update on otoacoustic emissions: basic science to clnical ... · update on otoacoustic emissions:...
TRANSCRIPT
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Update on Otoacoustic Emissions:
Basic Science to Clnical Application
Morning Session
Introductions
Historical evolution of OAEs
Cochlear physiology and OAEs
Prospects of clinical applications
Break
OAE types and taxonomy
Mechanisms of OAE generation
Complex generation of DPOAEs
DPOAEs and hearing thresholds
OAEs as early indicators of cochlear pathology
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• Overview of otoacoustic emissions
• Anatomy and physiology
• Classification of OAEs
• Instrumentation and calibration
• Clinical measurement of OAEs: procedures
• OAE analysis
• OAE applications in children
• OAE applications in adults
• Efferent auditory system and OAEs
• New directions in research and clinical
application
Otoacoustic Emissions Textbook
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Update on Otoacoustic Emissions:
Basic Science to Clnical Application
Afternoon Session
General hardware and software orientation
Calibration and probe placement
Break
Measurements with various parameters in diverse
clinical populations
Case studies: Participant cases
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OAEs in AUDIOLOGY TODAY: Main Points
OAEs are important in the diagnostic audiologic
assessment of children and adults.
OAE findings and the audiogram do not always
agree … that‟s good … OAEs provide unique
information on auditory status.
Abnormal OAEs can be recorded with a normal
audiogram … and can detect cochlear dysfunction.
OAEs should be a part of the basic audiologic test
battery.
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Giuseppe Tartini (April 8, 1692 - February 26, 1770)
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George von Bekesy
(1899 - 1972)
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Thomas Gold
OAE Prophet
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OAE:
Classic Quote from Yesteryear by Thomas Gold
“I had discussed at length in 1948 with von Bekesy at
Harvard that the observations he made on the dead
cochlea were unrepresentative. But he wouldn‟t have
that!”
“It is shown that the assumption of a „passive‟ cochlea,
where the elements are brought into mechanical
oscillation solely by means of the incident sound, is not
tenable.”
“ … the nerve ending abstracts much energy from a
mechanical resonator.”
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William Rhode demonstrates cochlear
nonlinearity in the squirrel monkey in 1971.
Data from Ruggero et al., 1982
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David Kemp
“Discoverer of OAEs”
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Discovery of OAEs by David Kemp (Kemp DT. Stimulated acoustic emissions from within the
human auditory system. JASA 64: 1978.)
“A new auditory phenomenon has been identified in the
acoustic impulse of the human ear…
This component of the response appears to have its origin
in some nonlinear mechanism probably located in the
cochlea, responding mechanically to auditory stimulation,
and dependent upon the normal functioning of the cochlear
transduction process…
It is tempting to suggest that one of the functions of the
outer hair cell population is the generation of this
mechanical energy.”
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David Kemp (1978)
Threshold Microstructure (Elliot, 1958)
Spacing of Loudness Maxima (Kemp, 1979)
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William Brownell:
Discoverer of OHC Motility in Early 1980s
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Music
1750s
Audiology
today
Physics/Physiology
1978 –
Psychoacoustics
1805 –
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Historical Overview of OAEs:
Major Events Since Discovery (1)
1980s
Early studies of newborn hearing screening in UK and
Denmark
Introduction of ILO 88 “auditory neuropathy”
1990s
Research on DPOAEs in animals and humans
NIH Consensus Conference recommends UNHS in
1993, including use of OAEs
New DPOAE systems by major manufacturers in 1994
First CPT codes in 1995
OAEs in identification of ANSD
Automated OAE devices
Evidence on clinical applications grows
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Historical Overview of OAEs:
Major Events Since Discovery (2)
2000 to present
Two textbooks on OAEs
OAEs recommended by JCIH for screening
New applications of OAEs including:
Tinnitus
Ototoxicity monitoring
Noise/music cochlear dysfunction
Preschool and school age screening
Combination technologies
ABR and OAEs
Tympanometry and OAEs
New CPT codes for OAEs
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Update on Otoacoustic Emissions:
Basic Science to Clnical Application
Morning Session
Introductions
Historical evolution of OAEs
Cochlear physiology and OAEs
Prospects of clinical applications
Break
OAE types and taxonomy
Mechanisms of OAE generation
Complex generation of DPOAEs
DPOAEs and hearing thresholds
OAEs as early indicators of cochlear pathology
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OAEs: Differences between inner and outer hair cells (1)
Inner Hair Cells Outer Hair Cells
Single row 3 or 4 rows
N = 3500 N = 12,000 to 20,000
On spiral lamina On basilar lamina
Wine bottle shape Cylinder (test tube) shape)
No contact bet/ stereocilia Tallest stereocilia contact tectorial
and tectorial membrane membrane
95% of afferents innervate IHC 5% of afferents innervate OHCs
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Not motile Motile
Encompassed by support cells Supported only on top & bottom
Central nucleus Nucleus at base of cell
Single layer of endoplasmic Extensive subsurface reticulum
cisternae
Mitochondria scattered Mitochondria along throughout cell
perimeter
Efferents from lateral Efferents from medial superior olive
superior olive
OAEs: Differences between inner and outer hair cells (2)
Inner Hair Cells Outer Hair Cells
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Hermann Ludwig Ferdinand von Helmholtz
Overloading type
nonlinearity in the middle
ear.
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Site of Generation
Cochlea: observed delay in OAEs; recordings from BM
& auditory nerve.
Outer Hair Cells: concomitant ablation of OAEs and
OHC (e.g., Davis et. al., 2002); loss of OAEs due to
other insults associated with OHC damage (salicylate,
noise, etc.).
But where in the OHC?
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Lessons from Kemp, 1978
Same stimulus in human ear
shows response lasting beyond
10 ms – TEOAE.
We have to wait for the speaker
to stop ringing. Continues to be
the case; early TEOAE is not
recorded.
Different delays for responses
to tone bursts of different
frequencies – cochlear origin.
Random noise recorded when
closed cavity is stimulated with
a click.
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Site of Generation
Cochlea: observed delay in OAEs; recordings from BM
& auditory nerve.
Outer Hair Cells: concomitant ablation of OAEs and
OHC (e.g., Davis et. al., 2002); loss of OAEs due to
other insults associated with OHC damage (salicylate,
noise, etc.).
But where in the OHC?
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Cheatham et. al. (2004), J Physiol
Liberman et al., 2004
Prestin KO
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Cheatham et. al., (2004); J. Physiol
Verpy et. al., (2008); Nature
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Cochlea Outer Hair Cell
Stereocilia (transducer)
Soma (?amplifier)
Olivocochlear
efferents
Middle ear
transmission
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Why does it matter?
No amplifier: Recordable DPOAEs at high input levels.
Good candidate for acoustic amplification.
No transducer: DPOAEs not recordable. Good
candidate for electrical input.
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Auditory Anatomy Involved in the
Generation of OAEs
Outer hair cell motility
Prestin motor protein
Stereocilia
Motion
Stiffness
Tectorial membrane
Basilar membrane mechanics
Dynamic interaction with outer hair cells
Stria vascularis
Middle ear (inward and outward propagation)
Medial efferent pathways
External ear canal
Stimulus presentation
OAE detection
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Update on Otoacoustic Emissions:
Basic Science to Clnical Application
Morning Session
Introductions
Historical evolution of OAEs
Cochlear physiology and OAEs
Prospects of clinical applications
Break
OAE types and taxonomy
Mechanisms of OAE generation
Complex generation of DPOAEs
DPOAEs and hearing thresholds
OAEs as early indicators of cochlear pathology
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OAEs in Early Detection of Outer Hair Cell Dysfunction:
Rationale underlying many clinical applications
Abnormal
OHC
(OAEs)
Normal
OHC
(OAEs)
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CLINICAL APPLICATION OF
OTOACOUSTIC EMISSIONS (OAE): General advantages
Highly sensitive to cochlear (outer hair cell function)
Site specific (to outer hair cells)
Do not require behavioral cooperation or response
Ear specific
Highly frequency specific
Do not require sound-treated environment
Can be quick (< 30 seconds)
Portable (handheld devices)
Relatively inexpensive
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CLINICAL APPLICATION OF
OTOACOUSTIC EMISSIONS (OAE): Possible disadvantages
Susceptible to effects of noise
Affected greatly by middle ear status
Provide cochlear information only about outer hair cells
May be abnormal or not detected with normal audiogram
Are not detectable with hearing loss > 40 dB HL
Cannot be used to estimate degree of hearing loss
Not a measure of neural or CNS auditory function
Not a test of hearing
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Outer Hair Cells, Otoacoustic Emissions, and
Auditory Function
OHCs and OAEs are highly dependent on blood flow to
the cochlea, due to demands of metabolism
OAEs are pre-neural and, therefore, not affected by
retrocochlear auditory dysfunction
OHC motility contributes to:
enhanced auditory sensitivity
sharper tuning curves (increased frequency
selectivity or cochlear tuning)
normal growth of loudness
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OAEs after Sound Induced
Damage
11 chinchillas exposed to 100
dBA for 5 days
Davis et al., 2005
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And in humans…
Avan & Bonfils (2005)
evaluated DPOAEs in 27
noise-exposed workers
with clear notches in their
audiograms.
(in most ears)
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still from Avan & Bonfils (2004)
(in 11 ears)
DPOAE
Thd
TEOAE
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Recreational Exposure
• 21 participants listened to 1 hour of music from personal music players.
Repeated six times.
• No change in DPOAE or hearing thresholds even in those listening at >
75% of volume setting (97 – 102 dBA).
• TEOAE show statistically significant shift in these listeners of -0.47 dB
at 2 kHz and -0.70 dB at 2.8 kHz.
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338 volunteers (US Navy) evaluated before and after 6-month
training where they were noise exposed.
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On average hearing thresholds did not change in a group of 75
volunteers.
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Significant (-0.66 dB) change in TEOAE amplitude.
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Significant (-1.28 dB) change in DPOAE amplitude. Greatest
change at lowest stimulus level.
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In 18 ears with PTS, the likelihood of PTS increased with decreasing OAE
amplitude.
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Hair cell response returns to normal; Long term synaptic loss and loss of neural
amplitude; Loss of ganglion cells is delayed even more.
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Six Reasons Why OAEs Will Never Replace the
Audiogram nor Accurately Estimate Hearing Loss
(1-3)
OAEs measurement is dependent on inward and outward
propagation of energy through the middle ear (e.g.,
abnormal OAEs with normal hearing sensitivity)
OAEs are more sensitive to cochlear dysfunction than
the audiogram (e.g., abnormal OAEs with normal hearing
sensitivity)
OAEs are electrophysiologic measures while the
audiogram is behavioral (e.g., normal OAEs with
abnormal audiogram)
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Six Reasons Why OAEs Will Never Replace the
Audiogram nor Accurately Estimate Hearing Loss
(4-6)
OAEs are produced by OHCs, whereas the audiogram is
dependent on IHCs (e.g., normal OAEs with abnormal
audiogram)
OAEs are pre-neural, whereas the audiogram is
dependent on retrocochlear pathways (e.g., normal
OAEs with abnormal hearing sensitivity)
OAEs reflect OHC integrity, whereas the audiogram
measure hearing (e.g., normal OAEs with abnormal
audiogram)
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Otoacoustic Emissions in Audiology Today:
Limitations in use of OAEs by clinical audiologists
Over reliance on screening protocols, e.g.,
Recording within a limited frequency region
Simple “pass” versus “fail” outcome
Questionable techniques for measurement and analysis, e.g.,
Single trial or run (remember … “If your OAEs do not repeat, your test is not complete!”
Failure to achieve lowest possible noise levels (< 95%ile for adult normal subjects)
Analysis limited to “present” or “absent”
Not applied in a variety of patient populations
Only used as a screening technique for newborn infants
Not applied routinely in the initial diagnostic audiologic assessment of most patients (children and adult)
False assumption
OAEs will provide the same information that is available from the audiogram … “I know the patient has a sensorineural hearing loss … why should I perform OAEs? …
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Update on Otoacoustic Emissions:
Basic Science to Clnical Application
Morning Session
Introductions
Historical evolution of OAEs
Cochlear physiology and OAEs
Prospects of clinical applications
Break
OAE types and taxonomy
Mechanisms of OAE generation
Complex generation of DPOAEs
DPOAEs and hearing thresholds
OAEs as early indicators of cochlear pathology
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But That’s Not the Entire Story
(See Chapter 3 of Dhar & Hall, 2012)
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Shera, 2009
Phase is a Factor in the Generation of OAEs
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Regular Spacing of Spontaneous OAEs
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base apex
stapes
input
Coherent Reflection Filtering Zweig, Shera (1995 on)
Incoming signal is “reflected”
randomly by outer hair cells;
some reflections are coherent
and contribute to the outward-
traveling energy.
Coherent reflectors near the peak
region of the traveling wave have
enough magnitude to contribute
significantly to ear-canal OAE.
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Inhibition (Suppression) of Otoacoustic Emissions:
Role of the Efferent Auditory System (See Chapter 9 of Dhar & Hall, 2012)
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Classification S
TIM
UL
US
M
EC
HA
NIS
M
Without stimulation Spontaneous
Stimulated Transient,Distortion product,Stimulus frequency
Distortion Reflection Spontaneous
Mixed
DPOAEs
TEOAEs
SFOAEs
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Types of OAEs:
Conventional Classification
Type Stimulus Prevalence
Spontaneous none < 70%
Evoked
transient click or tone burst > 99%
distortion product two pure tones > 99%
stimulus frequency continuous tone ?? %
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Transient Otoacoustic Emissions
(TEOAE)
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Distortion Product Otoacoustic Emissions
(DPOAEs)
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Update on Otoacoustic Emissions:
Basic Science to Clnical Application
Morning Session
Introductions
Historical evolution of OAEs
Cochlear physiology and OAEs
Prospects of clinical applications
Break
OAE types and taxonomy
Mechanisms of OAE generation
Complex generation of DPOAEs
DPOAEs and hearing thresholds
OAEs as early indicators of cochlear pathology
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Update on Otoacoustic Emissions:
Basic Science to Clnical Application
Morning Session
Introductions
Historical evolution of OAEs
Cochlear physiology and OAEs
Prospects of clinical applications
Break
OAE types and taxonomy
Mechanisms of OAE generation
Complex generation of DPOAEs
DPOAEs and hearing thresholds
OAEs as early indicators of cochlear pathology
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Update on Otoacoustic Emissions:
Basic Science to Clnical Application
Morning Session
Introductions
Historical evolution of OAEs
Cochlear physiology and OAEs
Prospects of clinical applications
Break
OAE types and taxonomy
Mechanisms of OAE generation
Complex generation of DPOAEs
DPOAEs and hearing thresholds
OAEs as early indicators of cochlear pathology
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f1 f2 oute
r ear
mid
dle
ear
f2 f1
Mixed DPOAEs
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oute
r ear
mid
dle
ear
f2 f1
nonlinear
reflection composite
model Talmadge, Long, Tubis & Dhar (1999); JASA
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Talmadge, Long, Tubis & Dhar (1999); JASA
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Hearing Level in dB HL
-10 0 10 20 30 40 50 60
OAE
Amplitude
WNL
(Amplitude > 95%ile)
No OAE
(OAE – NF < 6 dB)
Normal
Present
but not
normal No OAE
Relation Between OAE Amplitude and Hearing Loss
DPOAE 65/55 dB SPL TEOAE 80 dB SPL
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Be
st b
et fo
r th
resh
old
pre
dic
tio
n: In
pu
t/O
utp
ut
Fu
nctio
ns
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Improving Predictions
Using I/O Functions
Plot DPOAE pressure (in
Pascals not dB SPL).
Fit linear function to first few
points reliably above the noise
floor.
Threshold is the stimulus level
that yields 0 Pa DPOAE
amplitude per the fitted line.
(Boege & Janssen, 2002)
Two slope method (Neely et al.,
2009) leads to further
improvement.
Neely et al., 2009
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Gorga et al., 1997
Prediting thresholds from DPOAE
levels has not been successful.
Categorization of ears works to
some extent. Screening works the
best.
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Gorga et al., 1997
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Gorga et al., 1997
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OAEs:
Abnormal OHCs and loudness recruitment
“The phenomenon of loudness recruitment appears
to be the psychoacoustic expression of the loss of
a large component of outer hair cells and the
concurrent preservation of a large component of
inner hair cells and type I cochlear neurons.”
Schuknecht HF. Pathology of the Ear (2nd ed). 1993, p. 91
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Diagnostic Application of OAEs:
Findings for multiple frequencies vs. normal region
Normal
region
Noise
floor
Screening = pass (DP – NF = > 6 dB)
Diagnostic = abnormal
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Analysis of DPOAE Amplitude:
Diagnostic Applications
Normal Present but
Abnormal
No
OAE
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Steps in Analysis of DPOAE Findings
Perform analysis at all test frequencies
Verify adequately low noise floor (< 90% normal limits)
Verify replicability of DPOAE amplitude (+/- 2 dB) from at least two runs
Is DP - NF difference > 6 dB?
Yes? DPOAEs are present
No? There is no evidence of DPOAEs
Is DP amplitude within normal limits?
Yes? DPOAEs are normal
No? DPAOEs are abnormal (but present)
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EAR CANAL FACTORS INFLUENCING
OAE MEASUREMENT
Non-pathologic
probe tip placement, size, or condition
probe insertion depth
standing waves
cerumen or debris
vernix casseous (healthy newborn infants)
Pathologic
stenosis
external otitis
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CLINICAL APPLICATION OF
OTOACOUSTIC EMISSIONS (OAE): Trouble-shooting
Minimizing the effects of noise on OAE recordings
eliminate extraneous noise sources in test room
close door to test room
insert probe deeply
secure probe cord
instruct patient to remain quiet and still (if feasible)
position test ear away from equipment
modify protocol (to frequencies > 2000 Hz)
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VENTILATION TUBES and OAEs
Daya et al. (1966). Otoacoustic emissions: Assessment of hearing after tympanostomy tube insertion. Clin Otolaryngol 21: 492-494.
Owens, McCoy, Lonsbury-Martin, Martin. (1993). Otoacoustic emissions in children with normal ears, middle ear dysfunction, and ventilating tubes. Amer J Otol 14: 34-40.
Tilanus. Stenis, Snik.(1995). Otoacoustic emission measurements in evaluation of the effect of ventilation tube insertion in children. Annals of ORL 104: 297-300.
Richardson, Elliott, Hill. (1996). The feasibility of recording transiently evoked otoacoustic emissions immediately following grommet insertion. Clin Otolaryngol 21: 445-448.
Cullington, Kumar, Flood. (1998). Feasibility of otoacoustic emissions as a hearing screen following grommet insertion. Brit J Audio 32: 57-62.
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AUDIOGRAM & DPOAEs:
Pre-ventilation tubes (5 y.o. girl)
20
40
60
80
0
.50 1K 2K 3K 4K 6K 8K
dB
HL
KHz
AC
BC
20
40
60
80
0
8K 6K 4K 3K 2K 1K .50
Right Ear Left Ear
ST = 20
ST = 40
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AUDIOGRAM & DPOAEs:
Ventilation tubes (4 mos. later before APD eval.)
20
40
60
80
0
.50 1K 2K 3K 4K 6K 8K
dB
HL
KHz
AC
BC
20
40
60
80
0
8K 6K 4K 3K 2K 1K .50
Right Ear Left Ear
ST = 15 ST = 15
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Non-factors in OAE Interpretation
Non-Factors
diurnal effects (time of day)
genetics
body temperature
body position
anesthetic agents (w/ normal middle ear status)
state of arousal (attention to stimulus)
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Hearing Level in dB HL
-10 0 10 20 30 40 50 60
OAE
Amplitude
WNL
(Amplitude > 90%ile)
No OAE
(OAE – NF < 6 dB)
Normal
Present
but not
normal No OAE
Relation Between OAE Amplitude and Hearing Loss
DPOAE 65/55 dB SPL TEOAE 80 dB SPL
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Diagnostic Application of OAEs:
Findings for multiple frequencies vs. normal region
Normal
region
Noise
floor
Screening = pass (DP – NF = > 6 dB)
Diagnostic = abnormal
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Analysis of DPOAE Amplitude:
Diagnostic Application
Normal Present but
Abnormal
No
OAE
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Six Reasons Why OAEs Will Never Replace the
Audiogram nor Accurately Estimate Hearing Loss
(1-3)
OAEs measurement is dependent on inward and outward
propagation of energy through the middle ear (e.g.,
abnormal OAEs with normal hearing sensitivity)
OAEs are more sensitive to cochlear dysfunction than
the audiogram (e.g., abnormal OAEs with normal hearing
sensitivity)
OAEs are electrophysiologic measures while the
audiogram is behavioral (e.g., normal OAEs with
abnormal audiogram)
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Six Reasons Why OAEs Will Never Replace the
Audiogram nor Accurately Estimate Hearing Loss
(4-6)
OAEs are produced by OHCs, whereas the audiogram is
dependent on IHCs (e.g., normal OAEs with abnormal
audiogram)
OAEs are pre-neural, whereas the audiogram is
dependent on retrocochlear pathways (e.g., normal
OAEs with abnormal hearing sensitivity)
OAEs reflect OHC integrity, whereas the audiogram
measure hearing (e.g., normal OAEs with abnormal
audiogram)
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2f1-f2
Otoacoustic Emissions:
Current Research Topics
(See Chapter 10. Dhar & Hall, 2011)
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Lateral and Medial Efferent Auditory Pathways
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Functional Role of Auditory Efferents
Protection from noise.
Disrupted function in neuropathy.
Role in learning and learning
disability.
Signal detection and localization in
noise.
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Three categories of guinea pigs
with varying MOC reflex strength.
Animals with a strong
reflex show least damage.
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Hood et. al., 2003
Patients with auditory
neuropathy have grossly
reduced MOC reflex.
TEOAE
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Hood et. al., 2003Hood et. al., 2003
Garinis et. al., 2008
Adults with learning disabilities have
atypical pattern of MOC reflex.
TEOAE
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Efferent activation alters
both basilar membrane
vibration magnitude and
phase.
Cooper & Guinan, 2006
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Liberman et. al., 1996
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CAS leads to reduction in SOAE magnitude
and increase in SOAE frequency
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Distortion Product OAEs
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Siegel & Kim, 1982
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Sun, 2008
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Wagner et al., 2007
The lure of a change of
greater magnitude has
led to the suggestion of
only evaluating the “MOC
reflex” at dips.
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General Methods
• 8 normal-hearing young adults.
• Best estimate of middle ear muscle reflex > 90 dB
SPL.
• DPOAE recorded using stimulus tones swept in
frequency between 1 and 4 kHz.
• Broad band noise (0.1 - 10 kHz) presented in
contralateral ear at 60, 70, and 80 dB SPL.
• +CAS conditions bracketed by two -CAS conditions.
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overlap
CF DPOAE
-CAS
overlap
CF DPOAE
+CAS
Greater reduction in CF component could
explain DPOAE enhancement in valleys.
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The magnitude of the CF component is reduced
more than the magnitude of the overlap
component on efferent stimulation (also observed by Abdala et
al., 2009).
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Purcell et al., 2008
Efferent stimulation
also causes fine
structure patterns to
shift toward higher
frequencies. (Mauermann & Kollmeier,
2004; Sun, 2005, 2008; Purcell et al., 2008, Abdala, 2009)
A differential reduction in DPOAE component
magnitudes cannot account for frequency shifts
in fine structure patterns.
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Clinical Considerations
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Stuck at one frequency
Large but inconsistent effects at valleys/dips/minima. Smaller but less inconsistent effects at
peaks/maxima.
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Following a peak
Consistent and systematic changes at
peaks/maxima.
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Tracking frequency shift
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Practically speaking...
∆f
f
f / ∆f ≃ 16
f ± (f/4)
f ± (f/8)
At least one of four
strategically spaced
measurements will be near
peak/maximum.
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Efferent modulation of OAEs can be
complex with changes in both magnitude
and phase.
Both clinicians and scientists appear
to be interested in the phenomenon and
its reliable measurement.
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Questions?