Effect of Bone Conduction Transducer Placement on Distortion Product Otoacoustic Emissions

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EFFECT OF BONE CONDUCTION TRANSDUCER PLACEMENT ON DISTORTION PRODUCT OTOACOUSTIC EMISSIONS

DISSERTATION

Presented in Partial Fulfillment of the Requirements for the Degree Doctor of

Philosophy in the Graduate School of The Ohio State University

Julie L. Hazelbaker, M.A.

*****

The Ohio State University 2004

Dissertation Committee: Approved by Professor Lawrence Feth, Advisor

Professor Pamela Mishler ______Professor Stephanie Davidson Lawrence L. Feth Advisor, Department of Speech & Hearing Science

ABSTRACT

The purpose of this study was to develop a technique to determine the magnitude of bone conducted sound in the cochlea when stimuli are delivered from three different locations on the head.

Distortion product otoacoustic emissions (DPOAE) at 1000 and 2000 Hz were used as tools to determine cochlear response to stimuli introduced via air conduction and bone conduction in three subjects. The bone conduction transducer was moved to three head locations (ipsilateral mastoid, contralateral mastoid and forehead). The intensity of the emissions elicited was compared. The differences in DPOAE magnitude created by varying the location of the bone conduction transducer were compared with behavioral threshold differences with the same transducers at the same locations.

It was assumed that results of behavioral measures would provide a prediction of the relationship between air and bone conducted DPOAE. However, in the current study, this was not the case.

Behavioral bone conduction threshold data did not predict differences in DPOAE at different bone conduction transducer locations. This was a somewhat surprising result and should be considered further in future studies examining the properties of DPOAE elicited by bone conduction.

Additionally, a wide band noise masker was introduced to the non-test ear when bone conducted stimuli were introduced to make DPOAE and behavioral test conditions as similar as possible. No great suppression effects were noted across subjects for either frequency. This was likely due to the shape and intensity of the contralateral masked used.

For Ella:

The happiness and satisfaction I feel as I complete my doctorate could never compare with the joy you have brought me the last 14 months. Thank you for helping me keep things in perspective.

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ACKNOWLEDGMENTS

First and foremost, I would like to express my sincere appreciation to my advisor, Dr.

Lawrence Feth. His guidance, patience and encouragement throughout this process have been abundant. His knowledge of hearing science and his willingness to teach and share it with his students is truly amazing. He will always have my utmost respect as a scientist and as a teacher.

I would like to thank members of my generals and dissertation committees, Dr. Pamela

Mishler, Dr. Stephanie Davidson, Dr. Patrick Feeney and Dr. Wayne King for their help and encouragement. My gratitude is also expressed to my fellow doctoral students for their advice and support, especially Dean Hudson who was so kind to volunteer hours of his time. Special thanks also to my co-workers at Columbus Speech and Hearing for always cheering me on, especially Kim Shorr.

I would like to thank my parents and my sister who have always provided love, support and unwavering confidence in my abilities, especially when I doubted them myself. Finally, I would like to thank my wonderful husband, Jason. Words cannot express how blessed I am to have such a supportive, loving and kind partner. His willingness to sacrifice to help get me to this point will never be forgotten.

VITA

December 9, 1973………………………….. Born, Portsmouth, Ohio

1996…………………………………………B.A. Speech and Hearing Science The Ohio State University

1998…………………………………………M.A. Speech and Hearing Science The Ohio State University

1998-present……………………………..… Clinical Audiologist Columbus Speech and Hearing Center

FIELDS OF STUDY

Major Field: Speech and Hearing Science

TABLE OF CONTENTS

Page

Abstract………………………………………………………………………………..ii

Dedication………………………………...... iii

Acknowledgments………………………………...... iv

Vita………………………………...... v

List of Tables………………………………...... viii

List of Figures…...…………………………...... ix

Chapters:

1. Introduction………………………………...... 1

1.1 Bone Conduction………………………………………………………....1 1.2 Importance of Bone Conduction Research……………………………….2 1.3 Otoacoustic Emissions……………………………………………………4 1.4 The Current Study………………………………………………………...4

2. Review of Literature………………………………...... 6

2.1 How We Hear…………………………………………………………….6 2.2 Bone Conduction………………………………...... 7 2.3 Clinical Audiometry……………………………………………………..12 2.3 Clinical measures of bone conduction………………...... 13 2.3 Calibration of bone conduction transducers.……...... 16 2.4 Otoacoustic emissions………………………………...... 17 2.5 Suppression of otoacoustic emissions…………………………………...20 2.6 Previous Bone Conduction Work using OAE…………………………..22 2.6 The Current Study..……………………...... 25

3. Methods………………...…………...... 26

3.1 Subjects………………………………...... 26 3.2 Behavioral Threshold Measurements…………………………………...26 3.3 Otoacoustic Emission Testing…………………………………………...27 3.4 Calibration……………………………………………………………….32 3.5 Test Sessions………………………………...... 33 3.6 Test Conditions…………………………...... 34

4. Results…..………………………………...... 39

4.1 Behavioral Threshold Data……………………………………………...39 4.2 DPOAE Input/Output Functions………………………………………...41 4.3 Results for Fc=1000 Hz…………………………………………………42 4.4 Results for Fc=2000 Hz…………………………………………………57 4.5 Comparison of Behavioral Thresholds and DPOAE Data………………67 4.6 Contralateral Masking…………………………………………………...69 4.7 Effects of Contralateral Masking, 1000 Hz……………………………..76 4.8 Effects of Contralateral Masking, 2000 Hz……………………………..82 4.9 Summary of Results……………………………………………………..84

5. Summary and Conclusions…………………...... 85

5.1 Behavioral Threshold Data……………………………………………...85 5.2 Effect of P2 Location……………………………………………………85 5.3 Effects of Contralateral Masking……………………………………..…88 5.4 Sources of Variability ………………………………………………..…89 5.5 Conclusions……………………………………………………………...95 5.6 Implications for future research………………………...... 96

Bibliography………………………………...... 97

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LIST OF TABLES

TABLE PAGE

1. 1000 Hz Behavioral Threshold Data……………………………………………...40

2. 2000 Hz Behavioral Threshold Data...... 41

3. Values of Input/Output Function Shifts, Fc=1000 Hz………………...... 56

4. Values of Input/Output Function Shifts, Fc=2000 Hz………………...... 66

5. Average Differences in DPOAE Input/Output Functions and Behavioral Threshold Data for 1000 Hz...... 87

6. Average Differences in DPOAE Input/Output Functions and Behavioral Threshold Data for 2000 Hz...... 87

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LIST OF FIGURES

FIGURE PAGE

1. Diagram of the Auditory System……………………………………………...... 8

2. Tonndorf’s Circuit Model of Bone Conduction Hearing………………………...10

3. Sample Screen from SigGen Signal Generation Program……………...... 27

4. Hardware Configuration for Collection of DPOAE………………...... 29

5. Sample Screen from BioSig Data Collection Program...... 30

6. Calibration Set-up...... 32

7. Calibration of the Bone Conduction Transducer………………………………...32

8. Air/Air Test Condition.…………………………………………………..………33

9. Air/Air (with masking) Test Condition.…………………………...……..………34

10. Air/Ipsi Test Condition.………..……………………………….………..………34

11. Air/Ipsi (with masking) Test Condition.………...………...……...……..………35

12. Air/Contra Test Condition.….……………………………….………..………...35

13. Air/Contra (with masking) Test Condition.………...………...….……..…….…36

14. Air/Forehead Test Condition.………………………………….………..………36

15. Air/Forehead (with masking) Test Condition.………...……...….……..……….37

16. Input/Output Functions of all P2 Placements, Fc=1000 Hz, Subject 1……...…45

17. Input/Output Functions of all P2 Placements, Fc=1000 Hz, Subject 2………....46

FIGURE PAGE

18. Input/Output Functions of all P2 Placements, Fc=1000 Hz, Subject 3…………47

19. Illustration of Input/Output Function Matching Technique……………………..48

20. Ipsilateral Placement, Fc=1000 Hz, All Subjects……………………………….51

21. Contralateral Placement, Fc=1000 Hz, All Subjects…………...……………….53

22. Forehead Placement, Fc=1000 Hz, All Subjects………………………………..54

23. Input/Output Functions of all P2 Placements, Fc=2000 Hz, Subject 1………....58

24. Input/Output Functions of all P2 Placements, Fc=2000 Hz, Subject 2………....59

25. Input/Output Functions of all P2 Placements, Fc=2000 Hz, Subject 3………....60

26. Ipsilateral Placement, Fc=2000 Hz, All Subjects……………………………….61

27. Contralateral Placement, Fc=2000 Hz, All Subjects…………...……………….62

28. Forehead Placement, Fc=2000 Hz, All Subjects………………………………..63

29. Scatter plots of Behavioral Threshold Differences and Differences in OAE Input/Output Functions……………………………68-69

30. Contralateral Masker Effects, Fc=1000 Hz, P2 via Air Conduction, All Subjects…………………………………………….72

31. Contralateral Masker Effects, Fc=1000 Hz, P2 at the Ipsilateral Placement, All Subjects……………………...…………….73

32. Contralateral Masker Effects, Fc=1000 Hz, P2 at the Contralateral Placement, All Subjects…………...……...…………….74

33. Contralateral Masker Effects, Fc=1000 Hz, P2 at the Forehead Placement, All Subjects……………………....…………….75

FIGURE PAGE

34. Contralateral Masker Effects, Fc=2000 Hz, P2 via Air Conduction, All Subjects…………………………………………….78

35. Contralateral Masker Effects, Fc=2000 Hz, P2 at the Ipsilateral Placement, All Subjects……………………...…………….79

36. Contralateral Masker Effects, Fc=2000 Hz, P2 at the Contralateral Placement, All Subjects…………...……...…………….80

37. Contralateral Masker Effects, Fc=2000 Hz, P2 at the Forehead Placement, All Subjects……………………....…………….81

38. Comparison of L2 in the Ear Canal at Different P2 locations, Fc=1000 Hz, All Subjects……………………………………..91-92

39. Comparison of L2 in the Ear Canal at Different P2 locations, Fc=2000 Hz, Subjects 1 and 2………………………………….....93

CHAPTER 1

INTRODUCTION

1.1 Bone Conduction

Normally, airborne acoustic energy enters the outer ear, travels through the eardrum and the middle ear prior to entering the inner ear. However, sound can reach the inner ear by more than one pathway. The concept of bone conduction, with regard to hearing, refers to sound entering the inner ear predominantly through vibrations of the skull. Bone conduction hearing is a process that interests auditory researchers because it provides the potential for examining the properties of the inner ear with minimal contributions from the outer and middle ears.

We know from von Bekesy’s (1960) work on cadavers that when acoustically stimulated, the inner ear response does not change, even when mode of stimulation

(air or bone conduction) is varied. These investigations laid the groundwork for the

implementation of clinical bone conduction testing. The comparison of air conducted

hearing thresholds with bone conduction thresholds allowed the hearing specialist

(audiologist) to localize where in the audiotory system a problem exists in a hearing- impaired person.

For instance, if air conduction thresholds indicate a hearing loss but bone conduction

thresholds are within the normal hearing range, a problem with the outer or middle

ear is inferred. Today bone conduction stimulation of the cochlea is widely used

clinically to differentiate between conductive and sensorineural hearing impairments.

1.2 Importance of Bone Conduction Research

Two important reasons to continue bone conduction research are the bone anchored hearing aid (BAHA) and noise control. The BAHA is emerging as an alternative for hearing-impaired patients--especially those suffering from chronic middle ear or outer ear pathologies which complicate the use of traditional air conduction hearing aids. The BAHA is connected to an osseo-integrated titanium fixture, which is implanted into the temporal bone behind the pinna. Vibrations from the transducer go directly to the skull bone, excluding the skin from the vibration pathway (Carlsson & Hakansson, 1997). Since this system is relying entirely on stimulation via bone conduction, several aspects of bone conduction hearing have been extensively studied by those involved in the design and implementation of the

BAHA (Hakansson, et.al, 1997, 1998, 1999)

Bone conduction with respect to noise control is also of interest. Zwislocki

(1957) examined bone and body conducted thresholds. Results indicated that when the ear canal is effectively shielded from noise exposure (with earplugs) further measures to attenuate air conducted sound are futile if the body conduction limit has been reached. Noise exposure will occur through bone and body conduction. More recent research has confirmed that hearing protection worn by workers exposed to high noise levels effectively reduces air conducted sound, but that bone conducted 2

noise may still be harmful (Berger, 1983, 2003). When the maximum amount of air

conduction attenuation is obtained with earplugs, no further air conduction

attenuation is effective in reducing noise levels, as the noise is now entering through

bone and body conduction. This is true for any situation in which humans may be in

the presence of loud noise, occupationally or recreationally. Similar implications extend to the medical field where current functional magnetic resonance imaging

(fMRI) techniques emit sound levels reaching the hazardous range (Ravicz &

Melcher, 2001). Prior to implementing any successful measures of attenuating bone conducted noise, knowledge of the magnitude and phase of the actual stimulation in the inner ear is required. This may require a closer look at the interaction of air and bone conducted sounds and their additive contribution to the cochlear response.

In addition to noise control and bone conducted amplification, further bone

conduction research is necessary simply to provide audiologists with knowledge of what a bone conducted hearing threshold means. Specifically, what do bone conduction thresholds reveal about the cochlea? There are three placements commonly used clinically to measure bone conducted thresholds: ipsilateral mastoid, contralateral mastoid and forehead. We know from previous research that there are slight differences in behavioral threshold measurements when transducer placement is varied (Studebaker, 1962). However, are there differences in the cochlear responses when the skull is stimulated at different locations? The contributions of the outer and middle ears are reported to vary at the three locations (Dirks, 1978). Can the inner ear component at the different placements be isolated?

1.3 Otoacoustic Emissions

Normally-hearing, healthy ears generate low-level sounds known as

otoacoustic emissions (OAE). OAE are produced by the normal workings of the

inner ear (cochlea) and can occur spontaneously or in response to acoustic

stimulation. By placing a specially constructed probe with miniature microphones in the ear canal, OAE can be recorded and studied. OAE are thought to reflect the activity of active biological mechanisms within the cochlea. Before emissions were discovered by David Kemp in 1978, the only methods to explore the inaccessible structures of the cochlea involved invasive, and thus damaging, experiments.

1.4 The Current Study

The purpose of this study was to develop a technique to determine the

magnitude of bone conducted sound in the cochlea when stimuli are delivered from

three different locations on the head. Specifically, the research questions addressed in

this study are:

1. Are there differences in the cochlear response when the skull is stimulated at different locations?

2. Are objective measures of the cochlear response consistent with subjective, behavioral measures?

3. Does the introduction of contralateral noise affect the cochlear response?

OAE testing was used as a tool to determine cochlear response to stimuli

introduced via air conduction and bone conduction. OAE elicited with air and bone

conduction stimuli can provide insight into the magnitude of bone conducted stimuli

at the cochlea. Otoacoustic emissions were obtained via air conduction and with a 4

combination of air and bone conducted stimuli. The bone conduction transducer was

moved to three head locations (ipsilateral mastoid, contralateral mastoid and

forehead). The intensity of emissions elicited was compared. The differences in varying the location of the bone conduction transducer for OAE testing was compared with behavioral threshold differences with the same transducer at the same locations.

Additionally, a wide band noise masker was introduced to the non-test ear and it’s effects on OAE level were examined.

The current study was influenced by a series of studies by Purcell, et al,

(1998, 1999, 2003). It is hoped that this study will lead to future research which can quantify the relative contributions to bone conduction hearing of the external, middle and inner ear. In addition, it is hoped that knowledge gained about bone conduction and inner ear stimulation provide useful information for clinical audiologists and those with interest in BAHA and noise control.

CHAPTER 2

REVIEW OF LITERATURE

This chapter contains a review of the literature relevant to the present study.

This review includes discussions of the normal auditory processes, air conduction

hearing, bone conduction hearing, and otoacoustic emissions and their properties.

2.1 How We Hear

The three main parts of the ear, the external ear, middle ear and inner ear have

separate functions in audition. The external ear or outer ear includes the pinna and the external auditory canal. The outer ear essentially acts as a funnel to channel sound into the middle ear. The eardrum (tympanic membrane) and the ossicles, in an air-filled space, comprise the middle ear. The middle ear increases the efficiency by which sound travels from the air-filled to fluid-filled spaces. The inner ear, the cochlea, converts sound waves into electrical potentials that travel to the brain via the auditory nerve.

Sound enters the external auditory canal and vibrates the tympanic membrane.

Movement of the drum in turn mobilizes the ossicles, the three bones in the middle ear space, the malleus, incus and stapes. Movement of the stapes in and out of the oval window transfers sound energy into the inner ear (cochlea). The surface ratio of

eardrum to oval window (20/1) allows an adequate energy transfer of the sound pressure between the air and the fluids of the inner ear. The middle ear can be

considered as an impedance adapter - without it about 98% of energy would be

reflected back.

To this point, all of the sound energy is passed from one air-filled space to

another. From the stapes inward, sound travels through fluid-filled spaces. The

sound energy creates what can be thought of as a traveling wave, moving the fluid

and the structures inside the cochlea. The traveling wave moves down the basilar

membrane, which extends the length of the cochlea and separates two of the three

chambers of the inner ear. Distortions of the basilar membrane produced by the

traveling wave stimulate the hair cells or sensory cells, which, in turn, electrically

stimulate the auditory nerve. These electrical potentials travel to the auditory cortex

of the brain so the stimulus is “heard”.

2.2 Bone Conduction

In the early 20th century the route of stimulation by a bone conducted sound was

uncertain. However, a very important study by Bekesy in 1932 proved that bone

conducted sounds stimulate the cochlea by creating a cochlear traveling wave, just as

air conducted sounds do.

Bekesy (1932, 1960) also asserted that the primary vibratory energy pathway

from the skull to the inner ear was through bone (completely osseous). Other studies

(i.e. Wever & Lawrence, 1954) emphasized the osseous pathway taken by bone

conducted sounds and the minimal contribution of the non-osseous pathways via

tissue and other skull contents.

Outer Ear Middle Ear Entrance to Cochlea Inner ear

Figure 1. Diagram of the Auditory system. From Inter University Research Center’s website, Promenade ‘round the Cochlea. http://www.iurc.montp.inserm.fr/cric/audition/english/start2.htm

Tonndorf (1966) found that some energy was conducted as surface waves

along the skin and soft tissues of the head and that some energy may pass through the

skull as pressure waves and act on the cochlea through the cochlear aqueduct.

However, this pathway was thought to provide a minimal contribution to the

detection of bone conducted sound. Tonndorf reported three major osseous routes of

bone conducted sound (see Figure 2). The outer ear component, often called the

osseo-tympanic component, is created as skull vibrations radiate into an occluded external meatus producing sound waves which act on the tympanic membrane, just as in air conduction. This “occlusion effect” is greater for lower frequency stimuli and is negligible for frequencies 2000 Hz or greater. The middle ear component, called the inertial component, occurs due to the relative motion between the vibrations of the cochlear shell and the ossicular chain. This motion leads to the same type of cochlear fluid displacement produced by air conducted sounds. The compressional/distortional inner ear component is created by vibration of the temporal bone which in turn creates deformation in the cochlear bony shell and fluid displacements in and out of the cochlear windows. The round window augments the response and the oval window reduces the amount of energy acting on the cochlear partition. The sum total of all communications of the intracochlear spaces acts as a “third window”

(Tonndorf, 1968). This energy in the form of a traveling wave, creates basilar membrane displacement and excitation of the outer hair cells.

Figure 2 (redrawn from Tondorff, 1968) is a circuit model of the auditory system stimulated via bone conduction. Note that the circuit is a parallel one, which illustrates that when a bone conducted sound is introduced, all three parts of the auditory system respond in some fashion.

This model shows that when the skull is vibrated with a transducer, some of the energy does indeed travel directly through the bones to the inner ear. However, some of the acoustic energy also travels through the skull into the outer ear and middle ear where a portion of the energy is absorbed, and a portion of the energy travels along the “normal” air conduction pathway.

The mechanism of bone conduction is more complex than von Bekesy believed.

Further investigation, especially with respect to the cochlear response to the

interaction of air and bone conducted sounds is required.

Z I. II. III.Skull skin bone content Bone conduction Temporal vibrator bone

walls TM ossicles air O.W. sc. vestib. external TM air phase opening cushion inverter air cushion R.W. sc. tymp. 1. External canal 2. Middle ear 3. Cochlea

Figure 2. Tonndorf’s circuit model of bone conduction hearing.

More recent research by Freemen, Sichel & Sohmer (2000) indicates that

there is indeed a significant contribution of bone conducted sound via a non-osseous

pathway. They contend that bone conduction transducer vibrations may induce sound

pressure waves in brain tissues and cerebral spinal fluid which can be communicated via fluid channels (possibly in the cochlear and vestibular aqueducts) to the fluids of the inner ear. Ultimately, the stimulus at the cochlea is a combination of energy from several pathways, the sum of which is dependent upon the relative phase and magnitude of each signal.

An assumption of linearity is often made when examining any system. When considering vibration of the skull, this assumption has been tested and validated by a number of researchers (Corliss & Coidan, 1955; Flottorp & Solberg, 1976;

Hakansson Brandt, Carlsson, Tjellstrom, 1994) for the 0.1- to 10 kHz frequency range at normal hearing levels. However, some investigations have reported that sound propagation through the skull is nonlinear. Khanna, Tonndorf & Queller, (1976) reported second harmonic distortion below 2 kHz in a series of cancellation experiments. Arlinger, Kylen & Hellqvist, (1978) also found that in the lower frequencies, second and third harmonic distortion was present in levels ranging from

60-65 dB HL. However, the measurement techniques of these previous studies may have been confounded by equipment limitations. A more recent study, Hakansson.

Carlsson, Brandt, Stenfelt, (1996) investigated the linearity of sound propagation through the skull using the titanium studs of a person implanted with the bone anchored hearing aid (BAHA) system. Results showed no indication of nonlinear properties up to 77 dB HL in the 0.1 to 10 kHz frequency range. Linearity of bone conducted sound at high levels (>77 dB HL) has not been studied. At high levels, it is possible that the skull is driven into nonlinearity.

Bone conducted signals may also reach the cochlea via body conduction.

Zwislocki (1957) examined bone and body conducted thresholds and protection of the ear at high noise levels. Results indicated that when the ear canal is effectively shielded from noise exposure (for example with earplugs) further measures to attenuate air conducted sound are futile if the bone conduction limit has been reached.

These results were supported by Berger (1983, 2003) and Ravicz & Melcher (2001).

Berger estimated the bone conduction limit by measuring behavioral thresholds of

subjects wearing both insert ear plugs (deeply inserted) and large lead earmuffs. Due

to the large amount of ear canal attenuation with these measures, the obtained

thresholds were due to sound perceived through the head and body. Thus, noise

exposure will occur through bone and body conduction.

2.3 Clinical Audiometry

Pure tone audiometry is the standard behavioral method for determining auditory sensitivity. Using a clinical audiometer, frequency is varied (usually octave frequencies, 250 – 8000 Hz). The intensity required for a listener to just detect a tonal stimulus is recorded. Two types of transducers are used for air conduction audiometry. Insert earphones have foam tips that are inserted into the listener’s ear canal. Supra-aural headphones completely cover the pinna, or outer ear. Any sound that travels through the outer, middle and inner ear is heard by air conduction. In clinical audiology, human hearing is tested by two sound pathways, air conduction and bone conduction. Transducers used for bone conduction testing are headbands with an attached bone vibrator or oscillator (the terms vibrator and oscillator are used interchangeably in clinical audiology when referring to bone conduction transducers).

Recommended application force of the vibrator to the head is approximately 550 grams (ANSI S3.43-1992) at all frequencies, so that variability of responses due to force against the head is minimized.

2.4 Clinical Measures of Bone Conduction

Clinically, there are numerous factors that can modify the bone conduction response, including force of the transducer against the head, contact area of the oscillator, placement of the oscillator, and calibration of the oscillator. In general, the more force that is applied to the bone oscillator, the less intensity needed to elicit a bone conduction response. Dean (1930), Studebaker (1962) and Dirks (1964), among others have examined the effects of oscillator placement on the measurement of bone conduction thresholds. Although vertex of the skull and teeth have been examined, forehead and mastoid placement are the most popular sites for bone conduction testing.

Bone conduction responses from the frontal bone vs. the mastoid were examined by Dirks in 1964. Results revealed that frontal bone sensitivity was consistently poorer than thresholds obtained with mastoid placement. The magnitude of the difference in the two measures was frequency dependent. As frequency increased, the difference between the two threshold measures decreased. However,

Dirks also found that test-retest reliability was better with forehead placement.

Studebaker, 1962 also demonstrated that forehead placement had less test-retest variability and higher inter-subject reliability. These studies indicated that forehead placement was superior due to fewer variations produced by vibrator to skull pressure and less artifact produced by abnormalities of the sound-conducting mechanism in the middle-ear. In addition, the effect of the inertial component of bone conduction is more pronounced with mastoid oscillator placement. At low frequencies, motion of the ossicular chain is activated to a greater degree when the oscillator is placed at the

mastoid (Studebaker, 1962).

Despite these advantages of forehead placement, the main disadvantage is that the dynamic range is smaller since thresholds are typically greater. Therefore, mastoid placement is favored clinically due to the greater dynamic range.

Additionally, it is often reported that there is no interaural attenuation to consider in bone conduction testing (Martin, 1997), that the signal reaches both cochleae at equal magnitudes. This is not completely true for mastoid oscillator placement. Interaural attenuation values can be as much as 15 dB at 2000 Hz and 20 dB at 4000 Hz, which is a second advantage for ipsilateral mastoid placement (Silman & Silverman, 1991).

Although clinical bone conduction thresholds are assumed to be inner ear thresholds, changes in bone conduction thresholds have been reported in patients with various middle ear disorders. For example, patients with otosclerosis, or ossification of the bones in the middle ear space, often show a greater bone conduction loss at

2000 Hz. This notch first described by Carhart (1950) is now known as “Carhart’s notch”. Upon surgical repair, bone conduction thresholds return to normal, not due to cochlear changes, but due to mechanical changes in the ossicular chain. The presence and disappearance of Carhart’s notch emphasizes the role the middle ear plays in bone conduction. An improvement in bone conduction thresholds has been documented in patients who have undergone radical mastoidectomies. There have also reported cases of otitis media creating changes in bone conduction thresholds, with low frequency thresholds being enhanced, and higher frequency thresholds worsening (Hulka, 1941). Results of many investigations have shown that bone conduction thresholds can be altered by manipulating middle ear status with air

pressure changes in the external meatus, loading of the tympanic membrane (Allen &

Fernandez, 1960) and the occlusion of the external canal (Bekesy, 1932; Tonndorf,

1966).

It has been known for many years that the cochlear mechanism by which we hear sounds transmitted through vibrations of the skull is the same as that with airborne sounds. However, when air and bone conduction responses are recorded clinically, the responses are interpreted differently. Air conduction thresholds are a reflection of the total hearing system via the outer, middle and inner ear. If a disorder exists in one or more of these areas, hearing loss will likely result. Bone conduction is thought to

bypass the outer and middle ear and provide a measure of the integrity of the

sensory/neural system. However, this is not entirely accurate. Clinical bone

conduction testing has primarily been used for differential diagnosis of

conductive/mixed losses from sensorineural ones. However, in order to ensure that

appropriate referrals and recommendations are made, clinical diagnostic evaluations

should be comprehensive, so that pathologies requiring medical treatment can be

appropriately identified. More information regarding the outer, middle, and inner ear

contributions to bone conduction hearing is needed.

In summary, there are many limitations with clinical bone conduction testing,

several of which are due to equipment. For clinical testing, bone vibrators have a

reduced frequency response, when compared to air conduction. A mechanical

resonance is also present in the 200-600 Hz range, which can affect low frequency

threshold measurements (Arlinger, et al., 1978). The dynamic range of a bone

oscillator is also limited, especially when a forehead placement is used. Reliability of

bone conduction testing has also been questioned, due to inter- and intra-subject variability (Dirks, 1964). Clinically, air conduction thresholds are typically measured at octave frequencies from 250 Hz-8000 Hz. Bone conduction thresholds are obtained at octave frequencies, 250 Hz-4000 Hz (Bess & Humes, 1990).

Bone conduction hearing is complex. The bone conduction pathway is predominantly osseous, but sound propagation through fluid and tissue is also likely.

When the bone conduction limit is reached, noise exposure is possible through head and body vibrations. Bone conduction is not independent of the status of the outer and middle ear.

2.5 Calibration of Bone Conduction Transducers

Calibration of bone conduction oscillators is challenging. The development of the artificial mastoid which simulates the mechanical impedance of the average human mastoid process has standardized calibration of bone oscillators making it more accurate than previously used methods (ANSI, 1997). Artificial mastoids like the Breul & Kjaer type 4930, became commercially available in the 1960s.

International standards state that the reference amount of vibratory energy from the oscillator is to be equal to the energy required to elicit a threshold from an otologically healthy young person (0 dB HL). Because the mechanical impedance of the artificial mastoid is a population estimate of human mastoid impedance, a fairly objective measure of the force exerted on a similar mastoid is possible. This is an invaluable tool for calibrating bone conductors--especially in the clinical setting.

Bone vibrators themselves must meet additional standards of contact shape and area

and must be applied with the appropriate force (ANSI S3.43-1992). The most

commonly used bone vibrators are the Radioear B-71 and B-72.

Because the artificial mastoid impedance is based on population estimates,

differences in the actual magnitude of the bone conducted stimulus will exist for any

given individual. Any particular individual may not receive the bone conducted tone

at the expected magnitude, due to anatomical differences. There have also been

concerns raised about the accuracy of bone conduction standards used to calibrate

audiometers (Lightfoot & Hughes, 1993) and the use of artificial mastoids as

specified in the standards. Because of these concerns, a more reliable and patient-

specific way of calibrating bone vibrators is needed for clinical testing. A novel bone

oscillator calibration technique (Purcell, 1999) will be discussed later in this paper.

2.6 Otoacoustic Emissions

The understanding of frequency analysis in the inner ear has gone through

three main periods (Dallos, 1992). The first was dominated by Helmholtz’s

assertions that spectral analysis in the cochlea was performed by spatially ordered,

mechanically resonant elements. By the second period in the mid 20th century, measurement of wave propagation characteristics through the cochlear partition had been well studied. von Bekesy’s (1960) experiments had provided important information about cochlear mechanics. Direct measurements of basilar membrane movement were made at moderate and high levels with live and post mortem animal studies. However, the most sensitive direct measurement techniques failed to give data within 50 dB of hearing thresholds. Mechanical tuning properties described by

Bekesy were broader than those of neural tuning recorded from the VIII nerve

(Kiang, et al., 1965). As new techniques were used for measurement of basilar membrane movement, the agreement between mechanical and neural “tuning curves” improved (Rhode, 1971; Rhode, 1978; Sellick et al., 1982). Cochlear insults such as anoxia or ototoxicity proved to broaden the tuning, similar to results obtained by

Bekesy (Rhode, 1971; Sellick et al., 1982). These observations led to the conclusion that the sharp frequency tuning in the human cochlea is based on a physiologically vulnerable mechanism.

Studies using the Mossbauer technique suggested that the cochlea exhibits nonlinear vibration characteristics predominantly at low stimulus levels (Rhode,

1971). Several models of nonlinear cochlear behavior were then developed (Hubbard

& Geisler, 1972; Kim et al., 1973; Hall, 1974). Many investigators at that time proposed a “second filter” in the auditory system distinct from movement of the cochlear partition which would increase human sensitivity and frequency selectivity

(Evans & Wilson, 1973).

The amazing sensitivity and frequency selectivity of the human auditory system was proposed many years ago to depend on a cycle-by-cycle amplification of sound induced vibrations in the organ of Corti (Gold, 1948). He proposed that traveling wave amplification was possible due to mechanical energy release. Among the cells in the organ of Corti, only outer hair cells (OHC) have been shown to have electro-motility and mechanical nonlinearity capable of ‘generating’ sound

(Brownell, 1983).

Now we are in the third period of understanding of cochlear frequency

analysis. It is now believed that von Bekesy’s traveling wave is enhanced by a local electromechanical amplification process which is often referred to as the cochlear amplifier. The outer hair cells are implicated in this amplification process and appear to serve as both sensors and mechanical feedback elements. The result of this cochlear amplifier is the remarkable performance of the human auditory system.

Otoacoustic emissions (OAE) were discovered in 1978 by D. Kemp. OAE are low level acoustic signals thought to be generated in the cochlea by this same cochlear amplifier. Mechanical energy follows a reverse transmission through the middle ear and into the ear canal where sounds can be recorded by a microphone.

Numerous reports have indicated a cochlear origin of OAE. Not only can they be measured while neural responses to sound are absent, but even if the VIII nerve is

severed (Siegel & Kim, 1982). Evoked OAE are frequency dispersive (higher

emission frequencies have shorter latencies). OAE are susceptible to noxious agents,

such as intense noise, anoxia, and ototoxic drugs, all of which are known to affect the cochlea. Finally, OAE are absent in the frequency regions where a cochlear hearing

loss exists and present at frequencies of normal hearing sensitivity.

There are two broad classes of OAE: spontaneous and evoked. The most

clinically utilized OAE are the distortion product otoacoustic emissions (DPOAE).

DPOAE are evoked emissions elicited by two simultaneous tones, termed primaries,

which differ slightly in frequency (f1

occur at predictable frequencies related to the primaries (Lonsbury-Martin & Martin,

1990; Probst et al., 1991). The most robust distortion product is the cubic difference

tone, 2f1-f2. It is now established that the 2f1-f2 component is highly correlated with a functioning cochlear amplifier (Brown et al., 1989; Whitehead et al., 1992).

DPOAE are considered to be relatively narrow-band responses and therefore are considered by many to be a valuable tool for probing cochlear frequency resolution

(Brown & Kemp, 1984; Lonsbury-Martin et al., 1987; Harris et al., 1989; Whitehead et al., 1990).

DPOAE measurement’s success in differentiating normal from hearing impaired ears depends on the recording parameters used. The frequency ratio (f2/f1) and the relative levels of the two primaries (L1 and L2) will affect the magnitude of the DPOAE obtained. The consensus for the separation of normal from hearing impaired ears is that a frequency ratio of f2/f1~1.2 (Harris et al., 1989) and level differences of L2-L1=10-15 dB (Hauser & Probst, 1991; Whitehead et al., 1995) be utilized.

OAE and specifically, DPOAE have emerged as a powerful clinical tool for the objective measurement of cochlear status. Availability of commercial devices for

measuring OAE is widespread. Although limitations remain, OAE are effective

screening and diagnostic audiologic tools.

2.7 Suppression of OAE

When a stimulus (that falls within certain frequency and intensity

requirements) is simultaneously presented with OAE eliciting stimuli, suppression of

the OAE results (Harris & Glattke, 1992). Suppression of otoacoustic emissions has

been used to confirm the cochlear origin of OAE and also to study frequency

selectivity. Suppression experiments have been conducted with transient OAE

(Kemp, 1979; Wit & Ritsma, 1980; Folsom et al., 1995), spontaneous OAE

(Bargones & Burns, 1988; Long et al., 1993) and stimulus frequency OAE (Kemp &

Chum, 1980) as well as with DPOAE (Brown & Kemp, 1984; Harris et al., 1992;

Kummer et al., 1995; Abdala et al., 1996).

Suppression of distortion product otoacoustic emissions (DPOAE) is achieved by simultaneously adding a third tone (suppressor tone) to the two stimulating primary tones. The level of the suppressor tone is varied until the maximum reduction of DPOAE amplitude is achieved. The suppressor level as a function of

DPOAE suppression is known as a DPOAE iso-suppression tuning curve (STC).

STCs have been shown to be very similar in shape to phychophysical tuning curves.

These similarities have led investigators to predict that STCs provide insight into the gain of the cochlear amplifier (Mills, 1998). STCs elicited with low primary levels reveal the sharpest tuning and the greatest suppressor effects due to the greater contribution of the cochlear amplifier at low levels.

Suppression studies have been done strictly via air conduction, however, advantages may exist to conducting suppression experiments with the DPOAE primaries delivered through bone conduction. Suppressor tones are combined electrically with one of the primaries in a single speaker in the probe. This has the potential of creating distortion and affecting results. Using primaries delivered via bone conduction, the suppressor tone can be alone in the ear canal and therefore, the possibility of distortion/interaction between primary and suppressor tones is eliminated. A second potential practical advantage is that the bone conducted

primaries will elicit a bilateral response, or, if a “better” ear exists, the resultant

DPOAE will be from the better cochlea. This may result in a larger suppression effect and therefore, more valid suppression data.

Although these advantages appear to be promising, the major limitation for use of bone conduction stimuli is the calibration of the oscillator (as discussed previously). If appropriate primary levels cannot be achieved, or even worse, are believed to be achieved, but aren’t, poor data will result. In addition, maximum

intensity limits of bone oscillators are reduced compared to air conduction

transducers. This would likely not routinely be problematic, however, if suppressor

levels need to be increased beyond bone oscillator capabilities, complete STCs would

be impossible.

2.8 Previous Bone Conduction Work using Otoacoustic Emissions

Perhaps the major advantage of bone stimulated OAE is that (at least a portion

of) the stimulus is away from the ear canal. Emissions are often very small in

magnitude and a greater dynamic range of the digitizer used to record the response is

possible with any reduction in the ear canal stimuli (Purcell et al., 1998). A second

property of bone stimulated OAE is that both cochleae are stimulated simultaneously,

which may be practical for screening applications.

There are very few researchers reporting bone conduction delivery of the

stimuli for eliciting otoacoustic emissions (OAE). The first two studies to stimulate

OAE through bone conduction were done in 1988 (Rossi and Solero, 1988; Rossi et

al., 1988). These researchers investigated transient otoacoustic emissions (TEOAE)

by bone conduction. TEOAE are emissions evoked with brief acoustic stimuli. They

are frequency dispersive responses following a click or a tone burst. In these studies,

bone conducted TEOAE showed the same characteristics as those elicited by air

conduction. In addition, the TEOAE were stable over time for a given individual.

Collet, Hellal, Gartner and Morgon (1989) also studied bone conducted TEOAE and reported similar results.

In 1998, Purcell and colleagues demonstrated that distortion product otoacoustic emissions (DPOAE) could be stimulated by bone conduction. Purcell, et al., 2003 used DPOAE to develop an objective technique to estimate bone conduction

signals at the cochlea. DPOAE and models of the auditory periphery were used to

estimate the magnitude and phase of sinusoidal bone conducted sounds at the cochlea.

The middle ear model employed was that based on the work of Zwislocki (1962) which was later extended by Giguere and Woodland (1994). An electrical analogue model was used to estimate the magnitude and phase of steady state sinusoidal signals at points in the ear where they could not be measured non-invasively. The magnitude of the bone conducted signal at the cochlea was estimated using a bone conducted

DPOAE calibration technique developed by Purcell and colleagues in 1999. In this calibration, input/output (I/O) functions of DPOAE stimulated through air conduction were compared to I/O functions of bone stimulated DPOAE. The investigators relied on the assumption that when equal magnitude DPOAE are recorded, the stimulus levels via the two modes are equal at the cochlea. In order to equate the two I/O functions, magnitude and mode of one stimulus tone (L2) was varied while all other parameters ( f1, f2, L1) remained constant. By correlating the I/O functions, the bone

oscillator was objectively calibrated at the f2 frequency. Each value of the bone

conducted L2 was mapped to an equivalent emission generating value of the air

conducted L2. They estimated phase by relying on models of the acoustic probe, the

ear canal and the middle ear. The phase of the DPOAE primaries was determined at

the electrical output of the microphone used to elicit the DP, as well as the pressure

phase of the DPOAE as it entered the measuring microphone. The phase at the base

of the cochlea was estimated by employing DPOAE generation site theories which state that the DP inherits the phase of its stimuli at the generation site in the same way

the DP frequency is determined. Details of these estimates are beyond the scope of

this study. However, the resulting bone conduction transfer functions created by

these estimations and actual measurements reflect the multiple contributions made to

the total bone conducted signal at the cochlea. With physical measurements of the

signal in the ear canal obtained, the transfer function was separated into ear canal and

middle/inner ear components.

In addition to the air and bone I/O function procedure, Purcell et al., (1999)

used a subjective phase cancellation technique to test the validity of the objective

calibration. Subjects performed phase cancellation between sinusoidal stimuli at the

P2 frequency through a bone conduction transducer and a speaker in the ear canal

probe. Subjects were asked to adjust the loudness of the two stimuli (one via air and one via bone conduction) until they were perceived as equal. Then the subjects would adjust the phase of the air conducted signal until a loudness minimum was perceived. Results of this portion of the study indicated agreement between

subjective phase cancellation data and objective I/O function shifts.

2.9 The Current Study

One way to reduce the amount of middle ear contribution to the bone

conducted response is to move the stimulation from the mastoid to the forehead

(Dirks and Malmquist, 1969). This was done in the current study and I/O functions

of the air and bone conducted OAE were compared. In previous work with bone

conduction DPOAE a subjective phase cancellation procedure was employed (Purcell

et al., 1999). However, results were not compared with behavioral thresholds. In the

current experiment, behavioral threshold testing with air and bone conduction transducers was completed. The bone conduction transducer was moved to the three placements used for DPOAE testing and thresholds were recorded. Air and bone conduction behavioral thresholds were compared to the DPOAE elicited with air and bone conducted stimuli.

CHAPTER 3

METHODS

3.1 Subjects

Three adults (ages 36, 30 and 30 years) participated in this study. Two of the

listeners were male and one was female. Their participation in this experiment was

voluntary. All had normal hearing and normal middle ear functioning bilaterally.

For the purposes of this study, normal hearing acuity was defined as audiometric

thresholds of 20 dBHL or better for 250Hz to 8000Hz. Normal middle ear function was defined as normal middle ear pressure and compliance as measured by a clinical tympanogram. The three subjects were screened prior to starting this experiment and were found to have present and robust distortion product otoacoustic emissions at the test frequencies 500-8000Hz bilaterally using the ILO 88 clinical test system. The right ear was used as the test ear for all three subjects.

3.2 Behavioral Threshold Measurements

Behavioral thresholds were recorded using a Grayson-Stadler model 61

clinical audiometer. Subjects were seated in a double walled Industrial Acoustics

Company, Inc. (IAC) sound attenuating room and instructed to press a button when

they could hear the stimuli. Pure tones at 1000 Hz and 2000 Hz were delivered

through an ER 3A insert earphone for air conduction thresholds, and via a radio ear

B-71 bone vibrator for bone conduction thresholds. The bone vibrator was moved

from ipsilateral to contralateral mastoid and to forehead placements, in random order.

Narrow band maskers were introduced into the non-test ear for the bone conduction thresholds. The 3A insert phone was left in the subject’s test ear (right ear)

throughout bone conduction threshold testing. This was done to simulate the OAE

testing conditions where the 10C probe remained in the subjects’ ears for delivering

P1 and recording the DPOAE. Thresholds were measured in dB HL and then

converted to dB SPL so they may be compared to DPOAE levels recorded.

3.3 Otoacoustic emission testing

Primary tones for the distortion product otoacoustic emissions (DPOAE) were generated in SigGen, a Tucker Davis System II signal generation program (see Figure

3).

Figure 3. SigGen signal generation program sample screen. From tucker- davistechnologies.com 27

DPOAE primary tones were generated at frequencies where the second primary (P2)

was 1.2 times greater in frequency than the first primary (P1) (Harris et al., 1989;

Gaskill & Brown, 1990). For the purposes of this study, the primary tones were

centered around two frequencies (Fc), 1000 and 2000 Hz. Therefore, P1 was

generated at Fc * .909 and P2 at Fc * 1.09. The level (L1) of P1 was held constant at

60 dB SPL. The level (L2) of P2 was varied from 30 to 75 dB SPL. Higher levels

were attempted but not achieved due to distortion generated by overdriving the bone

transducer. Level was manipulated by SigGen via two external PA-4 attenuators

[Tucker-Davis System II]. The two primaries were then put through separate channels of a headphone buffer and delivered into the ear via an Etymotic Research

ER-10C probe system (See Figure 4). The tones were not combined until they reached the ear canal of the subject. The 10C probe also served as the recording instrument for the distortion product (DP). A signal at the 2f1-f2 frequency was considered a valid DPOAE if it was at least 3 dB above the extrapolated noise floor.

Four placements and two transducers were used to stimulate the DP. When the DP was being elicited via air/air (meaning both P1 and P2 were air conducted), the primaries were put into the two channels of the 10C probe. When the condition was air/bone, the transducer for P2 was changed to the bone vibrator. P1 was always introduced via air conduction and through channel 1 of the 10C probe. The transducer of P2 was varied from channel 2 of the 10C probe to the bone vibrator, depending upon the desired condition. In some conditions, wide band Gaussian noise was introduced to the non-test ear. The noise was produced by a Tucker-Davis 28

wave generator (WG 2) with a flat spectrum, a 20 kHz bandwidth, rolling off above

20 kHz at a rate of 18 dB/octave. The level of the noise was no greater than 50 dB

SPL in any condition, as measured on a Larson-Davies model 810B sound level meter. An Etymotic Research ER-10A insert earphone was used as the transducer for the noise. See Figures 8-15.

Sound booth DA1 PA4-1 1 In Out HB6 2 Ch 1 Trig In Out 10C probe / mic Channel 1 Ch 2 PA4-2 In Out 10C probe / mic Channel 2 TG6 In Out or bone transducer 1 2 3 WG2 Out 4 5 6 10A insert earphone AD1 MA2 10C probe / mic box 1 Trig In Out

Figure 4. Hardware configuration for collection of DPOAE.

The DPOAE testing was administered through BioSig, a Tucker-Davis

System II diagnostic program designed for recording electrophysiologic potentials.

See Figure 5.

Figure 5. Sample BioSig data collection screen for electrophysiologic potentials.

In this program, SigGen signals are utilized to stimulate electrophysiologic potentials, in this study, DPOAE. Order and number of the conditions can be changed, repeated, paused and stopped in BioSig. Signal averaging of the response also occurs in

BioSig. For this study, the number of averages was set at 2000 or 3000. The level of the noise floor was evaluated for each subject for each condition. If the noise floor was deemed to be too high, such that a dp although present, may be buried in the noise, the number of averages was increased. Averages were never increased beyond

3000 due to the additional time required for a higher number of averages. A

hamming window output of the primaries and the resulting DPOAE as well as the noise floor was displayed upon completion of each condition. This output spectrum

displayed level in arbitrary units. However, L1 in the ear canal was calibrated and known to be 60 dB SPL. L1 was used as the “reference” from which to measure the

L2, the noise floor and the level of the dp in the ear canal. See the appendix for a chart of how levels were determined.

3.4 Calibration

A 1 volt rms signal at each of the center frequencies was routed through

transducer, coupled to the 10C microphone with a Zwislocki coupler attached to a

Larson-Davies sound level meter to measure the equivalent dB SPL (See Figure 6).

This SPL value was entered into the SigGen program for calibration of the system. In

addition, the levels of the two primaries in BioSig were confirmed. L1 was measured

as 60 dB SPL through the 10C microphone in a Zwislocki coupler and L2 varied from

75dB to 30 dB SPL. Before subjects were tested, an initial calibration procedure in

BioSig was conducted with the 10C probe transducer. Tones of fixed voltage were

presented to the 10C transducer at 1000 and 2000 Hz and the resulting SPL of these

tones was recorded in the ear canal. Based on this information, an equalization of

output levels was performed for each subject to achieve target stimulus levels from

this transducer.

10C probe

SigGen SLM & BioSig TDT hardware 10C Probe / Mic Zwislocki System coupler

Figure 6. Calibration set-up.

Additionally, the Radio-Ear B-71 clinical bone vibrator, used in this

experiment as the bone transducer, was calibrated with a Bruel & Kjaer Type 4930 artificial mastoid and a Quest model 155 sound level meter.

Radio ear b-71 oscillator

SigGen TDT SLM & BioSig hardware

Artificial mastoid

Figure 7. Calibration set-up of the bone ocillator.

Prior to data collection, the 10C probe was inserted into each subject’s test ear

and the microphone calibration level tested. No microphone calibration adjustment

was needed among the subjects at the two test frequencies.

3.5 Test Sessions

Listeners were tested one at a time in a single-walled IAC sound attenuating

booth. They were seated in a reclining chair and instructed to relax. The 10C probe

was inserted into the test ear and depending on the test condition, the bone vibrator

(seated on the ipsilateral mastoid, the contralateral mastoid or the forehead) and the insert earphone with masking noise in the non-test ear may also have been used (see

Figure 8). In total, sixteen conditions were measured, the eight conditions listed below at two center frequencies, 1000 and 2000 Hz.

3.6 Test Conditions

ER 10-C Probe / Mic TE

Subject

Figure 8. Condition 1. Air/Air: The 10C probe is placed in the test-ear and delivers both of the primaries for eliciting the DPOAE.

ER 10A Insert earphone in NTE ER 10-C Probe / Mic TE NTE

Subject

Figure 9. Condition 2. Air/Air (with masking): The 10C probe is placed in the test- ear and delivers both of the primaries for eliciting the DPOAE. Masking noise is delivered via one ER-10A insert earphone into the non-test ear.

Radio Ear b-71 headband

Radio Ear b-71 oscillator on TE mastoid

ER 10-C Probe / Mic TE NTE

Subject

Figure 10. Condition 3. Air/Bone-Ipsi : The 10C probe is placed in the test-ear and delivers P1. The radio ear B-71 transducer is placed on the ipsilateral (test-ear) mastoid and delivers P2 via bone conduction.

Radio Ear b-71 headband

Radio Ear b-71 oscillator on TE mastoid

ER 10A Insert earphone TE NTE in NTE ER 10-C Probe / Mic Subject

Figure 11. Condition 4. Air/Bone-Ipsi (with masking): The 10C probe is placed in the test-ear and delivers P1. The radio ear B-71 transducer is placed on the ipsilateral (test-ear) mastoid and delivers P2 via bone conduction. Masking noise is delivered via one ER-10A insert earphone into the non-test ear.

Radio Ear b-71 headband

Radio Ear b-71 oscillator on NTE mastoid

ER 10-C Probe / Mic TE NTE

Subject

Figure 12. Condition 5. Air/Bone-Contra : The 10C probe is placed in the test-ear and delivers P1. The radio ear B-71 transducer is placed on the contralateral (non test-ear side) mastoid and delivers P2 via bone conduction.

Radio Ear b-71 headband

Radio Ear b-71 oscillator on NTE mastoid

ER 10A Insert earphone TE NTE in NTE ER 10-C Probe / Mic Subject

Figure 13. Condition 6. Air/Bone-Contra (with masking) : The 10C probe is placed in the test-ear and delivers P1. The radio ear B-71 transducer is placed on the contralateral (non test-ear side) mastoid and delivers P2 via bone conduction. Masking noise is delivered via one ER- 10A insert earphone into the non-test ear.

Radio Ear b-71 oscillator Radio Ear b-71 headband on forehead

TE NTE ER 10-C Probe / Mic

Subject

Figure 14. Condition 7. Air/Bone-Forehead : The 10C probe is placed in the test- ear and delivers P1. The radio ear B-71 transducer is placed on the forehead and delivers P2 via bone conduction.

Radio Ear b-71 oscillator Radio Ear b-71 headband on forehead

ER 10A Insert earphone in NTE ER 10-C Probe / Mic TE NTE Subject

Figure 15. Condition 8. Air/Bone-Forehead (with masking) : The 10C probe is placed in the test-ear and delivers P1. The radio ear B-71 transducer is placed on the forehead and delivers P2 via bone conduction. Masking noise is delivered via one 2 insert earphone into the non-test ear.

Approximately eight test sessions were required for completion of the data.

Each session was 1.5 to 2 hours in length. When possible, the transducers were not disturbed during a test session, however, for the conditions when the bone vibrator was used, subjects usually became uncomfortable and it was necessary to remove the transducers. Effort was made to reposition the transducers similarly within the conditions and among test sessions, however, each placement was necessarily unique and this potentially created variability in the response. To minimize this variability,

levels in BioSig were monitored within and among sessions to attempt to keep levels

in the ear canal as constant as possible in each subject. Although this does not ensure

that the levels reaching the cochlea are constant, it does provide a confidence that

large effects noted in the data are not completely due to test/retest and placement

variability.

Input/output functions were created for each subject with non-test ear and without non-test ear masking to observe the effects of contralateral masking on the

DPOAE. Input/output functions for the air/air conditions were compared to those for the air/bone conditions at the three placements. A calibration technique similar to that used by Purcell, et al., 1999, was employed to match the input/output functions.

CHAPTER 4

RESULTS

This chapter contains the results of behavioral threshold and distortion product

otoacoustic emission (DPOAE) testing for three subjects. The data consists of

DPOAE input/output functions when both primaries (P1 and P2) are delivered via air conduction and when the higher frequency primary (P2) is routed through bone conduction. The effects of varying the location of the transducer delivering the bone

conducted P2 can be observed. In addition, threshold data are compared with

DPOAE differences at the different P2 placements. Finally, the effects of non-test ear

masking are presented.

4.1 Behavioral threshold data

Tables 1 and 2 list behavioral thresholds (in dB SPL) for the three subjects

with air and bone conduction transducers. First, threshold measurements were made

via air conduction with an insert earphone in the test ear at both Fc values (1000 and

2000 Hz). Bone conduction threshold measurements were also recorded with a bone vibrator at three locations: ipsilateral mastoid, contralateral mastoid and forehead at both frequencies. All bone conduction behavioral threshold measurements were made with contralateral masking in the non-test ear to ensure threshold was recorded from the test ear. Also, an insert earphone was placed in the test ear for bone 39

conduction threshold measurements to simulate the acoustics of the occluded ear when the DPOAE probe delivered P1 to the test ear. Occlusion of the ear canal can affect the outer ear’s contribution to the bone conducted response in the lower frequencies (1000 Hz and lower),Tonndorf, 1963. Bone conduction thresholds may be lower when the ear canal is “blocked” with a probe or insert earphone. In DPOAE testing with P2 delivered by bone conduction, P1 was always delivered and the

DPOAE was recorded by a probe in the test ear. The same acoustic conditions were desired for behavioral threshold and DPOAE testing. If DPOAE were affected by necessarily occluding the test-ear with the probe, the effect is desired in the behavioral threshold measurements as well.

1000 Hz Air Ipsilateral Contralateral Forehead

Subject 1 10.5 19.5 16.5 32.5

Subject 2 6.5 -0.5 -2.5 1.5

Subject 3 18.5 8.5 15.5 15.5

Average 11.83 9.33 9.83 16.5 threshold

Table 1. Behavioral thresholds in dB SPL, at 1000 Hz, for all P2 locations. A 1 dB step size was used in determining threshold.

2000 Hz Air Ipsilateral Contralateral Forehead

Subject 1 12.5 13.5 21.5 15.5

Subject 2 13.5 7.5 6.5 14.5

Subject 3 -0.5 9.5 8.5 7.5

Average 8.8 10.17 12.17 12.5 threshold

Table 2. Behavioral thresholds in dB SPL, at 2000 Hz, for all P2 locations. A 1 dB step size was used in determining threshold.

4.2 DPOAE Input/Output Functions

Input/output functions were generated by plotting the nominal level (L2) of P2 in dB SPL on the abscissa and the level of the observed DPOAE on the ordinate. The level (L1) of P1 was kept constant at 60 dB SPL. In all of the graphs in the chapter, the abscissa is labeled “nominal” dB SPL because the voltage delivered to the transducer is known, but the actual SPL has to be estimated. In the air/air conditions, this is also the level delivered into the ear canal and finally, into the cochlea; however, in the air/bone conditions, this may not always be the case. The actual level delivered to the cochlea will vary depending on head size and skull density as well as placement of the bone vibrator. Sources of variability will be explored further in the discussion section of this document. For consistency and clarity, the abscissa is labeled in this manner for all input/output functions presented. Additionally, the scales for the graphs throughout the results section have differences in the range on the ordinate. This was done intentionally. The graphs are formatted such that the

DPOAE level differences and differences in shape of the input/output functions when 41

P2 was delivered by bone conduction are easily visible. For this study, level of the measured DPOAE is not as important as the shape of the functions. In one test condition, both primaries were introduced via air conduction. In the other three

conditions, P1 was introduced via air conduction and P2 via bone conduction. Three

placements (ipsilateral mastoid, contralateral mastoid and forehead) of the bone

vibrator were used. When conditions are referred to in this chapter as air, ipsi, contra

or forehead, it can be assumed that these are indications of location of P2.

4.3 Results for Fc=1000 Hz

Figures 16, 17 and 18 show the input/output functions for four transducer

locations of P2 at 1000 Hz. P2 was delivered via air conduction and an insert

earphone into the test-ear, and at three head locations (ipsilateral mastoid,

contralateral mastoid and forehead) via bone conduction using a clinical bone

vibrator. P1 was always delivered via air conduction. The black lines with circle

symbols indicate that P2 is being delivered via air conduction. The red lines with

diamond symbols indicate P2 is delivered via bone conduction on the ipsilateral (test-

ear) mastoid. The green lines with triangle symbols represent the condition where P2 is delivered via bone conduction with the transducer on the contralateral (non-test ear)

mastoid and the blue lines with square symbols indicate P2 is being delivered via

bone conduction at the forehead placement. These graphs illustrate the differences in

input/output functions due to changing the location of P2. Typical input/output

functions for DPOAE are an inverted “U” shape. As L2 increases and gets closer to

L1, the DPOAE intensity increases. The DPOAE level is generally highest around a

level difference of L1-L2 = 10 dB (Hauser & Probst, 1991; Whitehead et al., 1995).

When L2 surpasses this optimal level difference, the DPOAE begins to decrease in intensity.

Figure 16 shows the data for subject 1 at 1000 Hz. All four plots for the transducer location look similar, in the level of DPOAE obtained, however, L2 appears to be horizontally shifted for the conditions where P2 was delivered via bone conduction. Similarities in the data for subjects 2 and 3 (figures 17 and 18) are not as apparent. Subject 2 has input/output functions that deviate from the expected shape slightly. The conditions in which P2 is delivered via bone conduction are harder to compare to the functions in which P2 is delivered by air conduction. A horizontal shift is not as easy to visualize with this data. The forehead placement (blue line with square symbols) for Subject 2 did not yield measurable DPOAE at levels below the nominal SPL value of 55 dB. The data for Subject 3 (Figure 18) reveal that at two of the bone conduction conditions (contra and forehead), the DPOAE were not as intense as those obtained for the air/air and air/ipsi conditions.

Figure 19 illustrates a calibration technique (Purcell et al., 1999) for the conditions where P2 is delivered through bone conduction. Input/output functions with bone conducted P2 are compared to the air/air condition input/output functions and the DPOAE levels at different L2 conditions are “matched”. In Figure 19, the plot for Subject 1, (Fc=1000 Hz, P2 delivered at the ipsilateral mastoid) is shifted

11dB to match the air/air function. The underlying assumption is that equal magnitude of DPOAE recorded in the ear canal are stimulated by equivalent stimulus levels in the cochlea. This technique uses input/output functions to compare DPOAE

elicited through bone conduction with those obtained via air conduction. The best match is obtained when the two curves overlap each other as well as possible. In most cases, the input/output functions were aligned using the quadratic curve fit function in Sigma Plot 2000 for Windows (Version 6.0 from SPSS, Inc.). Using the

2 formula y=yo + ax + bx , the y-intercept and values of a and b were calculated with

the curve fit function in Sigma Plot. These values were then entered into a program

which finds roots of second order polynomials using the equation:

x = [-b ±√(b2-4ac)] / 2a

This root finder program was obtained from the internet and can be found on

the Contra Costa County Office of Education website,

(http://www.cccoe.k12.ca.us/javamath/algebra/root.htm). After obtaining the two x-

intercepts (roots) the lower intercept from the P2 via air conduction input/output

curve was subtracted from the lower intercept of the P2 via bone conduction curve.

This difference was used to shift the bone conducted curve in (nominal) dB SPL on

the graph. In a few instances, a linear fit of the most linear portions of the two curves

appeared visually to be a more appropriate technique to fit the data. The linear fit

function applying the equation, y = yo + ax in Sigma Plot was used for these matches.

The x-intercept from the P2 via air conduction input/output curve was subtracted

from the intercept of the P2=bone curve in order to shift the functions the appropriate

amount. There were also a few instances where neither the quadratic nor the linear

fits appeared to appropriately match the curves due to the absence of measurable

DPOAE at some L2 conditions or due to differences in the shapes of the two

functions. In these cases, dp levels were subjectively compared. The bone conducted

-2

-4

dpoae level (dB SPL) Air -6 Ipsi Contra -8 Forehead

-10 30 35 40 45 50 55 60 65 70 75 L2 level (nominal dB SPL)

Figure 16. Subject 1, 1000 Hz. Input/output functions of all P2 placements.

-5

dpoae level (dB SPL) (dB dpoae level Air Ipsi -10 Contra Forehead

-15 30 40 50 60 70 80 L2 (nominal dB SPL)

Figure 17. Subject 2, 1000 Hz. Input/output functions of all P2 placements.

dpoae level (dB SPL) (dB dpoae level 0 Air Ipsi -5 Contra Forehead

-10 30 40 50 60 70 80 L2 (nominal dB SPL)

Figure 18. Subject 3, 1000 Hz. Input/output functions of all P2 placements.

input/output function was shifted in nominal dB SPL until the DPOAE SPL levels were as visually similar as possible to the air/air function. These types of calibration or “matching” are done in figures 20-22 for all subjects, all placements, using quadratic curve fits, unless otherwise noted. Specific information of individual subjects’ curve shifts will be discussed later in the text.

8 A 6

2 0

-2

-4

(dB SPL) dpoae level -6

-8

-10 30 35 40 45 50 55 60 65 70 75 nominal dB SPL

8 B 6

dpoae level (dB SPL) level (dB dpoae -2 Air/Air Air/Ipsi -4 Shifted Air / Ipsi

-6 20 30 40 50 60 70 80 nominal dB SPL

Figure 19. Subject 1, 1000 Hz, Illustration of the matching technique. A. Quadratic curve fits done in Sigma Plot for the Air/Air function (black line/black circles) and for the Air/Ipsi function (red line/red diamonds). B. Difference of two x-intercepts used to shift the Air/Ipsi curve 11 dB. 48

In Figure 20, the ipsilateral placement functions were shifted to match the air/air functions for each subject at Fc equal to 1000 Hz. The black input/output curves with circle symbols indicate P2 was delivered by air conduction. The red curves with diamond symbols indicate P2 was delivered by bone conduction/ipsilateral placement. All curves were shifted using quadratic curve fits.

For subject 1 (A), the air/ipsi curve was shifted 11 dB. For subject 2 (B), the air/ipsi curve was shifted 8 dB. For Subject 3 (C), the air/ipsi curve was shifted 7 dB.

Although the amount of shift required to match the two curves is close for all three subjects, there are individual differences among the curves and in the “fit” of the shifted functions. Visual inspection reveals good agreement in the air/air and air/ipsi curves for subjects 1 and 3 (A and C). There is more of a discrepancy between the two curves for subject 2 (B), although goodness of fit statistics have not been applied for any of the data due to the varying number of data points available. A consistent number of data points could not always be achieved. Lower L2 did not yield measurable DPOAE in many instances. This was especially true when the bone conduction transducer was placed at the contralateral mastoid and at the forehead.

The varying number of data points made comparisons of the curves more difficult from a statistical standpoint.

In Figure 21, the contralateral placement functions were shifted to match the air/air functions for each subjects at Fc equal to 1000 Hz. The black input/output curves with circle symbols indicate P2 was delivered by air conduction. The green upright triangles indicate P2 is delivered by bone conduction/contralateral placement.

The pink curve with upside down triangles in B is the P2 via bone/contra curve

matched to P2 via air using a linear fit, otherwise, the curves were fit using quadratic curve shifts. For subject 1 (A), the air/contra curve was shifted 10 dB.

For subject 2 (B), the air/contra curve was shifted 15 dB using a quadratic curve fit or

10 dB using a linear fit. Visually, the linear fit appears to more accurately align the two functions. For Subject 3 (C), the air/contra curve was shifted 20 dB. No good match is possible for the two curves for subject 3 due to the marked difference in

DPOAE level when P2 is at the contralateral placement. Although the amount of shift required to match the two curves is within 10 dB among the subjects, there are

individual differences among the curves and in the “fit” of the shifted functions.

Visual inspection reveals good agreement in the air/air and air/contra curve for

subject 1 (A). There is more of a discrepancy between the two curves for subject 2

(B), since the contralateral placement condition yielded more robust DPOAE than the

air/air placement at many L2 conditions. It appears subjectively that for subject 2, the

linear fit is a more appropriate match for the two functions. The DPOAE levels for

subject 3 (C) at the contralateral placement did not reach those observed when P2 was

via air conduction. DPOAE levels are much less robust. Therefore, no good match is

possible for these two functions.

18 A

6 Air / Air Air / Ipsi 4

0 20 30 40 50 60 70 80

10 B 8

SPL) 6

(dB

l 4 eve l

2 Air / Air poae poae

d Air / Ipsi 0

-2 20 30 40 50 60 70 80

18 C

6 Air / Air Air / Ipsi 4

0 20 30 40 50 60 70 80 nominal dB SPL

Figure 20. Match for P2 at the ipsilateral placement at Fc=1000 Hz. A. Subject 1, shifted 11 dB. B. Subject 2, shifted 8 dB. C. Subject 3, shifted 7 dB.

In Figure 22, the forehead placement functions are shifted to match the air/air

functions for each subject at Fc equal to 1000 Hz. The black input/output curves with circle symbols indicate P2 is delivered by air. The blue curves with square symbols indicate P2 via bone conduction/forehead placement. All curves were shifted using quadratic curve fits. For subject 1 (A), the air/forehead curve was

shifted 12 dB. For subject 2 (B), the air/forehead curve was shifted 21 dB. For

Subject 3 (C), the air/forehead curve was shifted 34 dB. The amount of shift required

to match the two functions varied greatly among the subjects. Visual inspection

reveals good agreement in the air/air and air/forehead curves for Subject 1 (A).

Subject 2 also had fairly good agreement between the matched curves. Subject 3’s

bone conduction, this time at the forehead placement. These DPOAE did not reach

the magnitude of the DPOAE when P2=air. It appears that only a portion of the

forehead placement input/output curve was obtained. The “curve” is shifted vertically on the graph. It appears that if greater levels could have been delivered

through the transducer for bone conduction, more robust dopoae may have been

observed.

8 A 6

-2 Air / Air Air/Contra -4

-6 20 30 40 50 60 70 80

12 B 10 ) PL

S 8 dB ( 6

Air / Air dpoae level Air / Contra-quadratic curve fit 2 Air / Contra-linear fit

0 20 30 40 50 60 70 80

25 C 20

0 Air / Air Air / Contra -5

-10 20 30 40 50 60 70 80 nominal dB SPL

Figure 21. Match for P2 at the contralateral placement at Fc=1000 Hz. A. Subject 1, shifted 10 dB. B. Subject 2, shifted 15 dB using a quadratic curve fit and 10 dB using a linear fit. C. Subject 3, shifted 20 dB. In C., no good match is possible due to the marked difference in DPOAE level when P2 is at the contra placement.

8 A 6

-2

Air / Air -4 Air/Forehead

-6

-8 20 30 40 50 60 70 80

10 B

5 SPL)

0 (dB

l eve l -5 poae

d -10 Air / Air Air / Forehead

-15 20 30 40 50 60 70 80

25 C 20

0 Air / Air Air / Forehead -5

-10 10 20 30 40 50 60 70 80 nominal dB SPL

Figure 22. Match for P2 at the forehead placement, Fc=1000 Hz. A. Subject 1, shifted 12 dB. B. Subject 2, shifted 21 dB. C. Ssubject 3, shifted 34 dB. Subject 3 shows a marked difference in DPOAE level when P2 is at the forehead placement.

As discussed in Chapter 2, it is expected that differences in air conduction and ipsilateral (ipsi) v. contralateral (contra) mastoid bone conduction behavioral thresholds are negligible, near 0 dB (Studebaker, 1962 ; Dirks, 1964). Forehead thresholds are more variable and are generally 10 dB different (greater) than ipsi or contra thresholds (Nilo, 1965; Martin, 1997), although some studies have found no difference in forehead versus mastoid behavioral thresholds in normal ears (Dirks,

1969). The assumption, then, is that when recording DPOAE, differences in the OAE at the different placements would be similar to behavioral differences. Shifts in

DPOAE bone conduction functions to match air conduction functions would be similar to those observed in behavioral threshold testing. Very little difference is expected between functions when P2 is delivered via air conduction and at the ipsi and contra placements. Accordingly, forehead DPOAE functions may be expected to be shifted on the order of 10 dB. The preceding 1000 Hz DPOAE data acquired in this study do not support this assumption.

1000 Hz P2=Ipsilateral P2=Contralateral P2=Forehead

Subject 1 11 10 12

Subject 2 8 15Q 21

10L

Subject 3 7 20 34

Average Shift for 8.67 14.17 22.33 3 Subjects Subscripts: Q=quadratic fit, L=linear fit. When no subscript is listed, quadratic fits were performed.

Table 3. Values of the “shifts” in dB SPL used at Fc=1000 Hz to match the bone conduction to air conduction input/output functions. **If more than one type of shift was used (i.e.: linear and quadratic, Subject 2) both numbers were averaged for that subject and this value was used to calculate the overall average for the three subjects.

Table 3 lists the shifts in dB SPL for each subject and each bone vibrator location at 1000 Hz. The numbers in the table indicate the dB SPL shift needed to align the bone conduction input/output curve with the air conduction input/output curve. In most cases, these numbers were determined by using quadratic curve shifts, however, for some conditions linear fits were also used, since they appeared, upon visual inspection, to provide a better “match”. Due to small sample size, statistical analysis of the data was not performed, however, data in Table 3 (Fc=1000 Hz) shows similar correction factors for all subjects at the ipsilateral (within 4 dB) and contralateral (within 10 dB) placements. The forehead placement shifts varied up to

22 dB.

Considering individual subject data, Table 3 illustrates that Subject 1 had consistent shifts (within 2 dB) across P2 location when Fc=1000 Hz. Subjects 2 and

3 had shifts which increased as P2 placement was moved from ipsilateral to contralateral to forehead locations. Average shifts in dB SPL among the 3 subjects for 1000 Hz are listed in the table. The difference in ipsilateral vs. contralateral placement is approximately 5 dB and nearly 13 dB vs. forehead placement.

4.4 Results for Fc=2000 Hz

Figures 23, 24 and 25 show the input/output functions for four transducer

locations of P2. P2 was delivered via air conduction and an insert earphone into the

test ear, and at three head locations (ipsilateral mastoid, contralateral mastoid and

forehead) via bone conduction using a clinical bone vibrator. P1 was always

delivered via air conduction. The symbols for these graphs are the same as for the

1000 Hz data. The black lines with circle symbols indicate that P2 is being delivered via air conduction. The red lines with diamond symbols indicate P2 is delivered via

bone conduction on the ipsilateral (test ear) mastoid. The green lines with triangle

symbols represent the condition where P2 is delivered via bone conduction with the

transducer on the contralateral (non-test ear) mastoid and the blue lines with square

symbols indicate P2 is being delivered via bone conduction at the forehead

placement. These graphs illustrate the differences in input/output functions due to

changing the location of P2.

-2

-4

dpoae level (dB SPL) (dB dpoae level Air -6 Ipsi Contra -8 Forehead

-10 30 35 40 45 50 55 60 65 70 75 L2 (nominal dB SPL)

Figure 23. Subject 1, 2000 Hz. Input/output functions of all P2 placements.

-2

-4

-6

-8

-10

dpoae level (dB SPL) (dB dpoae level -12 Air Ipsi -14 Contra Forehead -16

-18 30 40 50 60 70 80 L2 (nominal dB SPL)

Figure 24. Subject 2, 2000 Hz. Input/output functions of all P2 placements.

0 Air dpoae level (dB SPL) -5 Ipsi Contra Forehead -10

-15 20 30 40 50 60 70 80 L2 (nominal dB SPL)

Figure 25. Subject 3, 2000 Hz. Input/output functions of all P2 placements.

8 A 6

-2 Air / Air Air/Ipsi-quadratic fit -4 Air / Ipsi-linear fit

-6 20 30 40 50 60 70 80

4 B 2

-2

-4

-6

-8 dpoae level (dBSPL) Air / Air -10 Air / Ipsi--subjective best fit

-12 35 40 45 50 55 60 65 70

24 C 22

8 Air / Air Air / Ipsi 6

4 20 30 40 50 60 70 80 nominal dB SPL

Figure 26. Match of P2 at the ipsilateral placement at Fc=2000 Hz. A. Subject 1, shifted 3 dB using a quadratic curve fit and 11 dB using a linear fit. B. Subject 2, shifted 10 dB using a subjective “best fit”. C. Subject 3, shifted 7 dB using a quadratic curve fit. 61

8 A 6

-2 Air / Air -4 Air / Contra

-6 20 30 40 50 60 70 80

2 B

-2 SPL) -4

(dB -6

l -8 eve l -10

-12 poae poae d -14 Air / Air Air / Contra--subjective best fit -16

-18 35 40 45 50 55 60 65 70

25 C 20

-5 Air / Air Air / Contra--quadratic fit -10 Air / Contra--linear fit

-15 -20 0 20 40 60 80 nominal dB SPL

Figure 27. Match of P2 at the contralateral placement at Fc=2000 Hz. A. Subject 1, 15 dB using a quadratic curve fit. B. Subject 2, shifted 10 dB using a subjective “best fit”. No objective curve fit could appropriately match the two curves due to lack of measurable dpoae at many L2 values. C. Ssubject 3, shifted 21 dB using a quadratic curve fit and 33 dB with a linear fit.

8 A 6

-2 Air / Air Air / Forehead -4

-6 20 30 40 50 60 70 80

4 B 2 ) 0 PL S -2 dB ( -4

-6

-8 dpoae level Air / Air -10 Air / Forehead--subjective best fit

-12 35 40 45 50 55 60 65 70

25 C 20

0 Air / Air Air / Forehead -5

-10 0 1020304050607080 nominal dB SPL

Figure 28. Match of P2=forehead placement at Fc=2000 Hz. A. Subject 1, shifted 21 dB B. Subject 2, data point shifted 20 dB using a subjective “best fit”. No objective curve fit could appropriately match the data due to lack of measurable DPOAE at many L2 values. C. Subject 3, shifted 28 dB.

Figures 26, 27 and 28 show differences due to changing placement of P2.

Symbols used for these figures are the same as those used in Figures 13, 14 and 15.

In Figure 26, the ipsilateral placement functions were shifted to match the air/air functions for each subject. The curves were aligned using quadratic curve shifts unless otherwise noted. For subject 1 (A), the air/ipsi curve was shifted 3 dB using a quadratic curve fit or 11 dB using a linear fit. Upon visual inspection, it appears that neither the quadratic nor the linear fit is able to align data well. For subject 2 (B), the air/ipsi curve was shifted 10 dB using a subjective “best fit”. It should be noted that subject 2’s

DPOAE at 2000 Hz were not as robust as those at 1000 Hz. None of the bone conducted input/output functions at any P2 location could be fit by quadratic or linear equations to

“match” the air conduction input/output functions. For Subject 3 (C), the air/ipsi curve was shifted 7 dB. Although the amount of shift required to match the two curves is similar (3-10dB) among the subjects, there are individual differences among the curves and in the “fit” of the shifted functions. Visual inspection reveals good agreement in the air/air and air/ipsi curve for subject 3 (C). There is more of a discrepancy between the two curves for subjects 1 and 2 (A and B). The shape of the air/air and the air/ipsi input/output functions for subject 1 (A) are different. It appears from visual inspection that the linear fit does a better job aligning the two curves, however, no good match is achieved due to the differences in curve shapes. Matching the two functions for subject 2

(B) is also problematic since the ipsilateral placement condition yielded more robust dpoaes than the air/air placement at two L2 conditions. No goodness of fit statistics have been applied to the data due to varying number of measurable dpoae at the different P2 locations. 64

Contralateral results (Figure 27) varied more dramatically (10-21 dB) among subjects. For subject 1 (A), the air/contra curve was shifted 15 dB using a quadratic curve fit and 11 dB using a linear fit. For subject 2 (B), the air/contra curve was shifted

10 dB using a subjective “best fit”. For Subject 3 (C), the air/contra curve was shifted 21 dB using a quadratic curve fit or 33 dB with a linear fit. It appears that the best alignment of these two functions would occur somewhere between the quadratic and linear fits.

Visual inspection reveals good agreement in the air/air and air/contra curve for subject 1

(A) and fairly good agreement for subject 3 (C). There is more of a discrepancy between the two curves for subject 2 (B). Matching the two functions for subject 2 (B) is difficult since the contralateral placement condition yielded measurable DPOAE at only two L2 values (60 and 65 nominal dB SPL). Subject 2’s dpoae levels did not reach those observed in the air condition.

The forehead placement (Figure 28) was the most difficult condition to obtain robust DPOAE, especially in Subject 2 where only one L2 level (75 dB SPL) yielded a measurable DPOAE. The 3 subjects “correction factors” spanned 20 to 28 dB at the forehead placement. For subject 1 (A), the air/forehead curve was shifted 21 dB. For subject 2 (B), the air/forehead data point was shifted 20 dB using a subjective “best fit”.

For Subject 3 (C), the air/forehead curve was shifted 28 dB. Visual inspection reveals fairly good agreement in the air/air and air/forehead curves for subjects 1 and 3 (A and

C). Little can be said about the “match” for subject 2, since an input/output function was unable to be obtained.

2000 Hz P2=Ipsilateral P2=Contralateral P2=Forehead

Subject 1 3Q 15 21

11L

Subject 2 10S 10S 20S

Subject 3 7 21Q 28

33L

Average Shift for 3 8 17.33 23 Subjects Subscripts: Q=quadratic fit, L=linear fit, S=subjective “best fit”. When no subscript is listed, quadratic fits were performed.

Table 4. Values of the “shifts” in dB SPL used at Fc=2000 Hz to match the P2=bone conduction to P2=air conduction input/output functions. **If more than one type of curve shift was used (i.e.: linear and quadratic, Subject 1 and Subject 3) both values were averaged for that subject and this average was used in the overall average for the three subjects.**

Table 4 (Fc=2000 Hz) shows correction factors or shifts for the different P2 placements. In most cases, these numbers were determined by using quadratic or linear fits. For one subject (Subject 2) subjective “best fit” alignments were made due to insufficient data points. Not enough L2 values yielded measurable DPOAE so that curve fittings could be applied. Due to small sample size, statistical analysis of the data was not performed. The ipsilateral (within 8 dB) and forehead (within 7 dB) placements, have similar shifts. However, the contralateral placement showed greater variability with a span of 23 dB among the 3 subjects.

Considering individual subject data, Table 2 illustrates that Subject 1 had shifts

which increased as P2 placement was moved from ipsilateral to contralateral to forehead locations. Similar results can be seen for Subject 3. Subject 2 had the same shifts for the ipsilateral and contralateral placements and a 10 dB difference in the forehead placement.

The average shifts in dB SPL among the 3 subjects show a difference in ipsilateral vs.

contralateral placement of approximately 9 dB and 15 dB vs. forehead placement. More

of a difference is noted between ipsilateral and contralateral placements when compared

to data for 1000 Hz. However, ipsilateral vs. forehead conditions are very similar for the

two frequencies. In addition, differences in contralateral and forehead correction factors

are similar when Fc=2000 Hz (~6 dB) compared to Fc=1000 Hz (~8 dB).

4.5 Comparison of Behavioral Thresholds and DPOAE Data

For this study, the experimenter assumed that DPOAE differences or “shifts” in

DPOAE input/output functions at different P2 locations would be similar to shifts in behavioral thresholds recorded with the transducer at the same P2 locations. Reported differences in air conduction and ipsilateral and contralateral bone conduction thresholds

are negligible and up to 10 dB of difference can be expected with forehead placement.

(Nilo, 1965; Martin, 1997) In Figure 29, differences in air conduction and bone

conduction behavioral thresholds at the three locations are compared to the observed

shifts in DPOAE input/output functions for the three subjects. Differences in behavioral

bone conduction threshold (in dB SPL) at the three placements (ipsilateral mastoid,

contralateral mastoid and forehead) from behavioral air conduction threshold are on the

abscissa. Shifts (in dB SPL) used to align the input/output functions when P2 is via bone

conduction at the three placements are on the ordinate. Ipsilateral placement is indicated

with diamond symbols, contralateral with triangle symbols and forehead with square

symbols.

Subject 1 data are in black, Subject 2 in blue and Subject 3 in red. The top panel

(A) is data for 1000 Hz, (B) for 2000 Hz. DPOAE shifts at the varying P2 locations are not comparable with behavioral thresholds. No relationship is found among the data points at either frequency.

40 A

OAE input/output curve shifts (dB SPL) -10

-10 0 10 20 30 40 Behavioral threshold differences (dB SPL)

Figure 29. Scatter plots of behavioral threshold differences and differences in OAE input/output functions in dB SPL. A. Fc=1000 Hz. B. Fc=2000 Hz. Diamonds=ipsi placement, triangles=contra, squares=forehead. Black symbols=Subject 1, Blue=Subject 2, Red=Subject 3. The dashed line represents where data points would be if behavioral threshold differences were equal to differences in OAE input/output functions.

(Continued)

Figure 29: Continued

30 B

0 OAE input/output curve shifts (dB SPL) (dB shifts curve input/output OAE

-10 -10 0 10 20 30 Behavioral threshold differences (dB SPL)

4.6 Contralateral Masking

The following data (Figures 30-37) illustrate effects of a wide band (0-20 kHz)

Gaussian noise masker. The masker was introduced into the contralateral or non-test ear via an ER 10A insert earphone. Colors and symbols are consistent with the previous graphs (Figures 16-28), with one exception. Open symbols are now present in all plots indicating when non-test ear masking is employed. Masking was initially introduced to simulate behavioral threshold test conditions. It was known that suppression of the

DPOAE was possible. The effect on the emission level was uncertain, since most

DPOAE suppression studies have focused on producing the maximum amount of

suppression by varying the level of the suppressor, rather than L2 (Brown & Kemp, 1984;

Harris et al., 1992; Kummer et al., 1995, Abdala et al., 2001). Additionally, a greater

number of suppression studies have used tonal suppressors of varying frequency rather

than noise suppressors. Input/output functions were constructed as previously described

with constant level masking (40 dB SPL) in the non-test ear. Masker level was increased

to 46 dB SPL in one condition for one subject to see if a greater masking effect was

noted. The effect of this masking on the level of the observed DPOAE varied with

varying L2 values. This was not surprising since previous research with wide band noise

suppressors found that varying the primary levels affected the suppressor level required

to produce DPOAE suppression (Puel & Rebillard, 1990; Kujawa et al., 1993).

In suppression studies, a criterion of DPOAE difference is chosen to represent a

“suppression effect”. This indicates that the DPOAE level is reduced due to the suppressor and not simply due to normal test/retest variability. This criterion is not consistent across studies and ranges from 1 to 10 dB SPL (Brown & Kemp, 1984; Puel &

Ribillard, 1990; Kujawa et al., 1993; Abdala et al., 1996).

DPOAE levels are stable in individual subjects upon test/retest (Beattie et al.,

2003). It is expected that measured DPOAE levels at the frequencies used in the current

study, will only vary 1-3 dB when test/retest occurs on the same day. When there is more

time between test sessions, 5-10 days, DPOAE levels are expected to be within 5 dB.

Using bone conduction for DPOAE stimulation potentially adds to the test/retest

variability, although no study has confirmed this. The experimenter is unable to precisely

control the force of the vibrator against the head. Additionally, although great care was taken to place the bone vibrator in the same location for different conditions, each placement of the transducer is necessarily unique. Because of this potential for greater variability, a 6 dB suppression criteria was set for this study.

Most suppression studies focus on finding the suppressor which maximally reduces the DPOAE level (Brown & Kemp, 1984; Harris et al., 1992; Kummer et al.,

1995, Abdala et al., 2001). The current experiment is not a “suppression study” therefore, the contralateral masker employed, was not designed nor manipulated to produce maximum DPOAE level changes. It was not expected that large levels of suppression would be observed. In suppression studies which used wide band noise (Puel

& Ribillard, 1990; Kujawa et al., 1993) levels of DPOAE suppression were between 1-3 dB.

20 A

WITHOUT contralateral masking WITH contralateral masking -5

-10 30 35 40 45 50 55 60 65 70

20 B 15

SPL) 10

(dB

5 level

0 dpoae -5 WITHOUT contralateral masking WITH contralateral masking

-10 30 40 50 60 70 80

25 C 20

WITHOUT contralateral masking -5 WITH contralateral masking

-10 30 40 50 60 70 80 L2 (nominal dB SPL)

Figure 30. Contralateral masker effects when P2 was delivered via air, Fc=1000 Hz. A. Subject 1. B. Subject 2. C. Subject 3.

20 A

WITHOUT contralateral masking -5 WITH contralateral masking

-10 40 45 50 55 60 65 70

20 B 15

SPL) 10

(dB

5 el v le

dpoae WITHOUT contralateral masking -5 WITH contralateral masking

-10 30 40 50 60 70 80

20 C 15

WITHOUT contralateral masking -5 WITH contralateral masking

-10 30 40 50 60 70 80 L2 (nominal dB SPL)

Figure 31. Contralateral masker effects when P2 is at the ipsilateral placement, Fc=1000 Hz. A. Subject 1. B. Subject 2. C. Subject 3.

20 A 15

0 WITHOUT contralateral masking WITH contralateral masking -5

-10 35 40 45 50 55 60 65 70 75

20 B

SPL) 10

(dB

5 el v le

dpoae WITHOUT contralateral masking -5 WITH contralateral masking

-10 40 45 50 55 60 65 70 75 80

20 C

-5 WITHOUT contralateral masking WITH contralateral masking

-10 40 45 50 55 60 65 70 75 L2 (nominal dB SPL)

Figure 32. Contralateral masker effects when P2 is at the/contralateral placement, Fc=1000 Hz. A. Subject 1. B. Subject 2. C. Subject 3.

20 A

WITHOUT contralateral masking -10 WITH contralateral masking

40 45 50 55 60 65 70 75

20 B

dpoae level (dB SPL) WITHOUT contralateral masking -10 WITH contralateral masking

50 55 60 65 70 75 80

20 C

WITHOUT contralateral masking -10 WITH contralateral masking

50 55 60 65 70 75 80 L2 (nominal dB SPL)

Figure 33. Contralateral masker effects when P2 is at the forehead placement, Fc=1000 Hz. A. Subject 1. B. Subject 2. C. Subject 3.

4.7 Effects of Contralateral Masking at 1000 Hz

Figure 30 shows contralateral masking effects for the three subjects when P2 is

introduced via air conduction. The Fc is equal to 1000 Hz. Again, in Figures 30-37,

closed symbols indicate no contralateral masking was used, open symbols indicate that

40 dB SPL of wide band Gaussian noise was presented to the non-test ear via an ER-10A insert earphone. Subject 1 (A) showed DPOAE level differences at some L2 values.

However, only at the lowest L2 tested, L2=35 dB SPL, was the criteria for suppression

met. At L2=35 dB, 11.3 dB of suppression was observed. Subject 2 (B) exhibited 7 dB

of suppression when L2=60 dB. Suppression was not evident at other L2 conditions.

Subject 3 (C) had consistent levels (2-4 dB) of DPOAE intensity changes across L2

values, however, these changes are attributed to test/retest variability.

Figure 31 shows contralateral masking effects for the three subjects when P2 is

introduced via bone conduction at the ipsilateral placement. The Fc is equal to 1000 Hz.

Subject 1 (A) had no changes in DPOAE level which met suppression criteria. Subject 2

(B) exhibited the greatest difference in DPOAE level at the highest L2 tested in this

condition, L2=70 dB SPL, at which level the DPOAE suppression effect was 5.8 dB. No

other suppression effects were observed. No measurable DPOAE could be recorded at

L2 conditions below 50 dB (nominal) SPL. Subject 3 (C) did not exhibit DPOAE level

changes which met suppression criteria.

Figure 32 shows contralateral masking effects for the three subjects when P2 is

introduced via bone conduction at the contralateral placement. The Fc is equal to 1000

Hz. No DPOAE level differences met suppression criteria for Subject 1 (A). Subject 2

(B) exhibited DPOAE suppression at the highest L2 tested in this condition, L2=75, at

which level the DPOAE suppression effect was 5.7 dB. Subject 3 (C) had a suppression

effect at L2=55 dB SPL, where the DPOAE was reduced 6 dB re: the same P2 placement

without masking.

Figure 33 shows masking effects for the three subjects when P2 is introduced via

bone conduction at the forehead placement. The Fc is equal to 1000 Hz. Suppression effects were observed in Subject 1 (A) at L2=55 dB (10.4 dB DPOAE level difference) and at L2=50 where the DPOAE was suppressed by 9.3 dB. No suppression effects were noted for Subject 2 (B). Subject 3 (C) had 7 dB of DPOAE suppression at 75 dB. No

suppression was noted at other L2 values for Subject 3.

A 20

WITHOUT contralateral masking -10 WITH contralateral masking

30 35 40 45 50 55 60 65 70

20 B

-10 dpoae level (dB SPL) dpoae WITHOUT contralateral masking WITH contralateral masking

-20 35 40 45 50 55 60 65 70

25 C 20

0 WITHOUT contralateral masking -5 WITH contralateral masking WITH a greater amount of contralateral masking

-10

20 30 40 50 60 70 80 L2 (nominal dB SPL)

Figure 34. Contralateral masker effects when P2 is delivered via air conduction, Fc=2000 Hz. A. Subject 1. B. Subject 2. C. Subject 3.

A 20

WITHOUT contralateral masking WITH contralateral masking -10

35 40 45 50 55 60 65 70 75

B 20

dpoae level (dB SPL) WITHOUT contralateral masking WITH contralateral masking

-10

58 60 62 64 66 68 70 72 74 76

25 C 20

WITHOUT contralateral masking -5 WITH contralateral masking

-10

20 30 40 50 60 70 80 L2 (nominal dB SPL)

Figure 35. Contralateral masker effects when P2 is at the ipsilateral placement, Fc=2000 Hz. A. Subject 1. B. Subject 2. C. Subject 3.

20 A

-10 WITHOUT contralateral masking WITH contralateral masking

45 50 55 60 65 70 75 80

20 B

-10 dpoae level (dB SPL) (dB level dpoae WITHOUT contralateral masking WITH contralateral masking

-20 64 66 68 70 72 74 76

20 C

-10 WITHOUT contralateral masking WITH contralateral masking

20 30 40 50 60 70 80 L2 (nominal dB SPL)

Figure 36. Contralateral masker effects when P2 is at the/contralateral placement, Fc=2000 Hz. A. Subject 1. B. Subject 2. C. Subject 3.

A 20

WITHOUT contralateral masking WITH contralateral masking -10 45 50 55 60 65 70 75 80

B 20

0 WITHOUT contralateral masking dpoae level (dB SPL) WITH contralateral masking

-10 40 50 60 70 80

C 20

WITHOUT contralateral masking -5 WITH contralateral masking

-10 30 40 50 60 70 80 L2 (nominal dB SPL)

Figure 37. Contralateral masker effects when P2 is at the forehead placement, Fc=2000 Hz. A. Subject 1. B. Subject 2. C. Subject 3.

4.8 Effects of Contralateral Masking at 2000 Hz

Figure 34 shows contralateral masking effects for the three subjects when P2 is

introduced via air conduction. The Fc is equal to 2000 Hz. Again, in Figures 30-37,

closed symbols indicate no contralateral masking was used, open symbols indicate that

40 dB SPL of wide band Gaussian noise was presented to the non-test ear via an ER 10A insert earphone. Across the input/output function, Subject 1 (A) shows definite suppression effects. DPOAE suppression occurs at the “tails” of the function where L2 is

at the highest and lowest levels. The DPOAE is suppressed approximately 7 dB at L2

levels of 35, 40, 45, 65 and 70 dB SPL. Subject 2 shows suppression at one level (65 dB)

on the input/output function. The DPOAE was suppressed 9.5 dB. No suppression was observed for Subject 3 (C). In addition to open symbols, Figure 34 has a curve with circle symbols with ‘+’ signs. This curve indicates that the suppressor tone in the non-

test ear was increased to 46 dB SPL (from 40 dB). However, no further suppression of

the DPOAE was noted, therefore, for the remainder of the conditions, 40 dB SPL of noise

was used.

Figure 35 shows masking effects for the three subjects when P2 is at the

ipsilateral placement at 2000 Hz. For Subject 1 (A) an 8.7 dB suppression effect was

noted when L2 was highest (70 dB). Subject 2 (B) also exhibited DPOAE suppression at

the highest L2 tested in this condition, L2=75 dB SPL, at which level the DPOAE

suppression effect was 8.9 dB. At L2=70 dB, 5.5 dB of suppression was noted. No

measurable DPOAE could be recorded at L2 conditions below 70 dB (nominal) SPL.

Subject 3 (C) had no suppression of the DPOAE.

Figure 36 shows contralateral masking effects for the three subjects when P2 is at

the contralateral placement at 2000 Hz. Subject 1 (A) had levels DPOAE suppression

effects ranging from 6.5 to 9.9 dB at L2 values of 55-75 dB. No measurable DPOAE

could be recorded at L2 conditions below 55 dB (nominal) SPL. Subject 2 (B) did not

exhibit suppression of the DPOAE at either of the two L2 values where DPOAE could be

measured. Subject 3 (C) did not exhibit suppression effects.

Figure 37 shows contralateral masking effects for the three subjects when P2 is

introduced via bone conduction at the forehead placement. The Fc is equal to 2000 Hz.

Subject 1 (A) had levels DPOAE suppression effects between 6-7 dB when high L2

values (65-75 dB SPL) were used. No suppression effects were noted at other L2 values.

Only one L2 (75 dB) produced a measurable DPOAE for Subject 2 (B) in this condition.

Suppression of this DPOAE was not observed when contralateral masking was

introduced. Subject 3 (C) exhibited no DPOAE suppression.

This experiment was not designed to be a DPOAE suppression study. As

expected, only islands of suppression were observed in the data. Based on previous data,

(Brown & Kemp, 1984) it is expected that when the masker is within 5 dB of L2 in the cochlea and near F2 in frequency, the maximum amount of suppression will be observed.

A more effective suppressor which varied in frequency and in level would likely have

produced greater effects.

4.9 Summary of Results

Results of the current study reveal no obvious relationship between behavioral threshold differences and differences in air and bone conducted I/O functions for the three subjects in this experiment. This is surprising since the cochlear response to air and bone conduction is thought to be comparable (von Bekesy, 1955; Lowy, 1942; Tonndorf,

1966, Zwislocki, 1953). This also was an unexpected result when considering subjective phase cancellation data (Purcell et al., 1999) which supported the values obtained from objective I/O function shifts. In addition, no great suppression effects were noted across subjects for either frequency. This is likely due to the shape and intensity of the contralateral masker employed.

CHAPTER 5

SUMMARY AND CONCLUSIONS

5.1 Behavioral Threshold Data

Large differences were not observed in average behavioral thresholds for the three subjects at the different transducer locations at either frequency. Air and bone

conduction thresholds, in the absence of a hearing disorder, should be equal (Hood,

1979). Average data in the current study do not show large differences in air and bone

conduction thresholds. For the forehead location, a 10 dB increase in bone conduction

thresholds was expected (Nilo, 1965; Martin, 1997). Participants did not exhibit a 10 dB

difference in behavioral thresholds when the bone conduction transducer was moved to

the forehead location at 2000 Hz. Although thresholds were elevated at this location, the

average magnitude of the difference from ipsilateral and contralateral placements was on

the order of 2 dB. For 1000 Hz, the average difference was approximately 7 dB, which is

more consistent with the difference expected when the transducer is moved to the

forehead location.

5.2 Effect of P2 Location

The average amount of “shift” needed to match air input/output (I/O) functions with bone I/O functions was similar at the three placements for the three subjects.

Average shifts for ipsilateral placement were 8.67 dB at 1000 Hz and 8 dB at 2000 Hz. A

greater shift was necessary to match the contralateral I/O functions with the air

conduction I/O functions. The average shift at 1000 Hz was 14.17 dB and 17.33 dB for

2000 Hz. Forehead placement required the greatest amount of shift for all three subjects.

The average shift was 22.33 dB at 1000 Hz and 23 dB for 2000 Hz.

No consistent differences in effect of P2 location were noted between 1000 and

2000 Hz. Comparison of 1000 and 2000 Hz reveals the largest difference in the average

shifts was 3 dB for the contralateral placement. The average ipsilateral and forehead

placement shifts were within 1 dB. Although shifts between frequencies were greater as

placement was moved from ipsilateral to contralateral to forehead positions, the average

magnitude of the difference between ipsilateral and contralateral placements was on the

order of 1 dB at 1000 Hz and 2 dB at 2000 Hz. Average magnitude of the difference of

the two frequencies between contralateral and forehead placements was 6.67 dB at 1000

Hz and 0.3 dB at 2000 Hz.

Air and bone conducted I/O functions have been matched in the current study and in previous studies (Purcell et al., 1999, 2003). This matching is done with the assumption that equal magnitudes of DPOAE are elicited by equivalent stimulation in the cochlea. This is not an unreasonable premise since previous experiments have shown that the cochlea responds to air and bone conducted sound in the same manner (Lowy

1942, von Bekesy, 1955). The basilar membrane traveling wave is not affected by the mode of stimulation (Zwislocki, 1953). With this in mind, it could further be assumed that the shifts to “equalize” or match the air and bone conducted I/O functions would be predictable by measuring each subject’s behavioral threshold differences at the same

head locations. The air channel is predictable. If the only difference in air and bone

conduction stimulation is the level of the stimuli that actually reaches the cochlea, then

results of DPAOE shifts should be predictable with shifts in behavioral thresholds.

Surprisingly, this was not true for the participants in the current study. (See Tables 5 and

6). Based on the current data, the assumption that DPOAE stimulated via bone conduction can be correlated with DPOAE via air conduction, must be questioned.

1000 Hz Ipsilateral Contralateral Forehead

DPOAE I/O Shifts 8.67 13.75 22.33 to match bone I/O functions with air I/O functions Behavioral -2.67 -2 4.67 threshold differences from air conduction thresholds

Table 5. Average differences in DPOAE I/O functions and in Behavioral threshold data for 1000 Hz.

2000 Hz Ipsilateral Contralateral Forehead

DPOAE I/O Shifts 7.75 19.75 23 to match bone I/O functions with air I/O functions Behavioral 1.67 3.67 4 threshold differences from air conduction thresholds

Table 6. Average differences in DPOAE I/O functions and in Behavioral threshold data for 2000 Hz.

5.3 Effects of Contralateral Masking 87

The current study was not designed to study DPOAE suppression effects.

However, it is known that by adding a contralateral stimulus, suppression of the DPOAE may occur. Therefore, these effects were measured. Criterion for suppression was set as a 6 dB or greater decrease in the DPOAE magnitude. This limit was set somewhat arbitrarily, although based on previous research. Brown and Kemp (1984) recommended a 5 dB criterion for suppression studies. It is expected that measured DPOAE levels at the frequencies used in the current study, will only vary 1-3 dB when test/retest occurs on the same day. When there is more time between test sessions, 5-10 days, DPOAE levels are within 5 dB (Beattie et al., 2003). Using bone conduction for DPOAE stimulation potentially adds to the test/retest variability, although no study has confirmed this.

Because of this potential for greater variability, a 6 dB suppression criterion was set for this study.

In general, the masker was not an effective suppressor of the DPOAE. Isolated instances of suppression were noted for all subjects when Fc=1000 Hz. Subject 1 exhibited suppression at one L2 value in both the air conduction and forehead placement

conditions. Subject 2 displayed a suppression effect at one L2 value in the air conduction

condition. Subject 3 exhibited the criterion amount of suppression also at one L2 level in

the forehead condition.

Subject 1 exhibited greater suppression effects at 2000 Hz. This is not surprising

based on the type of contralateral masker used. The wide band noise masker could

produce a greater suppression effect at 2000 Hz since the bandwidth of the masker is

constant but the critical band at that frequency is greater than at 1000 Hz. Suppression

was noted at five L2 values in the air conduction condition, at one L2 value in the

ipsilateral condition and at two L2 values in both the contralateral and forehead

conditions. Subject 2 displayed a suppression effect at one L2 value in the air conduction

condition and at two L2 values in the ipsilateral condition. Subject 3 did not exhibit the criterion amount of suppression in any condition at 2000 Hz.

5.4 Sources of Variability

Bone conduction testing results in greater variability. Large inter- and intra-

subject variations in bone conduction are known to occur (Studebaker, 1962). Variability

is due mostly to the complexity of bone conduction hearing. Characteristics from the

geometry, configuration, dynamics and mechanical properties of the skin, tissues, and

skull are different for every human. Studies measuring resonant frequencies (Hakansson

et al., 1994) and mode shapes (Khalil et al., 1979) of the human skull found that each

skull is unique. There are also large variations in skin/skull mechanical impedance

(Flottorp and Solberg, 1976). Thickness of skin and subcutaneous tissue layers do not

have direct correlation with transmission of vibration from the surface of the head to the

skull (Mylanus et al., 1994).

Variability was certainly introduced by head size. Application force below 5.4N

with a standard bone conductor can cause increased variability (Dirks, 1994). Different

head sizes would create varying levels of force with the non-adjustable headband on the

clinical B-71 bone transducer used in the study.

Additionally, it was not possible to complete all conditions of this study in one

test session. The bone oscillator and headband became uncomfortable and subjects

needed to remove it after 1-1.5 hours of testing. Individual conditions were always

completed with one placement of the bone oscillator (i.e.: complete input/output

functions for each condition were obtained prior to moving the oscillator). Great care

was taken to replace the transducer in the same location as had been previously used,

however, each placement of the transducer would realistically be unique. Many studies

have recorded variability due to bone conduction transducer placement (Dirks, 1964;

Weston et al, 1967). Khanna et al. (1976) found that the sound pressure level measured

in the ear canal varied by as much as 25 dB when transducer placement position was

varied on the forehead. The sound pressure level of P2 was measured and recorded in

the Tucker-Davis program BioSig. These levels were monitored and recorded in an

effort to reduce (as much as possible) the variability introduced by placement and

replacement of the transducer. Figures 38 and 39 compare the level (L2) of P2 in the ear canal at the different P2 locations when Fc=1000 Hz and 2000 Hz, respectively.

70 A

40 Contra WITHOUT masking Contra WITH masking Forehead WITHOUT masking L2 in the ear canal (dB SPL) Forehead WITH masking 30 Ipsi WITHOUT masking Ipsi WITH masking

30 40 50 60 70 80

Nominal transducer level (dB SPL)

70 B

Contra WITHOUT masking Contra WITH masking 60 Forehead WITHOUT masking Forehead WITH masking Ipsi WITHOUT masking 50 Ipsi WITH masking

L2 in the ear canal (dB SPL) (dB canal ear the in L2 30

20 30 40 50 60 70 80 Nominal transducer level (dB SPL)

Figure 38. Comparison of L2 in the ear canal at the different P2 placements. Fc=1000 Hz. A. Subject 1. B. Subject 2. C. Subject 3. (Continued) 91

Figure 38: Continued

70 C Ipsi WITH masking Ipsi WITHOUT masking Contra WITHOUT masking 60 Contra WITH masking Forehead WITHOUT masking Forehead WITH masking 50

40 L2 in the ear canal (dB SPL) (dB canal ear the in L2

30 40 50 60 70 80 Nominal transducer level (dB SPL)

55 A 50

Ispi WITHOUT masking 30 Ipsi WITH masking Contra WITHOUT masking L2 in the ear canal (dB SPL) the ear canal (dB L2 in Contra WITH masking 25 Forehead WITHOUT masking Forehead WITH masking 20 45 50 55 60 65 70 75 80 Nominal transducer level (dB SPL)

70 B 60

Ipsi WITHOUT masking 20 Ipsi WITH masking

L2 in the ear canal (dB SPL) ear canal the L2 in Contra WITHOUT masking 10 Contra WITH masking Forehead WITHOUT masking Forehead WITH masking 0 30 40 50 60 70 80 Nominal transducer level (dB SPL)

Figure 39. Comparison of L2 in the ear canal at the different P2 placements and varying L2. Fc=2000 Hz. A. Subject 2. B. Subject 3. Data for Subject 1 were not recorded due to an experimenter error.

In Figures 38 and 39, the dB SPL going into the transducer is on the abscissa and

L2 (dB SPL) in the ear canal measured in BioSig is on the ordinate. Red diamond

symbols indicate ipsilateral placement of the bone conduction transducer. Green triangle

symbols represent contralateral placement and blue square symbols represent forehead

placement. Closed symbols for each condition indicate that no contralateral masking was

introduced, open symbols indicate masking was presented to the non-test ear. These symbols are consistent in both figures.

Linear fits were done with the curve fit function in Sigma Plot 2000 for Windows

(Version 6.0 from SPSS, Inc.). The linear fit function applied the equation, y=yo + ax, to fit the lines. The x-intercepts from all functions were compared to quantify the range of variability in L2 in the ear canal due to placement of the transducer. In Figure 38

(Fc=1000 Hz), plots for Subject 1 (A) indicate no greater than a 9 dB difference in sound

pressure level (SPL) measured in the ear canal across conditions. This implies that the

position of the bone transducer did not introduce a great deal of variability from condition

to condition. Considerably more variability is noted in Subject 2 (B). The greatest

difference in the linear functions, not including the ipsilateral condition without masking,

was 22 dB. This indicates that changes in DPOAE levels at the different P2 locations, were likely affected by the placement and replacement of the bone transducer. L2 in the ear canal for the ipsilateral condition without masking (red lines with closed diamond

symbols) was unlike the L2 values for the masked condition. It is possible that the

transducer shifted during testing due to subject movement / head turning.

Subject 3 (C) shows 16 dB of variability in the ear canal SPL across conditions. The

position of the bone transducer was fairly stable for this subject and did not introduce a

large amount of variability.

Figure 39 shows graphs for two of the three subjects when Fc=2000 Hz. L2 ear

canal SPL values were not recorded for Subject 1 due to an experimenter error. Subject 2

(A) shows 23 dB of variability in the ear canal SPL across conditions. Again, positioning

and repositioning of the bone transducer did create variability in the response. Linear fits

of the forehead conditions were not possible since only one data point was acquired for

these conditions. Subject 3 (B) shows 17 dB of variability in the ear canal SPL across

conditions. Comparisons of the x-intercepts with both ipsilateral conditions (6 dB) and both contralateral conditions (6 dB) show less variability. Only 1 dB of variability exists between the two forehead functions, consistent with previous studies which reported greater test/retest reliability with the forehead placement (Studebaker, 1962; Dirks,

1964).

It should be noted that simply changing the location of the transducer will likely affect the measurable SPL in the ear canal. Therefore, some differences in the levels measured may not be due to variability in the position of the transducer. However, this appears to be the main source of difference in the L2 values in Figure 32 (C). Overall, the L2 in the ear canal for the individual placements are fairly stable. Tracking the L2 in the ear canal was a way to have some handle on the variability during test conditions. If it was noted during testing that L2 in the ear canal was significantly different than what was expected, position of the transducer was changed and the condition repeated.

5.5 Conclusions

In conclusion, the present study demonstrates that DPOAE can be measured with

one primary via bone conduction at different locations on the head (ipsilateral mastoid,

contralateral mastoid and forehead). Behavioral bone conduction threshold data do not

predict the differences in DPOAE at the different locations. In this study, for these three

subjects, behavioral thresholds do not coincide with DPOAE differences with different

transducer placements. This is somewhat surprising and should be considered further,

especially since a subjective phase cancellation procedure did correlate with DPOAE data

in a previous study (Purcell, 1999).

5.6 Implications for Future Research

This study is limited in its ability to generalize information due to the small

subject size. More data is needed on a greater number of subjects. With more subjects,

individual differences in functions due to head size and force of the transducer against the

head will be minimized. Statistical analysis would be also possible with a greater number of subjects. Additionally, a procedure that would decrease the amount of time the subject has to wear the bone conduction transducer would be helpful. The headband of the

Radio-Ear B-71 grew quite uncomfortable and had to be removed in every test session for each subject. Less variability in the response could be achieved if the transducer was not

moved during the testing.

Suppression studies may be the next step in looking at bone conducted sounds in

the cochlea. A well designed DPOAE suppression study with one (or more) bone

conducted primaries may provide insight into cochlear frequency selectivity that has not

been revealed in the current study.

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