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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


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SLIDE 1

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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SLIDE 2
  • 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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SLIDE 3

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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SLIDE 4
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SLIDE 5

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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SLIDE 6

Giuseppe Tartini (April 8, 1692 - February 26, 1770)

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SLIDE 7

George von Bekesy (1899 - 1972)

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SLIDE 8

Thomas Gold OAE Prophet

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SLIDE 9

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

  • scillation solely by means of the incident sound, is not

tenable.” “ … the nerve ending abstracts much energy from a mechanical resonator.”

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SLIDE 10

William Rhode demonstrates cochlear nonlinearity in the squirrel monkey in 1971.

Data from Ruggero et al., 1982

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SLIDE 11

David Kemp “Discoverer of OAEs”

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SLIDE 12

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

  • uter hair cell population is the generation of this

mechanical energy.”

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SLIDE 13

David Kemp (1978)

Threshold Microstructure (Elliot, 1958) Spacing of Loudness Maxima (Kemp, 1979)

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SLIDE 14

William Brownell: Discoverer of OHC Motility in Early 1980s

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SLIDE 15

Music 1750s Audiology today Physics/Physiology 1978 – Psychoacoustics 1805 –

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SLIDE 16

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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SLIDE 17

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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SLIDE 18

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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SLIDE 19
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SLIDE 20

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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SLIDE 21

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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SLIDE 22
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SLIDE 23

Hermann Ludwig Ferdinand von Helmholtz Overloading type nonlinearity in the middle ear.

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SLIDE 24

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

  • ther insults associated with OHC damage (salicylate,

noise, etc.).

 But where in the OHC?

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SLIDE 25

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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SLIDE 26

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

  • ther insults associated with OHC damage (salicylate,

noise, etc.).

 But where in the OHC?

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SLIDE 27
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SLIDE 28

Cheatham et. al. (2004), J Physiol

Liberman et al., 2004

Prestin KO

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SLIDE 29
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SLIDE 30

Cheatham et. al., (2004); J. Physiol Verpy et. al., (2008); Nature

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SLIDE 31

Cochlea Outer Hair Cell Stereocilia (transducer) Soma (?amplifier) Olivocochlear efferents Middle ear transmission

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SLIDE 32

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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SLIDE 33

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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SLIDE 34

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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SLIDE 35

OAEs in Early Detection of Outer Hair Cell Dysfunction: Rationale underlying many clinical applications

Abnormal OHC (OAEs) Normal OHC (OAEs)

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SLIDE 36

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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SLIDE 37

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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SLIDE 38

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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SLIDE 39

OAEs after Sound Induced Damage

11 chinchillas exposed to 100 dBA for 5 days

Davis et al., 2005

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SLIDE 40

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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SLIDE 41

still from Avan & Bonfils (2004)

(in 11 ears)

DPOAE Thd TEOAE

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SLIDE 42

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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SLIDE 43
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SLIDE 44

338 volunteers (US Navy) evaluated before and after 6-month training where they were noise exposed.

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SLIDE 45

On average hearing thresholds did not change in a group of 75 volunteers.

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SLIDE 46

Significant (-0.66 dB) change in TEOAE amplitude.

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SLIDE 47

Significant (-1.28 dB) change in DPOAE amplitude. Greatest change at lowest stimulus level.

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SLIDE 48

In 18 ears with PTS, the likelihood of PTS increased with decreasing OAE amplitude.

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SLIDE 49

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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SLIDE 50

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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SLIDE 51

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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SLIDE 52

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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SLIDE 53

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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SLIDE 54

But That’s Not the Entire Story (See Chapter 3 of Dhar & Hall, 2012)

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SLIDE 55

Shera, 2009

Phase is a Factor in the Generation of OAEs

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SLIDE 56

Regular Spacing of Spontaneous OAEs

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SLIDE 57

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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SLIDE 58

Inhibition (Suppression) of Otoacoustic Emissions: Role of the Efferent Auditory System

(See Chapter 9 of Dhar & Hall, 2012)

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SLIDE 59

Classification

STIMULUS MECHANISM

Without stimulation Spontaneous Stimulated Transient,Distortion product,Stimulus frequency Distortion Reflection Spontaneous Mixed DPOAEs TEOAEs SFOAEs

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SLIDE 60

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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SLIDE 61

Transient Otoacoustic Emissions (TEOAE)

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SLIDE 62
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SLIDE 63
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SLIDE 64
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SLIDE 65

Distortion Product Otoacoustic Emissions (DPOAEs)

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SLIDE 66
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SLIDE 67
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SLIDE 68
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SLIDE 69
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SLIDE 70
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SLIDE 71

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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SLIDE 72

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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SLIDE 73

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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SLIDE 74

f1 f2

  • uter ear

middle ear

f2 f1

Mixed DPOAEs

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SLIDE 75
  • uter ear

middle ear

f2 f1

nonlinear reflection composite

model Talmadge, Long, Tubis & Dhar (1999); JASA

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SLIDE 76

Talmadge, Long, Tubis & Dhar (1999); JASA

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SLIDE 77
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SLIDE 78

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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SLIDE 79

Best bet for threshold prediction: Input/Output Functions

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SLIDE 80

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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SLIDE 81

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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SLIDE 82

Gorga et al., 1997

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SLIDE 83

Gorga et al., 1997

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SLIDE 84
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SLIDE 85

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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SLIDE 86

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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SLIDE 87

Analysis of DPOAE Amplitude: Diagnostic Applications

Normal Present but Abnormal No OAE

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SLIDE 88

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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SLIDE 89

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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SLIDE 90

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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SLIDE 91

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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SLIDE 92

AUDIOGRAM & DPOAEs: Pre-ventilation tubes (5 y.o. girl)

20 40 60 80 .50 1K 2K 3K 4K 6K 8K

dB HL KHz

AC BC 20 40 60 80 8K 6K 4K 3K 2K 1K .50

Right Ear Left Ear

ST = 20 ST = 40

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SLIDE 93
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SLIDE 94
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SLIDE 95
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SLIDE 96

AUDIOGRAM & DPOAEs: Ventilation tubes (4 mos. later before APD eval.)

20 40 60 80 .50 1K 2K 3K 4K 6K 8K

dB HL KHz

AC BC 20 40 60 80 8K 6K 4K 3K 2K 1K .50

Right Ear Left Ear

ST = 15 ST = 15

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SLIDE 97

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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SLIDE 98

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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SLIDE 99

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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SLIDE 100

Analysis of DPOAE Amplitude: Diagnostic Application

Normal Present but Abnormal No OAE

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SLIDE 101

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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SLIDE 102

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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SLIDE 103

2f1-f2

Otoacoustic Emissions: Current Research Topics (See Chapter 10. Dhar & Hall, 2011)

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SLIDE 104

Lateral and Medial Efferent Auditory Pathways

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SLIDE 105
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SLIDE 106

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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SLIDE 107

Three categories of guinea pigs with varying MOC reflex strength. Animals with a strong reflex show least damage.

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SLIDE 108

Hood et. al., 2003

Patients with auditory neuropathy have grossly reduced MOC reflex. TEOAE

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SLIDE 109

Hood Hood Garinis et. al., 2008

Adults with learning disabilities have atypical pattern of MOC reflex. TEOAE

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SLIDE 110
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SLIDE 111
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Efferent activation alters both basilar membrane vibration magnitude and phase.

Cooper & Guinan, 2006

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SLIDE 113

Liberman et. al., 1996

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CAS leads to reduction in SOAE magnitude and increase in SOAE frequency

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SLIDE 118

Distortion Product OAEs

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Siegel & Kim, 1982

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SLIDE 120

Sun, 2008

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SLIDE 121

Wagner et al., 2007

The lure of a change of greater magnitude has led to the suggestion of

  • nly evaluating the “MOC

reflex” at dips.

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SLIDE 122

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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SLIDE 123
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SLIDE 124
  • verlap

CF DPOAE

  • CAS
  • verlap

CF DPOAE

+CAS

Greater reduction in CF component could explain DPOAE enhancement in valleys.

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SLIDE 125

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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SLIDE 126

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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SLIDE 127

Clinical Considerations

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SLIDE 128

Stuck at one frequency

Large but inconsistent effects at valleys/dips/minima. Smaller but less inconsistent effects at peaks/maxima.

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SLIDE 129

Following a peak

Consistent and systematic changes at peaks/maxima.

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SLIDE 130

Tracking frequency shift

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SLIDE 131

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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SLIDE 132

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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SLIDE 133

 Questions?