Update on Otoacoustic Emissions: Basic Science to Clnical Application. Morning Session

Transcription

1 Update on Otoacoustic Emissions: Basic Science to Clnical Application Introductions Morning Session 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

2 Otoacoustic Emissions Textbook 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

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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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.

6 Giuseppe Tartini (April 8, February 26, 1770)

7 George von Bekesy ( )

8 Thomas Gold OAE Prophet

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 oscillation solely by means of the incident sound, is not tenable. the nerve ending abstracts much energy from a mechanical resonator.

10 William Rhode demonstrates cochlear nonlinearity in the squirrel monkey in Data from Ruggero et al., 1982

11 David Kemp Discoverer of OAEs

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 outer hair cell population is the generation of this mechanical energy.

13 David Kemp (1978) Spacing of Loudness Maxima (Kemp, 1979) Threshold Microstructure (Elliot, 1958)

14 William Brownell: Discoverer of OHC Motility in Early 1980s

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

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

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

18 Update on Otoacoustic Emissions: Basic Science to Clnical Application Introductions Morning Session 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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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

21 OAEs: Differences between inner and outer hair cells (2) Inner Hair Cells Not motile Encompassed by support cells Central nucleus Single layer of endoplasmic Mitochondria scattered Efferents from lateral Outer Hair Cells Motile Supported only on top & bottom Nucleus at base of cell Extensive subsurface reticulum cisternae Mitochondria along throughout cell perimeter Efferents from medial superior olive superior olive

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

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 other insults associated with OHC damage (salicylate, noise, etc.). But where in the OHC?

25 Lessons from Kemp, 1978 Random noise recorded when closed cavity is stimulated with a click. 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.

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 other insults associated with OHC damage (salicylate, noise, etc.). But where in the OHC?

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28 Cheatham et. al. (2004), J Physio Prestin KO Liberman et al., 2004

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

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

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.

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

34 Update on Otoacoustic Emissions: Basic Science to Clnical Application Introductions Morning Session 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

35 OAEs in Early Detection of Outer Hair Cell Dysfunction: Rationale underlying many clinical applications Normal OHC (OAEs) Abnormal OHC (OAEs)

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

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

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

39 OAEs after Sound Induced Damage 11 chinchillas exposed to 100 dba for 5 days Davis et al., 2005

40 And in humans Avan & Bonfils (2005) evaluated DPOAEs in 27 noise-exposed workers with clear notches in their audiograms. (in most ears)

41 still from Avan & Bonfils (2004) Thd DPOAE TEOAE (in 11 ears)

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 ( dba). TEOAE show statistically significant shift in these listeners of db at 2 khz and db at 2.8 khz.

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44 338 volunteers (US Navy) evaluated before and after 6-month training where they were noise exposed.

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

46 Significant (-0.66 db) change in TEOAE amplitude.

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

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

49 Hair cell response returns to normal; Long term synaptic loss and loss of neural amplitude; Loss of ganglion cells is delayed even more.

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)

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)

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?

53 Update on Otoacoustic Emissions: Basic Science to Clnical Application Introductions Morning Session 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

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

55 Phase is a Factor in the Generation of OAEs Shera, 2009

56 Regular Spacing of Spontaneous OAEs

57 Coherent Reflection Filtering Zweig, Shera (1995 on) stapes base input apex Incoming signal is reflected randomly by outer hair cells; some reflections are coherent and contribute to the outwardtraveling energy. Coherent reflectors near the peak region of the traveling wave have enough magnitude to contribute significantly to ear-canal OAE.

58 Inhibition (Suppression) of Otoacoustic Emissions: Role of the Efferent Auditory System (See Chapter 9 of Dhar & Hall, 2012)

59 STIMULUS MECHANISM Classification Without stimulation Spontaneous Stimulated Transient,Distortion product,stimulus frequency Distortion Reflection Spontaneous Mixed DPOAEs TEOAEs SFOAEs

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?? %

61 Transient Otoacoustic Emissions (TEOAE)

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65 Distortion Product Otoacoustic Emissions (DPOAEs)

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71 Update on Otoacoustic Emissions: Basic Science to Clnical Application Introductions Morning Session 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

72 Update on Otoacoustic Emissions: Basic Science to Clnical Application Introductions Morning Session 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

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

74 outer ear middle ear Mixed DPOAEs f1 f2 f2 f1

75 outer ear middle ear f2 f1 composite reflection nonlinear Talmadge, Long, Tubis & Dhar (1999); JASA model

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

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78 Relation Between OAE Amplitude and Hearing Loss DPOAE 65/55 db SPL TEOAE 80 db SPL OAE Amplitude Normal WNL (Amplitude > 95%ile) Present but not normal No OAE No OAE (OAE NF < 6 db) Hearing Level in db HL

79 Best bet for threshold prediction: Input/Output Functions

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

81 Prediting thresholds from DPOAE levels has not been successful. Categorization of ears works to some extent. Screening works the best. Gorga et al., 1997

82 Gorga et al., 1997

83 Gorga et al., 1997

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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

86 Diagnostic Application of OAEs: Findings for multiple frequencies vs. normal region Screening = pass (DP NF = > 6 db) Diagnostic = abnormal Normal region Noise floor

87 Analysis of DPOAE Amplitude: Diagnostic Applications Normal Present but Abnormal No OAE

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)

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

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)

91 VENTILATION TUBES and OAEs Daya et al. (1966). Otoacoustic emissions: Assessment of hearing after tympanostomy tube insertion. Clin Otolaryngol 21: Owens, McCoy, Lonsbury-Martin, Martin. (1993). Otoacoustic emissions in children with normal ears, middle ear dysfunction, and ventilating tubes. Amer J Otol 14: Tilanus. Stenis, Snik.(1995). Otoacoustic emission measurements in evaluation of the effect of ventilation tube insertion in children. Annals of ORL 104: Richardson, Elliott, Hill. (1996). The feasibility of recording transiently evoked otoacoustic emissions immediately following grommet insertion. Clin Otolaryngol 21: Cullington, Kumar, Flood. (1998). Feasibility of otoacoustic emissions as a hearing screen following grommet insertion. Brit J Audio 32:

92 db HL AUDIOGRAM & DPOAEs: Pre-ventilation tubes (5 y.o. girl) Right Ear KHz Left Ear.50 1K 2K 3K 4K 6K 8K.50 1K 2K 3K 4K 6K 8K ST = ST = 20 AC BC

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96 db HL AUDIOGRAM & DPOAEs: Ventilation tubes (4 mos. later before APD eval.) Right Ear.50 1K 2K 3K 4K 6K 8K KHz.50 1K Left Ear 2K 3K 4K 6K 8K ST = 15 ST = AC BC

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)

98 Relation Between OAE Amplitude and Hearing Loss DPOAE 65/55 db SPL TEOAE 80 db SPL OAE Amplitude Normal WNL (Amplitude > 90%ile) Present but not normal No OAE No OAE (OAE NF < 6 db) Hearing Level in db HL

99 Diagnostic Application of OAEs: Findings for multiple frequencies vs. normal region Screening = pass (DP NF = > 6 db) Diagnostic = abnormal Normal region Noise floor

100 Analysis of DPOAE Amplitude: Diagnostic Application Normal Present but Abnormal No OAE

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)

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)

103 Otoacoustic Emissions: Current Research Topics (See Chapter 10. Dhar & Hall, 2011) 2f1-f2

104 Lateral and Medial Efferent Auditory Pathways

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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.

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

108 TEOAE Patients with auditory neuropathy have grossly reduced MOC reflex. Hood et. al., 2003

109 TEOAE Adults with learning disabilities have atypical pattern of MOC reflex. Garinis et. al., 2008

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112 Cooper & Guinan, 2006 Efferent activation alters both basilar membrane vibration magnitude and phase.

113 Liberman et. al., 1996

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

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118 Distortion Product OAEs

119 Siegel & Kim, 1982

120 Sun, 2008

121 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.

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 ( khz) presented in contralateral ear at 60, 70, and 80 db SPL. +CAS conditions bracketed by two -CAS conditions.

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124 Greater reduction in CF component could explain DPOAE enhancement in valleys. overlap overlap DPOAE CF DPOAE CF -CAS +CAS

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).

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.

127 Clinical Considerations

128 Stuck at one frequency Large but inconsistent effects at valleys/dips/minima. Smaller but less inconsistent effects at peaks/maxima.

129 Following a peak Consistent and systematic changes at peaks/maxima.

130 Tracking frequency shift

131 Practically speaking... f ± (f/8) f ± (f/4) f f f / f 16 At least one of four strategically spaced measurements will be near peak/maximum.

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.

133 Questions?