EFFECTS OF INTENSE ACOUSTIC NOISE
ON COCIILEAR FUNCTION IN INFANT AND
ADULT GUINEA PIGS
HARVEY BRUCE ABRAMS
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
AC KNO WL LLDGEMEN'I: S
The author wishes to express his deepest appreciation to
and respect for Dr. Teas, Chairman of his supervisory committee
and academic advisor, whose guidance and patience have been a
continual source of encouragement and inspiration throughout
The author also wishes to express his sincere gratitude
to Drs. William E. Brownell and William HI. Cutler, for their
valuable assistance. The writer is indebted to the Veterans
Administration which provided a traineeship during his doctoral
studies at the University.
TABLE OF CONTENTS
ACKNOWLEDGEMENTS . . . . . . . .... .. .. .ii
ABSTRACT . . . . . . . ... . . . . iv
I. INTRODUCTION . . . . . . . . .. . 1
II. METHOD . . . . . . . . . . ... 12
Animals . . . . . . . .. .. . .. . 12
Surgical Procedure . . . . ... .. ... .12
Signal Generation . . . . . . . . 16
Noise Stimulus Generation . . . . . .. 19
Recording . . . . . . . . . .... 19
Procedure . . . . . . . . . .... 24
Histology . . . . . . . . ... .. .25
III. RESULTS . . . . . . . . . . . 27
Preexposure . . . . . . . . .. .. . 27
Response Waveform . . . . . . . . 27
Threshold . . . . . . . ...... 30
Effects of Frequency and Intensity on N1 and
P4 Response Amplitudes . . . . . ... .33
Effects of Frequency and Intensity on N1 and
P4 Response Latencies . . . . . ... .41
Postexposure . . . . . . . .. 48
Effects of Noise on Threshold .......... 48
Effects of Noise Exposure on Response
Amplitude and Latency . . . . . ... .52
Histology . . . . . . .. ... . 70
IV. DISCUSSION . . . . . . . . . . . 80
Development of the Auditory System . . . .. 80
Effects of Noise on the BSR . . . . ... 83
Susceptibility . . . . . . . . . .85
LIST OF REFERENCES . . . . . . . . ..... 88
BIOCRAPHICAL SKETCH . . . . . . . . . .. 94
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
EFFECTS OF INTENSE ACOUSTIC NOISE
ON COCHLEAR FUNCTION IN INFANT AND
ADULT GUINEA PIGS
HARVEY BRUCE ABRAMS
Chairman: Donald C. Teas
Major Department: Speech
Brain stem responses (BSR) to filtered acoustic clicks were ob-
tained from four groups of guinea pigs, two newborn and two adult,
with chronically implanted recording electrodes. One adult group
and one newborn group were exposed to two hours of a 108 dB SPL
narrow band of noise centered at 4 kHz. The two other groups served
as controls. After one month following the exposure, BSRs were again
obtained, the animals sacrificed and the cochleae prepared to deter-
mine the number of missing hair cells. Threshold, response amplitude
and response latency values were analyzed for the N1 and P4 waves of
the BSR for all animals. Preexposure results indicated that while
the N1 response functions in the adult and newborn groups were gener-
ally similar, the P4 functions differed between the two groups.
Postexposure results indicated a greater N1 and P4 threshold shift
for the exposed newborn group in response to the 6 kHz filtered
click than for the adult group. In addition, the postexposure
N1 and P4 response amplitude functions of the newborns showed a
greater relative decrease in response to the 6 klz filtered click
than did the adult functions. Postexposure latency measures did
not indicate differences between the groups although the latencies
of N1 and P4 in response to the 1 kHz filtered click were longer
at higher click intensity levels than those obtained prior to the
noise exposure. Histological analysis failed to show any differ-
ences in the number of missing hair cells among the exposed adults
and newborns. The results of this study are discussed in relation
to maturation of the auditory system, effects of noise on the BSR
and susceptibility to noise-induced hearing loss.
Modern man pays a price for technological progress in the form
of industrial iand environmental related health disorders. The effects
of noise on the auditory system are of considerable interest today and
have been studied since the early 19th century. Fosbroke (1831) identi-
fied individuals suffering noise-induced hearing loss on the basis of
their exposure to weapon fire and forge operations. Yoshii (1909) was
able to identify the hair cell region of the cochlea as the principle
site of noise-induced damage. Investigations through the 1950's were
directed toward the quantification of cochlear damage as a function of
stimulus intensity and frequency (Crowe, Guild and Polvogt, 1934;
Davis, Derbyshire, Kemp, Lurie and Upton, 1935; Lurie, Davis and
Hawkins, 1944; Wever and Smith, 1944; Davis and Associates, 1953;
Ever and Lawrence, 1955). Throughout the last several decades the
effects of noise upon cochlear electrophysiology have received atten-
tion (Eldredge, Bilger, Davis and Covell, 1961; Price, 1968, 1972,
1974; Simmons and Beatty, 1962; Benitez, Eldredge and Templer, 1972;
Mitchell, Brummett and Vernon, 1973; Eldredge, Mills and Bohne, 1973)
as has the normal anatomical and physiological development of the
cochlea (Nakai and llilding, 1968; Pujol and llilding, 1973).
The efforts of these and many other investigators have added much
to our knowledge of the effects of intense noise on the auditory sys-
tem. We know, for instance, that the cochlear structures principally
affected by high noise levels are the outer hair cells (Luric et al.
1944; Davis et al. 1935). As the intensity or duration of the noise
increases the extent of injury increases and may include other struc-
tures such as the inner hair cells and afferent nerve fibers. It is
generally accepted that the location of damage within the cochlea is
related to the frequency of the stimulus. Hiigh frequency, high in-
tensity noise causes damage to the basal end of the cochlea whereas
lower frequency noise affects more apical portions of the cochlea
(Wever and Smith, 1944). It has also been shown that damage to the
structures of the cochlea results in electrophysiological changes
such as a decrease in the magnitude of the cochlear microphonic
(Price, 1968, 1972, 1974) and in the whole-nerve action potential
(Mitchell, Brummett and Vernon, 1973, 1977). Although the effects
of noise on cochlear structure and function have been well studied
and documented, the specific mechanisms of cochlear damage remain
Spoendlin (1976) suggested that the specific mechanisms of noise-
induced cochlear damage are a function of the intensity of the stimu-
lus and its duration. Spoendlin described two critical intensities
with respect to their effect upon the cochlea. Below 90 dB (critical
intensity I) there appears to be little structural damage regardless
of the duration of the exposure. Above 130 dB (critical intensity II)
the structures of the cochlea undergo severe irreversible damage even
with very short durations. As the duration of the exposure increases
at 130 dB and above, the damage to the cochlea does not increase in
proportion to the duration. The mechanism of damage at these levels
is apparently mechanical as evidenced by separation of the organ of
Corti from the basilar membrane. The hair cells in the detached por-
tion often have a normal looking appearance. The motion of the basilar
membrane at high intensities is apparently so violent that the organ of
Corti separates from the membrane. Between these two critical intensi-
ties (90-130 dB) the duration oF exposure is an important consideration.
As duration increases for moderately intense stimuli, cochlear damage
increases. The specific mechanisms of damage between the two critical
intensities have been the subject of considerable investigation
(Spoendlin, 1970, 1971; Ward and Duvall, 1971; Beagley, 1965; Lipscomb
and Roettger, 1973; Bohne, 1972, 1976).
One theory proposes that cochlear damage to moderately intense
noise is the result of what Spoendlin (1976) calls metabolic decompen-
sation. Hair cells examined after noise exposure show damage that is
consistent with the effects of changes in the metabolic activity of the
cells. These changes include distortion or swelling of the cell bodies
(Spoendlin, 1970, 1971) fusion of sterocilia (Spoendlin, 1971; Ward and
Duvall, 1971) and an increase in the number of lysosomes in the outer
hair cells (Beagley, 1965; Ward and Duvall, 1971). A second theory
suggests that vascular changes occur as a result of noise exposure re-
sulting in an interruption of blood supply, oxygen and nutrients to
the cells. Lipscomb and Roettger (1973) found evidence of constriction
and decrease in red blood cells in the vessels below the basilar mem-
brane following noise exposure. Spoendlin (1971) discovered swelling
of the afferent nerve fibers following noise exposure. This finding
is similar to that seen after an interruption of the blood supply to
A third theory, the Ionic Theory, as proposed by Bohne (1972,
1976) suggests that damage to the structure of the organ of Corti is
caused by the communication of perilymph-like fluid of the organ of
Corti (low potassium, high sodium ion content) with endolymph of the
scala media (high pot;lss i m, low sodium ion content) through the nor-
mally impermeable reticular lamina. Bohne theorized that noise expo-
sure somehow increases the permeability of the reticular lamina re-
sulting in communication of the two fluids. To test her hypothesis,
Bohne exposed chinchillas to a one hour exposure of 108 dB SPL octave
band noise centered at 4 kHz and sacrificed the animals at different
postexposure intervals to determine the course of injury over time.
She discovered that while there was little evidence of damage shortly
after the exposure (< one hour) at one month postexposure there was
total degeneration of a 1 mm segment of the organ of Corti approxi-
mately 4 mm from the base. Bohne discovered small holes, the size of
missing hair cells, in the reticular lamina two hours postexposure
which were large enough to allow leakage of the endolymph into the
organ of Corti fluid spaces. These holes later healed resulting in
scars formed by the enlarged phalangeal processes. Some indirect
support for Bohne's theory is provided by Goldstein and Mizukoshi
(1967) who suspended outer hair cells in artificial endolymph and
perilymph and found swelling in those cells placed in the endolymph
whereas those cells placed in the perilymph retained their shape.
Stronger support is provided by Duvall, Sutherland and Rhodes (1969)
who nicked the endolymphatic surface of the organ of Corti and dis-
covered increasing damage to the ulstrastructure of the organ of
Corti as the time increased following the procedure.
A second unresolved issue in noise-induced hearing loss is the
possibility that susceptibility to noise-induced trauma varies among
organisms within the same species. There is, as yet, no way to de-
termine susceptible individuals within a population. As a result,
those susceptibility studies which have been particularly valuable
have dealt not so much with individual as with group susceptibility.
The target for several of these investigations has been the very young.
Falk, Cook, Haseman and Sanders (1974) exposed two-day, eight-
day and eight-month old guinea pigs to 30 hours of white noise at 119-
20 dB SPL and found that the younger animals suffered significantly
greater pathology as measured by hair cell loss. Price (1976) found
a greater loss of cochlear microphonic (CM) as measured at the round
window among kittens than among adult cats after an exposure to an
intense 5 kHz pure tone for 50 minutes. The correlation between
histological results and the CM measurements were somewhat inconsistent
but the overall results suggested a positive relation between the two
measures. Bock and Saunders (1977) proposed a critical period theory
to explain the results of a study in which hamsters, 27-55 days of age,
appeared to exhibit an increased susceptibility to noise trauma as mea-
sured by CM sensitivity. The authors suggested that there may be de-
velopmental changes in the young cochlea which increase the suscepti-
bility to noise trauma. Danta and Caiazzo (1977) exposed newborn and
adult guinea pigs to a 115 dB SPL narrow band of noise centered at
4 kHz for one hour and discovered an increased susceptibility to tem-
porary threshold shift (TTS) among the newborns as measured behaviorally.
Dodson, Bannister and Douek (1978) in attempting to simulate incubator
conditions in a newborn nursery, exposed one week old guinea pigs to
white noise at 76 dB SPL for seven days. They found appreciable
loss of outer hair cells in these animals as compared with a control
group. These results suggest that young organisms may be more sus-
ceptible to noise-induced hearing loss than adult specimens. Of
particular significance is the case of human infants remaining for
weeks in incubators. If infants show similar susceptibility, these
individuals may be undergoing noise-induced damage to cochlear hair
The basis for noise-induced permanent hearing loss is structural
damage to the fine detail of the organ of Corti. Only in recent
years, with the use of electron microscopy, has the fineness of de-
tail required to effectively study noise-induced damage become suffi-
ciently documented. It is hair cell damage that must be assessed in
noise trauma and the central question is the relation between hair
cell damage and the parameters of the traumatic stimulus. However,
hair cell damage can only be assessed post-mortem. If one could de-
termine the relation between an ante-mortem assay of hair cell loss,
an estimate of the state of hair cell integrity might then be possible.
For this reason, there has been much interest in studying response
activity in preparations subjected to stimuli which were chosen to in-
duce acoustic trauma. One might expect, for example, that behavioral
threshold would be a good correlate for hair cell damage if we assume
that behavioral thresholds accurately reflect the integrity of coch-
lear structures. However, Eldredge, Mills and Bohne (1973) showed
that in the chinchilla there was a poor correlation between threshold
sensitivity and hair cell loss.
The CM discovered by Wever and Bray (1930) and defined by Saul
and Davis (1932) has been used frequently as an index for noise-in-
duced cochlear damage. The CM is a stimulus-related cochlear poten-
tial with waveform which duplicates the displacement-time pattern of
the cochlear partition (Dallos, 1973). The input-output function of
the CM is characterized by three segments. The first segment is a
linear one in which output voltage is directly proportional to the
stimulus intensity. CM output has been measured as low as .005 my
(Wever, 1966). The second segment is characterized by a departure
from linearity toward the maximum output of the CM. The third seg-
ment consists of a roll-over effect in which increases in stimulus
intensity result in decreases in CM output. The CM has traditionally
been measured by two techniques: a single electrode placed on or
near the round window (RW), and the differential recording technique
(Tasaki and Fernandez, 1952) which utilizes two active electrodes
placed in the same cochlear turn. The RW technique has the advantage
of relative ease of recording but it has a serious drawback in that,
in the case of low frequency stimulation, it cannot be determined
whether the electrode is picking up proximally or distally generated
CM. Another problem with the RW technique is that the electrode picks
up the whole-nerve action potential (AP) with the CM. Under many
stimulus conditions it is difficult to visually separate the two re-
sponses which originate from different anatomical sources. The
differential electrode technique, on the other hand, permits the study
of locally generated CM and the separation of whole-nerve AP and CM
components but it requires a more surgically invasive technique than
RW recording. Unfortunately, RW recordings tend to yield little
difference in the reduction of CM sensitivity as a function of test
frequency (Simmons and Beatty, 1962; Price, 1968). In noise exposure
experiments (Smith and Wever, 1949; Price, 1968) the frequency at which
maximum depression of the CM occurred tended to be below the exposure
frequency. Iurrant (1976) concludes that, ". . the loss of CM sen-
sitivity and maximum output appear to be rather limited indicators of
the detailed mechanisms involved with acoustic trauma, based on cur-
rently available data" (p. 192).
In contrast to the CM, the neural responses may be a more sensi-
tive index of the degree of and perhaps the location of noise trauma
(Davis and Associates, 1953; Benitez, Eldredge and Templer, 1972;
Mitchell, Brummett and Vernon, 1977; Pugh, Horowitz and Anderson,
1974). The use of the eighth nerve action potential to gain frequency
specific information was earlier felt to be limited since the prevail-
ing thought was that the response reflected only synchronous activity
in the basal portion of the cochlea. Analysis of the whole-nerve re-
sponse with analytic procedures shows that some resolution of frequency
representation can be obtained. The use of tone-pips (Davis, Fernandez
and McAuliffe, 1950), filtered clicks (Aran, 1971; Zerlin and Naunton,
1975), click-pips (Coats, 1976) and selected masking of broadband click
evoked AP (Teas, Eldredge and Davis, 1962; Eldredge, Mills and Bohne,
1973) have enabled investigators to obtain substantial frequency speci-
fic information from the whole-nerve response. The whole-nerve AP
appears to correlate well with anatomical data. Eldredge and his
associates (1973) concluded that, "The close rank oreder correlation
between loss of whole-nerve AP . and the loss of hair cells is
very gratifying in terms of a quest for reliable physiological indices
of injury. The N, peak voltages as a function of input sound pressure
may be a more sensitive index for loss of hair cells than any measure
of threshold simply because this function examines responses over a
wider dynamic range" (p. 79).
The whole-nerve response in man is recorded most clearly with a
transtympan i c electrode rest ing on the promontory. The response can
also be recorded with a wick electrode in the external auditory mea-
tus, but with some loss of clarity. The whole-nerve response is also
included in the Brain Stem Response (BSR) as wave I.
Jewett and his associates (Jewett, Romano and Williston, 1970;
Jewett, 1970; Jewett and Williston, 1971), recording from the vertex
of the scalp, described a series of waves consisting of seven peaks
which appeared in the first nine msec after the onset of a click
stimulus. Their evidence strongly suggested that wave I was generated
by the eighth nerve while waves II through VII represented auditory
evoked brain stem activity. The waves have since been referred to as
the Brain Stem Response.
In an attempt to correlate the individual waves with specific
brain stem structures, Lev and Sohmer (1972) recorded intracranially
in cats and concluded that waves I through V represented activity of
the cochlear nerve, cochlear nucleus, superior olivary complex, and
the inferior colliculus (waves IV and V) respectively. Buchwald and
Iluang (1975) dissected various auditory brain stem structures in the
cat and came to similar conclusions regarding the generator sites of
the BSR with the exception that wave IV appeared to represent activity
in the ventral nucleus of the lateral lemniscus. In a similar inves-
tigation, Henry (1979) concluded that the sources of the BSR in the
mouse closely resemble those in the cat.
Wave V is of particular interest as it is the most prominent
peak when recorded from the human scalp. Recent investigations have
attempted to demonstrate relationships between wave I and wave V
(Elberling, 1976; Klein and Teas, 1978). lilberling has shown that,
regardless of the intensity, the latency of wave V varies as a con-
stant (4.2 4.4 msec) when compared to the latency of wave I for a
2 kHz acoustic transient. Elberling suggests that this relationship
is indicative of the close approximation of frequency specificity
between the two waves. The significance of this relationship is two-
fold. First, the clinician's task for measuring responses close to
threshold is made easier with the larger wave V and secondly, infor-
mation may be obtained which can add to our knowledge concerning the
relationship between peripheral and central auditory processing.
The use of BSR is rapidly becoming a valuable objective method
for differentially diagnosing auditory pathway disorders (Sohmer,
Feinmesser and Szabo, 1973; Sohmer, Feinmesser, Bauberger-Tell, Lex
and David, 1972; Berry, 1976; Davis, 1976; Davis and Hirsh, 1977).
At present, however, few studies have investigated the effects of
intense noise on these brain stem neuri potentials.
In one study, Sohmer and Pratt (1975) studied the effects on the
BSR in human subjects produced by noise exposure. The noise produced
a temporary threshold shift (1TS). The BSR to a click showed a greater
latency and amplitude change for the earliest negative deflection (N1)
than the later waves which showed little change in the TTS condition.
The authors suggested that this finding indicated that TTS is a peri-
pheral, electrophysiologic event.
As humans cannot be used in permanent threshold shift (PTS)
studies, the guinea pig has long been considered one of the animals
of choice for several reasons: low cost, ease of procurement, surgi-
cal accessibility of the auditory structures, and as Davis and
Associates wrote in 1953, "In any extrapolation of . d:ta to
the probl em( of acoustic trauma in man we can prohhIbly assume with
some confidence that the organ of Corti in man has about the same
mechanical strength that it has in the guinea pig. The size and
structure are very similar, particularly if we compare the corres-
ponding regions that are most sensitive to the same frequency. For
given amplitudes of movement of the footplate of the stapes we should
expect rather similar injurious effects on the hair cells and similar
probabilities of mechanical failure of supporting structures" (p. 1188).
The use of the guinea pig also has produced considerable data of in-
trinsic interest quite apart from their direct applicability to man.
That is, the principles of function are also of interest.
The purpose of this study was to contrast the effects of noise
which produces PTS on the BSR's of newborn and adult guinea pigs.
Specific data are presented on (1) the effect of age on the suscep-
tibility to noise-induced hearing loss as measured by the BSR, (2)
on the effects of PTS on the amplitude and latency of the early and
late waves of the BSR and the relations among these waves, (3) on
the correlation between noise-induced changes in the early and late
BSR and hair cell loss, and (4) on the suitability of filtered clicks
as a frequency-specific stimulus.
ME'101)S AND PROCEDURElS
An i ma s
Four groups of guinea pigs, 16 animals, were used. Five animals
were in the adult experimental group (305-957 gms) and five animals
were in the newborn experimental group (96-112 gms). Three animals
were in the adult control group (407-508 gms) and three animals were
in the newborn control group (107-132 gms). In this study an animal
under 72 hours of age was considered newborn. The adult animals were
procured, fed, and managed by the Animal Resources Department of the
University of Florida and caged in a laboratory. The newborns were
born in this room and stayed with their mothers. The ambient noise
level in the room was approximately 48 dBA and consisted mostly of
animal vocalizations and movement within the cages. No frequency
analysis of the ambient noise was done.
Normal auditory acuity was determined by the presence of Pryor's
Reflex (this reflex was often weak and/or missing in the newborns),
normal otoscopic examination and acceptable BSR (first negative wave)
threshold to broad band clicks. Pilot studies had determined this
threshold to be approximately 30 dB SPL + 5 dB.
The animal was anesthetized with Nembutal (0.5 cc/kg of body
weight). A supplemental dose (1/3 of initial dose) was given after
two hours if the animal showed signs of discomfort or excessive
movement. Temperature and heart rate were monitored continuously.
Temperature was maintained between 36-380 C. In order to eliminate
the contribution of the contralateral ear to the BSR the test ear
(Taniguchi, Murata and Minami, 1976; Teas and Niclsen, 1975) the
left cochlea was destroyed by rupturing the round and oval windows
transtymp;nically and draining the cochlear fluids.
Under clean, non-sterile conditions, a 2-3 cm anterior to pos-
terior incision was made along the midline of the scalp. After the
tissue was retracted to expose the skull, one hole was drilled at
the parietal crest and another was drilled approximately 3 mm
superior to the external auditory meatus (EAM). In the adults,
mounting screws (0.80" x 1/16") were screwed into these holes and
platinum wires were wrapped about each screw (.008" diameter + .003"
diameter teflon coated except for 2 mm of its tip). In the newborn,
the tips of the electrodes were inserted directly into the drilled
holes since the newborn skull was too thin to accept the screws.
With the wires attached to a small socket, the implant was fixed
onto the skull with cranioplastic cement. Figure 1 illustrates the
location of the electrodes in the skull. Soon after implantation
was completed the animals were returned to their cages (the newborns
to their mothers) and allowed to recover approximately 48 hours be-
fore BSR measurements were made.
One postsurgical complication found during pilot studies was
that vestibular disturbances due to the contralateral labyrinthectomy
could be so severe that feeding is inhibited. This occurred in one
newborn animal which eventually died despite attempts at supplemental
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feeding. It was found that if damage to the non-test cochlea was kept
to a minimum, the animals would quickly recover from vestibular prob-
lems (nystagmus and loss of balance). Another complication was the
loosening and eventual loss of the implant plug in the newborn animals
as a result of a rapid skull growth during the one month postexposure
period. This problem was solved by periodically adding a small amount
of cranioplastic to the perimeter of the implant during the one month
A simplified block diagram illustrating the equipment used in
this study is shown in Fig. 2. A Grass stimulator produced the square
wave pulse which had a repetition rate of 10 pulses/sec and a duration
of 120 msec. After being delivered to a buffer, attenuator and mixer,
the signal was amplified (McIntosh, MC 40) attenuated and fed into an
IAC single wall, sound-treated room enclosed by a concrete block wall.
The filtered clicks were generated by activating a band-pass filter
(Krohn-Hite, 3100) with the pulse. The filter cutoffs were adjusted
to produce the desired waveform of approximately four cycles in length
with its plateau being reached within the second cycle. The filter
imposed a frequency dependent delay between the synchronizing pulse
and the signal at the transducer which ranged from .18 msec for the
filtered click (FC) centered at 8 kHz to .89 msec for the 500 Hz
centered FC. All latency measures reported in this study are corrected
for this filter delay. The filtered clicks drove a Bruel and Kjacr
(BSK) 1/2 in condenser microphone (type 4133) coupled to the opening
of the guinea pig's EAM by a 1 mm diameter speculum. The spectra of
the filtered clicks (Fig. 3) were found by measuring the acoustic
output from a speculum with a 1/8" condenser microphone (B&K 4138)
connected to a sound-level meter (B&K 2209) with 1/3 octave filter
(B&K 1616). The output of the meter was fed to a graphic level re-
corder (BfIK 2306) which plotted the data semi-automatically. The
spectra were corrected for ear canal effects as measured previously
in this laboratory (Teas and Nielsen, 1975) and for the difference
in repetition rates used for calibration (90/sec) vs. the rate used
during the experiment (10/sec). The spectrum SPL at the ear drum at
0 dB attenuation was determined by subtracting 10 X Log of the band-
width (bandwidth being determined at 6 dB down from the peak) from
the averaged SPL values of those data points within 6 dB of the peak.
Noise Stimulus Generation
The stimulus for the narrow band noise exposure was generated by
a Grason-Stadler 455C Noise Generator. After being filtered (Krohn-
Hite, 3100) and amplified (McIntosh, 4C40) the filtered noise was de-
livered to an Altec, 802 D acoustic transducer whose cone was placed
2 cm from the EAM of the animal. The signal was calibrated before
and after each exposure by a Ballantine, 320A True RMS meter and by
a BUK Precision Sound Level Meter (model 2209) with a 1/2 in conden-
sor microphone (type 4135) placed at 00 incidence to the center of
the cone's opening. The spectrum of this noise is shown in Fig. 4.
The two leads from the skull implant were connected to a Grass,
model IIIP511B high impedance cathode follower connected to a Grass P5
Series AC Preamplifier (gain set at 10k, band passed from 30 llz to
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3 kiHz) and Krohn-llite model 3100 filter (also band passed from
30 Hz to 3 kHz). The head holder served as ground. The filtered
response was delivered to the A/D converter (40 psec bin width) of
a Computer Automation mini-computer which performed the averaging
of the BSR activity. The single responses were monitored on the
Tektronix 565 oscilloscope to note changes in the waveform which
would indicate equipment malfunction or excessive movement.
The animal was placed in a head holder immediately after the
anesthetic had taken effect and the implant was connected to the
cathode follower. After the speculum had been placed into the open-
ing of the EAM, intensity functions were performed with broad-band,
0.5, 1, 2, 4 and 8 kHz filtered clicks in that order. As the signal
to noise ratio was poorest at the lowest frequencies, the averages
tended to be satisfactory at these low frequencies while the animal
was most heavily anesthetized. Intensity of the clicks was varied
from 0 dB of attenuation to threshold, in 6 dB steps, for each
stimulus. At 0 dB attenuation the calculated SPL was 89 dB at 8 kHz,
86 dB at 6 kHz, 75 dB at 4 kHz, 70 dB at 2 kHz, 77 dB at 1 kliz and
82 dB at 500 Hz. The attenuators were linear over the range utilized.
The number of responses averaged for each stimulus varied depending
upon the intensity and CF of the stimulus. This number ranged from
32 responses for the higher frequency FCs at 0 dB of attenuation to
2038 responses at threshold. Threshold was determined as the point
between the level at which the response was just visually detectable
in the average and the level at which it was no longer visually
detectable for 2048 repetitions. The responses were recorded on
data cassettes for later processing.
After completion of the baseline measurements, the experimental
groups were exposed to a narrow band of noise centered at 4 kHz at
108 dl SPI, for two hours. Following the four-week interval, input-
output functions were again performed, the procedure for which was
identical to that described for the baseline measurements. A four-
week interval was selected as there is no indication of additional
anatomical damage beyond this time in the chinchilla (Bohne, 1976)
and pilot work did not indicate additional damage as measured elec-
trophysiologically in the guinea pig.
Immediately following the one month postexposure measures, the
cochleae were processed for analysis by surface preparation (Engstrom,
Ades and Anderson, 1966; Smith and Vernon, 1976). The animals were
administered an overdose of Nembutal IP. As soon as respiration
ceased, the animals were decapitated and the temporal bones removed
and placed in vials of formalin fixative. Under a dissecting micro-
scope at 12X magnification, the bulla was opened to expose the cochlea.
A small hole was made in the apex and the cochlear windows were care-
fully ruptured to allow gentle perfursion of fixative throughout the
cochlea by means of a Pasteur pipette. The perfused cochlea remained
in fixative for at least 48 hours. After two 10 minute rinses in
phosphate-buffered solution, the cochlea were gently perfused several
times with 1 percent 0s04 for 2 hours. After removal of the 0,04,
the cochlea were rinsed twice with 35 percent alcohol, twice with 50
percent alcohol (at 5 minutes per rinse) and left to stand, and re-
frigerated in 70 percent alcohol until dissected.
Dissection was performed under a stereomicroscope. Beginning
at the apex and continuing through the upper three turns, the hone
portion of the cochlea was removed, followed by the stria vascularis
and tectoriial membrane. The organ of Corti was separated from the
osseous spiral lamina with a capsule knife in 1/2 to full turns and
placed in a vial of glycerol. The section was then placed in a drop
of glycerol centered on a glass slide, covered with a glass cover
slip, and sealed with permount. Due to the tenacity with which the
organ of Corti adheres to the spiral ligament in the basal turn, the
capsule knife was used to separate the organ of Corti from both the
ligament and lamina. The tissue was carefully lifted out from the
base in 1/4 turn sections for mounting.
The specimens were viewed under phase-contrast microscopy at
1000X magnification. Missing hair cells were counted for each turn.
The results of this study are presented in preexposure and post-
exposure sections. Within each section the threshold measures and
the effects of frequency and intensity upon response amplitude and
latency will be shown. Histological results will be presented in a
final section. Except for the threshold measures, where data are
presented for all filtered clicks, the results will focus upon the
responses to the 1 kHz and 6 kHz FC's. Response amplitude and
latency contrasted sharply as a function of click intensity and in
the effects of the noise exposure for these two signals. Responses
to the 4 and 8 kHz FC's were often similar to those of the 6 kHz
signal. The 500 Hz FC often elicited a small dynamic range and the
2 kHz FC contained strong resonant energy at 4 kHz (Fig. 3).
The BSR waveform is shown in Figure 5 and consists of four posi-
tive and four negative peaks. The parietal lead was positive with
reference to the EAM. For the purpose of this study the first nega-
tive peak (N1) and the fourth positive peak (P4) were analyzed as
they were the earliest and latest waves that varied systematically
and consistently in amplitude and latency with changes in stimulus
intensity. A cursor was used to measure peak amplitude and latency
Figure 5. Representative BSR waveforms produced by FC's of different
center frequencies. A, 500 Hz; B, 1000 lHz; C, 2000 Hz; D, 4000 Hz;
E, 6000 Hlz; F, 8000 Hz; G, broad-band. All waveforms are shown at
0 dB of attenuation. The number of average responses varied from 32
for waveforms C thru G to 128 for waveform A.
values. Amplitude of N1 was measured from baseline to its most
negative value and the amplitude of P4 was measured from the most
negative value of N3 to the most positive value of P4. Latency was
measured from the onset of the signal at the transducer to the N1
and P4 peaks at their most negative and positive amplitude values
In one pilot study electrode locations were varied. As the
more caudal electrode was moved away from the external canal to more
medial positions, the amplitudes of the later BSR waves increased.
For this study the electrode configuration was chosen (Fig. 1) in
order to emphasize the amplitudes of the earliest BSR waves. The
waveforms in Figure 5 show that the amplitudes of the NI, N2 complex
are larger than the later deflections. However, the latencies could
be read easily with the cursor at all locations in the BSR waveform.
Figure 6 illustrates the mean NI and P4 preexposure threshold
values and + 1 Standard Deviation (SD) for each FC. The solid line
in each pair of curves represents the averaged responses of 5 experi-
mental plus three control animals. The broken line represents the
averaged responses of the three control animals measured 1 month
following exposure of experimental animals. Thus, the threshold
measurements over time are stable and the control group measures appear
to be valid estimates of preexposure sensitivity. In all cases thres-
holds measured 1 month following exposure were within 1 SD of the pre-
exposure threshold values. However, the P4 thresholds of the newborn
control animals measured 1 month after birth showed a decrease in
) l C
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threshold for frequencies of 1 kllz and above. The average decrease
in thresholds to the 5 filtered clicks (from 1 kllz to broad band) was
3.1 dB. There was no change in threshold for the 0.5 kliz FC. No
differences occurred in threshold for P1' in the adult control groap
ind only a slight difference occurred in the N1 responses in the new-
horn control group. All four sets o0 curves showed maximumlt sensi-
tivity to the 4 kiHz FC, and there was a tendency for the thresholds
to higher FC's to be slightly higher. The most extreme difference
in the visual detection level among the frequencies of the FC's
occurred in the adult group for P4 which showed a difference of
6 dB between 4 and 6 kilz. With the exception of the P4 response from
the newborn group, the absolute threshold levels for N1 and P4 were
very similar among the newborn and adult animals. The maximum
threshold values were approximately 67-69 dB SPL at 500 Hz and de-
creased to a minimum of 28-29 dB SPL at 4 kHz. The mean P4 threshold
values of the 8 newborn animals for FC's of 1, 2 and 4 kHz were 3 to
4 dB higher than the adults. The thresholds of the 3 newborn control
animals measured one month later, however, were consistent with all
other threshold measurements.
Effects of Frequency and Intensity on N1 and P4 Response Amplitudes
Figure 7 illustrates the preexposure response amplitude vs. signal
intensity for the N1 (Fig. 7A) and P4 (Fig. 7B) peaks produced by the
1 kHfz and 6 kllz FC's averaged over the 8 adult animals. Figure 7A
shows that N1 rises very steeply for the first 6 dB above threshold
and then more gradually with increases in intensity of the 6 kHz FC.
lTe N1 response to the 1 kilz FC requires greater intensity for
Figure 7. Average preexposure response amplitude in the adult group
(N=8) as a function of click intensity. Panel A illustrates the N1 amp-
litude function; Panel B, the P4 amplitude function. The solid circles
represent response to the 6 kHz FC; the cross marks, responses to the
1 kHz FC. See Figure 9 for variance data.
.- 6 kHz
50 70 90" 30 50
CLICK INTENSITY (dB SPL)
detection and is lower in amplitude at all intensity levels above
threshold. At suprathreshold intensities response magnitude in-
creases at a slower rate for the 1 klHz FC than for 6 kliz. The in-
tensity functions for P4 contrast with those for N1. Ilhe threshold
for the P4 responses are the same as for N1. Except near threshold,
the ampilitudes of the PI' responses are lower than the N1 responses
at respective intensities, probably because of the electrode con-
figuration used. The slope of the function of P4, 6 kflz is less
than that for the 1 kHz FC, but its maximum response is greater.
The intensity functions for the newborn group are shown in
Figure 8. The functions for N1 compare well with those for the
adults. However, those for P4 differ in some respects. The re-
sponse magnitudes and the slopes of the intensity functions are
lower. Unlike the adult responses there is little difference in
slope between the 1 and 6 kHlz FC's for the P4 responses.
Figure 9 shows the coefficient of variation (CV) for the pre-
exposure response amplitude as a function of click intensity for
the 1 kHz and 6 kHz FC's. The CV's for the adult animals (Fig. 9A)
in response to 6 kHz are nearly 1.0 near threshold and decreases to
about 0.5 by 18 dB above threshold and remains at about that level
throughout the intensity range. For 1 kHz, the threshold is higher
and the CV varies around the 0.5 value throughout the intensity
function. The CV's for N1 and P4 responses are similar in the adult.
The CV's for newborns are shown in Figure 9B. The wide variation in
CV for the responses from newborns contrasts with the consistency
shown by the adults responses. In a broad sense the CV's for the
two responses, N1 and P4, to each stimulus resemble each other.
Figure 8. Average preexposure response amplitude in the newborn group
(N=8) as a function of click intensity. The legend is the same as
that for Figure 7.
.02- 6 kHz
A I kHz
0 30 SO 70 90 30 SO
CLICK INTENSITY (dBSPL)
p r4 q
N N N
I I I
O CD tp r NJ
For 1 kHlz, N1 and P4 show maximum variation at 53 dB SPL. For
6 kHz each response shows a peak at 32 dB SPL. However, there are
also differences between N1 and P4 and, in general, the variation
in responses from the newborns is relatively large.
iEflcts of Frequency a nd Intensity on N and 14 Response Latencies
Response latency is reported to be a very stable measure of N1
and BSR while amplitude may vary due to electrode contact and other
procedural effects. Figure 10 illustrates the response latencies
for N1 and P4 for the 1 kHz and 6 kHz FC's from adults and newborns.
The latencies for N1 and P4 are plotted on overlapping coordinates
that have a constant 3.0 msec difference. The ordinate for N1 ranges
from 1 to 2.4 msec, and for P4 from 4 to 5.4 msec. The changes in
latencies with intensity of N1 and P4 are similar in the adult re-
sponses. For the 1 kHz FC the average difference between N1 and P4
for the adult group is 3 msec, for the infant group it is 3.13 msec.
For the 6 kHz FC the average N1 and P4 difference is 3.27 msec for
adults and 3.34 msec for the newborns. However, the N1 latency func-
tions for the .5 kHz FC in adults and newborns have very similar
values and, while an average difference is appropriate for the adults,
for infants the N1 and P4 latency difference is larger at 68 dB than
at 38 dB. No such divergence in N1 and P4 latency occurs for the
1 kHz FC. Apparently, P4 lags the changes in latency of N1 in the
newborn group while for the adults, P4 follows the latency decreases
in N1 as stimulus intensity increases. Figure 11 shows the functions
in Figure 10 redrawn with the 1 and 6 kHz FC's as the parameter. For
the responses from both the adult and the newborn, the latencies are
similar when the stimul i are strong. The ini num latencies at 88 and
Figure 10. Average preexposure response latency as a function of click
intensity and FC center frequency. Latency values for N1 and P4 are
plotted on overlapping coordinates having a 3.0 msec difference. Solid
circles represent the P4 latency functions; cross marks, the N1 latency
functions. Panels A thru D illustrate, respectively, the following
latency functions: Adult, 1 kilz; Adult, 6 kIIz; Newborn, 1 klHz; Newborn,
6 kIHz. N=8 for both groups. See Table 1 for variance data.
X-- N| 1
30 0 70 90 30 50
CLICK INTENSITY (dB SPL)
II I II
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NEWBORN LATENCY- ADULT LATENCY (MSEC)
-D o J
-T 0 0 0,
In '- U i
92 dB are slightly shorter in the adults than in newborns. On the
right side of Figure 11, in panel E, the differences between the N1
responses in adults and newborns for each signal are shown directly.
All the infant latencies are longer than the adult but the differences
for the 1 kilz IC below 66 dB are the smallest, i.e., the infant re-
sponses are most similar to tle adult. Above 06 dB, the differences
become larger abruptly, rising to 1.7 msec at 72 dB. For the 6 klHz
FC, the infant responses gradually approach the adult values, i.e.,
the differences become less with increases in intensity.
For P4 the latency functions for the two signals cross at about
64 dB. For signals greater than 64 dB, the responses to 1 kHtz FC
showed a shorter latency than those to 6 kHlz, while at intensities
less than 64 dB, P4 for 1 kHz has a longer latency than for 6 kHlz.
The latency functions also cross for the infant responses, but the
functions appear to be truncated, i.e., while the latencies for
weak signals are similar to the adult latencies, the infant P4 re-
sponses do not become as short as in the adults. The right-hand
panel F shows the differences in P4 responses between adult and
newborn groups. As for N1, infant responses lag the adult. The
sharp increase in P4 delay for infants seen for N1 is paralleled in
the data on P4. However, the difference for 6 kHz is minimal at
weak intensities and reaches a fairly constant value at 0.2 msec
as intensity increases.
Table 1 shows the average SD for the N1 and P4 latency measure-
ment for the adult and newborn groups. The overall variance was
similar between the two populations (.227 msec for adults vs. .22
Averaged S.I). for N1 and 1'4 Ltcncy Meoasurements (mscc)
N1 P4 N1 P4
1kHz .259 .238 .210 .294
6kHz .143 .266 .120 .256
msec for newborns). Within populations, N1 latency displayed less
variance than P4 in both groups, the difference being larger among
the newborns. Response variance to the 6 kllz FC was less than to
the 1 kllz FC, for both groups.
The preexposure threshold, iamp litude and latency data consis-
tently illustrated that the N1 response functions in the adult and
newborn were generally similar whereas the P4 functions differed
between the two groups.
Effects of Noise on Threshold
Figure 12 illustrates the mean N1 (Fig. 12A) and P4 (Fig. 12B)
threshold shift as a function of center frequency of the FC's for the
two groups of guinea pigs. The solid lines represent the responses
from experimental animals and the dashed lines represent control re-
sponses measured one month following exposure of the experimental ani-
mals. For both control groups, the threshold shifts for N1 and P4
were no more than + 6 dB from their preexposure values. Figure 12A
shows that the average threshold shift of N1 for the adult experimental
group increased with increasing center frequency for the FC to a maxi-
mum of 15 dB for the 8 kHz FC. The N1 threshold for the newborn group
also decreased with increasing frequency and exceeded the threshold
shift in adults. The threshold shift for the newborns showed a maximum
shift of 31 dB at 6 kllz. The shift in threshold for P4, shown in
Figure 121, shows the same trend of increasing shift with increasing
center frequency of the PC. The P4 threshold for newborns reached a
maximum shift of 30 dB for the 6 kilz FC and the P4 threshold for adults
LI) 0 c-'p
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postexposure threshold shift (dB SPL).
N1 cont. I4 cxper. P4 cont.
(N=3) (N=5) (N=3)
reached a maximum shift of 19 dB at 4 kHz. Except for the 6 kHz FC,
the difference between newborn and adult threshold shift was less
for P4 than for N1.
Effects of Noise Eixposure on Response Amplitude and Latency
Response amplitude. Figures 13 and 14 illustrate the relations
between postexposure response amplitude and signal intensity for the
N1 and P4 peaks produced by the 1 kHz and 6 kHz FC's averaged over
the five adult (Fig. 13) and five newborn (Fig. 14) experimental
animals. The preexposure equivalent measures are shown in Figures
7 and 8. As in the preexposure amplitude functions, response ampli-
tude was a continuously increasing function of stimulus intensity.
The postexposure curves of N1 for 6 kIlz show a greater decrease in
response amplitude from preexposure values than the curves for 1 kHz.
Both intensity functions show a shift to the right, i.e., requiring
greater intensities to reach a given amplitude, but the greatest
change occurs for the 6 kHiz curve. The response threshold to the
6 kHiz FC is elevated and a larger response was required for detection.
There is less postexposure change in the N1 response amplitudes for
the 1 kliz FC. The curves for P4 (adults) show relations similar to
those described for N1. For the newborns, however (Fig. 14), the
postexposure curve for N1 to the 6 kHz FC is shifted so far to the
right that it coincides with the intensity function for 1 kHz,
corresponding to the maximum threshold shift seen in Figure 12 (about
30 dB). Only very strong signals evoked P4 responses in the post-
Figure 13. Average postexposure response amplitude in the adult group
(N=5) as a function of click intensity. See Figure 7 for comparison
with preexposure functions and legend and Table 3 for variance data.
50 70 90 30
50 70 90
CLICK INTENSITY (dB SPL)
Figure 14. Average postexposure response amplitude in the newborn group
(N=5) function of click intensity. See Figure 8 for comparison with pre-
exposure functions and legend and Table 3 for variance data.
. 6 kHz
---X I kHz
70 90 30
Standard ldeviat ion for postexposulre response :inpl i tnlde (pV).
1 kliz (N=5)
-- -N F--
Newborn 1.31 1.15
6 kliz (N=5)
The differences in response amplitude between preexposure and
postexposure conditions are shown in absolute values in Figures
15 A-D and in relative values in 15 F and F. Relative shift was
computed by dividing postexposure response ;amplitude by preexposure
response amplitude, subtracting the result from 1 and multiplying by
100 to obtain a percentage shift. The results shown in Figure 15 in-
dicate that the noise exposure produced little change in the responses
to the 1 kHz FC but substantial change in response to the 6 kHz FC.
The absolute postexposure shift in the N1 response to the 6 kHz FC
was greater than that for the 1 kHlz FC in both the adult and newborn
populations. Similarly, response amplitude of P4 showed a greater
shift in response to the 6 kHz FC than to the 1 klHz in both groups
but to a lesser amount than N1. Figures 15 E and F show the post-
exposure response amplitudes in relation to the preexposure control
responses. The N1 and P4 response amplitudes to the 6 kHz FC in the
newborn group decreased more than did the responses of the adults.
Except at low intensities, the N1 and P4 responses decreased about
the same amount in the newborn group whereas the N1 response in the
adults shifted more, relative to the preexposure control responses
than did the P4 response.
Response latency. Figure 16 illustrates the postexposure
latencies vs. signal intensity for the N1 and P4 peaks produced by
the 1 kHz and 6 kHz FC's averaged over the five experimental adults
(Figs. 16 A and B) and five newborns (Figs. 16 C and D). The ordi-
nate for P4 is labeled so that there is a 3.0 msec constant between
N1 and P4. The corresponding preexposure measures are shown in
41 W 0
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od 420 x X-4
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1. '-4 Z e 1.i :-
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Figure 16. Averaged postexposure response latency as a function of
click intensity and FC center frequency. See Figure 10 for comparison
with preexposure functions and legend and Table 4 for variance data.
N=5 for both groups.
NI 4 ADULT
24 54- kHz 6 kHz
>- I //__,_ // .
w N P4
S24 54- NEWBORN
J 22 52- 1 kHz 6 kHz
14 44- *---* 4
1.2 42- POSTEXPOSURE
30 50 7 90 30 5 70 90
CLICK INTENSITY (dB SPL)
Standard deviation for averaged postexposure response latency (mscc).
1 kliz (N=5)
N6 k1 (N'-5
Figure 10. As in the preexposure functions, response latency for
all stimulus conditions was a continuously decreasing function of
stimulus intensity. There are relatively fewer data points for the
newborn population ldue to the restricted dynamic range caused by the
increase in postexposure threshold.
The slopes of the postexposure response latencies from adult
1 kHz functions are not as steep as the corresponding preexposure
curves (.016 msec/dB postexposure vs. .03 msec/dB preexposure).
By contrast, the slopes of adult 6 kiz functions (Fig. 16B) for pre
and postexposure are similar, but the postexposure latency values
are shorter than the preexposure measures. It is difficult to ob-
serve definite trends in the postexposure response latencies for the
newborn groups because of the relatively few data points. The post-
exposure latency function for N1 in response to the 6 kHz FC (Fig.
16D) is very similar but earlier (shifted left) than the preexposure
measure. The P4 response latency function shows a large decrease in
postexposure latency values throughout the intensity range and re-
quires signals greater than 56 dB for detection.
The postexposure N1 and P4 shift in latency as a function of FC
intensity is shown in Figure 17. Figures 17 A and B illustrate
latency shifts in the adult and Figures 17 C and D show the shifts
in the newborn group. The latencies for the control groups (dashed
lines) decreased for both the 1 kilz and 6 klIz FC's. The N1 and P4
postexposure response latencies to the 6 kilz FC for adults and the
N1 responses in the newborns also decreased in latency by a similar
amount. The latency of P4 from newborns increased in the responses
to 6 kilz. However, the postexposure latencies to the 1 kilz FC shows
4-J C, ~
0k '4 4
LC -~ 0
qv. u3 0
.0 0 ~
ri e ... r
c~ CI rf-
(33 SIl) ,3 N31V9
an increase in latency with increasing signal intensity for N1 and
throughout the intensity range for P4 for both adult and newborns.
Even though the N1 response to the 1 kHlz FC changed little in magni-
tude (Figs. 15A and 15C), the latency increase for the postexposure
measures was consistent. The response latency to the 6 kHlz IC also
decreased but less than for the I kH z FC, even though the amp litude
change was large. The P4 functions in the newborn group (Fig. 17D)
differ from the others in that there is a large decrease in latency
for the experimental group in response to the 6 klz FC as compared
with the control group. Also, the response latency to 1 kilz de-
creased at all signal levels except at the highest intensity, al-
though the function becomes less negative with increasing signal
Figure 18 illustrates the P4 N1 latency differences as a func-
tion of click intensity. For the adult responses to 1 kHz (Fig. 18A)
the postexposure P4 N1 differences are larger than the precxposure
differences, but for the responses to 6 kHz (Fig. 18B) there is no
change in the P4 N1 latency differences. For the newborns (Figs.
18C and 18D) postexposure P4 N1 differences are shorter than pre-
exposure values for both stimuli. Although N1 latencies for the
adult responses to the postexposure 1 kHz FC were slightly longer
than the preexposure latencies, a greater increase in latency occurred
for P4. No systematic latency effect occurred for responses to the
6 kHz FC.
The latencies from newborns showed shorter P4 N1 latency
differences following exposure to the 4 kHz narrow band noise. The
differences were consistent across the full range of intensities that
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4 -1 H &
4! -H O U
* CC'.- 0
o a o
(_3s ) IN--Nd
could be measured. The P4 N1 latency differences in response to
the 1 kHlz FC in the adult control group (Fig. 18A) (measured one month
following the exposure) to the experimental group were longer than the
preexposure mioasures at the higher signal intensities. As intensity
of the stimulus decreased, the latency differences of the control
group approached those of the preexposed experimental group. The
P4 N1 latency differences in response to the 6 kHz FC in the adult
control and preexposure groups (Fig. 18B) showed little differences.
Similarly, the P4 N1 latency differences for the newborn control
group measured one month following exposure to the experimental group
were similar to the preexposure measures (Figs. 18C and 18D).
The postexposure electrophysiological data show that exposure to
a narrow band of noise centered at 4 kHz produced a larger threshold
and amplitude shift in the N1 and P4 responses to the 6 kHz FC than
to the 1 kHz FC. The postexposure response latencies to the 1 kHz FC
increased as compared to the response to the 6 kHz FC. The results
also show that the newborn group experienced greater threshold and
relative amplitude shift than did the adults.
Figure 19 is a photomicrograph of a healthy section of turn III
of animal CI3, a control newborn animal. The three rows of outer
hair cells, their sterocilia and supporting structures can be clearly
seen. The inner hair cells are more difficult to see but their line
of sterocilia are just visible. A damaged portion of turn II of ani-
mal EA6 is seen in Figure 20. Missing outer hair cells are visible
in all three rows.
*ft t -I> \ -
>j ^h% ^Ai) 1"
Figure 21 illustrates the averaged number of missing hair cells
as a function of distance along the cochlear partition for the four
categories of preparations. In general, both groups exhibited only
minimal hair cell damage (in terms of missing cells). The adults
(Fig. 21A) showed damage at the base in all four rows of hair cells
with the amount of missing cells decreasing toward the apex. Oute r
hair cell row 3 exhibited the greatest amount of damage throughout
most of the cochlea although the first outer hair cell row was the
most damaged at the base. The newborn experimental group (Fig. 21B)
exhibited maximum damage at the apex in the third outer hair cell
row and minimum hair cell loss in the other turns and toward the base.
The control animals showed very little hair cell loss throughout the
There appears to be little correlation between histological and
electrophysiological data. The newborn group showed greater postex-
posure threshold shift (Fig. 12) and relative amplitude shift (Fig.
15) than the adult group in response to the 6 kllz FC. The histological
data, however, do not demonstrate greater hair cell loss for the new-
borns. On the contrary there are fewer missing hair cells toward the
basal end of the cochlea for the newborns than than for the adults.
Much of the histopathology in the adult group was statistically influ-
enced by one animal, EA6, which exhibited extensive hair cell loss in
the lower turns. It is thought that this damage existed prior to ex-
posure as EA6 was the oldest and largest (957 gins) animal used in this
study. Furthermore, EA6 demonstrated minimal postexposure electro-
physiologic changes. If the influence of EA6 is eliminated from the
0 r -, '
-4. 0 0 0
4-J E U ,
,- e ,
0 0 .-4 0 )
C) o C)
u U cl
r-4 0 O
0 0 C0.
U o rt
40 4 (I
0 0 *OC
O *H 0
) 3 t- c
C 0 0 Q
C0 Pt :o C
o Co -4
3 H0 0
V) C4- ) r
i0 '-4 0 ,'-'+
i ct z o
< > '0 3 -
4-J S O- '
Ud Ci -C C
P &, 3 0
*H C )
V) 4J U U F-4
H *0 oZ
-4 CZ (1)
*2 0 F20
0 3 k 0
0 Fi 0
UU C, E
Standard deviation for averaged number of missing hair cells.
Newbonmbe oft Adlt, hair
adult group, there is little difference between the number of missing
hair cells for the two groups. There does not appear to be a system-
atic relationship between postexposure latency changes and hair cell
loss. Figure 17 showed an increase in N1 response latency in response
to a 1 kilz FC for both the adult and newborn groups as compared with
preexposur meIasures. The histological data in Figure 21 show maximum
hair cell loss in the 3rd and 4th turns for the newborns and the 1st
and 2nd turns for the adults. The histological data for the control
groups are shown in panels 21C and 21D. Only minimal hair cell loss
was seen for both the adult and newborn groups.
Development of the Auditory System
Recordings of the BSR in humans and animals provide information
concerning the maturity and integrity of the auditory system. The
origins of the BSR peaks have been previously discussed. In the pre-
sent study, N1 as recorded in the adult and newborn guinea pig, is
thought to represent the synchronous discharges of auditory nerve
fibers. P4 is thought to represent the synchronous discharges of more
centrally located auditory neurons. The basis for these assignments
of origin depend upon peak latency, increase in amplitude and decrease
in latency with increasing stimulus intensity, and repeatability of
the waveform. The difference in the number of peaks (4 in the present
study vs. 5 in most human studies) may be due to electrode configura-
tion (implanted) recording technique (differential), or species differ-
ences. Taniguchi et al. (1976) also recorded four positive peaks in
the guinea pig utilizing a similar electrode configuration, and 4 peaks
are seen in cat's responses (Buchwald and Huang, 1975).
The gross similarity of the waveforms recorded from the adult and
newborn animal might suggest a high degree of auditory system maturity
at birth. On closer inspection, however, differences are apparent in
the latencies and amplitudes of responses from the two populations.
The preexposure measures suggest an immaturity of the central auditory
system of the guinea pig if P4 is interpreted to represent brain stem
activity. Figure 6, for example, illustrates the similarity of
threshold sensitivity for N1 in the adult and newborn groups as con-
trasted with P4 threshold sensitivity in newborn animals. P4 is de-
tectable at lower intensities as animals age and Figures 7 and 8 show
greater response magnitudes for the P4 responses in the adults than in
the newborns. Ilowever, the N1 response magn i tudes are similar in the
two groups. Preexposure latency measures (Figs. 10 and 11) also sup-
port the interpretation of developmental immaturity of higher auditory
brain stem structures. The P4 responses lagged the changes in N1
latency as a function of increasing intensity in the newborn group,
whereas P4 followed the latency decrease in N1 in the adult group.
The structural and physiological development of the peripheral
auditory system of the fetal and newborn guinea pig has been well
documented (Nakai and Ililding, 1968; Pujol and lHilding, 1973). In
the latter study the investigators discovered synaptic bars and cis-
ternae in hair cells opposite nerve endings, myelination of nerve
fibers, increasing numbers of mature synapses, and integration of
stia vascularis epithelium as indices of cochlear maturation of the
fetal guinea pig. Physiological evidence of peripheral maturity
which was reported included mature CM and whole-nerve action poten-
tials at birth. Although the preexposure N1 responses of the new-
born animals in the present study suggest relative maturity of the
peripheral auditory system, the evidence described above indicates
less than complete maturity. For example, the N1 response amplitude
in the newborn animals is lower than that of the adult, particularly
at high intensity levels (Figs. 7 and 8). Also, N1 latencies in the
newborns were found to be longer than those of the adults (Figs. 10
BSR investigations with human subjects have examined the rela-
tionship between chronological age and latency of the BSR waves as an
indication of auditory system maturity. Ilccox and Galambos (1974)
found decreasing latencies in wave V responses to broad hand clicks
as the age of human infants increased from three weeks to 18 months.
The authors suggested that incomplete myelination of the auditory
system may be partly responsible for the longer latencies near birth.
Salamy and McKean (1976) investigated the latency changes in wave I
and in the I to V difference as a function of age in newborn to one
year old human infants and interpreted their findings to suggest that
maturation of the peripheral (Wave I) and the central (Waves I-V
difference) auditory system occurred at different rates. The newborn's
wave I reached adult latency by six weeks of age whereas central trans-
mission latency did not reach adult values until one year of age. The
authors suggest that the paucity of myelinated fibers in the inferior
colliculus (Rourke and Riggs, 1969) may be responsible for the lengthened
latency at birth. Starr, Anlie, Martin and Sanders (1977) measured BSR
latencies in preterm and newborn human infants ranging in gestational
age from 25 to 44 weeks and found, as in the other studies, a decrease
in wave V and I to V difference with an increase in age. In the present
study, maturation of the central auditory system is suggested by the
decrease in P4 thresholds in the one month control animals as compared
with their thresholds ;as newborns (Fig. 6). Central auditory system
maturation is not reflected, however, in the growth in P4 response
amplitude in the one month control animals (Fig. 15). Nor does there
appear to be any demonstrable decrease in latency of the P4 response
or decrease in the P4 N1 latency difference in the one month control
animals (Figs. 18C and 1SI)). 'There are several possibility s to
account for these observations:
1. The change in electrophysiologic threshold is a more sensi-
tive indicator of maturation in the central auditory system of the
guinea pig than response amplitude or latency, or
2. Changes in response amplitude and latency are not seen in the
guinea pig until after one month of age, or
3. The number of control animals was too small to demonstrate
significant changes in amplitude and latency. There does, however,
appear to be substantial evidence in the literature and in the present
study to support the idea that the auditory system is not mature at
birth and that the central system reaches maturity later than the
periphery. Whether this delay is the result of incomplete myelination
or some other developmental factor is yet to be determined.
Effects of Noise on the BSR
Few studies have investigated the effects of noise on the later
BSR waves and the findings, thus far, are contradictory. Sohmer and
Pratt (1975) in their temporary threshold shift (TTS) study found that
the decrement of the later BSR waves was much smaller than the N1 de-
crement. Babighian, Moushegian and Rupert (1975) also used noise which
produced TTS and found a greater decrement in the collicular than in
the peripheral response. TTS is a fatigue phenomenon and does not re-
sult in durable structural damage to the cochlea or nerve fibers.
Thresholds usually recover within several minutes. The effects of
structural damage resulting from permanent threshold shift are last-
ing and apparently can be observed at higher levels in the auditory
system. In addition, the frequency specific effects of noise exposure
is seen for the P4 as well as for the N1 response, i.e., the greatest
clectrophysiologic cha;ngs in threshold, response asmplitude and
latency are seen in response to filtered clicks with a center frequency
similar to that of the center frequency of the noise stimulus. These
changes are observed in both the peripheral and central BSR waves.
The decrease in postexposure response amplitude and, consequently,
threshold sensitivity is thought to result from the disruption of the
mechanoelectrical coupling of the damaged hair cells to afferent 8th
nerve fibers. This disruption results in a loss of synchronous firing
of the nerve fibers with an accompanying decrease in whole-nerve AP
magnitude and, apparently, in response magnitudes from brain stem
The greatest decrease in threshold sensitivity and postexposure
magnitude was found in response to the 6 kHz FC, near the center fre-
quency of the noise stimulus whereas postexposure responses to the
1 kHz FC were not demonstrably different from preexposure levels.
The value of the FC's to reveal the frequency-specific nature of
noise-induced cochlear damage is also supported by the postexposure
latency measures. Figure 17 illustrates the increase in postexposure
N1 latency with increasing click intensity in response to the 1 kilz
FC whereas postexposure response latency to the 6 kHz FC showed little
change. This finding supports the interpretation that at high inten-
sities a 1 kilz FC stimulates nerve fibers toward the basal end of the
cochlea due to the wide traveling wave envelope (note the similarity
of latencies at high intensities in response to the 1 kHz and 6 kHz
FC in Fig. 11). When hair cells in the basal region are damaged by
high intensity narrow band noise, a 1 klHz FC stimulates healthy hair
cells more apically in the cochlea resulting in an increase in post-
exposure latency measures. This finding also confirms the belief
that the interpretation of responses to low frequency filtered clicks
presents problems, particularly at high intensities since the re-
sponses include activity from basal locations in the cochlea.
Although this study was not able to confirm a simple pattern of
extensive hair cell damage in the basal portion of the cochlea,
neither have previous studies. Eldredge et al. (1973) discovered that
the fractional loss of the whole-nerve AP in noise-exposed chinchillas
significantly exceeded the fractional loss of hair cells. Apparently
hair cell loss is not an accurate measure of cochlear damage. Bohne,
Eldredge and Mills (1973) discovered the following characteristics of
remaining hair cells in noise-exposed chinchillas: misshapen outer
hair cells; loss of mitochondria; increase in vesicles, vacuoles and
smooth endoplasmic reticulum in the efferent nerve fibers in the
affected region. It is entirely possible that such changes occurred
in the hair cells of the guinea pigs in the present study but were
not observed under light microscopy.
The findings of this study support the interpretation that the
newborn guinea pig suffers greater noise-induced damage to the audi-
tory system, as measured by changes in the BSR, than the adult animals.
The susceptibility of the newborn to noise-induced trauma is consis-
tent with findings of previous investigations which compared hair
cell loss between newborn and adult animals (Falk et al., 1974;
Dodson et al., 1978; Bock and Sanders, 1977) It has been theorized
that a critical period exists in the developing) ;aiditory system which
makes the system iunsunaIlly susceptible to the effects of noise (Bock
and Saunders, 1977). In the guinea pig it appears that the first
few days after birth are within this critical period. Although the
guinea pig auditory system is relatively mature at birth there is
considerable evidence, as discussed previously, that the system is
still developing. An exposure to a moderately high level of noise
for a sustained period of time is sufficient to cause more damage
to the newborn than would ordinarily be experienced by an adult
guinea pig. The cause of increased susceptibility in infants is
now known. This increased susceptibility, however, has serious
implications for newborn humans placed in incubators for extended
periods of time. The noise levels in incubators vary greatly but
can reach levels as high as 75-80 dB SPL. The source of the noise
is usually the ventilation fan and the noise level is often intensi-
fied by the resonance effects of the closed chamber. Although these
levels are not considered noise-hazardous by present damage-risk
criteria, it must be remembered that these criteria were formulated
for an adult population. The noise levels found in incubators may,
in fact, present a potential hazard for the susceptible newborn.
Another important consideration involves the finding that the effects
of noise-induced trauma is reflected in the activity of higher brain
stem structures. This observation also presents serious implications
for the infant as the central auditory system provides integrative
functions that are important for signal recognition and language
This investigation, a;s well ;is others deal ing with the problem
of susceptibility, h;is presented evidence which indicates that the
nI(wlor'ni ;nI itolry systIem is more suscc ptibl Ie than the adilt': ; to
noise-induced damage. Additional investigation needs to be conducted
to determine a set of damage-risk criteria for the human infant.
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llHarvey Bruce Abrams was born on November 25, 19)18, in Brooklyn,
N.Y. lie was graduated from Sheepshead Bay High School in June,
1966. In June, 1970, aided by a U.S. Office of Education Fellow-
ship, he received the degree of Bachelor of Arts with a major in
speech pathology and audiology from the George Washington University.
Mr. Abrams received the degree of Master of Arts with a major of
audiology in August, 1971, from the University of Florida. Aid
afforded by a Social Rehabilitative Services traineeship enabled
him to complete this aspect of his education. After serving four
years as an audiologist in the U.S. Army, Mr. Abrams returned to
the University of Florida in January, 1976, to pursue work toward
the degree of Doctor of Philosophy with a major in speech, aided
by a Veterans Administration Traineeship.
Mr. Abrams is an audiologist with the Veterans Administration
Medical Center at Bay Pines, Florida. He is a member of the Ameri-
can Speech-Language and Hearing Association, the Acoustical Society
of America and the Military Audiology and Speech Pathology Society.
He is married to the former Catherine L. Breder of Washington,
D.C., and is the father of three children -- Lydia, Jesse and Emily.
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.
Donald C. Teas
Professor of 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, s a dissertation for the
degree of Doctor of Philosophy.
I 1 am E. Browh 1
Asst. Professor Neuroscience
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.
William II. Cutler
Adjunct Asst. Professor, Dept.
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.
Dean, Graduate School