Clin Aud I Handout

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Card number_____ 1
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Syllabus for Clinical Audiology I, CD
5701
Instructor:
Martin 58

Robert de Jonge, Ph.D.,

Text:
Audiology: Diagnosis, RJ Roeser, M
Valente, and H Hosford-Dunn (eds).
Exams: There are three exams, all multiple
choice. The final is not comprehensive and will
also have a practical component based upon obtaining a valid masked audiogram (using a simulator).
Attendance: Class attendance policy is consistent with University policy. In addition, four absences are allowed for
whatever reason (approved or not, at your discretion). Beyond this the final grade is reduced by 1/4 of a letter grade for
each additional absence. The final grade will be increased by 1/4 for each of the allowed absences that is not used. Perfect
attendance improves performance by one full letter grade.

Exam 1: Masking (Section I)

Exam 2: SISI, ABLB, OAEs, Tone decay, Bksy (Section II)
Exam 3: Diagnostic uses of speech audiometry, introduction to ABR, and functional testing (Sections III-V)
Topics
In general it is assumed that you understand the basic evaluation. Also, It's helpful to learn about hearing disorders and
the "gold standard" for identifying acoustic nerve tumors (MRI and CT scans). As an introduction, read Chapters 11 (Pure
Tone Tests), 5 (Disorders of the Auditory System), and 6 (Radiographic Imaging in Otologic Disease).
I.
Clinical Masking. We will discuss the methods for obtaining a valid masked audiogram: normal procedures,
(valid) shortcuts, dilemmas, and masking for speech and other special procedures. Also, we will investigate the
theoretical basis of masking as it relates to the clinical setting.
Read Chapter 12 (Clinical Masking)
II.
Behavioral and physiologic site-of-lesion tests specifically related to cochlear pathology: loudness and the
difference limen for intensity (SISI, ABLB, MLB) and the direct evaluation of OHC functioning (OAEs). Behavioral tests
related to neural function, the phenomenon of adaptation: tone decay procedures and Bksy audiometry.
Read Chapters 1 (Diagnostic Procedures in the Profession of Audiology), 21 (Otoacoustic Emissions).
III.
Diagnostic uses of speech audiometry/central evaluation: the extrinsic redundancy of speech vs. intrinsic
redundancy of the auditory system.

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Read Chapters 13 (Speech Audiometry), 15 (Diagnosing Central Auditory Processing Disorders in Children), 16
(Diagnosing Central Auditory Processing Disorders in Adults)
IV.
Basics of the auditory brainstem response (ABR). The focus will be upon the use of the ABR in detecting
retrocochlear pathology. Also, some attention will be given to the ABR for threshold estimation.
Read Chapter 19 (The Auditory Brainstem Response)
V.

Pseudohypoacusis, the test procedures for evaluating non-organic hearing loss.

Read Chapter 14 (Audiologic Evaluation of Special Populations), the section on Pseudohypoacusis p. 329-333.

card fld "Introduction"

Introduction
The major focus of the class is on diagnostic audiometry
-identifying what is wrong with the system
-which facilitates appropriate management
Objectives
-understand the theory behind the procedures
-be able to implement, interpret procedures (protocols)
-feel free to practice on your own, use clinic materials
Background
Audiology began as a field with a focus on rehabilitation
-Carhart, WWII veterans
Advances in otology in the 1950s and 60s spurred interest in precise assessment of the auditory periphery
-tympanoplasty for reconstructing ears ravaged by inflammatory disease
-eliminating conductive component of otosclerosis via fenestration, stapedectomy
-early identification and surgical excision of acoustic neuromas
Distinguishing conductive from cochlear from retrocochlear was very important Different sites imply different
surgical procedures.
Importance of valid (masked) audiometric thresholds for establishing cochlear reserve was appreciated
The 1960s saw the development, or refinement of many behavioral, psychoacoustic tests for site of lesion
-ABLB, recruitment
-SISI, difference limen
-Bksy and tone decay, adaptation
-speech recognition testing
1970s was the era of impedance audiometry

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-objective technique for evaluating middle ear status, cochlear, retrocochlear status
-tympanogram
-acoustic reflex threshold, decay
1980s saw measurement of auditory evoked potentials (especially ABR) become clinically feasible
-ABR, the audiologic test of choice for detecting acoustic neuromas
-ABR for threshold determination in difficult to test
1990s will, perhaps, be the decade of otoacoustic emissions (OAEs)
-objective measure of OHC function
-audiometric screening (problems with OAE screen missing auditory neuropathy)
-site of lesion: While OAEs seem to be the ideal tool for identifying VIII N. tumors (i.e., SN hearing loss in the presence of
normal OAEs), OAEs are absent in many tumor patients.
-confounding effect of middle ear pathology
Some issues
A general trend toward replacing subjective procedures with objective
Sensitivity/specificity and (now) cost are key issues
The impact of high resolution imaging system (CT scans, MRI) on the need for audiologic procedures
-cost/benefit analysis provides rationale for using less sensitive tests (like ABR) especially considering that VIII N.
tumors grow slowly and are not a medical emergency
-what role exists for even less sensitive procedures (e.g. ABLB, SISI)?
-conventional MRI measures structure, not function, ABR abnormalities can be good corroborating evidence
-fMRI can measure function (oxygenated blood images differently from deoxygenated blood), but not very quickly

card fld "Cochlear Reserve"

Cochlear reserve is a euphemism for how well the hair cell/nerve fiber population is preserved. Good cochlear reserve
implies normal cochlear functioning.
Bone conduction has routinely been used to estimate cochlear reserve, but bone thresholds are "contaminated" by middle
ear effects as illustrated by Carhart's notch in stapedial fixation.
The SISI test and ABLB were developed, in part, as alternative methods for estimating cochlear reserve.

card fld "Sensitivity - Specificity"

Sensitivity The percentage of abnormals identified by the test as being abnormal

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SpecificityThe percentage of normals identified as being normal (or, non-abnormals identified by the test as not being
abnormal)
A perfect test has 100% sensitivity and 100% specificity
Generally, as sensitivity of a test increases, the specificity decreases (and vice-versa)

card fld "Other Assignments"

Masking
A major goal of the class is to make certain that you can obtain a valid masked audiogram. To facilitate this, two stacks
have been developed
-Masking Model
-Audiometric Simulator
Audiometric Simulator will help you practice masking techniques during the remaining 2/3 of the semester
A portion of the final exam will be a practical exam on masking
See the text Clinical Masking Procedures by WS Yacullo
-It contains the same information as lecture and readings, but expanded
-It contains many examples
Central auditory evaluation
Testing for CAPD is often difficult
Many different tests with involved protocols
Interpretation of the results is more ambiguous than other audiologic tests (like ABR, OAEs, ABLB, etc.)
Meaningful recommendations often involve a team approach (e.g., SLP, neuropsychologist, classroom teacher)
You should find the following text very useful:
Bellis, Teri James, Assessment and Management of Central Auditory Processing Disorders in the Educational Setting:
From Science to Practice, Singular Publishing Group, Inc., San Diego - London, 1996.
Otoacoustic Emissions
We have software which simulates OAE testing with the ILO88, and contains many examples of actual cases from the
Rhode Island project on infant hearing screening.
See the 486 computer in the ear impression lab. The software is in a program group accessible via Windows 3.1.

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Protocol for the ABLB
Purpose:
To determine how loudness in the variable ear
(ear with hearing loss) changes relative to the
reference ear (ear with normal hearing)
To place the ear with hearing loss into one of the
categories:
1. No recruitment (normals, conductives, ?
retro)
2. Complete recruitment (cochlear)
3. Partial recruitment (? cochlear)
4. Decruitment (strongly retrocochlear)
5. Hyper-recruitment (strongly cochlear)
Requirements:
one ear with normal hearing (< 25 dB HL)
other ear with hearing loss (> 25 dB HL)
more that a 20 dB separation between ears
2 channel audiometer (or, independent levels)

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Procedure:
1. select (any) frequency, instruct patient
2. alternate tone between ears, 3 times
present 20 dB SL tone to reference ear
present ? dB SL tone to variable ear
3. obtain patient judgement about variable ear
softer
equally loud
louder
4. repeat #2 to #3 until
you have covered range from softer to louder
obtain point of equal loudness
5. repeat #2 to #4 until
you have covered dynamic range
20, 40, 60, 80, perhaps 100 dB SL

Note:
You can shorten the ABLB significantly by defining the normal hearing ear as the variable ear, the "bad" ear as the
reference ear
How cochlear vs. conductive's losses respond to loudness on the ABLB is very similar to differences in performance on
the
ABR latency-intensity functions
Acoustic reflex sensation levels
Should you mask with the ABLB? Probably not:
the loudness of the tone that has crossed over is negligible when combined with the loudness of the tone in the
impaired ear
this small increase in loudness could not create a test result suggesting recruitment

Protocol for the MLB

exactly the same for the ABLB, but
tones are administered to the same ear
exchange reference tone for reference ear
exchange variable tone for variable ear
A major problem with the test
people have trouble ignoring pitch differences and attending to loudness

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Theories of Recruitment
Originally, Schuknect believed that two conditions are necessary for recruitment
1. Damage to the hair cell population
2. Relatively intact neural supply to cochlea
Tonndorf related recruitment to a loss of hair cell ciliary stiffness
Relevant considerations:
Loudness is encoded as the total number of neural impulses (spikes)
OHCs are primarily responsible for sensitivity in the 0 to 40 dB HL range (boosting the input to the IHC)
95% of the afferent supply innervates IHC population
So,
A 40 to 50 dB loss can still have near normal total number of neural impulses for more intense signals complete
recruitment (Killion's Type I hearing loss).
Losses > 40-50 dB cannot produce a normal number of neural impulses for more intense stimuli partial recruitment
(Killion's Type II hearing loss).

The End

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card fld "Instructions"

Tell me when you think the tone in your left
ear is
louder
softer
the same
as the tone in your right

card fld "Info"

Turn the audiometer on, select the
"Alternate" button, and simulate a loudness
balance
Where you depress the interruptor switch
has a lot to do with the result of the loudness
judgment

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Question:
How much insertion gain (for a hearing aid) would be required to normalize loudness for the impaired ear?

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card fld "Phon"

Psychoacoustics
The study of our internal representation of
external stimuli
Don't ask a guy who has been operating a
jack hammer for 15 years without HPDs
if he's exposed to loud noise.

Loudness (phons & sones)

Phon scale
Loudness level in phons (Lp) used for making relative loudness judgements
reference: A 1000 Hz tone at 40 dB SPL has a loudness level of 40 phons
-a 57 dB SPL 1000 Hz tone = 57 phons
-a 80 dB SPL 1000 Hz tone = 80 phons
Compare loudness of a car horn to the loudness of a 1000 Hz tone, say 82 phon
Compare loudness of a door bell to the loudness of a 1000 Hz tone, say 63 phon
Compare loudness of a door bell to the loudness of a car horn (19 phon difference)
Equal loudness contours
-The 80 phon contour, for example, shows all combinations of frequency/SPL judged to be equally loud
-Loudness contours are like isobar maps used in meteorology, or elevation contours around mountains
The 0 phon contour is usually described as the threshold sensitivity curve, assuming 0 dB SPL is threshold at 1000 Hz
but it isn't.

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The 4.2 phon contour is approximately the threshold senstivity curve (binaural) in the sound field (MAF). The
equivalent contour under headphone is the MAP curve. The MAP curve defines normal hearing and is used to calibrate
audiometers.
One goal of a successful hearing aid fitting is to restore normal loudness perception for as large a frequency range as
possible.

card fld "Sone"

Sones
The sone scale is used for making absolute loudness judgements
The reference is a 1000 Hz tone, 40 dB SL re: threshold for a normal hearing person has a loudness of 1 sone
-SL is sensation level (the number of dB above threshold)
How does loudness change with SPL?
-For every 10 dB increase in SPL the loudness doubles (approximately)
___________________________________
Loudness phons Loudness in sones
Lp
Ls
___________________________________
20
0.25
30
0.5
40
1
50
2
60
4
70
8
80
16
90
32
100
64
Ls = 2^((Lp - 40)/10)
This is useful for performing a listening check of the calibration of an audiometer
Also notice how rapidly loudness is changing between 80 and 100 dB SPL (PEL = 90 dBA, AL = 85 dBA)
Recruitment
Recruitment is usually described as an abnormal rate of loudness growth that is associated with cochlear pathology (i.e.,
damage to the hair cells)

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For example, compare the results for a normal hearing person, a 40 dB HL conductive hearing loss, and a 40 dB HL
cochlear hearing loss. Each person judges the tone to be equally loud
Normal
80 dB HL
Conductive 120 dB HL
Cochlear 80 dB HL
Ears with recruitment don't hear soft sounds very well, but hear more intense sounds normally
-This makes it difficult to fit hearing aids. Amplification that makes the soft sounds audible makes the more intense
sounds too loud.

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The SISI test developed from difference limen (Latin for threshold) testing: the minimal difference in stimulus magnitude
needed for the listener to perceive a difference between two stimuli. DLs were commonly measured for frequency and
intensity. The DL is probably a reflection of the fundamental process initially used for analyzing the speech signal.
Protocol for the SISI
Purpose:
To determine if the pure-tone DL for intensity is 1.0 dB at a 20 dB SL (the modified SISI uses a different SL)
About the increments
-the increments have a 50 msec rise-decay
time, 200 msec at plateau
-they occur at 5 second intervals
-they are presented at a 20 dB SL re: threshold
To place the ear with hearing loss into one of the categories:
1. Negative SISI (normals, conductives, retro)
0 - 20%
2. Questionable SISI (?)
25 - 65%
3. Positive SISI (cochlear)
70 - 100%
Requirements:
can be used with bilateral hearing loss
can test any frequency
audiometer with SISI mode

Procedure:
1. select (any) frequency, instruct patient
caution them that the "jumps" will be small
listen carefully
2. Training phase
present carrier tone @ 20 dB SL
present 5 dB increment to elicit response
present 4, 3, 2 dB increments
3. Actual test
present 20, 1 dB increments
(10 increments can be used if the patient
exhibits all-or-none behavior)
4. Check response behavior
if first 5 identified, present an empty trial

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if first 5 missed, present a larger increment

to elicit response
5. Score test
5% for each increment identified correctly
1. Negative SISI (normals, conductives, retro)
0 to 20%
2. Questionable SISI (?)
25 to 65%
3. Positive SISI (cochlear)
70 to 100%
Note:
the probability of obtaining a positive SISI is related to the amount of hearing loss
positive SISI scores are more often found for higher frequencies

Modified SISI
Generally, everything is the same except for the
20 dB SL
the carrier tone is increased to a dB HL (usually around 75 dB HL) high enough to elicit a positive SISI
negative SISI responses suggest retrocochlear pathology, especially if
-hearing in the suspect ear is fairly good
-the other ear has a positive SISI (i.e., there is ear asymmetry)

Do the SISI and the ABLB measure the same thing?

Owens (1965) found that of 72 ears with recruitment, 70 (97%) had positive SISI
Martin (1970) used a group of unilaterals to perform the SISI at 4000 Hz under 2 conditions:
1. 20 dB SL in good ear & equal loudness in poorer ear (a lower overall loudness level)
2. 20 dB SL in poorer ear & equal loudness in better ear (a higher overall loudness level)
-SISI scores were not the same in each condition, despite the fact that loudness level was the same
-He concluded that ABLB & SISI probably measure different aspects of cochlear physiology
-the tests are not duplicative
Does tone decay invalidate the SISI?
when the carrier tone fades away, the increment appears to "pop out of nowhere"

The End

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card fld "card field id 9"

from Pratt & Egan (1968): Otosclerosis
Group A: post-op air was better than pre-op
bone, "over-closure" of the ABG (60 patients)
Group B: post-op air equal to or poorer than
pre-op bone (6 patients)
Group C: post-op air equal to or poorer than
pre-op bone (9 patients)

card fld "Point"

The main point:
A +SISI (other tests, too) is an indication of cochlear pathology.

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An ear with cochlear pathology may be more "fragile" and not able to withstand the trauma of surgery the result
being additional damage which may manifest as poorer post-op word recognition.
Consider options before operating on an ear with
evidence of cochlear pathology.

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Otoacoustic emissions
OAEs are sound, measured with a sensitive
microphone sealed in the ear canal
measurement assembly is much like an
impedance probe assembly
the spectrum of the OAE gives information
about hearing
OAEs can occur spontaneously (SOAEs) or they can be evoked by different stimuli
by a single, long duration frequency (SFOAE)
by a brief tone, a tone burst (TBOAE)
by a transient, a click (TEOAE or CEOAE)
by the distortion product associated with two long duration frequencies (DPOAE)
-f1 and f2, f2 > f1
-f2 is usually 1.25*f1
-the SPL of the distortion product is measured, the frequency of the DP is 2*f1 - f2, the cubic distortion product
-the origin of the OAE is associated with the geometric mean of f1 and f2

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Site of origin is within the cochlea, the OHCs. As the OHCs change in length: mechanical energy is imparted to: the
basilar membrane, the fluid within the cochlea, to the footplate of the stapes, through the middle ear, to the eardrum
which radiates acoustic energy into the ear canal.
the OHC response is preneural, no latency, present if the VIII is severed
the strength of each OHC response is proportional to the stimulus strength
the OHC response is nonlinear, it is a distortion product. In a linear system, if two frequencies (or more) enter the
system, the same two frequencies (or more) exit the system. In a nonlinear system, additional frequencies are present in
the output.
the acoustic spectrum of the OAE corresponds to the place and strength of the OHC response. For example
-if energy is present at 1000 Hz in the OAE, it originated from OHCs at the "1000 Hz" place on the basilar membrane
-a larger SPL at 1000 Hz in the OAE is associated with a more vigorous OHC response at the "1000 Hz" place
-the strength of the OHC response is directly related to the intensity of the stimulus, and to the number of functioning
OHCs
-the number of functioning OHCs is directly related to the audiogram threshold in the range from 0 to 40-50 dB HL
- see DPOAE Scatterplots.JPG
A complete absence of OHCs results in a hearing loss of approximately 50 dB, and results in an absent OAE
lesser amounts of hearing loss (thinning of the OHC population) result in a lower SPL for the OAE
So, by reducing stimulus intensity, and observing the diminution of the response, you should be able to predict
threshold. But,
predicting audiogram threshold from the OAE is, however, difficult and often unsuccessful due to variability in
-transmission loss through the middle ear
-variation in ear canal size
-noise in the measurement
-perhaps surviving OHCs with absent IHCs
-see OAE 25% - 75% Dist 1.JPG and
OAE 25% - 75% Dist 2.JPG
-see Interpreting OAE SN.JPG

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Neonatal ears produce OAEs with a much higher SPL than children, and especially adults probably because neonates
have smaller ear canals.
Conductive hearing loss can obliterate OAEs. The stimulus is attenuated by the ABG, the response is attenuated by the
ABG
OAEs can be used to document normal cochlear functioning in cases where the hearing loss is produced by retrocochlear
damage (as in auditory neuropathy, brainstem pathology)
no point in using a hearing aid
OAEs are sometimes present, sometimes not in ears with acoustic nerve tumors. Robinette (1992) found: Of 61 acoustic
neuromas
TEOAEs were present in 31 (51%)
only 12 (20%) had OAEs despite mild to moderate hearing loss (i.e., a good part of the hearing loss should have been
neural, not cochlear)
OAEs were only 20% sensitive to VIII N. lesions
acoustic neuromas affect cochlear function
The presence of OAEs indicates no more than a slight cochlear loss (provided the stimulus level is chosen appropriately,
not too high)
assuming the rest of the auditory system is normal (not a correct assumption with auditory neuropathy)
The absence of OAEs indicates more than a mild cochlear hearing loss
but does not tell you the magnitude of the hearing loss (identify magnitude of loss with ABR)
providing there is no conductive lesion
OAEs are effective in detecting higher frequency cochlear hearing loss, but usually not effective in detecting low
frequency cochlear hearing loss
noise is a major problem below 1000 Hz
stimulus energy is often low below 1000 Hz
with transients, energy may be low for high frequencies, > 4 kHz
OAEs can be useful for identifying pseudohypacusics
OAE can be useful for evaluating special cases, for example:
a perilymphatic fistula was suspected in a case of sudden, profound unilateral hearing loss
presence of OAEs did not support a peripheral site of lesion
final diagnosis was multiple sclerosis

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TEOAEs show great promise for the screening of neonates (day 1 or day 2) before hospital discharge
presence of OAEs to 80 - 85 dB clicks indicates hearing levels 30 dB HL or better
TEOAEs and DPOAEs are believed to derive from the same cochlear mechanism
the two procedures are generally equivalent in providing information about hearing loss
Gorga et al. (1993) found CEOAEs better at 1000, 2000 Hz. DPOAEs better at 4000 Hz.
-they found a poor correlation between OAE SPL and audiogram threshold
-presence of noise obscures the relationship
which procedure is better depends upon the signal-to-noise ratio of the OAE
both procedures ineffective at 500 Hz due to noise contamination.
Stover and Norton (1993) found that aging had little effect on the OAE, providing effects of hearing loss were removed
Equipment:
ILO88, ILO92, ILO288 (Institute of Laryngology and Otology, David Kemp's research)
Virtual (out of business)
CUBDIS (Etymotic Research)
Biologic Scout/AudX
Grason Stadler GSI-60

From Robinette (1992)

ILO88 TEOAEs
Results for 105 men, 160 women, 20 to 80 years of age (mean 42 years), normal hearing (T < 25 dB HL, 0.5 to 6 kHz)
80 sec pulses, 50/sec, 80 dB pe SPL
nonlinear clicks presented in blocks of 4: 3 condensation, 1 rarefaction, 3x larger
-summed ear canal response is 0 for each block
-nonlinear response remains (OAE)
2 stimulus sets of 1040 pulses (260 blocks) each are averaged (A and B buffers)
Mean SD Range
Stimulus peak
SPL
81.0 dB 2.7 75.0- 93.0
TEOAE SPL
8.6 dB 4.3 0.1- 22.3
Reproducibility 84.5% 13.4 31.0- 99.0
Canal noise
32.4 dB 1.6 28.8- 40.3
Test time
63.0 sec 2.0 59.0-197.0

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card fld "Missouri Legislation"

PERFECTED
HB 401 -- SCREENING FOR HEARING LOSS IN NEWBORNS (Barry)
Effective January 1, 2002, this bill establishes a screening
program for hearing loss in newborn children and children less
than 3 months old who are born in Missouri.
Authorized facilities, physicians, and other persons providing
pediatric care to newborns are required to provide parents or
guardians of newborns with information from the Department of
Health about screening for hearing loss and implications for
treatment or non-treatment before the examination is conducted.
The bill also specifies the type of hearing technology to be
used; the facilities, physicians, and other persons who are
required to ensure that the screening test was completed and
reported to parents and the department; and regulations
regarding the exemption of newborns.
If the newborn fails the screening test, authorized facilities,
physicians, and other persons are required to provide
educational information to parents or guardians promoting
further diagnostic assessments and the identification of
community resources. Authorized facilities, physicians, and
other persons who voluntarily provided screening examinations to
newborns prior to January 1, 2002, are required to report the
results to the department.
The Department of Health is required to provide administrative
and technical assistance to facilities implementing the
screening program. The department is also required to establish
and maintain a newborn hearing screening surveillance and
monitoring system for newborns reported with a hearing loss and
to establish follow-up, referral, and reporting procedures for
newborns reported with a possible hearing loss. The department
can disclose confidential information to authorized persons and
agencies for follow-up examinations without parental or guardian
consent.
The director of the Department of Elementary and Secondary
Education in conjunction with Part C of the Individuals with
Disabilities Education Act data system is required to monitor
and to annually report the results of early intervention
services to the Department of Health. The bill authorizes the

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establishment of a non-compensated, 12-member, Newborn Hearing

Screening Advisory Committee and specifies the composition of
the committee. The committee is to advise and assist the
Department of Health in the operation and evaluation of the
hearing screening program.
Various health insurance policies are required to provide
coverage for hearing screening examinations and additional
diagnostic examinations. Co-payments and deductible amounts are
required to remain similar to other health care services
contained in the policies. Newborns eligible for other medical
assistance or the children's health insurance program will also
be covered. Specific insurance policies are excluded from the
requirement to provide coverage for the hearing loss screening
tests as stated in the bill.
FISCAL NOTE: Estimated Net Cost to General Revenue of $164,144
to Unknown in FY 2000, $178,686 to Unknown in FY 2001, and
$359,576 in FY 2002. Estimated Net Income to Insurance
Dedicated Fund of $14,450 to $28,900 in FY 2000, $0 in FY 2001,
and $0 in FY 2002. Estimated Net Cost to Highway Funds of $0 in
FY 2000, $0 in FY 2001, and $41,177 in FY 2002.
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Tone Decay and Bksy Audiometry
Two procedures based upon adaptation
(abnormal tone decay)
TD is a reflection of the inability of the
cochlear nerve to maintain a constant firing
rate in response to a continuous, pure tone
General description of a tone decay procedure
(Carhart's, 1957 original procedure)
1. Instruct the patient to respond as long as the tone is heard
2. Present the tone (continuously on) below threshold, increase level in 5 dB steps until patient responds.
3. Begin timing. If tone is heard for full minute, discontinue test, and report 0 dB of tone decay.
4. If subject loses tone, record duration for which tone was heard, immediately increase level 5 dB, reset stopwatch to
zero, continue timing.

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5. The test is terminated when

the tone is heard for 1 full minute, or
30 dB SL re: Starting Level is reached
6. The amount of TD is the dB SL where the tone is heard for 1 full minute.
7. Excessive amounts of TD associated with VIII N. pathology

Characteristics of adaptation
Adaptation (tone decay) is similar to fatigue (noise-induced temporary threshold shift, TTS) in that the presence of the
stimulus causes poorer hearing. But the underlying processes are quite dissimilar.
adaptation occurs only for pure tones that are continuously on
adaptation does not occur for pulsed tones,
narrow-band noise, broad-band noise, speech
fatigue occurs for all types of signals

adaptation occurs very rapidly, within seconds; it must be measured while the tone is on
fatigue can be measured after the stimulus is off

adaptation can be very large (90 dB even) within a very short period (1 minute)
fatigue requires hours to produce fairly low levels (20 to 40 dB, typically)

adaptation recovers very rapidly, within 200 milliseconds, approximately (the off-time of the Bksy pulsed tone; no
adaptation occurs for the the pulsed tone)
fatigue can take up to 14 hours to recover

a stimulus producing adaptation does not cause damage, the tissue is not harmed
a stimulus producing fatigue can cause permanent damage

adaptation is a neural phenomenon, usually associated with compression, or stretching of the auditory nerve
fatigue is a sensory, end organ process, associated with TTS, or permanent NIHL

Clin Aud I Handout

The End

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card fld "card field id 2"
A Brief History of Tone Decay
1881, in March, Lord Rayleigh demonstrated
to Helmholtz how a high frequency 10 kHz
tone (gas bag driving a bird whistle) would
soon disappear. Waving your hand in front of
it would cause it to return!
1890 Corradi found this phenomenom
occurred for bone conduction
1893 Gradenigo, using a "telephonic audimeter," measured TD by gradually increasing dB level as perception faded. TD
was marked in cases of trauma, or compression (neuritis) of the VIII N.
1905 Shafer insisted that not everyone has decay. He could hear Rayleigh's bird whistle indefinitely.
1944 K. Shubert "rediscovered" TD, but was not optimistic about its clinical value
1957 Carhart develops his TD procedure. Still used essentially unchanged (when used) today.

The End

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card fld "card field id 2"
Various Tone Decay Procedures
Following Carhart's TDT there were many
modifications:
-Allow or disallow a rest period?
-Duration of tone/total test
-Check for audibility or tonality?
-Begin at threshold or higher dB SL?
-Measure the amount of time tone is audible at
each presentation level?
Hood (1956), similar to Carhart's (1957) procedure
if tone becomes inaudible, give a 60 sec rest period
continue increasing level until patient hears tone "indefinitely"
Rosenberg's (1958) modification (MTDT) of Carhart's procedure
entire test lasts 60 seconds, do not restart stopwatch

Clin Aud I Handout

Sorenson (1962)
patient must hear tone for 90 seconds
Green (1963) modification of Rosenberg's procedure, evaluates "tone perversion"
increase level to maintain constant tonality and audibility
instruct patient to put arm vertical (tonal), at 45 (perverted), down (inaudible)
Owens (1964) measured duration of decay
20 second rest period
terminated test after 20 dB SL reached
classified TD into Type I (normal & conductive), II (cochlear), and III (neural)
Type II: tone heard for longer durations at increased dB SL
Type III: tone heard for same, relatively short duration at increased dB SL
Palva, Karja, and Palva (1967) modification of Rosenberg's procedure
3 minute duration, sometimes longer
Sung, Goetzinger, and Knox (1969) KU TDT
modified Bksy procedure
subjects tracked tone for 2 minutes, maintaining constant loudness & tonality
Olsen & Noffsinger (1974) modification of Carhart's TDT
initial tone presented at 20 dB SL
found same results as with Carhart's TDT
Jerger & Jerger (1975) STAT procedure
a 110 dB SPL tone presented for 60 seconds
tone fading to inaudibility was STAT+

The End

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card fld "card field id 2"
Tone Decay: General Principles
TD is greater when
the presentation level of the tone is greater
the duration of the tone is greater
the frequency of the tone is higher
By manipulating variables to increase sensitivity
of the test (to find more VIII N. lesions), you reduce
the specificity (classify cochlears as VIII N. lesions).

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TD is basically a neural phenomenom, but mild to moderate amounts will occur for cochlears. But
cochlears hear the tone longer (than VIII N.) at greater dB SLs
False positives are more likely at higher audiometric frequencies
TD at 500 or 1000 Hz is more significant
TD can be reversible, when the lesion is healed.
TD is generally greater with larger tumors, but it is not the tumor size that is important. The important factor is how the
tumor is affecting (compressing or stretching) the nerve.
TD is greater with greater amounts of hearing loss. Controlling for hearing loss, tumor size does not affect the amount
of TD.
Other lesions (eg., vascular loops) can produce tone decay

The End

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card fld "card field id 2"
Bksy Audiometry
Began in 1947 with Bksy's description of a
new audiometer. Bksy is still popular in
industrial hearing testing
the audiometer was subject controlled
the signal could be fixed in frequency, or
slowly varying
the dB level continuously increased (2
dB/sec in 2 dB step sizes) until the subject pressed a button, then the level would decrease (as long as the button was
pressed)
a plotter tracked the subjects responses resulting in a saw tooth pattern
the midpoint of the tracings were equal to conventional audiogram threshold
normal tracking width is approximately 6 to 9 dB (ranging from 5 to 20 dB)
Bksy noted that tracking width was reduced (2 to 3 dB) in cases with recruitment

Clin Aud I Handout

he felt this reflected a reduced DLI, and could be useful as a site-of-lesion tool
Early research with Bksy (1947 - 1960)
1. Relationship between Bksy and conventional thresholds
found good correlation
2. Relating tracking width to presence of recruitment
found good trends in group data
too many confounding variables to make it clinically useful
-attenuation rate,
-subject reaction time, and
-recruitment/DLI
3. Do Bksy tracings reflect adaptation? That is, will tracings become poorer with time?
Conclusion yes, if the equipment would vary level in fine enough step size
Bksy's original equipment used a 2 dB step size
the Grason-Stadler E-800 used a 0.25 dB step size

Later research from 1960

Jerger in 1960 changed Bksy interpretation
Subjects traced thresholds for 2 tone types: continuous and interrupted
interrupted pulsed 2 times per second, duration of 250 msec, 50% duty cycle
adaptation would occur for continuous, but not interrupted
emphasized site-of-lesion
Original Bksy types
Type I
C & I interweaved
normal, conductives, some cochlears
Type II

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C & I interweaved at lower frequencies

curves separated (about 5 to 20 dB) at higher frequencies
at higher frequencies, tracking width was reduced
cochlear pathology
With revised type II, curves can separate anywhere, but there is less than 25 dB separation
Type III
Continuous curve plummets to the limits of the audiometer
retrocochlear pathology
Type IV
C & I separate below 1000 Hz
retrocochlear
With revised type IV, curves can separate anywhere, but there is more than 25 dB separation

Type V (added in 1961)

C is better than the I
kind of a reversed type IV
malingering

The End

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card fld "Info"

Roll-over is determinded by obtaining a
performance-intensity function for
phonetically balanced words (PI-PB)
usually, % correct as a function of dB SL, at
10 dB intervals re: SRT
PBmax, the maximum word recognition
score (WRS) is usually obtained at 30 to 40 dB
SL, or at a level close to MCL in cases with poor threshold and reduced dynamic range
PBmin, the poorest WRS is obtained at the highest SL testable, usually the UCL, or 5 dB less

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you can shorten the test by just presenting words at two levels
When comparing VIII N. with Mnire's patients
convention WRS showed too much overlap between groups
PBmax - PBmin showed less overlap, but still too much to be clinically useful
(PBmax - PBmin)/PBmax showed the least overlap
Jerger and coworkers, and Dirks found a roll-over index RI .45 as a good indication of retrocochlear pathology

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card fld "Info"

Central Auditory Evaluation
definite organic pathology (tumors, CVA,
trauma, etc.)
MRI, CT scan excellent locators of structural
change
CAE provides functional information
central auditory processing disorders
(learning disabilites), CAPD, LD
ADD, attention deficit disorder
ADHD, attention deficit hyperactivity disorder
auditory selective attention, figure-ground, sequencing, memory: listening skills
hyperacousis? hyperacusis? hypersensitivity?
Is middle ear pathology a factor?
-conductive attenuation creates sensory deprivation
-lack of stimulation causes CANS development to lag (see ABR & OME pic)
-mice raised with surgically created unilateral conductive losses show smaller diameter neurons in most brainstem
nuclei
Some points about CANS pathology
Loss in pure-tone sensitivity is not associated with CANS pathology
Conventional speech recognition ability is often normal
not challenging enough
Symptoms are usually (except in very low brainstem pathology) contralateral

Clin Aud I Handout

Some lesions can be imaged, some cannot

Aging produces significant effects
the young system myelinates, matures, in a caudal to rostral fashion
the elderly system deteriorates
The CANS defined
periphery
cochlea & VIII N.
low brainstem
cochlear nuclei, superior olivary complex, lateral lemniscus (i.e., up to wave V of the ABR)
high brainstem
inferior colliculus, medial geniculate body
intra-axial vs. extra-axial
lesion inside or on the surface of the brainstem
cortical
gray matter (cell bodies) in periphery of brain, cerebral cortex
Heschl's gyrus, primary auditory cortex, auditory reception cortex
secondary adjacent association areas
hemispheric
lesion affecting gray matter and white matter (myelinated fiber tracts)
interhemispheric
corpus callosum (this structure myelinates last)
A simple model of the CANS
Each ear has an ipsilateral path to cortex
Each ear has a more dominant contralateral path to cortex
Contralateral path begins at low brainstem (i.e., superior olive)
The left hemisphere is dominant for language
The right hemisphere is dominant for extracting nonspeech pitch, duration contours from the signal
corpus callosum connects the hemispheres
verbal responses require participation of the left hemisphere
So, for words (or other speech material)
presented to the right ear, goes directly to left hemisphere for processing
presented to the left ear, goes to right hemisphere, shuttled to left hemisphere via corpus callosum
-a weaker ipsilateral path can also get speech to left hemisphere

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-probably, the nondominant hemisphere can perform some simple processing

deficits occur when stimuli are presented to the ear contralateral to involved hemisphere, especially when a competing
message (CM) is present in opposite ear
-CM keeps the noninvolved hemisphere "busy"
For tonal materials (frequency, duration patterns)
the right hemisphere analyzes information
the left hemisphere verbally reports the results of the analysis
lesions in one hemisphere produce deficits in both ears (if a verbal response is required)
-a right hemisphere lesion produces a bilateral deficit (the pattern cannot be decoded)
-a left only hemisphere lesion produces a bilateral deficit (the pattern is analyzed but cannot be verbalized correctly, but
could be hummed)
Types of deficits
neurological
tumors & other brain lesions, disease
developmental
structural, functional abnormalities; i.e. microgyri as with autism
individual permanently affected
maturational
delayed myelination
person eventually develops ability
Knowledge base for audiologists
understand neuroanatomy, dissection work is helpful
clinical experience with a wide variety of patients
understand brain pathology and common CANS disorders
knowledgeable about theories of speech perception
know about learning disorders and language development
be familiar with the CAP tests
how to administer
scoring and interpretation
test sensitivity and specificity
The conceptualization
the CANS functions to analyze, decode complex stimuli (like speech), remove noise
vary extrinsic redundancy (all those factors which reduce the intelligibility of speech) to expose loss in intrinsic
redundancy (disruption caused by lesion)
Typical protocols

Clin Aud I Handout

Present stimuli to the RE and LE simultaneously, and ask the subject to repeat them
tests for cortical lesions, above brainstem
stimuli can be speech (usually) or nonspeech
Distort the speech stimulus in some way, add:
white or speech noise,
competing message (other speech, multitalker babble),
low-pass filter it,
speed it up (time compression),
chop it up (in time),
choose unintelligible speaker (like Rush Hughes)
Present the stimulus (pure speech, or speech in "noise") to one ear
Present the "noise" to the other ear (contralateral, CCM) to test for higher lesions
Present the "noise" to the same ear (ipsilateral, ICM) to look for lower lesions
Look for a deficit in performance in ear contralateral to lesion
Some CANS tests
dichotic digits (2 RE; 5 LE or 2,4 RE; 5,8 LE)
competing sentences, dichotic sentences
dichotic chords
dichotic CVs
dichotic rhyme test
SSW
Willeford battery
Rush Hughes/W-22 difference score
alternating speech, RASP
binaural fusion
low-pass filtered speech
pure tone or speech MLD
SSI-ICM
SSI-CCM
PSI-ICM/CCM
SCAN (filtered speech, speech in noise, dichotic words) and SCAN-A
time compressed speech
PI-PB
localization
lateralization, SBMPL
fused auditory image, FAI
ABLB, SISI
acoustic reflexes
frequency (pitch) pattern test
duration pattern test

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W-22s in white or speech noise

ABR
MLR
late potentials
P300, mismatched negativity
Typical patters of results
The brain is highly redundant, interpretation of results is difficult, confusing, often contradictory
Brainstem lesions
ABR and AR involve low brainstem pathways
PI-PB, SSI-ICM can be useful
MLD is more sensitive to brainstem lesions than cortical
dichotic digits, time compressed speech, filtered speech, competing sentences may be sensitive to both brainstem and
cortical/hemispheric lesions
frequency pattern test seems to be less sensitive to brainstem lesions
intra-axial lesions tend to produce contralateral symptoms
extra-axial lesion tend to produce ipsilateral symptoms
rostral lesions tend to produce contralateral symptoms; caudal lesions produce ipsilateral
larger lesions (CN to LL 3 cm) can produce bilateral deficits
Cortical/hemispheric lesions
According to Musiek, "none of the currently available tests is sensitive to problems in these areas to the exclusion of
brainstem or peripheral lesions."
dichotic speech tests show poorer performance with signal presented to ear contralateral to lesion (SSW, dichotic digits,
SSI-CCM, competing sentences, etc.)
monaural low redundancy speech tests show poorer performance with signal presented to ear contralateral to lesion
(time compressed speech, speech in noise, filtered speech, etc.)
frequency or duration pattern tests show bilateral deficits
Interhemispheric lesions (posterior portion of corpus callosum)
left ear deficit for dichotic speech, right ear scores may be enhanced
bilateral deficit for verbal reporting of frequency patterns
low redundancy monaural speech tests usually not affected
A suggested evaluation protocol
All tests are screening tests whether labeled so or not
detailed case history
peripheral evaluation
present a battery that assesses the entire system
SCAN test is useful for screening for CAPD in children, SCAN-A for adults
Brainstem lesions
ABR, AR, MLD, SSI-ICM

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All sites
dichotic digits, SCAN (filtered speech, monosyllabic words in noise, competing words)
Cortical/hemispheric, interhemispheric
competing sentences, SSW, SSI-CCM, frequency pattern test
MLR: Pa (thalamo-cortical projections, 1 cortex)
The ideal situation
Administer the CAE with a well defined protocol
each test is normed for age
the interpretation is objective
sensitivity and specificity are known
Findings of the CAE are interpreted
site of lesion is established
type of dysfunction is described
Results of CAE have implications for follow-up
medical/surgical treatment
rehabilitative strategies
decide which strategy is most effective
Offer a prognosis based upon known treatment efficacy
Recommendations from the CAPD battery
The audiologist is not solely responsible for management, but is part of a team (classroom teacher, LD specialist, parents,
SLP, counselor, neuropsychologist, etc.).
-usually the main concern is academic performance
-often a language problem coexists
-ADHD may coexist. ADHD may make it difficult to administer the CAPD battery. Modify test protocol, allow breaks,
etc.
A diagnosis of CAPD can sensitize parents and school personnel to the existence of a real problem or disability. They
may believe the child is just not trying hard enough, is being obstinate, or oppositional.
A diagnosis of no CAPD can allow personnel to focus on academic, behavioral, or language issues as the problem.
Management strategies focus on providing a highly redundant learning environment
-optimize S/N ratio, eliminate auditory distractions, FM systems (personal or group) for those children having poor
access to information be sure to follow-up and document benefit
-provide clear, slowed, well articulated speech (i.e., "clear speech")
-rephrasing, repeating information
-work to other, stronger modalities; for example provide written directions
-ensure you have the child's attention before giving important information
-pre-teach critical skills or concepts

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Therapeutic strategies provide experiences which directly challenge the deficits: perhaps to encourage myelination,
arborization, or to develop alternate neural circuits to compensate for the damaged areas. The existence of neuroplasticity
and neuromaturation even the formation of new neurons requiring stimulation is the rationale. For example:
-therapy may involve listening tasks similar to those the child exhibited difficulty with during the evaluation
-auditory closure tasks (missing words in sentences)
-interhemispheric exercises, music therapy, singing to music
Another strategy is to focus on the practical consequences of the deficit and attempt to build those skills. For example, if
CAPD results in language delay, do therapy for language acquisition.
For more information on this topic, see Bellis' chapters 7 and 8 (interpretation and management of auditory processing
disorders)

Card number_____ 35
card fld "card field id 1"
Check each item that is considered to be a concern by
the observer:
Has a history of hearing loss.
Has a history of ear infection(s).
Does not pay attention (listen) to instruction 50% or
more of the time.
Does not listen carefully to directions - often
necessary to repeat instructions.
Says "Huh?" and "What?" at least five or more times per day.
Cannot attend to auditory stimuli for more than a few seconds.
Has a short attention span.
(If this item is checked, also check the most appropriate time frame.)
___ 0-2 minutes ___ 5-15 minutes
___ 2-5 minutes ___ 15-30 minutes
Daydreams - attention drifts - not with it at times.

Clin Aud I Handout

Is easily distracted by background sound(s).
Has difficulty with phonics.
Experiences problems with sound discrimination.
Forgets what is said in a few minutes.
Does not remember simple routine things from day to day.
Displays problems recalling what was heard last week, month, year.
Has difficulty recalling a sequence that has been heard.
Experiences difficulty following auditory directions.
Frequently misunderstands what is said.
Does not comprehend many words - verbal concepts for age/grade level.
Learns poorly through the auditory channel.
Has a language problem (morphology, syntax, vocabulary, phonology).
Has an articulation (phonology) problem.
Cannot always relate what is heard to what is seen.
Lacks motivation to learn.
Displays slow or delayed response to verbal stimuli.
Demonstrates below average performance in one or more academic area(s).

Components of Auditory Processing:

Association
Localization
Attention
Long Term Memory
Attention Span
Motivation
Auditory-Visual Integration
Performance
Closure

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Recognition
Comprehension
Sensitivity
Discrimination
Sequential Memory
Figure-Ground
Short Term Memory
Identification
Speech-Language Problems
The norming group consisted of 280 K-6th graders. Allowing 4% per item not checked, the mean score was 86.8% (SD =
18.2%). A score of 72% suggested followup. Performance actually became poorer with age, suggesting that behaviors
acceptable in younger children became problems with age.
Group Mean Score
Kindergarten 92%
1st
90%
2nd
87%
3rd
86%
4th
86%
5th
87%
6th
80%

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card fld "Info"
ABR results for DK, a 27 year old male with
normal hearing.

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before test
check disk space, format new data disk
do listening check on headphones
set up, check test parameters (or use default settings)
check electrodes for shorts
placing electrodes The goal is a low impedance connection between electrode and skin
look at what you are doing and think about it
remove excess oil with alcohol (avoid contaminating reservoir, spreading bacteria from patient to patient)
remove excess dead skin with omni prep
saturate skin at electrode site with electrode paste
avoid putting paste over too large an area (trouble with tape sticking)
place electrode over site prepared
check impedance A good result is low impedance (<1000 ), and balanced across electrodes
a low impedance helps ensure a high signal level going to preamp, a better quality tracing
recheck impedances during test
check locations of active (non-inverting), reference (inverting), and common (ground) in preamp
Instructions
no muscle tension in neck or back, forehead
do not clench jaw
DK's parameters
ipsilateral earlobe to high forehead montage, ground electrode on contralateral earlobe
alternating clicks at 19.1/sec: 75 dB nHL
(up to 37.7/sec is acceptable)
filter settings: 150 - 3000 Hz
gain: 100,000
each tracing: average of 1024
Peak picking
each tracing is immediately replicated, to assess reliability
peak must be present in both tracings
the presence of a peak can be ambiguous
if there is a peak
at the proper time
it probably is a peak
determining the exact location of the peak can be ambiguous
moving a few pixels over can change value by a SD
picking a shoulder of wave V vs. the peak affects absolute and relative latencies

About parameters
vertex to nape of neck is a better location
vertical orientation of neural generators

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enhances wave V amplitude

a horizontal montage enhances wave I
horizontal location of generators
reducing click rate improves quality of the tracing (say, 11.1/sec)
increasing click rate degrades quality, and increases latency (beyond about 30/sec)
sometimes better ABR waveforms are obtained for rarefacting (usually) or condensation clicks; if you have no ABR,
repeat test using rarefacting clicks
Increasing the number of samples averaged improves quality, but increasing from 100 to 1000 samples produces the
same improvement as going from 1000 to 10,000 however, the increase in time to complete test is excessive.
the SNR improves with n^.5*SNR in original sample

Choosing presentation level

Present clicks at 75 dB nHL, or higher
at least 15 to 20 dB SL re: audiogram threshold at 3000 to 4000 Hz, or at limits
try to avoid an unnecessarily high level
tenses patient
PAM artifact?

Interpreting the ABR

A retrocochlear interpretation is generally based upon the effects the lesion has upon transmission time. But, remember
to consider effects (non-retrocochlear) peripheral hearing loss can have on the ABR.

Retrocochlear pathology
Complete absence of the ABR, typical
Normal Wave I, no subsequent waves
with high frequency loss, usually there is no Wave I
Abnormal interaural latency difference (ILD)
ILD > 2/2.5/3 SD
usually this is .3 to .45 msec

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Abnormal interpeak latencies (IPL, or interwave intervals, IWI)

Wave I is normal, subsequent waves are delayed
Wave morphology may be abnormal: reduced amplitudes or wave V smaller amplitude than wave I
abnormal I-V IPL, IPL > Mean + 2.5 SD is a typical criterion
-roughly IPL > 4.5 msec
Effects of peripheral hearing loss
Conductive hearing loss will increase Wave V latency, but IPL should not be affected
interpret Wave V latency as if the presentation level were reduced by the ABG

Cochlear hearing loss will increase Wave V latency

Precipitous hearing loss (very poor high frequency sensitivity) adds to the latency by the time it takes the traveling wave
to travel to apical regions of the basilar membrane
The following methods have been suggested to adjust latencies to account for the severity of cochlear hearing loss
- Subtract 0.1 msec (from wave V latency) for every 10 dB audiogram threshold is poorer than 50 dB @ 4000 Hz (Selters
& Brackmann, 1977).
- Subtract 0.1 msec (from wave V latency) for every 10 dB audiogram threshold is poorer than 30 dB @ 4000 Hz
(Rosenhamer et al., 1981).
- Or you can adjust the presentation level and interpret wave V ILD normally:
PTA for 1000, 2000,
and 4000 Hz
Click Intensity Level
0-19
70
20-39
80
40-59
90
60-79
100

If you can interpret the ABR in such a way that it is normal, it probably is normal

The End

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card fld "Parameters"

Recording the Middle Latency Response
Use 10 alternating clicks per sec or less.
Filter the response from 10 - 1500 Hz and
display in a 60 msec window.
Electrode montage is the same as with the
ABR.
Pa occurs at about 25 msec and is generated by the thalamus (medial geniculate body) and the 1 auditory cortex.
Pa is susceptible (diminished by) to sleep and CNS suppression; i.e., drugs. The response is not adult-like until age 8 to
10 years.

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card fld "Info"
Sensitivity The percentage of abnormals
identified by the test as being abnormal
SpecificityThe percentage of normals
identified as being normal (or, non-abnormals
identified by the test as not being abnormal)
A perfect test has 100% sensitivity and 100%
specificity
Generally, as sensitivity of a test increases, the specificity decreases (and vice-versa)

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card fld "Info"
Clinical performance of audiological and
related diagnostic tests; R. Turner, N. Shepard,
and G. Frazier. Ear & Hearing, 1984
Tumors of the CPA was authors' operational
definition of retrocochlear:
78% acoustic tumor (8 to 10% of all
intracranial tumors)
6% meningioma
6% primary cholesteatoma
6% glomus body tumors
History Information with tumors of the CPA:
initial symptom is auditory 77% of the time, either hearing loss (69%) or tinnitus (8%)
presenting complaint is auditory 57% of the time, vestibular (6%)
tumor is usually a vestibular schwannoma
95% of the tumors originate from the IAC, 5% develop in CPA
10% of cases with progressive unilateral loss are acoustic tumors
an incidence of 7 per 1,000,000 in general population

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Generally, the individual author's definition of a positive result for the test was used. They reviewed over 170 papers
published from 1968 thru 1983.
Guidelines:
ABLB: + if no recruitment or decruitment
SISI: + if 70%
Bksy: + if types III or IV
Tone Decay (TDT): + results > 30 dB
STAT+ based upon 500, 1000, 2000, or 4000 Hz
Speech Discrimination: + results < 30%
Acoustic Reflexes: + results were elevated HL, or decay
ABR: + results based on ILD, I-V interval, usually
ENG: based only upon calorics, UW 25%

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