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thesis entitled
Auditory Brain—stem Responses and Delayed

auditory Feedback in Dyslexic Readers

presented by

Kalpana M. Joshi

has been accepted towards fulfillment
of the requirements for

M.A degree in “Audiology

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mane-9.1

 

 

 

AUDITORY BRAIN-STEM RESPONSES AND DELAYED
AUDITORY FEEDBACK IN DYSLEXIC READERS

BY

Kalpana M. Joshi

A THESIS

Submitted to
Michigan State University
in partial fulfillment of the requirements
for the degree of

MASTER OF ARTS

Department of Audiology and Speech Sciences

May, 1994

 

 

ABSTRACT

AUDITORY BRAIN-STEM RESPONSES AND DELAYED AUDITORY
FEEDBACK IN DYSLEXIC READERS

BY

Kalpana M. Joshi

A Reading disorder is a symptom that is often categorized
under the general heading of Learning Disability. Often
the etiology remains unknown until autopsy or minimum brain
dysfunction is suspected. Children with dyslexia often do
not show consistent deficits on neurological examination
(Golden, 1982). There are very few data using techniques
which assess brain stem functionally, and that which exists
are not conclusive. The aim of this research project was
to investigate central auditory processing mechanisms
through Auditory Brain-stem Responses (ABR), and the
behavioral effects of Delayed Auditory Feedback (DAF) in

children diagnosed as having a reading disorder (Dyslexia).

Investigation of reading as a central process under DAF
revealed that control group was affected most at delay of
200 ms, whereas the experimental group continued to be
affected beyond 200 ms. Statistically significant
differences emerged between the two groups. The results
indicate that the dyslexic readers need more processing

time.

 

 

iii

DEDICATION

In memory of Chief Justice Thurgood Marshall
who made it possible for students to fight
educational inequalities and injustices.

This study is dedicated to all the dyslexic
children around the world who encounter
reading difficulties every day, and to their
dedicated teachers who make learning possible.

 

 

 

iv

ACKNOWLEDGEMENT

Special thanks to Dr. Ernest J. Moore, Professor,
Department of Audiology & Speech Sciences,
Michigan State University, for his guidance and
support during the research process. I extend
thanks also to Dr. Leo Deal, Professor Emeritus,
Department of Audiology & Speech Sciences, and
Dr. Ida Stockman, Professor, Michigan State
University, for their unfailing guidance as
Committee Members.

 

V

TABLE OF CONTENTS

Title Page ............................... i
Abstract ............................... ii
Dedication ............................... iii
Acknowledgements ............................... iv
Table of Contents ............................... v
List of Figures ............................... vii
List of Tables ............................... viii
Chapter I. INTRODUCTION ......................... 1
Dyslexia and Temporal Integration ... 3
Discussion of the Problem ............ 5
Theoretical Framework ............... 6
Rationale ........................... 7
Chapter II. REVIEW OF LITERATURE ................ 9
Introduction ........................ 9
Sub-types of Dyslexia ................ 9
Dyslexia and Learning Disorders ...... 12
Reading Processes and the Brain ..... 14
Normal Brain Asymmetries ............ 18
Dyslexia and Brain Morphology ....... 20
Laterality Studies .................. 23
Auditory Brain Stem Responses
and Dyslexia ..................... 30
Delayed Auditory Feedback ............ 32
Chapter III. METHODOLOGY ........................ 39
Description of Subjects .............. 39
Selection Criteria ................... 39
Description of Screening Tests ....... 40
Audiometric Procedures ............... 4O
Tympanometry ......................... 41
Audiometric Threshold Testing ........ 42
Speech Reception Threshold Testing ... 42
Description of Test Procedures ........ 43
Auditory Brain-stem Responses ........ 43
Delayed Auditory Feedback ............ 47
Reliability and Validity ............. 50
Statistical Analysis .................. 51
Expected Outcomes ................... 52

Clinical Implications ................ 52

Chapter IV.
Chapter V.

Chapter VI.
REFERENCES

APPENDIX A

vi

RESULTS ..............................
DISCUSSION ...........................
Effects of Delayed Auditory
Feedback Upon Reading Rates ...........
Effects of Delayed Auditory
Feedback Upon Repetitions .............
Effects of Delayed Auditory
Feedback Upon Prolongations ........
Comparison With other DAF Studies .....
Summary of Combined Effects ..........

SUMMARY AND CONCLUSIONS ...............

Samples of Reading Materials from
Bader Reading & Language Inventory ....

53
129

130
132
134
136
139
142

147

162

 

Figure III—1.
Figure III-2.
Figure IV-l.
Figure IV-2.
Figure IV~3.
Figure IV—4.
Figure IV—5.
Figure IV—6.
Figure IV—7.
Figure IV-8.
Figure IV—9.
Figure IV-lO.
Figure IV—ll.
Figure IV—12.

Figure IV—13.

 

LIST OF FIGURES

Block diagram of ABR instrumentation .. 44

Block diagram of DAF instrumentation .. 48

Samples of ABR waveforms .............. 55
Absolute latencies for ABR wave I ..... 57
Absolute latencies for ABR wave V ..... 62

Absolute latencies for ABR wave VI ... 66
Absolute latencies for ABR wave VII ... 70
Inter—peak latencies for waves I—V ... 75
Inter-peak latencies for waves 1—VI ... 79
Inter-peak latencies for waves I-VII .. 83
Inter—peak latencies for waves V—VI .. 88
Inter—peak latencies for waves V—VII .. 93
Reading rates under DAF .............. 97
Repetitions under DAF .. ........ .... 113

Prolongations under DAF ... ........... 119

 

Table IV—2A.

Table IV—ZB.

Table IV-3A.

Table IV-3B.

Table IV-4A.

Table IV—4B.

Table IV-SA.

Table IV-5B.

Table IV-6A.

Table IV—6B.

Table IV-7A.

Table IV-7B.

Table IV-8A.

Table IV-BB.

LIST OF TABLES

Absolute latencies for Wave I:

(Control Group) .................. 59

Absolute latencies for Wave I:

(Experimental Group) ............... 59

Absolute latencies for Wave V:

(Control Group) ................... 64

Absolute latencies for Wave V:

(Experimental Group) ............... 64

Absolute latencies for Wave VI:

(Control Group) ................... 68

Absolute latencies for Wave VI:

(Experimental Group) ............... 68

Absolute latencies for Wave VII:

Control Group) ................... 72 /
Absolute latencies for Wave VII: /
(Experimental Group) ............... 72 '

Inter—peak latencies for waves I-V:

(Control Group) .................. .. 77
Inter-peak latencies for Waves I-V:
(Experimental Group) ............... 77
Inter—peak latencies for waves I—VI:
(Control Group) ....... . ............ 81
Inter—peak latencies for Waves I-VI:
(Experimental Group) ............. 81
Inter-peak latencies for Waves I-VII:
(Control Group) ................. 85
Inter—peak latencies for Waves I—VII:
(Experimental Group) ............. 85

 

Table IV—9A.

Table IV—9B.

Table V—lOA.

Table IV-lOB.

Table IV-llA.

Table IV—11B.

Table IV—11C.

Table IV—llD.

Table IV-llE.

Table IV—llF.

Table IV-llG.

Table IV-llH.

Table IV—llI.

Table IV-llJ.

Table IV—12A.

Table IV—12B.

Table IV-13A.

Table IV—13B.

 

ix
Inter—peak latencies for Waves V—VI:
(Control Group) ...................... 90

Inter—peak latencies for Waves V-VI:
(Experimental Group) ................. 90

Inter—peak latencies for Waves V—VII:
(Control Group) ........... . .......... 95

Inter-peak latencies for Waves V—VII:
(Experimental Group) ................ 95

Reading rates under DAF:
(Control Group) ....... . .......... .. 99

Reading rates under DAF:
(Experimental Group) .............. 99

Range and mean reading rates
under DAF (Control Group) .......... 101

Range and mean reading rates
under DAF (Experimental Group) ..... 101

Difference from normal reading
rates ............. ... .............. 109

Analysis of difference from normal
reading rates (Control Group) ...... 109

Analysis of differences from normal
reading rates (Experimental Group) ... 109

Inter-delay differnces in reading
rates under DAF ...................... 110

Analysis of differences in reading
rates under DAF (Control Group) ...... 110

Analysis of differences in reading
rates under DAF (Experimental Group)...110

Episodes of repetitions under the
effects of DAF (Control Group) ....... 115

Episodes of repetitions under the
effects of DAF (EXperimental Group)... 115

Episodes of prolongations under the
effects of DAF (Control Group) ...... 121

Episodes of prolongations under the
effects of DAF (EXperimental Group) .. 121

 

—I—-————f“

Chapter I

INTRODUCTION

Introduction: Dyslexia is defined as a disorder manifested
by difficulty in learning to read despite conventional

instruction, adequate intelligence, and sociocultural

opportunity. It is dependent upon fundamental cognitive

disabilities which are frequently of constitutional origin

(American Medical Association, 1989).

Many children experience difficulties not asssociated with
brain dysfunction or other neurological, motor or

physiological problems. Most of them do not have peripheral

auditory or visual acuity problems. These children often

exhibit above average intelligence, normal language
development and oral productions, yet their reading deficit

defines them as "learning disordered" and they are referred

to special education classes. Parents and teachers often

get confused and alarmed at the reading disorder exhibited

and the prognosis for future academic achievement (Doris,
1986).

DYslexia is more common in males than in females (ratio of
3:1). may be related to socioeconomic status and family

Size, and it may have a genetic origin. It occurs two to

 

 

 

2
three times more in urban areas than in rural populations
(Snowling, 1987). It is estimated that about 3—6% of all
school-aged children suffer from dyslexia. other problems
co—occuring with dyslexia include poor visual spatial
skills, co—ordination, temporal orientation, spelling, color
identification, linear tracking, mixed cerebral dominance
and failure to develop "leading eye.“ Many dyslexic
readers, however, do not exhibit all of these problems

(American Medical Association, 1989).

Dyslexia may be congenital or acquired (Geshwind, 1962).
Kussmaul (1877) coded the terms "word deafness“ and "word
blindness“ for inability to understand spoken and written
words respectively. Dejerine (1892) stated that the lesions
of angular gyrus produced word blindness (Pirozzolo, 1979).
morgan (1896-1897) described the first documented case of
congenital word blindness, and Kussmaul (1881) described a
case of acquired word blindness (Orton, 1925). Later,
Henshelwood (1917) published his seminal paper on “word-
blindness". His results, based upon post—mortem
examinations, attributed this condition to lesions in the

angular gyrus due to trauma, disease or genetic factors.

Orton (1928) observed frequent reversals in dyslexic
children and coined the term "sterephosymbolia'I or twisted
symbols. Damage or defective development of the angular

gyrus was implicated in alexia (word blindness) and also

 

 

 

 

3
the failure of the dominant hemisphere in establishing
language dominance. He recommended teaching reading
disabled children rules of directionality and grapheme

to phoneme correspondence through phonics.

Dyslexia and Temporal Integration: Oral reading involves

both visual and auditory temporal integration (Orton, 1929).
Both modalities function in units of 250 ms. It requires
approximately 200-250 ms for visual integration (Lovegrove
et al., 1986). The human auditory system requires also 200
to 250 ms for sound integration (Durrant and Lovirnic, 1984).
Tones of higher intensity require less duration compared to
sounds of lower intensity. It seems as if the sounds were
analyzed in terms of frequency and intensity components and
measured in terms of sound energy. Beyond 200 ms the
relationship seems to fall apart (Green, 1971). The
doubling of duration leads to a 3 dB decrease in the
threshold of hearing (Sheeley and Bilger, 1964). The
auditory system in effect integrates (summates) the power of
the stimulus over time. The theory of temporal integration
takes into account the effect of stimulus duration on the
threshold for hearing. Loudness increases with duration of

the stimulus up to about 200 ms (Zwislocki, 1960).

The reason some sounds are attended to better than others

is due to their temporal duration and the energy present.

 

 

 

 

 

 

l:

 

4
For tones of shorter duration, more energy is required for
audibility. The human ear assesses the amount of energy in
every sound within 250 ms (Durrant and Lovirnic, 1984).
Thus, in the human auditory system, time and energy are
innately related. By reducing duration by one tenth, the
threshold for audibility is increased by 8 to 10 decibels.
Conversely, by increasing duration ten fold, less signal
intensity is required for signal detection (Miskolczy—Fodor,
1958). There exists controversy among various investigators

about the exact site of this power integration. Gerken et

 

al. (1991) stated that the integration takes place at the

level of the inferior colliculus or even at higher centers.

Snowling (1980) conducted tests of audio-visual

 

integration on 18 dyslexic (14 boys, 4 girls; i=12.1
years) and 36 normal children (15 boys and 21 girls: ié9.5
years). The results of the study indicated that dyslexic

readers had problems with visual-auditory integration.

Shapiro et al. (1990) investigated temporal processing in

15 dyslexic and normal children (5 males and 10 females;
.ié12.2 years). Short words (3—4 letters) and long words
(7-9 letters) were presented at durations of 100 and 300 ms.
Dyslexic readers showed slight decreases in correct
identification as word length was increased. The mean
number of correct words, however, was decreased at 300 ms

for short words, whereas the normal group showed a slight

 

 

5
increase in performance at 300 ms. For longer words the
normal readers showed increases in number of correct words,
whereas the dyslexic readers failed to show much difference.
Based upon these results the investigators speculated about
the use of simultaneous processing and reduced sequential
processing due to bilateral representation of these

different strategies in the two hemispheres.

A study conducted on reading impaired children (7-12 years
of age) on dichotic listening tasks involving stop

consonants and vowels with differing onset times of 0, 30,

 

90 or 150 ms showed that the impaired readers required more

processing time (Dickstein and Tallal, 1987). Tallal et al.

 

(1980) found that reading impaired children showed poor
auditory discrimination between speech sounds when the

temporal delay between them was less than 500 ms.

Discussion of the Problem: Brain morphology studies have
indicated differences between normal and dyslexic readers
(Galaburda, 1993). As can be seen from these studies,

however, generalizations cannot be made from a few studies.

 

A systematic study of peripheral auditory mechanisms
utilizing standard audiometric procedures could help
identify differences between normal and impaired readers in
terms sound conduction mechanisms. Electrophysiologic
techniques such as ABR could further identify the locale in

the delay Of sound transmission from first to third order

 

 

6
neurons. Analysis of waves VI and VII could test sound
transmission to the thalamus and the primary auditory cortex
(Stockard and Rossiter, 1977). Oral reading involves both
visual and auditory integrative processes (Orton, 1929).
The words are matched for their phonological and linguistic
familiarity and productions are monitored via auditory
feedback. A failure to do so results in dyslexia (Orton,

1929).

Feedback mechanisms operate in terms of units of time
segments (Whitaker, 1971). Varying temporal aspects of
delayed auditory feedback, during oral reading would

facilitate the observations of visual, phonological

 

decoding, and articulator segments of the reading process.

 

A study incorporating subjects without visual or auditory
deficits reading under the various temporal aspects of
delayed auditory feedback could reveal differences between

normal and dyslexic readers.

Theoretical Framework: It is proposed that a study involving

normal and reading impaired subjects should focus on

 

answering the following questions :

1) Are auditory brain—stem responses of children manifesting
dyslexia different from normal reading children ?

2) What are the effects Of Delayed Auditory Feedback on
(a) reading rates, (b) repetitions, and (c) prolongations

between the dyslexic and non-dyslexic readers ?

 

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7
The main purposes of the investigation are two—fold:
(1) If the peripheral auditory system is intact, could
the brain-stem be involved in the delayed neuronal
transmission to the cortical centers of dyslexic
children ?
Auditory brain—stem response studies are therefore included
as part of this research.
(2) If the auditory feedback loop is involved, then
by changing the temporal parameters of auditory
feedback, are there changes in the reading rates, number

of repetitions and prolongations in dyslexic children ?

Delayed auditory feedback studies are incorporated in this
research paradigm. It is therefore proposed that there are
critical periods of time in which auditory signals are
processed by dyslexic children. Information derived from a
combination of ABR and DAF are included in order to address

this hypothesis.

Rationale: The peripheral auditory system will be
investigated by use of standard audiometric tests. These
include otoscopy, pure tone and speech audiometry. The
integrity of the tympanic membrane, and the middle ear
(Stapedial muscle and ossicles) will be assessed through
tympanometry and impedance audiometry. These tests will
ensure the integrity of the mechanical transmission within

the auditory system.

 

 

 

 

 

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Only children without congenital anomalies involving outer
or middle ear will be included in the study. Peripheral
and central auditory system will be assessed through
analysis of ABR latencies for waves I through VII.

The absolute and interpeak latencies of waves I and II
would give data regarding the efficiency of transmission
of the first order afferents. The integrity of second
order afferents, the cochlear nucleus and the superior
olivary complex, will be indicated by the presence of
waves III and IV and their absolute and interpeak
latencies. The integrity of higher brain-stem neurons
will be established by latencies of waves V, VI and VII

(Stockard and Rossiter, 1977).

Investigation of oral reading under the effects of delayed
auditory feedback at different temporal delays would
delineate the differences between the experimental and the
control groups. It may also highlight the temporal delays
of feedback at which both groups may exhibit reduced

reading rates, increased number of repetitions and

prolongations.

 

 

 

 

 

 

 

 

 

 

 

 

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Chapter 11
REVIEW OF LITERATURE

Introduction: In this chapter, I will review the areas of
relevance to the study of dyslexia. Even though the main
purpose of the present study is to investigate auditory
brain-stem responses in normal and dyslexic readers and the
analysis of oral reading under various temporal parameters
of delayed auditory feedback, this chapter would not be
complete without including studies in normal brain
asymmetries, morphologic studies on dyslexic brains and
studies conducted on laterality. Oral reading involves
visual integration, language processing, oral productions
and feedback mechanisms, therefore, an extensive study of

literature is included in this section.

§Ebz§¥pe§ of Dyslexia: Attempts to classify dyslexia into
various types have been made by different investigators.
These were based upon whether these readers used the
grapheme to phoneme conversion efficiently, read by whole

word gestalts or the dominant hemispheric participation in

reading.

Boder (1973) outlined three types of developmental dyslexics.

These were — dysphonetic and dyseidetic, and alexic.

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10
Dysphonetic dyslexics read by "whole word gestalts", but
display problems with the grapheme to phoneme conversions,
and "sound/symbol integration." Dyseidetic dyslexics use
grapheme to phoneme conversions in reading and have
difficulty forming "whole word visual gestalts." The third

group, the alexics, display mixed problems.

Flynn and Deering (1989) using neurophysiologic techniques
(EEG) were able to identify dyseidetic dyslexics

(Boder, 1973). There was an increase in theta activity over
the left temporal-parietal area, corresponding to the
angular gyrus, in frustration reading and spelling
recognition tasks. These investigators emphasize the
importance of quantitative neurophysiologic techniques such

as EEG in diagnosis of disorders of reading.

Marshall and Newcombe (1973) categorized dyslexia into
surface and deep dyslexia. The symptoms Of surface dyslexia
are similar to dyseidetic dyslexia and deep dyslexia is
similar to dysphonetic dyslexia described by Boder (1973).
They include impaired grapheme to phoneme conversion,
problems with word endings, low imageablity and function
words. These readers are often visual readers and work with

visual gestalts (Boder, 1973). Dysphonetic dyslexia was

estimated to be 4-5 times more prevalant than the dyseidetic

dyslexia (Zenhausern, 1987).

 

 

 

 

 

 

 

 

 

 

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11
A case of developmental deep dyslexia was described by
Johnston (1983). The subject, an eighteen year old female
had awareness of initial sounds of words but was confused
about word endings, low imageability words, non-words,
rhyming and function words and semantics. The general
difficulties encountered were correlating graphemes to
phonemes. Accordingly, the problems encountered by the
subject could have been due to a “transmission" difficulty
between word reception and its motor production. The
possibility of brain dysfunction was suspected. It could
not be ascertained, however, if the subject suffered from
pure dyslexia due to brain lesions. This seems to be a
general problem with most studies on dyslexic subjects as
poor reading performance cannot with certainity be

attributed to specific brain disorders.

Bakker (1981) classified dyslexics into two types. Type P
dyslexic readers attended to the perceptual aspects of
written words to the detriment of the auditory-linguistic
components. Type L dyslexic readers concentrated on the
auditory-linguistic component of written words to the
detriment of visuo—spatial information. This classification
was based upon dichotic listening tests which revealed the
better ear, the hemisphere opposite to it was the assumed to
be the dominant cerebral hemisphere for language and speech.

The above investigator hypothesized that the P-type

 

 

 

 

Ca

12

he

 

 

12

dyslexics had right cerebral control of form and letter
perception and language and speech. The reading tendencies
of these dyslexics are marked by slowness and
fragramentations, prolongations and repetitions. The L—type
dyslexics on the other hand, display left hemisphere control
for language and speech, and ambivalent control for form and
letter perception. They are fast readers compared to P—type

dyslexics and exhibit numerous omissions, substitutions.

Caution was advised by Forness (1982) in diagnosing and
labelling dyslexic children. He stressed the fact that
tools used to assess reading disorders lack “sound empirical

basis“ and that "conventional notions of dyslexia and its

 

diagnosis are in need Of some revision.“

Reversals according to Forness could be due to lack of
directionality in a child or due to inadequate instruction
regarding word or letter formations, and lack of attention
instead of being a causative factor, could be the side

effect of dyslexia.

Dyslexia and Learning Disorders: Dyslexia often gets

categorized under the general heading of learning disability
or attention disorder. These misnomers get attached even
though some children with attention deficits may not exhibit

reading disorders (Conners, 1990).

 

 

13
The Federal Government's definition of "Learning
Disabilities“ is as follows : “A disorder in one or more of
the basic psychological processes involved in understanding
or in using language, spoken or written, which may manifest
itself in an imperfect ability to listen, think, speak,
read, write, spell or do mathematical calculations. The
term includes such conditions as perceptual handicaps, brain
injury, minimlal brain dysfunction, dyslexia, and
developmental aphasia. The term does not include children
who have learning problems which are primarily the result of
visual, hearing or motor handicaps: of mental retardation:
or of environmental, cultural or economic disadvantage."

[P.L. 94—142, 121a, 5 (9)].

 

Conners (1990) divided children with academic problems into
three categories. These were — hyperkinetic, learning
disabled, and mixed types. All three groups performed well
in mathematics and exhibited short attention span,
distractibility, impulsiveness, hyper or hypo—active
behavior, clumsiness, and had other academic problems
related to reading, writing. The learning disabled and
mixed group exhibited greater tendency towards dyslexia,
dysorthographia (spelling disability), and dysgraphia

(writing disability).

Since 1890’s reports of children had surfaced who failed to

read but had good mathematical skills. The suspected

 

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14

problem area was the angular gyrus in the left cereberal
hemisphere (Ceci, 1986). Children exhibiting various
academic problems were categorized under the general

heading of “learning disabilities" since the 1970's and
1980's (Goldberg et al., 1983). Thus learning disability
has become a global term of which dyslexia may be a part.
Both trace their etiologies to the anamolies of brain, which
in some cases remain suspect throughtout the individual's

life, and may or may not be revealed upon autopsy.

Reading Processes and the Brain: Reading consists of five
steps which include visual encoding, word recognition,
sentence level and text-level comprehension and
metacognition (Aaron, 1989). Cortical process involved in
reading were outlined by Geshwind (1972). These consist of
transmission of visual information from visual cortex to the
angular gyrus, phonological and linguistic processing in
Wernicke's area and articulatory control in Broca’s area

(Geshwind, 1972).

Visual encoding stage involves visual integration. Reading
consists of a series of saccades (20-50 ms) and fixations
(200—250 ms) regulated by higher congnitive centers, with
one word processed during each fixation (Lovegrove et al.
1986). Words are processed simultaneously and in parallel.

Beginnings and endings are processed first and then the

 

 

 

 

 

 

15
middle parts. Suffixed words require longer processing
time. After visual integration, the word is retained in a
temporary buffer called the "icon" for approximately 250 ms
while it is being correlated to its pronounciation and word
meaning, after which it becomes part of short term memory

with a duration of five to six seconds (Aaron, 1989).

Word recognition involves use of auditory memory or “working
memory." This memory is important in converting graphemes
into phonemes by utilizing phenomenon of "chunking" or
syllabication (Aaron, 1989). It has a capacity of about
seven to nine digits and helps in word recognition either
through direct access to semantic lexicon or through a
phonological route (Baddeley, 1978). Models of lexicons
have been proposed by researchers to understand exact
processes involved in meaning retrieval. Feature models of
lexicon are based upon the hypothesis that words are
represented by their phonological, orthographic and semantic

features.

A morphemic code of logogen is activated during word
detection when several features match (Aaron, 1989). Search
models of lexicon take into account the morpheme markers
which could become activated by the perception of the first
letter of the morpheme. This model assumes that words are
stored without prefixes and suffixes. Omissions of suffixes
by dyslexic readers is attributed to a failure at the

lexical level.

 

 

 

 

 

16

The subset model of lexicon is based upon the assumption
that a word—specific phonological lexicon exists which is
referred during the word retrieval stage which could take
place by direct word recognition or addressed phonology or
through phonological subset or assembled phonology (Aaron,
1989). In the comprehension stage, sentences are broken
down into meaningful clauses which are stored in working
memory and later converted into propositions. Important
facts are organized into "schema" while unimportant details
are obliterated (Kintsch, 1977). Metacognition involves
compensatory strategies to ensure effective comprehension.
Cognitive processes are understood and corrective procedures
are undertaken to ensure correct understanding of facts

(Aaron, 1989).

Reading process refers to "decoding" or conversion of
graphemes into phonemes. According to Snowling (1980),
there are presumably two routes to word meanings. The
direct semantic route involves visual perception of word as
gestalt which leads to direct semantic access and the
phonemic route utilizes grapheme to phoneme conversion for
semantic access. The former route improves with age and
usage according to Snowling (1980). Kimura (1993) stated
that experienced readers utilize direct semantic route
whereas beginning readers use the grapheme to phoneme

conversion for semantic access.

 

 

 

 

 

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Whitaker (1971) delineated the cortical areas involved in
language processing and correlated them with Brodmann's
classification of brain areas. Reading involves the primary
visual input which is transmitted to the primary and
secondary visual cortex (Brodmann’s areas 18, 19) and
relayed to the angular gyrus (Brodmann’s area 39), which is
described by Pirozollo (1979) as the "center for visual
images for letters." Wernicke’s area (Brodmann’s area 42),
auditory association area (Brodmann's area 22),
Supramarginal gyrus (Brodmann’s areas 40, 22) and angular
gyrus (Brodmann's area 39) are important components in

semantic/syntactic analysis (Whitaker, 1971).

The information is transmitted to Broca’s area (Brodmann's
area 44) for articulatory control. Thalamic contributions
were established by Whitaker (1988) for motor productions.
The motor and temporal cortex connect with the putamen,
which in turn sends fibers to the globus pallidus. The
information is transmitted to the ventral lateral thalamus

and the motor areas.

Whitaker (1988) emphasized the importance of the thalamus in
language functions. The motor areas (Broca's area) and the
temporoparietal decoder areas are connected via arcuate
fasciculus. Both send fibers to the caudate nucleus which
has connections with globus pallidus and ventral anterior

thalamus. The latter also receives connections from the

 

 

 

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reticular formation. The temporoparietal area connects to
the pulvinar and through the internal medullary lamina of
thalamus to the ventral anterior nucleus. According to
Whitaker (1971), layer VI of the neocortex has spindle
shaped cells with short and long association fibers and it
is this layer which has excess inter-connections with the
thalamus. Layer V of the neocortex is composed of large
pyramidal cells with longer axons which project into the
white matter. Layer IV is composed of star pyramids, which
inter-connect with various layers of the neocortex. In
layer III large pyramidal cells inter-connect with various
specific cortical areas. Small granular and pyramidal cells
send projections to layer I which is composed of apical

dendrites.

Penfield and Roberts (1959) delineated areas involved in
articulatory errors of hesitations and slurring which follow
the configuration of the main language areas delineated by
Whitaker (1971). The exact cortical sites for repetition of
syllables or words is unknown (Kimura, 1993). Whitaker
(1971) has highlighted the importance of feedback mechanisms

in language productions.

Normal Brain Asymmetries: Geshwind and Levitsky (1968)
conducted autopsies on one hundred normal brains and
discovered the planum temporale to be larger in the left

hemisphere in 65 % of the population studied. The right

 

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19
planum temporale was larger in 11%, with 24 % with a
symmetrical planum. Le May and Culebras (1972) studied
morphological differences between hemispheres by carotid
arteriography. The middle cerebral artery supplies the
lateral surfaces of the hemispheres. They found the left
parietal operculum to be highly developed in 38 out of 44
patients studied. Narrower arches of the left middle
cerebral arteries were Observed in the left hemisphere than
the right. Fifteen left—handed patients had symmetrical

arches in both hemispheres.

Witelson and Pallie (1973) studied 14 neonatal and 16 adult
brains and found the left planum temporale to be larger in
86 % of neonatal brains and in 81 % of adult brains. This
asymmetry is directly correlated to language acquisition and

hand dominance and is probably of biological significance.

LeMay (1976) using the CT scan technique studied one hundred
human brains and noticed the right frontal width to be
greater in 70 % of the brains, with 8.6 % showing greater
left frontal width. Sixty three percent of the brains had
wider left occipital lobe width, with 16.5 % showing the
opposite asymmetry. Sixty nine percent had greater left

occipital length and 9 % had greater right occipital length.

Pieniadz and Naeser (1984) correlated CT scan studies with

post mortem analysis of brains of fifteen right-handed males

 

 

J

21

(age range 46—71 years), 11/15 or 73 % had larger left
planum temporale. This is in comparison with 65 % of brains
with larger left planum temporale Observed by Geshwind and
Levitsky (1968). Twelve of fifteen subjects had larger left
occipital area compared with 63 % in LeMay (1976) study.
Over six percent had reversed occipital length in right
hemisphere compared to 9 % in a study conducted by LeMay

(1976).

Galaburda, Snides and Geshwind (1978) studied four brains
and found the left planum temporale to be larger in three
out of four or 75 % of brain specimens in their study.

The measurements in planimetric units were 171:55: 153:68;
and 156:114, with one brain showing larger right planum
temporale (118:136). All four brains had larger volumetric
areas in the left planum temporale 254:35: 151:69; 101:73; &
108:95. The above investigators were able to correlate
planum temporale with Brodmann’s area 22 and establish
association between reduced planum temporale and
lateralization. The degree of asymmetry could be related to
the degree of language specialization in the human brain,
whereas the lack of typical asymmetry could explain the

disorders of language functions.

D slexia and Brain Mor holo : Galaburda and Kemper (1979)

reported one case of developmental dyslexia. The subject

had above average intelligence, but suffered from noctural

21
seizures, disoriented movement, delayed speech development,
problems with directionality. The brain was studied after
the patient died as a result of fall at the age of twenty,
which revealed symmetrical planum temporale, deformed poly-
microgyria confined to the posterior region of Heschl’s
gyrus and left planum temporale, smaller language areas in
both hemipsheres, scattered large neurons, abnormal fused
gyri, cortical dysplasias and disordered cortical layers in
the left hemisphere. In describing the same patient in a
paper written in colloboration with Eidelberg in 1982,
Galaburda described the thalamic abnormalities. Myelinated
bands separated the main body of the medial geniculate
nucleus from abnormal large cells which were scattered all

over instead of being confined to their usual anterior and

dorsomedial position.

Galaburda et al. (1985) discussed cytoarchitectonic
'abnormalities found in the brains of four dyslexic readers.
Cellular distortions inteferred with the columnar
organization, particularly in the left planum temporale,
which had an excessive number of large neurons, folded and
fused laminae. All four subjects had symmetrical planum
temporale in both hemispheres which led the investigators to

speculate about the causal relationship between symmetrical

Planum temporale and the prevalance of dyslexia. Three out

Of four dyslexic brains had thalamic abnormalities. Brains

of subjects no.1 and 2 exhibited abnormalities of medial

 

 

22
geniculate nucleus. The former had distortions of posterior
lateral nuclei, bilaterally, whereas brains of subjects no.1

and 4 had large scattered neurons.

Kaufman and Galaburda (1989) found similar results from five
brains of dyslexic studied post mortem. All five brains
showed symmetrical plana, with major dysplasias and ectopias
in the left hemisphere. The anomalies were greater in the
left hemisphere than the right. Disordered neurons had
migrated to the subarchnoid space and intermingled with the
mesenchymal layers and the meninges. In ten normal brains
studied for comparisons, the left planum temporale was

larger in eight out of ten brains (80 %).

Galaburda (1989) investigated eight brains (six males and
two females) for microneural anamolies involved in dyslexia.
He Observed a symmetrical planum temporale, absence of neural
pruning leading to enlarged right planum, and excess neurons
due to faulty elimination processes. Focal cortical scars
were attributed to lesions occuring between the second
trimester of pregnancy to the second year of life. There
was disorganization of cortical plate involving ectopic
neurons and glial cells, and myelinated scars and neuron—
free regions in the cortical plates, abnormal axonal
connections, and pyramidal cell abnormalities in Ammons's
horn, a region involved in declarative memory function

(Galaburda, 1989).

 

 

23

Galaburda (1993) outlined the neuronal deficits contributing
to Visual deficits in dyslexia. He attributed the visual
deficits to the problems with the magnocellular system. The
brains of eleven dyslexic readers revealed magno cells to be
smaller by 27 %. The above investigator discussed faulty
neural migration during the second trimester of pregnancy,
genetics and environmental factors as probable causes of the
microdysgenesis and the symmetrical planum temporale

observed in dyslexic readers.

The cause of anamolous lateralization according to Galaburda
(1993) could be due to immunopathic lesions causing
transplacental migration of antibodies which may lead to
involvement of the lateral geniculate nucleus and thalamic
abnormalities. At present, past research seems to be
inadequate as to the specific loci which could lead to
reading problems. Dyslexia could well be one of the several
symptoms of failure of intersensory integration at the
thalamic level or it could be related to lack of hemspheric

dominance of language as Orton (1931) suggested.

Laterality Studies: Kimura (1961) conducted studies on
auditory laterality utilizing dichotic digits to one hundred
and twenty epileptic patients at the Montreal Neurological
Institute. One hundred and seven had Speech represented in
the left hemisphere and thirteen in the right hemisphere, as

revealed by sodium amytal tests.

 

 

24
The left hemisphere dominant group exhibited greater
accuracy for the digits presented to the right ear, and the
right hemisphere dominant group greater accuracy for the
left ear. This established a correlation between the
hemispheric superiority and contra-lateral ear advantage.
Of the left hemisphere dominant group, 93 right—handed and
10 left—handed subjects had greater accuracy for the right
ear. In the right hemisphere dominant group, three right-
handed and 9 left-handed subjects had greater left ear
superiority. Witelson (1977) conducted tests of laterality
on 85 dyslexics and 156 normal subjects (age range 6-14
years). The dichhaptic tests included placing figures and
letters in both hands and their correct identification. For
figures, the normal subjects exbited a left hand
superiority, indicating right hemisphere processing of that
stimuli, but the dyslexic subjects revealed no superiority
for either hand, thereby indicating lack of hemispheric
specialization. For letter stimuli, the normal subjects had
greater accuracy in identifying letters placed in the right
hand indicating left hemisphere superiority in processing
the stimuli. The dyslexic group revealed greater left hand
accuracy indicating the right hemisphere processing of

linguistic stimuli.

For visual stimuli (human figures), the control group had
greater accuracy in the left hemifield, indicative of right

hemisphere advantage in processing visuo-spatial stimuli.

 

 

25
The dyslexic group showed no preference for any hemifield.
This, according to Witelson (1977) revealed bilateral
representations of Visuo-spatial functions in dyslexic
readers along with the fact that they failed to show
hand/hemispheric advantage in the dichhaptic tests. In
dichotic listening tasks, both groups exhibited a right ear
advantage. The lower accuracy of dyslexic group compared to
normals indicated a left hemisphere dysfunction in the
former group. Based upon these tests Witelson (1977)
concluded that dyslexics may have bilateral representaion of
visual-spatial functions and less specialization for
language, linguistic processing. It is as though the

dyslexic readers had "two right hemispheres and none left."

Garren (1980) divided eighty children (age range between 8—
10 years) into four groups, according to their reading
performance on the Reading Recognition Subtest of the
Peabody Individual Achievement Test. Group I consisted of
control group, group II consisted of children with reading
deficits 12-17 months below the chronological age, group III
exhibited a reading delay of 18-23 months and group IV was
two years below their age level in reading. The stimuli
consisted of twenty four—letter words borrowed from the
Secondary Reading Inventory, presented 30 mm to the left or
right of the center. The duration of words was 150 ms.
Group I had greater accuracy scores for the right visual

field, while groups II, III and IV showed very slight

 

 

 

 

26

preference for the left visual field. Analysis of data
could be interpreted as a slight left visual field
preference by dyslexic readers or could be indicative of

lack of lateralization for linguistic stimuli.

Pirozzolo and Rayner (1979) investigated the hemispheric
involvement in tasks involving facial recognition, four
letter words in upper case and five letter words in lower
case presented in different visual fields of eighteen
dyslexic and normal readers. Their data showed that for
facial recognition, both groups performed with accuracy when
the stimuli was in the left visual hemifield rather than the

right hemifield.

For word recognition, normal readers exhibited more accuracy
for words presented in the right visual field whereas the
dyslexic readers exhibited no such asymmetry. In group
comparisons for unilateral and bilateral presentation of
stimuli, the dyslexic group exhibited greater visual errors
in left visual field and greater phonetic errors in the
right visual field compared to normal reading group. In
bilateral presentation of stimuli, the visual errors were
reduced while the number of phonetic errors increased in the
right visual field. The normal reading subjects showed
greater visual errors than phonetic errors in all visual

fields. This study seems to confirm Witelson’s hypothesis

 

 

 

 

27

of bilateral representation of spatial functions in dyslexic

readers.

Duara et al. (1991) used magnetic resonance imaging
techniques to delineate neuroanatomic differences between
twenty one dyslexic (12 males, 9 females, Yé35.3 years) and
twenty nine normal readers (15 males and 14 females, 3:39.1
years), right handed subjects. The areas of brain were
segmented into six regions: anterior polar (APL 10),
anterior (ANT 20), anterior central (ANC 20), posterior
central (PTC 20), posterior (PTR 20) and posterior polar
(PPL 10). Dyslexics differed from normals in the mid—
posterior region (PTR 20), encompassing the angular gyrus

and the posterior pole.

Males had larger brain segments in the mid—frontal and
midposterior locations representing larger premotor and
angular gyrus regions than females. Dyslexics had the
larger splenium compared to normals, but the females in all
the groups the exhibited largest spleniums. The
significance of the finding is not known. This study
revealed reversed asymmetry in the posterior brain segment

corresponding to angular gyrus in dyslexic subjects.

Yeni—Komishian et al. (1975) conducted research on 19
dyslexics (11 males and 8 females, §¥12.8 years) and 9 males

and 10 females, §=ll-8 years).

 

 

 

 

 

28
The test included dichotic listening of digits, visual
presentation of numbers 0,6,7, centrally and 1 to 9 in
either visual hemifield and visual visual presentation of
words. The results revealed no gender differences, but the
scores of dyslexic group was significantly poorer than the
normal group. On dichotic listening test, both groups

revealed a right-ear advantage.

 

There was a greater right hemifield superiority for both
groups on the number test, but the dyslexics had poorer
performance on left visual field. Dyslexics had nearly
equal scores on number and words in both visual fields
(139.10:139.36) compared to normals (144.63:155.66). The
experimental group also had less accuracy compared to normal
readers in foveal field for words (65.26: 73.16). Both
groups showed greater accuracy for numbers than words in the
foveal field (80.21:90.10). Based upon these results, Yeni-
Komishian et a1. (1975) stated that dyslexic readers suffer
from some kind of processing deficit in the right hemisphere
and that in dyslexic readers, the transmission from the

right hemisphere to the left could be degraded. They also
postulated a bilateral model Of reading which requires
participation by both hemispheres. The right hemisphere
could be involved in abstracting physical features from

words, such as length and spelling patterns and transmit the
information to the left hemisphere for phonological analysis

and speech activation.

 

 

 

 

29
Naylor, Wood and Flowers (1990) conducted regional blood
flow studies on 40 dyslexic readers divided into three
groups depending upon their scores on Gray Oral reading Test
(GORT), and the Wide Range Achievement Reading Sub-test
(WRAT). The reading disabled group was two standard
deviations below the means for normals on both tests. The
non—reading disabled group scored one standard deviation
below the normal means on the above tests and the borderline
group consisted of those who did not fulfill any of the
above criteria (or had medium scores). Despite the
confusing terminology used, the Reading Disabled group had
the lowest scores on both GORT and WRAT, followed by the

borderline group.

Regional blood flow activity was measured while subjects
indicated with a bi—manual finger response where words heard
binaurally were exactly four letter long. In the normals,
increased blood flow was found bilaterally in Broca’s and
wernicke’s area in the left and right hemispheres. The
reading disabled group had reduced blood flow in the left
hemisphere, but a slightly low area Of activation in the
right angular gyrus area. In the borderline group, there
were two areas of increased cerebral blood flow,
corresponding to wernicke's area and the inferior parietal-
occipital region, with two broad areas of activation in
right angular gyrus and hand—motor area of right hemisphere.

The non-reading disabled group displayed three cortical

 

 

 

30

areas of activation — Broca’s area, Wernicke's area and the
inferior parietal—occipital region. In the right hemisphere
there was only one area of activation with a sharp peak,
namely, the angular gyrus area. Based upon these results,
Naylor et al. (1990) postulated that the greater blood flow
in the angular gyrus area in the reading disabled group was
indicative of alternative compensatory strategies used,

probably due to a structural insufficiency.

Auditory Brain-stem Responses and Dyslexia: Few studies have

been conducted on dyslexia using brain-stem techniques and
those that exist are inconclusive. Grant (1980) in her
doctoral thesis on dyslexia was unable to find significant
differences between the experimental and control group in
terms of absolute or interpeak latencies. However,
significant differences were obtained for the frequency
following reponses to tonal stimuli. These findings could
not be analyzed conclusively due to lack of norms regarding

ABR responses.

Welsh, Healy and Cooper (1982) studied brain—stem responses
in conjunction with tests of central auditory function
(competing sentences, binaural fusion, filtered and
compressed speech). They found no differences in absolute
latencies for wave V in nine out of twelve dyslexic
subjects. This study did not take into account interpeak

latencies which could have provided further information

 

 

 

 

 

31
regarding the intengrity of the brain-stem function. Eighty
five percent of dyslexic subjects failed the test of
binaural fusion and fifty percent on the filtered speech
test. Based upon this, the researchers advocated the use of

central auditory tests in diagnosis of dyslexia.

Tait, Roush and Johns (1983) obtained normal auditory brain—
stem responses from 20 dyslexic children tested both in
terms of mean absolute latencies and interpeak latencies.
However their subjects ranged from nine years to fourteen
years of age. Maturational effects beyond the age of eleven
could have significant effects on auditory brain—stem
responses. In our View, the two groups should not be tested

together.

Grontved, Walter and Gronberg et al., (1988) found no
differences in twenty—four dyslexic children and twenty one
normal readers (range 10-17 years) in terms of absolute and
interpeak latencies in response to rarefaction clicks with
repetition rates of twenty clicks per second. Sound
intensity was between 100 to 110 dB spl. The brain-stem
responses at different levels of attenuation were not

studied.

None of the above studies have systematically studied graded
auditory responses to attenuated stimuli nor compared intra-

aural results in terms of absolute and interpeak latencies

 

 

 

 

 

32
(I-III, I-V, III—V) to assess the transmission function of

brain—stem in dyslexic children.

Stockard and Rossiter (1977) correlated normal brain—stem
responses from 129 normal and 100 neurological patients.

The electrode placements were Cz and M1 and M2, with
stimulus intensities ranging from 40, 60 and 80 dB SPL, at
500,000 amplification. In their analysis, Wave I is result
of direct contribution from the auditory nerve. Wave II
originates from the pontomedullary junction, involving
regions of the cochlear nucleus. Wave III has contributions
from pons (caudal region). Wave IV from mid-brain region or
pons (rostral). Wave V also had contributions from the mid-
brain regions. Wave V1 is due to the thalamic contributions

and Wave VII, thalamus and primary auditory cortex, area A1.

Delayed Auditory Feedback: Black (1950) studied the effects
of delayed side-tone upon vocal rate and intensity on
twenty—two enlisted army personnel. Ten delay periods were
used - 0.0, 30, 60, 90, 120, 150, 180, 210, 240, 270 and

300 ms.

The rate of utterances became slower as delays times were
increased from 0.0 to 180 ms. At 180 ms, the reading rates
were the slowest which the researcher attributed to the

syllabic effect (220 ms). The reading rates became steadily

 

 

 

 

33
fast beyond that. The above researcher attributed longer
duration time to the phonemic effect at 60 ms. Intensity
of productions increased with delay times and at the maximum

delay of 300 ms the intensity increased by 6.4 dB.

Interestingly, the intensity reached a plateau between 120
to 210 ms. There were two periods of maximum increment —
one as delay time was increased from 0—30 ms (intensity
increased by 2.4 dB) and another at 90 ms (intensity
increased by 2.2 dB) relative to earlier recorded mean
intensity level. The significance of these findings is not

known.

Delayed auditory feedback induced artificial stuttering in
normal speaking and reading subjects (Lee, 1951). Delays of
40, 80, 140, and 280 ms slowed rates of production,
increased intensities, repetitions and reflexive

repetition of syllables. These effects were caused due to
an interference with the feedback loop, according to the
above researcher. Repetitions of whole sentences was
attributed to clarity. This investigator did not find
independent repetitions of phonemes in subjects studies

under the effects of DAF.

Fairbanks (1955) studied the effects of delayed auditory
feedback upon articulation, duration of phrases, intensity

of productions and changes in fundamental frequency.

 

 

 

 

34
All sixteen college students showed maximum articulatory
errors and increases in sound intensities, maximum reduction
in rate of reading at 200 ms delay. The frequency effect
showed no significant changes for the various delay

parameters.

The changes in duration of phrases and articulatory errors
were categorized as primary effects and increases in
intensity and fundamental frequency as the secondary
effects of delayed auditory feedback by the investigator.
Further data analysis by Fairbanks and Gutman (1958) showed
increased number of errors of substitution, ommissions and

additions at the delay time of 200 ms.

 

 

Yates (1963) cited the importance of feedback loops in
monitoring speech productions. The repetitions of part of
the incoming stimuli is to give the summating system more
processing time. The feedback loop includes both the
afferent and efferent systems in speech productions and

reading.

Roode (1968) gave an outline of the sensory processing
mechanisms and intermodality integration involved in reading
and delayed auditory feedback. The three sensory modalities
act as sensory analyzers. In the auditory mechanisms
relative to speech, this analysis takes place in the form of

intensity, frequency and pitch analysis. The auditory

 

i

 

 

 

35
components are further analysed in terms of phonemes and
meaningful units (morphemes). Further, feedback loops from
all the three sensory modalities (audition, vision and
articulatory) are integrated at the level of angular gyrus
after having completed the feedback loop involving posterior
(Wernicke's area), anterior (Broca's area) and finally
premotor areas for speech production. The investigator
hypothesized about the malformation of angular gyrus
bilaterally which would interfere with efficiency of

integration of the input from different sensory modalities.

Effects of delayed auditory feedback upon fifteen dyslexic
college students and five normal readers was studied by Jack
and Herbert (1975). The dyslexic group differed
significantly in terms of the number of errors in reading
from the control group. The mean number of errors for the
former group was five times that of normal reading group.
Under effects of delayed auditory feedback the number of

errors were three times for control group (1:3).

Approximately, the same ratio was maintained by the dyslexic
group (5:14). However, when the differences of means was
compared, there was significant difference between the two
groups (2:9). This study failed to categorize the types of
articulatory errors exhibited making it ineffective for
comparison with other studies using delayed auditory

feedback.

 

36
Performance of ten patients with left hemispheric lesions
(mean age 55.1 years) and nine with right hemispheric
lesions (mean age 50.7 years) on tasks involving counting
digits, repeating high and low probability sentences,
tapping at a steady rate and rythmic pattern using morse
code for the letter "x", under conditions of delayed
auditory feedback at 360 ms was investigated by Vrtunski et
al. (1976). Both groups showed reduced effects of DAF for
functions affected by the site of lesions. Subjects with
left hemisphere lesions revealed increases in duration on
non-verbal tasks and their intensities did not show
significant change. The right hemisphere lesioned group
showed greater increases in duration for verbal tasks and
increases in intensities on nonverbal tasks. The control
group was affected by delayed auditory feedback and showed
greater increases in duration and intensities on all the

tasks.

Kavik et al. (1991) studied the effects of delayed auditory
feedback upon thirty—eight English speaking students
learning Japanese and Spanish in first and second year of
college. The highest increases in intensities and duration
of phrases were observed for spanish language under the
effects of delayed auditory feedback. In terms of error
analysis the number of repetitions, substitutions,
omissions, insertions, hesitations and self-corrections

increased by approximately 185 percent in Spanish compared

 

 

 

37
to 300 percent in English. For the Japanese language, under
the effects of delayed auditory feedback, the errors Of
repetitions, insertions, hesitations and self—corrections
actually declined giving a ratio of 156:165 for the number
of errors under delayed auditory feedback. The above
investigators failed to take into note the non-syllabic
character of Japanese language and further that an
ideographic language would have a different cerebral route

for integration.

Gillis and Sidlauskas (1978) discovered that reading rates
of dyslexic children (EEB.I years) improved when frequency
modulated delayed auditory feedback was presented primarily
through the right ear. According to the above researchers
in normal listening conditions, dyslexic children do not
exhibit a right ear advantage. Requiring these children to
listen with the right ear may facilitate an efficient neural

pathway to the left hemisphere.

In conclusion, research in the field of dyslexia has
concentrated primarily on laterality and formulating schema
of the reading processes without taking into account the
cross modality effects of the integrative functions. The
majority of the studies focused on just one modality —
auditory or visual. Few studies take into account the
reading rates of subjects under different temporal

parameters. The Assessment of cross modal integrative

 

 

functions

(Epstein,

reveal the
integratio
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are rare.

could reve
strategies
rates, nui
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functions involved in reading deserve thorough investigation
(Epstein, 1991). Reading under various temporal delays will
reveal the effects of those parameters on cross modality
integration of visual and auditory processes and the
feedback loop. Studies utilizing DAF on dyslexic readers
are rare. Segments of delay which affects dyslexic readers
could reveal the mechanisms involved and the reading
strategies used by these readers. An analysis of reading
rates, number of repetitions and prolongations could

indicate the delay parameters which affect the dyslexic
readers the most. Utilization of the brain stem response
techniques will facilitate the study of the efficiency of
transmission from the auditory nerve up to the inferior
colliculus. Central auditory processes involved in dyslexia
deserve through investigation and this cannot be done using

just one modality.

 

 

Descripti

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39

Chapter III

METHODOLOGY

Description of Subjects:
Three right—handed children, aged 8 to 11 years with

reading rates between 150 — 200 words per minute (Bader,
1983) composed the control group. Three right—handed
fourth grade children (8-11 years), with reading disorders
of no known etiology, composed the experimental group.

All children were screened on the Bader Language Test
Battery for reading. Only children performing less than
30% (two frustration levels below the grade) were included
in the experimental group. The control group consisted of

children with accuracy scores of 95 to 100 % on the graded

reading level.

Selection Criteria:

 

All children were administered routine audiometric tests:
otoscopy, tympanometry and immittance, puretone testing,
word reception, and speech discrimination. Any child

failing otoscopy or suffering from conductive or

sensorineural hearing loss was exempted from the study.

Thus, measures of auditory function were used to rule out

any peripheral auditory problems.

 

 

Bader Rea
was desig
Michigan

by the Li
diagnosti
Validatic
bY Dr. Da
Montana,

1981. T11
aPproxime
Words per
used for

utilize 1

Mp1

otoscope
examined
The Stat]
subJ'ects
in the p

 

40

Description of Screening Tests

Bader Reading and Langpage Inventory (1983): This test

was designed by Dr. Lois Bader, Professor of Reading,
Michigan State University. It is being used extensively
by the Literacy Coalition in Lansing, Michigan, both as a
diagnostic and remedial tool for the reading impaired.
Validation evaluation of this test was conducted in 1981
by Dr. Daniel Pierce, Eastern Montana College, Billings,
Mbntana, on elementary and secondary school children in
1981. The reading passages are graded with norms for
approximate reading rates (WPM) at each grade level.
WOrds per minute rather than syllables per minute were
used for reading rate assessment. Many reading tests

utilize these criteria.

Audiometric Procedures

QLQSQQBI: Otoscopy was conducted using an illuminated
otoscope. The orifice or the opening to the ear canal was

examined for presence of cerumen or other foreign bodies.

The status of the tympanic membrane was evaluated. Only

subjects passing the otoscopic examination were included

in the present study.

 

 

 

 

jympanome'

was used '
consisted
which emi
controlli
sound ref
was accon
ipsilater
sound emi
recording
1illlllpanome
in amplit
0r oonfig
Linden's

tympanoq.

(normal )

A Conduc
acoustic
t0 obscu
as to ru
a Stapea

inCIuded

 

 

Tympanometpy: A Middle Ear Analyzer (Grason—Stadler 1723)
was used to test middle ear impedances. This instrument
consisted of a control panel attached to a stimulus probe
which emitted a tone of 226 Hz, a manometer capable of
controlling air pressure, and a microphone to detect the
sound reflected back from the tympanic membrane. The unit
was accompanied by a head set with an outlet for
ipsilateral testing and an earphone for contralateral
sound emission. A pen drew the tympanogram on a
recording chart. The tympanograms were analyzed for
tympanometric pressure peak, static impedance as reflected
in amplitude or height of the tympanogram, and,the shape
or configuration of the tympanogram (Katz, 1985).
Linden’s (1969) and Jerger’s (1970) classification of
tympanograms was used. Only children with a type A

(normal) tympanograms were included in the present study.

A Conductive hearing loss can at times interfere with the
acoustic reflex. An air bone gap of 10 dB is sufficient
to obscure the reflex 80 % of the time (Katz, 1985). SO
as to rule out that possibility, only children exhibiting
a stapedial reflex response between 80 to 100 dB spl were

included in the present research.

 

 

 

hudiometrV

 

used. AN:
audiomete:
performed

instrumen‘

Audiometr
protocol

Academy 0
The resul
Symbol sy
frequenci
0n a line
equal to

each freq
The Pr0t(
for Audie
demonstr;
between (
250 to 8(

in the p]

reFiat a
The SRT :
(Puretm

 

 

42
Audiometry: An audiometer (Grason & Stadler 1701) was
used. ANSI standards 83.6 (1969) which pertain to
audiometers were followed. Listening checks were
performed daily to ensure proper working of the

instrumentation.

Audiometric Threshold Testing: The Hughson and Westlake
protocol for hearing testing approved by the American
Academy of Opthamology and Otolaryngology (1944) was used.
The results were recorded on a standard audiogram and the
symbol system recommended by ASHA (1989) was used. The
frequencies were represented on a log scale and intensity
on a linear scale. The space for one octave was thus
equal to 20 dB on the intensity scale. Thresholds for
each frequency were obtained and plotted on the audiogram.
The protocol followed was according to the ASHA guidelines
for Audiometric testing (ASHA 1978). Only children
demonstrating normal hearing thresholds bilaterally,
between 0 — 20 dB HL for octave test frequencies between
250 to 8000 Hz, including 1500 and 6000 Hz were involved

in the present study.

Speech Reception Threshold Testing: Subjects were asked to

repeat a list of spondee words (CID W—l Auditory Tests).
The SRT scores obtained were within 5-6 dB of the PTA
(puretone average) (Hodgson, 1980). WOrd recognition

scores were obtained for all subjects. Only children

 

 

 

 

obtaining
list were

protocol 1

Auditory i
system fo:
et al., (
diagram 0
(H12) sti
(Technics
(PC-AT) (3
consisted
capable c
research
Used. A]

were ade'

The freq1
the rate)
attenuatr

Stimul i .

The anall
reCeiVe -

ESE“) at

 

 

43
obtaining a score of 100 % on NU—6 (Northern University)
list were included in the present study. The ASHA (1987)

protocol for speech audiometry was utilized.
Description of Test Procedures

Auditory Brain Stem Responses: The microcomputer based
'system for auditory evoked potentials described by Moore
et al., (1989, 1992) was used. Figure III—1 shows a block
diagram of the ABR instrumentation. A Modular Instruments
(M12) stimulus generator, attached to a power amplifier
(Technics SE — 9060) and filter, was coupled to an IBM
(PC—AT) computer (Intel 80287). The click generator unit
consisted of a dual function generator with 16 KB memory
capable of generating various waveforms. For this
research purposes, clicks of alternating polarity were
used. Alternating click stimuli at the rate of 11.1/s

were administered through an earphone (Madsen MSH 300).

The frequency counter (Hewlett—Packard 5314 A) monitored
the rate/frequency of the test stimuli. The dual
attenuator (MI 108) controlled the intensity level of the

stimuli. The responses were averaged over 2048 sweeps.

The analog section consisted of two banana plugs to
receive three gold plated disc electrodes (Grass type

ESGH) attached to a preamplifier (Data Inc. 2124, Mod 2).

 

 

 

 

 

Fiwlre I]

 

 

44

 

Figure III-1: Block diagram of ABR instrumentation

 

basil/ii

 

LOeODCDOLo. I LOeOLOCOWTlfi

ZO\1P<L|ZMK\<JW\KWZ\ kqu

-lIIlIJ.

3

 

45

 

 

 

 

 

tossed

L

 

 

 

A

 

 

 

 

 

 

 

 

totoi

 

 

 

 

 

 

1

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

tc:
[V 65:00 ieobodrcoo i notcoE
area
$727594
med
. N a 1
odoomoEomO fiflwflocoa
i
eoczdrcii tobozcote. .ml roboeocoo

 

 

 

 

 

 

 

 

ZOEdfiszDmemZ mm<

 

 

 

 

 

 

 

 

The gain
filter wa

HZ.

The digit
analog to
the IBM c
in the cc
and calcu

data was

The monit
(Textroni
reSponsee
Connecter
t0 Print
abOUt thr
asked to
mOVement
and A1 a]
e16Ctrod.
disc elei
then Scr
Electrod‘

were SEC

46

The gain was set to 180,000 amplifiction. The high cut
filter was set at 100 Hz and the low cut filter at 3,000

Hz.

The digital section (MI 202) converted responses from

analog to digital and back to analog for final display on
the IBM computer screen. The data was analyzed and stored
in the computer memory; and after final analysis of waves
and calculation of absolute and inter-peak latencies, the

data was printed on a dot matrix printer (IBM 5152002).

The monitor section consisted of the oscilloscope
(Textronix D15) to display the test stimuli and the
responses from the subject. A plotter (IBM 6180)
connected to a dot matrix printer (IBM 5153001) was used
to print the data obtained. The subjects were instructed
about the test protocol and electrode placements, and were
asked to relax or take a nap, but not engage in excessive
movement. Areas of the head, Cz (vertex), FPz (forehead),
and A1 and A2 (earlobes) received gold plated disc
electrodes (Grass,type ESGH). The areas receiving the
disc electrodes were cleaned with disinfectant swabs and
then scrubbed with a cleansing solution (Omni-prep).
Electrode gel was applied to the disc electrodes and they

were secured with a porous adhesive (3M tape).

 

The impede
the low v:
commenced
Clicks of
earphones
ear. Aft
the inten
consecuti
Waves I t
inter-pea
measureme
latencies
With inte

(Stockard

”Mm
Verb p111,

testing,
For this
used- Tl
delays by
SDEed de'

effects

In the p

“059 pa

47
The impedances of the electrodes were checked, and only when
the low values were obtained (< 3000 ohms) was testing
commenced. The primary stimulus was at 115 dB SPL.
Clicks of alternating polarity were administered through
earphones, first to the left ear and then to the right
ear. After the waveforms were replicated at this level,
the intensity was attenuated in 10 dB SPL levels, two
consecutive times to 105 dB P.E. SPL and 95 dB P.E. SPL.
Waves I through V were analyzed for their absolute and
inter-peak latencies (I-III, I-V, III-V) and inter—ear
measurements (Moore, 1983). Analysis of absolute
latencies for waves VI and VII were also conducted along
with interpeak latencies between VI-VII, V—VI and V-VII

(Stockard and Rossiter, 1977).

Delayed Auditory Feedback: DAF equipment (Alexis Quadra
Verb Plus) was used for the delayed auditory feedback
testing. It was coupled to a tape recorder (JVC KD-15).
For this particular research, the "ping—pong" delay was
used. This delay type was selected over mono — and stereo
delays because it facilitated equal sound reflection at a

Speed determined by the delay time, without modulation

effects (see Figure III-2).

In the present study, the subjects were asked to read a

prose passage from the Bader Reading & Language Inventory.

 

 

Figure I]

 

 

 

Figure III—2: Block diagram of DAF instrumentation

 

 

zoe ~ <~ ZTW\~\<\VJA/\ \

1!.wa

r\/\hi\

 

49

 

 

 

tootooom
odoe

 

 

 

 

 

 

e

 

 

 

th L<Q

 

 

e

 

<

 

resaE<

 

 

 

 

 

 

 

 

ZOF<HZMEDWCWZI I1<Q

 

 

 

Their pro
earphones
and 500 m
delay tin

of repeti

19M
audiograi
impedance
as tympax
behaviore
increasee
At each 1
‘13 dOWn :

Possibil;

In the De
eliminati
t0 actua
AhalyZed
repetiti.

independ

The (Illal
andiomet

to 8000

 

 

50
Their productions were amplified and fed back to them via
earphones. The delay times were 0, 50, 100, 200, 300, 400
and 500 ms. Recordings of their readings under different
delay times were made and analyzed for reading rates, errors

of repetition and prolongations.

Reliability and Validity: For audiometric testing, the
audiograms were used to record data. The results of
impedance testing involving the middle ear were displayed

as tympanograms. Tympanometry of course does not require

 

behavioral responses. Reliability on the latter test was

increased by the use of the Hughson & Westlake procedure.

 

At each frequency, the thresholds were established by 10
dB down and 5 dB up procedure, thereby, minimizing the

possibility of errors.

In the Delayed Feedback paradigm, the learning effect was
eliminated by multiple readings of the text passages prior
to actual collection of data. Subsequent readings were
analyzed in terms of (a) words per minute, (b) number of
repetitions and (c) prolongations per reading. Two

independent judges scored the taped readings.

The qualifications of judges were that they had normal
audiometric thresholds for octave frequencies between 250

to 8000 Hz, SRT within normal limits and excellent word

 

 

recogniti
speech pr
reading p
neurologi
told abou
in this I

the subje

ABR respc
has no or
by the it
Was strel
starting
replicat¢
latencie:
Prefessi.

of readi
The t~te
Means an
auditory

within a

 

 

 

51

recognition scores (100 %). The judges had knowledge of
speech production and audiometry, and mechanics of the
reading process. They did not have any motor,
neurological or mental impairment. The judges were not
told about the expected outcomes or hypothesis involved
in this research nor did they have any information about

the subjects tested.

ABR responses are neural responses over which the subject
has no control. The possibility of error was eliminated
by the involuntary nature of the responses, and validity
was strengthened by use of established protocols. At the
starting level, 115 dB P.E. SPL, the wave form was
replicated twice and analyzed for absolute and inter—peak
latencies. The waveforms were stored and analyzed by two
professionals with a combined experience of twenty seven

years and compared with the normative data.

Statistical Analysis: Comparisons of mean and variances

of reading rates, repetitions and prolongations were made.
The t-test was used to establish the level of significance.
Means and variances were obtained for the latencies of
auditory brain—stem responses. Comparisons were made

within and across ears.

 

 

 

 

mm

were that
lowest at
dyslexic
the 200 1:
included
VII, and

V-VI and

m
this res<
central i
It could

processe;

Problems

 

 

 

52

Expected Outcomes: The results expected from this study

 

were that the reading rates of normal readers would be
lowest at the 200 ms delay level (Black, 1951), whereas
dyslexic readers would not be significantly affected by
the 200 ms temporal delay. Expected outcomes for ABR
included prolonged absolute latencies for waves V, VI and
VII, and prolonged interpeak latencies (I-V, I—VI, I—V and

V—VI and V—VII) for the dyslexic group.

Clinical Implications: It is expected that the results of
this research will establish the validity of DAF as
central auditory processing test for dyslexic children.

It could establish that in Dyslexia integrative central
processes are involved, rather than language or perceptual

problems.

 

 

 

 

This rese
1. Are a
manii

norm:

2. What
(a) 1
(6)1

non-1

A child‘
1- The
2- Was
3~ Achi

(me

Norm

A child
1~ The I
the c_
2- Was a
3- Achi€
mimn

DYSl<

 

53
Chapter IV

RESULTS

This research attempted to answer the following questions:
1. Are auditory brain—stem responses of children
manifesting Dyslexia different from those of

normal reading children ?

2. What are the effects of Delayed Auditory Feedback on
(a) reading rates, (b) repetitions and
(c) prolongations between the dyslexic and

non—dyslexic readers ?

A child was considered a normal reader if:

1. The reading level matched the grade level.

2. Was able to read the test material with 100 % accuracy.

3. Achieved a minimum reading rate of 160 words per minute
(wpm) on the reading passage.

Normal readers were referred to as N81, N82 and N83.

A child was selected for the experimental group if:

1. The reading level was at least two or more years below
the grade level.

2. Was able to read the test material with 80 % accuracy.

3. Achieved a minimum reading rate of 140 words per
minute (me) on the reading passage.

Dyslexic subjects were referred to as D31, D32 and D53.

 

 

 

 

Morpholoo‘
for ABR w
group. A
the waves
component
included
observed
studied.
included
important
neurons v
COMponeni
Significz

did the t

m
Figure I
for the .
intensjt

5 IV-zm

for the

fr°m 1.9

 

54

Results for ABR

Morphology_of Waves: Figure IV—l shows sample wave forms
for ABR waves I—VII for the control and the experimental
group. All ABR wave forms had excellent morphology with
the waves I—V clearly distinguishable, including the 1'
component preceding the wave I. In the pilot study which
included subjects in the age range of 8—10 years, I' was
observed to be missing in 100 % of the pilot wave forms

0

studied. It was present in 100 6 of the wave forms

 

included in the present study. This discrepancy raises
important questions about the maturational development of
neurons within the time frame and the presence of this
component. Intensity of the stimulus did not reveal any
significant differences between the two groups: neither

did the conduction times between waves I through VII.

Wave I Absolute Latencies

Figure IV—2 displays latencies including standard error
for the control and experimental groups for wave I at
intensities of 95, 105 and 115 dB P.E. SPL. Tables IV—2A
& IV—ZB list absolute latencies, means and standard error

for the control and the experimental groups, respectively.

 

At 95 dB P.E.SPL the absolute latencies for wave I ranged

from 1.96 (N81) to 2.28 ms (N53) for the control group.

   

 

Figure I‘

 

55

 

Figure IV—1. Sample of ABR waveforms for normal reader
(N81) and dyslexic reader (D82) at

intensity levels of 105 and 115 dB P.E. SPL.

 

 

:\/|~ mm><>> “\0 \PMVOJOTxQWxOV/x ummq

 

56

 

..Qm mo. mo n: .0 =>I. wo>03 mm< ”mm:

+
s .
u e =
.EV...\/ ... .e:
a .

§ '

.\... .1, u
1.. ..e
X. . .I. _ + .— w . _ 3|.
fees _ s _ .l 2.3.... ....K
=> .. ... \ = ......
u e x ..
. xer _= .
...». .2
> ..

 

 

. III .II'I

..am we mu n: so .31. 3.6; mm? ”82

c

a... -
..st ... .. __
\ 7.0/...>..#.>>
_> .c. «((4%
. _ _ _ I. _ _ __ _
Km]...
>—
.. \
5
..am we mu no. .o .51. $3... mm? H.mz
...E... .. .
.../i.
. .l .>

p-

? .
wax / x 3m):
/._\ __. Axe/l...
s - .w «I

.. .P
..j _ x. _ _ _ . q.
. g.
= \

:>l. mm><>> .10 >OODOIQKO§ ”mm;

 

 

 

Figure I

Figure IV—2:

ABR Wave I absolute latencies for the normal
(NR) and dyslexic readers (DR), at intensity
levels of 95, 105 and 115 dB P.E. SPL. The
open circles represent the latencies for the
control group, and filled circles for the
experimental group. The error bars
represent the standard error of the mean.
Circle without the standard error bar
indicates that the standard error was too

small to be represented on the graph.

2.5 I

_
flu.
2

Amt/C m5;

TIME (MS)

26

[\D
C)

t5

58

ABR¢WAVEI

 

.—

j/

 

85

l l l l

90

l l I l l l l l I l l I I l l l I l l l

q
.—
c:

95 100 105 no 115
INTENSITY (dB PE SPL)

ONR
.DR

LLJIIIIIIi]lllillllillllillllillllillll

120

q

)/

 

125

Table IV-2A

59

Absolute Latencies for Wave I: Control Grogp

Intensity in dB P.E. SPL

 

 

Time in M8

 

 

 

 

 

I
isubject I
I I
{N81 1.96 1.84 1.86 {
{N82 2.12 1.96 1.84 {
:NSB 2.28 2.10 _ 1.90 {
{Mean 2.12 1.97_— 1.87 {
— 0.13 0.11 0.025 :
I

Table IV-ZB

Absolute Latencies for Wave I: Experimental Group

Intensity in dB P.E. SPL

 

w

 

 

 

 

 

 

 

 

I
:Subject 95 105 115

1

{D81 1.86 1.60 1.42

{D82 2.14 1.68 1.68

{D83 2.28 2.24 2.00

(IE; __________ EST" 1.84 1.70

{SE —————— 0:1; ______ 0.28 0.24

l

 

For the I
2.28 ms

SPL inte‘
the stan
experime

0.17.

At 105 d
latencie
2.10 ms
ms and 5
readers,
ms (DS3)

the star

The intI
latenciI
The 1119a]
0.025.

readers
mean Wa:
Signifi.

the abs.

60

For the experimental group, they ranged from 1.86 (D81) to
2.28 ms (D83). The mean latency for Wave I at 95 dB P.E.

SPL intensity level for the control group was 2.12 ms and

the standard error was 0.13. The mean for the

experimental group was 2.09 ms, with a standard error of

0.17.

At 105 dB P.E. SPL level, the normal readers had absolute
latencies for Wave I which ranged from 1.84 (N81) to

2.10 ms (N83). The mean latencies for this group was 1.97
ms and a standard error of 0.11. For the dyslexic
readers, the latencies ranged from 1.60 ms (D81) to 2.24
ms (D83). The mean latency for this group was 1.84, and

the standard error was 0.28.

The intensity level of 115 dB P.E. SPL gave absolute
latencies which ranged from 1.84 (N82) to 1.9 ms (N83).
The mean for this group was 1.87, with a standard error of

0.025. The range of latencies for Wave I for the dyslexic

readers ranged from 1.42 ms (D81) to 2.0 ms (D83). The

mean was 1.70, with a standard error of 0.24. No

significant differences emerged between the two groups for

the absolute latencies for wave I.

 

M2
Figure I‘
error fo
levels 0
experime
latencie
shows th

experime

At 95 d1?
ranged i
mean was
were fn

and the

The latI
“‘5 (N33
The ma
error 0:
for WavI
The mea:

above 1

61

Absolute Latencies for Wave V

Figure IV-3 shows a comparative graph including standard
error for absolute latencies for Wave V at intensity
levels of 95, 105 and 115 P.E. SPL for the control and the
experimental groups. Table IV—3A gives the absolute
latencies for Wave V for the control group. Table IV—3B
shows the latencies for the above intensity level for the

experimental group.

At 95 dB P.E. SPL, the absolute latencies for Wave V
ranged from 5.76 ms for (N82) to 6.12 ms for (N83). The
mean was 5.89, with a standard error of 0.16. The ranges

were from 5.82 ms (D81) to 6.1 ms (D82). The mean was 5.98

and the standard error was 0.12.

The latencies for Wave V ranged from 5.46 ms (N82) to 5.94
ms (N83) at the intensity level of 105 dB P.E. SPL.

The mean was 5.75 for the control group, with a standard
error of 0.21. For the experimental group, the latencies
for Wave V ranged from 5.74 ms (DSl) to 5.86 ms (D82).

The mean was 5.81, with a standard error of 0.05 at the

above intensity level for the experimental group.

 

 

 

 

 

L_____-_ -

Figure l

Figure IV—3:

62

ABR Wave V absolute latencies for the normal
readers (NR) and dyslexic readers (DR). The
open circles represent the standard error

for the control group, and the filled circles,
for the experimental group at 95, 105 and

115 dB P.E. SPL.

 

6.5 —.

 

 

 

 

 

 

Amt/C m2;

 

TIME (MS)

65

6.0

5.5

63

 

 

 

 

ABR—WAVE V
l T T T I I l I l T I l I T ‘TlfiI V IN T I l I h I I T I T T T T Ti

_ 0 NR .

.. . DR ..
/ /
/( I

I l l l I l l l l I l iLLl 1 14—11—14 141—.L L414 1 LI 14 1_LIJ_1 l -
85 90 95 100 105 110 115 120 125

INTENSITY (dB PE SPL)

 

 

 

Table IV‘

 

Absolute

In_t_en_5it

 

---
———

~
~.
_-
—

‘~~-‘
—

 

 

~~~“

 

64

Table IV-BA

Absolute Latencies for wave V: Control Group

 

 

 

 

 

 

 

 

Intensity in dB P.E. SPL Time in MS

I ______________ __ ____ _
:Subject 95 105 115

}N81 - 5.80 5.86 5.84

:NSZ 5.76 5.46 5.64

:NSB 6.12 5.94 5.84

IMean 5.89 5.75 5.77

ISE — — 0.16 0.21 0.094

I

 

 

 

Table IV—3B

Absolute Latencies for Wave V: Experimental Group

 

 

 

 

 

 

 

 

 

 

_——-——--“_~-—__— — - ——— ————

 

Intensity in dB P.E. SPL Time in MS
I __ _ ________________________________________ |
ISubject 95 105 115
I _____________________________

{D81 5.82 5.74 5.44
{D82 6.1 5.86 5.84
{D83 6.02 5.82 5.60
{Mean 5.98 5.81 5.63
I

I

I

 

—‘~*~fl——fl~*~fl~fl

 

The inte]
Wave V f:
to 5.84

latencie
latencie
(DSl) to
error 0.

the two

lb§glhim
Figure I
standarI
experim
dB P.E.
and sta
IP-BO)

error f

ht inte
Centre:
The me;
The mg
7.54 m

and th

 

The intensity of 115 dB P.E. SPL produced latencies for

wave V for the control group which ranged from 5.64 ms (N82)
to 5.84 ms for N81 and N83, respectively. The mean
latencies were 5.77, and standard error 0.094. The
latencies for the experimental group ranged from 5.44 ms
(D81) to 5.84 ms (D82). The mean was 5.63, and the standard
error 0.16. No significant differences emerged between

the two groups for different intensity levels for wave V.

Absolute Latencies for Wave VI

Figure IV—4 shows a comparison of absolute latencies plus
standard error for Wave VI between the control and the
experimental groups at intensity levels of 95, 105 and 115
dB P.E. SPL. Table IV—4A shows absolute latencies, means
and standard error for the control group. Table IV—4B
(p.80) tabulates the latencies, mean and the standard

error for the experimental group.

At intensity of 95 dB P.E. SPL, the latencies for the
control group ranged from 7.12 ms (N82) to 7.70 ms (N83).
The mean was 7.48 and the standard error was 0.26.

The experimental group had latencies which ranged from
7.54 ms (D82) to 7.82 ms (D83). The mean latency was 7.67

and the standard error 0.12 at 95 dB P.E. SPL.

 

Figure IV—4:

66

ABR Wave VI absolute latencies for the normal
readers (NR) and dyslexic readers (DR). The
open circles represent the standard error for
the control group, and the filled circles,
for the experimental group at 95, 105 and

115 dB P.E. SPL. Circle without the standard
error bar indicates that the standard error

was too small to be represented on the graph.

 

5.
7
Amt/C 0.2;

 

 

 

TIME (MS)

67

 

 

 

 

ABR-WAVE VI
8-0 ""I“"I' I 'I Ifi‘l Tn' T
_ 0 NR
. DR
7.5 — -
7.0 // //
// //
1 111111111 lllillgbLilglAllJlM 1 LI l_1 Iii L i;
85 90 95 100 105 110 115 120 125

INTENSITY (dB PE SPL)

 

solute

’—

Intensit

 

Ab

032
Mean

 

Table IV-4A

68

Absolute Latencies for Wave VI: Control Group

Intensity in dB P.E. SPL

Time in H8

 

 

 

 

 

 

 

 

 

 

I
ISubject 95 105 115
I
{N81 7.62 7.54 7.42
{N82 7.12 7.46 7.26
{N83 7.70 7.56 7.18
{Mean— 7.48 7.52 7.29
{SE ————— 0.26 0.043 0.10
I

Table IV-4B

Absolute Latencies for Wave VI: Experimental Group

Intensity in dB P.E.SPL

Time__in_H_§

 

 

 

 

I
ISubject 95
I

IDSl 7.64
IDSZ 7.54
IDS3 7.82
{Mean 7:67
I 0.12
I

 

 

 

 

105 115

7.70 7.30

7.30 7.20

7.54 7.22
'''''' ;:.5_;_________;:24 '

0.16 ___—0.043

 

 

 

 

 

 

——~—~—~fl~fl~—~fl—

 

 

 

 

 

 

 

 

 

 

 

 

 

The inte
which re
mean 1aI
The expe
7.30 ms

this ng

At 115
from 7 .
with a
The lat
The mea
There w
TOUps

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I Stand;
1evels
list t

for th.

The intensity level of 105 dB P.E. SPL produced latencies
which ranged from 7.46 ms (N82) to 7.56 ms (N83). The
mean latency was 7.52, with a standard error of 0.043.
The experimental group had latencies which ranged from
7.30 ms (D82) to 7.70 ms (D81). The mean latency for

this group was 7.51, and the standard error was 0.61.

At 115 db P.E. SPL intensity level, the latencies ranged
from 7.18 ms (N83) to 7.42 (N81). The mean was 7.29,

with a standard error of 0.10 for the control group.

The latencies ranged from 7.20 ms (D82) to 7.30 ms (D81).
The mean for the experimental group was 7.24 and SE 0.043.
There were no significant differences between the two

groups for Wave VI latencies at intensities of 95, 105

and 115 dB P.E. SPL.

Absolute Latencies for Wave VII

Figure IV-5 shows a graph of comparative latencies
(standard error) between groups for Wave VII at intensity
levels of 95, 105, 115 dB P.E. SPL. Table IV—5A & IV—5B
list the absolute latencies, means and the standard error

for the control and the experimental group, respectively.

 

F TTTT

Figure IV—5:

70

ABR Wave VII absolute latencies for the normal
readers (NR) and the dyslexic readers (DR).
The open circles represent the standard error
for the control group, and the filled circles
for the experimental group at 95, 105 and

115 dB P.E. SPL.

 

10.0 I

0
g

Amt/Q HEP

 

8.5

 

 

 

 

 

'HME(MS)

10.0

9.5

L0
CD

8.5

71

ABR— WAVE VII

 

 

 

 

I I I I I I I I I I I I I I I I I I I I I—l—F fI ITTTIV I I I T I I I
_ C)NR -
DR

. C 1

- a

I .

- i
// /j
/( /

I I I I I I i l J._I_ IJ_L I LI 1; 1414—1 I_L I4L I_L l_L I L J_I
85 90 95 100 105 110 115 120 125

INTENSHW’(dB PE SPL)

 

 

 

 

Table IV

 

Absolute

 

Intensii

“-~—

‘~~-

72

Table IV-5A

Absolute Latencies for Wave VII: Control Group

 

 

 

 

 

 

 

 

 

 

 

Intensitv in dB P.E.SPL Time in MS

I _ _ __
ISubject 95 105 115

I _ l
{N81 8.50 8.72 9.12

{N82 9.16 9.26 8.5

{N83 8.76 _ 8.62 8.86

{Mean _ 8.81 8.87 8.83

{SE 0.27 0.28 0.25

I

Table IV—SB

Absolute Latencies for Wave VII: Experimental Group

———-—————-—-——.’——\—-—-i—-h-"-

 

 

 

 

 

 

 

SE 0.12 0.14 0.23

Intensity in dB P.E. SPL Time in MS
I _

ISubject 95 105 115

I _ ___ _
{D81 9.12 9.0 9.0
IDSZ 8.82 9.0 9.04
{D83 8.94 8.7 8.54
{Mean 8.96 8.9 8.86

I

I

I

 

 

 

 

 

 

 

 

 

 

At 95 d1
for the
The meal
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from 8.
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level w

At 105

8.62 TE
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group I

Intens
ranged
was 8.
0.25.

from I
and a
emerge

Have I

At 95 dB P.E. SPL intensity level, the range of latencies
for the control group was from 8.50 ms (N81) to 9.16 (N82).
The mean latency was 8.81 ms, and the standard error

was 0.27. The experimental group had latencies which range
from 8.82 ms (D82) to 9.12 (D81). The mean latency for the
experimental group for wave VII at 95 dB P.E. SPL intensity

level was 8.96, with a standard error of 0.12.

At 105 dB P.E. SPL, the latencies for Wave VII ranged from
8.62 ms (N83), to 9.26 ms (N82). The mean latency for the
control group at this intensity level was 8.87 ms, and the
standard error was 0.28. For the experimental group, the
latencies ranged from 8.7 ms (D83) to 9.0 ms for D81 and

D82, respectively. The mean latency for the experimental

group was 8.9 ms and the standard error was 0.14.

Intensity level of 115 db P.E.SPL produced latencies which
ranged from 8.5 ms (N82) to 9.12 ms (N81). The mean latency
was 8.83 ms and the standard error for the control group was
0.25. The experimental group had latencies which ranged
from 8.54 ms (D83) to 9.04 ms (D82). The mean was 8.86 ms,
and a standard error of 0.23. No significant differences

emerged between the two groups for the absolute latency for

wave VII.

 

 

 

 

 

 

 

74
Inter—peak Latency, Wave I—V
Figure IV-6 shows inter—peak latencies for Waves
I—V including standard error for the control and
experimental groups. Table IV—6A & IV—6B list the same for

the control and the experimental group, respectively.

At 95 dB P.E. SPL intensity level, the control group had
inter—peak latencies for Waves I—V which ranged from 3.64
ms (N82) to 3.84 ms for (N81) and (N83), respectively.
The mean inter—peak latency was 3.77 and the standard
error was 0.09. The experimental group had inter-peak
latencies which ranged from 3.74 ms (D83) to 3.96 ms
(D82). The mean latency for this group was 3.85 ms and

the standard error was 0.09.

Intensity level of 105 dB P.E. SPL produced latencies

which ranged from 3.50 ms (N82), to 4.02 ms (N81), for the
control group. The mean latency was 3.79 ms, and SE 0.22. I
The experimental group had inter—peak latencies which ranged I
from 3.58 ms (D83), to 4.18 ms (D82). The mean latency was I

3.97 ms and the standard error was 0.27.

Intensity of 115 dB P.E SPL produced inter—peak latencies
between Waves I-V which ranged from 3.80 ms (N82), to
3.98 ms (N81) for the control group. The mean latency at

115 dB P.E. 8P1 was 3.91 ms and the standard error was 0.08.

 

   

 

Figure IVF6:

75

Inter—peak latencies for waves I—V for the
control group (NR) and experimental group
(DR). The open circles represent standard
error for the normal readers and filled
circles for the reading impaired group at

intensity levels of 95, 105 and 115 dB P.E.

SPL.

 

 

 

 

TIME (MS)

76

ABR¥WAVES I—V (INTER—PEAK LATENCIES)

 

4.5 IIIIIIIIIIIIIIIIIFTIIIIIIIIIIIIITIIIIII
0 NR
0 OR

4.0 —

3.5 —

 

LIllllIIIllIIIIIIllIIAIllIIIlLLIJlIIJlI/f

85 9O 95 100 105 110 115 120 125
INTENSITY (dB PE SPL)

 

 

Table IV—6A

Inter-Peak Latencies for Waves I—V: Control Group

 

 

 

 

Intensity in dB P.E.SPL Time in MS

I _ ____ _______ __
ISubject 95 105 115

INSl 3.84 4.02 3.98 —- —
INSZ 3.64 3.50 3.80

INSB 3.84 3.84 3.94

IMean -—- 3.77 3.79 3.91 -—

 

 

 

 

 

Table IV-6B

Inter—peak Latencies for Waves I-V: Experimental Group

 

 

 

 

 

 

 

 

 

 

 

 

 

Intensity in dB P.E.SPL Time in MS
I ____________ _ __ _
ISubject 95 105 115

I ____________

IDSl 3.86 4.14 4.02
IDSZ 3.96 4.18 4.16
IDS3 3.74 3.58 3.60
{Mean 3.85 3.97 3.93

I

I

I

—fl——’—-f——fl~d-fl-—fl-

 

78

The experimental group had inter-peak latencies for wave I—V
at the above intensity level which ranged from 3.60 ms
(D83), to 4.16 ms (D82). The mean inter-peak latency for
this group was 3.93 ms, with a standard error of 0.24. There
were no significant differences between the two groups for

wave I—V inter—peak latencies.

Inter-peak Latency. Wave I-VI

Figure IV—7 shows graph of inter—peak latencies for waves
I-VI including standard error for the control and the
experimental groups. Tables IV—7A & 78 list the inter-peak
latencies for individual subjects, means and standard

error for the control and the experimental groups,

respectively.

At 95 dB P.E. SPL, the control group had inter-peak
latencies for waves I—VI which ranged from 5.00 ms (N82),
to 5.66 ms (N81). The mean inter-peak latency for wave
I-VI, for this group was 5.36 ms and the SE 0.27. The
experimental group showed inter-peak latencies for wave

I-VI, which ranged from 5.40 ms (D82), to 5.78 ms (D81).

The mean was 5.57 ms and the standard error was 0.16.

79

Figure IV-7: Inter—peak latencies between waves I-VI for
the control group (NR) and the experimental
group (DR). The open circles represent
standard error for the normal readers and
the filled circles for the reading impaired

group at intensity levels of 95, 105 and 115

dB P.E. SPL.

 

 

TIME (M8)

6.5

6.0

5.5

5.0

80

ABR—WAVES I—Vl (INTER—PEAK LATENCIES)

 

 

(IIIIIlIIIIIIQIIIIIIIIJIIILJIIILIIIJEIAII

85 90

I I I I I I

I I I I I I I I I I I I T? I I I I I I I ‘r I I I I I I I I
0 NR -
0 DR

\\.
i

 

95 100 105 110 115 120 125
INTENSITY (dB PE SPL)

 

81

Table IV-7A

Inter—peak Latencies for Waves I—VI: Control Group

 

 

 

 

 

 

Intensity in dB P.E. SPL Time in MS
I _ _

ISubjectS 95 105 115

I __ _
INSl 5.66 5.70 5.56
INSZ 5.00 5.50 5.42
INS3 5.42 5.46 5.28
IMean 5.36 5.55 5.42
ISE 0.27 0.11 0.11—
l

—fl~fl~’~fl~fl-—~fl—

 

Table IV-7B

Inter-peak Lgtencies for Waves I-VI: Experimental Group

 

 

 

 

 

 

 

l U1
m
0
O
H
ox
O
w
L»)
O
O
N
\D

 

 

Intensity in dB P.E. SPL Time in MS

I

ISubjects 95 105 115

I _ _ __
IDSl 5.78 6.10 5.88

IDSZ 5.40 5.62 5.52

IDSB 5.54 5.30 5.18

IMEan 5.57 5.67 5.53

I —————— — — — -- — _
I

I

 

_’~*~fl~*~fl*flafl-

 

82

At 105 dB P.E. SPL intensity, the control group had inter—
peak latencies between waves I~VI which ranged form 5.46 ms
(N83) to 5.70 ms (N81). The mean inter-peak latency at the
above intensity level was 5.55 ms with a S.E. of 0.11. The
experimental group exhibited inter-peak latency for wave
I—VI, which ranged from 5.30 ms (D83), to 6.10 ms (DSl).
The mean inter-peak latency for this group was 5.67 ms and

the inter—peak latency was 0.33.

At 115 dB P.E. SPL, the inter—peak latencies for waves I—VI
ranged from 5.28 ms (N83), to 5.56 ms (N51). The mean
inter—peak latency at above intensity level for wave I—VI
was 5.42 ms and the standard error was 0.11. The
experimental group exhibited inter-peak latencies which
ranged from 5.18 ms (D83), to 5.88 ms (D81). The mean
inter-peak latency for waves I—VI at 115 dB P.E. SPL was
5.53 ms and the standard error was 0.29. No significant
differences were observed between the groups at intensity
levels of 95, 105 and 115 dB P.E. SPL inter—peak latencies

for waves I—VI.

Inter-peak Latency- Wave I—VII

Figure IV-8 shows comparative data for inter—peak

latencies for waves I—VII including standard error between
the control and the experimental groups at intensity levels

of 95, 105 and 115 dB P.E. SPL. Tables IV-8A & IV-8B list

the same for the two grouPS-

 

 

 

Figure IV—8:

83

Inter—peak latencies between waves I—VII for
normal readers (NR) and the dyslexic readers
(DR) at intensity levels of 95, 105 and 115 dB
P.E. SPL. The open circles represent the
standard error of latencies for the control
group and the filled circles for the

experimental group.

 

TIME (MS)

84

ABR-WAVES I—VII (INTER-PEAK LATENCIES)

 

 

 

 

 

75 ""I""ITTI'T"" ""—I"TI+“"T""
0 NR
0 DR
7.0 — ~
6.5 — T —
j/ ‘/
/
// /
I I I I I I PLI 1+1 IJ__I l 14 I—Ll I_LI I I I L I LI Ll I J_I_1__L
85 90 95 100 I05 110 II5 IZO I25

INTENSITY (dB PE SPL)

 

85

Table IV—8A

Inter—peak Latencies for Waves I—VII: Control Group

 

 

 

 

 

 

Intensity in dB P.E. SPL Time in MS

I I
' I
a I
ISubject 95 105 115 I
I T" ————— I
INSl 6.54 6.88 7.26 I
INSZ 7.04 7.30 6.66 I
IN53 6.48 6.52 6.96 I
IMean 6.69 6.90 6.96 I
ISE 0.25 0.32 0.24

I

 

 

Table IV—8B

Inter-peak Latencies for Waves I-VII: Experimental Group

 

 

 

 

 

 

 

 

Intensity in dB P.E.SPL Time in MS

I __ __I
ISubjects 95 105 115 I
I “I
IDSl 7.26 7.40 7.58 I
IDS2 6.68 7.32 7.36 I
IDS3 ~— _ —_E;EE -------- 6.46 _ 6.54 _-__I
Igfig _________ 6.87 _ ~_— 7.06 7.16 ————— I
ISE 0.28 0.43 0.45

I

 

86

At 95 dB P.E. SPL, the inter-peak latencies between waves I-
VII ranged from 6.48 ms (N53), to 7.04 ms (N82). The mean
inter-peak latency was 6.69 ms and the standard error was
0.25. The experimental group had inter-peak latencies which
ranged from 6.66 ms (DS3), to 7.26 ms (DSl), at the above
intensity level. The mean for this group was 6.87 ms and

the standard error was 0.28.

At 105 dB P.E. SPL the inter—peak latencies between waves
I-VII for the control group ranged from 6.52 ms (N53), to
7.30 ms (N82). The mean inter-peak latency was 6.9 ms and
the standard error was 0.32. The experimental group had
inter-peak latencies for waves I-VII which ranged from
6.46 ms (DS3), to 7.40 ms (DSl). The mean inter—peak

latency was 7.06 ms and the standard error was 0.43.

At 115 dB P.E. SPL intensity level, the control group had
latencies which ranged from 6.66 ms (N82), to 7.26 ms
(N31). The mean inter-peak latency was 6.96 ms and the
standard error was 0.24. The experimental group had
inter—peak latencies which ranged from 6.54 ms (D33), to
7.58 ms (D31). The mean inter—peak latency for wave I—VII
was 7.16 ms and the standard error was 0.45. No
significant differences emerged between the two groups at

different intensity levels.

 

 

87

Inter—peak Latency; Wave V—VI

Absolute latency of wave VI was studied because according
to Stockard and Rossiter (1977), this wave originates in
the thalamus. Integrity of the neuronal pathway from
higher brain—stem to the thalamus was investigated by
studying inter—peak latency between wave V and VII.
Figure IV—9 shows comparative data for inter—peak
latencies including standard error at intensity levels of
95, 105, and 115 dB P.E. SPL levels. Tables IV-9A & 9B
list inter-peak latencies for individual subjects, mean
and the standard error for the control and the

experimental groups, respectively.

At 95 dB P.E. SPL, the inter-peak latencies for waves V—VI
for the control group ranged from 1.36 ms (N32), to 1.82
ms (N31). The mean inter-peak latency was 1.59 ms and the
standard deviation was 0.19. The experimental group had
inter—peak latencies which ranged from 1.44 ms (D32), to
1.82 ms (D31). The mean inter—peak latency was 1.69 ms,

and the standard error was 0.17.

At 105 dB P.E. SPL, the inter—peak latencies for the
control group ranged from 1.62 ms (N33), to 2.0 ms (N32).
The mean inter—peak latency at above intensity level was

1.77 ms and the standard error was 0.17.

 

 

Figure IV—9:

88

Inter—peak latencies between waves V—VI for
control group (NR) and the experimental
group (DR). The open circles represent data
for the normal readers and the filled circles
represent data for the dyslexic readers at

intensities of 95, 105 and 115 dB P.E. SPL.

 

TIME (M8)

2.5

2.0

1.5

89

ABR WAVES V-VI (INTER—PEAK LATENCIES)

 

/
/

I

 

IIIIIIIIIIlllnglIIIIIIIIJ—I—IIILLIIJJll

— \yl
\\

 

 

85 90 95 100 105 I10 115 120
INTENSITY (dB PE SPL)

 

125

 

 

90

Table IV-9A

Inter—Peak Latencies for Waves V-VI: Control Group

 

 

 

 

 

 

 

 

 

Intensity in dB P.E. SPL Time in MS
I _ __________ _ _ ______________ I
ISubject 95 105 115 I
I T _______________ T I
INSl 1.82 1.68 1.58 I
INSZ 1.36 2.00 1.62 I
INSB 1.58 1.62 1.34 I
Iié'QTT-W"TEEEE::EZEE:::-.1.-51 __ ’ I
ISE 0.19 0.17 0.12 I
I

 

Table IV—9B

Interepeak Latencies for Waves V—VI: Experimental Group

 

 

 

 

 

 

 

Intensity in dB P.E.SPL Time in MS

I_ _ _______ _ _____________________
ISubject 95 105 115

IDSl --- 1.82 1.96 1.86 ————————————————
IDSZ 1.44 1.44 1.36

IDSB 1.80 1.72 1.62

’Nean 1:69 1.71 1.61 TTTTTTTTTTTTTTT

 

 

 

 

91

The experimental group had latencies which ranged from
1.44 ms (D32), to 1.96 ms (031). The mean inter-peak

latency fOr this group was 1.71 ms and the standard error

was 0.21.

At 115 dB P.E. SPL, the control group exhibited inter—peak
latencies between wave V—VI which ranged from 1.34 ms
(N33), to 1.62 ms (N32). The mean inter—peak latency was
1.51 ms, with a standard error of 0.12. The experimental
group had inter-peak latencies which ranged from 1.36 ms
(D32), to 1.86 ms (D31). The mean inter—peak latency
between wave V—VI for this group was 1.61 ms, with a
standard error of 0.20. No significant differences were
found between the control and experimental groups for
inter-peak latencies between waves V and VI at intensity

levels of 95, 105 and 115 dB P.E. SPL.

Inter—peak Latency. Wave V—VII

The rationale for studying absolute latencies of waves VI
and VII is given by Stockard and Rossiter (1977).
According to these researchers, the above waves are
attributable to thalamic activity, with wave VII
reflecting supplemental contributions of the primary
auditory cortex. Inter—peak latencies between waves V and
VII were investigated for the efficiency of the neuronal
transmission from the higher auditory brain-stem to the

thalamus and the primary auditory cortex.

 

 

 

92
Figure IV—lO shows comparative inter—peak latencies between
waves V-VII including standard error, at intensity levels of
95, 105, and 115 dB P.E.SPL levels for the control and the
experimental groups. Tables IV—IOA & 103 list inter—peak

latencies, mean and standard error for the above groups.

At intensity of 95 dB P.E. SPL, the control group had
inter—peak latencies for waves V—VII, which ranged from
2.64 ms (N33), to 3.40 ms (N32). The mean inter—peak

latency for waves V—VII for the above group was 2.91 ms

 

and the standard error was 0.35. The experimental group
had latencies which ranged from 2.72 ms (D32), to 3.30 ms
(D31). The mean inter—peak latency for this group was

2.98 ms, with a standard error of 0.24.

The intensity of 105 dB P.E. SPL, produced inter-peak
latencies which ranged from 2.68 ms (N33), to 3.80 ms
(N32), for the control group.' The mean inter-peak latency
was 3.11 ms and the standard error was 0.49. The
experimental group exhibited latencies which ranged from
2.88 ms (D33), to 3.26 ms (D31). The mean inter-peak
latency for wave V-VII at 105 dB P.E. SPL for this group

was 3.09 ms, with a standard error of 0.16.

 

At 115 dB P.E. SPL produced inter—peak latencies for waves
V—VII for the control group, which ranged from 2.86 ms

(N32), to 3.28 ms (N31).

 

 

 

Figure IV-lO:

93

Inter—peak latencies between waves V—VII for
control group (NR) and the experimental
group (DR) at intensity levels of 95, 105
and 115 dB P.E. SPL. The open circles
represent latencies for the normal readers

and filled circles for the reading impaired

group.

 

 

 

 

TIME (MS)

94

ABR-WAVES V-Vll (INTER—PEAK LATENCIES)

 

 

 

 

4.0 IIIIIIIIIITIIII Iw—rr I [Tr I
— ONR -
_ .DR
5.5 — _
3.0 ~ _
2.5 — _.
7 j/
//
/ f
IIIII_I;LI141_I_I #11_JJ_JJ_JJ_IJ_14LIJI_ILIII_I#LI

 

85 9O 95 100 IO5 HQ 115 120 I25
INTENSITY (dB PE SPL)

 

 

Table IV—IOA

Inter—Peak Latencies for waves V—VII: Control Group

Intensity in dB P.E.SPL Time in MS

 

E
U
(‘D
0
fl
\D
01
p
0
U1

 

 

 

 

I I
I _ 115 I
INSl 2.70 2.86 3.28 I
Ist 3.40 3.80 2.86 I
INS3 2.64 2.68 3.02 I
IMean 2.91 3.11 3.05 I
ISE 0.35 0.49 0.17 I
| I

 

Table IV—10B

 

Inter—peak Latencies for Waves V—VII: Experimental Group

Intensity in dB P.E. SPL Time in MS

 

 

U}
5
u.
(D
0
d‘
RB
0'1

105 115

 

U D U
U: U)
N I-'
N w
\I to
N 0
Lu.)
I
N
O)
w
01
ON
“__I—'I—I—I—fl—fif-u-P—

U:
u
N
KO
N
N
I
00
m
N
o
s

 

3 I
(DI
all
a I
N
m
m
u
o
w
u
N
u

U! I
H
O
U
N
b
O
I
1.4
0')
O
I
N
U'I

———~—-—-—~*~fl~fl-——U-

 

 

96

The mean was 3.05 ms with a standard error of 0.17. The
experimental group had inter-peak latencies for waves V—VII
for the above intensity level which ranged from 2.94 ms
(D33), to 3.56 ms (D31). The mean inter-peak latency for
this group was 3.23 ms, with a standard error of 0.25. No
significant differences were observed for inter—peak
latencies for waves V—VII at intensity levels of 95, 105,

115 dB P.E. SPL levels.

The mean absolute latency for wave VI for the control and
experimental groups was 7.48 ms and 7.67 ms, respectively.
The mean absolute latency for wave VII for the control and
experimental group was 8.81 ms and 8.96 ms, respectively.
These values are in accordance with the norms obtained by
Stockard and Rossiter (1977). Therefore, the inter—peak
latency of waves VI and VII were not included in the

present research.

Results of DAF:

Figure IV—ll is a graph of reading rates for the control
and the experimental groups for temporal delays of 0, 50,
100, 200, 300, 400 and 500 ms. Table IV-11A gives
individual reading rates, mean and standard error for the
normal readers. Table IV-11B lists the same for the
reading impaired subjects. The reading rates of normal

readers ranged from 96 to 147 words per minute.

 

 

 

Figure IV—11:

97

Graph shows reading rates for the normal
(open circles) and dyslexic readers
(filled circles) at delayed auditory
feedback of 50, 100, 200, 300, 400 and
500 ms. NR and DR denote normal and
dyslexic readers, respectively. Circles
without the standard error bars indicate
that the standard error was too small to

be represented on the graph.

 

 

READING RATES (WPM)

120

100

80

98

DAF - READING RATES

 

I T I I I I I I I I I I I I j I I I I l I l I I I I I I

ONR
.DR I

NH
0 /\I

IIIJIII

 

 

I I I I

 

 

;
/
/ I
I L 14L 1; I4 J_I 1.1—1 4 I I L I I J J_I I J L; PL I
0 I 00 200 300 400 500 500

TIME (MS)

 

99

Table IV-llA

mean Reading Rates (WPM) Under Delayed Auditory Feedback
Control Group

Delay Time in MS

 

 

 

 

 

 

 

l I
ISubject 0 50 100 200 300 400 500 I
INSl 172 145 135 96 134 121 122 I
INSZ 173 141 109 120 145 141 147 I
IN53 170 137 123 140 141 137 135 I
IMean 171.7 141 122.3 118.7 140 133 134.7 I
ISE 1.25 3.27 10.62 18.0 4.55 8.64 10.20 I
I I

 

Table IV-llB

Mean Reading Rates (WPM) Under Delayed Auditory Feedback
Experimental Group

Delay Time in MS

 

 

 

 

 

 

 

 

 

I
________ _ _ ___ _ __I
SE 5.19 7.07 5.31 13.14 18.24 16.78 11.59 I

____________________________ __ _ _______I
I

I

ISubject 0 50 100 200 300 400 500 I
IDSl 156 112 99 139 118 137 103 I
IDS2 145 97 86 108 75 100 85 I
IDS3 156 97 93 116 86 103 113 I
IMean 152.3 102 92.7 121 93 113.3 100.3

I
I

I

 

 

 

100

The lowest reading rate of 96 words per minute (wpm) was
attained by NSl at a delayed time of 200 ms. The highest
reading rate (147 wpm) was attained by N32 at a delay of 500
ms. The range of reading rates for the dyslexic readers
ranged from 75 to 139 words per minute. The lowest reading
rate in this group (75 wpm) was achieved by D32 at a
temporal delay of 300 ms, and the highest reading rate

(139 wpm) was attained by D31 at delay of 200 ms.

Tables IV~11C & IV—11D give an analysis of range and means
of reading rates at different auditory feedback delays for
the control and the experimental group, respectively. The
reading rates ranged between 96 to 147 words per minute
for the normal readers. The range of reading rates for
dyslexic readers was between 75 to 139 words per minute.
The mean reading rates under different temporal parameters
for normals was 133.2 wpm. whereas that for dyslexic

readers was 98.1 wpm.

Reading Rates Under Different Temporal Delays

Table IV—11A lists reading rates, mean and standard error
for the control group. Table IV—llB lists individual
reading rates, means and standard error for the

experimental group.

 

 

101

Table IV—llC

Analysis of Range and Means of Reading Rates Under DAF
Control Group

 

 

 

 

 

 

 

I I
ISubject Range means I
I T I
INSl 96~145 125.5 I
INSZ 109—147 138.8 I
IN33 123—141 135.5 I
IControl Group 96-145 133.2 I
I “““““““ I ““““““““““““ I
Table IV—D

Analysis of Rapge and Means of Reading Rates Under DAF
Experimental Group

 

 

 

l I
ISubject Range Means I
I I
IDSl 99-139 118 I
IDSZ 75—108 91.8 I
IDS3 86-116 84.6 I
I

I

I

I
Experimental Group 75—139 98.1 I
I

—-_—_--—-——_—-—-—-———-w—n——-———————_————_———

 

102

At 0 ms DAF, the reading rates of normal readers ranged
from 170—172 wpm, whereas that of reading impaired group
ranged from 145 to 156 wpm. The mean reading rates for
the normal readers at 0 ms delayed auditory feedback was
171.7 wpm (SE 1.25). The mean reading rates for the
reading impaired group for the same temporal delay was

152.3 wpm (SE 5.19).

At 50 ms delay, the normal readers had reading scores that
ranged between 137 to 145 wpm (x = 141 wpm; SE = 3.27). The
dyslexic group had reading ranged from 97 to 112 at the same
temporal delay (2 = 102; SE = 7.07). Lowest reading rates
in the normal group was for subject N83, whereas the two
subjects D52 and D83 registered the lowest reading rates for
the same temporal parameter for the dyslexic group. Both
groups exhibited reduced reading rates at 50 ms delayed
auditory feedback compared with the reading rates at 0 ms
delay. The control group had mean reading rates of 141 wpm

compared to 102 wpm for the experimental group.

At delayed auditory feedback of 100 ms the normal readers
had reading rates that ranged from 109 to 123 wpm
(mean = 122.3; SE = 10.62). The lowest reading rates were

achieved by N32 at 109 and the highest by N81.

 

 

 

103
The dyslexic readers had reading scores that ranged from 86
to 99 wpm. The lowest mean reading rate (86 wpm) was
obtained by D82, whereas the highest reading rate was
obtained by D31 (99 wpm). The reading rates of both groups
were further reduced at 100 ms delay compared with reading
rates at 50 ms. The mean reading rate of the experimental
group was lowest at the temporal delay of 100 ms (mean
122.3) compared to the mean reading rate for the control

group (92.7).

At 200 ms DAF, the reading rates of normal readers ranged

from 96 me (N81) to 140 wpm (N83). The mean of reading

rates at this temporal delay was 118.7 me, with a

standard error of 18.0. For the dyslexic group, the

reading rates at this delay ranged from 108 (D52) to 139

me (D81). This gave a mean of 121 wpm and a standard

error of 13.4. As seen from Figure IV—11, both the

control and experimental group had nearly identical ‘
reading rates at delayed feedback of 200 ms.

The delay of 300 ms produced a mean of 140 wpm for the

normal readers with standard error of 4.55. The reading

rates ranged from 134 to 145 wpm for normal readers, with
the lowest reading rate attained by subject N51 and the
The

highest reading rate for this temporal delay by NS2.

experimental group had means of 93 wpm, with a standard

error of 18.24 at this temporal delay.

 

104
Their scores ranged from 86 wpm (DS3) to 118 wpm (DSl). At
300 ms delayed auditory feedback, the mean reading rates of
the control group increased to 140 wpm, whereas the
experimental group had their lowest mean reading rates of

93 wpm.

At 400 ms delayed feedback level, the reading rates of
normal readers ranged from 121 (NSl) to 141 me (N52),
giving a mean of 133 wpm and a standard error of 8.64.

The dyslexic readers attained reading rates that ranged
from 103 (DS3) to 137 wpm (DSl). The mean of their
reading rates at this level was 113.3 and a standard error
of 16.78. At 400 ms delay, the mean reading rate of the
control group was 133 me, whereas the experimental group

had mean reading rate of 113.3 wpm.

The temporal delay of 500 ms produced reading rates that
ranged between 122 wpm (N51) to 147 wpm (N32). The mean
reading rate was 134.7 wpm and the standard error was 10.20.
At the same level, the reading rates of dyslexic readers
ranged from 85 wpm (D82) to 113 wpm (DS3). Their mean
reading rates for this level was 100.3 wpm, with a standard
error of 11.59. The mean reading rates of the control group
remained nearly the same at 300 and 400 ms delay (133:134.7
me), whereas the experimental group had reduced mean
reading rate of 100.3 wpm, compared to 113.3 wpm at 400 ms

delay.

105
Tables IV—11C & IV—11D list the range and means of reading
rates for the control and experimental groups at feedback
delays of 50, 100, 200, 300, 400 and 500 ms. The reading
rates of N51 ranged from 96—145 wpm. N52 had reading rates
which ranged from 109-147 wpm and N53 had reading rates
which ranged from 123-141 wpm. The range for the control

group was from 96-145 me, with a mean of 133.2 wpm.

The experimental group had reading rates which ranged from
75-139, with a mean reading rate of 98.1. D51 had reading

rates for the above temporal delays which ranged form 99-139

 

wpm. D52 had reading rates which ranged from 75-108 wpm and

D53 had reading rates which ranged from 86-116 wpm.

As may be seen from Figure IV~11, there were two delay
segments which significatly affected the reading rates of
the control group. These delay segments extended from 100
ms (N52 and N53) to 200 ms (N51). Lowest reading rates
were recorded at these temporal two temporal delays of 100
and 200 ms for the control group. Immediately after this
delay time, the reading rates seem to recover
significantly followed by the plateau effect extending
from 400 to 500 ms. The curves obtained from normal
readers have a single trough (lowest reading rates)
followed by a period of recovery followed by a plateau

(nearly constant reading rates).

 

106

As can be seen from Figure IV-ll, the reading rates of
dyslexic readers follow a bi-modal curve. The delays of 100
ms and 500 ms were equally significant for D51 and D52 as
revealed by their low reading scores in Table IV-B. For D51
the reading rates at these temporal delays were 99 and 103
words per minute. For D52, the reading rates remained
nearly same (86 and 85 wpm) at delays of 100 and 500 ms,
respectively. Dyslexic readers D52, D53 were affected most
by the temporal delay of 300 ms as evidenced by their lowest

reading rates 75 and 86 wpm respectively.

Dyslexic readers exhibited two periods of recovery, one at
200 ms and the other at 400 ms. At these periods, their
reading rates improved substantially. The surprising fact
is that the reading rates at the period of recovery at 200
and 400 ms were nearly identical for all three dyslexic
readers. D51 attained reading rates of 139 and 137 wpm:
D52 108 and 100 wpm; and D53 106 and 104 me at feedback

delays of 200 and 400 ms.

It is to be noted that the reading rates exhibited by
dyslexic readers are almost mirror-like in their
replication between 100, 300 and 500 ms. With the reading
rates at 100 ms (lowest reading rates) replicated at 500
ms and those at 200 ms at the 400 ms delay level, with the

mid point at 300 ms. Thus, reading rates between 0 ms

 

 

feedback delay and different feedback parameters reveal
significant differences between the normal and dyslexic
readers. No significant differences emerged between the
mean reading rates for the control and experimental groups
at 200 ms. However, it should be noted that the reading
rates at 200 ms represent the highest mean reading rates

for the experimental group, whereas it represents the lowest

mean reading rates for the control group.

Differences Between Control and Experimental Groups at

0 ms DAF Table IV~11E lists the differences from reading
rates at 0 ms delayed auditory feedback. In the control
group, the highest difference from normal reading rates
occurred for subject N51, at DAF of 200 ms (—76 wpm).

N52 had maximum reduction in reading rates at 100 ms delay
(—64 wpm). N53 had maximum reduction in reading scores at
100 ms (-47 me). For all normal subjects, the slowest
reading rates (maximum.difference) occured at 200 ms

feedback delay (N51 and N52) and 100 ms (N53).

Among the dyslexic readers, the largest differences from
reading rates at 0 ms feedback occurred for subjects D52
and D53 at delays of 300 ms. Both attained identical
differences of -70 wpm from the original reading means.
D51 had maximum reduction in reading rates from 0 ms

feedback delays of 100 me and 500 ms.

 

 

 

 

108

As can be seen from Table IV—11F, the control group
exhibited reduction in reading rates which ranged from
-26 to —64 me from the normal reading rates or reading
rates at 0 ms delay. Table IV—G shows the differences

in reading rates from the reading rates at 0 ms feedback

 

 

 

 

delay for the experimental group. The effects ranged

from —17 to -70 me, with a mean reduction of —48.9 wpm.

Inter—delay Differences in Reading Rates

Analysis of differences of reading rates under different

 

delays is presented in table IV—11H. Based upon these
figures, there is significant difference in reading rates
between normal readers and dyslexic readers. The control
group had greatest reduction in reading rates in change of

delay from 50 to 200 ms (—39, -32, —33).

Change of delay from 200 and 300 ms produced an increase
in the rate of reading. This is shown by a positive
reading rate increase of +38, +25, and +1 wpm for N51,
N52 and N53, respectively. All normal readers showed

this positive trend between 200—300 ms.

Table IV—11H reveals that all dyslexic readers eXhibited
maximum reduction in reading rates at change of delays
from 0 to 50 ms (~44, ~48, -59 wpm) for D51, D52 and D53,

respectively. All of them have positive scores from 100 to

—¥

 

109

Table IV-llE

Difference From Normal Reading Rates

Delay Times in M5

 

 

 

U3
LI.)
I
01
KO
I
O)
u
I
uh
O
I
\I
O
I
01
w
I
uh
LII.)

 

 

I I
:5ubject 50 190 200 300 400 500_}
I I
:N81 -27 -37 -76 -38 -51 -50 I
{N82 -32 -64 -53 -28 -32 -26 {
{N83 -33 -47 -30 “29 —33 -35 {
{D81 -44 -54 -17 “38 -19 —53 {
{D82 -48 -59 -37 -70 -45 —60 i
In I
I I

Table IV-llF

Analysis of Differences From the Normal Reading Rates
Control Group

 

 

 

I
lSubject Range Hean Difference }
I I
{N81 —27 to —51 -46.5 1
{N82 -26 to -64 ~39.1 {
{N83 ~29 to -49 — _—36.1 {
{Control Group ~26 to ~64 . —40.5 t
I ’ I

 

Table IV-llG

Analysis of Differences From the Normal Reading Rates

Experimental Group

 

 

 

 

 

 

 

 

 

__ _ I
:Subject Range _ Mean Difference I
I " _‘ I
{D51 ~17 to ~54 ~39.1 I
{D52 ~37 to ~70 ~53.1 I
{D53 ~43 to ~63_ _ —54.6 _ I
{Experimental Group _ ~17 to ~70 ~48.9 I
I I

 

 

 

 

 

 

110

Table IV—11H

Inter-Delay Difference in Reading Rates

 

Delay times in milliseconds

 

 

I I
}5ubject 0-50 50-100 100—200 200-300 300-400 400-500 :
:N81 -27 -10 -39 +38 -13 +1 }
:N82 -32 —32 +11 +25 -4 +6 }
}N83 -33 -14 +17 +1 —4 -2 :
:D81 -44 -13 +40 -21 +19 -34 :
:D82 -48 —11 +22 ‘33 +25 -15 }
:D83 -59 —4 +23 -30 +17 +10 }
I I

 

 

Table IV—111

Analysis of Differences in Reading Rates Under DAF: Control

Group
I

 

 

 

 

 

 

I
Iffféfft Range mean Difference E
I ——————————— ' ‘
{N31 ~39 to +1 -50 I
IN32 -32 to +25 -38 I
{“33 __ _ ~33 to +17_ _______ _25 _ _ I
{Control Group ~39 to +25 ~37.6 t
I I

 

Table IV.11J Analysis of Differences in Reading Rates Under
DAE; Experimental Group

 

 

 

 

 

 

I I
IfgbjeCt Range Mean Difference I
:DSl “ -44 to +19 -53 1
}D32 ~48 to +25 -60 }
:PSB ~59 to +23 —43 I
IExperimental Group ~59 to +25 ~52 I
I I

111
200 ms and from 300—400 ms. This is evidenced by their
significant improvement in reading rates at those temporal

delays.

Table IV—llI gives ranges and mean difference in reading
rates at temporal delays of 50, 100, 200, 300, 400 and 500
ms for the control group which ranged from ~39 to + 25 wpm

with a mean difference of ~37.6 wpm.

Table IV—11J lists the range of reading rates, range and
means at different temporal delays for the experimental
group, which was ~59 to +25 me, with a mean difference of

~52 wpm.

As may be seen from these tables, no significant
differences emerged between the two groups in terms of
recovery of reading rates. The differences existed at the
lower limits of reading rates, with the dyslexic readers
being more affected by the delayed feedback (~59) compared
to the normal readers (~39). This produced observable
differences in mean reduction of reading rates for the two
groups (~37.6:~52 wpm). The control group showed reduced
reading rates for delayed feedback between 50 to 200 ms,
whereas the experimental group exhibited poor reading
rates from 50 to 100 ms and at 300 and 500 ms, but they

obtained the best reading rates at 200 ms.

 

 

112

Episodes of Repetitions Under the Effect of DAF

Figure IV—12 is a graph of number of repetitions for the
control and experimental groups. Tables IV—12A & IV~1ZB
list episodes of repetitions, including standard error at
auditory feedback delays of 50,100, 200, 300, 400 500 ms.
The number of repetitions for the control group at delayed
auditory feedback of 50 ms ranged from 1 (N51) to (8) for
N52. The mean was 3.7 and the standard error was 3.09.
Dyslexic readers had episodes of repetitions which ranged
from 6 (D53) to 11 (D52). The mean number of repetitions
for this group at delayed auditory feedback of 50 ms was
9, with a standard error of 2.16. At 50 ms delayed
auditory feedback, the mean number of repetitions for the
control group was 3, compared to 9 for the for the

experimental group.

At 100 ms delayed auditory feedback, the number of
repetitions for the control group ranged from 2 (N53) to 4
(N52). The mean number of repetitions at this delay was 3,
with a standard deviation of 0.82. The experimental group
had repetitions which ranged from 5 (D52) to 11 (053). The
mean number of repetitions was 7.7, with a standard error
of 2.49. At 100 ms delay, the mean number of repetitions
for the control group was 3 compared to the 7.7 for the

experimental group.

 

113

Figure IV—12: Number of repetitions for the control

(open circles) and experimental group

 

(closed circles). NR and DR denote

normal and dyslexic readers, respectively.

 

REPETITIONS (EPISODES)

3O

25

N
O

—k
U‘I

O

01

114

DAF - REPETITIONS

 

I T l I I I I l I I I—FT I I T T I l‘fiil I I I I
0 NR

.DR

Illlll'lrllllll

I'll

(LA—llIILIAIlIIAILLIlALLgIIJJildif
O

100 200 300 400 500 600
WME(MS)

 

 

 

115

Table IV—12A

Episodes of Repetitions Under the Effects of DAF

 

 

 

 

 

Control Group _
De_lay_111_1fi

Subject 50 100 200 300 400 500
N31 1 3 2 8 10 7
N82 8 4 15 12 12 8
N83 2 2 4 6 6 4
Mean 3.7 3 7 8.7 9.3 6.3
SE 3.09 0.82 5.72 2.49 2.49 1.7

 

 

Table IV—12B

Episodes of Repetitions Under the Effects of DAF

Experimental Group

 

 

 

 

w

I
Subject 50 100 200 300 400 500 {
D81 10 7 5 7 8 14 {
D82 11 5 12 24 13 12 {
D83 6 11 6 20 9 11 {
Mean 9 7.7 7.7 17 10 12.3 {
SE 2.16 2.49 3.09 7.26 2.16 1.25 I

I

 

 

   

 

116

Delayed auditory feedback of 200 ms produced episodes of
repetitions for the control group which ranged from 2 (N51),
to 15 (N52). The mean number of repetitions was 7, with a
standard deviation of 5.72. The experimental group had
repetitions at this temporal level, which ranged from 6

(D53) to 12 (052), with a mean of 7.7 and SE 3.09.

At 200 ms, the mean number of repetitions for the

control and the experimental groups were nearly equal
(7:7.7). At 300 ms delayed auditory feedback, the number
of repetitions for the control group ranged from 6 (N53),
to 12 (N52). The mean for this group was 8.7, with a
standard error of 2.49. The number of repetitions for the
experimental group ranged from 7 (D51), to 24 for D52 and
20 for DS3. The mean number of repetitions at the above

temporal delay was 17, with one standard error of 7.26.

Delayed auditory feedback of 400 ms produced number of
repetitions which ranged from 6 (N53) to 12 (N52). At
300 ms the mean number of repetitions for the control
group was 8.7, compared to 17 for the experimental group.
The mean number of repetitions for control group at 400 ms
delayed auditory feedback was 9.3 with a standard error of
2.49. The experimental group had episodes of repetitions

which ranged from 8 (051) to 13 (D52). The mean number of

 

 

repetitions for this group was 10, with a standard error of
2.16. At 400 ms, the mean number of repetitions for the
control group was 9.3 compared to 10 for the experimental

group.

At 500 ms delayed auditory feedback level, the number of
repetitions for the control group ranged from 4 (N53) to 8
(N52) and 7 (N52). The mean for this group was 6.3, with a
standard error of 1.7. The experimental group at the above
temporal delay exhibited episodes of repetitions which
ranged from 11 (D53) to 14 (D51) and 12 (D52). The mean
number of repetitions for this group was 12.3, with one
standard error of 1.23. The mean number of repetitions at
delayed auditory feedback of 500 ms was 6.3 compared to 12.3

for the experimental group.

Figure IV—12 shows the number of repetitions including
standard error for the normal and dyslexic readers. It
shows a nearly flat configuration for the control group,
with a sharp uni-modal peak at 300 ms for the experimental

group. This was reflected in their slower reading rates

at 300 ms.

 

 

118
Episodes of Prolongations Under the Effects of DAF
Tables IV—13A and IV—13B show the mean number of
prolongations at delayed auditory feedback levels of 50,
100, 200, 300, 400 and 500 ms for the control and the
experimental groups. Figure IV—13 shows the graph of
prolongations under DAF. Delay of 50 ms produced number
of prolongations which ranged from 7 (N53) to 13 (N51).
The mean number of prolongations were 10, with a standard
error of 2.45. For the dyslexic group, the number
prolongations ranged from 25 (D51) to 40 (D53). The mean
was 33, with a standard error of 6.16. At 50 ms delay,
the mean number of prolongations for the control group

was 10, compared to 33 for the experimental group.

At 100 ms delay, the number of prolongations for the
control group ranged from 8 (N53) to 16 (N52). The mean
was 11 with a standard error of 3.40. For the
experimental group, the number of prolongations at this
level were 43 for D51, to 44 for D52 and D53, respectively.
The mean for this group was 44, with a standard error of
0.47. At 100 ms delayed auditory feedback, the mean number
of prolongations for the control group was 11, compared to

44 for the experimental group-

Feedback delay of 200 ms produced prolongations which ranged
from 7 (N53) to 20 (N51) for the control group. The mean was

14, with one standard error of 5.35.

 

 

 

119

Figure IV—13: Graph for the number of prolongations
for the control (open circles) and
experimental group (closed circles).
NR and DR denote normal and dyslexic
readers, respectively. Circles
without the error bars indicate that
the standard error of the mean was

was too small to be represented on

the graph.

 

 

 

 

 

PROLONGATIONS (EPISODES)

50
45

40

L24
UT

<II|IIIIIIIrTIIIlIlIIIIIIIIllIIIIlIIIIlITITIITII

3O

25

20

IO

U'l

120

DAF — PROLONGATIONS

 

 

LL14!IJIQIIIJLIIIIIIIJLLIIf

O

‘ I

I‘VIIIIIUI’lIrIIlTI

II II I I
ONR
.DR

/\/%\H ‘

IOO

 

200 300 400 500 500
WME(MS)

 

 

Table IV—13A

121

Episodes of Prolongations Under the Effects of DAF

Control Group

Delay Time in M5

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

I I
{Subject _ 53 _100 ___EEE__ 300 400 500 { i
{N51 13 1o 20 9 11 8 { I
{N52 10 16 15 10 13 10 {
{N83 7 8 — 7 13 __ 9 9 {
{Mean 10 11 __ 14 11 11 9 {
{SE 2.45 3.40 5.35 1.7 1.63 0.82 {
' —_ — — - I
Table IV‘lBB
Episodes of Prolongations Under the Effects of DAF
Experimental Group
Delay Time in MS
I ____________ _ __.
{Subject 50 100 200 300 400 500 {
g... g. "7;" I; 31 15 17 {
{D82 34 44 30 45 32 37 {
{D83 40 44 31 37 30 __27—_-{
{N;;;—__-——-_—33 —————— 44 —————— 25 38 26 _ 27 {
{SE 6.16 0.47 _6t98 5.73 7.59 8.16 {
I
I

122

For the dyslexic group, the number of prolongations was from
13 (D51) to 30 and 31 for (D52) and (D53), respectively. The
mean number of prolongations was 25, with a standard error
of 6.98. The fewer number of prolongations for the
experimental group increased the reading rates at 200 ms. At
200 ms delayed auditory feedback, the mean number of
repetitions for the control group was 14, compared to 25 for

the experimental group.

At the 300 ms level, the number of prolongations for the
control group ranged from 9 (N51) to 13 (N53). The mean was
11 with a standard error of 1.7. For the experimental group
the same delay produced prolongations which ranged from 31
(D51) to 45 (D52). The mean number of prolongations was 38,
and a standard error of 5.73. At delay of 300 ms, the mean
number of prolongations for the control group was 11,

compared to 38 for the experimental group.

The delayed auditory feedback at 400 ms produced
prolongations which ranged from 9 (N53) to 13 (N52). The
mean was 11, and the standard error was 1.63. The
experimental group had episodes of prolongations which
ranged from 15 (D51) to 32 (D52). The mean was 26 and
standard error was 7.59. The mean number of prolongations
for the control group at 400 ms delay was 11, compared to

26 for the experimental group.

 

 

 

123

The delay of 500 ms gave a mean of 9 (S.E. 0.82) for the
normal group. The prolongations ranged from 8 (N51) to 10
(N52). The experimental group had a mean of 27 and a
standard error of 8.16. The number of prolongations ranged
from 17 (D51) to 37 (D52). The mean number of prolongations
for the control group at delayed auditory feedback of 500 ms

was 9, compared to 27 for the experimental group.

Figure IV—13 shows a comparative graph for the episodes of
prolongations between the control and the experimental
groups. The normal readers exhibit a flat curve, whereas
the dyslexic readers have bi~modal peaks at the delay

segments of 100 and 300 ms.

Tests of Statistical Sigmificance

The sample size dictated the use of non—parametric
statistical test of significance. Mann—Whitney U—Test was
used to measure the level of statistical significance.
This test took into account the difference of reading
rates at 0 ms delayed auditory feedback and different
temporal delays. Kendall’s Coefficient of Concordance was
used to obtain values of W indicating agreement among
judges who scored the reading rates, repetitions and

prolongations.

 

 

 

 

124
Reading rates
Mann—Whitney U—Test was used to test the level of
significance. The U1 for control group was 228 and U2 for
the experimental group was 96. At an alpha of 0.025 on a
one-tailed level of significance or 0.05 on a two—tailed
level of significance, the values for U were greater than
value of U2. Therefore, the null hypothesis was rejected
at an alpha level of 0.05. Thus, it can be said that this
group of normal readers and dyslexic readers did not
represent the same population. Delayed auditory feedback
affected the reading rates of dyslexic readers more than
the normal readers. These differences were statistically

significant at an alpha level of 0.05.

Test for Correlation

Kendall's Coefficient of Concordance gave values for W
which were highly significant at 50 ms (.95), and 300 ms
(.97), with perfect accord at 100 and 500 ms (1), with
above average values of significance at 200 ms (.87) and
at 400 ms (.78). This is indicative of high agreement

between the judges in terms of assessing reading rates.

Repetitions

The critical values obtained for U at an alpha of 0.25,
were greater than those obtained for U2 (81). The null
hYpothesis was therefore rejected. This sample of normal

readers and dyslexic came from different populations.

 

 

 

125
Delayed auditory feedback caused statistically greater
number of repetitions in the experimental group than in the
control group. These differences were statistically

significant at an alpha level of 0.025.

Test for Correlation

Kendall’s Co—efficient of Concordance Test yielded a value
of W (.81) at DAF of 50 ms and 200 ms (.79) which were
greater than the norms given indicating high agreement
among judges. However, at 100 ms the agreement between
judges was significant at a 20 % level and at 10 % level
at 300 ms as indicated by values for W which were (.54)
and (.77) respectively. At 400 ms, the value for W
indicated poor accord among judges (.34); but at 500 ms, the
value of W was greater than the values given by Kendall at
5, 10 and 20 % level of significance. It must be stressed
-again, that values closer to (1) signify high agreement,

whereas those closer to (0) indicate low agreement.

Prolongations At an alpha level of 0.002, the critical
values obtained for U were greater than U2 (8). The null
hypothesis was rejected in favor of the alternate, that
these two samples of normal and dyslexic readers did not
represent the same population. The number of prolongations
were greater for dyslexic than normal readers at different
temporal delays. These differences were statistically

significant at an alpha level of 0.002.

 

 

 

 

126

Test for Corrrelation

Kendall's Co-efficient for Concordance gave values for W
which were highly significant at 50 ms (.83), 200 ms (.87)
and at 500 ms (.88). These values indicate high agreement
between judges. The values of W at 100 ms (.66), at 300 ms
(.74) and at 400 ms (.76) were significant at 5, 10 and 20 %
level. All values obtained were closer to (1) than (0)

indicating high level of agreement among judges.

Summary

In summary, the results of Auditory Brain-stem Responses

 

in terms of absolute latencies for waves I, V, VI and VII
did not reveal significant differences between the normal
readers and the dyslexic readers. All the differences
fell within one standard error. The same was true for

inter-peak latencies between waves I—V, V—VI and V-VII.

However, statistically significant differences emerged
between the control and experimental groups under the
effects of delayed auditory feedback. The statistical
analysis for the reading rates at different delays showed
significant differences between the two groups for an

alpha level of 0.05. These differences indicate that the
experimental group was more affected by the delayed auditory

feedback than the control group.

 

The normal readers were significantly affected by delayed
auditory feedback up to 200 ms. Beyond this temporal
segment, the delay did not have significant effect upon
them. Their reading rates curve (standard error) shows a

uni-modal pattern.

The reading impaired group continued to be affected by
delays beyond 200 ms, and their reading rate curve

(standard error) reveals a bi—modal pattern. For the
control group, the number of repetitions did not reveal a
significant difference between subjects. Graph IV~12 with
means and standard error shows a nearly flat configuration.
The mean number of repetitions was nearly the same at 50 and
100 ms for the control group (3.7 and 3.0). However,
comparisons between groups revealed that the number of
repetitions were nearly twice at delay of 50 and 100 ms, and
300 and 400 ms. The number of repetitions remained nearly
the same at 200 ms (7 & 7.7) and 400 ms (9.3 & 10) for the

control and experimental group, respectively.

For the experimental group, the graph reveals a sharp
increase in number of repetitions at 300 ms. There were
statistically significant differences between the two

groups at an alpha level of 0.025. The standard error

 

128

graph for prolongations for the control group had a nearly
flat configuration. However, the dyslexic group had bi—
modal pattern for the graph of prolongations. The peaks
or periods of maximum number of prolongations corresponded
to the delay periods where the reading rates were
significantly low. Based upon the above results, the
control and eXperimental groups were differentially
affected by the temporal delays of auditory feedback at
every observed temporal delay. The experimental group was
more significantly affected by the delayed auditory

feedback than the control group.

 

 

129
Chapter V
DISCUSSION
The human auditory system was investigated for possible
relation with dyslexia in three children with suspected

dyslexia and three normal readers without dyslexia. The

integrity of the peripheral auditory system was assessed by

 

using otoscopy, tympanometry, stapedial reflex testing and
standard audiometry using pure tones and speech stimuli.
The ABR was used as an index of electrOphysiologic
functioning. The results indicate that the peripheral

auditory mechanisms are not implicated in reading disorders.

Analysis of ABR waves I—VII showed no significant
differences between the control and experimental groups.
The results suggest that dyslexic readers in this study
had efficient neuronal transmission from first order
neurons of the auditory nerve to the primary auditory
cortex (Stockard and Rossiter, 1977). Thus, brain stem
and up to the primary auditory cortex are not involved in
reading disorders manifested in the three dyslexic

subjects tested by ABR in the present study.

 

130
Delayed auditory feedback during reading tasks, however,
revealed significant differences between the two groups at
temporal delays of 50, 100, 200, 300, 400 and 500 ms.
These delays slowed the reading rates and increased
dysfluencies as measured by the number of repetitions and

prolongations.

The following sections discuss the implications of the three
parameters of oral reading i.e. visual integration,
phonological decoding and oral production of words under the
influence of delayed auditory feedback for understanding
reading disorders. Included in the discussion is how the

three parameters are affected by delayed auditory feedback.

Effects of Delayed Auditory Feedback Upon Reading Rates
The results show that the control group had lowest reading

rates at a temporal delay of 200 ms and that their reading

rates improved beyond that delay.

The dyslexic readers, however, had two segments of reduced
reading rates. The first segment was at 100 ms, and the
second at 300 ms. Contrary to the normal readers, their
reading rates actually improved at 200 ms. This implies
that these readers were affected most by the delayed
auditory feedback in visual processing segment of words

and their grapheme to phoneme correspondence. The fact

 

 

 

 

 

 

131

that they continued to be affected by later delays lends

 

strength to the proposition that dyslexic readers required
longer processing time compared to the normal readers. It
is well known that oral reading involves both visual and

auditory integration (Geshwind, 1972). It requires

 

approximately 200 ms for visual integration, one word
processed during each fixation (Joula et al., 1982:
Lovegrove, 1993). Auditory integration is also completed

by 200 ms (Durrant and Lovirinic, 1984). The fact that the
reading rates of the control group were low at DAF of 50 and

100 ms and lowest at 200 ms implies that the DAF may have

 

interfered with their visual processing strategy. For
normal readers, feature detection (Kimura, 1993) and
phonological decoding operate simultaneously (Baddley, 1978).
If this is true, then the greatest reduction at 200 ms could
be attributed to the DAF affecting phonological decoding

processes in the Wernicke's area.

The experimental group had problems with phonological

decoding of words and were mainly sight readers. They

 

showed greater mean reduction in reading rates at DAF of
50 ms than the control group compared to reading rates at
0 delayed auditory feedback. However, at 100 ms, the
experimental group had the lowest mean reading rate.

This implies that DAF at 100 ms may have interferred with
the early visual processing. Unlike the control group, the

reading rates of dyslexic readers improved at 200 ms and did

 

 

 

 

 

132

not maintain a plateau effect at later delays. In fact, the
mean reading rates at DAF of 300 ms were similar to those at
100 ms. For the normal readers, the temporal delays beyond
200 ms remained nearly the same, whereas the dyslexic
readers continued to be affected by the later delays. This
indicates perhaps that the processing of visual material
continued beyond 200 ms for the dyslexic group. In other
words, the dyslexic readers may have required more
processing time compared to the normal readers. Thus the
results indicate that the reading material is processed
differently by the dyslexic readers when compared to the

normal readers.

Effects of Delayed Auditory Feedback Upon Repetitions

The delayed auditory feedback caused repetitions of
phonemes or whole words such as articles in both the
control and experimental groups. What is interesting is
the fact that the number of repetitions do not complement
the reading rates under different levels of DAF. For the
control group, the least number of repetitions occured at
feedback delays of 50 and 100 ms. The largest number of
repetitions occurred at 400 ms despite the fact that the
reading rates at 400 and 500 ms had reached a plateau
effect. Contrary to expectations, the number of repetitions

were not the greatest at 200 ms.

 

 

 

 

 

 

133
Thus, episodes of repetitions did not complement the reading
rates under different temporal delays for the control group.
For the experimental group however, the first segment with
reduced reading rates (100 ms) produced the least number of
repetitions, whereas the second segment (300 ms) produced

the greatest number of repetitions. It can be stated that

 

the parameters responsible for repetitions in the two

segments were not related to each other.

Interestingly, even though the reading rates did not level

off at later delays of 400 and 500 ms, the number of

 

repetitions nearly did. The experimental group was affected
nearly three times as much as the control group by DAF at

50 ms, and twice as much at delays of 100 ms, 300 ms, and
500 ms. The least number of repetitions occurred at a DAF

of 100 and 200 ms for the experimental group.

Bakker et al. (1981) have classified dyslexia into two
types ~ P—type and L~type. The former according to them

exhibit primarily right hemisphere strategies for form

 

perception and grapheme to phoneme correspondence. The
P-type dyslexics are slow readers and exhibit greater number
of fragramentations, repetitions and prolongations. The
L~type dyslexic readers reveal left cerebral dominance, with
probably ambivalent control for form perception. The
reading style of L~type dyslexics is relatively fast, but

they make more substantative errors, omissions or additions.

 

 

 

134

The three dyslexic readers in my study exhibited problems
with phonological decoding and were mainly sight readers.
Their reading strategies were similar to the P~type
dyslexics described by Bakker (1981) and their problems
with phonology categorizes them as dysphonetic dyslexics

of Boder (1973).

Syllabic repetition was attributed by Lee (1951) to
involuntary forces. He did not observe any phonemic

repetition. In my study, both groups exhibited greater

 

number of mean repetitions at temporal delays of 300 ms
(dyslexic readers) and 400 ms (normal readers). This
could be due to reflexive motor interaction between the
sensory afferents receiving the delayed feedback and the

efferent system of motor control situated in Broca’s area.

Effects of Delayed Auditory Feedback Upon Prolongations

The number of prolongations complement the graph for reading
rates under the effects of delayed auditory feedback. The
control group had maximum mean number of prolongations at

200 ms and least at 500 ms. At precisely the same temporal
delays (100 and 300 ms) where the subjects in the
experimental group had the lowest reading rates, the number
of prolongations were greatest. This indicates that for
both groups, the reduced reading rates were directly related

to the increased number of prolongations.

135
The cortical areas involved in reading are also the ones
implicated in slurring or hesitations (Penfield and Roberts,
1959). The present study, the number of prolongations were
maximum in temporal areas of delayed feedback where the
reading rates were greatly reduced. 50 that the number of
prolongations contributed to reduced reading rates in both
groups under the influence of delayed auditory feedback. It
is thus hypothesized that DAF influenced the processing in
the cortical areas that are significant to reading in both

the control and experimental groups.

It could be that the processing was affected due to the
proximity of Heschl’s gyrus to Wernicke’s area, so that the
feedback reaching the former affected the linguistic
processing in the latter by causing an interference effect
at 200 ms for the control group and at 300 ms for the
experimental group. The increased number of prolongations
in the early visual processing segment for the experimental
group implies that delayed auditory feedback may have caused
interference in the visual processing in the dyslexic, but
not the control group. The fact that the control group
exhibited maximum prolongations and reduced reading at one
temporal parameter (200 ms) suggests that that particular
parameter was significant to the processing of reading
material for this group. This could be due to a direct
access route used by these readers from.word feature
detection to phonological and semantic access (Ostrosky~

Solis et al., 1987: Kimura 1993).

 

 

136
Comparison With Other DAF 5tudies_:
Black (1950) found increased intensity and duration of
phrases in 22 normal subjects reading under the influence of
DAF. Increased intensities were observed at feedback delays
beyond 200 ms, whereas the duration showed maximum increases
at 180 ms (slowest reading rate), with gradual decrease in
duration (recovery) beyond that point. The normal subjects
in my study exhibited lowest reading rates at 200 ms and
slight recovery beyond that point, a finding which

substantiates the findings of Black (1950).

 

Lee (1951) observed that under the effects of delayed
auditory feedback, normal readers speak like stutterers.
DAF causes normal readers to increase intensity, slow down
the rate of productions, halt or repeat syllables and
sentences. He found an absence of phonemic repetition in
his study. This is at variance with our observations.

The subjects in our study repeated phonemes and articles
and sometimes whole sentences. The latter, according to
Lee (1951), is voluntary and is exercised by subjects

under DAF for clarity.

Vrtunski et al. (1976) found duration of sentences to
nearly double in 10 left hemisphere damaged subjects
under the influence of delayed auditory feedback. The
dyslexic subjects in my study showed increases in number
of prolongations at temporal delays of delayed auditory

feedback where the reading rates were the slowest.

137
Fairbanks (1955) observed that 16 college students showed
reduced accuracy in reading, had greatest number of
articulatory errors on words, longest duration (slowest
speed), highest sound pressure and fundamental frequency
at delayed feedback of 200 ms. Articulatory errors and
increased duration were analyzed by the above researcher
as direct effects, and increase in fundamental frequency
and intensity were seen as indirect effects of delayed
auditory feedback. Our sample showed increased duration
(reduced reading rates) and greatest number of prolongations
at 200 ms for normal readers, but the DAF had opposite
effect for dyslexic readers. The number of repetitions and
prolongations for the experimental group were maximum at
300 ms. The control group had greatest number of
repetitions at 400 ms. 50 the repetitions did not slow them
down, but the prolongations did. These findings are at
variance with those of Jack and Herbert (1975) who found

error rates in spoken words to be nearly four times the

 

normal error rate at DAF of 120 ms in five dyslexic subjects

and ten normal readers.

Fairbanks and Guttman (1958) attributed an increase in
articulatory errors and duration as direct effects of DAF
and increase in intensity and frequency as indirect effects
of delayed auditory feedback. They found increased
duration, repetitions and articulatory errors at 200 ms in

16 normal readers.

 

 

 

138
The present study supports these observations. For normal
readers, the reading rates were lowest, and prolongations
were greatest at 200 ms. The number of repetitions were
maximum at 400 ms. Delayed auditory feedback affected
reading processes differently in normal and dyslexic
readers. This could be due the interference effect of
the DAF on visual processing in the primary segment of the
reading process or due to interference effect caused by
auditory afferent receptors in the Heschl’s gyrus with the
linguistic processes conducted in Wernicke’s area. The
proximity of these two areas in the temporal lobe bears
credence to this hypothesis (Geshwind, 1972; Pirozzolo,

1979).

In both groups a correlation exists between reduced
reading rates and prolongations. The increased mean
repetition in late segment at 300 ms could be due to
interference effects caused by auditory cortical afferents
in Heschl’s gyrus, decoding processes in wernicke’s area
and/or the efferent articulatory command center in Broca’s
area. The exact cause of repetitions is unknown (Kimura,
1993). Hutchinson et al. (1973) obtained lowest reading
rates and mean phonation times for normal speakers and
stutterers at 100 ms delay, with increased number of pauses
at 200 ms for both groups. In our study, this was true of

the reading impaired group which showed slowest reading

rates at 100 ms.

 

 

 

 

139

5mmmamy of Compined Effects

In summary, delayed auditory feedback affected the reading
rates of dyslexic readers more than it affected normal
readers. The reduced reading rates were due to increased

number of prolongations.

The repetition rates complemented the reading rates only
for delayed auditory feedback of 300 ms, where they were
greatest. This could be due to the interaction of
auditory sensory afferents and the motor efferent system.
The experimental group had enhanced reading rates at 200 ms
whereas the control group had the lowest reading rates at

this temporal delay.

The control group exhibited reduced reading rates between
50 to 200 ms, with greatest reduction at 100 and 200 ms.
The dyslexic readers showed excessive reduction at 50 and
100 ms, with recovery at 200 ms. All these parameters
fall well within the time frame for visual integration.

In other words, the readers see the word before they can
sound it out in reading. For the normal readers the
feature detection (Kimura, 1993) and phonological decoding

work simultaneously (Baddley, 1978).

This particular group of dyslexic readers relied more on

visual gestalt at the expense of phonological decoding.

 

 

140

The DAF interferred with the visual processing as is
evidenced by reduced reading rates and increased number of
prolongations at 50 and 100 ms for the experimental group.
The fact that prolongations increased as the reading rates
decreased for both groups indicates that the DAF affected
areas of significance in the reading processes and the

modes utilized.

The control group probably read by simultaneous feature
detection using semantic and phonological access (Kimura,
1993). They were greatly influenced by the DAF at 200 ms.
For the experimental group, the reading strategy may have
first involved independent feature detection. The fact
that DAF in early visual processing temporal frame
affected them the most at 100 ms leads one to suspect that
visual processing for these readers may be a totally a
disconnected phenomenon and that they could be utilizing
letter—by—letter identification strategy (Joula et al.,
1978). The reduction in reading rates, but increased
prolongations and repetitions under the influence of
delayed auditory feedback of 300 ms may imply that the
second stage of reading ~ phonological and semantic
assessment — may be taking place at a later temporal

delay for the dyslexic readers.

 

Various investigators have proposed different models of
processing used by dyslexic readers. Witelson (1977)
hypothesized about the lack of lateralization in dyslexic
readers. Coltheart (1980) has posited a bilateral
processing model for reading in deep dyslexia, with
feature detection in the right hemisphere with language
decoding and motor control in the left hemisphere.
Whether one or both hypotheses pertain to the experimental

group in this study is not now known.

 

142

CHAPTER VI

SUMMARY AND CONCLUSIONS

Oral reading is a visuo~auditory integrative process
(Orton, 1929). Graphemes are converted into their
meanings based upon their phonological and linguistic
familiarity, and then matched via auditory feedback for
correct production. A failure to do so results in
dyslexia (Orton, 1929). This cross modality integration

is a reflection of cerebral processing time which has not

 

been well studied (Merzenich et al., 1993). Geshwind
(1972) has outlined the processes involved in reading.
The visual features are first transferred to the primary
and secondary visual cortex, and then to the angular
gyrus. A semantic match between the visual features and
their phonological—semantic match is made in the
Wernicke’s area. The information is then conveyed to the

Broca’s area for motor activation of articulators.
Since oral reading involves the visual and auditory
integration, language processing and production, this

study was aimed at answering the following questions:

1. Are auditory brain—stem responses of children

 

manifesting dyslexia different from those of

normal reading children ?

143

2. What are the effects of Delayed Auditory Feedback on
(a) reading rates, (b) repetitions, (c)prolongations

between the dyslexic and non—dyslexic readers ?

To answer the first question, ABR responses were obtained
from three right—handed children aged 8 to 11 years
exhibiting dyslexia and three non—dyslexic children.

The intensity levels were 95, 105 and 115 dB P.E. SPL.
Clicks of alternating polarity were used and the gain was
set to 180,000 amplification. Three gold plated electrodes
were used. Gold plated electrodes were placed on areas of
head, Cz (vertex), FPz (forehead) and A1 and A2 (earlobes).
The data was stored and analyzed for absolute and inter—peak
latencies for waves I to VII for the right ear. In the
final analysis, only the ABR data for the right ear was

used.

The results indicate that there were no differences between
the dyslexic and non-dyslexic children in terms of absolute
and inter—peak latencies for waves I to VII. This may imply
an efficiency of neural transmission in this particular

group from the auditory nerve to higher auditory centers and

probably the thalamus (Stockard and Rossiter, 1977).

 

 

 

144
To answer the second question, DAF was administered to three
right—handed dyslexic and non—dyslexic children in the age
range of 8 to 11 years. Their oral productions were
amplified and replayed back to them via earphones at
randomized temporal delays of 50, 100, 200, 300, 400 and
500 ms. Their readings were taped and analyzed for reading
rates, number of repetitions and prolongations. The control
group read passages from the Bader Language Test Battery at
their grade level, whereas the experimental group read

passages two to three levels below their grade level.

 

Delayed auditory feedback affected the control and
experimental groups differently. Statistically significant
differences emerged between the two groups on the Mann —
Whitney U—Test. An alpha level of 0.05 revealed significant
differences between the two groups for reading rates,
whereas alpha levels of 0.025 and 0.002 showed statistical
differences between the two groups in terms of repetitions

and prolongations, respectively.

The normal readers were most affected by delayed auditory

feedback at 200 ms, whereas the dyslexic readers continued

 

to be affected by the later delay parameters. The results
of this study indicate that central processes could be
implicated in dyslexia. Delayed auditory feedback, a tool
which has been used effectively on stutterers, seems to

cause differences between the normal and dyslexic readers in

 

 

145

terms of reading rates, repetitions and prolongations. This
test, which has proved valuable previously (Black 1951:
Vrtunski 1976; Kavik et al., 1991), has proved to be a

valuable tool for this study.

DAF increased the number of repetitions and prolongations in
dyslexic readers. The number of prolongations may have

contributed to the reduced reading rates in the experimental
group but not in the control group. The temporal delays at

which the reading rates were lowest also produced maximum

 

number of prolongations in the dyslexic readers. The fact
that these readers showed an increase in the number of
repetitions and prolongations at 300 ms delay indicates that
they may have used a different reading strategy compared to
the non—dyslexic readers. DAF continued to affect the
dyslexic readers at later temporal delays which may also

reveal longer processing time required by these readers.

The applicability of DAF as an investigative tool is
supported by this study. Advancements in the field of
acoustics has led to development of equipment which is
superior by far compared to the ones used by earlier
researchers. The reduction of echo, standardization of tape
speeds, and stereophonic amplification systems have reduced

the number of variables and increased the validity of DAF

 

tests.

 

146
Suggestions for Future Research:
1. Dyslexia is not a homogenous entity and should not
be treated as such. It should be treated as a syndrome
(Ramaa, 1993). A thorough investigation of reading
strategies of subjects is pre—requisite before more

definitive conclusions can be made.

2. Lateralization studies should be conducted using
EEG, magnetic resonance techniques during the reading
process to investigate the contributions of both

hemispheres during reading.

3. Further studies need to be conducted using delayed
auditory feedback involving uni—lateral or bi—lateral
feedback during the reading process involving, a larger

sample group than was used in the present study.

4. Further research should be conducted on reading
impaired children who fail to visually differentiate

between words.

5. P300 latencies should be checked during reading
visually similar words (photo/phono) with one presented
as the odd-ball stimulus or a semantically meaningful
word paired with a visually similar non-word. Little
research has been done in this field using linguistic

stimuli.

 

 

 

 

 

147

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APPENDIX

 

 

 

 

 

APP

 

APPENDIX A:

162

Samples of Reading Materials
from Bader Reading and
Language Inventory (1983).

 

 

 

 

Here is a story a

One I
tainside
of a CH
flutter:
When‘
its bor
pain 8
eyes (
eyésg

the y

And

feath

tend

and

Comprehensi:

\ Who
\ WheI
K WhaI

- How

\- Wha
arro

\ Wha
'tok

\ Why

was

 

 

I

{ 163

I Here is a story about an Indian boy. 5th C (p. 141)
I

WAUKEWA'S EAGLE

I One morning when the boy called Waukewa was hunting along the moun-

 

 

I tainside, he found a young eagle with-a broken wing. It was lying at the base 33:30?

I b I A ES:

I ‘ - , .
of a cliff. The bird had fallen from a ledge and, being too young to fly, had Egsymm s

 

fluttered down the cliff. It was hUrt so severely that it was likely to die.

 

When Waukewa saw it, he was about to drive one of. his sharp arrows through
its body. But then he saw that the young eagleat his feet was quivering with
pain and fright. Waukewa slowly stooped over the panting eaglet. The wild

eyes of the wounded bird and the keen, dark eyes of the boy met. The boy’s

 

eyes grew gentler and softer as he gazed at the bird. Then the struggling of
the young eagle-stopped. The wild, frightened look passed out (if its eyes.-
And the bird allowed Waukewa'fto pass his- hand gently over its ruffled
feathers. The desire to fight, to defend-Its life, gave .way to the charm of the
tendernessand pity expressed in the boy’s eyes. From-that mo’ment'Waukewa

and the eagle were friends. (192 words)

Comprehension Questions

 

__ Who was Waukewa? (an Indian boy)
__ Where did he find the eagle? (at the base of a cliff)
__ What injury did the eaglet have when Waukewa found it? (broken wire)

 

__ How was the eagle’s wing broken? (in a fall)

__ What was Waukewa going to do to the eagle when he first saw it? (kill him -- put an
arrow through his body)

__ What made Waukewa change his mind about killing the bird? (he decided he wanted
- to keep the bird himself)

__ Why did the eagle decide not to fight and defend his life? (he realized that the boy
was not going to hurt him)

85

 

 

Here is a stc

loo?
1 h
kel

“P

Unpromp'

Please re
_— sa
‘ w

“.81

Interp

Memc

 

164

Here is a story about an old man. 1A (p. 131)

GIVE ME ROOM

I saw an old man get on the bus. He walked very slowly. He used a cane. I

 

 

looked at the cane with surprise. The man had a bike horn on it. I told him GRADED
. PASSAGES:
I had never seen a_'cane with a horn. “Have you ever been to the city mar- Eggymm's

 

ket?” he asked. I said that I had. “Then you know it is crowded,” he said.

 

“People did not give me room. Now I honk my horn and they move.” .

(81 words)

Unprompted Memories Comprehension Questions

I . _ Please retell the story. __ Who did the person see? (an old man)

I __ saw old man on bus _. What was the old man doing? (riding a bus)
I __ walked slowly using cane __ Describe the old man. (walked slow)
I

__ surprised at horn on cane (used a cane)

 

__.__ never saw a cane with horn __ Why was the person surprised? (had a horn
_ been to market, he asked? on a cane)

. __ What did the person say to the old man?
__ said yes

(never saw a cane with a horn on it before)
__ it is crowded, he said

_____ What caused the problem for the old man?
__ people didn’t give me room (crowded market) '

_ now honks and they move __ Why did the person understand the problem
at the market? (he had been there)

 

.... Why did he use a born? (to get people to
move)

Interpretive question: Why did peOple move when he honked?

Acceptable answer: Yes No

 

 

Memories: __ Un prompted

 

Prompted Organized retelling: ___ Yes No

 

65

 

 

 

Here is a story at

Isabel
blue car
“Corr
had big
was hu
“1 v
black

Tht

Unprompted I

Please retel
_ Isabe

‘ on 5?
car

‘ con
, N kitt
- big
K be
E Iv

His:

Interpr

Memo

165

Here is a story about a kitten and a girl named Isabel. 1C (p. 129)

ISABEL AND THE KITTEN

Isabel saw a kitten. It was on the side of the street. It was sitting under a
blue car.

“Come here, little kitten,” Isabel said. The kitten looked up at Isabel. It
had big yellow eyes. Isabel took her from under the car. She saw that her leg
was hurt.

“I will take care of you,” Isabel said. She put her hand on the kitten’s soft,
black fur. “You can come home with me.”

The kitten gave a happy meow. (80 words)

Unprompted Memories ‘ Comprehension Questions

Please retell the story. __ What did Isabel see? (kitten)

 

 

 

 

 

 

_ Isabel put hand on fur saw it was hurt? (I will take care of you)

 

come home with me

__ kitten meowed happily (take it home)

Isabel saw kitten __ Where was the kitten? (side of street)
on side of the street/under (under car) .
car __ What did Isabel first say to the kitten? (come
come here, Isabel said here, little kitten)
__ kitten looked up ____ What did the kitten look like? (yellow eyes)
' big yellow eyes, black fur __ (black fur)
her legxwas hurt ;_ What was the matter with the kitten? (hurt
__ I will take care of you leg)

__ What did Isabel say to the kitten when she

__ What did Isabel want to do with the kitten?

___ What did the kitten do? (meowed happily)

Interpretive question: Why was the kitten happy at the end of the story?

Acceptable answer: Yes

 

 

Memories: Unprompted __ Prompted Organized retelling: __ Yes

 

 

 

 

 

No

No

 

 

GRADED
PASSAGES:
EXAMINER'S
COPY

 

 

61

 

Here is a :

Unpromp

Please re
R Li
N Ill
\ h:

\h:

 

166

Here is a story about a little frog. ' 2C (p 132)

. -THE SONG QF LITTLE FROG
Little Frog lived by a lake. He did not have many things. He only had a

 

 

house to live in, a bed to sleep in, and an old pot to cook with. He had one GRADED
PASSAGES:
old book that he read again and again. Still Little Frog was happy. Eg’w'mm's

 

 

Near his house there were many pretty flowers. The birds sang all day.
Little Frog liked to- look at the pretty flowers. He liked to hear~ the birds

sing. Little Frog wanted to sing like the birds. But when he tried to sing, all

 

 

that came out wasa ribbit ribbit. (99 words)
Unprompted Memories Comprehension Questions
Please retell the story. __ Where did Little Frog live? (by a lake)
__ Little Frog (in a house)
lived by a lake __ What did he own? (pot)
__ had a house, bed, and pot __ (bed)
_ had an old book __ Why did he read the same book? (only had

one book)
__ How did Little Frog feel? (happy)

__ What things were near his house? (flowers)

read again and again

 

near house flowers, birds

 

__ he wanted to

 

sing like birds (birds)

when he tried __ Why did he like the birds? (they sang)
‘ . . . . . __ What happened when he tried to sing?

Just ribbit ribbit (ribbit ribbit)

 

Interpretive question: Why was Little Frog happy with just a few things?

Acceptable answer: No

Yes

 

 

Yes No

 

 

Un prom pted Prompted Organized retelling:

 

Memories:

 

67

 

I-v.. .3

 

I,
.3.
1‘ .

W.,

3'.. "'7' .

.,.. .~- t'u'r. .. ...,"

—~,~..‘ - Prrl _v
~ . .

u-pv .. v . ,

,h . "y\":1'~“'rrrA .

Y .rqw-ry‘vplrr.

_ _ ,5“, ...w r

 

.i<