Audiological Medicine

ISSN: 1651-386X (Print) 1651-3835 (Online) Journal homepage: http://www.tandfonline.com/loi/ihbc19

Otoacoustic emission suppression testing: A

clinician's window onto the auditory efferent
pathway

Louisa Murdin & Rosalyn Davies

To cite this article: Louisa Murdin & Rosalyn Davies (2008) Otoacoustic emission suppression
testing: A clinician's window onto the auditory efferent pathway, Audiological Medicine, 6:4,
238-248, DOI: 10.1080/16513860802499957

To link to this article: http://dx.doi.org/10.1080/16513860802499957

Published online: 11 Jul 2009.

Submit your article to this journal

Article views: 101

View related articles

Citing articles: 3 View citing articles

Full Terms & Conditions of access and use can be found at

http://www.tandfonline.com/action/journalInformation?journalCode=ihbc19

Download by: [University of Valencia] Date: 11 July 2017, At: 08:59

Audiological Medicine. 2008; 6: 238
248

Otoacoustic emission suppression testing: A clinicians window

onto the auditory efferent pathway

LOUISA MURDIN & ROSALYN DAVIES

Department of Neuro-otology, National Hospital for Neurology and Neurosurgery, London, UK

Abstract
There has been considerable progress in the last decade in understanding the role of the auditory efferent pathway. This is
exemplified by the development of tests for the suppressive effect of contralateral noise on the production of otoacoustic
emissions by the outer hair cells of the cochlea. Suppression of OAEs is demonstrably subserved by the auditory efferent
pathway, as carried in the inferior vestibular nerve. Advances in the development of testing the suppressive effects of noise
have been paralleled by application to a variety of relevant clinical scenarios, enhancing and refining the use of this test in
routine clinical practice. In particular, OAE suppression testing has been proposed in the assessment of cerebello-pontine
angle tumours, multiple sclerosis, myasthenia gravis, auditory neuropathy/dys-synchrony and auditory processing disorders.
This review considers these advances, along with practical issues and pitfalls in testing. OAE suppression testing is the most
widely accessible method of testing auditory efferent function in the clinic, but consensus has yet to be achieved as to a
standard protocol, and interpretation of this test, and elements of the underlying physiology remain incompletely
understood. It is a useful addition to the audiological test battery, allowing the clinician a window onto the auditory efferent
pathway.

Key words: otoacoustic emissions, auditory efferent pathway, contralateral suppression

Introduction Search strategy

Recording of otoacoustic emissions (OAEs) has been
used for more than a quarter of a century in the
evaluation of the peripheral auditory system (1).
Established applications for OAE testing are the
assessment of cochlear function in patients with
hearing loss and tinnitus; serial monitoring of
potential or progressive inner ear disorders; and in
screening for hearing loss in newborns and others in
whom behavioural audiological testing is difficult or
compromised (reviewed in (2)). Additional clinical
applications have been suggested by studying the
suppressive effect of noise on the amplitude of
OAEs, including evaluation of efferent pathway
integrity (3). This article describes the anatomy
and physiology which underlies application of this
technique, and describes how testing is carried out
and interpreted in routine clinical practice. This is
followed by a review of the literature regarding
clinical applications of OAE suppression testing,
and a case example is presented for illustrative
purposes.
A search was undertaken of Medline and Embase
databases, using the term otoacoustic emissions
(MESH and free text). All abstracts generated were
reviewed and relevant articles selected on the basis of
relevance to clinical practice. Reference lists of such
articles were also reviewed and suitable papers
retrieved, focusing primarily on papers highlighting
potential clinical applications.
Anatomy and physiology of the auditory
efferent pathway
The auditory efferent pathway is subserved by the
olivocochlear bundle originating in the brainstem at
the level of the superior olivary complex (SOC,
Figure 1). These neurons derive from the lateral
SOC (lateral olivocochlear bundle, LOC) or the
medial SOC (medial olivocochlear bundle, MOC).
There are ipsilateral and contralateral olivocochlear
reflexes. Both of these reflexes ascend from the
cochlea to the cochlear nucleus and traverse the

Correspondence: L. Murdin, Department of Neuro-otology, Box 127 National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N
3BG, UK. Tel: 0845 1555000, extn. 723386. Fax: 020 7829 8775. E-mail: louisa@murdin.com

(accepted 23 September 2008)

ISSN 1651-386X print/ISSN 1651-3835 online # 2008 Informa UK Ltd. (Informa Healthcare, Taylor & Francis As)
DOI: 10.1080/16513860802499957
 Otoacoustic emission suppression 239

CN: cochlear nucleus

TB: trapezoid body
SOC: superior olivary complex
OCB: olivocochlear bundle
ANF: auditory nerve fibre
IHC: inner hair cell
OHC: outer hair cell
Ascending pathways are shown as double lines. ........... .
Lateral olivocochlear path are shown as dashed lines. .
Medial olivocochlear path are shown as bold lines. ....

Modulation by higher centres

SOC SOC

TB
CN CN

Uncrossed
Crossed OCB
OCB
Floor of
4th ventricle

OCB in
inferior
Midline vestibular
ANF nerve

IHC OHC

Figure 1. Lateral olivocochlear pathway (LOC) is shown as dashed lines. Medial olivocochlear pathway (MOC) is shown as bold lines.

midline once in the trapezoid body (4). After
synapsing in the superior olivary complex, the
ipsilateral reflex then decussates again in the crossed
olivocochlear bundle at the floor of the fourth
ventricle. The contralateral reflex descends in the
uncrossed olivocochlear bundle. Both pathways
travel in the inferior vestibular nerve. In many
animals, the ipsilateral MOC reflex dominates, but
the relative contributions of ipsilateral and contral-
ateral reflexes in humans are less clear. MOC
fibres are mostly large and myelinated. The lateral
olivocochlear (LOC) bundle consists mainly of
smaller unmyelinated fibres, and is predominantly
ipsilateral. MOC neurons synapse directly onto
outer hair cells, whereas LOC neurons synapse
onto the afferent auditory nerve fibres (5). Both
pathways are subject to top down modulation by
the auditory cortex (6).
OAEs are thought to be the mechanical by-
product of outer hair cell activity in their role of
enhancing frequency specificity as modulators of
cochlear amplifier gain. Since MOC neurons sy-
napse directly onto the outer hair cells, it is not
surprising that changes in MOC activity influence
240 L. Murdin & R. Davies
OAE properties. Noise stimulation activates the
efferent pathway reflex thereby suppressing OAE
amplitude, and additionally causing a phase shift of
the response (7). This suppressive effect has been
demonstrated in spontaneous (8), transient evoked
(9), stimulus frequency (5) and distortion product
OAEs (10).
As the auditory efferent system travels in the
inferior vestibular nerve, its function could be
presumed to be disrupted with vestibular nerve
section, and indeed OAE suppression is lost in
subjects with vestibular deafferentation (11,12). To
demonstrate that the phenomenon is mediated via
the MOC and not the middle ear reflexes, the effect
has been observed in patients with Bells palsy and
other conditions with absent middle ear reflexes
(12). OAE suppression is highly frequency specific,
which is not a feature of middle ear reflexes, and has
been shown to be robust at intensities below the
acoustic reflex threshold (13). In addition, animal
studies have shown that crossed olivocochlear bun-
dle stimulation suppresses OAEs even when middle
ear muscles have been severed (14).
There are many hypotheses as to the physiological
function of the MOC system. It has been suggested
to shift the dynamic range of hearing to enhance
signal detection and frequency selectivity (15), to
protect from excessive noise (16,17), and aid in
selective attention (18).
Carrying out OAE suppression test in the clinic
Essentially, the OAE is recorded using an evoking
click or tone both with and without suppressive noise,
and the amplitude of the two responses is compared.
Parameters relating to both evocation of the OAE and
to the suppressive noise affect outcome.
OAE evoking stimulus parameters
Suppressive effects are larger as OAE level decreases,
because cochlear amplifier gain is largest at low
evoking stimulus presentation levels (19). A low
intensity stimulus also avoids the problem of con-
founding middle ear muscle contraction. However,
the stimulus must be adequate to evoke a recordable
OAE, and for the suppressive effect to be measur-
able. For transient click evoked OAE suppression in
normal hearing individuals, a click stimulus of
around 60dB SPL is suggested. The uniform click
is often selected in favour of the usual reverse-
polarity click to avoid distortions in response ampli-
tude (20). This means that more noise will be
included in the measured response, but since the
measurement is relative across two conditions (i.e.
with and without suppressive noise) this is thought
to be less important.
Suppressive noise stimulus parameters
The MOC can be activated by low (just audible)
levels of noise, and the suppressive effect increases
with higher intensities (3,7). As is the case for the
OAE evoking stimulus, the noise stimulus must use a
sound source intensity that is too small to elicit
middle ear muscle contraction, i.e. less than 75dB
SPL for broadband noise. One study has shown that
the greater the bandwidth of the noise, the greater
the resulting amount of suppression (21); 40dB SL
white noise was identified in one experiment to be
the highest intensity that can be used without
eliciting middle ear reflexes (less than 1% normal
subjects (22)). Many groups have found that white
or broadband noise at 30 to 40dB SL is adequate
(9,23
25). Testing can be performed using ipsilat-
eral, contralateral or bilateral noise, and most centres
have used contralateral noise (9,24,26,27). How-
ever, it is reported that the suppressive effect is
greatest using binaural noise, with a lesser effect
from ipsilateral noise, and contralateral noise caus-
ing the weakest suppression (28). Using ipsilateral or
binaural noise creates problems in distinguishing
signal from noise in the responses, and thus requires
more complex analysis or the use of forward masking
techniques, making the use of contralateral noise a
more technically straightforward procedure.
Which type of OAE?
It could be argued that for greatest frequency
specificity information, DPOAEs may be a preferred
technique. However, the main disadvantage of using
DPOAEs is that the effect of noise is not always
suppressive (29). The magnitude of the effect is also
small. These two factors mean that it is difficult to
interpret single measurements. Stimulus frequency
OAEs are technically more difficult to record, but
are perhaps more easily interpretable (5). Most
clinical work has been carried out using TEOAEs.
Parameters used for testing in general clinical
situations in our department are summarized in
Box 1.
Interpretation: what level of suppression is
normal?
Good test-retest reliability of OAE suppression in
young healthy military service subjects was demon-
strated using DPOAEs (10). However, significant
inter-individual and intra-individual variability of
contralateral suppression of TEOAEs has been

Box 1. National Hospital for Neurology and Neu-
rosurgery protocol for testing OAE contralateral
suppression.
The procedure is carried out in a sound treated
room with subjects seated in a comfortable chair.
1. Ensure external ears are clean and free of wax/
external debris.
2. Carry out tympanometry to confirm normal
middle ear function, and standard TEOAE
testing.
3. Set ILO88 software to Difference B on/off
function using the following parameters:
i. Uniform click (to evoke OAE): 60 /  The lack of an observed effect in this latter study
3dB SPL.
ii. White noise (contralaterally for suppres-
sion): 40dB SL via insert probe.
iii. 600 sweeps (60 10 autorepeat takes,
alternating with and without contralateral
noise).
iv. Noise rejection 48dB SPL.
4. The response is taken as the difference be-
tween the amplitude of the response with
contralateral noise (from AltF1 on the key-
board) and the amplitude of the response
without contralateral noise (from AltF2).
Adapted from Ceranic et al. (24).
reported in six healthy normal subjects aged 22
67
years (30). Another study confirmed the presence of
TEOAE suppression in 20 normal subjects, but in
some the suppression was weak, and in several cases
very asymmetrical (12). There was no difference
between left and right ears and no testing order effect
when results were averaged across all individuals. It
seems likely that factors such as repeatability vary
considerably, depending on the protocol selected, and
possibly also on subject factors such as age, gender
and handedness (see below).
The effect of benzodiazepines on OAE suppres-
sion has been studied, with the effect of oxazepam
being greater in the right ear (31). This group has
also noted asymmetries in MOC effects which co-
vary with gender and handedness in people under 34
years of age (32). Values of suppression are greater in
the right ear in right handed people, but this
asymmetrical effect is not seen in left handed people,
in whom both ears show values similar to the right
ear of right-handed people.
Using a similar procedure to that described in Box
1, a suppression level below 1.0dB is often taken as
abnormal. This figure gave a false negative rate of
Otoacoustic emission suppression 241
about 17% in extrinsic brainstem lesions (n 18)
and 0% in intrinsic brainstem lesions (n 11) (33).
Recent work in our department using the protocol
described in Box 1 on 39 healthy volunteers aged
18
60 years has yielded a lower cut-off point for
normal suppression (two standard deviations below
the mean) of 0.7dB (Murdin, unpublished observa-
tions).
What is the effect of age?
It has been reported that the suppressive effect is
smaller in older subjects than in a younger age group
(34). Conflicting reports exist, however, showing no
effect of age, using broadly similar protocols (35).
may have resulted from a lack of statistical power of
the chosen analysis technique, with subjects split
into age groups each containing 12 or fewer subjects.
A decrease in suppression of DPOAEs in middle and
older aged groups compared to younger subjects has
been reported (36). It seems likely that there is a
gradual fall-off in efferent system function with
increasing age, although it is hard to separate this
out from the effect of age on hearing levels. This may
be compared with the effect of age on TEOAE
amplitude, and the effect of noise on OAE suppres-
sion (see below).
At the other end of the scale, the phenomenon is
absent in many premature newborns up to around
34 weeks gestation and becomes increasingly appar-
ent with postnatal maturity (37). However, in this
study the afferent arm of the reflex was not assessed
independently, so it is not possible to determine
from these data whether this delay is related to the
known maturational effect in the afferent arm, or can
be localized to the efferent pathway.
What are the clinical applications of OAE
suppression testing?
Neurological disorders
Cerebello-pontine angle tumours. Four cases of vestib-
ular schwannoma (acoustic neuroma) have been
reported in which the amplitude of DPOAEs (with-
out suppression testing) was larger in the affected
than the unaffected side, suggesting a disinhibition
effect and, therefore, possible involvement of the
MOC system (38). Other work is broadly consistent
with this hypothesis, although these four cases were
selected retrospectively from a pool of 106 patients,
suggesting that the effect is not a common one. One
study compared TEOAE suppression by contralat-
eral noise in 17 patients with unilateral cerebello-
pontine angle (CPA) tumours with normal controls
242 L. Murdin & R. Davies
(39). There was no difference between ears in the
patient group. However, there was a difference
between control ears and patient ears (with or
without tumour), with normal control subjects
showing greater suppressive effects. This suggests
that there is impairment of the afferent and efferent
pathways on both sides occurring within the tumour
group. This may be explained by the diversity of
lesion size and neurological location. There are also
reports of paradoxical effects of noise on OAE
amplitude in patients with acoustic neuroma, i.e.
an increase in amplitude with noise stimulation (40).
The authors speculate that the pathology could
impact adaptation occurring at the level of efferent
nerve fibre transmitter release, enhancing outer hair
cell motion response instead of suppressing it.
In a study of the practical use of OAE suppression
as a diagnostic test, Prasher et al. studied OAE
suppression in patients with a variety of intrinsic and
extrinsic brain lesions (31). In those with CPA
tumours, the affected ear showed reduced suppres-
sion, and suppression was reduced bilaterally in
those with intrinsic brainstem lesions. Similarly, it
has been reported that OAE suppression can be
affected by cholesterol cysts of the midline petrous
apex (25).
Multiple sclerosis. In a comprehensive evaluation of 30
patients with multiple sclerosis, TEOAE suppression
was significantly reduced compared with normal
controls (41). Ninety per cent of subjects with
multiple sclerosis had abnormal suppression in at
least one ear, compared to only 4.5% of healthy
normal controls. It is worth noting that most of the
ears with abnormal suppression testing also had
abnormal auditory brainstem responses, so that the
lesion cannot be confidently localized to the efferent
pathway, although the authors argue that as the
mean pure tone audiometric thresholds for the
subjects were all within the normal range, significant
afferent dysfunction is unlikely.
Myasthenia gravis. In an elegant pharmacological
study, suppression of DPOAEs in patients with
myasthenia gravis was examined before and after
acetylcholinesterase inhibitor administration (27). In
the pre-administration condition there was no sig-
nificant suppression. After administration, however,
contralateral noise produced a significant decrease of
DPOAE amplitudes for middle frequencies (f2
between 1306 and 2600 Hz). The authors suggested
that the drug-induced increase in acetylcholine
availability facilitates outer hair cell function, and
that contralateral suppression of DPOAEs may be
useful in monitoring the effectiveness of treatment.
These results were confirmed by another study,
which reported that patients with myasthenia gravis
lose DPOAE suppression, but that such an effect
was not seen with TEOAEs (42). Apart from a
chance statistical aberration, a potential explanation
for this observation proffered by the authors is that
the frequency specificity of DPOAEs potentially
renders DPOAE suppression a more specific test
for some conditions.
Migraine. Migraine is a common neurological dis-
order characterized, in addition to typical headaches,
by heightened sensitivity to sensory stimuli (43).
Symptoms of phonophobia and photophobia form
part of the International Headache Society (2004)
criteria for diagnosis of migraine (44). Since OAE
suppression is postulated to have a role in regulation
of system gain in response to noise, it could be
hypothesized that OAE suppression testing may be
abnormal in migraineurs (see case example, Box 2).
One study has reported OAE data in migraineurs.
The authors record that there is a statistically
significant difference between TEOAE amplitude
in quiet and noise conditions in normal subjects, but
not in migraineurs (45). This result is of interest, but
there are methodological limitations. For example,
the eliciting stimulus was set at 83dB SPL, and a role
of middle ear reflexes cannot be excluded. Also, the
analysis depended on pooled data for noise and quiet
conditions, rather than making use of paired data for
each individual.
Auditory disorders
Exposure to hazardous noise. OAE suppression has
been examined in military personnel after impulse
noise exposure (46). Significant correlations were
obtained between audiometric threshold improve-
ment and contralateral TEOAE suppression, with
better recovery in subjects with greater MOC sup-
pressive action. The authors suggested that the MOC
system could play a role in post-traumatic auditory
threshold recovery. However, a similar study that
attempted to correlate temporary threshold shift in
healthy young men with a degree of contralateral
suppression of DPOAEs showed no such effect (10).
Solvent exposure differentially affects OAE suppres-
sion in noise-exposed workers (47). Classical musi-
cians have been shown to have a greater degree of
OAE suppression than non-musicians (48). This has
been postulated to relate to sound conditioning, the
phenomenon by which prior exposure to noise
protects from further noise damage. Dysfunction of
the MOC may be a factor in susceptibility to the
development of tinnitus or hyperacusis, especially in
the context of noise induced hearing loss (49).

Box 2. Case example.
An 18-year-old woman was seen in the neuro-
otology clinic. She experienced episodic dizziness
from the age of three years, occurring every three
months, associated with photophobia, nausea
and, more recently, unilateral tinnitus on the right
side. Additionally, she suffered attacks of migraine
with aura meeting International Headache Society
(2004) criteria (45). She has a stable mild hearing
loss present since childhood (Figure 2) with
normal auditory brainstem responses and stape-
dial reflexes. At assessment in July 2004 her
TEOAEs were robustly present with large ampli-
tudes (23.5dB SPL on the right; 23.2dB SPL on
the left) despite her hearing loss. Over subsequent
years, OAE suppression was measured on a
number of occasions. It was noted to be reduced
on the left or bilaterally when she was seen just
before an attack, but present on the right when
she was well (Figure 3). This pattern suggests a
fluctuating olivocochlear reflex deficit, and is
hypothesized to relate to her diagnosis of mi-
graine. She has abnormal suppression bilaterally,
with the right ear appearing to correlate with
symptoms.
Patients with noise-induced tinnitus have less sup-
pression than normal controls or those with tinnitus
due to other causes (50).
Tinnitus/hyperacusis. Patients with tinnitus after head
injury have been shown to have both larger TEOAE
amplitudes and less suppression than either normal
subjects or patients with head injury but no tinnitus
(23,24). Patients with acute tinnitus also had less
suppression of DPOAEs than normal controls,
although no difference in suppression was shown in
this study between symptomatic and asymptomatic
ears (26). It has been reported that OAE suppression
can be deficient in some cases of hyperacusis (9). A
review of studies of patients who have undergone
vestibular nerve section (and therefore presumed de-
efferentation) showed that the majority experienced
no increase in complaints of tinnitus (51). Never-
theless, in individual studies up to 60% of this
population does experience worsening of tinnitus
symptoms, and it is possible that efferent system
dysfunction is relevant to an unidentified subgroup.
Effects of vestibular nerve section on symptoms of
hyperacusis are less well documented, although one
study reported no effect on various psychoacoustic
Otoacoustic emission suppression 243
tests of loudness adaptation in a series of 15 patients
(52).
King-Kopetzky syndrome/obscure auditory dysfunction.
Patients with hearing difficulties in background noise
and normal audiograms (also known as King-Ko-
petzky syndrome or Obscure Auditory Dysfunction)
are another group in whom efferent dysfunction has
been proposed (53). This hypothesis is supported by
data from a small pilot study (54). In this study
suppression effects were more pronounced in right
ears than left, which may relate to the handedness
findings discussed above (32). Abnormal suppres-
sion of TEOAEs by contralateral noise has been
shown to be more common in children with an
auditory processing disorder than those without
(55,56). If the MOC has a role in selective attention
or noise suppression, it may be, perhaps rather
speculatively, hypothesized that MOC dysfunction
could have a role in the development of specific
language impairment by disrupting language access.
However, when this hypothesis was investigated
using TEOAE suppression by contralateral noise in
a fairly small sample of 20 diverse children with
specific language impairment, no evidence of such
an effect was found (57). Reduced suppression has
been noted in childhood selective mutism (58).
Auditory neuropathy/dys-synchrony. Reduced suppres-
sion is a common finding in auditory neuropathy/
dys-synchrony in patients with absent auditory
brainstem responses and robust TEOAEs (20).
This effect was demonstrable to an impressive extent
even with a small sample of nine cases. In this study,
there was no demonstrable difference in suppression
impairment between patients with normal pure tone
thresholds and those with poor pure tone thresholds.
One hypothesis to explain this observation is that
afferent dysfunction results in inability to activate the
efferent response (20,59). This is supported by the
report of a case of unilateral auditory neuropathy/
dys-synchrony, interpreting the pattern of abnorm-
alities across binaural, ipsilateral and contralateral
noise conditions (20).
Screening applications
Neonatal hearing loss. Neonates with normal
TEOAEs but risk factors for hearing loss showed
lower levels of suppression than full-term neonates
without risk factors (60). This observation may
relate to lower levels of neurological maturity in the
high-risk group, since, as discussed above, there is a
known maturational effect (61). The authors em-
phasize that this is a group effect and might not be
detectable in individual cases, but conjecture that
244 L. Murdin & R. Davies
Figure 2. Pure tone audiogram for case example.
reduced OAE suppression might be a risk factor for
developing hearing loss or auditory processing dis-
orders. Since the subjects were selected as being at
high risk for hearing loss, it remains to be proven that
abnormal OAE suppression testing could provide
information additional to what is known from the
clinical history.
Noise exposure
Section of the olivocochlear bundle in chinchillas
increases susceptibility to acoustic trauma (62). This
effect has also been demonstrated in guinea pigs
(17). These results have been taken to suggest that
the olivocochlear system may have a role in protec-
tion from noise exposure. OAE suppression is
reduced in human subjects exposed to noise (63),
and has even been mooted as a method of early
identification for at-risk workers (64), although there
is currently little evidence that suppression testing
would have any advantage over other methods such
as TEOAE measurement.
Ototoxic agents
Can OAE suppression predict susceptibility to
ototoxicity from drugs such as aminoglycosides or
other ototoxic drugs? Clinical studies are not yet
available to answer this question, but one animal
study suggested it may be possible (65). In guinea
pigs, rapid efferent adaptation of DPOAE predicted
both number of days before onset of deafness and
final threshold shift.
Some words of caution
Middle and outer ear factors have a potentially
significant effect on recording of OAEs, and sup-
pressive effects may be masked if recording condi-
tions are not optimal. It is prudent where possible to
make recordings where tympanometry is normal and
the external ear is clear of wax and debris. The
suppressive effect is observed during sleep but in
almost half of cases no suppression is seen at the
onset of sleep (66). Some authors recommend that
subjects read during testing to prevent any possible
reduction in effect due to drowsiness (22).
Direct electrical stimulation of MOC fibres is used
in animal studies, and MOC effects seem to be larger
in these experiments. When OAE suppression is
compared with cochlear neural responses as a
function of MOC stimulation, cochlear neural re-
sponses always show a greater response. In other
words, the use of OAE techniques to assess efferent
system activity is subject to some idiosyncrasy due to
the properties of TEOAEs (5). Some patients do not
lose suppression completely after vestibular neurot-
omy (12), suggesting either that some efferent fibres
do not travel in the vestibular nerve, or that middle
ear reflexes have a role to play in these circum-
stances.
TEOAE recordings, and so also suppression test-
ing, may be a window onto cochlear activity but it

3.00
2.00
imminent
attack
suppression / dB
1.00
0.00
-1.00
-2.00
31-MAR-2005
Figure 3. OAE suppression results for case example. OAE suppression values are plotted using squares (I) for the left ear and circles (k)
for the right ear.
should be recognized that the view is restricted and
the glass may be somewhat misty! Only a fraction of
the acoustic energy emitted by the cochlea is
analysed using OAEs, which are a by-product of
normal cochlear process. The use of suppression
testing to assay efferent function is clearly somewhat
indirect.
Discussion and areas for future research
Suppression of OAEs is a non-invasive and procedu-
rally straightforward test, although there are technical
challenges to its use in the clinic. In the presence of a
normal afferent arm, it can be used to assess integrity
of the efferent auditory pathway. It can be a useful
addition to the audiological test battery (case exam-
ple, Box 2). Despite the advances in development of
OAE suppression testing over the past decade, much
remains to be done. There is little consensus about
the optimal techniques for recording and calculating
suppression, or for interpreting normal values, espe-
cially in older people or those with hearing impair-
ment.
OAE suppression testing has been shown to be
useful in a number of different neurological and
audiological clinical scenarios. There is evidence that
loss of suppression may be a manifestation of
auditory system damage, e.g. in noise and solvent
damage and in the high risk neonatal population,
although inter-individual variability may limit its
Otoacoustic emission suppression 245
well
imminent imminent
attack attack
28-JUL-2005 26-OCT-2006 27-MAR-2008
date
usefulness. Preliminary animal studies have postu-
lated the test as a predictor of ototoxicity, suggesting
applications in chemotherapy or aminoglycoside
treatment.
A number of further areas for research suggest
themselves. The finding that OAE suppression is
weaker in neonates at high risk for hearing loss, and
in children with auditory processing disorders, raises
the possibility of a relationship between these find-
ings. Low levels of suppression in a newborn could
potentially be a risk factor for developing auditory
processing disorders (60).
Could OAE suppression testing be used to assess
conditions of the inferior vestibular nerve, which
carries the efferent arm of the reflex? Vestibular
evoked myogenic potentials (VEMPs) assess a reflex
arc transmitted via the saccule and inferior vestibular
nerve, and have been shown to be useful in predict-
ing outcome in vestibular neuritis in terms of the
development of posterior canal benign paroxysmal
positional vertigo (PC-BPPV) (67). Patients with
preserved VEMPs after vestibular neuritis have an
intact inferior vestibular nerve, which may mediate
symptoms of PC-BPPV. OAE suppression is also
mediated through the auditory efferent pathway via
the inferior vestibular nerve, so would similarly be
intact in the majority of cases in which the superior
vestibular nerve is affected. There is no difference in
TEOAE amplitudes between lesional and contral-
ateral sides after vestibular neuritis according to one
246 L. Murdin & R. Davies
retrospective study (68), although resting TEOAE
amplitude may not be as good an indicator of MOC
activity as OAE suppression.
Data from patients with hyperacusis, especially
those with head injury, suggest that OAE suppres-
sion may be useful in evaluating patients with
heightened auditory responsiveness. This is well
known to occur in some neurological conditions
such as migraine, in which attacks are commonly
associated with hyperacusis or phonophobia. Pre-
liminary data as discussed above have suggested a
significant effect but with some methodological
limitations. Hyperacusis is also noted to occur in
other conditions such as William syndrome and
multiple sclerosis (69), and OAE suppression testing
could help to further characterize these populations.
Acknowledgement
The authors wish to thank Professor D Stephens for
instructive critical comments on an early draft of the
manuscript.
Declaration of interest: The authors report no
conflicts of interest. The authors alone are respon-
sible for the content and writing of the paper.
References
1. Kemp DT. Stimulated acoustic emissions from within the
human auditory system J Acoust Soc Am. 1978;64:1386
91.
2. Lonsbury-Martin BL, Martin GK. Otoacoustic emissions.
Curr Opin Otolaryngol Head Neck Surg. 2003;11:361
6.
3. Collet L, Kemp DT, Veuillet E, Duclaux R, Moulin A,
Morgon A. Effect of contralateral auditory stimuli on active
cochlear micro-mechanical properties in human subjects.
Hear Res. 1990;43:251
61.
4. De Venecia RK, Liberman MC, Guinan JJ Jr, Brown MC.
Medial olivocochlear reflex interneurons are located in the
posteroventral cochlear nucleus: a kainic acid lesion study in
guinea pigs. J Comp Neurol. 2005;487:345
60.
5. Guinan JJ Jr. Olivocochlear efferents: anatomy, physiology,
function, and the measurement of efferent effects in humans.
Ear Hear. 2006;27:589
607.
6. Xiao Z, Suga N. Modulation of cochlear hair cells by the
auditory cortex in the mustached bat. Nat Neurosci. 2002;5:
57
63.
7. Ryan S, Kemp DT, Hinchcliffe R. The influence of contral-
ateral acoustic stimulation on click-evoked otoacoustic emis-
sions in humans. Br J Audiol. 1991;25:391
7.
8. Mott JB, Norton SJ, Neely ST, Warr WB. Changes in
spontaneous otoacoustic emissions produced by acoustic
stimulation of the contralateral ear. Hear Res. 1989;38:
229
42.
9. Collet L, Veuillet E, Bene J, Morgon A. Effects of contral-
ateral white noise on click-evoked emissions in normal and
sensorineural ears: towards an exploration of the medial
olivocochlear system. Audiology. 1992;31:1
7.
10. Wagner W, Heppelmann G, Kuehn M, Tisch M, Vonthein R,
Zenner HP. Olivocochlear activity and temporary threshold
shift-susceptibility in humans Laryngoscope. 2005;115:
2021
8
11. Williams E, Brookes G, Prasher D. Effects of olivocochlear
bundle section and otoacoustic emissions in humans: efferent
effects in comparison with control subjects Acta Otolaryngol.
1994;114:121
9.
12. Giraud AL, Collet L, Chery-Croze S, Magnan J, Chays A.
Evidence of a medial olivocochlear involvement in contral-
ateral suppression of otoacoustic emissions in humans. Brain
Res. 1995;705:15
23.
13. Veuillet E, Collet L, Duclaux R. Effect of contralateral
acoustic stimulation on active cochlear micromechanical
properties in human subjects: dependence on stimulus vari-
ables. J Neurophysiol. 1991;65:724
35.
14. Mountain DC. Changes in endolymphatic potential and
crossed olivocochlear bundle stimulation alter cochlear me-
chanics. Science. 1980;210:71
2.
15. May BJ, Budelis J, Niparko JK. Behavioural studies of the
olivocochlear efferent system: learning to listen in noise. Arch
Otolaryngol Head Neck Surg. 2004;130:660
4.
16. Brown MC, Kujawa SG, Liberman MC. Single olivocochlear
neurons in the guinea pig. II. Response plasticity due to noise
conditioning. J Neurophysiol. 1998;79:3088
97.
17. Maison SF, Liberman MC. Predicting vulnerability to
acoustic injury with a non-invasive assay of olivocochlear
reflex strength. J Neurosci. 2000;20:4701
7.
18. Hill JC, Prasher DK, Luxon LM. Evidence for efferent effects
on auditory afferent activity, and their functional relevance.
Clin Otolaryngol Allied Sci. 1997;22:394
402.
19. Moulin A, Collet L, Duclaux R. Contralateral auditory
stimulation alters acoustic distortion products in humans.
Hear Res. 1993;65:193
210.
20. Hood LJ, Berlin CI, Bordelon J, Rose K. Patients with
auditory neuropathy/dys-synchrony lack efferent suppression
of transient evoked otoacoustic emissions. J Am Acad Audiol.
2003;14:302
13.
21. Norman M, Thornton AR. Frequency analysis of the
contralateral suppression of evoked otoacoustic emissions by
narrow-band noise. Br J Audiol. 1993;27:281
9.
22. De Ceulaer G, Yperman M, Daemers K, van Driessche K,
Somers T, Offeciers FE, et al. Contralateral suppression of
transient evoked otoacoustic emissions: normative data for a
clinical test set-up. Otol Neurotol. 2001;22:350
5.
23. Attias J, Zwecker-Lazar I, Nageris B, Keren O, Groswasser Z.
Dysfunction of the auditory efferent system in patients with
traumatic brain injuries with tinnitus and hyperacusis. J Basic
Clin Physiol Pharmacol. 2005;16:117
26.
24. Ceranic BJ, Prasher DK, Raglan E, Luxon LM. Tinnitus after
head injury: evidence from otoacoustic emissions. J Neurol
Neurosurg Psychiat. 1998;65:523
9.
25. Hurley RM, Hurley A, Berlin CI. The effect of midline
petrous apex lesions on tests of afferent and efferent auditory
function. Ear Hear. 2002;23:224
34.
26. Riga M, Papadas T, Werner JA, Dalchow CV. A clinical study
of the efferent auditory system in patients with normal
hearing who have acute tinnitus. Otol Neurotol. 2007;28:
185
90.
27. Di Girolamo S, dEcclesia A, Quaranta N, Garozzo A, Evoli
A, Paludetti G. Effects of contralateral white noise stimulation
on distortion product otoacoustic emissions in myasthenic
patients. Hear Res. 2001;162:80
4.
28. Berlin CI, Hood LJ, Hurley AE, Wen H, Kemp DT. Binaural
noise suppresses linear click-evoked otoacoustic emissions
more than ipsilateral or contralateral noise. Hear Res.
1995;87:96
103.
29. Lisowska G, Smurzynski J, Morawski K, Namyslowski G,
Probst R. Influence of contralateral stimulation by two-tone

complexes, narrow band and broadband noise signals on the
2f1
f2 distortion product otoacoustic emission levels in hu-
mans. Acta Otolaryngol. 2002;122:613
9.
30. Graham RL, Hazell JW. Contralateral suppression of transient
evoked otoacoustic emissions: intra-individual variability in
tinnitus and normal subjects. Br J Audiol. 1994;28:235
45.
31. Morand-Villeneuve N, Veuillet E, Perrot X, Lemoine P,
Gagnieu MC, Sebert P, et al. Lateralization of the effects of
the benzodiazepine drug oxazepam on medial olivocochlear
system activity in humans. Hear Res. 2005;208:101
6.
32. Khalfa S, Veuillet E, Collet L. Influence of handedness on
peripheral auditory asymmetry. Eur J Neurosci. 1998;10:
2731
7.
33. Prasher D, Ryan S, Luxon L. Contralateral suppression of
transiently evoked otoacoustic emissions and neuro-otology.
Br J Audiol. 1994;28:247
54.
34. Castor X, Veuillet, Morgon A, Collet L. Influence of ageing
on active cochlear micromechanical properties and on the
medial olivocochlear system in humans. Hear Res. 1984;77:
1
8.
35. Quaranta N, Debole S, Di Girolamo S. Effect of ageing on
otoacoustic emissions and efferent suppression in humans.
Audiology. 2001;40:308
12.
36. Kim S, Frisina DR, Frisina RD. Effects of age on contralateral
suppression of distortion product otoacoustic emissions in
human listeners with normal hearing Audiol Neurootol. 2002;
7:348
57.
37. Chabert R, Guitton MJ, Amram D, Uziel A, Pujol R,
Lallemant JG, et al. Early maturation of evoked otoacoustic
emissions and medial olivocochlear reflex in preterm neo-
nates. Pediatr Res. 2006;59:305
8.
38. Gouveris H, Mann W. Increased amplitudes of distortion
product otoacoustic emissions in patients with unilateral
acoustic neuroma. ORL J Otorhinolaryngol Relat Spec. 2004;
66:302
5.
39. Ferguson MA, ODonoghue GM, Owen V. Contralateral
suppression of transient evoked otoacoustic emissions in
patients with cerebello-pontine angle tumour. Ear Hear.
2001;22:173
8.
40. Quaranta A, Gandolfi A, Fava G, Quaranta N, Zini C.
Paradoxical effects of contralateral white noise on evoked
otoacoustic emissions in ears with acoustic neuroma. Acta
Otolaryngol. 2000;120:227
30.
41. Coelho A, Ceranic B, Prasher D, Miller DH, Luxon LM.
Auditory efferent function is affected in multiple sclerosis. Ear
Hear. 2007;28:593
604.
42. Hamed SA, Elattar AM, Hamed EA. Irreversible cochlear
damage in myasthenia gravis: otoacoustic emission analysis.
Acta Neurol Scand. 2006;113:46
54.
43. Goadsby P, Lipyon R, Ferrari M. Migraine: current under-
standing and treatment. N Eng J Med. 2002;346:257
70.
44. International Headache Society Headache Classification
Committee. The International Classification of Headache
Disorders (second edition). Cephalalgia. 2004;24 (Suppl
1):1
160.
45. Bolay H, Bayazit YA, Gunduz B, Ugur AK, Akcali D,
Altunyay S, et al. Subclinical dysfunction of cochlea and
cochlear efferents in migraine: an otoacoustic emission study.
Cephalalgia. 2008;28:309
17.
46. Veuillet E, Martin V, Suc B, Vesson JF, Morgon A, Collet L.
Otoacoustic emissions and medial olivocochlear suppression
during auditory recovery from acoustic trauma in humans.
Acta Otolaryngol. 2001;121:278
83.
47. Prasher D, Al-Hajjaj H, Aylott S, Aksentijevic A. Effect of
exposure to a mixture of solvents and noise on hearing and
Otoacoustic emission suppression 247
balance in aircraft maintenance workers. Noise Health. 2005;
7:31
9.
48. Brashears SM, Morlet TG, Berlin CI, Hood LJ. Olivoco-
chlear efferent suppression in classical musicians. J Am Acad
Audiol. 2003;14:314
24.
49. Ceranic B. The value of otoacoustic emissions in the
investigation of noise damage. Audiol Med. 2007;5:10
4.
50. Attias J, Bresloff I, Furman V. The influence of the efferent
auditory system on otoacoustic emissions in noise induced
tinnitus: clinical relevance. Acta Otolaryngol. 1996;116:
534
9.
51. Baguley DM, Axon P, Winter IM, Moffat DA. The effect of
vestibular nerve section upon tinnitus. Clin Otolaryngol
Allied Sci. 2002;27:219
26.
52. Scharf B, Magnan J, Chays A. On the role of the olivocochlear
bundle in hearing: 16 case studies. Hear Res. 1997;103:
101
22.
53. Zhao F, Stephens D. A critical review of King-Kopetzky
syndrome: hearing difficulties, but normal hearing? Audiol
Med. 2007;5:119
24.
54. Zhao F, Ozcaglar H, Meredith R, Stephens D. Transient
evoked otoacoustic emission with contralateral stimulation in
King Kopetzky syndrome. J Audiol Med. 1997;6:36
44.
55. Sanches SG, Carvallo RM. Contralateral suppression of
transient evoked otoacoustic emissions in children with
auditory processing disorder. Audiol Neurootol. 2006;11:
366
72.
56. Muchnik C, Ari-Even Roth D, Othman-Jebara R, Putter-Katz
H, Shabtai EL, Hildesheimer M. Reduced medial olivoco-
chlear bundle system function in children with auditory
processing disorders. Audiol Neurootol. 2004;9:107
14.
57. Clarke EM, Ahmmed A, Parker D, Adams C. Contralateral
suppression of otoacoustic emissions in children with specific
language impairment. Ear Hear. 2006;27:153
60.
58. Bar-Haim Y, Henkin Y, Ari-Even Roth D, Tetin-Schneider S,
Hildesheimer M, Muchnik C. Reduced auditory efferent
activity in childhood selective mutism. Biol Psychiatry. 2004;
55:1061
8.
59. Berlin CI, Hood LJ, Morlet T, Wilensky D, St. John P,
Montgomery E, et al. Absent or elevated middle ear muscle
reflexes in the presence of normal otoacoustic emissions: a
universal finding in 136 cases of auditory neuropathy/dys-
synchrony. J Am Acad Audiol. 2005;16:546
53.
60. Durante AS, Carvallo RM. Contralateral suppression of
linear and non-linear transient evoked otoacoustic emissions
in neonates at risk for hearing loss. J Commun Disord. 2008;
41:70
83.
61. Gkoritsa E, Tsakanikos M, Korres S, Dellagrammaticas H,
Apostolopoulos N, Ferekidis E. Transient otoacoustic emis-
sions in the detection of olivocochlear bundle maturation. Int
J Pediatr Otorhinolaryngol. 2006;70:671
6.
62. Zheng XY, Henderson D, Hu BH, Ding DL, McFadden SL.
The influence of the cochlear efferent system on chronic
acoustic trauma. Hear Res. 1997;107:147
59.
63. Desai A, Reed D, Cheyne A, Richards S, Prasher D. Absence
of otoacoustic emissions in subjects with normal audiometric
thresholds implies exposure to noise. Noise Health. 1999;1:
58
65.
64. Sliwinska-Kowalska M, Kotylo P. Occupational exposure to
noise decreases otoacoustic emission efferent suppression. Int
J Audiol. 2002;41:113
9.
65. Halsey K, Skjonsberg A, Ulfendahl M, Dolan DF. Efferent-
mediated adaptation of the DPOAE as a predictor of
aminoglycoside toxicity. Hear Res. 2005;201:99
108.
248 L. Murdin & R. Davies
66. Collet L, Veuillet E, Moulin A, Morlet T, Giraud AL,
Micheyl C, et al. Contralateral auditory stimulation and
otoacoustic emissions: a review of basic data in humans. Br
J Audiol. 1994;28:213
8.
67. Murofushi T, Halmagyi GM, Yavor RA, Colebatch JG.
Absent vestibular evoked myogenic potentials in vestibular
neurolabyrinthitis: an indicator of inferior vestibular nerve
involvement? Arch Otolaryngol Head Neck Surg.
1996;122:845
8.
68. Gouveris H, Victor A, Mann W. Transient evoked otoacoustic
emissions in vestibular neuritis. Ann Otol Rhinol Laryngol.
2006;115:908
11.
69. Baguley DM. Hyperacusis. J R Soc Med. 2003;96:582
5.