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FORWARD MASKING OF AUDITORY NERVE (N1)
AND BRAINSTEM RESPONSES (WAVE V)
IN HUMANS
By
STEVEN JOHN KRAMER
A DISSERTATION PRESENTED TO THE GRADUATE COUNCIL OF
THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT
OF THE REQUIREMENTS FOR THE DEGREE OF
DOCTOR OF PHILOSOPHY
UNIVERSITY OF FLORIDA
1981
ACKNOWLEDGEMENTS
I would like to thank the chairman of my supervisory
committee, Dr. Donald C. Teas, for all his tireless efforts
and encouragements in helping me to conceive, organize,
and carry out this research. I would also like to thank
my committee members, Dr. W. Keith Berg, Dr. William E.
Brownell, Dr. F. Joseph Kemker, and Dr. Kenneth J. Gerhardt,
for their support and participation. In addition I would
like to express thanks to my friends and subjects without
whom this research would not have been possible and to
Mrs. Kathy Farley for her secretarial assistance. Finally,
I would like to express my appreciation to Kathleen Cannon
for all her help, encouragement and sacrifice and to whom
this project is dedicated.
TABLE OF CONTENTS
Page
ACKNOWLEDGEMENTS.
LIST OF TABLES. .
LIST OF FIGURES
. vii
. xi
ABSTRACT.
CHAPTER
I INTRODUCTION . . .
General Description of the AP. .
Forward Masking of the Whole-
Nerve Action Potential (AP) .
General Description of the ABR
Forward Masking of the Auditory
Brainstem Response (ABR) .
II METHODS . . . .
Subjects . . .
Equipment . . .
Stimuli . . .
Electrodes . .
Procedures . .
II RESULTS . . . .
"Standard" Recovery Function .
The Effect of Masker Duration..
The Effect of Masker Level .
The Effect of High-Pass Masking.
Derived Response . .
IV DISCUSSION . . .
. 14
S 17
. 28
. 32
S. 47
. 47
S. 48
. 48
. 54
S. 55
S. 58
S. 65
. 81
91
S. 99
119
S. 129
. ii
I
TABLE OF CONTENTS (Continued)
General Effects of Forward
Masking . . ... 132
Effect of Masker Duration and
Level . . . 134
Effects of Masker Low Frequency
Cutoff (High-Pass Masking) .138
Possible Mechanism Underlying the
Effects of Forward Masking on
N1 and Wave V . . 141
Wave V Amplitude . ... 142
V-N1 vs N1 Amplitude. ... 144
Central Physiological Evidence. 148
Explanation of Forward
Masking Effects on N1 .. 150
Relation to Psychophysics. .... 153
Summary and Conclusions. ... 154
BIBLIOGRAPHY. . . . .. 157
BIOGRAPHICAL SKETCH . . ... .172
LIST OF TABLES
Table Page
I Forward masking series received by
each of the subjects. (+) indicates
success and (-) indicates failure
in obtaining data for ABR/AP. .. 60
II Means and standard deviations
(S.D.) of wave V and N1 latencies
for the "standard" series . 72
III Means and standard deviations (S.D.)
of wave V and N1 amplitudes for the
"standard" series . ... .79
IV Means and standard deviations (S.D.)
of wave V, N1 and V-N1 probe response
latencies for the three masker
durations . . . .. 83
V Means and standard deviations (S.D.)
of wave V and N1 probe response
amplitudes for the three masker
durations . . . .. 89
VI Means and standard deviations of
wave V, N1 and V-N1, probe response
latencies for the three masker
levels. . . . . 94
VII Means and standard deviations of
wave V and N1 probe response
amplitudes for the three masker
levels. . . . ... 97
LIST OF TABLES (Continued)
Table Page
VIII Means and standard deviations (S.D.)
of wave V, N1, and V-N1 probe
response latencies for the four
masker low frequency cutoffs. . ... 110
IX Means and standard deviations (S.D.)
of wave V and N1 probe response
amplitudes for the four masker low
frequency cutoffs . . .. 118
X Summary of significant effects and
interactions of masker parameters
on wave V and N1 probe responses. ... .135
LIST OF FIGURES
Figure Page
1 Spectra of the masking stimuli (a)
and frequency response of the TDH-39
earphone (b) . . . .50
2 Simplified block diagram of the
stimulus generating and response
recording equipment . ... .52
3 Examples of unmasked control response
waveforms . . . 62
4 Example of ABR and AP probe response
waveforms as a function of AT for the
"standard" series . . ... .68
5 Mean and fl S.D. of wave V, N1, and
V-N1 latencies as a function of AT
(delay time) for the "standard"
series. . . . ... 69
6 Mean and 1 S.D. for wave V and N1
amplitude (uvolts) as a function of
AT for the "standard" series . 76
7 Mean wave V and N1 amplitude recovery
functions expressed as percent of the
mean unmasked control amplitude (100%)
for the "standard" series . .. 77
8 Summary comparison of wave V and N
for the "standard" series .. ... 80
9 Latency recovery functions for wave V,
N1 and V-N1 probe responses following
wide-band makers with durations of
30, 60, and 120 msec. . ... .86
vii
LIST OF FIGURES (Continued)
Figure rage
10 Amplitude recovery functions for
wave V probe responses following
wide-band makers with durations
of 30, 60, and 100 msec . ... .87
11 Amplitude recovery functions for
N1 probe responses following wide-
band makers with durations of 30,
60, and 120 msec. . . ... .90
12 Latency recovery functions for
wave V, N1, and V-N, probe responses
following 60 msec wide-band makers
with levels of +10 dB relative to
the "standard" series (referred to
as 0 dB). . . ... .. .. 93
13 Amplitude recovery functions for
wave V probe responses following
60 msec wide-band makers with
levels of 10 dB relative to the
"standard" series . . ... .96
14 Amplitude recovery functions for
N1 probe responses following 60
msec wide-band makers with levels
of 10 dB relative to the "standard"
series. . . . ... 98
15 Example of the probe ABRs as a
function of AT (top to bottom) for
the different masker low frequency
cutoffs (left to right) . ... 102
16 Example of probe APs as a function
of AT (top to bottom) for the
different masker low frequency
cutoffs (left to right) . ... 105
viii
LIST OF FIGURES (Continued)
Figure
Latency recovery functions for
wave V, N1, and V-N1 probe re-
sponses following 60 msec makers
with masker low frequency cutoffs
of .02, 2, 4, and 6 kHz . .
Wave V and N1 probe response
latencies as a function of masker
low frequency cutoff . . .
Amplitude recovery functions for
wave V probe responses following
60 msec wide-band makers with
masker low frequency cutoffs of
.02, 2, 4, and 6 kHz. . . .
Wave V probe response amplitude as
a function of masker low frequency
cutoff . . . .
Amplitude recovery functions for
N1 probe responses following 60
msec wide-band makers with masker
low frequency cutoffs of .02, 2,
4, and 6 kHz . . .
N1 probe response amplitude as a
function of masker low frequency
cutoff . . . .
Example of derived response
technique for the ABR . .
Example of the derived response
technique for the AP. . .
Mean latencies of wave V and N1
as a function of derived CF ..
106
107
113
114
116
. 117
. 122
. 124
. 125
Page
LIST OF FIGURES (Continued)
Figure Page
26 Mean amplitudes of wave V and
N1 as a function of derived CF. ... 127
27 V-N1 latency interval as a function
of % N1 control amplitude for the
different masker low frequency cutoffs
at each AT . . . 147
Abstract of Dissertation Presented to the Graduate Council
of the University of Florida in Partial Fulfillment of
the Requirements for the Degree of
Doctor of Philosophy
FORWARD MASKING OF AUDITORY NERVE (N1)
AND BRAINSTEM RESPONSES (WAVE V)
IN HUMANS
By
Steven John Kramer
June 1981
Chairman: Donald C. Teas
Major Department: Speech
In both psychophysical and electrophysiological inves-
tigations, it has been demonstrated that a response to one
sound (probe) can be influenced by another sound maskerr)
when the two sounds occur simultaneously or in a temporal
relation. The relation in which the masker precedes the
probe is called forward masking. Measurements of the probe
response as a function of the time interval following the
masker (AT) describe the forward masking recovery func-
tions.
In the present study, the effects of forward masking
were investigated on wave V of the ABR along with N1
responses recorded simultaneously (on a separate channel)
from the ear canal. Evoked potentials to 50 dB HL
broadband clicks were obtained for ATs of 6.2, 12.5, 25,
50, and 100 msec following short-duration noise makers.
Postmasking recovery functions were measured for different
masker durations, masker levels, and masker low frequency
cutoffs (high-pass masking).
The largest amount of masking occurred for the
shortest ATs and masking decreased as AT increased. The
effects on wave V were found to be different than on N1.
The primary effects of forward masking on the probe re-
sponses were decreases in N1 amplitude and increases in
wave V latency, neither of which were fully recovered by
AT=100 msec. Wave V amplitude recovered by AT=25 msec
and showed a robustness to the forward masking. Charac-
teristic changes in the recovery functions were found for
variations on masker parameters.
The relation between wave V latency and N1 amplitude,
along with other characteristics of the results, suggests
that underlying mechanisms include a recoding of the
neural input (N1) within the brainstem pathways generating
the wave V potential.
xii
CHAPTER I
INTRODUCTION
The effects that one sound may have on the perception of
another sound have been of interest to investigators ever since
Mayer (1876a,b) first described some aspects of this basic
phenomenon which has become known as masking. Masking is a
psychophysical term used to denote an elevation in threshold
of audibility for one sound (probe) in the presence of another
sound maskerr). Mayer observed that a watch-tick could be
obliterated by a louder clock-tick when the two ticks over-
lapped each other. By using two time-pieces running at
different speeds, Mayer also noticed that the quieter watch-
tick was obliterated by the clock-tick at instances when the
two ticks did not exactly overlap in time. Mayer's early
qualitative observations demonstrated that different temporal
relations among sounds could influence the perception of those
sounds and have since led to an abundance of research known,
in a general sense, as temporal masking. The masking situation
with the masker coincident with the probe is generally called
simultaneous masking. The term forward masking is used for
situations where the masker precedes the probe and backward
masking applies to situations where the masker follows the
probe. The time interval between the masker and the probe
is generally called AT. One problem with the simultaneous
masking paradigm is that nonlinear distortion products are
produced by the two stimuli with different frequencies, thereby
producing energy at frequencies other than the stimulus fre-
quencies (Rodenburg, Verschuure, and Brocaar, 1974; Shannon,
1975; Wightman, McGee, and Kramer, 1977; Moore, 1978; Vogten,
1978). A forward masking paradigm overcomes the distortion
problem since the two stimuli are not present at the same time.
Forward and backward masking paradigms have been used in
psychophysical investigations to describe the time course of
masking effects (Lusher and Zwislocki, 1947; Zwislocki, Pirodda,
and Rubin, 1959; Elliott, 1962; Plomp, 1964; Wilson and Carhart,
1971; Robinson and Pollack, 1973; Duifhuis,1973; Penner, 1974;
Fastl, 1976; Berg and Yost, 1976). In this procedure, the
threshold of the probe stimulus is measured as a function of
AT. As AT increases, less energy is required to detect
the probe signal and the plot of threshold vs At defines the
masking recovery function for stated masker-probe parameters.
In general, the decrement in sensitivity to the probe produced
by the forward or backward masker is greatest for shortest ATs
(least sensitivity) and then monotonically decreases (toward
greater sensitivity) as AT increases. The decrease in
sensitivity to the probe becomes greater for longer masker
durations and higher masker levels. The actual descriptions
of the recovery functions are not entirely agreed upon and
are dependent on stimulus parameters. Recovery from backward
masking occurs much faster than recovery from forward masking.
Backward masking will not be addressed any further in this
investigation.
In electrophysiological investigations, masking paradigms
have been adapted to provide correlatives to psychophysical
masking phenomena. The investigation of electrical potentials
evoked by acoustic stimuli has been of interest to auditory
researchers as a means of describing underlying physiological
phenomena that may possibly mediate some of the psychophysical
observations. The development of signal-averaging computers
in the 1960's greatly improved the ability to extract stimulus-
related electrical potentials from the random electrical back-
ground activity and has made it possible to record electrical
activity to auditory stimuli from remote sites within the
boundaries of the skull and scalp. Two such averaged evoked
potentials most applicable to humans are the whole-nerve
action potential (AP) and the Auditory Brainstem Response
(ABR), which are the subjects of the present study.
The term masking has been retained in electrophysiologi-
cal experiments and refers to a reduction in some measure of
neural response to one signal (probe) due to the presence of
another signal maskerr). In physiological masking, it has
been thought that the masker "subtracts" the contributions
(through refractory, adaptation, and/or desynchronizing
mechanisms) from certain areas of the cochlear partition
dependent on the level and spectral characteristics of the
masker. A response to the probe, recorded in the presence
of the masker, is considered to reflect the "unmasked" portion
of the cochlear partition (Teas, Eldredge, and Davis, 1962;
Elberling, 1974; Spoor, Eggermont and Odenthal, 1976; Don and
Eggermont, 1978; Parker and Thornton, 1978). The probe and
masker can be presented simultaneously or in a temporal
relation, e.g., forward masking.
In both psychophysical and electrophysiological masking
studies, there is general agreement that for relatively short
duration makers at levels below 80-90 dB Sound Pressure Level
(SPL) the decrement of probe response activity is due to some
short-term noncumulative effect. For makers above 80-90 dB
SPL the effects are different and involve some form of cumula-
tive "fatigue" (Hood, 1950; Gisselsson and Sorensen, 1959;
Coats, 1964a; Smith, 1977). This investigation is concerned
only with the short-term lower level effects of forward
masking.
Forward masking effects have been investigated by several
researchers in recordings of the whole-nerve response (AP)
(Hawkins and Kniazuk, 1950; Sorensen, 1959; Coats, 1964a,b,
1967, 1971; Spoor, 1965; Coats and Dickey, 1972; Eggermont
and Spoor, 1973a,b; Eggermont and Odenthal, 1974a; Spoor et al.,
1976; Charlet de Sauvage and Aran, 1976; Dallos and Cheatham,
1976; Harris, 1979; Huang and Buchwald, 1980; Abbas and Gorga,
1981). In general, these studies have shown that the amounts
of post masking recovery functions are dependent on the pro-
cedure, masker and probe levels, and masker durations. A re-
view of existing literature on forward masking of the AP is
presented in more detail in a later section.
A special case of forward masking is that of repetitive
stimuli. Responses to successive stimuli show a decrement
when the preceding stimuli have an extended effect. The re-
sponse to each stimulus can be measured for a pair of stimuli
or for a train of stimuli as a function of ISI. The amount
of response decrement for the AP has been shown to be greater
for shorter ISIs and the final amount of response decrement
is reached by the 4th or 5th stimulus (Sorensen, 1959; Kupper-
man, 1971; Yoshie and Ohashi, 1971; Eggermont and Spoor, 1973a;
Thornton and Coleman, 1975; Spoor et al., 1976; Don, Allen
and Starr, 1977). Since no further response decrement of
the AP occurs after the 5th stimulus in the stimulus-train
experiments, others have used repetition rate procedures
where the final averaged AP responses to fast repetition rates
are compared to responses using a slow repetition rate (Peake,
Goldstein, and Kiang, 1962; Yoshie, 1968; Teas and Henry, 1969;
Spoor et al., 1976). Response magnitude as a function of ISI
defines the recovery function in the repetitive stimuli para-
digm.
Forward masking paradigms have also been used to measure
masker and probe responses in single auditory nerve fibers
(Galambos and Davis, 1943; Kiang, Watanabe, Thomas, and Clark,
1965; Young and Sachs, 1973; Evans, 1976; Smith, 1977, 1979;
Bauer, 1978; Harris and Dallos, 1979; Abbas, 1979; Delgutte,
1980). These studies have shown that during continuous stimu-
lation (of constant intensity and frequency), e.g., by the
masker, the discharge rate of the nerve fiber responds
maximally at the onset then declines rapidly at first followed
by a more gradual decline until a quasi steady-state is reached
by 100-200 msec. This (normal) neural decrement is called
adaptation. Following the offset of a masker to which the
single fiber has adapted, the spontaneous neural activity
shows an immediate depression followed by a recovery to base-
line levels. The probe response following the masker offset
shows a decrement in discharge rate compared to its unmasked
value which then recovers as AT is lengthened. The recovery
of the probe response magnitude has been shown to be related
to the recovery of the spontaneous activity and this is pro-
portional to the driven onset (and average) discharge rate
which occurs for the masker. Both the adaptation and recovery
from adaptation have been shown to follow exponential recovery
functions; however, the time course of adaptation is much
faster than the time course of recovery from adaptation
(Harris and Dallos, 1979). In addition, the recovery func-
tions have been shown to have different time constants for
different species, e.g., they are about 2.5 times longer in
guinea pig than chinchilla. Single auditory nerve fiber
responses to increasing click repetition rate show decreases
in neural discharge rate and only small (0.1 msec) latency
increases (Kiang et al., 1965).
The actual mechanisms) responsible for the decrement
during adaptation and for the postmasking decrement of the
probe-evoked responses is not known. The source of the
mechanism has been attributed by most investigators to the
hair cell-nerve fiber synapse (Rosenblith, 1954; Hawkins and
Kniazuk, 1950; Sorensen, 1959; Peake et al., 1962; Young and
Sachs, 1973; Spoor et al., 1976; Prijs, 1980). The hair cell
cochlear microphonics (CM) do not change with repetitive
stimuli (Sorensen, 1959; Peake et al., 1962; Young and Sachs,
1973; Charlet de Sauvage and Aran, 1976; Huang and Buchwald,
1980) nor do the summating potentials (Dallos, Schoeny, and
Cheatham, 1972; Eggermont, 1976a). The efferent olivocochleo
bundle (OCB) was considered a partial contributor by Liebrandt
(1965) who demonstrated that the AP decrement observed with
repetitive tone-bursts was abolished after injections of
procaine into the internal auditory canal. Liebrandt (1965)
suggested that efferent activity may play a part in several
portions of the central nervous system in causing a decrement
in evoked potentials following repetitive stimuli. Others,
however, do not consider the efferent pathways responsible for
the AP decrements since their effect on the AP requires much
higher rates of stimulation, stimulation does not cause any
reduction of spontaneous activity in auditory nerve fibers,
the AP decrements are still observed following complete
sectioning of the auditory nerve, and contralateral stimula-
tion does not produce any response changes (Sorensen, 1959;
Kupperman, 1972; Young and Sachs, 1973; Don, Allen and Starr,
1977; Huang and Buchwald, 1980). Middle ear muscle activity
has also been ruled out on the basis that the postmasking
effect is present at levels below middle ear muscle reflex
threshold, contraction of middle ear muscles does not affect
click-evoked APs, and the postmasking effect can be observed
after sectioning the muscles or following high doses of
anesthesia (Hawkins and Kniazuk, 1950; S'rensen, 1959; Liebrandt,
1965; Coats, 1971; Young and Sachs, 1973). The refractory
period of auditory nerve fibers may be important for simul-
taneous masking phenomena, but cannot explain the effects seen
in forward masking for the long ATs (Rosenblith, 1950; Hawkins
and Kniazuk, 1950; Peake et al., 1962; Harris and Dallos,
1979; Huang and Buchwald, 1980).
Recently, the Auditory Brainstem Response (ABR) has
become popular as a noninvasive far-field electrophysiological
recording procedure for assessing a short-latency system of
the auditory nerve and brainstem pathways (Jewett and Williston,
1971; Picton, Hillyard, Krausz, and Galambos, 1974; Buchwald
and Huang, 1975; Starr and Hamilton, 1976). The ABR can pro-
vide information on peripheral as well as more central response
capabilities. The ABR to temporally related stimuli has not
been as extensively investigated as has the AP. Repetition
rate and stimulus-train paradigms have been applied to
measures of the ABR and some of the brainstem components have
been shown to behave differently than the auditory nerve
response (Jewett and Williston, 1971; Picton et al., 1974;
Terkildsen, Osterhammel, and Huis in't Veld, 1975; Thornton
and Coleman, 1975; Pratt and Sohmer, 1976; Zllner, Karnahl,
and Stange, 1976; Hyde, Stephens, and Thornton, 1976; Martin,
1976; Weber and Fujikawa, 1977; Don et al., 1977; Kodera,
Yamada, Yamane, and Suzuki, 1978; Scott and Harkins, 1978;
Klein and Teas, 1978; Chiappa, Gladstone, and Young, 1979;
Kevanishvilli and Lagidze, 1979; Despland and Galambos, 1980;
Harkins and Lenhardt, 1980). These studies will be described
in more detail in a later section.
The different behavior of the various brainstem components
to temporally related stimuli is potentially quite interesting
and may indicate that peripheral auditory information is coded
in different ways in the brainstem. Response differences to
repetitive stimuli have also been noted for the various brain-
stem nuclei (Kiang, 1968; Winklegren, 1968; Watanabe and
Simada, 1969; Kitahata, Amakata, and Galambos, 1969; Kitzes
and Buchwald, 1969; Webster, 1971).
Knowledge of the postmasking recovery properties of the
ABR and their relation to postmasking recovery properties of
the AP may be useful as a method for objectively assessing
a dynamic property of the auditory system at more than one
level in a noninvasive manner. Provided that the normal
postmasking recovery properties are known, certain altera-
tions in clinical populations may be of diagnostic value as
has been suggested by Charlet de Sauvage and Aran (1976) and
Zllner, Karnahl, and Stange (1976) for cochlear pathologies,
by Yoshie and Ohashi (1971) for detecting acoustic neuromas,
by Robinson and Rudge (1977) for cases involving multiple
sclerosis, and by Salamy, McKean, Pettett, and Mendelson
(1978), Fujikawa and Weber (1977), Rowe (1978), and Despland
and Galambos (1980) for different developmental states. In
addition, postmasking recovery may be a method to better
assess persons who have poor speech discrimination beyond
that which can be due to their loss of pure-tone sensitivity
(phonemic regression), a characteristic of some geriatric
persons. Since continuous speech involves alternations of
intense vowels with relatively weak consonants, frequent
pauses and silent intervals, onsets and offsets with different
rates of amplitude changes, short-time spectral changes, and
different sound durations (Shoup and Pfeifer, 1976; Stevens,
1980), knowledge of temporal masking effects may have
important implications for better understanding these dynamic
characteristics of speech discrimination. Since most auditory
experience does not consist of simple sounds in a quiet
background, it is of interest to understand how one sound
affects the response to a simultaneous or subsequent sound.
At the single auditory nerve fiber level, Delgutte (1980)
suggests the importance of temporally related effects for
speech discrimination in the following:
Consider a region of rapid spectral change
in a speech signal (transition interval)
preceded by a steady segment having most of
its energy over a limited frequency region.
This segment would adapt most of the units
whose CF is in that region, so that these
units would be less responsive to the follow-
ing transition interval /-and_. this decreased
responsiveness would occur even if there
were a 50-100 msec silent interval between
the adapting segment and the transition
interval. (p. 847)
Temporal intervals up to 150 msec are typical between transi-
tions at the release of a stop consonant and the preceding
vowel (Delgutte, 1980). It is of interest also to understand
how these temporal effects are manifested in evoked potentials
and how they relate at different levels of the auditory system
in order to more fully understand basic auditory processing,
as well as, a potential clinical technique to help differentiate
certain abnormalities.
The purpose of this investigation is to provide some
normative descriptions of the postmasking recovery functions
for the ABR (wave V) in humans. A forward masking paradigm
is used to measure the click-evoked potentials for various ATs
following a noise-burst masker. AP responses from the ear
canal are also measured simultaneously with the ABR in some
of the subjects so that a direct comparison of the postmask-
ing recovery functions at two levels of the auditory system
can be made. Recent evidence suggests that under certain
stimulus conditions (especially repetition rate) and certain
pathological conditions, the brainstem responses do not simply
follow events occurring at the auditory periphery (Pratt and
Sohmer, 1976; Coats, Martin, and Kidder, 1979; Kevanishvilli
and Lagidze, 1979); therefore, one of the emphases of this
investigation is to compare the forward masking effects on
the ABR to the forward masking effects on the AP. Since
longer duration makers increase the postmasking effect (Coats,
1964a; Harris and Dallos, 1979), this type of forward masking
may have a more pronounced effect than repetition rate experi-
ments on the ABR and may prove in future applications to be
more useful in assessing certain clinical abnormalities at
different levels of the auditory system once the normal
characteristics are known. The postmasking recovery functions
are described in this investigation for different masker
durations, masker levels, and masker frequency bands (high-
pass masking).
General Description of the AP
The whole-nerve action potential (AP) represents a
population of synchronously responding auditory nerve fibers
to an abrupt acoustic stimulus and reflects both hair cell
function and activity in the auditory nerve (Dallos, 1973).
Recording of the AP can be achieved with electrodes on the
auditory nerve (Derbyshire and Davis, 1935; Goldstein and
Kiang, 1958; Kiang, Moxon, and Kahn, 1976; Huang and Buchwald,
1980), within the cochlea (Tasaki, Davis, and Eldredge, 1954;
Teas, Eldredge, and Davis, 1962), near the round window
(Rosenblith, 1954; Peake et al., 1962; Eggermont and Odenthal,
1974a,b,c; Dallos and Cheatham, 1976), or from the external
ear canal (Yoshie, Ohashi, and Suzuki, 1967; Cullen, Ellis,
Berlin, Lousteau, 1972; Elberling, 1974; Coats, 1974, 1976;
Berlin and Gondra, 1976; Kramer and Teas, 1979).
Auditory stimulation at high intensities produces an AP
response that consists of an initial negative deflection, labe
Nl, which occurs about 1.5-2.5 msec poststimulus onset and
followed by a smaller positive deflection, then negative again
forming N2 about 1 msec after N1 (Derbyshire and Davis, 1935;
Teas et al., 1962). In humans, the N2 is not as prominent
as in animals (Elberling, 1976a; Yoshie, 1976; Spoor et al.,
1976; Kramer and Teas, 1979). Most descriptions of the AP
led
response involve measurements of the latency and amplitude
of the N1 components as a function of stimulus intensity.
In general, as intensity increases the latency of N1 decreases
and the amplitude increases.
The most common stimulus used for evoking the AP is the
broadband click because of its rapid onset, which produces
a highly synchronous response from a population of nerve fibers
over a wide span of frequencies. Since estimates of the
basilar membrane traveling wave velocity indicate that the
velocity is greatest at the basal end and progressively de-
creases towards the apex (Teas et al., 1962; Zerlin, 1969;
Eggermont, 1975), the neural discharges from the nerve fibers
in the basal region occur sooner than those from apical regions
and are more synchronous because many discharges occur within
a brief time period. In response to broadband clicks, these
more synchronous basal fiber discharges predominate when
responses are recorded with distant electrodes, as is the AP
response (Teas et al., 1962; Schmidt and Spoor, 1974;
Eggermont, Spoor and Odenthal, 1976). More recently, it has
been demonstrated that tone-bursts and filtered clicks with
abrupt rise-times are good compromise stimuli for providing a
more frequency-specific evaluation along the cochlear parti-
tion at low intensities (Eggermont, 1976b; Zerlin and Naunton,
1976; Eggermont et al., 1976; Coats, 1976; Kramer and Teas,
1979; Coats, Martin, and Kidder, 1979). For higher in-
tensities, the basal extension of events on the basilar
membrane results in a more limited frequency specificity due
to an inclusion of the more synchronous high frequency re-
sponding populations (Teas et al., 1962; Elberling, 1974;
Eggermont et al., 1976; Kramer and Teas, 1979). A technique
to obtain responses from more frequency-specific regions
along the cochlear partition, even at high intensities, is to
add high-passed noise makers which can exclude the dominant
high frequency region and allow a probe response from more
apical regions (Teas et al., 1962; Elberling, 1974; Eggermont
et al., 1976; Zerlin and Naunton, 1976; Kramer and Teas, 1979).
The recording of the AP response "threshold" has been
demonstrated to correspond fairly well with conventional be-
havioral thresholds (Aran, Charlet de Sauvage, and Pelerin,
1971; Yoshie, 1973; Eggermont, 1975; Montandon, Shepard, Mass,
Peake, and Kiang, 1975; Elberling and Salomon, 1976) and
characteristic differences in waveform and the latency and
amplitude input-output functions have been found between
normals and pathological patients (Odenthal and Eggermont,
1974; Montandon et al., 1975; Yoshie, 1976; Elberling and
Salomon, 1976; Coats et al., 1979).
Forward Masking of the Whole-Nerve
Action Potential (AP)
Early evidence of forward masking of the AP can be found
in the work of Derbyshire and Davis (1935) who were the first
to demonstrate a decline in the AP voltage recorded from a
gross electrode on the auditory nerve in cats during tonal
stimulation, a phenomenon termed equilibrationn." From con-
tinuous photographic records, Derbyshire and Davis (1935)
measured the amplitudes of the APs over time for different
stimulating frequencies. Although the APs continued to decline
in voltage up to 10 minutes following the onset of the tone,
the largest and most rapid decline occurred during the first
2 seconds. The amount of reduction for the first AP follow-
ing the "onset" AP was found to be negligible for frequencies
below 400 Hz. Above a critical frequency of 1000 Hz the
voltage declined abruptly until about 4000 Hz where synchronous
APs were not detectable. Derbyshire and Davis (1935) sug-
gested that the decline of the first AP after the "onset" AP
was a reflection of the "functional" refractory period of
individual auditory nerve fibers (1.0 msec) and the continued
decline over the following 2 seconds was due to prolongation
of the relative refractory period. Galambos and Davis (1943)
demonstrated that the AP amplitude decline during continuous
stimulation was due, primarily, to a decline in discharge
rate of individual auditory nerve fibers. Maximum discharge
rate of single fibers averaged about 400/sec; however, dis-
charge rates up to 1000/sec were possible. A decline in dis-
charge rate (adaptation) to about 25% of the maximum rate
occurred within 1.0 sec. Coats (1964a) explained these
original findings of Derbyshire and Davis (1935) and
Galambos and Davis (1943) in terms of forward masking, where
each cycle of the stimulating tone had a forward masking
effect on subsequent cycles and the amount of decline de-
pended on the period of the tone as well as the duration of
stimulation. Derbyshire and Davis (1935) were also the first
to report on masking of the click-evoked APs by continuous
noise or tones. A demonstration of forward masking was
apparent in their results which showed that the largest mask-
ing effect occurred when the click response coincided with
the peak of a low frequency tonal masker (in phase)i however,
some masking of the click-evoked AP occurred for certain other
phase relations.
Rosenblith, Galambos, and Hirsh (1950) and Rosenblith
(1954), although primarily interested in investigation of the
AP following intense prolonged noise makers, observed that
the click-evoked AP from the round window in cats had a
sizable reduction in amplitude following even a short ex-
posure to moderately intense tones.
The first quantitative description of the postmasking
recovery of the AP was by Hawkins and Kniazuk (1950) who
recorded from the round window in cats click-evoked APs pre-
ceded by a 1.3 msec noise or tonal masker. These authors
found that full recovery of AP amplitude did not occur until
300 msec following a 50 dB SPL masker and 1.0 sec following
a 70 dB SPL masker. Masker duration did not affect recovery
for the 50 dB SPL masker, but delayed recovery was found as a
function of masker duration for masker intensities above 50
dB SPL. For tonal makers, Hawkins and Kniazuk (1950) re-
ported that 4000 Hz was the most effective masker of the
click-evoked APs and resulted in the greatest delayed re-
covery from masking. That the masking effects extended over
a period far in excess of the refractory period of auditory
nerve fibers was an important observation and Hawkins and
Kniazuk (1950) suggested that the long postmasking effects
involved some mechanism which transmits excitation from the
hair cell to the nerve fiber.
Using a paired-click paradigm in the cat, Rosenzweig
and Rosenblith (1953), Rosenblith (1954), and Sorensen (1959),
all demonstrated that the AP to the second click was reduced
in amplitude and the reduction was dependent on the interval
between the clicks as well as the intensity of the first
click. AP amplitude was still reduced for intervals far in
excess of the refractory period of the nerve fibers.
Sorensen (1959) investigated the forward masking effects
in guinea pigs using a low level (40 dB SPL) 1.0 sec noise
masker preceding a click presented at different levels. Post-
masking recovery functions were found to be dependent on
masker level as well as on probe level. Recovery time in-
creased as the signal-to-noise ratio decreased and ranged from
50 to 600 msec for complete recovery. Results with tonal
makers showed a much smaller effect than the white noise
makers and no significant differences were observed as a
function of masker frequency. Latency changes of N1 were not
reported. Sorensen (1959) suggested two possibilities to
explain the postmasking effects observed for the AP. Either
(1) the decrease in N1 amplitude is due to a decrease in the
number of active nerve fibers while each fiber maintains a
constant firing rate, or (2) the decrease in N1 amplitude is
due to a decrease in firing rate of all the active fibers
while the number of active fibers remains constant.
Peake et al. (1962) recorded AP responses to repetitive
stimuli (clicks and brief noise-bursts) in cats with a wire
electrode near the round window. Following the onset of
the stimulus train, the AP amplitude to successive stimuli
systematically decreased until some steady-state level was
reached. The APs to successive stimuli were observed and
it was found that the amount of decline increased as the
repetition rate increased up to 3000/sec. For rates above
3000/sec (ISI=.33 msec) no stimulus-locked activity could be
detected after the "onset" response. For rates below 5/sec
(ISI=200 msec) there was little change in amplitude for pro-
longed stimulation. The amount of amplitude decline measured
after the steady-state level had been reached was compared
for the different repetition rates and revealed constant
amplitude for rates up to 10/sec and then exponentially decayed
(except for a "bump" between 300 and 800/sec) until no neural
response was observed above a rate of 3000/sec. It was also
observed that for rates between 10 and 50/sec the entire AP
waveform decreased in amplitude without any change of N1
latency. Between rates of 50 and 300/sec there was a continued
decrease in amplitude as well as a change in latency of the
components later than N1. Above rates of 300/sec interpretation
was difficult because of response overlapping. Huang and
Buchwald (1980), recording from the auditory nerve and
cochlear nucleus using repetitive tone-bursts, found that
evoked potential decrements were parallel at the two loca-
tions. A complex interaction of repetition rate and stimulus
duration was reported and was determined to be due to the
intertone interval. For intertone intervals greater than
100 msec, evoked potential decrements were not observed
regardless of stimulus duration and repetition rate.
In a series of articles, Coats (1964a,b, 1967, 1971)
described the time courses of AP recovery following tonal
and white noise makers in cats for different masker durations,
masker intensities, and probe-click intensities. The shortest
AT measured was 50 msec. Increasing the masker duration from
.3 to 3.3 sec resulted in a decrease in the AP recovery rate
(longer recovery with longer duration). Changing the duration
of the masker was found not to have any effect on the masked
AP amplitude under simultaneous masking conditions; therefore,
the "masking duration effect" acted only to slow the rate of
recovery following the masker. Increasing masker intensity
was shown to increase the amount of AP depression (amplitude
reduction), but the recovery functions had parallel time
courses until AP amplitudes were above 80% of control. In
addition, Coats reported that the maskerr duration effect"
was minimal for masker intensities below 50 dB SPL and in-
creased as a function of masker level above 50 dB SPL. In
contrast to the maskerr duration effect," the maskerr
intensity effect" was related to decreasing the AP amplitude,
but had no effect on the rate of recovery. Varying click
intensity was similar to the effect of changing masker in-
tensity on the amplitude of the AP. The latency of N1 was
found to change only slightly under the forward masking
conditions.
Kupperman (1971) found a close comparison between human
and guinea pig AP depression as a function of click repetition
rate except that the amount of amplitude reduction was less
pronounced in humans.
Yoshie (1968) investigated changes in N1 amplitude as a
function of repetition rate in humans using a needle electrode
inserted into the wall of the external ear canal. The clicks
were presented at 70 dB sensation level for rates of 1-200/sec.
Averaged steady-state amplitude remained unchanged up to
rates of 10/sec. A monotonic decline in amplitude was found
for rates above 10/sec, but the latency of N1 and the wave-
form configuration remained unchanged. Using a paired-click
paradigm, Yoshie (1968) measured AP amplitude as a function
of ISI and found that full recovery occurred after 100 msec,
which corresponded to the critical value found in the rate
function (10/sec). Yoshie and Ohashi (1971) compared normal
AP responses to click-trains to those obtained from a
patient having bilateral acoustic neuromas, moderate
sensorineural hearing loss, abnormal tone decay, and poor
speech discrimination. For the normal subjects, the ampli-
tude decrease across time was very rapid over the first
10-20 msec of the click-train followed by a more gradual
decrease. The amount of amplitude decline increased as ISI
decreased. In contrast, the patient showed a slower initial
amplitude decline and continued to decline over a longer time
period, up to 100 msec, i.e., no clear distinction could be
made between the early rapid decline and the later slower
decline as was seen in the normals. The locus of the abnormal
AP responses to the repetitive stimuli could not be estab-
lished, however, the authors suggest that the abnormal AP
decrement could be due to a mechanism of sensory cell-nerve
fiber synapse reflecting sensory cell damage as well as
properties of the nerve fibers.
Eggermont and his coworkers (Spoor, 1965; Eggermont and
Spoor, 1973a,b; Eggermont and Odenthal, 1974a; Spoor et al.,
1976) have provided an extensive description of forward mask-
ing effects on the AP using noise makers, stimulus-trains,
and repetition rates. They used 4000 and 6000 Hz tone-bursts
as the probe stimuli. The recovery functions under all three
conditions followed an exponential time course. Changes
were observed both in N1 latency and amplitude as a function
of repetition rate and as a function of AT; however, the
recovery took longer in the noise masking case due to the
duration effect (Coats, 1964a). Following the 500 msec
noise masker, the N1 amplitude reached full recovery after
250 msec in guinea pigs while the latency was fully recovered
by 64 msec. Masker levels below 60 dB SPL produced lesser
amounts of AP decrement at masker offset, but the slope of
the recovery functions became less steep as masker intensity
decreased. For masker levels above 70 dB SPL, the time for
full recovery increased to values beyond 250 msec. In addi-
tion, it was shown that N1 recovery was about 4 times longer
(up to 1000 msec) in man than in guinea pigs using the same
procedure. This was suggested to be due to different proper-
ties at the hair cell-nerve fiber synapse between the two
species. These authors also suggested that the forward mask-
ing effects of the AP are caused by adaptation properties
of each active individual nerve fiber resulting in a reduction
in discharge rate. The adaptation, in turn, allows spon-
taneous desynchronizing factors (synapse or membrane noise)
to contribute to the latency distribution function (Goldstein
and Kiang, 1958) and produce an increase in latency (because
of a broadening) and a decrease in N1 amplitude. The number
of potentially active nerve fibers remains the same and is
determined by the stimulus intensity and frequency. These
authors further suggest that the N1 recovery curve can only
be influenced by the refractory properties of the auditory
nerve fibers up to about 20 msec. For longer times, the
postmasking effects are primarily due to adaptation mechanisms.
Charlet de Sauvage and Aran (1976) investigated AP
responses to click-trains in normal adults and in patients
with various sensorineural hearing abnormalities. They used
a train of 5 clicks with an ISI of 8.5 msec and 100 msec
between click-trains. Only amplitudes were measured since,
in contrast to Eggermont and coworkers, they did not observe
any N1 latency shifts for the responses. (They attributed
this difference perhaps to the fact that clicks were used
instead of tone-bursts which were used by Eggermont and
coworkers.) Charlet de Sauvage and Aran (1976) showed that
AP decrements were most pronounced when the click-trains were
at 60 dB Hearing Level (HL), corresponding to the "knee" of
the input-output function. These authors suggested that if
the response amplitude of the 4th click is greater than 76%
or less than 36% of the response to the 1st click this should
be considered abnormal; however, they found that whenever
the response decrement was abnormal it was to the side of
being greater than 76% of the first click, i.e., less re-
sponse decrement. Response decrement of the click-trains
was found to be significantly different from normal only for
dissociated and recruiting ears. These authors suggested
that in those pathological ears which showed abnormal response
decrements there were, primarily, outer hair cell losses.
Since normals showed a much larger response decrement and the
decrement was maximal at 60 dB (the hypothetical point of
changeover from outer hair cell to inner hair cell response)
the pathological ears were apparently missing this mechanism.
In summary, it appears that a (simple) sound can clearly
affect the normal AP response to a following sound in a fairly
dramatic manner, i.e., a significant reduction in response
amplitude occurs for temporal intervals at least up to 100
msec. The effect on N1 latency is not entirely agreed upon.
The extended masking effects occur for temporal intervals
far in excess of refractory mechanisms. Recovery functions
at the underlying single fiber level closely parallel those
of N1 and provide evidence that a reduction in firing rate
of each individual fiber following a normal adaptation process
is a basic mechanism of forward masking at this level of the
auditory system. Since the AP is a population response, one
must consider that the sum total of the contributing single
fibers may be manifested in the AP in a complex fashion.
In addition, one cannot rule out the possibility that a re-
duction in number of nerve fibers plays a role in the
observed effects on the AP under forward masking conditions.
The source of the forward masking effects is not known; how-
ever, it is most likely related to a transduction mechanism
at the hair cell-nerve fiber synapse, and this basic normal
mechanism may be deficient in certain pathologic cases.
General Description of the ABR
The auditory brainstem response (ABR) was first described
by Sohmer and Feinmesser (1967) who observed a series of
potentials following N1 when recording from the external ear
canal and attributed them to brainstem sources. Soon after,
Jewett (1969, 1970),recording in cats, observed four positive
waves occurring between 2-7 msec following a click stimulus.
By simultaneously recording at various brainstem locations,
wave 1 was found to be synchronous with the auditory nerve
and wave 2 to activity of the cochlear nucleus. Regions
corresponding to waves 2 through 5 were found to have fast
and slow components, and since the slow components have longer
latencies, they could add to the activity from higher auditory
centers. Nevertheless, wave 3 was attributed primarily to
the superior olivary complex, wave 4 between the lateral
lemniscus and the inferior colliculus, and wave 5 to the in-
ferior colliculus. Similar conclusions were found by Buchwald
and Huang (1975), Huang and Buchwald (1977), and Achor and
Starr (1980) using ablation and depth recording techniques
in cats. Starr and Hamilton (1976) recorded ABRs in human
patients with confirmed brainstem pathologies and their
results indicated ABR sources which were in agreement with
those of previous investigators.
The most prominent and stable wave of the ABR is wave V,
which is the current wave of interest in most auditory in-
vestigations of the ABR. In response to a click at high
intensities, wave V shows a characteristic latency between
5.2 and 6.2 msec and can be reliably recorded from the
same subject over time (Jewett and Williston, 1971; Picton
et al., 1974; Starr and Achor, 1975). Schulman-Galambos and
Galambos (1975), Hecox and Galambos (1974), Salamy et al.
(1978), and Despland and Galambos (1980) demonstrated that
wave V was present by 30 weeks gestational age and that the
latency of wave V decreased with infant maturation until the
age of 12-18 months, at which time wave V latency was the
same as adult values. The ABR has also been shown to be
independent of level of consciousness or stage of sleep
(Amadeo and Shagass, 1973; Picton and Hillyard, 1974; Uziel
and Benezech, 1978) or levels of anesthesia (Starr, Hamilton,
and Achor, 1974; Gerull, Biesen, Mrowinski and Rudulph, 1974;
Bobbin, May and Lemoine, 1979).
Amplitude measures of the ABR have not been reported as
often as have the latencies of the waves. Amplitudes of the
ABR are very small (nanovolt range) and most investigators
have shown a large variability across subjects and within the
same subjects (Picton et al., 1974; Starr and Achor, 1975;
Rowe, 1978; Chiappa et al., 1979).
Investigation of the ABR centers, primarily, on the
relation of the latencies (especially wave V) to different
stimulus variables, e.g., the latency of wave V has been shown
to systematically decrease as the stimulus intensity is in-
creased. Stimulus frequency (Davis, 1976; Klein and Teas,
1978; Coats et al., 1979) and repetition rate (Jewett and
Williston, 1971; Pratt and Sohmer, 1976; Harkins et al., 1979)
also affect the ABR. The extent that the various ABR com-
ponents reflect activity occurring at the periphery is an
interesting question. This is extremely important if one
expects to use, say wave V, to approximate behavioral audio-
grams. The suggestion that wave V is closely linked to the
synchronous volley of nerve impulses occurring at the
periphery, except displaced in time has been made by some in-
vestigators (Davis, 1976; Elberling, 1976a;Klein and Teas,
1978; Kramer and Teas, 1979). However, some evidence exists
which indicates that wave V behaves differently than N1
under certain conditions, e.g., as a function of stimulus fre-
quency, repetition rate, or types of hearing loss (Thornton
and Coleman, 1975; Pratt and Sohmer, 1976; Kevanishvilli and
Lagidze, 1979; Coats et al., 1979; Kramer and Teas, 1979).
Certainly, peripheral activity serves as input to the brainstem
and therefore different contributing response areas along
the cochlear partition will produce different inputs. The
frequency specificity of wave V should be influenced by
the changing spatial distribution of N1. To more closely
partition out various spatial (and frequency) distributions,
high-pass masking has also been applied to the ABR and results
have indicated a close correspondence of wave V and N1
latency across frequency region (Don and Eggermont, 1978;
Kramer and Teas, 1979). However, the amplitude of wave V
remained fairly stable across frequency regions while N1
amplitude decreased for lower frequency regions (Don and
Eggermont, 1978; Parker and Thornton, 1978).
The relation between stimulus variables and latency is
precise enough to make the ABR useful for accurate
estimations of auditory thresholds (Davis, 1976; Galambos
and Hecox, 1977; Pratt and Sohmer, 1976), for evaluation of
auditory function in infants (Despland and Galambos, 1980),
and in the evaluation of neurological disorders (Stockard
and Rossiter, 1977; Starr and Achor, 1975; Stockard, Rossiter,
Wiederholt, and Kobayashi, 1976; Robinson and Rudge, 1977;
Stockard, Stockard, and Sharbrough, 1977; Shanon, Gold,
Himmelfarb, and Carasso, 1979; House and Brackman, 1979).
Forward Masking of the Auditory
Brainstem Response (ABR)
Interest in the effect of temporally related stimuli on
the ABR has been restricted to repetition rate or stimulus-
train paradigms. Generally, the concern has been for identify-
ing a repetition rate most applicable for routine clinical
testing, i.e., establishing a repetition rate that provides
a clear and stable response within the shortest time period.
Only recently have the effects of repetition rate per se been
quantitatively investigated in terms of assessing a dynamic
property of the brainstem pathways, with the implication
that certain disease states may cause a failure in adequate
conduction of impulses when driven at high repetition rates.
Jewett and Williston (1971) first demonstrated the
effect of click repetition rate on the ABR in normal hearing
adults. They reported that wave V showed no amplitude or
latency shifts as repetition rate increased from 2.5 to
50/sec, while earlier peaks were severely reduced in ampli-
tude, but showed no latency shifts. Wave V amplitude was
even shown to increase slightly at the higher repetition
rates. It was suggested that wave V could be a useful candi-
date for clinical measures since faster repetition rates could
be employed without affecting the amplitude of the response.
Picton et al. (1974) confirmed the findings of Jewett and
Williston (1971) for click repetition rates up to 60/sec.
Terkildsen, Osterhammel, and Huis in't Veld (1975) re-
corded ABRs in normal adults using tone-bursts (1,2,5 kHz)
at repetition rates of 5-40/sec. They found equal increases
in latency for waves I and V, but the amplitude of wave V
remained stable for the higher repetition rates while wave
I's amplitude was significantly reduced even at a repetition
rate of 10/sec. The effects of repetition rate were found
to be independent of tone-burst frequency. These authors
interpreted their findings as evidence for longer lasting
unit responses at the source of wave V, making wave V less
susceptible to desynchronizing factors.
A click-train paradigm was used by Thornton and Coleman
(1975) where ABRs were recorded to each click in the train
for ISIs of 15, 24, and 32.5 msec. These authors found that
the amplitude and latency changes of all the waves were
nearly complete by the 4th or 5th stimulus and the amount of
amplitude reduction increased with decreasing ISI and de-
creasing stimulus intensity. Wave V was found to show the
least amount of amplitude reduction compared to the earlier
waves. In addition, Thornton and Coleman (1975) reported that
the latency increases were smaller for the smaller amplitude
reductions, i.e., wave V showed the smallest latency increase
and wave I showed the largest latency increase. Thornton
and Coleman (1975) suggested that the decrement in wave I
amplitude is due to a reduction in firing rate of all active
nerve fibers while the number of nerve fibers remains con-
stant. In the brainstem, the reduced firing rate of incoming
fibers resultsin fewer responding cells because some cells
may not reach an adequate threshold level. This should re-
sult in amplitude decrements at each brainstem level parallel
with (or greater than) wave I. However, the amplitude
decrements become less at more rostral brainstem levels be-
cause of an increasing number of fibers and complex inter-
connections at each successive stage which results in a smaller
number of adapted outgoing fibers than the number of adapted
fibers at the input.
Pratt and Sohmer (1976) found, in humans, that as
click rate increased from 5 to 80/sec wave I amplitude
was significantly reduced, but showed no latency change,
and wave V latency increased, but showed only small ampli-
tude changes. The latency change of each wave was found to
be greater than the wave preceding it (accumulative). These
authors suggested that each wave is influenced by preceding
waves and "at a particular nucleus a smaller number of in-
coming fibers would be active and their synapses less effec-
tive, so that it would take longer for the excitatory
synaptic potential to reach the threshold of firing of
outgoing fibers" (p. 90). The amplitudes of later waves
remain stable because of increasing number of neurons
at higher levels which receive input from a smaller number
of lower-order fibers (divergence) as well as each higher-
order neuron receiving many endings from lower-order fibers
(convergence).
Don, Allen, and Starr (1977) studied the latency shift
of wave V in normal adults using click repetition rates of
10, 30, 50, and 100/sec at levels up to 60 dB HL and found
significant latency increases (up to 0.9 msec) for repetition
rates from 10 to 100/sec. This latency shift was found to
be equivalent to a 15-20 dB reduction in the stimulus level
and these authors felt that repetition rate should be con-
sidered carefully in interpreting response latencies. These
authors described the latency shifts as a linear function of
repetition rate, which they point out as being different
from the exponential shift of the AP latency found by Egger-
mont and coworkers. The different behavior of wave V compared
to N1 of the AP was interpreted by Don et al. (1977) to
possibly suggest different peripheral and central responsive-
ness to repetitive stimuli due to adaptation mechanisms along
the monaural pathway. However, Don et al. (1977) felt that
the locus of the wave V effects was at the auditory periphery.
Unfortunately, the resolution of waves I-IV was not clear
enough in the study of Don et al. (1977) to make any direct
comparisons of peripheral and central effects. The latency
increases with repetition rate were also found to be inde-
pendent of stimulus intensity. In another part of the same
study, Don et al. (1977) used click-trains with ISIs of 10
msec and demonstrated that the latency shift of wave V was
complete by the 5th stimulus. No latency shift of wave V
was observed in the click-train experiment when the ISI was
100 msec. A binaural central mechanism was ruled out in a
third experiment where they found no latency change to the 1st
and 20th click presented to the ipsilateral ear while the
2nd through 19th click were presented to the contralateral
ear (ISI=10 msec).
As the above studies show, there does not appear to be
complete agreement on the effects of increasing repetition
rate for the various components of the ABR. The effects of
click repetition rate on the ABR in normal adults have been
extensively studied by several other investigators for
repetition rates ranging from 2/sec to 100/sec (Pratt and
Sohmer, 1976; Zollner, Karnahl, and Stange, 1976; Hyde,
Stephens, and Thornton, 1976; Klein and Teas, 1978; Harkins,
McEvoy, and Scott, 1979; Martin, 1976; Weber and Fujikawa,
1977; Scott and Harkins, 1978; Chiappa, Gladstone, and Young,
1979). In general, the majority of these studies have shown
that the greatest effect of increasing click repetition rate
has been a large reduction of wave I amplitude and a sub-
stantial (up to about 0.9 msec) latency increase of wave V.
In contrast to the study by Don et al. (1977), most studies
describe the latency change of wave V as being a logrithmic
function of repetition rate. In contrast to Thornton and
Coleman's (1975) click-train study, most investigators report
that wave I latency does not increase or increases only
slightly at the higher repetition rate. Most investigators
agree that there is a cumulative latency increase for
successive peaks after wave I as a function of repetition
rate, suggesting that the latencies of successive waves are
influenced by the preceding wave. In contrast to Don et al.
(1977) and Thornton and Coleman (1975), the studies by
Zollner et al. (1976) and by Weber and Fujikawa (1977) have
shown that the effects of repetition rate are dependent on
stimulus intensity, i.e., greater effect at higher inten-
sities. The relatively large wave V at higher repetition
rates has enhanced the popularity of using wave V for ob-
jective clinical audiometry. However, as suggested by Zollner
et al. (1976), the examination of the waves earlier than
wave V, especially wave I, as a function of repetition rate
may be a more useful indicator of inner ear damage.
Bauer, Elmasian, and Galambos (1975) compared the
psychophysical loudness judgements with human ABRs for the.
second of two 0.2 msec 8 kHz tone-bursts separated by intervals
ranging from 100-400 msec. The psychophysical results showed
the expected "loudness enhancement" for some of the conditions
above 15 dB, but wave V latencies and amplitudes were not
affected under any of the conditions. The total response
power of the ABR was reduced which indicated a decrease in
the amplitude of the waves earlier than wave V since wave V
voltage was not altered (and loudness was enhanced).
These results suggest that the ABR does not correspond to
perceived loudness under certain conditions.
Kodera et al. (1978) compared the effects of repetition
rate on the ABR and the middle latency components using 500
and 1000 Hz tone-pips in order to determine which response
would be more suitable in routine clinical testing. It was
observed that as ISI decreased from 104 to 32 msec the
middle conponent's amplitude decreased significantly, while
wave V was not appreciably affected except for a slight
increase in amplitude at ISI=32 msec due to superpositioning
of responses from preceding stimuli. Latency increases were
found only for wave V as ISI decreased.
Huang and Buchwald (1980), on the other hand, showed
that in cats the amplitude of the later ABR waves (P3, P4)
decreased by the same amount as the earlier waves (PI, P2)
when repetition rate was increased. The amplitude de-
crease was gradual up to a repetition rate of 20/sec
then decreased sharply for rates up to 200/sec. All waves
showed a slight (0.1 msec) latency increase as repetition rate
was increased from 50 to 200/sec. Increasing the stimulus
duration beyond 10 msec caused an interaction with repetition
rate, i.e., using 100 msec tone-bursts at a rate of 10/sec
produced a larger amplitude reduction than seen for the
short duration stimuli at 10/sec. Duration-rate inter-
actions have also been shown to affect the wave V amplitude
in humans (Hecox et al., 1976).
In monkeys, Allen and Starr (1978) found no latency
shift of wave I, a significant (p < .05) latency shift of .1
msec for wave II, and 0.4 msec in wave IV (comparable to
wave V in humans) between click repetition rates of 10 and
100/sec. Significant interaction was found between rate and
stimulus intensity, i.e., at higher intensities wave IV
showed larger latency increases with increasing repetition
rate.
Kevanishvilli and Lagidze (1979) used a response con-
ditioning paradigm to study the temporal effects on the ABR
in humans. The conditioning click and the test click were
separated by ATs of 5 or 10 msec. By subtracting the re-
sponse to the conditioning click from the response to the
conditioning click-plus-test click, the contamination by
middle latency components and postauricular potentials was
eliminated. Their results showed, for a AT of 10 msec, that
wave I was significantly reduced in amplitude while wave V
was not affected. The latency changes of wave I and V were
the same. For AT=5 msec, wave V latency increased much more
than wave I latency. These authors attributed their find-
ings to peripheral desynchronizing factors which have
different effects on various waves depending on the durations
of neural contributions to each wave, i.e., wave V shows less
amplitude decrease because of its relatively longer response
component which makes it less susceptable to desynchroniza-
tion.
The effects of repetition rate on the ABR as a function
of age were first reported by Jewett and Romano (1972) for cats
and rats during the first 2-3 months of life. Young kittens
were found to be different from adult cats and young rat
pups in that the kittens did not show any responses to 100/sec
clicks until several days after ABRs were detectable at slower
repetition rates. Soon after 100/sec responses could be ob-
tained in the kittens (about 16 days old) subsequent stimula-
tion with clicks at 10/sec resulted in a lack of response
for several minutes, i.e., there was a "fatigability" factor
in the young kittens. For the rat pups and older cats,
stimulation at 100/sec produced decreased amplitude and in-
creased latency, which the authors suggested was due to some
manifestation of a "recovery cycle."
In humans, the effects of repetition rate on the ABR as
a function of age have not been firmly established. Fujikawa
and Weber (1977) compared wave V latency shifts as a function
of repetition rate in populations of 7-8 week old infants,
young adults, and geriatrics. All groups showed a latency
shift of wave V as repetition rate was changed from 33-67/sec,
and the amount of latency shift for the young adults and in-
fants was the same except for 67/sec where the infants showed
a greater latency shift. In contrast, the geriatric group
showed considerably longer wave V latencies than the adults
and infants at all the rates tested. The different behavior
of the geriatrics was attributed to a possible reduction in
the number of nerve fibers and/or cell count, whereas the
different behavior of the infants (at the highest rate) may
reflect a myelination factor. Salamy et al. (1978), on
the other hand, found that for infants from birth to 6 months
of age, the effects of increasing click repetition rate
from 10-80/sec (decreased amplitude of earlier waves and
increased latency of wave V) was not significantly different
from adults except for the newborns (24-27 hours). This
finding suggested that the mechanisms responsible for rate
effects are mature very shortly after birth. Despland and
Galambos (1980) found that responses to clicks up to 80/sec
could be measured in premature infants above 30 weeks
gestational age and that the latency shifts of wave V as a
function of repetition rate decreased with age from 270 usec
for each 10/sec increase in rate at the earliest age, down
to about 35 usec for each 10/sec increase in rate found in
adults. Wave I was also found to increase in latency as a
function of repetition rate; however, the amount of latency
shift was about one-half that seen for wave V. The rate
function of wave I across age paralleled wave V. These
authors state that one-half of the rate effects occur at
the periphery and one-half in the brainstem.
The effects of repetition rate on the ABR in clinical
patients have also not been extensively studied. Stressing
the system by increasing repetition rates (or other tem-
porally related stimuli) could be useful for differentiating
certain central brainstem pathologies. Stockard and Rossiter
(1977) and Stockard, Stockard, and Sharbrough (1977) found
that in patients with multiple sclerosis, a demyelinating
disease of the central nervous system, the ABRs to clicks at
10/sec were abnormal in all of them and showed increased
latency and/or reduced amplitude of various waves. Increasing
the repetition rate to 25-30/sec enhanced the sensitivity of
the test, i.e., greater response abnormality was found in
the patients with multiple sclerosis than could be accounted
for by the normal rate dependent changes. Since all the
patients had confirmed multiple sclerosis and all showed
abnormal responses at the 10/sec rate, there did not appear
to be any additional information obtained from the higher
repetition rate. Robinson and Rudge (1977), however, did
find that recording the ABR at high repetition rates was
useful in detecting and confirming patients with multiple
sclerosis. A unique procedure was used by Robinson and
Rudge (1977) for stressing the auditory system. The ABRs
were recorded to the first of a pair of clicks separated by
5 msec. In normals, when the pairs of clicks were presented
at a rate of 2.5/sec the latencies and amplitudes of all the
waves were the same as to a single click. When the pairs
of clicks were presented at a rate of 20/sec the response to
the first click showed significant increases in latencies of
waves I, III, and V, but wave I latency did not change
(changing repetition rate of single clicks from 2.5 to 20/sec
showed an increase in wave III latency only). Using this
paired-click paradigm presented at 20/sec in patients with
multiple sclerosis, Robinson and Rudge (1977) found that 55%
of those patients who had abnormal latencies to single clicks
and 57% of those patients who had abnormal amplitudes to
single clicks (and normal latency) showed an abnormal increase
in wave V latency to the paired-clicks. More importantly,
three patients who had normal ABRs to single clicks showed
either an abnormal increase in wave V latency or no response
at all to the first click of the pair. These authors suggest
that stressing the auditory system by combining paired-clicks
with a high rate of presentation (when either alone produced
no change) can reveal changes in the ABR which can be a
useful indicator of patients with unconfirmed or suspected
multiple sclerosis, even when normal ABRs or normal latencies
with reduced amplitudes are found to single clicks (20/sec).
In summary, the effects of preceding sounds on the ABR
response to another sound have been shown not to simply
parallel those changes that occur for the AP response. The
most obvious difference has been a stability of wave V ampli-
tude concomitant with a large increase in wave V latency,
whereas N1 has shown large amplitude reductions with only
slight latency changes. These differential manifestations
to repetitive stimuli at two levels of the auditory system
preclude the simple assumption that the perception of one
sound preceded by another sound is entirely due to peripheral
mechanisms which are "relayed" unchanged to higher centers.
Because ABRs do not always produce clear and stable waves
earlier than wave V, comparisons between waves are often
difficult to make. By simultaneously recording auditory
46
nerve activity from the ear canal, more direct comparisons
can be made. Further investigation of the effects of
temporally related sounds at different levels of the auditory
system appears warranted. Once the normal characteristics
are known more fully, application to clinical populations
may have more success in understanding normal auditory pro-
cessing.
CHAPTER II
METHODS
Click-evoked ABRs and APs were recorded using a forward
masking paradigm for delay times (AT) of 0 to 100 msec.
Responses obtained, as a function of AT, following a 60 msec
wide-band masker (.02-10 kHz) set at a level sufficient to
"fully" mask wave V of the ABR (AT=0 msec) are called the
"standard" series. In addition to the "standard" series,
responses were obtained (as a function of AT) for variations
of masker duration, masker level, and masker low frequency
cutoff.
Subjects
Fifteen normal hearing (ANSI, 1969) adults, 23-33 years
of age, served as volunteer subjects. All 15 subjects
received the "standard" series. For each variation in
masker, i.e., duration, level, or low frequency cutoff, 7
subjects were used. Six subjects were willing to return for
a second recording session, providing data for two different
variations of masker.
Equipment
Stimuli
The probe stimuli were 0.1 msec broadband clicks
generated by a shift-register pulse output with the duration
of the clicks controlled by a precision one-shot (logic
level). Intensity calibration for the probe clicks was based
on standard reference levels which have been in use at this
laboratory for the past 5 years. These levels were obtained
by determining the behavioral threshold to the clicks presented
at a repetition rate of 5/sec for a group of normal hearing
listeners. This was considered 0 dB HL (Hearing Level) to
which other intensity levelsware referenced. Calibration
levels were determined by measuring the voltage (and converting
to dB SPL) of the clicks at 60 dB HL presented at a repetition
rate of 250/sec on a true RMS voltmeter (Ballantine, 320).
Corresponding peak-to-peak voltage was measured on an oscillo-
scope (Tektronix, RM561A). Calibration levels for the 60 dB
HL broadband clicks were 72 dB SPL and .07 volts peak-to-peak.
An attenuator (Hewlett-Packard, 350D) provided control of the
click level as measured on the true RMS voltmeter. For this
investigation, the probe click intensity level was always
set at 50 dB HL.
The masker stimuli were obtained from a random noise
generator (Grason-Stadler, 455C). The duration of the noise,
onset-to-offset, was determined by another precision one-
shot and shaped by an electronic switch to produce nonlinear
rise-fall times of 10 msec. An attenuator (Hewlett-Packard,
350D) independently controlled the intensity of the noise
masker. The bandwidth of the noise was produced by feeding
the white-noise output of the noise generator into two
variable bandpass filter networks (Rockland, 816) wired in
series. Each bandpass filter had a rolloff of 48 dB/octave
with a resultant rolloff of 96 dB/octave. The high frequency
cutoff was always set at 10 kHz. The low frequency setting
of the noise could be changed to produce the desired makers,
e.g., .02-10 (referred to a wide-band), 2-10, 4-10, and 6-10
kHz. The frequency characteristics of the earphone (TDH-39)
produced additional filtering of the signals. The acoustic
outputs were measured in a standard 6-cc coupler with a
condenser microphone (Bruel and Kjaer, 4132) connected to a
sound level meter (Bruel and Kjaer, 2203). Spectral analysis
was performed by a software Fast Fourier Transform (FFT)
program. The noise spectra and earphone characteristics
are shown in Fig. 1.
A block diagram of the stimulus generation and masker-
probe timing relation are given in Fig. 2. To produce the
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forward masking paradigm, the click delay relative to the
masker was varied by another precision one-shot. The
delay time from the masker offset to the click onset was
defined as AT. The values of AT used were 0, 6.2, 12.5,
25, 50, 100 msec. These were determined by observation on
the oscilloscope display and setting of the one-shot. A
synch pulse (97 usec) to the computer was initiated at the
probe click onset. The masker-probe pairs were presented at
a repetition rate of 4/sec which resulted in an intermasker
interval (IMI), i.e., time between offset of one masker
and onset of subsequent masker, of 190 msec. For the series
where masker duration was varied, the repetition rate remained
constant (4/sec) resulting in different IMIs for each duration.
For the maximum AT (100 msec), the following masker occurred
90 msec later. This reduced any possible backward masking
effects. The probe and makers were fed sequentially to a
mixer, an amplifier (James B. Lansing, SE 400S), a final
attenuator (Hewlett-Packard, 350D), and then monaurally
presented through the earphone. The equipment allowed for
the presentation of the signal or noise separately or the
signal presented with (after) the noise. The signal and noise
levels could be varied independently or simultaneously.
Electrodes
Three silver/silver chloride scalp electrodes were used
for the ABR recordings. The electrical activity was recorded
between forehead and ipsilateral mastoid with the contra-
lateral mastoid serving as ground. The electrode sites were
abraded with electrode paste (Grass, EC-2) then taped to the
forehead and mastoids. Electrode resistance was checked with
a VOM meter and the electrodes were reattached if the resis-
tance was greater than 5 k Ohms.
The ear canal recording required a specially made elec-
trode. This was made of 6 inches of teflon coated silver
wire (diameter=.007 inches). The teflon was scraped off the
end and the stripped end of the wire then wrapped around the
end of a narrow (1/8th inch) piece of polyurethane surgical
rubber rubing (about 3/4 inch long). The tubing was then
bent in a "V" before inserting into the ear canal. After
the electrode was positioned inferiorly in the ear canal,
with the aid of an otoscope, earlight, and forceps, the tubing
was released so that it opened slightly to hold itself in
place against the walls of the ear canal. Good responses
were obtained only when the wire wrapped end of the ear canal
electrode was in contact with the canal wall. If poor re-
cordings were obtained the ear canal electrode was repositioned,
but if poor responses were still obtained after one or two
attempts at repositioning no further attempts were made and
ear canal recordings were not obtained. The reference
electrode for the ear canal recordings was the ipsilateral
mastoid and the ground was the contralateral mastoid.
Procedures
The subject laid on a bed in a sound treated room (IAC).
Two recording channels were used for independent monitoring
of the ABR and the AP. Each electrode configuration was
connected to a separate high-impedance cathode follower
(Grass, HIP 511E) and then to separate a.c. coupler high-
gain preamplifiers (Grass, P511). The gain of the amplifier
was set at 100,000 and bandpassed at 0.03-3 kHz.
The electrical activity from the ABR and ear canal
electrodes was recorded on separate channels of an FM tape
recorder (Ampex, FR 100A) bandpassed at 0-2500 Hz at 7 1/2
i.p.s. and kept for later off-line processing. Additional
response filtering (Krohn-Hite, 330M) was done ahead of the
computer with a bandpass of 70-1600 Hz. The subject's
electrical brain activity was also monitored on the oscillo-
scope. A general purpose computer (Digital Equipment,
PDP-8e) was used for the response averaging. Each response
represented the averaged stimulus-locked activity for 1200-1500
samples. A sweep duration of 10.0 msec (39 usec/point, 256
points) was used for the ear canal response. For the ABR,
a sweep duration of 20.2 msec (79 usec/point, 256 points)
was used. A toggle switch allowed processing of either the
ABR or the AP activity. However, after determining whether
or not the ear canal electrode was working properly, only
the ABR was monitored on-line and the averaged ABRs were
stored directly on floppy disks. The AP responses from the
ear canal were played back later off the FM tape and then
stored on the floppy disks. A feature of the averaging pro-
gram was variable artifact rejection, which was set by two
independent cursor lines. In these experiments, electrical
activity greater than 7 pvolts was rejected from the average
by the computer. This criterion excluded unwanted muscle or
movement artifacts from the averaged response.
In off-line processing, latencies and peak-to-peak ampli-
tudes were obtained by means of a cursor which could be set
at any location in the waveform and read from the monitor
display.
Each session began with the "standard" series which con-
sisted of a 60 msec wide-band (0.2-10 kHz) noise masker pre-
ceding the broadband probe click (50 dB HL). The level of
the wide-band masker was set (and measured) so that, with a
AT of 0 msec, the wave V response was as fully masked as
possible (not discernible in the averaged response). The
"standard" recovery function was obtained by recording the
probe responses for the different ATs. Following the
"standard" series, the subject received one of the following
series:
1. Masker duration was changed to 30 and then 120
msec and responses were recorded for each AT.
2. Masker level was changed -10 dB and then +10 dB
relative to the "standard" series and responses
were recorded for each AT.
3. The low frequency cutoff of the high-passed
masker (60 msec duration) was systematically
raised while maintaining a constant spectral
level set by the "standard" series. For each
of the makers 2-10, 4-10, and 6-10 kHz,
responses were recorded for each AT.
CHAPTER III
RESULTS
Auditory Brainstem Responses (ABRs) were collected on
a group of 15 normal hearing adults. In addition, whole-
nerve action potentials (APs) were simultaneously recorded
from some of the subjects. Using a forward masking paradigm,
responses were recorded only for the probe click. Not all
recording sessions produced usable AP data because of either
an inability to obtain proper placement of the ear canal
electrode after repeated attempts or the subject decided
against the use of the ear canal electrode. Out of 17 re-
cording sessions where an ear canal electrode was attempted,
9 produced usable AP data. One reason for difficulty with the
ear canal electrode was that the wrapped end often did not
make contact with the canal wall, e.g., the tubing would
"hang up" on a protruding edge of the canal or cerumen. In
addition, if the electrode was not positioned properly on
the first attempt it was difficult to reposition the electrode
(because it sprang open) without causing discomfort to the
subject. If the electrode could not be repositioned easily,
it was removed and only the ABR was collected.
58
Each subject received the "standard" series; 60 msec
wide-band masker set at an intensity level sufficient to
eliminate as completely as possible (fully mask) the wave V
peak of the ABR when .LT=0 msec. Responses to the probe
click were then obtained for each AT. All subjects received
the "standard" series which provide the largest amount of
data and which served as a reference for subsequent variation
of masker parameters. Three subjects (DR, TL, PD) received
two of the additional series, i.e., variation in masker dura-
tion, level, or low frequency cutoff in the same (extra long)
session and two subjects (DS, MO) were used for two of the
additional series on separate days. Table I summarizes the
recording series for each subject and includes whether or not
corresponding ear canal responses were obtained. ABR data as
a function of AT were obtained for 7 subjects for each of the
variations in masker parameter and AP data was obtained for
at least three subjects for each variation in masker.
Examples of the ABR and AP waveforms to the probe click
(50 dB HL) without the presence of the forward masker, i.e.,
unmasked control responses, are shown in Fig. 3. In the ABR
waveforms on the left of Fig. 3 the wave V peak is easily
identifiable in all of the examples. Peaks earlier than
wave V in the ABR can also be seen in some of the control
Table I. Forward masking series received by each of the
subjects (+) indicates success and (-)
indicates failure in obtaining data for ABR/AP.
Masking Condition
High-Pass Masking Masking "Standard"
Subject Masking Duration Level Series
KC +/+ +/+
DS +/+ +/- +/+
DR +/+ +/+ +/+
MO +/+ +/- +/+
TL +/+ +/+ +/+
PD +/- +/- +/-
NK +/- +/- +/-
BK +/+ +/+
KG +/- +/-
MS +/+ +/+
CB +/- +/-
SP +/+ +/+
SL +/- +/-
SW +/+ +/+
GC +/- +/-
Total 7/5 7/3 7/3 15/9
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responses, but are not as easily identifiable in all sub-
jects. Only the wave V peak was systematically measured.
The latencies were measured to the positive wave V peak
just prior to the characteristic sharp negative trough
occurring in the appropriate latency range for this response,
i.e., between 6 and 10 msec. In some instances wave V
appears as a shelf on the positive peak just before the
negative trough, an example of which can be seen for subject
KC in Fig. 3. The peak-to-peak wave V amplitudes were
measured from the wave V peak to the following negative
trough. For the 15 subjects, the mean latency and t 1
standard deviation (S.D.) for the unmasked control wave V is
6.815 .220 msec. The mean peak-to-peak amplitude of the
control wave V is .223 + .067. volts. The AP responses from
the ear canal, shown on the right portion of Fig. 3, corre-
spond to the simultaneously obtained ABRs shown on the left.
The AP shows an initial negative trough (Nl) followed by a
larger positive peak which is generally broader in time than
the N1 trough and has a negative-going dip superimposed on
the positive peak which never goes below baseline in any
of the subjects. There is also considerable variability in
the configuration of the ear canal AP across subjects. Those
subjects with smaller amplitudes have a broader waveform
and a less noticeable negative-going dip on the positive
peak, most likely a result of the relation of the electrode
position to the potential sources. Latency measurements of
the AP are made to the base of the N1 trough. For the
unmasked N1 controls, the mean latency is 2.864 .135 msec.
The peak-to-peak amplitudes are measured from the N1 trough
to the nearest following positive peak. The mean N1 control
amplitude is .461 .200 volts. Considerable intersubject
variability of N1 amplitude was apparent and was primarily
related to the position of the ear canal electrode. Intra-
subject N1 amplitude variability across the recording session
was relatively low. The AP waveforms are similar to those
found by other investigators from the ear canal (Coats, 1964a,
1976; Yoshie, 1968) except for the dominance of the positive
peak following N1 and a poorly defined N2 in the AP waveforms
of this investigation.
Comparisons between the unmasked control and the forward
masked responses are made as a function of the time interval
between masker termination and probe onset (AT) for both
the mean latencasand mean amplitude of wave V and Ni. The
recovery function, defined as the probe response magnitude
(latency or amplitude) as a function of AT, represents the
time course of recovery from forward masking and is described
below for the different masker variables.
"Standard" Recovery Function
The "standard" forward masking series was obtained for
the ABR in all 15 of the subjects and AP data were included
from 9 of the subjects. Only one "standard" series for each
subject was included in the analysis. Masker levels necessary
to "fully mask" wave V (AT=0 msec) ranged from 74 to 82 dB
SPL. Preliminary data on two subjects using a simultaneous
continuous wide-band noise masker resulted in about 8-9 dB
less masker level necessary to fully mask wave V than for
the pulsed (60 msec) masker at AT=0 msec. Leaving the
masker level constant and switching from continuous to pulsed
in the simultaneous presentation maintained the fully masked
condition. The levels of masker necessary to fully mask wave
V were considerably higher than needed to fully mask the N1
response. In fact, it was often difficult to be absolutely
certain when wave V was fully masked because of a seemingly
apparent resistance to masking, especially in a forward mask-
ing paradigm, or because of a relatively more "noisy" base-
line. As the masking noise was added to the recording
paradigm and the intensity raised, the most apparent effect
on wave V was an increase in latency. With additional in-
creases in masker level, the amplitude of wave V diminished.
In some cases, adding 2 or 3 dB of masker caused the wave V
peak to go from almost full amplitude (with longer latency)
to unobservable.
Figure 4 shows typical unmasked controls and forward
masked ABRs along with corresponding AP waveforms for the
"standard" series. The probe-evoked ABRs and APs show
alterations produced by the preceding wide-band masker.
Wave V is easily observed in the masked waveforms and shows
a considerable increase in latency (relative to control)
for short ATs. Wave V amplitude is not severely altered
except at the earliest ATs. In addition, the peaks earlier
than wave V are not clearly identifiable in the masked wave-
forms. (Only 1200-1500 samples were used for the averaged
responses and adding more samples may have improved the clarity
of the earlier peaks.) The N1 latency, on the other hand,
shows only a slight latency shift even for the shortest AT,
but the N1 amplitude is considerably reduced even for the
longest AT.
The "standard" latency recovery function based on the
mean values are plotted in Fig. 5 for wave V, N1, and the
computed latency difference between wave V and N1 (V-N1)
representing the central brainstem conduction time. The
unmasked control (CNTL) values are also included in Fig. 5
and subsequent figures. For wave V (top of Fig. 5), the
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latencies as a function of AT (delay time)
for the "standard" series. Unmasked con-
trols (CNTL) are indicated on the right in
this and subsequent figures.
maximum mean latency shift (increase) occurs at AT=6.2
msec and is 1.288 msec longer than the control latency.
For AT=0 msec, there are no wave V responses because of
the criterion (fully masked. As AT increases, the mean
latency of wave V systematically decreases towards the
control latency. The time course of wave V latency recovery
from forward masking can be described as a linear function
of log AT between the values of AT used in this investi-
gation, i.e., 6.2-100 msec. Although AT values above and
below 100 and 6.2 msec were not included, one may expect
deviations from the logrithmic function for other values of
AT. However, between ATs of 6.2 and 100 msec the equation
LATV = -.92 log AT + 8.867 fits the mean wave V latency
data quite well. For all ATs, the mean masked wave V
latency is greater than the mean control wave V latency.
For the "standard" series, as well as for each of the series
described in following sections for the different masker
variables, an analysis of the data was performed using
Statistical Analysis System (SAS) programs (University of
Florida Computer Center). An analysis of variance appro-
priate for unbalanced data (General Linear Systems, GLM)
was used and included partitioning out the variance due to
subjects as well as the different "treatment" variables. As
expected, for wave V latency for the "standard" series,LT
was found to be highly significant (F=191.24, df=5, 69
p < .001. The unmasked controls were not included in any of
the analyses of variance. In addition, whenever the ampli-
tudes of the responses were not measureable they were assigned
a value of 0 uvolts, but their corresponding latencies were
treated as "missing" in the analyses. An additional analysis
was performed in order to test which of the "treatment" means
are significantly different (p < .05) from the unmasked con-
trol mean, i.e., to determine where complete recovery occurs.
This was done using a paired-comparison procedure based on
least-square means (for unbalanced data) by SAS (LSMEANS/
PDIFF) for each possible comparison. (A Duncan Multiple
Range Test was also included to test for differences among
means (p < .05) and the results were in almost all cases
the same as the results for the LSMEANS test). Table II
gives the means and standard deviations of wave V latency
as a function of L T for the "standard" series. Also in-
cluded in Table II and subsequent tables are indicators
(*) for those masked response means which are significantly
different (p < .05) from the unmasked control response mean.
As Table II shows, wave V latency is significantly different
from control even for-LT=100 msec, i.e., complete recovery
has not occurred.
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The N1 "standard" latency recovery function is shown
in the bottom portion of Fig. 5. As for wave V, the maximum
mean latency shift of N1 occurs at the shortest AT; however,
the amount of maximum N1 latency shift, .444 msec, is only
about one-third that seen for wave V (1.288 msec). The time
course of the N1 latency function, like for wave V, can
also be described as a linear function of log AT between ATs
of 6.2 and 100 msec, but the slope of the N1 recovery func-
tion is much less steep than for wave V. The mean N1 latency
data as a function of AT fit the equation, LATN1 = -.16
log AT + 3.433. For NI, AT is also highly significant
(F=14.44, df=5, 35 p < .001). Table II includes the means
and corresponding statistics for N1 latency as a function
of A T. N1 latency has completely recovered by AT=50 msec.
The V-N1 latency interval (middle portion of Fig. 5)
also changes as a function of AT as expected due to the
longer latency changes of wave V relative to NI. The mean
unmasked V-N1 latency interval is 3.956 t .303 msec and is in
agreement with other investigators (Davis, 1976; Elberling,
1976; Rowe, 1978; Coats et al., 1979). Again, AT is highly
significant (F=14.56, df=5, 35 p< .001). The V-N1 latency
interval is equal to the control latency for ATs of 50 and
100 msec (see Table II).
The amplitude recovery functions, in uvolts, for wave
V and N1 are shown in Fig. 6. Although the variability is
large, there is a systematic increase in amplitude for both
wave V and N1 as -T increases. However, the masked wave V
amplitude is less than the wave V control amplitude only
for ATs below 25 msec, while the masked N1 amplitude is
dramatically reduced at all ATs. To describe the amplitude
recovery functions in another way,the mean amplitudes are
normalized by considering the amplitude of the mean unmasked
response as 100% and the mean amplitudes for the responses
at each LT are then expressed as a percent of the mean
unmasked response (% control amplitude). The percent con-
trol amplitude is used to describe the remainder of the
amplitude recovery functions. Figure 7 shows the amplitude
recovery functions for both wave V and N1 and one can easily
notice the different behavior of the two responses.
For wave V, the amplitude recovery function does not
follow a simple logrithmic function as was seen for the wave
V (and N1) latency recovery functions; however, a monotonic
growth function is apparent across AT. For wave V ampli-
tude, LT was a significant factor (F=8.72, df=5, 69 p < .001).
Wave V amplitude recovers from fully masked to 60% of con-
trol by AT=6.2 msec and has completely recovered (p < .05)
Fig. 6. Mean and l1 S.D. for wave V and N1 amplitude
voltst) as a function of AT for the
"standard" series.
8.40
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8 6 12 25 50 109
DELAY TIME Cmso.)
I-
j 88.8
0 O
81."
I / L
8 6 12 25 5o 1o8
DELAY TIME (msec)
Fig. 7. Mean wave V and N1 amplitude recovery
functions expressed as percent of the
mean unmasked control amplitude (1000%)
for the "standard" series.
by LT=25 msec (even though wave V latency is not recovered
even by ;T=100 msec). The slight supernormality of wave V
amplitude seen in Fig. 7 at LT=100 msec is not significantly
different from the control response. Table III gives the
means and corresponding statistics, as a function of 3T,
for wave V amplitude.
The effect of the forward makers on the amplitudes of
the N1 response was much greater than for wave V amplitudes.
As seen in Fig. 7, the mean amplitude (% control amplitude)
of N1 increases from fully masked to only 18% of the unmasked
control response at LT=6.2 msec and is only 65% of the control
by LT=100 msec. As expected, LT is a highly significant
factor for N1 amplitude (F=20.07, df=5, 37 p < .001). The mean
N1 amplitudes are significantly different from the control
response amplitude for all LTs, i.e., full recovery does
not occur for N1 amplitude by AT=100 msec (even though the
mean N1 latency is equal to control by AT=50 msec). The
N1 amplitude recovery function is less steep than the wave V
amplitude recovery function. Table III gives the summary
data for N1 amplitude along with the wave V data.
Figure 8 shows a summary comparison of wave V and N1
latency and amplitude behavior for the "standard" series
from which the following characteristics can be summarized:
L CN
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1. As AT increases, the latencies and amplitudes
of both wave V and N1 monotonically approach
the control response.
2. The most pronounced effects of the wide-band for-
ward masker are a decrease in the N1 amplitude
and an increase in the wave V latency.
3. The latency of wave V is not completely recovered
to the control response latency by AT=100 msec;
however, the amplitude of wave V is completely
recovered by AT=25 msec.
4. The latency of N1 is completely recovered by
AT=50 msec, but N1 amplitude is not recovered
even by AT=100 msec.
The Effect of Masker Duration
The effects of changing the duration of the wide-band
forward masker on the probe-evoked wave V response were investi-
gated in 7 subjects and comparable N1 data were obtained for 3
of those subjects. The mean values of the probe response
latency and amplitude were computed for each AT for each of
the three masker durations (30, 60, 120 msec). Recall that
changing the masker duration resulted in a change in the
intermasker interval (IMI) since the repetition rate remained
constant. In two of the subjects it was observed that there
were no noticeable differences in the wave V responses between
constant IMI (rate changes) and constant rate (IMI changes).
The effect of keeping IMI constant vs keeping rate constant
was not evaluated for the N1 response.
Figure 9 shows the mean latency recovery functions for
wave V and N1 for masker durations of 30, 60 ("standard"),
and 120 msec. For wave V there is a systematic increase in
the probe response latency as the masker duration increases
and nearly equal shifts of latency are observed at each T.
There is no significant interaction between masker duration
and ~T. Masker duration is a significant factor for wave V
latency (F=24.68, df=2, 85 p <.001); however, only the mean
responses to the 120 msec masker are significantly different
from the responses to the 30 and 60 msec makers. The time for
complete recovery of wave V latency increases with increasing
masker duration. The mean wave V latency is fully recovered
by AT=50 msec following the 30 msec masker, by LT=100 msec
following the 60 msec masker (for this smaller subgroup of
subjects this "standard" series is recovered by LT=100
msec, whereas for the larger group of subjects described
earlier wave V latency had not recovered by AT=100 msec),
and is not fully recovered by AT=100 msec following the 120
msec masker. Table IV gives the summary data for wave V
latency for the different masker durations.
In contrast to the mean wave V latency, the mean N1
latency does not show any significant difference as a function
of masker duration (F=0.00, df=2) and the mean N1 latency
8.5%
o 8.58
5.58
E
1- 4.S5"
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a 3 weC
0 68 uc
+128 asc
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L L/ L L k L.L L h .L I i- I
0 6 12 2Z 58 108 CNTL
DELAY TIME (msec)
Fig. 9. Latency recovery functions for wave V, N1,
and V-N1 probe responses following wide-band
makers with durations of 30, 60, and 120
msec. Level of the masker was set to "fully"
eliminate wave V response at AT=0 following
the 60 msec masker ("standard" series).
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recovery curves are the same for the responses following
all three duration makers (see Fig. 9). For all three
masker durations, it can be observed that the mean N1 probe
response latency increases slightly at the shorter ATs, but
the amount of N1 latency shift is much less than the wave V
latency shift. The mean N1 latency for this group of sub-
jects is fully recovered by.T=25 msec following all three
masker durations. As can be seen in the middle portion of
Fig. 9, the V-N1 latency interval increases with increasing
masker duration; however, the differences due to masker
duration are not significant (F=1.67, df=2). Table IV in-
cludes the summary data for N1 and V-N1 latencies for the
different masker durations.
The mean amplitude recovery functions for wave V are
shown in Fig. 10. For wave V amplitude, there is no signi-
ficant interaction between masker duration and!T on the
probe-evoked responses and the effect of masker duration is
significant (F=11.65, df=2, 99 p < .001), but only the mean
responses following the 30 msec masker are significantly
different from the responses following the 60 and 120 msec
makers. This is not consistent with differences found for
wave V latency, i.e., the mean response following the 120
msec masker was different from the mean response for the
A 39 moe
0 68 mec
S128 9s*c
WAVE V
20.0
28.0
0.8
I I I I I 1 I 1 | r |
6 12
25 58
188
Fig. 10.
Amplitude recovery functions for wave V probe
responses following wide-band makers with
durations of 30, 60, and 100 msec. Level
of the masker was set to"fully" eliminate
wave V response at AT=0 msec for the 60
msec masker.
DELAY TIME (msec)
30 and 60 msec makers. The recovery of the wave V ampli-
tude is faster following the 30 msec masker than following
the 60 and 120 msec makers which show similar recovery curves.
An interesting feature seen in Fig. 10 is an apparent super-
normality of the mean wave V amplitude forATs above 25
msec and this supernormality is most prevalent for the 30
msec masked condition. However, none of the supernormal
amplitudes are significantly different from the control
response. Wave V amplitude is equal to the control response
amplitude for all ZTs above 12.5 msec for the 60 and 120
msec masked conditions, and for ATs above 6.2 msec for the
30 msec masked condition. Table V gives the summary data
for wave V amplitude for the three masker durations.
The mean amplitude recovery functions for N1 for all
three masker durations are shown in Fig. 11. Increasing
masker duration results in a decrease in the postmasking
amplitude of the N1 probe response. For Ts below 25 msec,
the N1 responses were difficult to measure in all three
subjects for the 120 msec masked condition (and wave V was
easily observed). Unlike N1 latency, which showed no
significant duration effect, N1 amplitude is significantly
affected by masker duration (F=7.79, df=2, 33 p <.001) with
the difference occurring between the mean responses to the
|
|
PAGE 1
,FORWARD MASKING OF AUDITORY NERVE (N1) AND BRAINSTEM RESPONSES (WAVE V) IN HUMANS By STEVEN JOHN KRAMER A DISSERTATION PRESENTED TO THE GRADUATE COUNCIL OF THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY UNIVERSITY OF FLORIDA 1981
PAGE 2
,--ACKNOWLEDGEMENTS I would like to thank the chairman of my supervisory committee, Dr. Donald C. Teas, for all his tireless efforts and encouragements in helping me to conceive, organize, and carr y out this research. I would also like to thank my committee members, Dr. W. Keith Berg, Dr. William E. Brownell, Dr. F. Joseph Kemker, and Dr. Kenneth J. Gerhardt, for their support and participation. In addition I would like to express thanks to my friends and subjects without whom this research would not have been possible and to Mrs. Kathy Farley for her secretarial assistance. Finally, I would like to express m y appreciation to Kathleen Cannon for all her help, encouragement and sacrifice and to whom this project is dedicated. ii
PAGE 3
TABLE OF CONTENTS ACKNOWLEDGEMENTS . LIST OF TABLES. LIST OF FIGURES ABSTRACT. ii V vii xi CHAPTER I II III IV INTRODUCTION ...... 1 General Description of the AP. 14 Forward Masking of the WholeNerve Action Potential (AP) . 17 General Description of the ABR. 28 Forward Masking of the Auditory Brainstem Response (ABR). . . 32 METHODS . Subjects Equipment. Stimuli Electrodes. Procedures. RESULTS . 47 47 48 48 54 55 58 "Standard" Recover y Function . . 65 The Effect of Masker Duration. 81 The Effect of Masker Level. 91 The Effect of High-Pass Masking. 99 Derived Response . . . 119 DISCUSS ION. . 129 iii
PAGE 4
TABLE OF CONTENTS (Continued) General Effects of Forward Masking. . . . . 132 Effect of Masker Duration and Level . . . . . 134 Effects of Masker Low Frequency Cutoff (High-Pass Masking) . 138 Possible Mechanism Underlying the Effects of Forward Masking on N 1 and Wave V. . . . 141 Wave V Amplitude. . . 142 V-N 1 vs N1 Amplitude. . . 144 Central Physiological Evidence. 148 Explanation of Forward Masking Effects on N 1 . . 150 Relation to Psychophysics. Summary and Conclusions .. BIBLIOGRAPHY .... BIOGRAPHICAL SKETCH iv 153 154 157 172
PAGE 5
Table I II III LIST OF TABLES Forward masking series received by each of the subjects. ( +) indicates success and {-) indicates failure in obtaining data for ABR / AP ... Means and standard deviations (S.D.) of wave V and N1 latencies for the "standard" series Means and standard deviations (S.D.) of wave V and N 1 amplitudes for the "standard" series ....... IV Means and standard deviations (S.D.) of wave V, N1 and V-N 1 probe response latencies for the three masker durations V VI Means and standard deviations (S.D.) of wave V and N 1 probe response amplitudes for the three masker durations . . .... Means and standard deviations of wave V, N 1 and V-N 1 probe response latencies for the three masker levels. . . . . . VII Means and standard deviations of wave V and N 1 probe response amplitudes for the three masker levels .. .. V 60 72 79 83 89 94 97
PAGE 6
LIST OF TABLES (Continued) Table VIII IX X Means and standard deviations (S.D.) of wave V, N 1 and V-N 1 probe response latencies for the four masker low frequency cutoffs .... Means and standard deviations (S.D.) of wave V and N 1 probe response amplitudes for the four masker low frequency cutoffs ........ Summary of significant effects and interactions of masker parameters on wave V and N1 probe responses vi 110 118 135
PAGE 7
Figure 1 2 LIST OF FIGURES Spectra of the masking stimuli (a) and frequency response of the TDH-39 earphone (b) . . . Simplified block diagram of the stimulus generating and response recording equipment . ... 3 Examples of unmasked control response waveforms 4 Example of ABR and AP probe response waveforms as a function of ~T for the 5 6 "standard" series . . . Mean and ~l S.D. of wave V, Nl, and V-Nl latencies as a function of ~T (dela y time) for the "standard" series. . . . . . Mean and S.D. for wave V and N 1 amplitude (uvolts) as a function of . . T for the "standard" series . . 7 8 9 Mean wave V and N 1 amplitude recovery functions expressed as percent of the mean unmasked control amplitude (100%) for the "standard" series Summary comparison of ~ave V and N 1 for the "standard" series .... Latenc y recover y functions for wave V, N 1 and V-N 1 probe responses following wide-band maskers with durations of 30, 60, and 120 msec. . . .. vii 50 52 62 68 69 76 77 80 86
PAGE 8
LIST OF FIGURES (Continued) Figure 10 11 12 Amplitude recovery functions for wave V probe responses following wide-band maskers with durations of 30, 60, and 100 msec Amplitude recovery functions for N 1 probe responses following wide band maskers with durations of 30, 60, and 120 msec. . . Latency recovery functions for wave V, N 1 and V-N 1 probe responses following 60 msec wide-band maskers with levels of ~10 dB relative to the "standard" series (referred to as O dB) . . . . 13 Amplitude recovery functions for wave V probe responses following 60 msec wide-band maskers with levels of ~10 dB relative to the "standard" series 14 Amplitude recovery functions for 15 16 N 1 probe responses following 60 msec wide-band maskers with levels of :!:'10 dB relative to the "standard" series ... Example of the probe ABRs as a function of ,6. T ( top to bottom) for the different masker low frequency cutoffs (left to right) ..... Example of probe APs as a function of 6.T (top to bottom) for the different masker low frequency cutoffs (left to right) viii 87 90 93 96 98 102 105
PAGE 9
LIST OF FIGURES (Continued) Figure 17 18 Latency recovery functions for wave V, N 1 and V-N 1 probe re sponses following 60 msec maskers with masker low frequency cutoffs of .02, 2, 4, and 6 kHz ..... Wave V and N 1 probe response latencies as a function of masker low frequency cutoff. . . . 19 Amplitude recovery functions for wave V probe responses following 60 msec wide-band maskers with masker low frequency cutoffs of 20 21 .02, 2, 4, and 6 kHz ....... Wave V probe response amplitude as a function of masker low frequency cutoff. . . . ... Amplitude recovery functions for Ni probe responses following 60 msec wide-band maskers with masker low frequency cutoffs of .02, 2, 4, and 6 kHz. . . . 22 N 1 probe response amplitude as a function of masker low frequency cutoff. 23 24 25 Example of derived response technique for the ABR .. Example of the derived response technique for the AP. Mean latencies of wave V and N 1 as a function of derived CF .. ix 106 107 113 114 116 117 122 124 125
PAGE 10
LIST OF FIGURES (Continued) Figure 26 27 Mean amplitudes of wave V and N1 as a function of derived CF. V-N 1 latency interval as a function of% N 1 control amplitude for the different masker low frequency cutoffs at each 6. T . . . . . . . X 127 147
PAGE 11
Abstract of Dissertation Presented to the Graduate Council of the University of Florida in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy FORWARD MASKING OF AUDITORY NERVE (N1) AND BRAINSTEM RESPONSES (WAVE V) IN HUMANS By Steven John Kramer June 1981 Chairman: Donald C. Teas Major Department: Speech In both psychophysical and electrophysiological investigations, it has been demonstrated that a response to one sound (probe) can be influenced by another sound (masker) when the two sounds occur simultaneously or in a temporal relation. The relation in which the masker precedes the probe is called forward masking. Measurements of the probe response as a function of the time interval following the masker (6T) describe the forward masking recovery functions. In the present study, the effects of forward masking were investigated on wave V of the ABR along with N 1 responses recorded simultaneously (on a separate channel) from the ear canal. Evoked potentials to 50 dB HL broadband clicks were obtained for 6Ts of 6.2, 12.5, 25, xi
PAGE 12
50, and 100 msec following short-duration noise maskers. Postmasking recovery functions were measured for different masker durations, masker levels, and masker low frequency cutoffs (high-pass masking). The largest amount of masking occurred for the shortest t::,. Ts and masking decreased as t::,.T increased. The effects on wave V were found to be different than on N 1 The primary effects of forward masking on the probe responses were decreases in N 1 amplitude and increases in wave V latency, neither of which were fully recovered by t::,.T=l00 msec. Wave V amplitude recovered byt::,.T=25 msec and showed a robustness to the forward masking. Charac teristic changes in the recovery functions were found for variations on masker parameters. The relation between wave V latency and N 1 amplitude, along with other characteristics of the results, suggests that underlying mechanisms include a recoding of the neural input (N 1 ) within the brainstem pathways generating the wave V potential. xii
PAGE 13
CHAPTER I INTRODUCTION The effects that one sound may have on the perception of another sound have been of interest to investigators ever since Mayer (1876a,b) first described some aspects of this basic phenomenon which has become known as masking. Masking is a psychophysical term used to denote an elevation in threshold of audibility for one sound (probe) in the presence of another sound (masker). Mayer observed that a watch-tick could be obliterated by a louder clock-tick when the two ticks over lapped each other. By using two time-pieces running at different speeds, Mayer also noticed that the quieter watch tick was obliterated by the clock-tick at instances when the two ticks did not exactly overlap in time. Mayer's early qualitative observations demonstrated that different temporal relations among sounds could influence the perception of those sounds and ha~since led to an abundance of research known, in a general sense, as temporal masking. The masking situation with the masker coincident with the probe is generally called simultaneous masking. The term forward masking is used for situations where the masker precedes the probe and backward 1
PAGE 14
masking applies to situations where the masker follows the probe. The time interval between the masker and the probe 2 is generall y called .6.T. One problem with the simultaneous masking paradigm is that nonlinear distortion products are produced b y the two stimuli with different frequencies, thereby producing energy at frequencies other than the stimulus fre quencies (Rodenburg, Verschuure, and Brocaar, 1974; Shannon, 1975; Wightman, McGee, and Kramer, 1977; Moore, 1978; Vogten, 1978). A forward masking par a digm overcomes the distortion problem since the two stimuli are not present at the same time. Forward and b~ckward masking paradigms have been used in ps y choph y sical investigations to describe the time course of masking effects (Lilsher and Zwislocki, 1947; Zwislocki, Pirodda, and Rubin, 1959; Elliott, 1962; Plomp, 1964; Wilson and Carhart, 1971; Robinson and Pollack, 1973; Duifhuis,1973; Penner, 1974; Fastl, 1976; Berg and Yost, 1976). In this procedure, the threshold of the probe stimulus is measured as a function of .6.T. As .6.T increases, less energ y is required to detect the probe signal and the plot of threshold v s .6.t defines the mas k ing recover y function for stated masker-probe parameters. In general, the decrement in sensiti v it y to the probe produced b y the forward or backward masker is greatest for shortest .6.Ts (least sensiti v it y ) and then monotonicall y decreases (toward
PAGE 15
3 greater sensitivity) as L::.T increases. The decrease in sensitivity to the probe becomes greater for longer masker durations and higher masker levels. The actual descriptions of the recovery functions are not entirely agreed upon and are dependent on stimulus parameters. Recovery from backward masking occurs much faster than recovery from forward masking. Backward masking will not be addressed any further in this investigation. In electrophysiological investigations, masking paradigms have been adapted to provide correlatives to psychophysical masking phenomena. The investigation of electrical potentials evoked by acoustic stimuli has been of interest to auditory researchers as a means of describing underlying physiological phenomena that may possibly mediate some of the psychophysical observations. The development of signal-averaging computers in the 1960's greatly improved the ability to extract stimulus related electrical potentials from the random electrical back ground activity and has made it possible to record electrical activity to auditory stimuli from remote sites within the boundaries of the skull and scalp. Two such averaged evoked potentials most applicable to humans are the whole-nerve action potential (AP} and the Auditory Brainstem Response (ABR), which are the subjects of the present study.
PAGE 16
4 The term masking has been retained in electrophysiologi cal experiments and refers to a reduction in some measure of neural response to one signal (probe) due to the presence of another signal (masker). In physiological masking, it has been thought that the masker "subtracts" the contributions (through refractory, adaptation, and / or desynchronizing mechanisms) from certain areas of the cochlear partition dependent on the level and spectral characteristics of the masker. A response to the probe, recorded in the presence of the masker, is considered to reflect the "unmasked" portion of the cochlear partition (Teas, Eldredge, and Davis, 1962; Elberling, 1974; Spoor, Eggerrnont and Odenthal, 1976; Don and Eggermont, 1978; Parker and Thornton, 1978). The probe and masker can be presented simultaneously or in a temporal relation, e.g., forward masking. In both psychophysical and electrophysiological masking studies, there is general agreement that for relatively short duration maskers at levels below 80-90 dB Sound Pressure Level (SPL) the decrement of probe response activity is due to some short-term noncumulative effect. For maskers above 80-90 dB SPL the effects are different and involve some form of cumula tive "fatigue" (Hood, 1950; Gisselsson and Srensen, 1959; Coats, 1964a; Smith, 1977). This investigation is concerned
PAGE 17
only with the short-term lower level effects of forward masking. 5 Forward masking effects have been investigated by several researchers in recordings of the whole-nerve response (AP) (Hawkins and Kniazuk, 1950; srensen, 1959; Coats, 1964a,b, 1967, 1971; Spoor, 1965; Coats and Dickey, 1972; Eggermont and Spoor, 1973a,b; Eggermont and O~enthal, 1974a; Spoor et al., 1976; Charlet de Sauvage and Aran, 1976; Dallos and Cheatham, 1976; Harris, 1979; Huang and Buchwald, 1980; Abbas and Gorga, 1981). In general, these studies have shown that the amounts of post nasking recovery functions are dependent on the pro cedure, masker and probe levels, and masker durations. A re view of existing literature on forward masking of the AP is presented in more detail in a later section. A special case of forward masking is that of repetitive stimuli. Responses to successive stimuli show a decrement when the preceding stimuli have an extended effect. The r~ sponse to each stimulus can be measured for a pair of stimuli or for a train of stimuli as a function of ISI. The amount of response decrement for the AP has been shown to be greater for shorter ISis and the final amount of response decrement is reached b y the 4th or 5th stimulus (Srensen, 1959; Kupper man, 1971; Yoshie and Ohashi, 1971; Eggermont and Spoor, 1973a;
PAGE 18
Thornton and Coleman, 1975; Spoor et al., 1976; Don, Allen and Starr, 1977). Since no further response decrement of the AP occurs after the 5th stimulus in the stimulus-train experiments, others have used repetition rate procedures 6 where the final averaged AP responses to fast repetition rates are compared to responses using a slow repetition rate (Peake, Goldstein, and Kiang, 1962; Yoshie, 1968; Teas and Henry, 1969; Spoor et al., 1976). Response magnitude as a function of ISI defines the recovery function in the repetitive stimuli para digm. Forward masking paradigms have also been used to measure masker and probe responses in single auditory nerve fibers (Galambos and Davis, 1943; Kiang, Watanabe, Thomas, and Clark, 1965; Young and Sachs, 1973; Evans, 1976; Smith, 1977, 1979; Bauer, 1978; Harris and Dallos, 1979; Abbas, 1979; Delgutte, 1980). These studies have shown that during continuous stimu lation (of constant intensity and frequency), e.g., by the masker, the discharge rate of the nerve fiber responds maximally at the onset then declines rapidly at first followed by a more gradual decline until a quasi steady-state is reached by 100-200 msec. This (normal) neural decrement is called adaptation. Following the offset of a masker to which the single fiber has adapted, the spontaneous neural activity
PAGE 19
7 shows an immediate depression followed by a recovery to base line levels. The probe response following the masker offset shows a decrement in discharge rate compared to its unmasked value which then recovers as ~Tis lengthened. The recovery of the probe response magnitude has been shown to be related to the recovery of the spontaneous activity and this is pro portional to the driven onset (and average) discharge rate which occurs for the masker. Both the adaptation and recovery from adaptation have been shown to follow exponential recovery functions; however, the time course of adaptation is much faster than the time course of recovery from adaptation (Harris and Dallas, 1979). In addition, the recovery functions have been shown to have different time constants for different species, e.g., they are about 2.5 times longer in guinea pig than chinchilla. Single auditory nerve fiber responses to increasing click repetition rate show decreases in neural discharge rate and only small (O.l msec) latency increases (Kiang et al., 1965). The actual mechanism(s) responsible for the decrement during adaptation and for the postmasking decrement of the probe-evoked responses is not known. The source of the mechanism has been attributed by most investigators to the hair cell-nerve fiber synapse (Rosenblith, 1954; Hawkins and
PAGE 20
8 Kniazuk, 1950; Sorensen, 1959; Peake et al., 1962; Young and Sachs, 1973; Spoor et al., 1976; Prijs, 1980). The hair cell cochlear microphonics (CM) do not change with repetitive stimuli (Sorensen, 1959; Peake et al., 1962; Young and Sachs, 1973; Charlet de Sauvage and Aran, 1976; Huang and Buchwald, 1980) nor do the summating potentials (Dallas, Schoeny, and Cheatham, 1972; Eggermont, 1976a). The efferent olivocochleo bundle (OCB) was considered a partial contributor by Liebrandt (1965) who demonstrated that the AP decrement observed with repetitive tone-bursts was abolished after injections of procaine into the internal auditory canal. Liebrandt (1965) suggested that efferent activity may play a part in several portions of the central nervous system in causing a decrement in evoked potentials following repetitive stimuli. Others, however, do not consider the efferent pathways responsible for the AP decrements since their effect on the AP requires much higher rates of stimulation, stimulation does not cause any reduction of spontaneous activity in auditory nerve fibers, the AP decrements are still observed following complete sectioning of the auditory nerve, and contralateral stimula tion does not produce any response changes (Sorensen, 1959; Kupperman, 1972; Young and Sachs, 1973; Don, Allen and Starr, 1977; Huang and Buchwald, 1980). Middle ear muscle activity
PAGE 21
9 has also been ruled out on the basis that the postmasking effect is present at levels below middle ear muscle reflex threshold, contraction of middle ear muscles does not affect click-evoked APs, and the postmasking effect can be observed after sectioning the muscles or following high doses of anesthesia (Hawkins and Kniazuk, 1950; Sefrensen, 1959; Liebrandt, 1965; Coats, 1971; Young and Sachs, 1973). The refractory period of auditory nerve fibers may be important for simul taneous masking phenomena, but cannot explain the effects seen in forward masking for the long .t:i.Ts (Rosenblith, 1950; Hawkins and Kniazuk, 1950; Peake et al., 1962; Harris and Dallas, 1979; Huang and Buchwald, 1980). Recently, the Auditory Brainstem Response (ABR) has become popular as a noninvasive far-field electrophysiological recording procedure for assessing a short-latency system of the auditory nerve and brainstem pathways (Jewett and Williston, 1971; Picton, Hillyard, Krausz, and Galambos, 1974; Buchwald and Huang, 1975; Starr and Hamilton, 1976). The ABR can pro vide information on peripheral as well as more central response capabilities. The ABR to temporally related stimuli has not been as extensively investigated as has the AP. Repetition rate and stimulus-train paradigms have been applied to measures of the ABR and some of the brainstem components have
PAGE 22
10 been shown to behave differently than the auditory nerve response (Jewett and Williston, 1971; Picton et al., 1974; Terkildsen, Osterhammel, and Huis in't Veld, 1975; Thornton and Coleman, 1975; Pratt and Sohmer, 1976; z8llner, Karnahl, and Stange, 1976; Hyde, Stephens, and Thornton, 1976; Martin, 1976; Weber and Fujikawa, 1977; Don et al., 1977; Kodera, Yamada, Yamane, and Suzuki, 1978; Scott and Harkins, 1978; Klein and Teas, 1978; Chiappa, Gladstone, and Young, 1979; Kevanishvilli and Lagidze, 1979; Despland and Galambos, 1980; Harkins and Lenhardt, 1980). These studies will be described in more detail in a later section. The different behavior of the various brainstem components to temporally related stimuli is potentially quite interesting and may indicate that peripheral auditory information is coded in different ways in the brainstem. Response differences to repetitive stimuli have also been noted for the various brainstem nuclei (Kiang, 1968; Winklegren, 1968; Watanabe and Simada, 1969; Kitahata, Amakata, and Galambos, 1969; Kitzes and Buchwald, 1969; Webster, 1971). Knowledge of the postmasking recovery properties of the ABR and their relation to postmasking recovery properties of the AP may be useful as a method for objectively assessing a dynamic property of the auditory system at more than one
PAGE 23
11 level in a noninvasive manner. Provided that the normal postmasking recover y properties are known, certain altera tions in clinical populations ma y be of diagnostic value as has been suggested by Charlet de Sauvage and Aran (1976) and Z8llner, Karnahl, and Stange (1976) for cochlear pathologies, b y Yoshie and Ohashi (1971) for detecting acoustic neuromas, b y Robinson and Rudge (1977) for cases involving multiple sclerosis, and by Salamy, McKean, Pettett, and Mendelson (1978), Fujikawa and Weber (1977), Rowe (1978), and Despland and Galambos (1980) for different developmental states. In addition, postmasking recover y may be a method to better assess persons who have poor speech discrimination beyond that which can be due to their loss of pure-tone sensitivit y (phonemic regression), a characteristic of some geriatric persons. Since continuous speech involves alternations of intense v owels with relativel y weak consonants, frequent pauses and silent intervals, onsets and offsets with different rates of amplitude changes, short-time spectral changes, and di f ferent sound durations (Shoup and Pfeifer, 1976; Stevens, 1980), knowledge of temporal masking effects ma y have important implications for better understanding these d y namic characteristics of speech discrimination. Since most auditory e x perience does not consist of simple sounds in a quiet
PAGE 24
12 background, it is of interest to understand how one sound affects the response to a simultaneous or subsequent sound. At the single auditory nerve fiber level, Delgutte (1980) suggests the importance of temporally related effects for speech discrimination in the following: Consider a region of rapid spectral change in a speech signal (transition interval) preceded by a steady segment having most of its energy over a limited frequency region. This segment would adapt most of the units whose CF is in that region, so that these units would be less responsive to the follow ing transition interval L-andJ this decreased responsiveness would occur even if there were a 50-100 msec silent interval between the adapting segment and the transition interval. (p. 847) Temporal intervals up to 150 msec are typical between transi tions at the release of a stop consonant and the preceding vowel (Delgutte, 1980). It is of interest also to understand how these temporal effects are manifested in evoked potentials and how they relate at different levels of the auditory system in order to more fully understand basic auditory processing, as well as, a potential clinical technique to help differentiate certain abnormalities. The purpose of this investigation is to provide some normative descriptions of the postmasking recovery functions for the ABR (wave V) in humans. A forward masking paradigm is used to measure the click-evoked potentials for various ATs
PAGE 25
13 following a noise-burst masker. AP responses from the ear canal are also measured simultaneously with the ABR in some of the subjects so that a direct comparison of the postmask ing recovery functions at two levels of the auditory system can be made. Recent evidence suggests that under certain stimulus conditions (especially repetition rate) and certain pathological conditions, the brainstem responses do not simply follow events occurring at the auditory periphery (Pratt and Sohmer, 1976; Coats, Martin, arid Kidder, 1979; Kevanishvilli and Lagidze, 1979); therefore, one of the emphases of this investigation is to compare the forward masking effects on the ABR to the forward masking effects on the AP. Since longer duration maskers increase the postmasking effect (Coats, 1964a; Harris and Dallas, 1979), this type of forward masking may have a more pronounced effect than repetition rate experi ments on the ABR and may prove in future applications to be more useful in assessing certain clinical abnormalities at different levels of the auditory system once the normal characteristics are known. The postmasking recovery functions are described in this investigation for different masker durations, masker levels, and masker frequency bands (high pass masking).
PAGE 26
14 General Description of the AP The whole-nerve action potential (AP) represents a population of synchronously responding auditory nerve fibers to an abrupt acoustic stimulus and reflects both hair cell function and activity in the auditory nerve (Dallas, 1973). Recording of the AP can be achieved with electrodes on the auditory nerve (Derbyshire and Davis, 1935; Goldstein and Kiang, 1958; Kiang, Maxon, and Kahn, 1976; Huang and Buchwald, 1980), within the cochlea (Tasaki, Davis, and Eldredge, 1954; Teas, Eldredge, and Davis, 1962), near the round window (Rosenblith, 1954; Peake et al., 1962; Eggermont and Odenthal, 1974a,b,c; Dallas and Cheatham, 1976), or from the external ear canal (Yoshie, Ohashi, and Suzuki, 1967; Cullen, Ellis, Berlin, Lousteau, 1972; Elberling, 1974; Coats, 1974, 1976; Berlin and Gondra, 1976; Kramer and Teas, 1979). Auditory stimulation at high intensities produces an AP response that consists of an initial negative deflection, labeled N1, which occurs about 1.5-2.5 msec poststimulus onset and followed by a smaller positive deflection, then negative again forming N 2 about l msec after N 1 (Derbyshire and Davis, 1935; Teas et al., 1962). In humans, the N 2 is not as prominent as in animals (Elberling, 1976a; Yoshie, 1976; Spoor et al., 1976; Kramer and Teas, 1979). Most descriptions of the AP
PAGE 27
response involve measurements of the latency and amplitude of the N 1 components as a function of stimulus intensity. 15 In general, as intensity increases the latency of N1 decreases and the amplitude increases. The most common stimulus used for evoking the AP is the broadband click because of its rapid onset, which produces a highly synchronous response from a population of nerve fibers over a wide span of frequencies. Since estimates of the basilar membrane traveling wave velocity indicate that the velocity is greatest at the basal end and progressively de creases towards the apex (Teas et al., 1962; Zerlin, 1969; Eggermont, 1975). the neural discharges from the nerve fibers in the basal region occur sooner than those from apical regions and are more synchronous because many discharges occur within a brief time period. In response to broadband clicks, these more synchronous basal fiber discharges predominate when responses are recorded with distant electrodes, as is the AP response (Teas et al., 1962; Schmidt and Spoor, 1974; Eggermont, Spoor and Oienthal, 1976). More recently, it has been demonstrated that tone-bursts and filtered clicks with abrupt rise-times are good compromise stimuli for providing a more frequency-specific evaluation along the cochlear parti tion at low intensities (Eggermont, 1976b; Zerlin and Naunton,
PAGE 28
16 1976; Eggermont et al., 1976; Coats, 1976; Kramer and Teas, 1979; Coats, Martin, and Kidder, 1979). For higher in tensities, the basal extension of events on the basilar membrane results in a more limited frequency specificity due to an inclusion of the more synchronous high frequency re sponding populations (Teas et al., 1962; Elberling, 1974; Eggermont et al., 1976; Kramer and Teas, 1979). A technique to obtain responses from more frequency-specific regions along the cochlear partition, even at high intensities, is to add high-passed noise maskers which can exclude the dominant high frequency region and allow a probe response from more apical regions (Teas et al., 1962; Elberling, 1974; Eggermont et al., 1976; Zerlin and Naunton, 1976; Kramer and Teas, 1979). The recording of the AP response "threshold" has been demonstrated to correspond fairly well with conventional be havioral thresholds (Aran, Charlet de Sauvage, and Pelerin, 1971; Yoshie, 1973; Eggerrnont, 1975; Montandon, Shepard, Mass, Peake, and Kiang, 1975; Elberling and Salomon, 1976) and characteristic differences in waveform and the latency and amplitude input-output functions have been found between normals and pathological patients (Odenthal and Eggermont, 1974; Montandon et al., 1975; Yoshie, 1976; Elberling and Salomon, 1976; Coats et al., 1979).
PAGE 29
Forward Masking of the Whole-Nerve Action Potential (AP) 17 Early evidence of forward masking of the AP can be found in the work of Derbyshire and Davis (1935) who were the first to demonstrate a decline in the AP voltage recorded from a gross electrode on the auditory nerve in cats during tonal stimulation, a phenomenon termed "equilibration." From continuous photographic records, Derbyshire and Davis (1935) measured the amplitudes of the APs over time for different stimulating frequencies. Although the APs continued to decline in voltage up to 10 minutes following the onset of the tone, the largest and most rapid decline occurred during the first 2 seconds. The amount of reduction for the first AP following the "onset" AP was found to be negligible for frequencies below 400 Hz. Above a critical frequency of 1000 Hz the voltage declined abruptly until about 4000 Hz where synchronous APs were not detectable. Derbyshire and Davis (1935) sug gested that the decline of the first AP after the "onset" AP was a reflection of the "functional" refractory period of individual auditory nerve fibers (1.0 msec) and the continued decline over the following 2 seconds was due to prolongation of the relative refractory period. Galambos and Davis (1943) demonstrated that the AP amplitude decline during continuous
PAGE 30
18 stimulation was due, primarily, to a decline in discharge rate of individual auditory nerve fibers. Maximum discharge rate of single fibers averaged about 400/sec; however, dis charge rates up to 1000 / sec were possible. A decline in dis charge rate (adaptation) to about 25% of the maximum rate occurred within 1.0 sec. Coats (1964a) explained these original findings of Derbyshire and Davis (1935) and Galambos and Davis (1943) in terms of forward masking, where each cycle of the stimulating tone had a forward masking effect on subsequent cycles and the amount of decline de pended on the period of the tone as well as the duration of stimulation. Derbyshire and Davis (1935) were also the first to report on masking of the click-evoked APs by continuous noise or tones. A demonstration of forward masking was apparent in their results which showed that the largest mask ing effect occurred when the click response coincided with the peak of a low frequency tonal masker (in phase) 1 however, some masking of the click-evoked AP occurred for certain other phase relations. Rosenblith, Galambos, and Hirsh (1950) and Rosenblith (1954), although primarily interested in investigation of the AP following intense prolonged noise maskers, observed that the click-evoked AP from the round window in cats had a
PAGE 31
sizable reduction in amplitude following even a short ex posure to moderately intense tones. 19 The first quantitative description of the postmasking recovery of the AP was by Hawkins and Kniazuk (1950) who recorded from the round window in cats click-evoked APs pre ceded by a 1.3 msec noise or tonal masker. These authors found that full recovery of AP amplitude did not occur until 300 msec following a 50 dB SPL masker and 1.0 sec following a 70 dB SPL masker. Masker duration did not affect recovery for the 50 dB SPL masker, but delayed recovery was found as a function of masker duration for masker intensities above 50 dB SPL. For tonal maskers, Hawkins and Kniazuk (1950) re ported that 4000 Hz was the most effective masker of the click-evoked APs and resulted in the greatest delayed re covery from masking. That the masking effects extended over a period far in excess of the refractory period of auditory nerve fibers was an important observation and Hawkins and Kniazuk (1950) suggested that the long postmasking effects involved some mechanism which transmits excitation from the hair cell to the nerve fiber. Using a paired-click paradigm in the cat, Rosenzweig and Rosenblith (1953), Rosenblith (1954), and Sorensen {1959), all demonstrated that the AP to the second click was reduced
PAGE 32
20 in amplitude and the reduction was dependent on the interval between the clicks as well as the intensity of the first click. AP amplitude was still reduced for intervals far in excess of the refractory period of the nerve fibers. Sorensen (1959) investigated the forward masking effects in guinea pigs using a low level (40 dB SPL) 1.0 sec noise masker preceding a click presented at different levels. Post masking recovery functions were found to be dependent on masker level as well as on probe level. Recovery time in creased as the signal-to-noise ratio decreased and ranged from 50 to 600 msec for complete recovery. Results with tonal maskers showed a much smaller effect than the white noise maskers and no significant differences were observed as a function of masker frequency. Latency changes of N 1 were not reported. Sorensen (1959) suggested two possibilities to explain the postmasking effects observed for the AP. Either (1) the decrease in N 1 amplitude is due to a decrease in the number of active nerve fibers while each fiber maintains a constant firing rate, or (2) the decrease in N1 amplitude is due to a decrease in firing rate of all the active fibers while the number of active fibers remains constant. Peake et al. (1962) recorded AP responses to repetitive stimuli (clicks and brief noise-bursts) in cats with a wire
PAGE 33
electrode near the round window. Following the onset of the stimulus train, the AP amplitude to successive stimuli systematically decreased until some steady-state level was reached. The APs to successive stimuli were observed and 21 it was found that the amount of decline increased as the repetition rate increased up to 3000 / sec. For rates above 3000/sec (ISI=.33 msec) no stimulus-locked activity could be detected after the "onset" response. For rates below 5/sec (ISI=200 msec) there was little change in amplitude for pro longed stimulation. The amount of amplitude decline measured after the steady-state level had been reached was compared for the different repetition rates and revealed constant amplitude for rates up to 10/sec and then exponentially decayed (except for a "bump" between 300 and 800 / sec) until no neural response was observed above a rate of 3000/sec. It was also observed that for rates between 10 and 50/sec the entire AP waveform decreased in amplitude without any change of N1 latency. Between rates of 50 and 300 / sec there was a continued decrease in amplitude as well as a change in latency of the components later than N 1 Above rates of 300/sec interpretation was difficult because of response overlapping. Huang and Buchwald (1980), recording from the auditory nerve and cochlear nucleus using repetitive tone-bursts, found that
PAGE 34
22 evoked potential decrements were parallel at the two loca tions. A complex interaction of repetition rate and stimulus duration was reported and was determined to be due to the intertone interval. For intertone intervals greater than 100 msec, evoked potential decrements were not observed regardless of stimulus duration and repetition rate. In a series of articles, Coats (1964a,b, 1967, 1971) described the time courses of AP recovery following tonal and white noise maskers in cats for different masker durations, masker intensities, and probe-click intensities. The shortest ~T measured was 50 msec Increasing the masker duration from 3 to 3.3 sec resulted in a decrease in the AP recovery rate (longer recovery with longer duration). Changing the duration of the masker was found not to have any effect on the masked AP amplitude under simultaneous masking conditions; therefore, the "masking duration effect" acted only to slow the rate of recovery following the masker. Increasing masker intensity was shown to increase the amount of AP depression (amplitude reduction), but the recovery functions had parallel time courses until AP amplitudes were above 80% of control. In addition, Coats reported that the "masker duration effect" was minimal for masker intensities below 50 dB SPL and increased as a function of masker level above 50 dB SPL. In
PAGE 35
23 contrast to the "masker duration effect," the "masker intensity effect" was related to decreasing the AP amplitude, but had no effect on the rate of recovery. Varying click intensity was similar to the effect of changing masker in tensity on the amplitude of the AP. The latency of N 1 was found to change only slightly under the forward masking conditions. Kupperman (1971) found a close comparison between human and guinea pig AP depression as a function of click repetition rate except that the amount of amplitude reduction was less pronounced in humans. Yoshie (1968) investigated changes in N 1 amplitude as a function of repetition rate in humans using a needle electrode inserted into the wall of the external ear canal. The clicks were presented at 70 dB sensation level for rates of 1-200/sec. Averaged steady-state amplitude remained unchanged up to rates of 10 / sec. A monotonic decline in amplitude was found for rates above 10/sec, but the latency of N 1 and the wave form configuration remained unchanged. Using a paired-click paradigm, Yoshie (1968) measured AP amplitude as a function of ISI and found that full recovery occurred after 100 msec, which corresponded to the critical value found in the rate function (10 / sec). Yoshie and Ohashi (1971) compared normal
PAGE 36
24 AP responses to click-trains to those obtained from a patient having bilateral acoustic neuromas, moderate sensorineural hearing loss, abnormal tone decay, and poor speech discrimination. For the normal subjects, the ampli tude decrease across time was very rapid over the first 10-20 msec of the click-train followed by a more gradual decrease. The amount of amplitude decline increased as ISI decreased. In contrast, the patient showed a slower initial amplitude decline and continued to decline over a longer time period, up to 100 msec, i.e., no clear distinction could be made between the early rapid decline and the later slower decline as was seen in the normals. The locus of the abnormal AP responses to the repetitive stimuli could not be estab lished, however, the authors suggest that the abnormal AP decrement could be due to a mechanism of sensory cell-nerve fiber synapse reflecting sensory cell damage as well as properties of the nerve fibers. Eggermont and his coworkers (Spoor, 1965; Eggermont and Spoor, 1973a,b; Eggermont and Odenthal, 1974a; Spoor et al., 1976) have provided an extensive description of forward mask ing effects on the AP using noise maskers, stimulus-trains, and repetition rates. They used 4000 and 6000 Hz tone-bursts as the probe stimuli. The recovery functions under all three
PAGE 37
25 conditions followed an exponential time course. Changes were observed both in N 1 latency and amplitude as a function of repetition rate and as a function of 6T; however, the recovery took longer in the noise masking case due to the duration effect (Coats, 1964a). Following the 500 msec noise masker, the N 1 amplitude reached full recovery after 250 msec in guinea pigs while the latency was fully recovered by 64 msec. Masker levels below 60 dB SPL produced lesser amounts of AP decrement at masker offset, but the slope of the recovery functions became less steep as masker intensity decreased. For masker levels above 70 dB SPL, the time for full recovery increased to values beyond 250 msec. In addi tion, it was shown that N 1 recovery was about 4 times longer (up to 1000 msec) in man than in guinea pigs using the same procedure. This was suggested to be due to different proper ties at the hair cell-nerve fiber synapse between the two species. These authors also suggested that the forward mask ing effects of the AP are caused by adaptation properties of each active individual nerve fiber resulting in a reduction in discharge rate. The adaptation, in turn, allows spon taneous desynchronizing factors (synapse or membrane noise) to contribute to the latency distribution function (Goldstein and Kiang, 1958) and produce an increase in latency (because
PAGE 38
26 of a broadening) and a decrease in N 1 amplitude. The number of potentiall y active nerve fibers remains the same and is determined b y the stimulus intensit y and frequenc y These authors further suggest that the N 1 recovery curve can only be influenced by the refractory properties of the auditory nerve fibers up to about 20 msec. For longer times, the postmasking effects are primaril y due to adaptation mechanisms. Charlet de Sauvage and Aran (1976) investigated AP responses to click-trains in normal adults and in patients with v arious sensorineural hearing abnormalities. The y used a train of 5 clicks with an ISI of 8.5 msec and 100 msec between click-trains. Onl y amplitudes were measured since, in contrast to Eggermont and coworkers, they did not observe an y N 1 latenc y shifts for the responses. (The y attributed this difference perhaps to the fact that clicks were used instead of tone-bursts which were used b y Eggermont and coworkers.) Charlet de Sauvage and Aran (1976) showed that AP decrements were most pronounced when the click-trains were at 60 dB Hearing Level (HL), corresponding to the "knee" of the input-output function. These authors suggested that if the response amplitude of the 4th click is greater than 76 % or less than 36 % of the response to the 1st click this should be considered abnormal; however, the y found that whenever
PAGE 39
27 the response decrement was abnormal it was to the side of being greater than 76% of the first click, i.e., less re sponse decrement. Response decrement of the click-trains was found to be significantly different from normal only for dissociated and recruiting ears. These authors suggested that in those pathological ears which showed abnormal response decrements there were, primarily, outer hair cell losses. Since normals showed a much larger response decrement and the decrement was maximal at 60 dB (the hypothetical point of changeover from outer hair cell to inner hair cell response) the pathological ears were apparently missing this mechanism. In summary, it appears that a (simple) sound can clearly affect the normal AP response to a following sound in a fairly dramatic manner, i.e., a significant reduction in response amplitude occurs for temporal intervals at least up to 100 msec. The effect on N 1 latency is not entirely agreed upon. The extended masking effects occur for temporal intervals far in excess of refractory mechanisms. Recovery functions at the underlying single fiber level closely parallel those of N 1 and provide evidence that a reduction in firing rate of each individual fiber following a normal adaptation process is a basic mechanism of forward masking at this level of the auditory system. Since the AP is a population response, one
PAGE 40
28 must consider that the sum total of the contributing single fibers may be manifested in the AP in a complex fashion. In addition, one cannot rule out the possibility that a re duction in number of nerve fibers plays a role in the observed effects on the AP under forward masking conditions. The source of the forward masking effects is not known; how ever, it is most likely related to a transduction mechanism at the hair cell-nerve fiber synapse, and this b~sic normal mechanism may be deficient in certain pathologic cases. General Description of the ABR The auditory brainstem response (ABR) was first described by Sohrner and Feinmesser (1967) who observed a series of potentials following N1 when recording from the external ear canal and attributed them to brainstem sources. Soon after, Jewett (1969, 1970) ,recording in cats, observed four positive waves occurring between 2-7 msec following a click stimulus. By simultaneously recording at various brainstem locations, wave 1 was found to be synchronous with the auditory nerve and wave 2 to activity of the cochlear nucleus. Regions corresponding to waves 2 through 5 were found to have fast and slow components, and since the slow components have longer latencies, the y could add to the activity from higher auditory centers. Nevertheless, wave 3 was attributed primarily to
PAGE 41
29 the superior olivary complex, wave 4 between the lateral lernniscus and the inferior colliculus, and wave 5 to the in ferior colliculus. Similar conclusions were found by Buchwald and Huang (1975), Huang and Buchwald (1977), and Achor and Starr (1980) using ablation and depth recording techniques in cats. Starr and Hamilton (1976) recorded ABRs in human patients with confirmed brainstem pathologies and their results indicated ABR sources which were in agreement with those of previous investigators. The most prominent and stable wave of the ABR is wave V, which is the current wave of interest in most auditory in vestigations of the ABR. In response to a click at high intensities, wave V shows a characteristic latency between 5.2 and 6.2 msec and can be reliably recorded from the same subject over time (Jewett and Williston, 1971; Picton et al., 1974: Starr and Achor, 1975). Schulman-Galambos and Galambos (1975), Hecox and Galambos (1974), Salamy et al. (1978), and Despland and Galambos (1980) demonstrated that wave V was present by 30 weeks gestational age and that the latency of wave V decreased with infant maturation until the age of 12-18 months, at which time wave V latency was the same as adult values. The ABR has also been shown to be independent of level of consciousness or stage of sleep
PAGE 42
30 (Amadeo and Shagass, 1973; Picton and Hillyard, 1974; Uziel and Benezech, 1978) or levels of anesthesia (Starr, Hamilton, and Achor, 1974; Gerull, Biesen, Mrowinski and Rudulph, 1974; Bobbin, May and Lemoine, 1979). Amplitude measures of the ABR have not been reported as often as have the latencies of the waves. Amplitudes of the ABR are very small (nanovolt range) and most investigators have shown a large variability across subjects and within the same subjects (Picton et al., 1974; Starr and Achor, 1975; Rowe, 1978; Chiappa et al., 1979). Investigation of the ABR centers, primarily, on the relation of the latencies (especially wave V) to different stimulus variables, e.g., the latency of wave V has been shown to systematically decrease as the stimulus intensity is in creased. Stimulus frequency (Davis, 1976; Klein and Teas, 1978; Coats et al., 1979) and repetition rate (Jewett and Williston, 1971; Pratt and Sohmer, 1976; Harkins et al., 1979) also affect the ABR. The extent that the various ABR com ponents reflect activity occurring at the periphery is an interesting question. This is extremely important if one expects to use, say wave V, to approximate behavioral audio grams. The suggestion that wave Vis closely linked to the synchronous volley of nerve impulses occurring at the
PAGE 43
31 periphery, except displaced in time has been made by some in vestigators (Davis, 1976; Elberling, 1976a;Klein and Teas, 1978; Kramer and Teas, 1979). However, some evidence exists which indicates that wave V behaves differently than N 1 under certain conditions, e.g., as a function of stimulus fre quency, repetition rate, or types of hearing loss (Thornton and Coleman, 1975; Pratt and Sohmer, 1976; Kevanishvilli and Lagidze, 1979; Coats et al., 1979; Kramer and Teas, 1979). Certainly, peripheral activit y serves as input to the brainstem and therefore different contributing response areas along the cochlear partition will produce different inputs. The frequency specificity of wave V should be influenced by the changing spatial distribution of N 1 To more closely partition out various spatial (and frequenc y ) distributions, high-pass masking has also been applied to the ABR and results have indicated a close correspondence of wave V and Ni latenc y across frequency region (Don and Eggermont, 1978; Kramer and Teas, 1979). However, the amplitude of wave V remained fairl y stable across frequenc y regions while N1 amplitude decreased for lower frequenc y regions (Don and Eggermont, 1978; Parker and Thornton, 1978). The relation between stimulus variables and latency is precise enough to make the ABR useful for accurate
PAGE 44
32 estimations of auditory thresholds (Davis, 1976; Galambos and Hecox, 1977; Pratt and Sohmer, 1976), for evaluation of auditory function in infants (Despland and Galambos, 1980), and in the evaluation of neurological disorders (Stockard and Rossiter, 1977; Starr and Achor, 1975; Stockard, Rossiter, Wiederholt, and Kobayashi, 1976; Robinson and Rudge, 1977; Stockard, Stockard, and Sharbrough, 1977; Shanon, Gold, Himmelfarb, and Carasso, 1979; House and Brackman, 1979). Forward Masking of the Auditory Brainstem Response (ABR) Interest in the effect of temporally related stimuli on the ABR has been restricted to repetition rate or stimulus train paradigms. Generally, the concern has been for identifying a repetition rate most applicable for routine clinical testing, i.e., establishing a repetition rate that provides a clear and stable response within the shortest time period. Only recently have the effects of repetition rate per se been quantitatively investigated in terms of assessing a dynamic property of the brainstem pathways, with the implication that certain disease states may cause a failure in adequate conduction of impulses when driven at high repetition rates. Jewett and Williston (1971) first demonstrated the effect of click repetition rate on the ABR in normal hearing
PAGE 45
33 adults. They reported that wave V showed no amplitude or latency shifts as repetition rate increased from 2.5 to SO/sec, while earlier peaks were severely reduced in ampli tude, but showed no latency shifts. Wave V amplitude was even shown to increase slightly at the higher repetition rates. It was suggested that wave V could be a useful candidate for clinical measures since faster repetition rates could be employed without affecting the amplitude of the response. Picton et al. (1974) confirmed the findings of Jewett and Williston (1971) for click repetition rates up to 60/sec. Terkildsen, Osterhammel, and Hu~s in't Veld (1975) re corded ABRs in normal adults using tone-bursts (1,2,5 kHz) at repetition rates of 5-40/sec. They found equal increases in latency for waves I and V, but the amplitude of wave V remained stable for the higher repetition rates while wave I's amplitude was significantly reduced even at a repetition rate of 10/sec. The effects of repetition rate were found to be independent of tone-burst frequency. These authors interpreted their findings as evidence for longer lasting unit responses at the source of wave V, making wave V less susceptible to desynchronizing factors. A click-train paradigm was used by Thornton and Coleman (1975) where ABRs were recorded to each click in the train
PAGE 46
34 for ISis of 15, 24, and 32.5 msec. These authors found that the amplitude and latency changes of all the waves were nearly complete by the 4th or 5th stimulus and the amount of amplitude reduction increased with decreasing ISI and de creasing stimulus intensity. Wave V was found to show the least amount of amplitude reduction compared to the earlier waves. In addition, Thornton and Coleman (1975) reported that the latency increases were smaller for the smaller amplitude reductions, i.e., wave V showed the smallest latency increase and wave I showed the largest latency increase. Thornton and Coleman (1975) suggested that the decrement in wave I amplitude is due to a reduction in firing rate of all active nerve fibers while the number of nerve fibers remains constant. In the brainstem, the reduced firing rate of incoming fibers resultsin fewer responding cells because some cells may not reach an adequate threshold level. This should re sult in amplitude decrements at each brainstem level parallel with (or greater than) wave I. However, the amplitude decrements become less at more rostral brainstem levels be cause of an increasing number of fibers and complex inter connections at each successive stage which results in a smaller number of adapted outgoing fibers than the number of adapted fibers at the input.
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35 Pratt and Sohmer (1976) found, in humans, that as click rate increased from 5 to 80 / sec wave I amplitude was significantly reduced, but showed no latency change, and wave V latency increased, but showed only small ampli tude changes. The latency change of each wave was found to be greater than the wave preceding it (accumulative). These authors suggested that each wave is influenced by preceding waves and "at a particular nucleus a smaller number of in coming fibers would be active and their synapses less effec tive, so that it would take longer for the excitatory synaptic potential to reach the threshold of firing of outgoing fibers" (p. 90). The amplitudes of later waves remain stable because of increasing number of neurons at higher levels which receive input from a smaller number of lower-order fibers (divergence) as well as each higher order neuron receiving many endings from lower-order fibers (convergence). Don, Allen, and Starr {1977) studied the latency shift of wave Vin normal adults using click repetition rates of 10, 30, 50, and 100 / sec at levels up to 60 dB HL and found significant latency increases (up to 0.9 msec) for repetition rates from 10 to 100 / sec. This latency shift was found to
PAGE 48
36 be equivalent to a 15-20 dB reduction in the stimulus level and these authors felt that repetition rate should be con sidered carefully in interpreting response latencies. These authors described the latency shifts as a linear function of repetition rate, which they point out as being different from the exponential shift of the AP latency found by Egger mont and coworkers. The different behavior of wave V compared to Ni of the AP was interpreted by Don et al. (1977) to possibly suggest different peripheral and central responsive ness to repetitive stimuli due to adaptation mechanisms along the monaural pathway. However, Don et al. (1977) felt that the locus of the wave V effects was at the auditory periphery. Unfortunately, the resolution of waves I-IV was not clear enough in the study of Don et al. (1977) to make any direct comparisons of peripheral and central effects. The latency increases with repetition rate were also found to be independent of stimulus intensity. In another part of the same study, Don et al. (1977) used click-trains with ISis of 10 msec and demonstrated that the latency shift of wave V was complete by the 5th stimulus. No latency shift of wave V was observed in the click-train experiment when the ISI was 100 msec. A binaural central mechanism was ruled out in a third experiment where they found no latency change to the 1st
PAGE 49
and 20th click presented to the ipsilateral ear while the 2nd through 19th click were presented to the contralateral ear (ISI=lO msec). 37 As the above studies show, there does not appear to be complete agreement on the effects of increasing repetition rate for the various components of the ABR. The effects of click repetition rate on the ABR in normal adults have been extensively studied by several other investigators for repetition rates ranging from 2/sec to 100/sec (Pratt and II Sohmer, 1976; Zollner, Karnahl, and Stange, 1976; Hyde, Stephens, and Thornton, 1976; Klein and Teas, 1978; Harkins, McEvoy, and Scott, 1979; Martin, 1976; Weber and Fujikawa, 1977; Scott and Harkins, 1978; Chiappa, Gladstone, and Young, 1979). In general, the majority of these studies have shown that the greatest effect of increasing click repetition rate has been a large reduction of wave I amplitude and a sub stantial (up to about 0.9 msec) latency increase of wave V. In contrast to the study by Don et al. (1977), most studies describe the latency change of wave Vas being a logrithmic function of repetition rate. In contrast to Thornton and Coleman's (1975) click-train study, most investigators report that wave I latency does not increase or increases only slightly at the higher repetition rate. Most investigators
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38 agree that there is a cumulative latency increase for successive peaks after wave I as a function of repetition rate, suggesting that the latencies of successive waves are influenced by the preceding wave. In contrast to Don et al. (1977) and Thornton and Coleman (1975), the studies by Z~llner et al. (1976) and by Weber and Fujikawa (1977) have shown that the effects of repetition rate are dependent on stimulus intensity, i.e., greater effect at higher inten sities. The relatively large wave Vat higher repetition rates has enhanced the popularity of using wave V for ob jective clinical audiometry. However, as suggested by Zollner et al. (1976), the examination of the waves earlier than wave V, especially wave I, as a function of repetition rate may be a more useful indicator of inner ear damage. Bauer, Elmasian, and Galambos (1975) compared the psychophysical loudness judgements with human ABRs for the second of two 0.2 msec 8 kHz tone-bursts separated by intervals ranging from 100-400 msec. The psychophysical results showed the expected "loudness enhancement" for some of the conditions above 15 dB, but wave V latencies and amplitudes were not affected under any of the conditions. The total response power of the ABR was reduced which indicated a decrease in the amplitude of the waves earlier than wave V since wave V
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39 voltage was not altered (and loudness was enhanced). These results suggest that the ABR does not correspond to perceived loudness under certain conditions. Kodera et al. (1978) compared the effects of repetition rate on the ABR and the middle latency components using 500 and 1000 Hz tone-pips in order to determine which response would be more suitable in routine clinical testing. It was observed that as ISI decreased from 104 to 32 msec the middle conponent's amplitude decreased significantly, while wave V was not appreciably affected except for a slight increase in amplitude at ISI=32 msec due to superpositioning of responses from preceding stimuli. Latency increases were found only for wave Vas ISI decreased. Huang and Buchwald (1980), on the other hand, showed that in cats the amplitude of the later ABR waves (P3, P4) decreased by the same amount as the earlier waves (Pl, P2) when repetition rate was increased. The amplitude de crease was gradual up to a repetition rate of 20/sec then decreased sharply for rates up to 200/sec. All waves showed a slight (0.1 msec) latency increase as repetition rate was increased from 50 to 200/sec. Increasing the stimulus duration beyond 10 rnsec caused an interaction with repetition rate, i.e., using 100 msec tone-bursts at a rate of 10/sec
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40 produced a larger amplitude reduction than seen for the short duration stimuli at 10 / sec. Duration-rate inter actions have also been shown to affect the wave V amplitude in humans (Hecox et al., 1976). In monkeys, Allen and Starr (1978) found no latency shift of wave I, a significant (p < .05) latency shift of .1 msec for wave II, and 0.4 msec in wave IV (comparable to wave Vin humans) between click repetition rates of 10 and 100 / sec. Significant interaction was found between rate and stimulus intensity, i.e., at higher intensities wave IV showed larger latency increases with increasing repetition rate. Kevanishvilli and Lagidze (1979) used a response con ditioning paradigm to study the temporal effects on the ABR in humans. The conditioning click and the test click were separated by .6.Ts of 5 or 10 msec. By subtracting the re sponse to the conditioning click from the response to the conditioning click-plus-test click, the contamination by middle latency components and postauricular potentials was eliminated. Their results showed, for a .6.T of 10 msec, that wave I was significantly reduced in amplitude while wave V was not affected. The latency changes of wave I and V were the same. For .6,T=S msec, wave V latency increased much more
PAGE 53
41 than wave I latency. These authors attributed their find ings to peripheral desynchronizing factors which have different effects on various waves depending on the durations of neural contributions to each wave, i.e., wave V shows less amplitude decrease because of its relativel y longer response component which makes it less susceptable to desynchroniza tion. The effects of repetition rate on the ABR as a function of age were first reported by Jewett and Romano (1972) for cats and rats during the first 2-3 months of life. Young kittens were found to be different from adult cats and young rat pups in that the kittens did not show any responses to 100/sec clicks until several days after ABRs were detectable at slower repetition rates. Soon after 100 / sec responses could be ob tained in the kittens (about 16 days old) subsequent stimula tion with clicks at 10 / sec resulted in a lack of response for several minutes, i.e., there was a "fatigability" factor in the young kittens. For the rat pups and older cats, stimulation at 100 / sec produced decreased amplitude and in creased latency, which the authors suggested was due to some manifestation of a "recover y cycle." In humans, the effects of repetition rate on the ABR as a function of age have not been firml y established. Fujikawa
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42 and Weber (1977) compared wave V latency shifts as a function of repetition rate in populations of 7-8 week old infants, young adults, and geriatrics. All groups showed a latency shift of wave Vas repetition rate was changed from 33-67/sec, and the amount of latency shift for the young adults and in fants was the same except for 67 / sec where the infants showed a greater latenc y shift. In contrast, the geriatric group showed considerably longer wave V latencies than the adults and infants at all the rates tested. The different behavior of the geriatrics was attributed to a possible reduction in the number of nerve fibers and / or cell count, whereas the different behavior of the infants (at the highest rate) may reflect a m y elination factor. Salamy et al (1978), on the other hand, found that for infants from birth to 6 months of age, the effects of increasing click repetition rate from 10-80 / sec (decreased amplitude of earlier waves and increased latency of wave V) was not significantly different from adults except for the newborns (24-27 hours) This finding suggested that the mechanisms responsible for rate effects are mature very shortly after birth. Despland and Galambos (1980) found that responses to clicks up to BO / sec could be measured in premature infants above 30 weeks gestational age and that the latenc y shifts of wave Vas a
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43 function of repetition rate decreased with age from 270 usec for each 10 / sec increase in rate at the earliest age, down to about 35 usec for each 10 / sec increase in rate found in adults. Wave I was also found to increase in latency as a function of repetition rate; however, the amount of latency shift was about one-half that seen for wave V. The rate function of wave I across age paralleled wave V. These authors state that one-half of the rate effects occur at the peripher y and one-half in the brainstem. The effects of repetition rate on the ABR in clinical patients have also not been extensivel y studied. Stressing the s y stem b y increasing repetition rates (or other tem porall y related stimuli) could be useful for differentiating certain central brainstem pathologies. Stockard and Rossiter (1977) and Stockard, Stockard, and Sharbrough (1977) found that in patients with multiple sclerosis, a demyelinating disease of the central nervous s y stem, the ABRs to clicks at 10 / sec were abnormal in all of them and showed increased latenc y and / or reduced amplitude of various waves. Increasing th e repetition rate to 25-30 / sec enhanced the sensitivity of the test, i.e., greater response abnormalit y was found in the patients with multiple sclerosis than could be accounted for by the normal rate dependent changes. Since all the
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44 patients had confirmed multiple sclerosis and all showed abnormal responses at the 10/sec rate, there did not appear to be any additional information obtained from the higher repetition rate. Robinson and Rudge (1977), however, did find that recording the ABR at high repetition rates was useful in detecting and confirming patients with multiple sclerosis. A unique procedure was used by Robinson and Rudge (1977) for stressing the auditory system. The ABRs were recorded to the first of a pair of clicks separated by 5 msec. In normals, when the pairs of clicks were presented at a rate of 2.5 / sec the latencies and amplitudes of all the waves were the same as to a single click. When the pairs of clicks were presented at a rate of 20 / sec the response to the first click showed significant increases in latencies of waves I, III, and V, but wave I latency did not change (changing repetition rate of single clicks from 2.5 to 20/sec showed an increase in wave III latency only). Using this paired-click para1igm presented at 20 / sec in patients with multiple sclerosis, Robinson and Rudge (1977) found that 55% of those patients who had abnormal latencies to single clicks and 57% of those patients who had abnormal amplitudes to single clicks (and normal latency) showed an abnormal increase in wave V latency to the paired-clicks. More importantly,
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45 three patients who had normal ABRs to single clicks showed either an abnormal increase in wave V latency or no response at all to the first click of the pair. These authors suggest that stressing the auditory system by combining paired-clicks with a high rate of presentation (when either alone produced no change) can reveal changes in the ABR which can be a useful indicator of patients with unconfirmed or suspected multiple sclerosis, even when normal ABRs or normal latencies with reduced amplitudes are found to single clicks (20/sec). In summary, the effects of preceding sounds on the ABR response to another sound have been shown not to simply parallel those changes that occur for the AP response. The most obvious difference has been a stability of wave V ampli tude concomitant with a large increase in wave V latency, whereas N 1 has shown large amplitude reductions with only slight latency changes. These differential manifestations to repetitive stimuli at two levels of the auditory system preclude the simple assumption that the perception of one sound preceded by another sound is entirely due to peripheral mechanisms which are "relayed" unchanged to higher centers. Because ABRs do not always produce clear and stable waves earlier than wave V, comparisons between waves are often difficult to make. By simultaneously recording auditory
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46 nerve activity from the ear canal, more direct comparisons can be made. Further investigation of the effects of temporally related sounds at different levels of the auditory system appears warranted. Once the normal characteristics are known more fully, application to clinical populations may have more success in understanding normal auditory pro cessing.
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CHAPTER II METHODS Click-evoked ABRs and APs were recorded using a forward masking paradigm for delay times (.6.T) of Oto 100 msec. Responses obtained, as a function of .6.T, following a 60 msec wide-band masker (.02-10 kHz) set at a level sufficient to "full y mask wave V of the ABR (.6.T=0 msec) are called the "standard" series. In addition to the "standard" series, responses were obtained (as a function of .6.T) for variations of masker duration, masker level, and masker low frequency cutoff. Subjects Fifteen normal hearing (ANSI, 1969) adults, 23-33 years of age, served as volunteer subjects. All 15 subjects received the "standard" series. For each variation in masker, i.e., duration, level, or low frequency cutoff, 7 subjects were used. Six subjects were willing to return for a second recording session, providing data for two different variations of masker. 47
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48 Equipment Stimuli The probe stimuli were 0.1 msec broadband clicks generated by a shift-register pulse output with the duration of the clicks controlled by a precision one-shot (logic level). Intensity calibration for the probe clicks was based on standard reference levels which have been in use at this laboratory for the past 5 years. These levels were obtained by determining the behavioral threshold to the clicks presented at a repetition rate of 5 / sec for a group of normal hearing listeners. This was considered 0 dB HL (Hearing Level) to which other intensity levels wer-e referenced. Calibration levels were determined by measuring the voltage (and converting to dB SPL) of the clicks at 60 dB HL presented at a repetition rate of 250 / sec on a true RMS voltmeter (Ballantine, 320). Corresponding peak-to-peak voltage was measured on an oscillo scope (Tektronix, RM561A). Calibration levels for the 60 dB HL broadband clicks were 72 dB SPL and .07 volts peak-to-peak. An attenuator (Hewlett-Packard, 350D) provided control of the click level as measured on the true RMS voltmeter. For this investigation, the probe click intensity level was always set at 50 dB HL.
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49 The masker stimuli were obtained from a random noise generator (Grason-Stadler, 455C). The duration of the noise, onset-to-offset, was determined by another precision one shot and shaped by an electronic switch to produce nonlinear rise-fall times of 10 msec. An attenuator (Hewlett-Packard, 350D) independently controlled the intensity of the noise masker. The bandwidth of the noise was produced by feeding the white-noise output of the noise generator into two variable bandpass filter networks (Rockland, 816) wired in series. Each bandpass filter had a rolloff of 48 dB/octave with a resultant rolloff of 96 dB/octave. The high frequency cutoff was always set at 10 kHz. The low frequency setting of the noise could be changed to produce the desired maskers, e.g., .02-10 (referred to a wide-band), 2-10, 4-10, and 6-10 kHz. The frequency characteristics of the earphone (TDH-39) produced additional filtering of the signals. The acoustic outputs were measured in a standard 6-cc coupler with a condenser microphone (Bruel and Kjaer, 4132) connected to a sound level meter (Bruel and Kjaer, 2203). Spectral analysis was performed by a software Fast Fourier Transform (FFT) program. The noise spectra and earphone characteristics are shown in Fig. 1. A block diagram of the stimulus generation and masker probe timing relation are given in Fig. 2. To produce the
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z 0 <( z w <( co -0 0 30 60 2-10 kHz 0 2 4 8 16 FREQUENCY (kHz) Fig. 1. Spectra of the masking stimuli obtained through the earphone (TDH-39). V1 0
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Fig. 2. Simplified block diagram of the stimulus generating and response recording equipment. Inset shows the timing relation of the click and noise for the masking conditions.
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t JO i SC Ge,, o G en , One suot Noi s~ Uur 0 ne l snr Cli c k Dur. 0 n~ Shot 3 S ,,,. ch Fu l se I 1 0 '4o 1 0 190 5 tfo i se "/Cli-----t' ____ _, r b Ti m in g r e l ation of t he signal and n o ise used in t he mask ing con d i t ion s. Nu m bers ar e in msec R a t e o f pre s ent a tion is 9/s ec. -~ Elec. S1 / j t C j 4a S ti m ul us g e neratin g and respon s e r ec ording e quip me n t ; ~ J B L Attn . rt A,1;p r 2 h e aa pnone I ,.,. -r I A : tn I Scope R~S 2 Met er ?D? 8c I:: i 1 t e r i 3 o mputer ::.cope l . -, T ape ---G clS s ~ r 0ss Rec or ce r 1:;p t\ rr p l 2 ,, .,, + t.] i Scope .. 4 G D,, \ '-./ 5 Ul I\.)
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forward masking paradigm, the click delay relative to the masker was varied by another precision one-shot. The 53 delay time from the masker offset to the click onset was defined as ~T. The values of 6T used were 0, 6.2, 12.5, 25, 50, 100 msec. These were determined by observation on the oscilloscope display and setting of the one-shot. A synch pulse (97 usec) to the computer was initiated at the probe click onset. The masker-probe pairs were presented at a repetition rate of 4 / sec which resulted in an intermasker interval (IMI), i.e., time between offset of one masker and onset of subsequent masker, of 190 msec. For the series where masker duration was varied, the repetition rate remained constant (4 / sec) resulting in different IMis for each duration. For the maximum ~T (100 msec), the following masker occurred 90 msec later. This reduced any possible backward masking effects. The probe and maskers were fed sequentially to a mixer, an amplifier (James B. Lansing, SE 400S), a final attenuator (Hewlett-Packard, 350D), and then monaurally presented through the earphone. The equipment allowed for the presentation of the signal or noise separately or the signal presented with (after) the noise. The signal and noise levels could be varied independently or simultaneously.
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54 Electrodes Three silver / silver chloride scalp electrodes were used for the ABR recordings. The electrical activity was recorded between forehead and ipsilateral mastoid with the contra lateral mastoid serving as ground. The electrode sites were abraded with electrode paste (Grass, EC-2) then taped to the forehead and mastoids. Electrode resistance was checked with a VOM meter and the electrodes were reattached if the resis tance was greater than 5 k Ohms. The ear canal recording required a specially made elec trode. This was made of 6 inches of teflon coated silver wire (diameter=.007 inches). The teflon was scraped off the end and the stripped end of the wire then wrapped around the end of a narrow (1 / Sth inch) piece of polyurethane surgical rubber rubing (about 3 / 4 inch long). The tubing was then bent in a "V" before inserting into the ear canal. After the electrode was positioned inferiorly in the ear canal, with the aid of an otoscope, earlight, and forceps, the tubing was released so that it opened slightly to hold itself in place against the walls of the ear canal. Good responses were obtained only when the wire wrapped end of the ear canal electrode was in contact with the canal wall. If poor recordings were obtained the ear canal electrode was repositioned, but if poor responses were still obtained after one or two
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55 attempts at repositioning no further attempts were made and ear canal recordings were not obtained. The reference electrode for the ear canal recordings was the ipsilateral mastoid and the ground was the contralateral mastoid. Procedures The subject laid on a bed in a sound treated room (IAC). Two recording channels were used for independent monitoring of the ABR and the AP. Each electrode configuration was connected to a separate high-impedance cathode follower (Grass, HIP 511E) and then to separate a.c. coupler high gain preamplifiers (Grass, P511). The gain of the amplifier was set at 100,000 and bandpassed at 0.03-3 kHz. The electrical activity from the ABR and ear canal electrodes was recorded on separate channels of an FM tape recorder (Ampex, FR l00A) bandpassed at 0-2500 Hz at 7 1/2 i.p.s. and kept for later off-line processing. Additional response filtering (Krohn-Hite, 330M) was done ahead of the computer with a bandpass of 70-1600 Hz. The subject's electrical brain activity was also monitored on the oscillo scope. A general purpose computer (Digital Equipment, PDP-Se) was used for the response averaging. Each response represented the averaged stimulus-locked activity for 1200-1500 samples. A sweep duration of 10.0 msec (39 usec/point, 256
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56 points) was used for the ear canal response. For the ABR, a sweep duration of 20.2 msec (79 usec / point, 256 points) was used. A toggle switch allowed processing of either the ABR or the AP activity. However, after determining whether or not the ear canal electrode was working properly, only the ABR was monitored on-line and the averaged ABRs were stored directly on floppy disks. The AP responses from the ear canal were played back later off the FM tape and then stored on the floppy disks. A feature of the averaging pro gram was variable artifact rejection, which was set by two independent cursor lines. In these experiments, electrical activity greater than 7 volts was rejected from the average by the computer. This criterion excluded unwanted muscle or movement artifacts from the averaged response. In off-line processing, latencies and peak-to-peak ampli tudes were obtained by means of a cursor which could be set at any location in the waveform and read from the monitor display. Each session began with the "standard" series which con sisted of a 60 msec wide-band (0.2-10 kHz) noise masker pre ceding the broadband probe click (50 dB HL). The level of the wide-band masker was set (and measured) so that, with a ~T of O msec, the wave V response was as fully masked as
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57 possible (not discernible in the averaged response). The "standard" recovery function was obtained by recording the probe responses for the different ll.Ts. Following the "standard" series, the subject received one of the following series: 1. Masker duration was changed to 30 and then 120 msec and responses were recorded for each AT. 2. Masker level was changed -10 dB and then +10 dB relative to the "standard" series and responses were recorded for eachll.T. 3. The low frequency cutoff of the high-passed masker (60 msec duration) was systematically raised while maintaining a constant spectral level set by the "standard" series. For each of the maskers 2-10, 4-10, and 6-10 kHz, responses were recorded for each ~T.
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----------------------CHAPTER III RESULTS Auditory Brainstem Responses (ABRs) were collected on a group of 15 normal hearing adults. In addition, wholenerve action potentials (APs) were simultaneously recorded from some of the subjects. Using a forward masking paradigm, responses were recorded only for the probe click. Not all recording sessions produced usable AP data because of either an inability to obtain proper placement of the ear canal electrode after repeated attempts or the subject decided against the use of the ear canal electrode. Out of 17 recording sessions where an ear canal electrode was attempted, 9 produced usable AP data. One reason for difficulty with the ear canal electrode was that the wrapped end often did not make contact with the canal wall, e.g., the tubing would "hang up" on a protruding edge of the canal or cerumen. In addition, if the electrode was not positioned properly on the first attempt it was difficult to reposition the electrode (because it sprang open) without causing discomfort to the subject. If the electrode could not be repositioned easil y it was removed and onl y the ABR was collected. 58
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59 Each subject received the "standard" series; 60 msec wide-band masker set at an intensity level sufficient to eliminate as completely as possible (fully mask) the wave V peak of the ABR when ~T=O msec. Responses to the probe click were then obtained for each .6.T. All subjects received the "standard" series which provide the largest amount of data and which served as a reference for subsequent variation of masker parameters. Three subjects (DR, TL, PD) received two of the additional series, i.e., variation in masker dura tion, level, or low frequency cutoff in the same (extra long) session and two subjects (DS, MO) were used for two of the additional series on separate days. Table I summarizes the recording series for each subject and includes whether or not corresponding ear canal responses were obtained. ABR data as a function of .6.T were obtained for 7 subjects for each of the variations in masker parameter and AP data was obtained for at least three subjects for each variation in masker. Examples of the ABR and AP waveforms to the probe click (SO dB HL) without the presence of the forward masker, i.e., unmasked control responses, are shown in Fig. 3. In the ABR waveforms on the left of Fig. 3 the wave V peak is easily identifiable in all of the examples. Peaks earlier than wave Vin the ABR can also be seen in some of the control
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60 Table I. Forward masking series received by each of the subjects ( +) indicates success and (-) indicates failure in obtaining data for ABR / AP . Maskin9 Condition High-Pass Masking Masking "Standard" Subject Masking Duration Level Series KC + / + + / + DS + / + + / +/+ DR +/+ + / + + / + MO + / + + / + / + TL + / + +/+ + / + PD + / +/+/NK + / + / + / BK + / + + / + KG + / +/MS + / + +/+ CB + I +/SP + / + +/+ SL + / +/SW + / + + / + GC +/+ I Total 7 / 5 7 / 3 7 / 3 15 / 9
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Fig. 3. Examples of unmasked control response waveforms. Wave Vs and N 1 s are indicated on their respective waveforms. Note the different time and amplitude scales for the ABR and the AP.
PAGE 74
SUBt KC DR DS HO HS SP ABR. UNHSKED RESPONSES .4uvL 2 msec I msec I I I I I I I
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responses, but are not as easily identifiable in all sub jects. Only the wave V peak was systematically measured. The latencies were measured to the positive wave V peak 63 just prior to the characteristic sharp negative trough occurring in the appropriate latency range for this response, i.e., between 6 and 10 msec. In some instances wave V appears as a shelf on the positive peak just before the negative trough, an example of which can be seen for subject KC in Fig. 3. The peak-to-peak wave V amplitudes were measured from the wave V peak to the following negative trough. For the 15 subjects, the mean latency and~ 1 standard deviation (S.D.) for the unmasked control wave Vis 6.815 .220 msec. The mean peak-to-peak amplitude of the control wave Vis .223 .067 volts. The AP responses from the ear canal, shown on the right portion of Fig. 3, corre spond to the simultaneously obtained ABRs shown on the left. The AP shows an initial negative trough (N 1 ) followed by a larger positive peak which is generally broader in time than the Ni trough and has a negative-going dip superimposed on the positive peak which never goes below baseline in any of the subjects. There is also considerable variability in the configuration of the ear canal AP across subjects. Those subjects with smaller amplitudes have a broader waveform
PAGE 76
64 and a less noticeable negative-going dip on the positive peak, most likely a result of the relation of the electrode position to the potential sources. Latency measurements of the AP are made to the base of the N 1 trough. For the unmasked N 1 controls, the mean latency is 2.864 .135 msec. The peak-to-peak amplitudes are measured from the N 1 trough to the nearest following positive peak. The mean N 1 control amplitude is .461 .200 volts. Considerable intersubject variability of N 1 amplitude was apparent and was primarily related to the position of the ear canal electrode. Intra subject N 1 amplitude variability across the recording session was relatively low. The AP waveforms are similar to those found by other investigators from the ear canal (Coats, 1964a, 1976; Yoshie, 1968) except for the dominance of the positive peak following N 1 and a poorly defined N 2 in the AP waveforms of this investigation. Comparisons between the unmasked control and the forward masked responses are made as a function of the time interval between masker termination and probe onset (~T) for both the mean latenCESand mean amplitude; of wave V and N 1 The recovery function, defined as the probe response magnitude (latency or amplitude) as a function of ~T, represents the time course of recovery from forward masking and is described below for the different masker variables.
PAGE 77
65 "Standard" Recovery Function The "standard" forward masking series was obtained for the ABR in all 15 of the subjects and AP data -were included from 9 of the subjects. Only one "standard" series for each subject was included in the analysis. Masker levels necessary to "fully mask" wave V ( .6. T=0 msec) ranged from 74 to 82 dB SPL. Preliminary data on two subjects using a simultaneous continuous wide-band noise masker resulted in about 8-9 dB less masker level necessary to fully mask wave V than for the pulsed (60 msec) masker at .6.T=0 msec. Leaving the masker level constant and switching from continuous to pulsed in the simultaneous presentation maintained the fully masked condition. The levels of masker necessary to fully mask wave V were considerably higher than needed to fully mask the Ni response. In fact, it was often difficult to be absolutely certain when wave V was fully masked because of a seemingly apparent resistance to masking, especially in a forward mask ing paradigm, or because of a relatively more "noisy" base line. As the masking noise was added to the recording paradigm and the intensity raised, the most apparent effect en wave V was an increase in latency. With additional in creases in masker level, the amplitude of wave V diminished. In some cases, adding 2 or 3 dB of masker caused the wave V
PAGE 78
66 peak to go from almost full amplitude (with longer latency) to unobservable. Figure 4 shows typical unmasked controls and forward masked ABRs along with corresponding AP waveforms for the "standard" series. The probe-evoked ABRs and APs show alterations produced by the preceding wide-band masker. Wave Vis easily observed in the masked waveforms and shows a considerable increase in latency (relative to control) for short 6.Ts. Wave V amplitude is not severely altered except at the earliest 6,Ts. In addition, the peaks earlier than wave V are not clearly identifiable in the masked waveforms. (Only 1200-1500 samples were used for the averaged responses and adding more samples may have improved the clarity of the earlier peaks.) The N 1 latency, on the other hand, shows only a slight latency shift even for the shortest 6. T, but the N 1 amplitude is considerably reduced even for the longest 6.T. The "standard" latency recovery functiorabased on the mean values are plotted in Fig. 5 for wave V, N 1 and the computed latency difference between wave V and N1 (V-N 1 ) representing the central brainstem conduction time. The unmasked control (CNTL) values are also included in Fig. 5 and subsequent figures. For wave V (top of Fig. 5), the
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Fig. 4. Example of ABR and AP probe response waveforms as a function of b,, T for the "standard" series. The preceding masker was a 60 msec wide band noise burst set at a level sufficient to "fully" eliminate wave V for 6. T=O msec.
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UNti 6T 0 6.2. 12.5 25 50 100 'STANDARD' SERIES l( 2 msec l msec O'I OJ
PAGE 81
(\ 0 I E V >u z w t< .J 69 8.50 7 .50" WAVE V l I I 8.50' S.50 T 4.58 V-N 1 T X 1 3.58 T T r r B B Nt l l J. 2.58 0 6 12 25 50 100 CNTL DELA l TIME (,nsec) Fig. 5. Mean and S.D. of wave V, N 1 and V-N1 latencies as a function of ~T (dela y time) for the "standard" series. Unmasked con trols (CNTL) are indicated on the right in this and subsequent figures.
PAGE 82
70 maximum mean latency shift (increase) occurs at 6T=6.2 msec and is 1.288 msec longer than the control latency. For 6T=0 msec, there are no wave V responses because of the criterion ( fully maskedl. As 6 T increases, the mean latency of wave V systematically decreases towards the control latency. The time course of wave V latency recovery from forward masking can be described as a linear function of log 6 T between the values of 6 T used in this investi gation, i.e., 6.2-100 msec. Although 6T values above and below 100 and 6.2 msec were not included, one may expect deviations from the logrithmic function for other values of 6T. However, between 6Ts of 6.2 and 100 msec the equation LATv = -.92 log 6T + 8.867 fits the mean wave V latency data quite well. For all 6Ts, the mean masked wave V latency is greater than the mean control wave V latency. For the "standard" series, as well as for each of the series described in following sections for the different masker variables, an analysis of the data was performed using Statistical Analysis System (SAS) programs (University of Florida Computer Center). An analysis of variance appro priate for unbalanced data (General Linear Systems, GLM) was used and included partitioning out the variance due to subjects as well as the different "treatment" variables. As
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71 expected, for wave V latency for the "standard" series, L. T was found to be highly significant (F=l91.24, df=S, 69 p < .001. The unmasked controls were not included in any of the analyses of variance. In addition, whenever the ampli tudes of the responses were not measureable the y were assigned a value of O pvolts, but their corresponding latencies were treated as "missing" in the analyses. An additional analysis was performed in order to test which of the "treatment" means are significantly different (p < .05) from the unmasked con trol mean, i.e., to determine where complete recovery occurs. This was done using a paired-comparison procedure based on least-square means (for unbalanced data) by SAS (LSMEANS/ PDIFF) for each possible comparison. (A Duncan Multiple Range Test was also included to test for differences among means {p < .05) and the results were in almost all cases the same as the results for the LSMEANS test). Table II gives the means and standard deviations of wave V latency as a function of i..,. T for the "standard" series. Also in cluded in Table II and subsequent tables are indicators (*) for those masked response means which are significantly different (p< .05) from the unmasked control response mean. As Table II shows, wave V latency is significantly different from control even for ~ T=lOO msec, i.e., complete recovery has not occurred.
PAGE 84
Table II. Means and standard deviations (S.D.) of wave V and N! latencies for the "standard" series. Asterisks (*) are used in this table and subsequent tables to indicate which mean values are significantly different from the unmasked control mean (CNTL). Wave V N Mean-msec S.D. 0 15 NR NR 6.2 14 0.1 0 3* .318 Delay Time ( .6.T) rosec 12.5 25 50 15 7.878* .301 15 7.578* .296 15 7.300* .320 100 15 6.999* .266 CNTL 15 6.815 .220 -----------------------------------------N Mean-msec S.D. N Mean-rnsec S.D. NR NR NR NR NR NR 5 3.308* .141 5 4.611* .151 9 3.247* .269 9 4_599* .482 9 3.200* .222 9 4.372* .402 9 3.125 8 2.959 9 2.869 .23~3-'----~-~1~5~7 __ _.;._1 3~5 __ 9 4.142 490 8 4.012 .328 9 3.956 .353 -.J N
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73 The N 1 "standard" latency recovery function is shown in the bottom portion of Fig. 5. As for wave V, the maximum mean latency shift of N 1 occurs at the shortest ~T; however, the amount of maximum N 1 latency shift, .444 msec, is only about one-third that seen for wave V (1.288 msec). The time course of the N 1 latency function, like for wave V, can also be described as a linear function of log .6 T between 6. Ts of 6.2 and 100 msec, but the slope of the N 1 recovery func tion is much less steep than for wave V. The mean N 1 latency data as a function of 6T fit the equation, LATN 1 = -.16 log 6T + 3.433. For N 1 6T is also highly significant (F=l4.44, df=S, 35 p < .001). Table II includes the means and corresponding statistics for N 1 latency as a function of D T. N 1 latency has completely recovered by t,. T=50 msec. The V-N1 latency interval (middle portion of Fig. 5) also changes as a function of D T as expected due to the longer latency changes of wave V relative to N 1 The mean unmasked V-N 1 latency interval is 3.956: .303 msec and is in agreement with other investigators (Davis, 1976; Elberling, 1976; Rowe, 1978; Coats et al., 1979). Again, l..T is highly significant (F=l4.56, df=5, 35 p< .001). The V-N 1 latency interval is equal to the control latency for L Ts of 50 and 100 msec (see Table II).
PAGE 86
74 The amplitude recovery functions, inJUvolts, for wave V and N 1 are shown in Fig. 6. Although the variability is large, there is a systematic increase in amplitude for both wave V and N 1 as ~T increases. However, the masked wave V amplitude is less than the wave V control amplitude only for ~Ts below 25 msec, while the masked N 1 amplitude is dramatically reduced at all ATs. To describe the amplitude recovery functions in another way,the mean amplitudes are normalized by considering the amplitude of the mean unmasked response as 100% ~nd the mean amplitudes for the responses at each 6 T are then expressed as a percent of the mean unmasked response (% control amplitude). The percent con trol amplitude is used to describe the remainder of the amplitude recovery functions. Figure 7 shows the amplitude recovery functions for both wave V and N 1 and one can easily notice the different behavior of the two responses. For wave V, the amplitude recovery function does not follow a simple logrithmic function as was seen for the wave V (and N1) latency recovery functions; however, a monotonic growth function is apparent across bT. For wave V ampli tude, b T was a significant factor (F=B.72, df=S, 69 p < .001). Wave V amplitude recovers from fully masked to 60% of control by LT=6.2 msec and has completely recovered (p < .05)
PAGE 87
Fig. 6. Mean and ~l S.D. for wave V and N 1 amplitude (vol ts) as a function of T for the "standard" series.
PAGE 88
76 e.~ ... ,a..,.,s. a WAVE. V l&J 0-.2.9r Q ::> IJr 1-t .J 9'.,29" l CL J: < !> ILi e.ur > < :I e.w ~-49 0.39 I ... 0 Nt > ::, la.29 V ILi Q ::> Ie.2a1-t -J a. J: < 0 .10 z ra-.a 0 6 12 25 50 Ul0 DElAY TIME Cmae.c)
PAGE 89
w a :> IH J 0.. I: < J 0 (t: Iz 0 t) t2BJ3" 100.0 80Jl 68.0" 40.0' 20.0' 0 6 12 25 50 DELAY TIME Cm.sec) Fig. 7. Mea n wa v e V and N 1 amplitude reco v er y functions expressed as percent of the mean unmasked control amplitude (100 % ) for the "standard" series. 77 WA.VE V Nt 100
PAGE 90
78 by u T=25 msec (even though wave V latency is not recovered even by T=l00 msec). The slight supernormality of wave V amplitude seen in Fig. 7 at 6 T=l00 msec is not significantly different from the control response. Table III gives the means and corresponding statistics, as a function of LT, for wave V amplitude. The effect of the forward maskers on the amplitudes of the N 1 response was much greater than for wave V amplitudes. As seen in Fig. 7, the mean amplitude (% control amplitude) of N 1 increases from fully masked to only 18% of the unmasked control response at L T=6. 2 msec and is only 65% of the control by L:.T=l00 msec. As expected, L:. T is a highly significant factor for Ni amplitude (F=20.07, df=5, 37 p < .001). The mean N 1 amplitudes are significantly different from the control response amplitude for all DTs, i.e., full recovery does not occur for N 1 amplitude by 6T=l00 msec (even though the mean N 1 latency is equal to control by 6T=50 msec). The N 1 amplitude recovery function is less steep than the wave V amplitude recovery function. Table III gives the summary data for N 1 amplitude along with the wave V data. Figure 8 shows a summary comparison of wave V and N 1 latency and amplitude behavior for the "standard" series from which the following characteristics can be summarized:
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Table III. Means and standard deviations (S.D.) of wave V and N 1 amplitudes for the "standard" series. Delay Time { 6 T) msec 0 6.2 12.5 25 50 100 CNTL N 14 14 15 15 15 15 15 Wave V Mean-v .ooo* .135* .181* .222 .222 .242 .223 (% CNTL} (0) (60) ( 81) ( 99) ( 99) ( 108) (100) S .D. .000 .050 .070 .081 .069 .083 .067 N 9 7 9 9 9 8 9 Nl .ooo* .ass* .168* .193* .213* Mean-pv .300 .461 ( % CNTL) (O} (18) (36) ( 41) ( 46) (65) (100) S.D. .000 .062 .079 .102 .110 .132 .200 -...J I..O
PAGE 92
f\ a I E tk. H i 0 2 .. t< J t...51" til.l V t ,25" n i V NI ,..... z 1.J' R t11.r V ll J NI ,..... NI t_}S 0 .. V .. .... Nt g I.SB Nt tI H J IL ZI.I 8.2S J: V t!1 V ,( ... I.I V V V 6 12 188 6 12 2S SB DEL.Al Ill Casec) DEUl lD C uecl Fig. 8. Summary comparison of wave V and N 1 for the "standard" series. Latency shift refers to the increase in the mean masked response latencies relative to the unmasked control mean. Amplitude reduction is also relative to unmasked control mean. Darkened bars indicate complete recovery based on statistical tests (see text). The wave V amplitude value at L:i.T=lOO msec is slightly larger than control, i.e., a negative reduction. co 0
PAGE 93
1. As ,D.T increases, the latencies and amplitudes of both wave V and Ni monotonically approach the control response. 81 2. The most pronounced effects of the wide-band for ward masker are a decrease in the N 1 amplitude and an increase in the wave V latency. 3. The latency of wave Vis not completely recovered to the control response latency by .D.T=l00 msecf however, the amplitude of wave Vis completely recovered by .D.T=25 msec. 4. The latency of N 1 is completely recovered by .D.T=50 msec, but N 1 amplitude is not recovered even by .D. T=l00 msec. The Effect of Masker Duration The effects of changing the duration of the wide-band forward masker on the probe-evoked wave V responsewer:e investigated in 7 subjects and comparable N 1 data were obtained for 3 of those subjects. The mean values of the probe response latency and amplitude were computed for each .D. T for each of the three masker durations (30, 60, 120 msec). Recall that changing the masker duration resulted in a change in the intermasker interval (IMI) since the repetition rate remained constant. In two of the subjects it was observed that there were no noticeable differences in the wave V responses between constant IMI (rate changes) and constant rate (IMI changes). The effect of keeping IMI constant vs keeping rate constant was not evaluated for the N 1 response.
PAGE 94
82 Figure 9 shows the mean latency recovery functions for wave V and N1 for masker durations of 30, 60 ("standard"), and 120 msec. For wave V there is a systematic increase in the probe response latency as the masker duration increases and nearly equal shifts of latency are observed at eachilT. There is no significant interaction between masker duration and L. T. Masker duration is a significant factor for wave V latency (F=24.68, df=2, 85 p < .001); however, only the mean responses to the 120 msec masker are significantly different from the responses to the 30 and 60 msec maskers. The time for complete recovery of wave V latency increases with increasing masker duration. The mean wave V latency is fully recovered by L T=SO msec following the 30 msec masker, by LT=lOO msec following the 60 msec masker (for this smaller subgroup of subjects this "standard" series is recovered by LT=l00 msec, whereas for the larger group of subjects described earlier wave V latency had not recovered by ..:.T=lOO msec), and is not fully recovered by ilT=lOO msec following the 120 msec masker. Table IV gives the summary data for wave V latency for the different masker durations. In contrast to the mean wave V latency, the mean N 1 latency does not show any significant difference as a function of masker duration (F=0.00, df=2) and the mean N 1 latency
PAGE 95
(\ 0 I E V >u t<( _J 83 7 .50" ~AVE V X 6.58 38 uec 68 IISM: + 128 1KM: 5.50 4.50" V-N t X 3.50' ~ X Nt 2.50 0 6 12 25 50 100 CNTL DELAY TIME Crnsec) Fig. 9. Latenc y recover y functions for wave V, N 1 and V-N 1 probe responses following wide-band maskers with durations of 30, 60, and 120 msec. Level of the masker was set to "full y eliminate wave V response at 6. T=O following the 60 msec masker ("standard" series).
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Table IV. Means and standard deviations (S.D.) of wave V, Nl and V-N 1 probe response latencies for the three master durations. Delay Time ( 6 T} msec 0 6.2 12.5 25 50 100 CNTL Duration-msec 30 8.124* 7.830* 7.629* 7_437* 7.053 6.895 6.884 Wave V Mean-msec 60 NR 8.035* 7.843* 7_595* 7.245* 6.958 6.884 120 NR 8.369* 8.097* 7.840* 7_459* 7.116* 6.884 30 .271 .259 .287 .195 .149 .099 .247 Wave V S.D. 60 .000 .202 .202 .195 .180 .276 .247 120 .000 .486 .272 .234 .181 .142 .247 30 NR 3.223 3.357* 3.100 3.203 3.050 2.980 N1 Mean-msec 60 NR 3.127 3.300* 3.215 3.254 3.053 2.980 120 NR NR NR 3.296 3.242 3.118 2.980 30 .000 .221 .196 .082 .134 .067 .118 N1 S.D. 60 .000 .074 .418 .326 .309 .043 .116 120 .000 .000 .000 .202 .120 .042 .118
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Table IV (Continued) 0 6.2 30 NR 4.571* V-N1 4.742* Mean-msec 60 NR 120 NR NR 30 .000 .260 V-N1 S.D. 60 .000 .037 120 .000 .000 Delay Time 12.5 25 4.147 4.268 4_494* 4.237 NR 4.571* .133 .249 .571 .278 .000 .433 ( T) msec 50 100 3.828 3.822 3.934 3.951 4.210 4.071 .031 .067 .345 .079 .201 .066 CNTL 3.892 3.892 3.892 .184 .184 .184 en u,
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86 recovery curves are the same for the responses following all three duration maskers (see Fig. 9). For all three masker durations, it can be observed that the mean N 1 probe response latency increases slightly at the shorter ~Ts, but the amount of Ni latency shift is much less than the wave V latency shift. The mean N1 latency for this group of sub jects is fully recovered by .6.T=25 msec following all three masker durations. As can be seen in the middle portion of Fig. 9, the V-N 1 latency interval increases with increasing masker duration; however, the differences due to masker duration are not significant (F=l.67, df=2). Table IV in cludes the summary data for N1 and V-N 1 latencies for the different masker durations. The mean amplitude recovery functions for wave V are shown in Fig. 10. For wave V amplitude, there is no signi ficant interaction between masker duration and I.. T 0:1 the probe-evoked responses and the effect of masker duration is significant (F=ll.65, df=2, 99 p < .001), but only the mean responses following the 30 msec masker are significantly different from the responses following the 60 and 120 msec maskers. This is not consistent with differences found for wave V latency, i.e., the mean response following the 120 msec masker was different from the mean response for the
PAGE 99
w Q :J IH J (l I: < .J 0 tz 0 0 87 120.0' A '8 INC C 68 1AC + 128 INC 100.0 80.0 WAVE V 60.0' 40.0' 20.0 0.0 0 6 12 25 50 100 DELAY TIME C~) Fig. 10. Amplitude recover y functions for wave V probe responses following wide-band maskers with durations of 30, 60, and 100 msec. Level of the masker was set to"full y eliminate wave V response at ~T=O msec for the 60 msec masker.
PAGE 100
88 30 and 60 msec maskers. The recovery of the wave V ampli tude is faster following the 30 msec masker than following the 60 and 120 msec maskers which show similar recovery curves. An interesting feature seen in Fig. 10 is an apparent super normality of the mean wave V amplitude for.b.Ts above 25 msec and this supernorrnality is most prevalent for the 30 mse~ masked condition. However, none of the supernormal amplitudes are significantly different from the control response. Wave V amplitude is equal to the control response amplitude for all ~ Ts above 12.5 msec for the 60 and 120 msec masked conditions, and for ATS above 6.2 msec for the 30 msec masked condition. Table V gives the summary data for wave V amplitude for the three masker durations. The mean amplitude recovery functions for N1 for all three masker durations are shown in Fig. 11. Increasing masker duration results in a decrease in the postmasking amplitude of the N1 probe response. For ~ Ts below 25 msec, the N 1 responses were difficult to measure in all three subjects for the 120 msec masked condition (and wave V was easily observed). Unlike N 1 latency, which showed no significant duration effect, N 1 amplitude is significantly affected by masker duration (F=7.79, df=2, 33 p <.001) with the difference occurring between the mean responses to the
PAGE 101
Table V. Means and standard deviations (S.D.) of wave V and N 1 probe response amplitudes for the three masker durations. Dela::i Time { .6.T) msec 0 6.2 12.5 25 50 100 CNTL Duration-msec 30 .106* .131* .200 .241 .252 .262 .218 ( 48) (60) ( 92) ( 110) ( 115) (120) (100) Wave V Mean-uv 60 .ooo* .160* .161* .204 .200 .251 .218 ( % CNTL) ( 0) (73) ( 74) (93) ( 92) (115) (100) 120 .ooo* .120* .141* .206 .238 .218 .218 {0) {55) { 65) {94) {109} {100} {lOOL 30 .039 .027 .074 .079 .072 .069 .082 Wave V S.D. 60 .000 .041 .069 .094 .051 .097 .082 120 .000 .068 .085 .065 .075 .094 .082 30 .ooo* .130* .130* .186* .240* .300 .420 (0) ( 31) ( 31) (44) (57) ( 71) (100) N1 .166* .210* Mean-uv 60 .ooo* .113* .126* .123* .420 ( % CNTL) (0) (27) (30) ( 29) (40) (50) (100) 120 .ooo* .ooo* .033* .100* .136* .206* .420 {0) {0) {8) {24} {32) { 49) {100} 30 .000 .072 .095 .190 .115 .122 .280 N1 S.D. 60 .000 .105 .049 .092 .141 .140 .280 120 .000 .000 .057 .028 .115 .168 .280 0)
PAGE 102
la.I Q :J r H _J (l I: < ..J 0 ll'. r z 8 90 129.0 A 38 IIHC 0 60 IIHC 4' 128 IIHC 100.0" 80.0 60.0 40.0" 20.0' 0 .0' 0 6 12 25 50 100 DELAY TIME Ciasec) Fig. 11. Amplitude recover y functions for N 1 probe responses following wide-band maskers with durations of 30, 60, and 120 msec. Level of the masker was set to "full y eliminate the wave V response at t::,,. T=0 msec for the 60 msec masker.
PAGE 103
91 120 msec masked condition and the 30 and 60 msec masked conditions. The mean N1 amplitude recovery is fastest for the 30 msec masked condition which is statistically equal to the control response amplitude by ~T=lOO msec. The 60 and 120 msec masked conditions do not show response amplitude recovery equal to control response amplitude even by ~T=lOO msec. Table V includes the summary data for N 1 amplitude as a function of ~T for the three masker durations. In summary, the most prevalent effects on the probeevoked responses as a result of increasing the duration of the forward masker are as follows: 1. The latency of wave V increases and the amplitude of N1 decreases. 2. The recovery time increases as the masker duration increases. 3. N 1 latency does not show a significant effect due to masker duration. The Effect of Masker Level The effects of changing the level of the wide-band forward masker on the probe-evoked wave vwereinvestigated in 7 subjects and comparable N 1 data were obtained in three of those subjects. The masker levels were~ 10 dB relative to the level used for the "standard" series (referred to as O dB) and mean latency and amplitude values were computed for each ~T.
PAGE 104
92 Figure 12 shows the latency recovery functions for wave V, N1, and the V-N1 latency interval for the different masker levels. For wave V latency, the interaction between masker level and .6.T is significant (F=2.08, df=B, 81 p .05). The effect of masker level on the probe responses was evaluated at each ~ T (simple effects) and revealed that masker level was significant for ~Ts below 50 msec and all masker levels were significantly different from each other except at c T=25 msec where only the +10 dB masker was significantly different from the O and -10 dB masker. For all three masker levels, the probe response wave V latency is not fully recovered by LT=lOO msec. Since there are no significant differences in wave V latency due to masker level at.v.T=lOO msec, the effect of increasing masker level does not appear to cause an in crease in the time for complete recovery; however, complete recovery time is beyond AT=lOO msec. The effect of increas ing masker level serves to increase the postmasking latency immediately following the masker. Table VI gives the summary data for wave V latency for the conditions of varying masker level. In Fig. 12 (bottom) can be seen the N 1 latency recovery function. N 1 latency does show a significant effect due to the different masker levels (F=S.00, df=2, 20 p L .02). No interaction between masker level and.LT was present for
PAGE 105
(\ 0 4) E V >0 z w I4: ,j 93 8.50 7 .50" WAVE V X 6.50' A ""18 cl re 'slandcrd' 8 cl I + 1118 cl I 5.~ 4_50" V-N1 X 3.50 X 2.50 0 6 12 25 50 100 CNTL DELAY TIME Cmsec) Fig. 12. Latency recover y functions for wave V, N 1 and V-N1 probe responses following 60 msec wideb and maskers with levels of dB relative to the "standard" series (referred to as O dB).
PAGE 106
Table VI. Means and standard deviations of wave V, N1 and V-N 1 probe response latencies for the three masker levels. Delay Time { 6T} msec 0 6.2 12.5 25 50 100 CNTL Level dB -10 8.468* 7.919* 7.749* 7.450* 7.139* 6.983* 6.777 Wave V 0 NR 8.229* 7.922* 7.579* 7.320* 7.053* 6.777 Mean-msec +10 NR 8.650* 8.146* 7.781* 7.403* 7.200* 6.777 -10 .443 .584 .290 .268 .299 .173 .207 Wave V 0 NR .401 .318 .275 .309 .304 .207 S.D. +10 NR .362 .375 .471 .366 .339 .207 -10 NR 3.318* 3.187* 3.180* 3.114* 2.983 2.873 N1 0 NR 3.515* 3.224* 3.139* 3.185* 3.052 2.873 Mean-msec +10 NR NR 3.461* 3.328* 3.370* 3.179 2.873 -10 NR .138 .110 .140 .130 .137 .022 Nl 0 NR .241 .297 .082 .119 .180 .022 S.D. +10 NR NR .041 .073 .079 .053 .022 -10 NR 4.529* 4.476 4.177 3.880 3.969 3.895 V-N1 0 NR 4.437* 4.570* 4.234 3.898 3.781 3.895 Mean-msec +10 NR NR 4.439* 4.137 3.871 3.877 3.895 -10 NR .454 .059 .019 .221 .137 .149 V-N1 0 NR .231 .409 .067 .253 .124 .149 S.D. +10 NR .058 041 .094 .115 .089 .149
PAGE 107
95 N 1 latency. A significant difference occurs only between the +10 and -10 dB masked conditions for the N 1 mean latency. Complete recovery of the N 1 latency occurs by LT=l00 msec for the -10 and O dB maskers. The V-N1 latency interval, on the other hand, does not show any significant effects due to changing masker level (see middle of Fig. 12). Figure 13 shows the mean wave V amplitude recovery func tions. The effect o f changing masker level is significant (F=6.97, df=2, 95 p < .001); however, this significance is due only to the differences observed at ilT==0 msec between the mean amplitudes for the -10 dB condition and the other two levels which have 0 amplitude means. The interaction be tween masker level and L T, however, was not significant. The mean amplitude of wave V equals the control response amplitude by.D.T=l2.5 msec for all three masker levels. Table VII gives the summary data for wave V amplitude as a function of L T for the different masker levels. The N 1 amplitude recovery functions for the three masker levels are shown in Fig. 14. The 0 and -10 dB maskers show recovery functions which are not significantly different from the +10 dB masker recovery function. Again, a much more noticeable effect due to the forward maskers occurs for N 1 amplitude than was seen for N 1 latency (or wave V ampli tude). For this group of subjects, the mean N 1 amplitude
PAGE 108
lu a :) IH .J ll. I: < .J 0 lk: Iz 0 u 96 120 .0' A -10 dB r 'slcandar-d' a 0 dB I + +10 dB I 188.0 80.0' WAVE V 60.0' 48.0 20.0' 0 6 12 25 50 DELAY TIME Ctasec) Fig. 13. Amplitude recovery functions for wave V probe responses following 60 msec wide band maskers with levels of ~10 dB relative to the "standard" series. 100
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Table VII. Means and standard deviations of wave V and N 1 probe response amplitudes for the three masker levels. Delay Time { T} msec 0 6.2 12.5 25 50 100 CNTL Level dB -10 .097* .141* .198 .218 .245 .256 .234 Wave V ( 41) (60) ( 85) (93) ( 105) (108) (100) Mean-pv 0 .ooo* .098* .207 .245 .230 .220 .234 ( % CNTL) ( 42) ( 88) (105) (98) (104) (100) +10 .ooo* .092* .187 .228 .241 .239 .234 {39} {BO) { 97} (102} {98} {100) Wave V -10 .074 .030 .087 .091 .052 .040 .057 S.D. 0 .000 .029 .076 .073 .079 .052 .057 +10 .000 .058 .090 .089 .122 .052 .057 -10 .ooo* .186* .160* .130* .254* .270 .443 Nl (42) (36) (29) (58) (61) (100) Mean-pv 0 .ooo* .123* .180* .285* .246* .340 .443 ( % CNTL) (28) ( 41) (64) ( 5 5) (77) (100) +10 .ooo* .ooo* .090* .120* .166* .243* .443 {10) {27} p 7) ( 55 )____ (100} Nl -10 .000 .126 .060 .042 .160 .113 .247 S.D. 0 .000 .037 .115 .162 .100 .029 .247 +10 .000 .000 .095 .108 .076 .125 .247
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l&1 a :> tH J a.. I: < _J 0 l'.k: tz 8 98 129 .0' A -18 ell r 1 sl.cx1dard 1 a 8ci5 I + +19 I 100Jl 80.0' 60.0' 40Jl 29.0' 0.0 0 6 12 25 50 100 DELA'! TIME Ct1Sec) Fig. 14. Amplitude recovery functions for N 1 probe responses following 60 msec wide-band maskers with levels of dB relative to the "standard" series.
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99 is not significantly different from the mean control response amplitude at T=l00 msec for the -10 dB and 0 dB maskers even though the amplitudes are only between 60 and 75% of the control response amplitude. High variability and a small number of subjects makes interpretation of the N 1 amplitude data difficult, but compared to wave V amplitude obvious differences can be observed which are consistent with the previous observations shown in the "standard" series where a larger group of subjects was included. Table VII also includes the summary data for Ni amplitude as a function of T for the different masker levels. In summary, the most prevalent results of increasing the level of the forward masker are as follows: 1. Increasing the level of the forward masker pro duced increases in wave V latency and decreases in N 1 amplitude. 2. Wave V latency and N 1 amplitude were not recovered by T=l00 msec. The significant interaction of wave V latency and masker level at T=l00 msec may indicate that masker level does not influence recovery time. 3. The amplitude of wave V and the latency of N 1 did not significantly change as masker level was in creased over most Ts. 4. Wave V amplitude recovered quickly for all three masker levels, i.e., by 12.5 msec.
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100 The Effect of High-Pass Masking The high-pass masking series was performed on 7 subjects following the "standard" series and of those subjects N 1 data were obtained on 5 subjects. Keeping the spectral level of the masker constant (determined during the "standard" series), the ABRs and APs were obtained for each :'.' .T for the following masker low frequency cutoffs, .02 ("standard"), 2, 4, 6 kHz. The high frequency cutoff was maintained at 10 kHz. Figure 15 shows a typical example of ABR waveforms for the high-pass masking series. From left to right are the responses obtained for the different masker low frequency cutoffs and from top to bottom are the responses obtained for the different ATs. The unmasked control response is also in cluded in Fig. 15 and is repeated at the top of each column for ease of comparison to the masked responses as a function of ilT. Wave V is easily observable in all of the m3.sked waveforms of Fig. 15. The peaks earlier than wave V are not as easily identifiable and are often confounded by the base line activity. The earlier peaks are clearer in the masked waveforms for the longer ATs and higher frequency masker cut offs. As the masker low frequency cutoff increases (left to right in Fig. 15) and as AT increases (top to bottom in Fig. 15), the latency of wave V decreases. The amplitude of wave V increases as AT increases and, in this particular example, is largest for maskers with low frequency cutoffs of 2 and 4 kHz.
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Fig. 15. Example of the probe ABRs as a function of AT(top to bottom) for the different masker low frequency cutoffs (left to right). Unmasked responses are repeated at the top of each column for ease of com parison.
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UNM. L\T 0 12.5 25 50 100 .02-10 KHZ 2-10 KHZ ABR S:.DR 4-10 KHZ 6-10 KHZ I-' 0 Iv
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103 Figure 16 shows the corresponding AP waveforms for the high-pass masking series seen in Fig. 15 for wave V. The amplitude of N 1 increases systematicall y as ~T increases and as the masker low frequenc y cutoff increases. The N 1 responses are more distorted and more diminished in ampli tude than wave V, especiall y for the lower masker cutoff frequencies and for shorter ~Ts. Also noticeable in the AP waveforms of Fig. 16 is a more pronounced effect of the maskers on the baseline to N 1 amplitude than on the positive peak following N 1 peak is observed. In some wa v e f orms a double negative The behavior of the double negative peak was not found to be consistent within the same subject nor was it present in all of the subjects. Whenever a double negative peak was observed, measurement of N 1 was chosen as the most negative point immediately preceding the more prominent positive peak. In the top portion of Fig. 17 are plotted the mean latencies of wave Vas a function of ~T for each of the mas k er low frequenc y cutoffs. The same data are replotted in the top of Fig. 18 as a function of masker low frequenc y cutoff for each of the ~Ts. From these two figures it can be seen that as the masker low frequency cutoff increases from .02 to 2 kHz there is ver y little change in the mean
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Fig. 16. Example of probe APs as a function of .6T(top to bottom) for the different masker low frequency cutoffs (left to right). Unmasked responses are repeated at the top of each column for ease of comparison.
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UNM ~T 0 6.2 12.5 25 50 100 .02-10 KHZ .Ae S=-DR 2-10 KHZ 4-10 KHZ 6-10 KHZ I-' 0 u,
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(\ 0 I E V >u z w I4: 106 8.58 7 .50" X 6.50' a .82 r& YAVE V A 2 kHz 4 r& ... 6 r& 5.58 4.50" : t~ -i X 3.50" V-N1 : t? s: :$ %. X 2.50' Nt 0 6 12 25 50 100 CNTL DELAY TIME Cmsec) Fig. 17. Latenc y reco ve r y functions for wave V, N 1 and V-N 1 probe responses following 60 msec maskers with masker low frequenc y cutoffs of .02, 2, 4, and 6 kHz. The high frequency filter setting remained at 1 0 kHz.
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" 0 I E V > 0 z w t< ..J 107 8.56 7.50' X 6.50" a a IAC alav A 6,2 I 0 125 I I 5.50" V 2S I .. + S8 I f 188 I 4.50' 3.50" i RG!I t X 2.50 .02 2 4 6 CNTL MASKER LOW fREO CUTOFF CkHz) Fig. 18. Wave V and N 1 probe response latencies as a function of masker low frequency cutoff. The parameter is 6 T (msec delay)
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108 wave V latency, i.e., removing masker frequencies below 2 kHz does not cause any appreciable decrease in wave V latency. As masker low frequency cutoff increases above 2 kHz, the mean wave V latency decreases and the largest latency decrease occurs as the masker low frequency cutoff changes from 2 to 4 kHz. Further latency decreases of wave V occur as the masker low frequency cutoff changes from 4 to 6 kHz and (for the shorter ~Ts) between the masker low fre quency cutoff of 6 kHz and the unmasked control. The amount of latency decrease as a function of masker low frequency cutoff becomes less asilT increases, i.e., the greatest differentiation of mean wave V latency across masker low frequency cutoff occurs at AT=O msec and the amount of differentiation becomes less apparent as LT increases. As shown in Fig. 17, the mean wave V latency recovery functions are essentially the same for the .02-10 and 2-10 kHz maskers. The wave V latency recovery functions become progressively less steep for the 4-10 and 6-10 kHz maskers. For wave V latency, the interaction between masker low frequency cutoff and ilT is significant (F=9.27, df=l4, 124 p L.001) and this interaction is readily apparent in Figs. 17 and 18. In testing for simple effects it was found that masker low frequency cutoff is a significant factor for wave V latency
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109 for all A Ts except A T=l00 msec. For all A Ts, there are no significant differences between masker low frequency cutoffs of .02 and 2 kHz, but the differences between response means for the 2, 4, and 6 kHz masker low frequency cutoffs are significant. Comparisons of the mean masked wave V latencies to the mean control response latency reveal that for masker low frequency cutoffs of .02 and 2 kHz, the mean wave V probe response has not reached full recovery by AT=l00 msec. For the 4 kHz masker low frequency cutoff, full probe response recovery is obtained by A T=S0 msec. For the 6 kHz masker low frequency cutoff, full recovery of wave V latency occurs by AT=25 msec. Table VIII gives the summary wave V latenc;:y data as a function of AT for each of the masker low frequency cutoffs. The mean N 1 latency changes as a function of AT for the high-pass masking series are shown in the bottom portions of Figs. 17 and 18. Like for wave V, the largest latency shift of N 1 occurs at AT=0 msec; however, in contrast to wave V,very little differentiation across masker low fre quency cutoff can be seen and there is no significant interaction between masker low frequency cutoff and AT. No latency decreases are seen for N 1 until the masker low frequency cutoff increases from 4 to 6 kHz, and between
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Table VIII. Means and standard deviations (S.D.) of wave V, N1, and V-N 1 probe response latencies for the four masker low frequency cutoffs. 12 e J. 2a ::t Time ( ~T) msec 0 6.2 12.5 25 50 100 CNTL Low-Freq. Cutoff 8.203* 7_933* 7.132 .02 NR 7.708 7.471 6.867 Wave V 2 8.543* 8.194* 7.866* 7.685* 7.448 7.154 6.867 Mean-msec 4 7.561* 7.441* 7.459* 7.264* 7.166* 7.031 6.867 6 7.083* 7.110* 7.189* 7.057 6.985 6.938 6.867 .02 NR .443 .366 .397 .364 .308 .277 Wave V 2 .665 .318 .298 .446 .301 .309 .277 S.D. 4 .559 .449 .417 .353 .264 .290 .277 6 .314 .303 .455 .302 .358 .241 .277 .02 NR 3.092* 3.243* 3.172* 2.991 2.854 2.832 N1 2 NR 3.273* 3.239* 3.080* 2.971 2.909 2.832 Mean-msec 4 3.323* 3.229* 3.149* 3.148* 3.056* 2.981 2.832 6 3.075* 3.053* 3.016* 2.983* 2.961 2.874 2.832 .02 NR .096 .215 .233 .148 .137 .137 Nl 2 NR .358 .310 .136 .184 .167 .137 S.D. 4 .372 .420 .303 .298 .269 .248 .137 6 .283 .352 .287 .242 .217 .253 .137 .02 NR 5.053* 4.639* 4.506* 4.450* 4.224 4.000 V-N1 2 NR 4.875* 4.629* 4.535* 4.422* 4.200 4.000 Mean-msec 4 4.222* 4.157 4.229* 4.019 4.022 3.954 4.000 6 3.935 4.030 4.074 3.968 4.006 4.037 4.000 .02 NR .527 .478 .489 .446 .358 .390 V-N1 2 NR .421 .390 .539 .403 .415 .390 S.D. 4 .824 .719 .473 .431 .412 .411 .390 6 .461 .524 .740 .372 .534 .499 .390 I-' I-' 0
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111 masker low frequency cutoff of 6 kHz and the unmasked control latency, i.e., as frequencies above 4 kHz are excluded the latency of Ni decreases. The large latency changes seen for wave V between masker low frequency cutoffs of 2 and 4 kHz are not seen for the N1 response. Masker low frequency cutoff is a significant factor for the probe evoked N 1 latency (F=S.93, df=3, 73 p ~.005), and is mostly attributable to the 6 kHz masker low frequency cutoff which is significantly different from the other masker low frequency cutoffs. The time course of recovery for the mean N 1 latency is very similar for all of the masker low fre quency cutoffs (Fig. 17). Complete N 1 latency recovery occurs byuT=S0 msec for all the masker low frequency cutoffs. The amount of N 1 latency shift as a function of AT is considerably less than for wave V for the .02 and 2 kHz masker low fre quency cutoffs; however, the V-N 1 latency interval becomes less as the masker low frequency cutoff increases due to a larger decrease in wave V latency relative to N 1 latency. The V-N 1 latency interval is significantly different from the control response only for masker low frequency cutoffs of .02 and 2 kHz at 4Ts below 100 msec. Summary data for N 1 latency and V-N 1 latency interval are given in Table VIII as a function of ~T for the different high-pass maskers.
PAGE 124
112 The wave V amplitude recovery functions for the various masker low frequency cutoffs are given in Fig. 19 and re plotted in Fig. 20 as a function of the masker low frequency cutoff. Wave V amplitude is not severely affected by any of the maskers except at the shorter ~Ts. Wave V amplitude recovery is faster for the masker low frequency cutoffs of 2 and 4 kHz which show a larger response amplitude than the masked responses for the .02 and 6 kHz masker low frequency cutoffs. There is a significant interaction of masker low frequency cutoff and ~T for the wave V amplitude (F=2.26, df=lS, 128 p L.01). Testing for simple effects indicate that the only significant differences in response means occur be tween those for the masker low frequency cutoffs of .02 and 2 kHz at all ~Ts except 25 and 100 msec. It apparently takes a very large difference between means to met signifi cance and this is due to the large variability in masked wave V amplitudes. An additional feature of Gis. 22 and 23 is a supernormality of wave V amplitude, especially for the masker low frequency cutoffs of 2 and 4 kHz; however, none of the supernormal response means are significantly different from the mean control response amplitude, except 2 kHz at ~T-50 msec. All the wave V mean amplitudes for the various high-pass maskers are equal to the mean control amplitude
PAGE 125
ILi a :) r H J Q. I: < .J 0 r z 0 0 113 120.0' 108.0' WAVE V 88.0" 60.0" D ..92 kHz A 2 kHz f kHz 6 kHz 48.0' 20.0' 0.8 0 6 12 25 50 100 DELAY IDE Ctasec) Fig. 19. Amplitude recover y functions for wave V probe responses following 60 msec wide-band maskers with masker low frequenc y cutoffs of .02, 2, 4, and 6 kHz.
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w a J tH J 11. l: < J a lk: tz a u )t 114 128.0' 100.0' 80.0' WAVE V 60.0" D 8 uec delay 40.8 6~ 12..S V 2S + 58 20.0" f Ula .02 2 4 6 MASKER LO'f FREQ CU10ff CKHz) Fig. 20. Wave V probe response amplitude as a function of masker low frequenc y cutoff. The parameter is .6.T (msec delay)
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115 by ~T=l2.5 msec and the mean wave V amplitude for the 2 kHz low frequency masker cutoff is equal to the mean control amplitude by ~T=6.2 msec. The mean masked amplitudes are not different from the mean control amplitude for any of the A Ts for the 6 kHz low frequency masker cutoff. Summary data for wave V amplitude is given in Table IX. The mean N 1 amplitude data for the high-pass masking series are shown in Figs. 21 and 22. Unlike N 1 latency (and wave V amplitude), N1 amplitude is more sensitive to the changes in masker low frequency cutoff, i.e., as masker low frequency cutoff increases the N 1 amplitude increases (for all ~Ts). The largest amplitude increase of N 1 are seen as the masker low frequency cutoff increases above 4 kHz. The N 1 amplitude also increases as ~T increases and the recovery functions for N 1 amplitude (Fig. 21) be come less steep as the low frequency cutoff of the masker increases. As expected, masker low frequency cutoff is a significant factor for the mean N 1 amplitude (F=60.58, df=3, 81 p "'-.001). The interaction between masker low fre quency cutoff and ~Tis not significant. Comparisons of mean masked N 1 amplitudes reveal that response means for masker low frequency cutoffs of .02 and 2 kHz are not significantly different from each other, but which are different from masker low frequency cutoff of 4 kHz which
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w a ::, tH .J ll. I: < J 0 {l 8 120 .. 0' D .82 kHz 4 2 kHz .. kHz + 6 kHz 100.8 80.0' 88.8 40.0' 20.0' 0.0 0 6 12 25 50 DELAY TIME Ctasec) Fig. 21. Amplitude recover y functions for N 1 probe responses following 60 msec wide-band maskers with masker low frequency cutoffs of .02, 2, 4, and 6 kHz. 116 100
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w a J tH .J a. l: < .J a tz a 0 120'.0" a e IIAC delay A 6.2 ,. 12.S .. V 25 .. 100.0' + 58 .. .. + 188 .. 80.0" 80.8 40.0' Nt 29.0' 0.0 .02 2 4 6 MASKER LOil FREQ CUTOFF CkHz) Fig. 22. Ni probe response amplitude as a function of masker low frequenc y cutoff. The parameter is AT (msec dela y ). 117
PAGE 130
-----------------------------Table IX. Means and standard deviations (S.D.) of wave V and N 1 probe response amplitudes for the four masker low frequency cutoffs. Dela:i Time ( AT) msec 0 6.2 12.5 25 50 100 CNTL Low-Freq. Cutoff .02 .ooo* .155 .200 .241 .232 .291 .231 (O) ( 6 7) ( 87) (104) (100) ( 126) (100) Wave V 2 .162* .225 .272 .271 .302* .290 .231 Mean-uv (70) ( 97) (118) ( 11 7) (130) ( 126) (100) (% CNTL) 4 .191 .216 .261 .280 .282 .260 .231 (83) (54) ( 113) (121) ( 122) (113) (100) 6 .206 .188 .210 .261 .265 .266 .231 (89) ( 81) ( 91) (113) ( 115) (115) {100) .02 .000 .070 .084 .107 .073 .095 .060 Wave V 2 .101 .421 .390 .129 .088 .090 .060 S.D. 4 .030 .071 .062 .095 .100 .129 .060 6 .047 .064 .050 .078 .074 .041 .060 .02 .ooo* .065* .180* .206* .232* _375* .608 Nl (11) (30) (34) ( 38) (62) (100) Mean-uv 2 .ooo* .172* .224* .240* .296* .372* .608 ( % CNTL) (28) ( 3 7) (39) ( 49) ( 61) (100) 4 .258* .320* .348* .366* .390* .408* .608 (42) (53) ( 5 7) (60) (64) ( 6 7) (100) 6 .487* .430* .510 .515 .546 .693 .608 BO) (71) {84) (85) {90) {114) {100) .02 .000 .076 .059 .049 .103 .105 .216 N1 2 .000 .026 .032 .048 .068 .131 .216 S.D. 4 .093 .088 .113 .131 .149 .176 .216 6 .163 .217 .207 .329 .208 .270 .216 I-' I-' OJ
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119 is different from the 6 kHz masker low frequency cutoff. Full recovery of mean N 1 amplitude occurs only for the 6 kHz low frequency cutoff for ATs above 12.5 msec. For those conditions that show complete wave V amplitude re covery (and even show supernormality), the N 1 amplitude is still less than 60-70% of the control response amplitude. Derived Response In order to more completely describe the contributions of various spectral (and presumably cochlear) regions to the wave V and N 1 responses, a derived narrow-band procedure was used. This derived narrow-band technique was first used by Teas et al. (1962) for demonstrating derived frequency regions and their contributions to the AP in guinea pigs. Others have more recently used this technique to study the AP in humans (Elberling, 1974; Eggermont et al., 1976) and has been applied to the ABR by Don and Eggermont (1978) and Parker and Thornton (1978}. The procedure involves raising the level of a wide-band noise until the probe response is eliminated in the averaged waveform. Then, keeping spectral level of the noise constant, the responses are obtained for e~ch successive increase in the low frequency cutoff of the masker (high-pass masking). The derived response waveforms
PAGE 132
120 are obtained by subtracting, point-by-point (done by the computer), the averaged responses produced from successive raising of the masker low frequency cutoff. The derived response waveforms, theoretically, are representations of the contributions to the probe response in the defined frequency regions which were removed by the noise. The derived frequency regions have arbitrarily been assigned derived characteristic frequencies (CF) of 1, 3, 5, 7 kHz. Since all of the high-pass maskers showed the largest effect on the response when AT=0 msec, the largest derived narrow band response waveforms also occur for ~T=0 msec. Figure 23 shows an example of the derived technique on a series of ABR waveforms (AT=0). The derived ABR waveforms on the right of Fig. 23 show characteristic ABR waveforms. Wave V latency decreases as the derived narrow-band frequency region increases and is generally thought to reflect basilar membrane traveling wave time, i.e., longer latencies for lower frequency regions. It can also be observed that the amplitude of wave Vis quite prominent for the lower fre quency narrow-bands and is not apparent in the example in Fig. 23 for the frequency region 6-10 kHz which, theoreti cally, does not have any measureable contribution to the unmasked probe response, whereas, there is a large
PAGE 133
Fig. 23. Example of derived response technique for the ABR. Each derived waveform on the right was obtained by successive subtractions of waveforms on the left. Each response on the left was subtracted from the response immediately below it, e.g., the response with masker low frequency cutoff of .02 kHz was subtracted from the response with the masker low frequency cutoff of 2 kHz resulting in a derived response indicated by CF=l. Responses were obtained at AT=O msec.
PAGE 134
Masker low Fr~q cu.loff .02 2 4 6 Unm NASJ'ED ABR DERIVED 2 msec I msec
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123 contribution to the unmasked probe response from regions of .02-2 kHz and 2-4 kHz. Figure 24 shows an example of the derived narrow-band response waveforms for the AP from the same subject whose derived ABRs are shown in Fig. 23. As for wave V, the latency of N 1 decreases as the derived narrow-band frequency increases. In contrast to wave V, the largest contributions to N 1 appear for the higher narrow-band regions and no contribution is seen for the .02-2 kHz region. In Fig. 25 the mean wave V and N 1 latencies are plotted as a function of the derived narrow-band "CF." The mean latency of wave V systematically decreases as "CF" increases over the entire "CF" range. For "CF"=7 kHz, the mean wave V latency is less than the mean unmasked latency, suggesting that the latency of wave Vis most influenced by the fre quency region somewhere between "CFs" of 5 and 7 kHz. N 1 also show a decrease in latency as "CF" increases above 3 kHz. Derived N 1 responses are not measureable for "CFs" below 3 kHz. The unmasked latency of N 1 is closely approximated by the latency of the derived response for "CF"= 7 kHz. It can also be observed that the amount of latency decrease as a function of "CF" is less for N 1 than for wave V. In high-pass masking studies using simultaneous
PAGE 136
MASKED Ma.sk.~r Low Fr~q Culoff DERIVED .02 2 4 6 Unm CF=I CF=3 CF=7 Fig. 24. Example of the derived response technique for the AP (see Fig. 23 for details).
PAGE 137
" 0 I E V > (.) z w t< J 125 8 .50" 7.50" WAVE V X e_se5.50" 4.50' 3.50" X 2.S0 1 3 5 7 CNTL DERIVED "Cf' CKHzJ Fig. 25. Mean latencies of wave V and N 1 as a function of derived CF. Derived responses were ob tained for ~T=O msec.
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126 masking paradigm (Elberling, 1974; Eggermont et al., 1976; Don and Eggermont, 1978; Kramer and Teas, 1979), the latency changes of wave V and N 1 at least across high CFs have been shown to be parallel. The difference between wave V and Ni latencies observed in the derived response data shown for this study may be due to the forward masking procedure. The mean derived narrow-band amplitudes expressed as a percent of the unmasked mean amplitude for wave V and N 1 are shown together in Fig. 26 as a function of "CF." An obvious difference is noticed between the mean amplitude behavior of wave V and N 1 For "CFs" of 5 and 7 kHz, the mean amplitudes of wave V and N 1 are nearly the same and both wave V and Ni mean amplitudes are larger for "CF"= 5 kHz than for "CF"= 7 kHz, i.e., a large contribution to the unmasked wave V and Ni amplitude (to a 50 dB HL probe) occurs for the frequency region 4-6 kHz. For "CFs" below 5 kHz, the mean N 1 amplitude shows a sharp decline and is not measureable for "CF"=l kHz. Wave V, on the other hand, maintains its amplitude for the lower "CFs" and may even increase slightly for the lower "CFs." This is in agreement with the findings of Don et al. (1977) using a simultaneous high-pass masking sequence. Wave V shows a dominant response contribution over a wide frequency range which is not observable in the unmasked
PAGE 139
------------w a J tH .J a. < .J a Q: tz a t) 127 100.0' D WAVE V A Nt 80.0' 60.0' 40.0' 28.0" 0. 0' 3 5 7 DERIVED "Cf (kHz) Fig. 26. Mean amplitudes of wave V and N 1 as a function of derived CF. Derived responses were obtained for AT=O msec.
PAGE 140
128 response. N 1 has its dominant contribution from the fre quency region 4-6 kHz.
PAGE 141
CHAPTER IV DISCUSSION This investigation provides a description of the normal ABR and AP postmasking recovery functions for various maskerprobe parameters. The forward masking paradigm, previously used by others for single auditory nerve fiber, AP, and psychophysical investigations, is applicable for recordings of the human ABR as well. Ultimately, one would like to be able to make comparisons at all levels of the auditory sys tem in order to understand underlying mechanisms and their correlation with the perception of temporally related stimuli. A primary focus of this study is a direct comparison of gross potential recovery functions from the brainstem (wave V) and the periphery (N 1 ). The direct comparison of wave V and N 1 are weakened in this investigation by two problems. One problem is that N 1 was not obtainable for all of the subjects from whom ABR recordings were obtained. Proper placement of the ear canal electrode proved to be difficult because the electrode "hung up" on a protruding ledge or cerumen within the ear canal, or the subject became intolerant of the ear canal 129
PAGE 142
130 electrode before proper placement was achieved. The use of ear canal recordings in humans is fairly new to this laboratory and investigator (Kramer and Teas, 1979) and one would expect improvement with more experience and more ideal conditions, such as better lighting of the ear canal, proper method of cleaning the ear canal, and better control of electrode placement. Different electrode designs were initially tried; however, the concept of having the electrode attached to a piece of material that "springs open" (Coats, 1974) seemed to work the best, i.e., produced the largest and most stable responses when properly positioned in the ear canal. Currently, only Coats and his coworkers routinely use an ear canal recording procedure, their electrode being made of a thin piece of acetate which "springs open." Coats (personal communication) reports having very little diffi culty in obtaining good ear canal responses. An electrode made similar to the one Coats describes (1974) was not found oy this investigator to work any better than the one presently used which is made from the polyurethane tubing. Paid subjects and the use of a topical anesthetic in the ear canal might also be helpful in obtaining more success with the ear canal electrode in human subjects.
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131 The second problem concerns the variability of response amplitude which was found to be quite large for both wave V and Ni (see Fig. 6). The sources of amplitude variability may be different for wave V and N 1 The large intersubject amplitude variability of N 1 (especially the unmasked re sponse) along with a much smaller intrasubject variability (within the same session) of N 1 amplitude suggests that much of the variability is due to the placement of the ear canal electrode, i.e., placement closer to the tympanic membrane and with better contact with the canal wall produces larger response amplitudes. Since placement of the electrode is difficult, the result is a large range of amplitudes. Wave V, on the other hand, has a smaller intersubject ampli tude variabilit y than N 1 but the intrasubject variability is much larger for wave V than N 1 Since the ABR electrode attachments are presumably similar across subjects, there must be some inherent physiological source of amplitude variability in recordings of the human ABR. Only recently have investigators begun to systematically measure ABR amplitudes. New and improved methods of amplitude measure ment and recording procedures are needed to increase the usefulness of ABR amplitude data. Perhaps increasing the number of samples in the averaged response, repeated runs,
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132 anesthetized subjects, and/or the use of digital filter ing and response smoothing techniques would improve ampli tude measures of the ABR. General Effects of Forward Masking The largest amount of data were collected for the "standard" series. They afford a fairly accurate description of the effects of forward masking on the ABR and AP gross potentials in humans. Averages or broadband click re sponses following short-duration (60 msec) maskers show characteristic alterations, the magnitude of which depend upon AT. The largest effects on the probe responses pro duced by forward masking occur for the shortest AT and the masking decreases as AT increases. Over the range of .uT used in this study, forward masking produced clear and consistent changes in the N 1 and wave V probe responses. The results demonstrate that the most apparent effects of forward masking are, (1) a decrease in N 1 amplitude and (2) an increase in wave V latency, neither of which is fully recovered by ~T=l00 msec. The fast recovery of wave V amplitude compared to N1, even after complete elimina tion at ~T=0 msec, attests to the robustness of this com ponent of the ABR.
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~ ------------------------------~-----133 The results of this study for N 1 are, in a general sense, consistent with a number of studies of postmasking recovery of the AP (Hawkins and Kniazuk, 1950; Srensen, 1959; Coats, 1964a,b, 1967; Eggermont and Spoor, 1973,a,b,c; Spoor et al., 1976; Abbas and Gorga, 1981). Direct com parisons with previous investigations are difficult because of differences in stimulus parameters and species among laboratories. The only reported study of forward masking using noise maskers of the human AP is by Spoor et al. (1976). Their results show that N 1 to a 50 dB HL probe (6 kHz tone-burst) following a 400 msec noise-burst (S/N=~ 5 dB) is nearly eliminated for t:::.. Ts below 8 msec and the amplitude of N 1 is more than 50"/o reduced at t:::..T=l00 msec. Complete recovery of N 1 amplitude does not occur in the study of Spoor et al. (1976) until 1.0 sec after masker offset. The results of the present study are quite similar to those of Spoor et al. (1976) over the range of t:::.. Ts used. Since t:::.. Ts longer than 100 msec are not included in this investi gation, the time for complete amplitude recovery for N 1 cannot be determined. The decrease in N 1 amplitude along with the increase in wave V latency found in this study are also in agreement with results of other investigators for wave I (auditory
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nerve activity) and wave Vin ABR recordings using repetition rate or simulus-train paradigms (Terkildsen 134 et al., 1975; Thornton and Coleman, 1975; Pratt and Sohmer, 1976; Harkins et al., 1979; Kevanishvilli and Lagidze, 1979). Comparisons of wave I and wave Vin ABR recordings are difficult because often wave I is not clearly defined and there is a problem of superpositioning of responses peaks, especially for repetition rates above 30 / sec. The results of the present study, using an ear canal recording tech nique to provide a more detailed description of auditory nerve activity, strengthens the previous findings of the above ABR investigations using repetition rate procedures. This study also presents the first observations of the effects of changing masker parameters of temporally related stimuli on the wave V response. It is clearly demonstrated that the effects of forward masking are not the same for the N 1 and wave V probe responses. Table X summarizes those parameters which showed a significant effect on the latencies and amplitudes of N 1 and wave V. Effect of Masker Duration and Level Increases in the duration or the level of forward masking produce greater alterations in the ABR and AP probe responses which are primarily seen as increases in wave v
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135 Table X. Summary of significant effects and interactions of masker parameters on wave V and N 1 probe responses. Asterisk (*) indicates significant effect. Wave V N Amp. Lat. Amp. Lat. Delay Time ( ~T) * * Masker Duration * Duration X ~T Masker Level * Level X ~T Masker Low Frequency * Frequency X ~T *
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136 latency and decreases in N 1 amplitude. In general, complete recovery times of wave V latency and N 1 amplitude are beyond the range of .6.Ts investigated, i.e., recovery takes longer than 100 msec. Therefore, it is difficult to deter mine whether increasing masker duration or level increases the time for complete recovery or whether they merely in crease the point from which recovery begins, i.e., at masker offset. The absence of significant interaction be tween masker duration and ,6.T, for both wave V latency and N 1 amplitude (see Table X) ,suggests that increasing masker duration increases the time for complete recovery. For wave V latency, the effect of increasing masker duration does show increasing recover y times which are apparent within the range of .6.Ts used, i.e., recover y time increases from 50 to 100 msec as masker duration increases from 30 to 60 msec, and recover y time is greater than 100 msec for the 120 msec masker (see Table IV). Increasing recovery time as a function of increasing masker duration has been demon strated previously for N 1 in cats b y Coats (1964a) and in guinea pigs b y Eggermont (1975). In contrast to the effect of masker duration on recover y time, a significant interaction is apparent between masker level and .6.T for wave V latency. This interaction suggests
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137 that masker level increases the initial postmasking latency, but not the time for complete recovery (which is beyond 100 msec, see Table VI). The N 1 data do not support the idea that recovery time is independent of masker level since an increase in recovery time is seen as the masker level is raised 10 dB above the "standard" series level (see Table VII) and there is no significant interaction between masker level and .6.T. Other investigators, however, have shown that increasing masker level only increases the initial postmasking N 1 decrement and not the time for com plete recovery (Coats, 1964b; Spoor et al., 1976). The large Ni amplitude variability in this study may be the source of the discrepancy regarding masker level effects on N 1 It may also be possible that the changes in Ni at the +10 dB level (about 90 dB SPL) involve a different mechanism, such as some type of "fatigability." This could also account for the longer latency of N 1 seen at the highest masker level (see Fig. 12). Wave V amplitude recovers much faster than N 1 amplitude (and wave V latency) for all the masker durations and masker levels. Masker level does not have a significant effect on wave V amplitude recovery functions (see Fig. 13 and Table VII). Masker duration, on the other hand, does
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138 show a significant difference on wave V amplitude recovery, with faster recovery occurring for the 30 msec masker compared to the 60 and 120 msec maskers which have similar recovery functions. The effects of masker duration and level appear to be initiated peripherally and are subsequently reflected as changes in wave V latency. In fact, changes in wave V latency may provide a better indication of peripheral effects of changing masker duration and level since characteristic changes of wave V latency are more orderly than N 1 amplitude because of N 1 1 s greater variability (compare Fig. 9 with Fig. 11 and Fig. 12 with Fig. 14). Effects of Masker Low Frequency Cutoff (High-Pass Masking) The high-pass masking series shows systematic increases in N 1 amplitude and decreases in wave V latency as the masker low frequency cutoff is raised (see Fig. 22). The largest increases in N 1 amplitude occur as masker low frequency cutoff is raised above 4 kHz. For wave V latency (see Fig. 18), the largest latency decrease occurs as the masker low frequency cutoff is raised from 2 to 4 kHz. These systematic changes of N 1 amplitude and wave V latency are apparent for each 6-T; however, the magnitude of the change
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139 becomes less as .:6.T increases. Also apparent is a stable wave V amplitude across all of the masker low frequency cutoffs (see Fig. 20). This suggests that the wave V probe response (as reflected in the latency change and large amplitude) has a contribution from a wider frequency region than does the N 1 response (as reflected in the amplitude change). This is more clearly represented in the derived response data seen in Fig. 25 and Fig. 26 which show an increase in wave V latency and a stability of wave V ampli tude over the entire range of derived CF, whereas, N 1 response amplitude is drastically decreased at the lower derived CFs. High-pass masking has been used in simultaneous masking paradigms to partition out various frequenc y (and pre sumabl y spatial) contributions at the cochlear level to the AP response (Teas et al., 1962; Elberling, 1974; Eggermont et al., 1976; Kramer and Teas, 1979). As the low frequenc y cutoff of the high-pass masker is lowered it reaches a point where the masker begins to o v erlap those populations of fibers responding to the probe stimulus, which result in an N 1 amplitude reduction (and latency increase). Differences in the amplitudes of N 1 and wave V have been observed; wave V has a fairly stable response
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140 amplitude across a wide range of frequency regions, whereas, N 1 amplitude dramatically decreases for lower frequency regions (Don and Eggermont, 1978; Parker and Thornton, 1978; Kramer and Teas, 1979). The results of the present findings using forward masking are consistent with the simultaneous high-pass masking studies. The recovery functions for the different high-pass maskers show that for wave V latency the recovery time in creases as masker low frequency cutoff decreases (see Fig. 17). For wave V amplitude, recovery is completed very quickly for all the masker low frequency cutoffs (see Fig. 19); however, recovery time decreases as masker low fre quency cutoff increases (see Table IX). Recovery times for N 1 amplitude (see Fig. 21) are beyond the 100 msec range used (except for masker 6-10 kHz); therefore, the effect of low frequency cutoff on complete re covery time cannot be determined. However, since the interaction between masker low frequency cutoff and AT is not significant, this implies that Ni amplitude recovery time decreases as masker loN frequency cutoff increases.
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141 Possible Mechanism Underlying the Effects of Forward Masking on Ni and Wave V The paucity of data concerning the precise characteristics of the neural generators of the various ABR waves allows only conjectures for explaining the observed effects found in this investigation. The considerably longer latency increases of wave V compared to N 1 and the relative persistence of wave V amplitude, even when N 1 amplitude is significantly reduced, implies that wave V does not simply parallel, at a more central site, the activity of the cochlear output under conditions of forward masking. The differential effects of N 1 and wave V suggest that some neural recoding is manifested in the wave V response. Each auditory nerve fiber enters the cochlear nucleus and branches to innervate many cells (Lorente de N6, 1933) and along with interconnecting neurons offers the first opportunity for recoding of the auditory nerve fiber activity. Harkins et al. (1979) using click repetition rate compared interwave latencies of various ABR waves and found latency shifts with increasing repetition rate for successive interwave differences. The largest latency shift occurred between wave II and III suggesting that much of the change in central coding occurs very early in the
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142 brainstem. The actual mechanisms responsible for the central nervous system's latency changes under forward masking conditions are not known. Changes in central synaptic processes (Hyde et al., 1976; Don et al., 1977; Harkins et al., 1979) seem to be a more reasonable explanation than changes in central neural conduction velocities (Terkildsen et al., 1975). Wave V Amplitude Wave V was easily observable in all of the masked responses. The amplitude of wave V was quite large even at .6.T=6.2 msec. Full recovery of wave V amplitude was considerably faster than N 1 amplitude. Because of the robustness, wave V provides an easily obtainable response in which to assess the effects of forward masking. As discussed above, the variability of wave V amplitude is fairly large and the usefulness of wave V amplitude ~easures may, in themselves, be limited. However, the fact that wave Vis readily identified, along with the systematic latency shifts, is an advantage over N 1 record ings. Wave V may prove to be a useful nontraumatic method for evaluating a dynamic characteristic of the auditory system. Application of forward masking paradigms to clinical populations may produce characteristic differences
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in the recovery properties which could be of diagnostic importance. 143 An interesting feature apparent in the wave V amplitude recovery functions is that for some masked conditions the mean amplitude of wave Vis greater than the unmasked control (see Fig. 19). Although this supernormality of wave V ampli tude is not statistically significant (except for 2 kHz at AT=50 msec), it warrants some speculation. At least two possibilities exist. The first is that the masker in some way adds to the responsiveness of the system, perhaps as a delayed response to the masker or as a "sensitization" of the population responding to the probe. Another possibility is that the unmasked wave V response does not reflect the entire responding population. This second possibility can be ex plained as follows. The broadband probe stimulus excites a relatively wide frequency region along the cochlear partition. Responses over this wide frequency region are reflected in the derived ABR wave forms shown in Fig. 23. Wave Vat the lower derived CF is quite prominent and the latency increases as CF decreases. Because of the latency shift across derived CF the positive wave V peak for one derived response superimposes in time on the negative trough (following wave V) in another derived response. In the unmasked situation the response reflects the complex
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144 summation of all responding regions. When a high-pass masker is added to the probe, it eliminates the high fre quency responding regions whose negative trough was sub tracting from the positive wave V peak at the lower fre quency region, thus producing the larger than unmasked responses seen for masker low frequency cutoffs of 4 and 2 kHz. The robustness of wave V amplitude and the question of supernormality are interesting features of ABR and are in need of further investigation. Mechanisms underlying the robustness of wave V are not known. Increasing numbers of neural elements at successively higher auditory centers (divergence), complex interconnections and response pro perties, and a convergence of input to the source of wave V, may provide a partial answer. V-N1 vs N1 Amplitude It has become fairly well established, at least at the level of the auditory nerve, that there is a relation between stimulus intensity and N 1 response amplitude. Increasing stimulus intensity "recruits" a greater number of fibers primarily from the base which results in a more synchronous response of larger amplitude (and shorter latency). It
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145 is possible that the latency increases of wave V observed under forward masking conditions are reflecting a reduced input to the central nervous system as seen by the decrease in N 1 amplitude. Plots of V-N 1 latency interval versus N 1 amplitude (Martin, 1976) across different stimulus con ditions, e.g., masker frequency, masker level, masker duration, stimulus intensity, or repetition rate, could arbitrarily provide a common dimension (N 1 amplitude) for comparing different stimulus variables and their effect on the V-N 1 latency intervals. Comparisons of V-N 1 latency interval across different conditions which produce a certain value of N1 amplitude can be made. If the amplitude of N 1 determines the V-N 1 latency interval, then an N 1 of, say 50% should produce the same V-N 1 interval for all stimulus conditions. Differences would have to be explained by different underlying mechanisms. As an example, Fig. 27 shows the V-N1 latency interval plotted against the mean Ni amplitudes for the high-pass masking conditions. It can be seen that the V-N 1 latency interval versus N 1 amplitude is dependent on the low frequency cutoff of the masker. The .02-10 and 2-10 kHz maskers show nearly the same slope, but as the masker lod frequency cutoff increases above 2 kHz, the slope decreases. This indicates that for a
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Fig. 27. V-N 1 latenc y interval as a function of % N1 control amplitude for the different masker low f requenc y cutoffs at each T. Dashed lines represent linear fit of the data v alues for each masker low fr e quenc y cutoff. A constant N 1 amplitude across d i fferent masking conditions produces different V-N1 latenc y intervals.
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('\ 0 I I E V z I > 4.99 4.79 4.59 4.39 4. 19 3.99 3.79 3.59 0.0 147 A C .02 kHz B 4 2 II C 4 D + 6 20.0 40.0 60.0 80.0 100.0 X NI CONTROL AMPLITUDE
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148 certain N 1 amplitude, the V-N 1 latency interval systemati cally decreases as the masker low frequency cutoff increases. The effects of forward masking on the latency of wave V are not simply related to the observed decrease in N 1 amplitude. The fact that there is a slope to the V-N 1 latency interval vs N 1 amplitude of Fig. 21 for the masking conditions is in contrast to the effects of stimulus intensity which show a constant V-N 1 latency interv3l for decreasing N 1 amplitude (Martin, 1976; Coats, 1978) and suggests that a more complex interpretation of forward masking effects is needed to explain the observed results. Additional information is needed con cerning mechanisms underlying the responses to temporally re lated stimuli and their relation to gross potentials such as the ABR and AP. Central Physiological Evidence Neural responses from auditory brainstem nuclei to repetitive stimuli provide some underlying evidence in line with the observed latency increase and fast amplitude recovery of wave V found in this study. Increasing click rate has been shown to produce an increase in latency of the initial peak of the PST histogram in some c8chlear nucleus units (even greater than 1.0 msec) while auditory nerve fibers show only slight (0.1 msec) latency shifts with increasing repetition rate (Kiang, 1968). In the inferior
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149 colliculus (the presumed principle source of wave V) an increasing amount of inhibitory activity has been demon strated which results in a dominance of fast adapting neurons, e.g., "on," "off," "on-off" type neurons (Watanabe and Simada, 1969) and one might expect faster recovery of those units if the recovery period is dependent in any way on the time course of adaptation, as has been shown by Harris and Dallos (1979) for single auditory nerve fibers. Recovery from forward masking has been shown to occur fairly rapidly in single neurons in the cochlear nucleus and inferior colliculus (Watanabe and Simada, 1969) and evoked potentials from the inferior colliculus have been found to recover much faster (complete recovery by 10 msec) than evoked potentials from higher auditory centers (Kitahata et al., 1969). In addition, evoked potentials from the inferior colliculus to repeated stimulation show increased amplitude or no change at all in about 50% of the recordings compared to cochlear nucleus activity which amplitude decreases in over 70% of the recordings (Kitzes and Buchwald, 1969). One must be careful in ascribing effects found for wave V to underlying neural response characteristics until more information is available concerning the relation of averaged far-field potentials to their neural constituents.
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Explanation of Forward Masking Effects on N1 150 The mechanisms responsible for the observed reduction and recovery of N 1 under forward masking conditions are not entirely agreed upon nor understood. The AP can be repre sented as a weighted summation over the contributing single auditory nerve fibers which contribute equally, but which have a fluctuating latency distribution (Goldstein and Kiang, 1958). Reduction of N 1 amplitude, as a result of prior ex citation by the masking stimulus, can be explained by either a reduction in the discharge rate of each nerve fiber, a reduction in the number of contributing nerve fibers, degree of synchronization, or some combination of these factors. Spoor et al. (1976) suggest that changes in the receptor mechanism as a result of the masking stimulation cause a decrease in discharge rate to the probe of all the potentially active fibers (number of responding fibers remains the same). This process allows spontaneous desynchronizing fluctuations to play a more important role and results in a decrease in N 1 amplitude. Thornton and Coleman (1975) also favor the reduced firing rate of each nerve fiber as the major factor in reducing the amplitude of N 1 during repetitive click stimulation. On the other hand, Coats (1971) and Pratt and
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151 Sohmer (1976) support the hypothesis that a reduction in number of contributing nerve fibers occurs. An important consideration is that the N 1 most likely does not reflect more than a single discharge in each fiber in response to each click since the duration of N 1 approximately 1.0 msec, is close to the refractory period of each nerve fiber (Kiang et al., 1976; Elberling, 1976b;Kevanishvilli and Lagidze, 1979). If the number of discharges of each individual fiber is not important to the definition of N 1 the postmasking reduction of N 1 is better explained by either a reduction in the number of contributing fibers or desyn chronizing factors. The reduction or desynchronization of the responding fibers is most likely due to some synaptic alteration which produces a disruption of the highly syn chronous conditions necessary for observation of the com pound AP, i.e., the primary effect following prior stimula tion is on the probability of neural firing across the entire responding population. The small latency change of N 1 at shorter L::i.Ts is also in agreement with other studies which show either no latency change or small latency change following a masking stimulus, most likely due to a broadening of the N 1 waveform caused by desynchronization (Spoor et al., 1976).
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152 Forward masking at the level of auditory nerve fibers shows a decrease in the discharge rate during stimulation b y the mas k er (adaptation). Following the masker offset there is a depression of the spontaneous discharge rate followed b y a recover y process of the spontaneous activity which ma y last 100-200 msec (Harris and Dallos, 1979; Smith, 1979; Abbas, 1979; Delgutte, 1980). A probe re sponse during this recover y period shows a decrease in discharge rate. If one assumes that the AP is not influenced b y each fiber's discharge rate to the probe,as discussed abo v e, the initial discharge of the probe of each adapted fiber must somehow be affected in order to cause a reduction in N1 amplitude. Increasing click repetition rate has been shown to affect the initial portion of the poststimulus time histograms of auditor y nerve fibers more than later portions (Kiang et al., 1965; Kiang, 1968). Variations in recover y processes across the population of responding nerve fibers ma y result in a des y nchronization. In addi tion some fibers ma y not reach an adequate threshold of response following the masker, i.e., they adapt out com pletel y This des y nchronization and / or reduction in number of responding nerve fibers are reflected in a reduced N 1 amplitude.
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Relation to Psychophysics The present investigations are counterparts of psychophysical experiments on forward masking. An ade153 quate comparison between physiological masking and psycho physical masking is difficult for several reasons. Psycho physical observations reflect the perception of the entire system which integrates activity from several serial and/or parallel pathways. There is no reason to assume that responses from any one part of even all the parts will correlate with the behavior of the entire organism. Another difficulty is that different measurement criteria are used. Psychophysical experiments generally quantify the masking effect as thres hold shifts (in decibels) to the probe stimulus to the threshold is quiet. In the present experiment, alterations in response magnitude (amplitude and latency) to a supra threshold probe were measured. The relation between these two measures are unknown; however, there is a correlation between the two, i.e., an elevation in threshold produced by masking corresponds to a decrease in response amplitude (and increase in latency). Despite the difficulties in interpretation, the psycho physical data on forward masking are qualitatively similar to those found in this investigation for N1 amplitude and
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154 wave V latency. Although the characterization of the psychophysical recovery functions are not entirely agreed upon, the majority of studies reveal that complete recovery from masking is on the order of 100-300 msec (Elliott, 1962; Plomp, 1964; Wilson and Carhart, 1971; Penner, 1974; Fastl, 1976). In addition, these studies have indicated that increasing masking level does not influence the recovery time, whereas increasing masker duration lengthens the recovery time. The present findings are in general agreement with the psychophysical observations. Recovery times as fast as those seen for wave V amplitude (25 msec) have not been reported in the psychophysical literature. Summary and Conclusions This investigation has presented a description of the forward masking effects on human ABRs (wave V). An attempt has been made to compare the behavior of wave V to that of N 1 in the same subjects under identical stimulus manipula tions. While N 1 recordings from the ear canal proved to be difficult and amplitude measures of both wave V and N 1 showed considerable variability, the data suggest the following conclusions. 1. The primary effects of forward masking are re flected in a decrease in the probe-evoked N1 amplitude and an increase in wave V latency.
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2. N1 amplitude is the most affected measure and recovery time is considerably longer than 100 rnsec. 3. Wave V amplitude is the best affected measure and is fully recovered by 25 msec. 155 4. Increasing masker duration and masker level (over the range used) produces a greater effect on the probe responses. Since recovery times were generally beyond the maximum ~T used (100 msec), the effect of masker duration and masker level on recovery time cannot be accurately determined. 5. In general, increasing masker low frequency cutoff produces systematic increases in probe response amplitude and decreases in latency which are c8nsistent with stimulus-related events along the basilar membrane. Recovery times are different for the various low fre quency cutoffs. This may be due to different overlapping of populations excited by the masker and the probe, i.e., recovery takes longer when the entire population of units responsive to the probe are previously excited by the masker. 6. The differential effects of forward masking on N1 and wave V suggest that neural recoding of the input (N 1 ) occurs along the pathways re sponsible for the generation of wave V. 7. The effects of masker duration, masker level, and masker low frequency cutoff are initiated peri pherally and (following the coding changes) are reflected as parallel changes in wave V latency. 8. The possibility of a supernormal wave V response under certain conditions deserves further in vestigation.
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156 9. In response to a broadband click (50 dB HL) it appears that (at 6 T=0 msec) frequency regions below 4 kHz have large contributions to wave V and very little contributions to the N 1 re sponse. 10. The orderly changes of wave V latency and this component's robust amplitude affords an oppor tunity to measure forward masking effects in a noninvasive way. Provided the normal charac teristics as known, certain alterations may be of diagnostic significance.
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BIBLIOGRAPHY Abbas, P. J. (1979). "Effect of stimulus frequency on adaptation in auditory-nerve fibers," J. Acoust. Soc. Am. 65, 162-165. Abbas, P. J. and Gorga, M. P. (1981). "AP responses in forward-masking paradigms and their relationship to responses of auditory-nerve fibers," J. Acoust. Soc. Am. 69, 492-499. Achor, L. J. and Starr, A. (1980). "Auditory brainstem responses in cats, II.Effects of lesions," Electro enceph Clin. Neurophysiol. 48, 174-180. Allen, A. R. and Starr, A. (1978). ~uditory brainstem potentials in monkey (m. mulatta) and man," Electro enceph. Clin. Neurophysiol. 45, 53-63. Amadeo, M. and Shagass, C. (1973). evoked potentials during waking Psychophysiol. 10, 244-250. "Brief latency click and sleep in man," ANSI. (1969). "Specification for audiometers," 53.6-1969 (Arn. Natl. Stand. Inst., New York). Aran, J.M., Charlet de Sauvage, R., and Pelerin, J. (1971). "Comparison des seuils electrocochleographigues et de l'audiograrnme; etude statistique," Rev. Laryngel. (Bordeaux) 92, 477-491. Bauer, J. w. (1978) "Tuning curves and masking functions of auditory-nerve fibers in cat," Sensory Processes 2, 156-172. Bauer, J. w., Elmasian, R. O., and Galarnbos, R. (1975). "Loudness enhancement in man. I. Brainstem-evoked response correlatives," J. Acoust. Soc. Am. 57, 105-171. 157
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158 Berg, K. and Yost, W. (1976). "Temporal masking of a click by noise in dichotic and diotic listening conditions," J. Acoust. Soc. Arn. 60, 173-177. Berlin, c. I. and Gondra, M. I. (1976). "Extratyrnpanic clinical electrocochleography with clicks," in Electrocochleogr~, R. Ruben, C. Elberling, and G. Salomon, Eds. (University Park Press, Baltimore), pp. 457-469. Bobbin, R. P., May, J. G., and Lemoine, R. L. (1979). "Effects of pentobarbitol and kPtarnine on brainstem auditory potentials," Arch. Otolaryngol. 105, 467-470. Buchwald, J. and Huang, c. M. (1975). "Far field acoustic response: Origins in the cat," Science 189, 382-384. Charlet de Sauvage, R. and Aran, J. M. (1976). "Clinical value of adaptation measurements in electrocochleography," in Electrocochleoqraphy, R. Ruben, C. Elberling, and G. Salomon, Eds. (University Park Press, Baltimore), pp. 169-182. Chiappa, K. H., Gladstone, K. J., and Young, R.R. (1979). "Brainstern auditory evoked responses. Studies of waveform variations in 50 normal human subjects," Arch. Neural. 36, 81-87. Coats, A. C. (1964a). "Physiological observations of auditory masking. I. Effect of masking duration," J. Neurophysiol. 27, 988-1000. Coats, A. C. (1964b). "Physiological observations on audi tory masking. II. Effect of masking intensity," J. Neurophysiol. 27, 1001-1010. Coats, A. C. (1967). "Physiological masking in the peri pheral auditory system. III. Effect of varying test click intensity," J. Neurophysiol. 30, 931-948. Coats, A. C. (1971). "Depression of click action potentials by attenuation, cooling, and masking," Acta Otolaryngol. Suppl. 284, 1-19. Coats, A. C. (1974). "On electrocochleographic electrode design," J. Acoust. Soc. Arn. 56, 708-711.
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159 Coats, A. C. ( 1976) "Evaluation of 'click pips' as impulsive yet frequency-specific stimuli for possible use in electrocochleography" in Electrocochleography, R. Ruben, c. Elberling, and G. Salomon, Eds. (Univer sity Park Press, Galtimore), pp. 387-406. Coats, A. and Dickey, R. (1972). "Postmasking recovery of human click action potentials and click loudness," J. Acoust. Soc. Am. 52, 1607-1612. Coats, A. c., Martin, J. L., and Kidder, H. R. (1979). "Normal short-latency electrophysiological filtered click responses recorded from vertex and external auditory meatus," J. Acoust. Soc. Am. 65, 747-756. Cullen, J., Ellis, M., Berlin, C., Lousteau, R. (1972). "Human acoustic nerve action potential recordings from the tympanic mernbrance without anesthesia," Acta Otolaryngol. 74, 15-22. Dallas, P. (1973). The Auditory Periphery: Biophysics and Physioloqy (Academic Press, New York). Dallas, P. and Cheatham, M. (1976). "Compound action potential (AP) tuning curves," J. Acoust. Soc. Am. 59-591-597. Dallas, P., Schoeny, Z., and Ch~atham, summating potentials, descriptive Otoloryngol. Suppl. 302, 1-46. M. (1972) "Cochlear aspects, Acta Davis, H. (1976). "Principles of electric response audio metry," Ann. Otol. Rhinol. Laryngol. Suppl. 28, 1-96. Delgutte, B. (1980). "Representation of speech-like sounds in the discharge patterns of auditory-nerve fibers," J. Acoust. Soc. Am. 68, 843-857. Derbyshire, A. J. and Davis, H. (1935). "Action potentials of the auditory nerve," Am. J. Physiol. 113, 476-504. Despland, P.A. and Galambos, R. (1980). brainstem response (ABR) is a useful in the intensive care nursery," Ped. "The auditory diagnostic tool Res. 14, 154-158.
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BIOGRAPHICAL SKETCH Steven John Kramer was born in Culver City, California, on December 18, 1950. He grew up and attended school in Santa Barbara, California. He received a B.A. degree in speech and hearing from the University of California at Santa Barbara in June 1976. He continued his education at the University of Florida where he received an M.A. degree in speech in June 1978. He developed an interest in hearing science and obtained a Ph.D. degree in June 1980. He was married to Kathleen A. Cannon on April 11, 1981, and they are moving to Galveston, Texas where he has a position with the University of Texas Medical Branch. 172
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I certify that I have read this study and that in my opinion it conforms to acceptable standards of scholarly presentation and is fully adequate, in scope and quality, as a dissertation for the degree of Doctor of Philosophy ~ ~ -, ~ 2iJi2 ~ L ~ f/:, i~ Donald C. ;i;;,hairman Professor of Psychology and Speech I certify that I have read this study and that in my opinion it conforms to acceptable standards of scholarly presentation and is fully adequate, in scope and quality, as a dissertation for the degree q_ L DoctQr of Philosophy. /, / / -) (_ / c > ~ ~ ~ ~ -d l~W. Keith Berg 1 Associate Professor of Psychology I certify that L have read this study and that in my opinion it conforms to acceptable standards of scholarly presentation and is : Jully adequate, in scope and quality, as a dissertation f9r the degree of D~ctor of Philosophy. i I, -; -r I t ) 1 : / ~( ---' -~ --,...___.. Jl ____ ~am E. Brownell Assistant Professor of Neuroscience I certif y that I have read this study and that in my opinion it conforms to acceptable standards of scholarly presentation and is fully adequate, in scope and quality, as a dissertation for the degree of Doctor of Philosophy. ~ ~ :.. .... ~-' ---,,-.--=a <"--"' : ~ / c.....;;. -"-/ _ _,; / _____ Francis J. Kemker Adjunct Professor of Speech
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This dissertation was submitted to the Graduate Faculty of the Department of Speech in the College of Liberal Arts and Sciences and to the Graduate Council, and was accepted as partial fulfillment of the requirements for the degree of Doctor of Philosophy. June 1981 Dean for Graduate Studies and Research
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UNIVERSITY OF FLORIDA II I II IIIIII Ill Ill lllll lllll II 1 11 1 111 11 1 11111111 II 11111111111 111 1 3 1262 08553 5895
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