluating the validity of a recorded emission. For TEOAEs mainly three signal evaluation approaches are used. The first method is based on the calculation of the buffer correlation of the time domain averaged signals between two separate signal buffers (Kemp et al., 1990a). If the two buffers are completely identical, the correlation coefficient is 1 and thus the reproducibility 100%. A signal is commonly accepted as valid for a reproducibility exceeding a minimum of 60%. The second method relies on the computation of the spectral power ratio of the sum and the difference of the two signal buffers. denoted as the signal-to-noise ratio (SNR). The pass criterion for a valid signal is typically set to an SNR of 6 dB. The third signal validation procedure is based on a binomial statistical test, which determines the statistical probability that an emission has been recorded. Binomial statistics reduces the recorded signal to binary events, and uses knowledge on the expected distribution of these events (binomial distribution) (Giebel, 2001).


In the case of DPOAEs, commercially available systems perform mainly two different data validation procedures. The first method is based on the calculation of the noise-floor level by averaging the levels of several adjoining frequency components around the DPOAE frequency component, with the SNR being indicated by the difference between the emission level and the noise-floor level. Here also, the SNR criterion is usually set to 6 dB. The second data validation procedure is based on a phase statistics method, which checks the coupling of the DPOAE component phase to the phase of the primary-tones. The phase statistics average normalized phase vectors of the signal received at the known DPOAE frequency. Like the binomial statistics, the vector sum can be scaled in probability terms, providing defined and very high sensitivities. A typical level of significance exceeds 99% per single frequency test.


TEOAE/DPOAE reproducibility

The inter-individual variance of the TEOAE level is high (standard deviation > 10 dB)(Kemp et al., 1986, Probst et al., 1987, Bonfils and Uziel, 1989, Smurzynski and Kim, 1992). The intra-individual variance of the DPOAE level is much smaller (standard deviation < 2 dB) (Johnsen and Elberling, 1982b, Johnsen and Elberling, 1982a, Harris et al., 1991). Recently, Janssen et al. (2005a) showed that repetitive DPOAE measurements with unchanged sound probe position exhibited an exponentially increasing standard deviation of DPOAE level with increasing SNR. For example, at a SNR of 10 dB, the standard deviation amounts to 1.8 dB, at a SNR of 20 dB to 0.7 dB, and at a SNR of 40 dB to 0.1 dB. This means that the higher the SNR, the higher is the reliability of the DPOAE measurement. This finding is important with respect to the evaluation of small DPOAE changes. For clinical practice, however, repetitive OAE measurements with changed sound probe position are relevant. For example, the standard deviation when changing sound probe position amounted to about 1.6 dB (Müller et al., 2005).

DPOAEs are supposed to primarily reflect OHC activity at the f2 place. However, there is evidence that DPOAEs are generated by two distinct cochlear sources (Whitehead et al., 1992, Brown et al., 1996, Shera and Guinan, 1999). As already mentioned, the first source, the effect of which is actually intended to be measured, is located at the region of overlap of the traveling waves of the two primary-tones near the f2 place and is due to intermodulation distortion. The second source, which is unintentionally adding to the first source emission, is located at the characteristic frequency place of the emission at 2f1-f2 and is due to reflection of energy that has travelled apically from the overlap region near f2. Thus, energy from both interacting sources yield the composite DPOAE signal which is actually recorded in the outer ear canal. The influence of the second DPOAE source may be observed when monitoring the DPOAE level across frequency with narrow frequency spacing of f2 (DPOAE fine-structure). Due to either destructive or constructive superposition of the two DPOAE sources across frequency, a number of investigators have described a pattern of dips and peaks in the DPOAE fine-structure in normal hearing subjects (He and Schmiedt, 1993, He and Schmiedt, 1996, He and Schmiedt, 1997, Talmadge et al., 1999). However, for clinical evaluation of DPOAE I/O functions, the interference of the second DPOAE source makes the interpretability and the accuracy of deduced measures, such as DPOAE threshold and compression, difficult. There have been attempts to minimize the influence of the second source by presenting an additional suppressor tone near 2f1-f2 (Heitmann et al., 1998), or by using a time-windowing procedure, which is able to separate the two sources (Mauermann and Kollmeier, 2004).

The measured OAE presssure in the outer ear canal depends on the ear canal volume. Because of the smaller ear canal volume, OAE pressure in newborns is higher compared to that of adults (Norton, 1992, Lasky, 1998b, Lasky, 1998a, Abdala, 2000). As a consequence, OAEs in newborns are easier to measure.

OAE References

ABDALA, C. 2000. Distortion product otoacoustic emission (2f1-f2) amplitude growth in human adults and neonates. J Acoust Soc Am, 107, 446-56.

BARKER, S. E., LESPERANCE, M. M. & KILENY, P. R. 2000. Outcome of newborn hearing screening by ABR compared with four different DPOAE pass criteria. Am J Audiol, 9, 142-8.

BERG, A. L., SPITZER, J. B. & GARVIN, J. H., JR. 1999. Ototoxic impact of cisplatin in pediatric oncology patients. Laryngoscope, 109, 1806-14.

BILGER, R. C., MATTHIES, M. L., HAMMEL, D. R. & DEMOREST, M. E. 1990. Genetic implications of gender differences in the prevalence of spontaneous otoacoustic emissions. J Speech Hear Res, 33, 418-32.

BOEGE, P. & JANSSEN, T. 2002. Pure-tone threshold estimation from extrapolated distortion product otoacoustic emission I/O-functions in normal and cochlear hearing loss ears. The Journal of the Acoustical Society of America, 111, 1810-1818.

BOETTCHER, F. A. & SALVI, R. J. 1991. Salicylate ototoxicity: review and synthesis. Am J Otolaryngol, 12, 33-47.

BONFILS, P. & UZIEL, A. 1989. Clinical applications of evoked acoustic emissions: results in normally hearing and hearing-impaired subjects. Ann Otol Rhinol Laryngol, 98, 326-31.

BRAY, P. 1989. Click evoked otoacoustic emissions and the development of a clinical otoacoustic hearing test instrument. Dissertation at the University College and Middlesex School of Medicine, London.

BROWN, A. M., HARRIS, F. P. & BEVERIDGE, H. A. 1996. Two sources of acoustic distortion products from the human cochlea. J Acoust Soc Am, 100, 3260-7.

BROWN, A. M., WILLIAMS, D. M. & GASKILL, S. A. 1993. The effect of aspirin on cochlear mechanical tuning. J Acoust Soc Am, 93, 3298-307.

BROWNELL, W. E., BADER, C. R., BERTRAND, D. & DE RIBAUPIERRE, Y. 1985. Evoked mechanical responses of isolated cochlear outer hair cells. Science, 227, 194-6.

BURNS, E. M., KEEFE, D. H. & LING, R. 1998. Energy reflectance in the ear canal can exceed unity near spontaneous otoacoustic emission frequencies. J Acoust Soc Am, 103, 462-74.

DALLOS, P. 1992. The active cochlea. J Neurosci, 12, 4575-85.

DAVIS, H. 1983. An active process in cochlear mechanics. Hear Res, 9, 79-90.

DORN, P. A., KONRAD-MARTIN, D., NEELY, S. T., KEEFE, D. H., CYR, E. & GORGA, M. P. 2001. Distortion product otoacoustic emission input/output functions in normal-hearing and hearing-impaired human ears. The Journal of the Acoustical Society of America, 110, 3119-3131.

DOYLE, K. J., FUJIKAWA, S., ROGERS, P. & NEWMAN, E. 1998. Comparison of newborn hearing screening by transient otoacoustic emissions and auditory brainstem response using ALGO-2. Int J Pediatr Otorhinolaryngol, 43, 207-11.

FAUSTI, S. A., LARSON, V. D., NOFFSINGER, D., WILSON, R. H., PHILLIPS, D. S. & FOWLER, C. G. 1994. High-frequency audiometric monitoring strategies for early detection of ototoxicity. Ear Hear, 15, 232-9.

GIEBEL, A. 2001. Applying signal statistical analysis to TEOAE measurements. Scand Audiol Suppl, 130-2.

GORGA, M. P., NEELY, S. T., DORN, P. A. & HOOVER, B. M. 2003. Further efforts to predict pure-tone thresholds from distortion product otoacoustic emission input/output functions. J Acoust Soc Am, 113, 3275-84.

GORGA, M. P., NELSON, K., DAVIS, T., DORN, P. A. & NEELY, S. T. 2000a. Distortion product otoacoustic emission test performance when both 2f1-f2 and 2f2-f1 are used to predict auditory status. J Acoust Soc Am, 107, 2128-35.

GORGA, M. P., NORTON, S. J., SININGER, Y. S., CONE-WESSON, B., FOLSOM, R. C., VOHR, B. R., WIDEN, J. E. & NEELY, S. T. 2000b. Identification of neonatal hearing impairment: distortion product otoacoustic emissions during the perinatal period. Ear Hear, 21, 400-24.

GORGA, M. P., STOVER, L., NEELY, S. T. & MONTOYA, D. 1996. The use of cumulative distributions to determine critical values and levels of confidence for clinical distortion product otoacoustic emission measurements. J Acoust Soc Am, 100, 968-77.

GRANDORI, F. & RAVAZZANI, P. 1993. Non-linearities of click-evoked otoacoustic emissions and the derived non-linear technique. Br J Audiol, 27, 97-102.

GRANDORI, F., TOGNOLA, G. & ALESSIA, P. A speech-in-noise test for screening hearing ability in adults: the Speech Understanding in Noise (SUN) test. Auris Nasus Larynx, submitted.

HARRIS, F. P., PROBST, R. & WENGER, R. 1991. Repeatability of transiently evoked otoacoustic emissions in normally hearing humans. Audiology, 30, 135-41.

HATZOPOULOS, S., PETRUCELLI, J., MORLET, T. & MARTINI, A. 2003. TEOAE recording protocols revised: data from adult subjects. Int J Audiol, 42, 339-47.

HE, N. & SCHMIEDT, R. A. 1997. Fine structure of the 2 f1-f2 acoustic distortion products: effects of primary level and frequency ratios. J Acoust Soc Am, 101, 3554-65.

HE, N. J. & SCHMIEDT, R. A. 1993. Fine structure of the 2f1-f2 acoustic distortion product: changes with primary level. J Acoust Soc Am, 94, 2659-69.

HE, N. J. & SCHMIEDT, R. A. 1996. Effects of aging on the fine structure of the 2f1-f2 acoustic distortion product. J Acoust Soc Am, 99, 1002-15.

HEITMANN, J., WALDMANN, B., SCHNITZLER, H.-U., PLINKERT, P. K. & ZENNER, H.-P. 1998. Suppression of distortion product otoacoustic emissions (DPOAE) near 2f[sub 1] – f[sub 2] removes DP-gram fine structure — Evidence for a secondary generator. The Journal of the Acoustical Society of America, 103, 1527-1531.

JANSSEN, T., BOEGE, P., MIKUSCH-BUCHBERG, J. & RACZEK, J. 2005a. Investigation of potential effects of cellular phones on human auditory function by means of distortion product otoacoustic emissions. The Journal of the Acoustical Society of America, 117, 1241-1247.

JANSSEN, T., BOEGE, P., OESTREICHER, E. & ARNOLD, W. 2000. Tinnitus and 2f1-f2 distortion product otoacoustic emissions following salicylate overdose. J Acoust Soc Am, 107, 1790-2.

JANSSEN, T., GEHR, D. D., KLEIN, A. & MÜLLER, J. 2005b. Distortion product otoacoustic emissions for hearing threshold estimation and differentiation between middle-ear and cochlear disorders in neonates. J Acoust Soc Am, 117, 2969-79.

JANSSEN, T., KUMMER, P. & ARNOLD, W. 1998. Growth behavior of the 2 f1-f2 distortion product otoacoustic emission in tinnitus. J Acoust Soc Am, 103, 3418-30.

JANSSEN, T., NIEDERMEYER, H. P. & ARNOLD, W. 2006. Diagnostics of the cochlear amplifier by means of distortion product otoacoustic emissions. ORL J Otorhinolaryngol Relat Spec, 68, 334-9.

JOHNSEN, N. J. & ELBERLING, C. 1982a. Evoked acoustic emissions from the human ear. I. Equipment and response parameters. Scand Audiol, 11, 3-12.

JOHNSEN, N. J. & ELBERLING, C. 1982b. Evoked acoustic emissions from the human ear. II. Normative data in young adults and influence of posture. Scand Audiol, 11, 69-77.

JÜLICHER, F., CAMALET, S., PROST, J. & DUKE, T. A. J. 2003. Active amplification by critical oscillations. In: GUMMER, A. (ed.) Biophysics of the Cochlea: from Molecule to Models. New Jersey: World Scientific.

KEEFE, D. H., BULEN, J. C., AREHART, K. H. & BURNS, E. M. 1993. Ear-canal impedance and reflection coefficient in human infants and adults. J Acoust Soc Am, 94, 2617-38.

KEMP, D. T. 1978. Stimulated acoustic emissions from within the human auditory system. J Acoust Soc Am, 64, 1386-91.

KEMP, D. T., BRAY, P., ALEXANDER, L. & BROWN, A. M. 1986. Acoustic emission cochleography–practical aspects. Scand Audiol Suppl, 25, 71-95.

KEMP, D. T. & RYAN, S. 1991. Otoacoustic emission tests in neonatal screening programmes. Acta Otolaryngol Suppl, 482, 73-84.

KEMP, D. T., RYAN, S. & BRAY, P. 1990a. A guide to the effective use of otoacoustic emissions. Ear Hear, 11, 93-105.

KEMP, D. T., RYAN, S. & BRAY, P. 1990b. Otoacoustic emission analysis and interpretation for clinical purposes. In: GRANDORI, F., CIAFRONE, G. & KEMP, D. (eds.) Cochlear mechanisms and otoacoustic emissions. Karger.

KOPELMAN, J., BUDNICK, A. S., SESSIONS, R. B., KRAMER, M. B. & WONG, G. Y. 1988. Ototoxicity of high-dose cisplatin by bolus administration in patients with advanced cancers and normal hearing. Laryngoscope, 98, 858-64.

KUMMER, P., JANSSEN, T. & ARNOLD, W. 1998. The level and growth behavior of the 2 f1-f2 distortion product otoacoustic emission and its relationship to auditory sensitivity in normal hearing and cochlear hearing loss. Journal of the Acoustical Society of America, 103, 3431-3444.

KUMMER, P., JANSSEN, T., HULIN, P. & ARNOLD, W. 2000. Optimal L(1)-L(2) primary tone level separation remains independent of test frequency in humans. Hear Res, 146, 47-56.

LASKY, R. E. 1998a. Distortion product otoacoustic emissions in human newborns and adults. I. Frequency effects. J Acoust Soc Am, 103, 981-91.

LASKY, R. E. 1998b. Distortion product otoacoustic emissions in human newborns and adults. II. Level effects. J Acoust Soc Am, 103, 992-1000.

LIBERMAN, M. C. & DODDS, L. W. 1984. Single-neuron labeling and chronic cochlear pathology. III. Stereocilia damage and alterations of threshold tuning curves. Hear Res, 16, 55-74.

LONG, G. R. & TUBIS, A. 1988. Modification of spontaneous and evoked otoacoustic emissions and associated psychoacoustic microstructure by aspirin consumption. J Acoust Soc Am, 84, 1343-53.

LONSBURY-MARTIN, B. L. & MARTIN, G. K. 2001. Evoked Otoacoustic Emissions as Objective Screeners for Ototoxicity. Semin Hear, 22, 377,392.

MARGOLIS, R. H. 2002. Influence of middle-ear disease on otoacoustic emissions. In: ROBINETTE, M. S. & GLATTKE, T. J. (eds.) Otoacoustic emissions: clinical applications. 2. ed. ed. New York: Thieme.

MAUERMANN, M. & KOLLMEIER, B. 2004. Distortion product otoacoustic emission (DPOAE) input/output functions and the influence of the second DPOAE source. J Acoust Soc Am, 116, 2199-212.

MCFADDEN, D. & PASANEN, E. G. 1994. Otoacoustic emissions and quinine sulfate. J Acoust Soc Am, 95, 3460-74.

MCFADDEN, D. & PLATTSMIER, H. S. 1984. Aspirin abolishes spontaneous oto-acoustic emissions. J Acoust Soc Am, 76, 443-8.

MILLS, D. M. & RUBEL, E. W. 1994. Variation of distortion product otoacoustic emissions with furosemide injection. Hear Res, 77, 183-99.

MÜLLER, J. & JANSSEN, T. 2004. Similarity in loudness and distortion product otoacoustic emission input/output functions: implications for an objective hearing aid adjustment. J Acoust Soc Am, 115, 3081-91.

MÜLLER, J., JANSSEN, T., HEPPELMANN, G. & WAGNER, W. 2005. Evidence for a bipolar change in distortion product otoacoustic emissions during contralateral acoustic stimulation in humans. J Acoust Soc Am, 118, 3747-56.

MYERS, E. N. & BERNSTEIN, J. M. 1965. Salicylate ototoxicity; a clinical and experimental study. Arch Otolaryngol, 82, 483-93.

NEELY, S. T., GORGA, M. P. & DORN, P. A. 2003. Cochlear compression estimates from measurements of distortion-product otoacoustic emissions. J Acoust Soc Am, 114, 1499-507.

NORTON, S. J. 1992. The effects of being a newborn on otoacoustic emissions. The Journal of the Acoustical Society of America, 91, 2409-2409.

NORTON, S. J., GORGA, M. P., WIDEN, J. E., FOLSOM, R. C., SININGER, Y., CONE-WESSON, B., VOHR, B. R. & FLETCHER, K. A. 2000a. Identification of neonatal hearing impairment: summary and recommendations. Ear Hear, 21, 529-35.

NORTON, S. J., GORGA, M. P., WIDEN, J. E., FOLSOM, R. C., SININGER, Y., CONE-WESSON, B., VOHR, B. R., MASCHER, K. & FLETCHER, K. 2000b. Identification of neonatal hearing impairment: evaluation of transient evoked otoacoustic emission, distortion product otoacoustic emission, and auditory brain stem response test performance. Ear Hear, 21, 508-28.

PENNER, M. J., GLOTZBACH, L. & HUANG, T. 1993. Spontaneous otoacoustic emissions: measurement and data. Hear Res, 68, 229-37.

PENNER, M. J. & ZHANG, T. 1997. Prevalence of spontaneous otoacoustic emissions in adults revisited. Hear Res, 103, 28-34.

PICTON, T. W., JOHN, M. S., DIMITRIJEVIC, A. & PURCELL, D. 2003. Human auditory steady-state responses. Int J Audiol, 42, 177-219.

PROBST, R., LONSBURY-MARTIN, B. L., MARTIN, G. K. & COATS, A. C. 1987. Otoacoustic emissions in ears with hearing loss. Am J Otolaryngol, 8, 73-81.

RHODES, M. C., MARGOLIS, R. H., HIRSCH, J. E. & NAPP, A. P. 1999. Hearing screening in the newborn intensive care nursery: comparison of methods. Otolaryngol Head Neck Surg, 120, 799-808.

ROBINETTE, M. S. & GLATTKE, T. J. 2002. Transient evoked otoacoustic emissions. In: ROBINETTE, M. S. & GLATTKE, T. J. (eds.) Otoacoustic emissions: clinical applications. 2. ed. ed. New York: Thieme.

ROESER, R. J. 1996. Roeser’s audiology desk reference. A guide to the practice of audiology., New York, Stuttgart, Thieme.

RUGGERO, M. A., RICH, N. C., RECIO, A., NARAYAN, S. S. & ROBLES, L. 1997. Basilar-membrane responses to tones at the base of the chinchilla cochlea. J Acoust Soc Am, 101, 2151-63.

SHERA, C. A. & GUINAN, J. J., JR. 1999. Evoked otoacoustic emissions arise by two fundamentally different mechanisms: a taxonomy for mammalian OAEs. J Acoust Soc Am, 105, 782-98.

SIEGEL, J. H. 1994. Ear-Canal Standing Waves and High-Frequency Sound Calibration Using Otoacoustic Emission Probes. Journal of the Acoustical Society of America, 95, 2589-2597.

SMURZYNSKI, J. & KIM, D. O. 1992. Distortion-product and click-evoked otoacoustic emissions of normally-hearing adults. Hear Res, 58, 227-40.

STARR, A., PICTON, T. W., SININGER, Y., HOOD, L. J. & BERLIN, C. I. 1996. Auditory neuropathy. Brain, 119 ( Pt 3), 741-53.

STAVROULAKI, P., APOSTOLOPOULOS, N., SEGAS, J., TSAKANIKOS, M. & ADAMOPOULOS, G. 2001. Evoked otoacoustic emissions–an approach for monitoring cisplatin induced ototoxicity in children. Int J Pediatr Otorhinolaryngol, 59, 47-57.

TALMADGE, C. L., LONG, G. R., TUBIS, A. & DHAR, S. 1999. Experimental confirmation of the two-source interference model for the fine structure of distortion product otoacoustic emissions. J Acoust Soc Am, 105, 275-92.

VON SPECHT, H., GANZ, M., PETHE, J., LEUSCHNER, S. & PYTEL, J. 2001. Linear versus non-linear recordings of transiently-evoked otoacoustic emissions–methodological considerations. Scand Audiol Suppl, 116-8.

WHITEHEAD, M. L., LONSBURY-MARTIN, B. L. & MARTIN, G. K. 1992. Evidence for two discrete sources of 2f1-f2 distortion-product otoacoustic emission in rabbit: I. Differential dependence on stimulus parameters. J Acoust Soc Am, 91, 1587-607.

WHITEHEAD, M. L., MCCOY, M. J., LONSBURY-MARTIN, B. L. & MARTIN, G. K. 1995a. Dependence of distortion-product otoacoustic emissions on primary levels in normal and impaired ears. I. Effects of decreasing L2 below L1. J Acoust Soc Am, 97, 2346-58.

WHITEHEAD, M. L., STAGNER, B. B., LONSBURY-MARTIN, B. L. & MARTIN, G. K. 1995b. Effects of ear-canal standing waves on measurements of distortion-product otoacoustic emissions. J Acoust Soc Am, 98, 3200-14.

WHITEHEAD, M. L., STAGNER, B. B., MCCOY, M. J., LONSBURY-MARTIN, B. L. & MARTIN, G. K. 1995c. Dependence of distortion-product otoacoustic emissions on primary levels in normal and impaired ears. II. Asymmetry in L1,L2 space. J Acoust Soc Am, 97, 2359-77.

WIER, C. C., PASANEN, E. G. & MCFADDEN, D. 1988. Partial dissociation of spontaneous otoacoustic emissions and distortion products during aspirin use in humans. J Acoust Soc Am, 84, 230-7.

WILSON, J. & JUNGNER, G. 1968. Principles and practice of screening for disease. World Health Organization (WHO), Geneva.

ZWICKER, E. & SCHLOTH, E. 1984. Interrelation of different oto-acoustic emissions. J Acoust Soc Am, 75, 1148-54.