Otoacoustic Emissions
Table of contents
1. Introduction
2. The essence of OAE, its anatomy and physiology
3. Efferent and afferent systems
4. Types of OAEs
5. The measurement of OAEs
6. The clinical use of OAEs
7. Conclusion
8. References
9. Appendices
Introduction
Otoacoustic emission is which is generated from within the inner ear. The finding
of OAE was extremely important for the development of modern science since it
opened new opportunities for the research of the inner ear health. In fact,
measurements of OAE can reveal the current state of the patient’s inner
ear health that is very important since the inner ear was traditionally quite
difficult to research while the analysis of its health was even more difficult.
In such a situation, the discovery of OAE and its practical implementation could
be viewed as a real breakthrough, especially in the field of medicine. At the
same time, the potential of OAE still need to be researched further in order
to fully reveal its real potential. Consequently, it is important to discuss
the essence of OAE and reveal the possible ways of its clinical application.
In this respect, it is necessary to point out that nowadays there are a variety
of possibilities to find the clinical application to OAE, though, it is necessary
to admit that the full potential of OAE is still not revealed. This is why researches
in this field are very important.
The essence of OAE, its anatomy and physiology
Otoacoustic emission is a surprising and exciting auditory phenomenon which
allows us to explore peripheral hearing function in unprecedented depth and
detail. OAEs have given us new insights into deafness and new possibilities
for early intervention and treatment. People often ask what prompted the first
OAE measurement. It was to explain a set of complex and little known psychoacoustic
phenomena. Spontaneous subjective pure tones had been cited by Gold in 1948
as potential evidence for a cochlear amplifier (Lalaki, 2003, p.135). Anomolous
aural combination tone generation had been reported by Ward in 1952 involving
mysterious internal tones (Lalaki, 2003, p.149). Finally in 1958 Elliot reported
a periodic ripple pattern in the fine structure of the auditory threshold in
normal ears (Lalaki, 2003, p.201). All three were systematically linked together
but no rational explanation could be found. Only one physical model seemed to
fit the facts. It was that near to threshold levels the healthy cochlea behaved
like a “reverberating and resonating auditorium enhanced by a strange
PA system prone to feedback howl and distortion! It was an incredibly long shot
but in June of 1977 I put a microphone into my ear canal just to check. Through
the microphone came distortion products, spontaneous tones and echoes! The incredible
turned out to be true!” (Lalaki, 2003, p.216). Today clinical OAE measurements
are fast becoming a standard part of the audiometric test battery. OAEs have
already had a major influence on newborn hearing screening programs across the
USA. But twenty years after the first otoacoustic emission recordings were made
at the Royal National ENT Hospital London, many hearing care professionals still
feel OAEs to be unfamiliar new technology. It is true that OAEs are very different
from ABRs. The technical complexity of many scientific papers on OAEs has impeded
their assimilation. Commentaries which reproduced misleading and inaccurate
ideas about OAEs without scientific foundation have added to the problem.
Fortunately the essential facts about OAEs are not complex. Everyone in audiology
should be acquainted with them. The aim of this booklet is to re-present OAEs
in a form that is brief, balanced, practical and accurate. Hopefully it will
promote the more effective use of this powerful new audiometric tool.
Otoacoustic emissions are small sounds caused by motion of the eardrum in response
to vibrations from deep within the cochlea. The healthy cochlea creates internal
vibrations whenever it processes sound. Impaired cochleae usually do not. Some
healthy ears even produce sound spontaneously as internal sounds are processed
and amplified. As described later, the cochlea’s capacity to generate
sound is intimately associated with its achievement of normal auditory threshold,
and the underlying mechanism is very easily damaged. To record the sounds made
by the cochlea an earphone and microphone combination probe is fitted into the
ear canal.
The middle ear has to be working efficiently in order to conduct the minute
cochlear vibrations back to the ear drum - acting like a stethoscope. A good
fitting of the probe is important. Closure of the ear canal by the probe greatly
increases the sound pressure created by any ear drum vibration. It also excludes
unwanted external sounds. Normally the ear to be tested is given mild acoustic
stimulation to evoke an otoacoustic emission. Clicks, tones, noise and even
speech all elicit an OAE response. There is a unique OAE response to every stimulus.
Efferent and afferent systems
Obviously, OAE is quite complicated and it is very important that OAE functioned
properly. In this respect, it should be said that efferent and afferent systems
contribute consistently to the normal functioning of OAE. At this point, it
is necessary to briefly dwell upon efferent and afferent systems. Efferent system
is represented by efferent neurons, which are also known as motor or effector
neurons, carry nerve impulses away from the central nervous system to effectors
such as muscles or glands. Speaking about the inner ear, it should be said that
the efferent system involves the cilitated cells. Basically efferent system
provides relative connections between nervous structures.
As for afferent system, it is necessary to point out that this system is actually
the opposite to efferent system. To put it more precisely, this system is represented
by afferent neurons, or sensory or receptory neurons, carry nerve impulses from
receptors or sense organs toward the central nervous system. This system also
provides relative connections between structures.
In fact, efferent system serves to carry nerve impulses from the central nervous
system to the inner system, while afferent system provides the reverse action,
i.e. carrying the signal from the inner ear to the central nervous system. In
such a way, the interaction of both efferent and afferent systems produces a
profound impact on the functioning of OAE and is simply essential for its normal
functioning.
Types of OAEs
The two major classes of OAE technology -TEOAE and DPOAE - differ fundamentally
in the condition of the cochlear which they observe. In TEOAE testing the OAE
sound is recorded during the silence between brief stimuli - so that the relaxed
status of the outer haircells is observed. As most of the cochlea is excited
by a click, reports are simultaneously received from multiple sections of the
organ of Corti (Williams et al, 1994, p.196). This does not blur the picture
because each section responds at its own characteristic frequency. Signal processing
can simultaneously observed by DPOAEs. This is primarily because modern day
transducers produce more distortion than the cochlea if fed with multiple tones.
DPOAE measurements must therefore be repeated at several frequencies to get
a balanced overall picture. To match the cochlea’s natural bandwidth for
processing, a 3 points per octave DPOAE resolution is required as a minimum.
Higher resolution is desirable so as to overcome the misleading effects of standing
wave interference within the cochlea which occur with pure tones.
Both DP and TEOAE views of cochlea function are valuable and complementary.
Each technology has different advantages and disadvantages. TEOAE technology
has the advantages of sensitivity.
Several distortion products are generated simultaneously A DP-Gram and TE-Gram
compared. A high resolution TEOAE Spectrum easily separate the response from
each part. A 20ms sweep allows a frequency resolution of 50Hz, or 20 points
per octave from 1 to 2kHz. TEOAEs therefore test many parts of the cochlea individually
and simultaneously in a functional state close to threshold stimulation (Williams
et al, 1994, p.199). With DPOAEs a more restricted part of the cochlea is more
intensely stimulus and continuously driven so that the outer haircells are observed
in their working state.
The width of the region tested is not defined by the precision of the pure tone
frequency but by the natural bandwidth of the cochlea. The stimulated region
is quite extensive. Only one or two regions of the cochlea can be frequency
resolution and speed, but it fails to recover OAEs in adults much above 4kHz.
This is due to the shorter latency of high frequency OAEs. DPOAE technology
has the advantage of superior detection of high frequency OAEs but it suffers
from lower frequency resolution and lower noise immunity at low frequencies.
The technique is unable to capture primary OAE energy but a more serious practical
drawback is the dependence of DPOAE on the precise stimulus configuration (frequency
and level ratios).
Frequency specificity is very important to cochlea function but is often misrepresented
in OAE literature. It is the frequency specificity of the cochlea that is important
and not that of the stimuli. Clicks or tones are therefore equally suitable
stimuli with which to observe the cochlea. All OAEs are highly frequency specific
in that each frequency component of an OAE can be directly traced to a frequency
component in the stimulus. What is desirable and is often assumed to be true
of OAEs is that the response obtained to a specific stimulus frequency tells
about the status of a particular place in the cochlea.
This is probably true only in a very broad sense. The relation between OAEs
level and auditory threshold - or rather the lack of it – has already
been discussed. In the early days of DPOAE research it was common to define
a DPOAE threshold as the stimulus level at which the OAE equalled the noise
present in the instrument. OAEs do not have a threshold and this measure is
unsafe. Threshold is a property of the inner haircells and nerve synapase which
play no part in the creation of OAEs. A related and more meaningful measure
is the growth rate of DPOAE with stimulus level which appears to steepen as
auditory threshold is elevated.
Observations must however be averaged over a range of stimulus frequencies and
ratios. The concept of .passive. and .active. DPOAE responses arose from animal
observations and should be applied with caution to clinical work. Human ears
stand much higher levels of stimulation than rodents and .passive. cochlear
responses are very unlikely in response to stimuli of 70dBspl and below. What
is more likely is passive DP generation in the probe and instrumentation. DPOAE
systems should be checked in a test cavity, but a more powerful test is to measure
the latency of DPOAE found in the ear. Latencies of 3ms or greater are highly
indicative of a cochlear origin, and lower latencies of instrumentation distortion.
Finally, calibration. In the clinic OAEs systems are used as function detectors,
not as measuring systems - but calibration is still important to ensure proper
operation and data comparability. OAE systems display sound levels on screen,
so the microphone calibration can be quickly checked against a calibrated sound
level meter. Stimulus calibration presents special problems due to standing
waves in the ear canal. The sound level at the drum cannot be accurately set
from measurements at the probe. The problem becomes serious above 5kHz in adults.
It is less important in infants. Additionally, the decibel level of the OAE
also depends strongly on ear canal acoustics. Considerable technical progress
is needed before the ultimate OAEs system is designed.
Also, it is possible to mention Spontaneous OAE. The characteristic feature
of this OAE is the fact that it arise spontaneously, unlike other types of OAE.
This means that its appearance can hardly be evoked intentionally, nor there
is any clear system of its appearance and development. At the same time, there
are also Synchronized Spontaneous OAE (SSOAE). Basically, SSOAE are identified
as sustained activity in the TEOAE spectrum. It is worthy of mention that the
transient click stimulus used to TEOAEs entrains the SSOAE for a short time
after which the SSOAE slowly looses synchrony with the stimulus (Prasher, 1994,
p.249).
The measurement of OAEs
Depending on the nature of the sound presented, different signal processing
techniques are effective in extracting the OAE from the stimulus and other noises.
The common technologies are TEOAE when clicks or tone bursts are used, DPOAE
when dual tone stimuli are used, and SFOAE when single tone stimulation is used.
It is important to remember TEOAE, DPOAE and SFOAE instruments deliver different
views of the same auditory process and a combination of measurements is needed
to get a complete picture.
The essential fact about OAEs is that their presence is always good news about
cochlea and middle ear function. It usually means hearing is within normal limits
around the stimulus frequency evoking the response - but this is not guaranteed.
There can be problems further along the auditory pathway and there is much still
to learn about OAEs and cochlear physiology. In the following pages we look
at the use of OAEs today for newborn screening and for clinical investigation,
and at the auditory physiology and biophysics behind OAEs and OAE technology.
What could be simpler than testing an infant.’ hearing with an insertearphone.
It takes only a few seconds to record the transient otoacoustic emissions in
a quiet office from a typical newborn who has clean ear canals and a well drained
middle ear. If conditions are not ideal it can take longer - but 5 minutes is
an exceptionally long time for an experienced OAE screener to test a newborn
- and it would usually mean that the newborn was not ready to be tested. Transient
OAE technology is generally preferred for screening at this time because the
instrumentation provides very fast feedback to the screener on general probe
fit, noise and test outcome. DPOAEs can also be used effectively.
TEOAE screening has the advantage of testing a wide range of frequencies individually
yet simultaneously giving a continuous panorama of cochlear function with frequency.
Around 100 universal screening programmes in the USA currently use TEOAEs. A
1996 survey by the National Center for Hearing Assessment and Management (NCHAM)
showed referral rate of less than 5%. The reportedly very high sensitivity of
the technique for universal screening has not been challenged, despite many
hundreds of thousands of TEOAE screenings starting with the Rhode Island Hearing
Assessment Project in 1989.
There is an acknowledged learning curve for newborn screening with OAEs. Initial
attempts at newborn screening with OAEs can be disappointing unless a few important
guidelines are followed. Firstly, probe fitting is paramount. Inspect the ear
and select a suitable size of tip. Straighten the ear canal by gently pulling
the pinna. Insert the probe firmly and deeply. This opens up the ear canal and
excludes external noise contamination. The room need not be audiometrically
quiet but continuous background noise should be avoided.
Observe the noise received by a suspended probe relative to the instrument’s
noise artifact rejection range. If the background noise level exceeds 50dBA
do not attempt newborn screening. Expect to see some indication of an OAE response
in about ten seconds with a newborn. If not - and if both the baby and room
are quiet - then assume that the probe insertion has not fully opened up the
ear canal or that the disposable tip has become clogged with debris. If having
dealt with this there is still no OAE, assume that there is retained fluid still
to be cleared from the middle ear, and retest the baby later. Babies tested
on the first day of life more often fail to show an OAE as a result of mild
ear contamination - but they usually pass on retest hours later. When OAEs do
appear, continue collecting data until the required level of confirmation is
achieved. The screener must be trained to judge the technical adequacy of a
measurement and to recognise the need for a repeat test. Technical adequacy
includes the achievement of the specific statistical and signal-to-noise targets
needed to validate OAE responses.
Instrument signal processing and automation greatly assist in this process.
It is the responsibility of the audiologist or physician to set an appropriate
pass/refer criteria for the baby. The previous gold standard for hearing screening
- the ABR - accepted a proven wave V response of normal latency to the selected
level of click stimulation as sufficient proof of normal auditory function.
By the same standard, any technically valid OAE response within the speech range
in response to a click stimulus could be reasonably accepted as proof of adequate
cochlea function. In practice, most screening programmes set a more stringent
criteria than this. It is common to require OAE responses to be 3 or 6dB above
the noise in 2, 3 or more half octave bands between 1 and 4kHz. This exceeds
the stringency of the ABR test, and results in a higher refer rate. However
the widespread acceptance of multifrequency pass criteria for OAEs must be taken
to indicate an underlying dissatisfaction with the non-frequency specific nature
of screening ABR. It remains to be seen if such stringent multifrequency OAE
pass criteria persist and yield tangible benefits.
OAE screening has proven very effective in the detection of hearing impairment
in newborns, even though the neural pathway is not being assessed. Failure to
show an OAE is probably the single most important risk factor for hearing impairment
but other risk factors should never be ignored. Any risk of neurological significance
means an ABR test must also be conducted. To date, among the hundreds of thousands
of OAE screenings monitored by NCHAM the incidence of late onset hearing losses
missed by OAE screening appears to be very low - around 1% of the hearing impaired
population. OAEs appear to be ideal for the first stage of universal screening
programmes.
The impressive spiral construction of the cochlea (Figure 1) serves only to
make the hearing organ more compact. The really important physical feature of
the cochlea is the gradually tapering basilar membrane which runs the length
of the spiral and carries the organ of Corti with its sensory haircells (lower
right). This elastic membrane receives the sound energy delivered to the cochlear
fluid by the middle ear. All sounds entering the cochlea result in a ripple
wave along the basilar membrane which travels from base to apex. These waves
travel hundreds of times slower than sound in air, taking several milliseconds
to complete a journey of a few millimetres over the sensory haircells. Each
individual frequency component wave grows in intensity as it travels, eventually
reaching a peak before coming to a complete stop at a unique place on the basilar
membrane.
The peaking of cochlear travelling waves is crucial to the hearing process.
It serves to separate excitation at different frequencies - rather as a prism
separates the colors of light (right Figure 1). Paralleling the eye, the cochlea
acts to mould the raw material of sensation, in this case sound, into an image
which can be read as a spatial pattern by the array of sensory cells and translated
into neural code. The cochlear image projected along the organ of Corti physically
represents the external sound environment mapped according to the figure left
shows a computer simulated snapshot of waves travelling along the basilar membrane
in response to two tones f1 and f2 (Rajan, 1990, p.200).
This is representative of the situation during typical clinical DPOAE measurements.
Note how f1 and f2 excite a substantial region of the cochlea, even though their
frequencies are very precisely defined. F1 reaches further into the cochlea
than f2. Distortion products can only be generated in the region where f1 and
f2 overlap. The envelope of f2 defines this region which does not include the
geometric mean frequency often wrongly cited as determining the place of DP
generation. Higher DPs, such as 2f2-f1, need to be generated even more basally
in order to escape the cochlear.
The size of sound sources. Large objects radiating low frequencies are focused
at the apex, and high frequency sounds typically radiated from small structures
come to focus as the base. The sensitivity and resolution of the ear depends
on two things. One is the size and sharpness of cochlear travelling wave peaks
- much as visual acuity depends on the sharpness of focus of the eye. The second
is the efficiency of transduction to the auditory nerve. Sound image quality
in the ear appears to depend on the health of the outer three rows of haircells,
while the single inner row is responsible for the transduction and neural encoding
(lower right). Without active outer haircell function, sound energy is lost
from the travelling wave before it peaks.
Peaks broaden and are of reduced size. Outer haircells generate replacement
vibration which sustains and even amplifies the travelling wave, resulting in
higher and sharper peaks of excitation to the inner haircells. Most of the sound
vibration generated by the outer haircells becomes part of the forward travelling
wave, but a fraction escapes. It then travels back out of the cochlea to cause
secondary vibrations of the middle ear and the ear drum. The whole process can
take 3 to 15 milliseconds (Rajan, 1990, p.201). These cochlear driven vibrations
are the source of Otoacoustic Emissions. Important as OAEs are for probing cochlea
function it is ludicrous to suggest that auditory threshold can be reliably
measured by OAEs. The crucial mechanism of transduction in the inner haircell
is not involved in OAE generation.
Furthermore, the mechanism for the escape of energy resulting in OAEs plays
no part in the hearing process. This factor certainly accounts for much of the
wide variation in the intensity of the OAE responses between individuals and
across frequency in the same individual. We would not expect - and we do not
observe - more than a 30% correlation between OAEs level and audiometric threshold
- far too small for clinical use. But we do observe a very high correlation
between the existence of OAEs and audiometric thresholds falling within the
normal range. The implication is clear. Most cochlear pathologies involve outer
haircell disorder, making OAEs an ideal frequency specific screening test for
cochlear function.
The clinical use of OAEs
As a part of the audiological test battery, otoacoustic emissions can help to
differentiate between auditory pathologies and provide useful information for
the management of hearing impaired patients. As reviewed earlier, OAEs have
revealed that most cochlear threshold elevations involve a loss in mechanical
responsiveness of the basilar membrane to sound vibration. We had no way of
knowing this before. Cochlear hearing losses up to around 40dB may be solely
due to poor outer haircell performance. The corresponding depression of cochlear
travelling wave development and the degradation of the sound image would be
adequate to account for the loss in hearing sensitivity. Of course a complementary
type of cochlear loss must exist in which the travelling wave develops normally
but inner haircells fail to translate the excitory image into neural code. Clinical
research is needed to clarify this potential dichotomy. Some hydrops patients
do exhibit OAEs with elevated audiometric threshold but most threshold elevations
result in absent OAEs.
The logic for the incorporation of OAEs into the audiological test battery is
easy to work out once the scope of each test is clearly defined. The pure tone
audiogram tests the whole auditory system but includes unwanted central and
psychological factors. The ABR tests the auditory periphery and neural pathways
as far as the brain stem. OAEs test only the peripheral system - including the
organ of Corti - up to the point of excitation of the inner hair cells but not
the cells themselves.
Tympanometry tests the system up to the cochlea. When interpreting OAE data
it should always be remembered that the cochlea is a frequency specific organ.
OAEs – whether obtained by DPOAE or TEOAE - should be considered on a
frequency by frequency basis. For example, a patient with normal hearing up
to say 2kHz then a precipitous loss will still show OAEs - but only to stimuli
containing components in the normal threshold range. Clicks contain all frequencies
so will excite an OAE in such a patient - but the OAE response will not include
frequency components from within the hearing loss range. This is the meaning
of frequency specificity (Lalaki, 2003, p.78).
In general if there is a hearing problem and there are no other indications,
it makes sense for an OAE examination to be the first objective test performed.
It is fast and helps confirm normal middle ear and cochlear function. In all
except newborns an absent OAE should be followed by tympanometry. Absent OAEs
with a normal tympanogram usually indicate a cochlear dysfunction but this can
sometimes be quite minor. The click stimulus intensity normally used for TEOAEs
is around 55dB normal sensation level, but this still provides high sensitivity
to losses as small as 15-20dB and even to subclinical factors 4kHz in adults.
DPOAEs elicited with stimuli greater than 60dBspl are less sensitive to cochlear
dysfunction. 25-30dB loss is needed to abolish the DPOAEs but this sensitivity
is maintained up to higher frequencies. A two stage clinical OAE test is recommended
- TEOAEs followed by DPOAEs (Iurato, 1976, p.261). OAE testing cannot determine
auditory threshold. ABR testing is needed to estimate threshold if audiometry
is not possible. If OAEs are strongly present with substantial threshold elevation
this can indicate a retrocochlear loss, an inner haircell loss, or an inorganic
loss.
Auditory nerve pathology often coexists with absent OAEs so that the demonstration
of a cochlear component of a hearing loss by OAEs cannot be used to exclude
retrocochlear pathology. However, the presence of OAE with retrocochlear pathology
indicates an intact cochlea which may indicate a policy of cochlear preservation
during surgery. In a minority of congenital hearing losses cochlear function
remains intact. The provision of amplification to an intact cochlea has to be
seriously reconsidered.
OAE examination should always precede hearing aid fitment of infants, especially
if not used in the identification process. It has been found valuable to re-examine
very young and handicapped hearing aid users with OAEs to identify those who
actually have normal cochlear mechanical function.
Tympanometry primarily examines the stiffness of the eardrum using low frequency
tones. OAEs on the other hand require normal middle ear function from 1kHz to
6kHz. OAEs therefore provide evidence of normal middle ear function, strongly
biased towards the transmission properties of the middle ear at speech frequencies
rather than its sound reflection properties. This additional information is
of course available only where the cochlea is known to be normal.
The quality and integrity of surgical reconstruction of the middle ear could
be assessed using OAEs. Although there are wide individual differences in OAE
responses, these tend to be stable through time. Small changes in TEOAE patterns
not attributable to probe fitting changes, indicate a change in middle ear or
cochlear status. This may be used in monitoring chronic conditions or in detecting
the effect of occupational noise exposure or the ototoxic effects of drugs.
TEOAE monitoring is less effective than DPOAE above 4kHz, but even DPOAEs can
be unreliable above this range due to complex ear canal acoustics.
Conclusion
Thus, taking into account all above mentioned, it is possible to conclude that
OAE is very important. The great clinical significance of OAEs may be revealed
in the fact that they only occur in the normal cochlea or near normal hearing.
If there is damage to the outer hair cells producing mild hearing loss, than
OAEs are not evoked. At the same time, it is necessary to remember about certain
limitations of the utility of OAEs. For instance, OAEs are not very helpful
in Meniere’s disease because OAEs mainly test high frequencies, while
Meniere’s disease usually starts with low-frequency hearing loss. Nevertheless,
the further researches of OAEs is extremely important because the further researches
can reveal some new characteristics and opportunities of OAE. Consequently,
it would be logical to presuppose that, in such a case, the clinical application
of OAE may widen.
References
Iurato S. (1974). Efferent innervation of the cochlea. In Keidel W, Neff W (eds)
Handbook of sensory physiology. (pp 261-82). New York: Springer-Verlag.
Kim DO. (1968). Active and nonlinear cochlear biomechanics and the role of outer-hair-cell
subsystem in the mammalian auditory system. Hear Res 22: 105-14.
Kimiskidis VK., Lalaki P., Papagiannopoulos S., (2004). Sensorineural hearing
loss and word deafness caused by a mesencephalic lesion: clinicoelectrophysiological
correlations. Otol Neurotol 25: 178-82.
Kujawa SG., Glattke T., Fallon M., Bobbin RP. (1993). Contralateral sound suppresses
distortion product otoacoustic emissions through cholinergic mechanisms. Hear
Res 68: 97-106.
Lalaki P. (2003). Otoacoustic emissions in the assessment of the efferent auditory
system: clinical and experimental protocols. Greece: Aristotle University, Thessaloniki.
Liberman MC. (1991). The olivocochlear efferent bundle and susceptibility of
the inner ear to acoustic injury. J Neurophysiol; 65: 123-32.
Micheyl C, Collet L. (1996). Involvement of the olivocochlear bundle in the
detection of tones in noise. J Acoust Soc Am 99: 1604-10.
Morlet T., Collet L., Salle B., Morgon A. (1993). Functional maturation of cochlear
active mechanisms and of the medial olivocochlear system in humans. Acta Otolaryngol
(Stockh); 113: 271-7.
Muchnik C,, Ari-Even Roth D,, Othman-Jebara R, (2004). Reduced medial olivocochlear
bundle system function in children with auditory processing disorders. Audiol
Neurootol 9: 107-14.
Prasher D., Ceranic B., Sulkowski W., Guzek W. (2001)Objective evidence for
tinnitus from spontaneous emission variability. Noise Induced Hearing Loss:
Basic Mechanisms, Prevention and Control. (pp 471-83). Noise Research Publications,
London. Prasher
D, Ryan S, Luxon L.(1994). Suppression of Transiently Evoked Otoacoustic Emissions
and Neuro-Otology. Br J Audiol 28:247-54.
Pujol R. Lenoir M. (1986).The four types of synapses in the organ of Corti.
In Altschuler R, Bobbin R, Hoffman D (eds) Neurobiology of hearing: The cochlea.
(pp 161-72.) New York: Raven Press.
Rajan R. (1990). Electrical stimulation of the inferior colliculus at low rates
protects cochlea from auditory desensitization. Brain Res 506: 192-204.
Ryan S., Kemp DT, Hinchcliffe R. (1991). The influence of contralateral acoustic
stimulation on click-evoked otoacoustic emissions in humans. Br J Audiol 25:
391-97.
Ryan S., Piron JP. (1994). Functional maturation of the Medial Efferent Olivocochlear
System in human neonates. Acta Otolaryngol (Stockh) 114: 485-89.
Sahley T, Nodar R, Musiek F. (1997). Efferent Auditory System: Structure and
Function. (pp1-5). London : Singular Publishing Group.
Sahley T, Nodar R, Musiek F. (1997). Neuroanatomy of the auditory pathways.
Efferent Auditory System: Structure and Function. (pp 25-47). London: Singular
Publishing Group, Inc.
Sahley T, Nodar R, Musiek F. Clinical relevance. In Sahley T, Nodar R, Musiek
F (eds). “Efferent Auditory System: Structure and Function”, Singular
Publishing Group, Inc. San Diego, London. 1997c; pp 7-24.
Siegel J, Kim DO. (1982). Efferent neural control of the cochlear mechanics?
Olivocochlear bundle stimulation effects cochlear biomechanical nonlinearity.
Hear Res 6: 171-82.
Starr A, Picton T, Sininger Y, Hood L, Berlin C. (1996). Auditory neuropathy.
Brain 119: 741-53.
Subramaniam M, Henderson D, Spongr VP. (1993). Protection from noise induced
hearing loss: Is prolonged “conditioning” necessary? Hear Res 65:
234-39.
Tavartkiladge G, Frolenkov G, Kruglov A, Artamasof S. (1997). Ipsilateral suppression
of Transient Evoked Otoacoustic Emissions. Otoacoustic Emissions: Clinical Applications.
(pp110-29). New York: Thieme.
Tolbert L, Morest D, Yurgelun-Todd D. (1982). The neuronal architecture of the
anteroventral cochlear nucleus of the cat in the region of the cochlear nerve
root: Horseradish peroxidase labeling of identified cell types. Neuroscience.
7: 3031-52.
Veuillet E, Collet L, Duclaux R. (1991). Contralateral auditory stimulation
and active micromechanical properties in human subjects : Dependence on stimulus
variables. Neurophysiol 65 : 724-35.
Warr WB. (1992). Organization of olivocochlear efferent systems in mammals.
The mammalian auditory pathway: Neuroanatomy. (pp 410-48). New York: Springer-Verlag.
Warr WB, Guinan JJ. (1979). Efferent innervation of the organ of Corti: two
separate systems. 173: 152-5.
Warren EH III, Liberman CM. (1989). Effects of contralateral sound on auditory-nerve
responses. I. Contributions of cochlear efferents. Hear Res 37: 89-104.
Williams EA, Brookes G, Prasher DK(1994). Effects of contralateral acoustic
stimulation on otoacoustic emissions following vestibular neurectomy. Scand
Audiol 22: 197-203.


