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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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Page 1: Update on Otoacoustic Emissions: Basic Science to Clnical ... · Update on Otoacoustic Emissions: Basic Science to Clnical Application Morning Session ... acoustic impulse of the

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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st b

et fo

r th

resh

old

pre

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t/O

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ut

Fu

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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?


Recommended