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Title: Effects of intense acoustic noise on cochlear function in infant and adult guinea pigs /
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Permanent Link: http://ufdc.ufl.edu/UF00102825/00001
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Title: Effects of intense acoustic noise on cochlear function in infant and adult guinea pigs /
Physical Description: Book
Language: English
Creator: Abrams, Harvey Bruce, 1948-
Copyright Date: 1980
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Bibliographic ID: UF00102825
Volume ID: VID00001
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Full Text








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

this endeavor.

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.


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




March 1980

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

the cochlea.

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.



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.

Surgical Procedure

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


Signal Generation

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


c H

) a r) *1

r u &o 0

a) (a \I
($- 4 c >C

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cd ua

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U -H U-i
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t -I 0

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0 0 0 0 0 0
m (0 In V



'1* 0 Mi
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af) -1)
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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).


Response Waveform

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.

I 0mec




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

respect ively.

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
00 0

Su 0 0 F-

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.-4 -4 a -t
cd 0 4.

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cO -H !-i :
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c 0





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(idS 8P) G1OHS3BdH

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
>--~I kHz

50 70 90" 30 50

0 30

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.


3 -
W 6


V .08-



.02- 6 kHz
A I kHz

0 30 SO 70 90 30 SO




4-) Q.)

P 4-

p r4 q

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rr rr

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1N3131 -303


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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.

I kHz



I kHz

6 kHz

6 kHz


X-- N| 1

3 .-----------------------------

30 0 70 90 30 50

70 90


\/ '/

*O*0 0
rO bO3
o C) r-i V) i

c 0 uce U

S> o N-
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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


k -I

LI) 0 c-'p
0 p~ +

P 0) -
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0 1) 0 a) :

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Standard deviation


0.5 kHz


















for averaged

N1 cxper.













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-

exposed newborn.

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.




> .8-




Z .-
W .08-
LU 06-

1/ 4

50 70 90 30

50 70 90



6 kHz

I kHz

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

70 90

(dB SPL)




. I







Standard ldeviat ion for postexposulre response :inpl i tnlde (pV).

1 kliz (N=5)
-- -N F--

+.07 +.07

d SPI,
















Newb orn








Newborn 1.31 1.15


















Adul t














6 kliz (N=5)
N1 1'4

+.18 +.06

.34 .23

.32 .45

.5 .63


.54 .5

.2 .12

.5 .68

.52 .05

.39 .69

.37 .1

.19 .66

.58 .25

.37 .58

.82 .16

.57 .4

.71 .27















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

H V) ;
V) 0

r -4r-4 C1 V)
a)- 0 x<
4-) i)W
4J t.O
*Hi 42 V ) r-
,-q r- 0 cd
.-4 S .

Li H 4-J GI

00c P1

o 0
C1VQ) 4

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, 42 1. 42 CH L

*-O S-l -4 U) 0
U') z ~ -4 ai) 0-
V L i r4 '-4 t
Li) *HH t
4-J 42 L. -4 -4

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*H0~~ 42

'I, L) 0 cz r- r
in 'o -4 1 00
M~ 4- WJ. P, U
Q u 0
o- CLOr ) Q

LHC(L) 0

'd 0 N c- 'H

(4-4 -4 >4-J t
U- $-4 Ct

4J Q) 0 ',
Li) 4> 4- L) C' 3
0o C : -

u. -4 r- tio
(1) 0 U
-,q c d~

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Cd 41 0 4 0 x

4- -4 (U (1
>p.,!- - P4-4 X
-4 CISH 4

0 0
U41 -l 4-J -

R( ;r L4 4-40
V) Lf)~

42 -0. F- 4
od 420 x X-4

0-al *0 "
LrQ) 0yJW;c
'-4 O Li) OH 4
1. '-4 Z e 1.i :-
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0o o
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o o
o (MI "r


31n-i s8v

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.

24 54- kHz 6 kHz

22 5.2-

20 50-

IB 48-

1.6 46-

14 44-

12 4.2

1.0 40-
>- I //__,_ // .

z C
w N P4

J 22 52- 1 kHz 6 kHz

20 5.0-

1.8 48-

1.6 46-

14 44- *---* 4

1.0 40-

30 50 7 90 30 5 70 90



Standard deviation for averaged postexposure response latency (mscc).

1 kliz (N=5)
































N6 k1 (N'-5
N1 1











































.192 .499


































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




0 0

*4-J 0r
r- C)


4-) 0

4-J C, ~
4 t

U ,-

~4-4 4~

0 --

O ~
rZ 'ci

*H 0


0k '4 4
LC -~ 0

qv. u3 0
*-4 0-
.0 0 ~
'A *H
>,U 0
0 r
0 '-

ri e ... r


u'- x-s
0~ 0

0 *H.-
0-.-.In -
O.< UT-

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0 0~



c~ CI rf-

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0X 0


I IN31V-1

(33 SIl) ,3 N31V9




t 0O I I

dX3J3td --dX:ISOd


.0 (





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

<-I II

C 0

C 0 4-)

S3 0


0 0
C 10
4- U) t4)

C *0O
*H C ra

C 0 C

*H 4 C) yh

*H 0 4-4

0 0
H r- "U

O u 0
ro ;-1 c0 0

0 44 U0

) C 3 HI c

0 0 0

V1< 4 -J
) *- C C O
4- U U
C) 0C C

0 o
(1) u p -i 0
4 4)
004- C C -H 4 C)

tr SC 0U

0 C- PO 0
o ,-1 o

0 3
4 -1 H &

oCL, Cl.4

4! -H O U

4rJ 2-4
* CC'.- 0


o a o
(_3s ) IN--Nd








- 4


(03SV) IN-i-d

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.





4-J tV)

,f-- x.


w *H




0 )o

'H p
-4 4-
(1) 0r

bAD u

4 -a


, 1


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>j ^h% ^Ai) 1"


V f


. A

~L-- ,i~J


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0 V


0 Q

U '-4

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o -

4-c, -



"-4 .

FPr~ip~ ,-IIF~F19~1-


~L~c~~ .I

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 ,

SC) C)

4U 4-
dr X

,- e ,

0 I

U 0-

0 0 .-4 0 )
0 *H0

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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
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i ct z o

< > '0 3 -
.,-1 0
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P &, 3 0

*H C )

V) 4J U U F-4

o -00.0
H *0 oZ

-4 CZ (1)

*2 0 F20

0 3 k 0
*0 0i 0 Fi 0



o 0


Standard deviation for averaged number of missing hair cells.

Newbonmbe oft Adlt, hair

Newborn, exp.

+ 1.9




Newborn, cont.

+ 3.7




Adult, exp.

+ 22.8




Adult, cont.

+ 2.5







OliC 2


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

and 11).

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.
of Speech

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

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