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Abstract:

One must understand how, when, and why the brains of individuals with autism
are thrown off track during development. Identifying what goes awry in the
developing brain of children with autism is the first step.

The search for the brain basis of autism started out as a hunt for a particular
place in the brain where the problem could be located. Though the limbic system,
cerebellum and other structures showed abnormalities in some studies, these
findings were not always consistent or explanatory. Rather than any one
structure being affected, researchers now think that the defect may lie within the
neural circuitry, the way the brain is wired together. One critical link between
brain circuitry may be the increasingly replicated finding of larger brain size in
autism and increased white matter volume.

This paper will discuss specific brain structures, natural process of


communication and dysfunction of brain due to larger brain size and increased
white matter in autism and developmental language disorder.

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Introduction

Language is a system of communication in which ideas and feelings are encoded


into signals of sounds, gestures, signs, or marks that convey meaning within a
group or community.
Language consists of two components – words and grammar. A word is an
arbitrary association between a signal and a meaning. Grammar is a system that
specifies how words can be combined and how the meaning of a combination of
words can be determined.

Language Acquisition in Children

Humans are born with the ability to perceive the full range of phonemes (the
smallest unit of speech sound). Babies make language-like sounds at 5-7
months, babble in well-formed syllables at 7-8 months, and gibber in sentence-
like streams by 12 months. They can discriminate speech sounds, even ones not
used in their parents’ language, in their first months. By 10 months, they
discriminate only phonemes used by their parents. By age one, babies can begin
to comprehend words and have a 30-50 word vocabulary. By age three, children
speak in full sentences and have a rich vocabulary, but still have difficulty with
grammar. Older children build up understanding of grammatical structure, rather
than simply imitating the speech of others. By age 6, children comprehend about
13,000 words, and high school graduates know 60,000 words.
Language development in children led Noam Chomsky to hypothesize in the late
1950’s that the human brain has evolved an innate neural circuitry dedicated to
the acquisition of language. Some psychologists and linguists disagree, believing
that the capacity for language is one expression of a general cognitive ability to
learn patterns, rather than a specific system for language. Whichever view is
correct, it is clear that language is an ability that is both innate and learned.
There are no homolog to human language in other species of the animal
kingdom. The lack of animal models for language has limited our ability to
understand the neural basis of language. Consequently, most of our knowledge
about which brain regions are involved in
language processing and how they function derives from the description of
language disorders, or aphasias, caused by focal brain lesions, most frequently
stroke or head injury.

Specific brain structures and their functions:

The brain has many parts including the cerebral cortex, brain stem, and
cerebellum. There are four lobes in the cerebral cortex: Frontal lobe, Parietal
lobe, Temporal lobe, Occipital lobe. It is important to understand that the brain
functions as a whole by interrelating its component parts. Below is a list of
functions and deficits or problems revealed when injury occurs at particular
locations.

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CEREBRAL CORTEX

Frontal Lobe: Most anterior, right under the forehead.

Functions:

• How we know what we are doing within our environment (Consciousness).


How we initiate activity in response to our environment. Judgments we
make about what occurs in our daily activities. Controls our emotional
response. Controls our expressive language. Assigns meaning to the
words we choose. Involves word associations.
• Memory for habits and motor activities.

Observed Problems:

• Loss of simple movement of various body parts (Paralysis). Inability to


plan a sequence of complex movements needed to complete multi-
stepped tasks, such as making coffee (Sequencing). Loss of spontaneity
in interacting with others. Loss of flexibility in thinking. Persistence of a
single thought (Perseveration). Inability to focus on task (Attending).
Mood changes (Emotionally Labile). Changes in social behavior.
Changes in personality. Difficulty with problem solving.
• Inablility to express language (Broca's Aphasia).

Parietal Lobe: near the back and top of the head.Functions:

• Location for visual attention. Location for touch perception. Goal directed
voluntary movements. Manipulation of objects.
• Integration of different senses that allows for understanding a single
concept.

Observed Problems:

• Inability to attend to more than one object at a time. Inability to name an


object (Anomia). Inability to locate the words for writing (Agraphia).
Problems with reading (Alexia). Difficulty with drawing objects. Difficulty in
distinguishing left from right. Difficulty with doing mathematics
(Dyscalculia). Lack of awareness of certain body parts and/or
surrounding space (Apraxia) that leads to difficulties in self-care. Inability
to focus visual attention.
• Difficulties with eye and hand coordination.

Occipital Lobes: Most posterior, at the back of the head.Functions:

• Vision

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Observed Problems:

• Defects in vision (Visual Field Cuts). Difficulty with locating objects in


environment. Difficulty with identifying colors (Color Agnosia). Production
of hallucinations Visual illusions - inaccurately seeing objects. Word
blindness - inability to recognize words. Difficulty in recognizing drawn
objects. Inability to recognize the movement of an object (Movement
Agnosia).
• Difficulties with reading and writing.

Temporal Lobes: Side of head above ears.Functions:

• Hearing ability Memory aquisition Some visual perceptions


• Catagorization of objects.

Observed Problems:

• Difficulty in recognizing faces (Prosopagnosia). Difficulty in


understanding spoken words (Wernicke's Aphasia). Disturbance with
selective attention to what we see and hear. Difficulty with identification of,
and verbalization about objects. Short-term memory loss. Interference with
long-term memory Increased or decreased interest in sexual behavior.
Inability to catagorize objects (Catagorization). Right lobe damage can
cause persistant talking.
• Increased aggressive behavior.

Relation between language and brain:

Currently there is more work and less agreement in neurolinguistics. The results
of neuropsychophysiological research investigations are often contradictory. To
make a comparison of these studies which generally lack uniformity is an
exacting task.
The studies differ in terms of the variables under examination, experimental
tasks, methodological procedures, criteria for subject selection, measures
employed for testing, scoring and analysis, etc. Occasionally even with uniformity
in the above, the results are conflicting.
The major causative factor for the disagreement and conflicting results could be
the lack of amenability of brain processes to experimental control. Experimental
control is very easily exercised, in comparison, on environmental variables.
Accordingly, in spite of vast and intensive research and consequent varied
evidence, it is still very difficult to conclude as to what part of the brain controls
and to what extent, a certain human behaviour such as language.
Also this non-agreement on the morphology of the cortical structures and the
functions subserved by them is an indication of the very complexity of the human
behaviour, in relation to its neurophysiology. This has led to Whitaker's (Whitaker

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1971) observation that the only thing that is certain is that language is
represented in brain. Research in science, however, does not stop at these
uncertainties and it should go on, with empirical data and systematic exploration
towards controlled generalizable interpretations, with the hope that at one time in
the not so distant future the studies would have covered the major steps towards
the ultimate truth.
There is a great amount of literature, rapidly expanding too, on the maturation of
the central nervous system focusing on the ontogeny of speech and language.
Language is said to be lateralized to one of the hemispheres and, more
commonly, to the left than to the right hemisphere.
Various tests are availed to determine the dominant hemisphere for language
processing. Some of them include reaction time studies, dichotic listening tests,
tachistoscopic viewing technique, the wada technique, etc. Averaged evoked
potential techniques have also been added to the repertory. Biochemical,
electrophysiological and morphological criteria are all availed of to draw
interpretations concerning the neuropsychophysiology of language.

Language Components and Human Brain:


It is generally observed that the different levels or components of language are
differentially distributed in brain with respect to their structure and function
(Whitaker 1978).
Various localizationistic and functional models of brain have proposed. The
recent view is indicative of a combined approach. It has been found that different
parts of the brain, each small in area, subserve a particular function and that
damage to certain areas of the brain result in certain deficits in language
functioning.
The different cortical structures contribute differently to total language
performance. Whitaker (1978) terms it as "performance grammar", the
components of which are differentially distributed in the brain. A small area in the
brain subserves several functions and a single function is contributed by a
number of such small areas.
This simple observation would indicate the intricacy and the complexity of the
brain mechanism in relation to human behavior.
Small areas in frontal, parietal, temporal and occipital lobes are responsible
together for language function and most part of the cortex does not contribute to
performance grammar. The classical zones like Broca's and Wernicke's areas,
supramarginal gyrus, angular gyrus and other motor and sensory cortical
structures are responsible for functions like speech, audition, reading, writing,
etc.
The evidence for differential distribution of language components comes from
studies on individuals with brain damage who exhibit a dissociated linguistic
disability. Some present a linguistic picture of deficient performance at the
syntactic level and/or at the semantic level or at the lexical level where the

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problem may be either in the use of content words or function words depending
on some crucial factors.
Any modality or language skill among the four important ones could be disturbed
at the central level. Even within the modalities, there might be a differential
picture of the two languages of a bilingual. For instance, within the broad
category of writing, an individual can present a dissociated disability between the
phonetically based writing systems and visually based one thus indicating a
differential localization of the two writing systems (Sasanuma, 1975).
There are cerebral Lateralization measures that suggest that asymmetry in
hemispheric dominance could be brought about by language-specific factors.
Particularly strong is the evidence that different orthographic system (Syllabic or
alphabetic versus ideographic) left to right versus right to left may enhance
different cerebral organization (Albert and Obler 1978).

Left versus right hemisphere:

The left hemisphere, rather than the right, is considered dominant for language
functions in majority of right handed humans, Schnitzer (1978) asserts that the
left hemisphere, rather than the right hemisphere, is endowed from birth with a
greater facility for learning certain crucial aspects of natural language.

Neuroanatomical evidence is offered by many for left hemisphere preference.


Geschwind and Levitsky (1968) report the presence of a larger temporal planum
(the area behind Heschl's gyrus) in contrast with the right temporal planum in
hundred adult brains. In addition, the neuroanatomical evidence for prenatal and
paranatal asymmetry has also been reported.

Wada, Clarke and Hamm (1975) find evidence of morphological asymmetry of


both the temporal planum and the frontal operculum (adjacent to Broca's area) in
the twenty-ninth week of gestation, when those of the left hemisphere are found
to be larger than those of right hemisphere in 90% of the adults and fetuses. This
has been supported by many, thus erasing the notion that Lateralization is a
function of language or that there is a strict cause and effect relationship between
the two.

In addition to such neuroanatomical asymmetry, behavioral asymmetry has


also been widely reported. Dennis and Whitaker (1976) studied the linguistic
abilities of 10 year old children with complete hemisphererctomy prior to 4 ½
months of age. The isolated normal left hemispheres and the isolated normal
right hemisphere of matched groups were compared along various phonological,
semantic and syntactic tasks. Syntax seemed to be the most affected in left
hemispherectonized individuals. On the basis of the findings it was concluded
that the right hemisphere was deficient in the following abilities:

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1. Understanding language auditorily especially when meaning was
conveyed by syntactic diversity.
2. Detecting and correcting error in surface structures.
3. Repeating stylistic variation of sentences.
4. Forming tag questions from presented statements.
5. Determining sentence implications.
6. Combining syntactic and semantic information for replacement of missing
pronoun, and
7. Judging the relationships among words in sentences.

It was noted that the right hemisphere was less endowed hierarchical abilities
rather than any lack in its conceptual and/or semantic abilities.

The right hemisphere was viewed as being holistic, spatial, gestalt, synthetic,
simultaneous, continuous, context dependent a positional and time independent
where as the left hemisphere is viewed as analytical, verbal, logical, sequential,
categorical, context independent, prepositional, time dependent by many
(Galloway 1981).

Schnitzer (1976) argues that phonology is not so closely embedded in language


structure as other linguistic aspects. This was in view of the finding that while
children learn or acquire language(s), they do so without a foreign accent
whereas most of the adults learning a second language would retain their mother
tongue accent in the newly acquired language. Schnitzer (1978) is also of the
opinion that, of all the linguistic components, phonology can be mastered by the
right hemisphere to a relatively comparable level as the left hemisphere. One can
infer from all these findings that right hemisphere is capable of processing some
of the crucial language aspects.

Lateralization of language processing:


Early studies of people with stroke or brain trauma found correlations between
patients’ language deficits and the brain areas that had been damaged,
determined by an autopsy at the time of death. These studies led to the
discovery that most language processing goes on in one hemisphere, called the
“dominant” hemisphere. In over 90% of people (98% in right-handed people and
about 65% of left-handed people) the left hemisphere processes grammar,
lexicon, phonetics, and speech production.

Lateralization of the brain:

The functional lateralization of the cerebral cortex was first suggested by


Geshwind and Levitsky (1968), who discovered that about 60% of human brains
display anatomical differences between the two hemispheres in the posterior
temporal lobe (the region which encompasses Wernicke’s area). In line with
these anatomical observations, language was the first function that was

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demonstrated to be lateralized in the human cerebral cortex. More recently,
various other anatomical and functional differences have been documented
between the two cerebral hemispheres.
The study of “split-brained” subjects in the late 20th century provided a great deal
of information on the specific roles of the two hemispheres. This condition results
from complete lesion of the corpus collosum, known as commissurotomy.
Because the collosum is severed, the two hemispheres can no longer
communicate with each other and there is no transfer of auditory, visual, or
sensory information from one hemisphere to the other. Commissurotomy is
sometimes the only treatment available for patients with intractable epilepsy. The
procedure can diminish the number and severity of the patients’ seizures.

The corpus collosum is essential for melding the actions of each hemisphere into
a unitary whole. Once the collosum is bisected, the hemispheres appear to act
independently. The study of this phenomenon has led to some surprising findings
in the field of perception and in trying to understand human consciousness. Split-
brain experiments often employ a tachistoscope, an instrument that presents
visual stimuli only to the patient’s left or right visual field (LVF or RVF,
respectively). Information about an image presented to the LVF of a split-brain
subject only reaches the RIGHT cerebral hemisphere, and vice versa. When the
image of an object is projected onto the RVF, the subject can easily name the
object because the information is accessible to the left, dominant, language
hemisphere. When the image is projected onto the LVF, the subject cannot
verbally identify it and may even deny ever seeing it - the language areas of the
left hemisphere are unaware of the image. However, the patient can readily
identify the object non-verbally, such as pointing to it with the left hand, or using
tactile cues to distinguish it from several other unseen objects. This suggests that
while the right hemisphere cannot talk, it is able to perceive, learn, remember,
and issue commands for motor tasks, even when the subject is not consciously
aware of these processes.

In another set of experiments, the split-brained patients’ ability to identify written


words was examined. Words presented to the RVF were easily read out loud. On
the other hand, the patients were unable to pronounce the word if it was
presented to the LVF. Interestingly, some patients could write words projected
onto the LVF, but not the RVF. This finding demonstrates that some people

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possess language skills in the right hemisphere, and that writing may require
non-dominant hemisphere skills such as creativity or artistic ability.

Language acquisition and critical period:

It is known that language acquisition is a natural process of mastering a


language that requires a certain level of cortical maturation and hemispheric
Lateralization, which in itself is an on going process. A biological barrier is
erected guiding the quality of language acquisition before and after the critical
period in specific ways.

Penfield and Roberts (1959) and Lenneberg (1967) conceived of Lateralization


as the dominance of the left hemisphere over the right (and in some, the reverse)
that place in the course of a chronological continuum and was completed within a
specific period. The process of Lateralization and the critical period were
considered simultaneous and both were considered to be conterminous around
puberty.

The age at which Lateralization takes place is still a matter of wide controversy.
One major record widely found is that Lateralization does take place in childhood.
One of the supporting notions is that cerebral Lateralization for language(s)
acquisition is not complete until the age of nine - twelve years (Penfield and
Roberts 1959). However, this has been widely refuted.

Lenneberg (1967) asserted that language Lateralization was complete by 11-14


years. Krashen (1973) cited evidence that language Lateralization was complete
by age four or five. Molfese (1972), and Molfese, Freeman and Palermo (1975)
found evidence to support that Lateralization took place at birth or even beyond.
Baser (1962) studied 102 cases of hemisplegia of early onset. He concluded that
language Lateralization occurred early, be it to the left or right, and that both the
hemispheres participated in language processing before the Lateralization was
complete.

Thus, the only certainty until now, and the traditional view, was jeopardized with
the advent of the proposal that Lateralization was present by birth. This fact
would cut at the roof of the simultaneity notion of Lateralization and critical
period. Lateralization, if present at birth, would, thus remain independent of the
so called critical period.

Critical Period:

Critical period was viewed as the congenial period for language acquisition when
the child's brain is highly receptive and plastic. However, this traditional idea of
the critical period is undergoing a radical change with the advent of recent
studies which argue that there are multiple critical periods instead of only one.

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Those critical periods are actually states of plasticity of cortical structures for
acquisition of certain functions.

The new interpretation (Seliger, 1978) given to the Lateralization and critical
period concepts is that Lateralization is a continuing process which stretches
much beyond the time span specified by Lenneberg (1967) and others.

In this interpretation, the term "critical period" refers to the gradual loss of
plasticity in various parts of the brain for different functions over most of one's life
time. In this light, Lateralization effects are those of both intra and
interhemispheric nature. The evidence for Seliger's (Seliger 1978), multiple
critical period hypothesis stemmed from age dependent aphasia and universal
second language inabilities which were taken to be indicative of both the state of
localization process and the gradual loss of plasticity.

Plasticity

According to Schnitzer (1978), although upto some point of development, the


brain is "plastic" and "transfer" from left hemisphere to the right hemisphere is not
done as proficiently as it is done by the intact left hemisphere. Schnitzer further
remarked that although the brain is lateralized for language functions from before
birth, it is relatively "plastic" for the first 5 years of life so that language could be
shifted to the contralateral hemisphere in the event of neuropathology during this
period. He later again asserted that the brain is never completely "plastic".

What Can We Infer From These Studies?

One may infer from the majority of the studies that traces of Lateralization are
present prior to or at birth and that the brain is more plastic in the first few years
of life than later to the extent that cortical structures can change and assume a
function different from the originally intended ones in the event of pathology to
the predetermined areas in the cortex and perform well, though not to the same
extent managed by left hemisphere. Disuse of certain areas for a long time would
naturally preclude the revival of the functions to the original extent. Thus,
probably, the previously uncommitted or differently committed right hemisphere
could be less capacitated to start all over again with a new function. However, we
notice in normal right hemisphere dominant individuals from birth that there is
normal performance equivalent to the left hemisphere functioning.

Literacy Skills

Literacy (reading and writing) skills are said to enhance left hemisphere
dominance. Even in an adult second language learner the left hemisphere might
play a major role although in the initial stages the right hemisphere may
participate. State of acquisition, manner and modality of acquisition are observed

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to be important variables in the cerebral organization of L2 in the adult second
language learning (Galloway 1981).

A controlled comparison of child and adult second language performances would


yield some information on the strategies adopted and the cerebral organization in
second language performance. A comparison of matched groups with and
without current formal schooling (where reading and writing skills are
emphasized) would also help in this venture to understand the extent of
contribution of literacy factor in hemispheric Lateralization.

The Wernicke-Geschwind model of language comprehension


and speech production

The other major discovery revealed by study of patients with aphasias was that
two cerebral cortical areas – Broca’s area in the lateral frontal lobe and
Wernicke’s area in the posterior superior temporal lobe – are major neural
substrates of language. A useful, if somewhat simplified, model for understanding
how the two language areas interact is the Wernicke-Geschwind model. This
model has been quite successful in predicting the effects of damage in several
brain regions and how visual information is processed in naming an object.

The model posits that Broca’s area, which is connected to regions of motor
cortex that control the face and tongue, is involved in planning the motor
execution of speech, and that Wernicke’s area, which is connected to auditory
cortex, is involved in recognizing and representing the sound pattern of words.
Within this model, the arcuate fasciculus is a unidirectional pathway that brings
information from Wernicke’s area to Broca’s area.
According to the Wernicke-Geschwind model, there is a clear, linear flow of
information through these two cortical areas for the recognition and production of
speech. Wernicke’s area contains the auditory codes for words - what they sound
like Broca’s area contains the articulatory codes for words - the motor commands
that tell the mouth and larynx how to articulate each word. The behavior of
repeating a spoken word exemplifies how the Wernicke-Geschwind model
understand language processing. When a spoken word is heard, the sound is
processed in auditory cortex and then transmitted to Wernicke's area.

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There the sound is matched to its auditory code, and it’s meaning can be
interpreted by other association areas of the cerebral cortex. The auditory code
is transmitted to Broca's area through the arcuate fasciculus, where the
articulatory code for the word is activated and sent to motor cortex for speech
production.
Reading comprehension also requires Wernicke’s area in the Wernicke-
Geschwind model. Visual information is sent to the angular gyrus which
translates the visual code to a form accessible by Wernicke’s area. Wernicke’s
area then matches the word to its auditory code, as for spoken speech. Thus,
according to this model, reading requires the phonological recoding of words in
Wernicke’s area.

The Wernicke-Geschwind model provided a framework for understanding the


neural mechanisms of the aphasias. Patients with damage to Broca’s areas
cannot produce speech, but they can still comprehend speech because
Wernicke's area is intact. Damage to Wernicke's area, on the other hand,
produces no problems in speech production because Broca’a area is unaffected,
but the meaning of the speech of others is improperly understood, and the
patient’s own speech has virtually no meaning.

Other brain areas and pathways involved in language

Despite its success predicting clinical outcomes, the Wernicke-Geschwind model


has significant limitations. New lesion studies, research in neuropsychology and

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linguistics, functional imaging (PET, fMRI), and direct neural recording
techniques (event-related electrical potentials, direct intraoperative recordings
from human cerebral cortex) have better defined the brain areas and pathways
involved in language processing.

It is now clear that there is a direct connection between the parieto-occipito-


temporal association cortices and Broca’s area. These pathways are involved in
the understanding and repetition of written language (i.e., visual recognition).
Thus, read words do not need to be transformed into auditory representations.
Instead, Broca’s area and other higher order association areas can handle this
information directly.
In addition, while Broca’s and Wernicke’s areas are important structures for
language, they do not operate independently for language production and
comprehension to the extent hypothesized in the Wernicke-Geschwind model.
The arcuate fasciculus is in fact a bidirectional pathway that connects Broca’s
and Wernicke’s areas to many other regions of cortex in the dominant
hemisphere. The prefrontal, premotor, and supplementary motor cortices in the
frontal lobes are necessary for higher order aspects of speech planning and
production, and for proper syntax of language comprehension and production.
Some areas of insular cortex are also related to speech articulation.
Wernicke’s area has reciprocal connections with the supramarginal and angular
gyri of the parietal lobe as well as with areas in the temporal lobe in the dominant
hemisphere. These regions are important for language comprehension, and also
participate in the mapping of the sounds of words to their meanings. The angular
gyrus in the language dominant hemisphere contributes to the understanding of
written language. Finally, several sub-cortical structures, such as the thalamus
and basal ganglia of the dominant hemisphere, are also critical for language
processing.

The non-dominant language hemisphere is also involved in many aspects of


language. Lesion studies and studies in split-brain patients reveal that the non-
dominant hemisphere can understand many words and can take on responsibility
for many aspects of language in children with damage to the dominant
hemisphere. In normal function, the non-dominant language hemisphere
participates in the emotional aspects of comprehension and speech production
(e.g., inflections, tone of voice, timing) and in the pragmatics of language (e.g.,
contextually appropriate speech). It has been suggested that the non-dominant
hemisphere codes information in a more general way, representing the overall
structure of a stimulus.

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FIG: Pathways involved in language

For instance, the right hemisphere is involved in determining if a statement is


funny, which involves analyzing the content of that statement as a whole rather
than the individual words.

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WHAT IS AUTISM?

Autism is one of the autism spectrum disorders, a group of conditions that vary in
their severity and the age at which a child first may show symptoms. Autism
spectrum disorders fall under a broader category known as pervasive
developmental disorders (PDDs). PDDs cause delays in many areas of childhood
development, such as the development of skills to communicate and interact
socially.

Autism typically is diagnosed during a child’s second year and is lifelong,


although symptoms may lessen over time. There is no cure for autism, but
appropriate treatments can help a child develop life skills to function more
independently.

Autism and developmental language disorder (DLD) are both behaviorally


defined disorders that emerge in early childhood. Both involve language
impairment, and autism additionally involves impaired social reciprocity as well
as repetitive or restricted behaviors (American Psychiatric Association, 1994;
Rapin and Dunn, 2003; Rapin et al., 2003).

How does autism affect communication?

The word “autism” has its origin in the Greek word “autos,” which means “self.”
Children with autism often are self-absorbed and seem to exist in a private world
where they are unable to successfully communicate and interact with others.
Children with autism may have difficulty developing language skills and
understanding what others say to them. They also may have difficulty
communicating nonverbally, such as through hand gestures, eye contact, and
facial expressions.

Not every child with an autism spectrum disorder will have a language problem.
A child’s ability to communicate will vary, depending upon his or her intellectual
and social development. Some children with autism may be unable to speak.
Others may have rich vocabularies and be able to talk about specific subjects in
great detail. Most children with autism have little or no problem pronouncing
words. The majority, however, have difficulty using language effectively,
especially when they talk to other people. Many have problems with the meaning
and rhythm of words and sentences. They also may be unable to understand
body language and the nuances of vocal tones.

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Below are some patterns of language use and behaviors that are often found in
children with autism.

• Repetitive or rigid language: Often, children with autism who can speak
will say things that have no meaning or that seem out of context in
conversations with others. For example, a child may count from one to five
repeatedly. Or a child may continuously repeat words he or she has
heard, a condition called echolalia. Immediate echolalia occurs when the
child repeats words someone has just said. For example, the child may
respond to a question by asking the same question. In delayed echolalia,
the child will repeat words heard at an earlier time. The child may say “Do
you want something to drink?” whenever he or she asks for a drink.

Some children with autism speak in a high-pitched or singsong voice or


use robot-like speech. Other children with autism may use stock phrases
to start a conversation. For example, a child may say “My name is Tom,”
even when he talks with friends or family. Still others may repeat what
they hear on television programs or commercials.

• Narrow interests and exceptional abilities: Some children may be able


to deliver an in-depth monologue about a topic that holds their interest,
even though they may not be able to carry on a two-way conversation
about the same topic. Others have musical talents or an advanced ability
to count and do math calculations. Approximately 10 percent of children
with autism show “savant” skills, or extremely high abilities in such as
calendar calculation, music, or math.

• Uneven language development: Many children with autism develop


some speech and language skills, but not to a normal level of ability, and
their progress is usually uneven. For example, they may develop a strong
vocabulary in a particular area of interest very quickly. Many children have
good memories for information just heard or seen. Some children may be
able to read words before 5 years of age, but they may not comprehend
what they have read. They often do not respond to the speech of others
and may not respond to their own names. As a result, children with autism
sometimes are mistakenly thought to have a hearing problem.

• Poor nonverbal conversation skills: Children with autism often are


unable to use gestures—such as pointing to an object—to give meaning to
their speech. They often avoid eye contact, which can make them seem
rude, uninterested, or inattentive. Without meaningful gestures or the
language to communicate, many children with autism become frustrated in
their attempts to make their feelings and needs known. They may act out
their frustrations through vocal outbursts or other inappropriate behaviors.

In autism there is increasing evidence that the disorder is associated with a


tendency towards large brain volume in childhood (Bailey et al., 1998;

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Fombonne, 2000; Aylward et al., 2002), driven predominantly by increased
white matter (Courchesne et al., 2003; Herbert et al., 2003a).

In DLD, brain investigations have largely focused on language regions of the


brain, although the few published whole-brain morphometric studies include
some reports of increased brain volume in this disorder as well (Filipek et al,.
1992; Woodhouse et al,. 1996; Herbert et al,. 2003b).

Working in the laboratory on a series of brains of children with autism and


DLD has identified multiple similarities between these two groups, though with
modest differences in degree: both share a pervasive morphometric anomaly-
notably, larger than normal brain and white matter volumes- but it is more
pronounced in autism (Herbert et al,. 2004). The white matter enlargement is
non uniformly disturbed, involving sub cortical radiate white matter but
sparing the corpus collosum (Herbert et al,. 2004). Thus, the volume
comprising intrahemispheric connection is disproportionately enlarged
compared to intrahemispheric white matter, and this may have an impact on
brain asymmetry.

Data are drawn from a comprehensive researched study of a segmentation of


the entire brain and a parcellation of the cerebral cortex, allowing analyses at
multiple nested anatomical levels. First, they examined large-scale patterns of
asymmetry in the hemispheres, in the principal grey and white matter
structures of the brain, in the cerebral lobular partitions and in aggregated
cortical parcellation units (PUs). Secondly, because they parcellated the entire
cortex, they were able to explore asymmetries in groupings of PUs
approximating the primary sensorimotor cortex, unimodal association cortex
and higher-order association cortex. It has been proposed that more complex
processing is impaired in autism (Minshew et al., 1997), and that rapid
processing is impaired in DLD (Benasich and Tallal, 2002). Association cortex
may provide an anatomical correlate for complex or rapid processing
impairments in these disorders. The hypothesis is that because cortical
components of neural systems with greater interconnectivity are likely to be
preferentially affected by abnormalities of white matter, one should therefore

17
see greater differences from controls in volume asymmetry in higher-order
association cortex. In addition, because language impairments are found in
both autism and DLD, they also looked for differences among groups in a
subset of association cortex PUs that are considered to be involved in
language functions. Since these brains are the products of atypical
development, it may be that functional divisions will differ from controls in
unknown ways, or that anatomical underpinnings of abnormalities in complex
processing (including language) may involve widely distributed circuit-
disrupting abnormalities. They therefore performed a comparison of
asymmetry patterns across the entire cerebral cortex, and hypothesized that
these three groups would differ from each other at this level. This study is thus
the first comprehensive whole-brain survey of volume asymmetry in high-
functioning autism and DLD.

Result:

To determine whether differences in asymmetry between autistic, DLD and


control boys were specific to PU involved in associational processing, the PU
were classified according to general functional type. Based on previously
published PU classifications (Rademacher et al., 1992), researchers were
able to classify 40 of the PUs as being predominantly (i) primary sensory or
motor cortex (six PUs), (ii) unimodal association cortex (17 PUs) or (iii) higher-
order association cortex (17 PUs). The remaining eight PUs could not be
clearly classified because of overlapping functions within the defined
boundaries of the PUs.

Analyses of asymmetry were performed for anatomical regions in a nested


hierarchy that included (i) total brain volume, (ii) all segmented divisions of
total brain volume (cerebral cortex, cerebral white matter, cerebellum,
caudate, globus pallidus–putamen, diencephalon, brainstem), (iii) lobes of the
cerebral cortex (derived by grouping cortical PUs according to lobe) and (iv)
individual cortical PUs for the entire cerebral cortex. A symmetry index was
calculated for anatomical units at each of these levels. To classify each
structure as being significantly left- or right-asymmetrical, one-sample
Student's t tests were used to assess the probability that the mean SI for each
segmented structure or PU was non-zero (i.e. significantly asymmetrical).
Since these one-sample tests were used only for general classification,
adjustments for multiple comparisons were not performed. For those
structures with significant asymmetry, the sign of the asymmetry index
determined classification as left-asymmetrical or right-asymmetrical.
Structures or PUs for which the one-sample t-test was not significant were
classified as being symmetrical.

18
Fig. Asymmetries of segmented structures. The x axis indicates percentage asymmetry to
the left or the right. *Asymmetry is significantly different from zero.

A GLM-CD (General linear models for correlated data) showed significant


overall differences between autistic, DLD and control boys regarding
asymmetry in language-related cortical areas.

When language-related PUs were removed from the two significant models,
the omnibus group difference was no longer significant for unimodal PUs,
while the overall group difference remained significant for higher-order PUs,
albeit to a lesser degree of significance.

In this whole-brain evaluation of cortical asymmetries in high-functioning boys


with autism and DLD, the main findings are that patterns of cerebral symmetry
are closely similar in the brains of autistic children and children with DLD, but
differ substantially from brains of controls. Thus, in neither autism nor DLD is
there asymmetry at the levels of major grey and white regions or the cerebral
cortical lobes. However, nested within their overall and lobar cortical lack of
asymmetry, in both autistic and DLD samples we see a substantial increase
compared with controls in the aggregate amount of cortical PU asymmetry. In
particular, right-asymmetrical cortex is substantially increased in autism and
DLD; at the same time, while there is a decrease in the volume of left-
asymmetrical cortex in DLD, there is no such loss relative to controls in the

19
autistic brains. This leads to a similar reversal of the right : left cerebral cortex
asymmetry ratio in the autistic and DLD samples compared with the controls.

Regarding the regional distribution of cortical asymmetry alterations,


researchers found that there are significant differences among the groups in
unimodal and higher-order association cortex, but not in primary sensory-
motor cortex. Language-related cortical PUs appear to drive the differences at
the level of unimodal association cortex, while higher-order association cortex
differences are more robust, showing differences beyond those PUs
considered to be related to language function. They also found that in their
patterns of significant asymmetry throughout the cerebral cortex, children with
autism or DLD differed from controls but were very similar to each other.

These findings invite several observations. First, researchers see an intriguing


disconnection in the asymmetry findings between the different levels of
analysis, asymmetries being increasingly masked as the size of the units of
analysis increases. Secondly, while the increase in rightward asymmetry is in
keeping with prior reported findings, the increase in total asymmetry of
aggregated cortical PUs is different from the loss of asymmetry that has been
commonly reported and that we have found at our larger-unit levels of
analysis. Finally, the differences from controls are not only more pronounced
in higher-order association areas but also for the most part the same in both
autism and DLD groups. If the widespread atypical asymmetries found in
these two disorders were not so similar, the perturbations outside of language
areas might be dismissed as random, or as ‘fluctuating asymmetry’
(Rasmuson, 2002). That the two samples are so similar not only implies a
relationship between these disorders, but also suggests that these changes
reflect systematic and similar alterations in neural systems. The widely
distributed significant asymmetry shifts in these two groups of brains may also
indicate that meaningful asymmetries are widespread in the cerebral cortex.

The loss of overall asymmetry of total cerebral cortex in autism and DLD, as
measured by grey–white segmentation, may in fact be consistent with the
gain in aggregate asymmetry of the cerebral cortex when it is subdivided into
PUs. The autism and DLD brains showed an increase in the number (and
volume) of cortical PUs with rightward asymmetry, but at the same time they
showed either no loss (autism) or only a small loss (DLD) in the number (and
volume) of cortical PUs with leftward asymmetry. The combined effect
appears to be that the increase in rightward cortical asymmetry in autism and
DLD has cancelled out the leftward asymmetry, so that the cortex taken as a
whole (in the segmentation measure) appears symmetrical.

Resting regional cerebral blood flow asymmetry was shifted from


predominantly left to predominantly right in both an autistic (Chiron et al.,
1995) and a dysphasic(childhood speech disorder) group (Chiron et al., 1999).
However, this ratio shift had a different origin in each group. In the autism

20
group this reversal of the right : left ratio was driven by regional cerebral blood
flow that was no different from controls on the right but diminished on the left,
while in the dysphasia group the left regional cerebral blood flow was largely
unchanged while the right was increased. There thus appears to be less
overall cerebral blood flow in the autistic sample and more in the dysphasic
one. In the findings we currently report, the shift in right : left ratios of volume
asymmetry is driven wholly in autism and predominantly in DLD by an
increase in aggregate volume of asymmetrical PUs on the right. If the volume
asymmetries similar to the ones we report here were present in subjects from
both groups in the studies by Chiron, this would suggest that volume and
metabolic rates have a different relationship in dysphasia than in autism.

Widespread abnormalities in white matter, connectivity and asymmetry may


relate to the functional abnormalities in autism and DLD, but because they do
not understand the mechanisms by which these anatomical changes may
exert their functional impacts, researchers do not assume that there is a direct
correlation between the magnitude of anatomical changes and the magnitude
of functional impact. In DLD, where asymmetry in language regions has
received greater study, the existence or magnitude of asymmetry has not
correlated consistently with diagnosis (Gauger et al., 1997; Preis et al., 1998).
In the face of more widespread asymmetry abnormalities that go beyond
regions associated with the deficits specifically characterizing either disorder,
formulating the possible significance of such widespread changes would
minimally require systematic correlation with behavioural data that goes
beyond the scope of this paper. However, researchers would argue that it also
and more fundamentally requires going beneath the defining behavioral
features of the disorders.

From a cognitive neuroscience vantage point, the behaviours and deficits that
define autism and DLD may be surface manifestations of underlying
processing abnormalities (Morton and Frith, 1995; Belmonte et al., 2004). It
has been proposed that the features of the autistic behavioural phenotype
emerge from an underlying deficit that can be characterized as ‘weak central
coherence’ (Shah and Frith, 1993) or a ‘generalized impairment in complex
processing’ (Minshew et al., 1997), and that the language as well as the wide-
ranging though subtle non-language impairments (Bishop, 2002; Kail, 1994) in
DLD may arise from an underlying pervasive processing disorder (Kail, 1994;
Johnston et al., 1997). While the presence of language abnormalities in both
disorders and the behavioral and social interaction impairments additionally
found in autism (American Psychiatric Association, 1994 Rapin and Dunn,
2003; Rapin et al., 2003) have invited a search for underlying focal brain
abnormalities, the regional anatomical abnormalities that have been reported
are not consistently replicated, while increased brain volume, which has been
found frequently, challenges modular approaches to structure–function
correlation (Herbert, in press). It may be that volume and white matter
increases are anatomical correlates of underlying processing abnormalities.

21
The tissue abnormalities leading to increased white matter volume could lead
to suboptimal connectivity, and this could in turn lead to poor coordination
among individual components of neural circuits, resulting in pervasive
processing abnormalities (Just et al., 2004). Because higher-order
associational activity involves greater integration than unimodal associational
processing, areas with greater interconnections would, in this model, have
heightened vulnerability to connectivity abnormalities.

Cortical areas related to language function are embedded in the unimodal and
higher-order association areas that showed significant differences in their
analysis. It may thus be the case that language functions are not specifically
targeted by the underlying pathogenesis in either disorder, but rather are
prominently affected because they are so highly reliant on associational
processing (Mesulam, 1998). It may also be the case that the functions of
social interaction and behaviour additionally impaired in autism are similarly
vulnerable because of their dependence on complex associational
processing. If this is the case, then since the behavioural abnormalities would
eventuate from systems perturbations rather than only from focal
disturbances, the magnitude of asymmetries in individual PUs may be less
salient regarding functional significance.

There is a further temporal component of vulnerability: the brain and white


matter enlargement found in both groups appears to occur substantially
postnatal. This postnatal growth pattern has been documented for autism
(Lainhart et al., 1997; Courchesne et al., 2003), and it may be inferred for
DLD as well, since in both the autism and DLD samples, white matter
enlargement is not only present (Herbert et al., 2003a, b) but is greater in
areas that myelinate later (Herbert et al., 2004). These abnormal volumes and
growth trajectories may create pressures towards asymmetry that amplify
over time.

Thus, while the increased number of cortical regions with rightward


asymmetry may have significant consequences in terms of altered
functionality, this phenomenon may not be primary in terms of pathogenesis.
Altered cortical asymmetries may instead emerge as a response or adaptation
to an abnormal brain and white matter growth trajectory. While increased
volume and its associated dysfunctional connectivity may together lead to
greater lateralization, the increased and aberrant lateralization may then
further degrade the functioning of the cortical networks that already, due to
white matter abnormalities, have suboptimal connectivity.

The asymmetry alterations researchers report, seen in the context of the


volume changes they accompany, may thus be the consequence of a positive
feedback loop: increased volume results from white matter tissue changes
that may impair connectivity, favoring lateralization and local processing.
Moreover, the volume increase itself may on its own create a bias towards

22
lateralization. These two dynamics may in turn combine to promote a
progressive divergence from the norm regarding functions requiring
associational activity. Such divergence may lead to processing and
localization that are dysfunctional, and that in turn feed back into and amplify
the ongoing dynamics. Added to this mix, and perhaps driving it, at least in
part, may be abnormal or noisy neuronal activity (Rubenstein and Merzenich,
2003) that their data cannot address.

While researchers' multivariate analysis found that differences among the


groups were most robust in higher-order association areas, their analysis
provided a lens into the pervasiveness of the asymmetry alterations, both in
showing that they are widely similar between autism and DLD, and in showing
that they go beyond our initial functional classifications. These widespread
alterations in anatomical asymmetry suggest that neural systems disruption in
these disorders is pervasive, rather than limited to functionally relevant
circuits. In this light, the instances of atypical functional localization that have
been documented, such as in autism where the fusiform face area may
(Hadjikhani et al., 2004) or may not (Schultz et al., 2000; Pierce et al., 2001)
activate normally for face processing, may actually be parts of more
widespread but largely not yet identified neural systems abnormalities
(Belmonte and Yurgelun-Todd, 2003; Hadjikhani et al., 2004; Herbert et al.,
2004). The variable but common presence of additional non-language-based
neurological and processing abnormalities such as clumsiness (Trauner et al.,
2000; Hill, 2001; Hardan et al., 2003; Herbert et al., 2003a, b; Rubenstein and
Merzenich, 2003), often seen in these two groups, may be further
consequences of these widespread abnormalities, and in that light not purely
coincidental. Given these anatomical and processing abnormalities, one
would predict that functional imaging or electrophysiological measures
sensitive to altered timing would find reduced coordination among regions.
This has been addressed theoretically (Brock et al., 2002) and documented in
a few metabolic and functional studies in autism (Horwitz et al., 1988;
Belmonte and Yurgelun-Todd 2003; Castelli et al., 2002; Luna et al., 2002).

The microanatomical underpinnings of grossly measurable cortical


asymmetries have been the subject of an increasing body of research, but
these studies have mainly focused on language regions, where differences in
cytoarchitectural organization appear to be related to asymmetries in cortical
processing capacities (Anderson et al., 1999; Hutsler, 2003; Hutsler and
Galuske, 2003). Researchers' findings demonstrate asymmetries in cortical
PUs that are not only widely but also similarly (and hence probably
systematically) distributed throughout the brain in two separate samples. This
may suggest functionally meaningful hemispheric differences in cortical
microstructure in brain regions other than those that are associated with
language. Even though these increased and shifted asymmetries could also
be dysfunctional (Escalante-Mead et al., 2003), their apparent systematic
distribution remains of interest.

23
cognitive abnormalities, many of which resemble mild forms of autistic
features (Bishop & Rosenbloom, 1987). Abnormal patterns of hemispherical
asymmetry have been suspected in autism, and early work hypothesized left
hemisphere dysfunction due to the language deficits involved. However, as in
semantic-pragmatic disorder, it is delay in language development and
abnormal use of language that characterize communication in autism, and the
condition can be found in the presence of relatively intact language form.
Autistic children show deficits in the areas of prosody, the social use of
language and the ability to read emotional expression in language. To the
extent to which these functions are lateralized in normal adults, it is the right
hemisphere, and not the left, that is involved (Prior & Bradshaw, 1979;
Springer & Deutsch, 1989). Fein, Humes, Kaplan, Lucci and Waterhouse
(1984) argued that language deficits are not primary in autism, and that many
of the characteristic social-affective abnormalities can more plausibly be
linked with right hemisphere deficits. Goodman (1989) considered the relative
contribution of the two cerebral hemispheres to the features of autism and
Asperger's syndrome, noting that language in such individuals is deviant in
the domains of pragmatics and prosody. He suggests that innate deficits in
the expression and comprehension of non-verbal communication could
underpin social/play impairment, and that this 'blindness to the subjective'
could correspond, from a cognitive point of view, to lack of a 'theory of mind'
(Frith, 1989).

Damage to the right hemisphere which is suffered early in life, or inherited,


gives rise to a similar constellation of deficits characterised by emotional and
interpersonal difficulties, shyness, visuospatial difficulties, and inadequate
paralinguistic communicative abilities. These patients lack eye contact and do
not use normal prosody or gesture. They perform worse on aurally presented
story recall tests than on paired associative learning tasks (Weintraub &
Mesulam, 1983; Voeller, 1986). Weintraub and Mesulam (1983, p.468) feel
that:

the integrity of the right hemisphere may be essential for the emergence of
interpersonal skills and of what Rymes (1971) has labelled communicative
competence'. It is possible that among the population of children who show
deficiencies in interpersonal skills there may be some whose symptoms have
a neurologic rather than an emotional or social basis.

Another condition around which debate continues about the possible effects
of cortical hemisphere function is that of dyslexia. Theories put forward
include a lack of cerebral dominance for language, a maturational lag in such
dominance, a left hemisphere deficit or interference in left hemisphere
functioning by the right hemisphere. Dyslexic children have difficulty in
decoding the form of written language, but have a normal ability to extract
meaning from text. In contrast, some children from both the semantic-
pragmatic disorder group and the autistic group have been observed to show

24
'hyperlexia', where tests such as the Neale Analysis of Reading Ability (Neale,
1958) reveal their good scores for reading accuracy, accompanied by poor
scores for reading comprehension. The autistic children had no decoding
problem, but failed to use semantic context in the absence of syntactic cues.
This failure could not be attributed to a failure of semantic access to individual
words, nor to a syntactic failure. This tendency to ignore context (to be field
dependent) had been noted in other cognitive tasks (Shah & Frith, 1983) and
seemed to be a general characteristic of their behaviour. Their failure in
reading for meaning could be seen as related to their failure in making use of
redundancy (Hermelin & O'Connor, 1970; Hermelin & Frith, 1971), yet there
seemed to be no problem in making use of the context for processing syntax.

The hypothesis of a failure to make use of redundancy has been suggested to


explain many of the handicaps of autistic children (Aurnhammer-Frith, 1969;
Hermelin & Frith, 1971). This notion of use of redundancy relates closely to
notions of use of context in perception and especially in reading (Frith &
Snowling, 1983).

Sperber and Wilson (1986) proposed the theory of relevance, which has been
used to explain the communication difficulties of autism. The communication
difficulties displayed by both some patients with acquired right hemisphere
lesions and children with semantic-pragmatic language disorder indicate a
failure to understand the processes of inference. These patients can cope
with the encoding and decoding aspects of communication, and can extract
meaning from the basic sound (or letter) patterns of speech (or writing), but
they are unable to deduce the speaker's informative intention so as to bridge
the gap between the 'surface' meaning of sentences and the 'deeper'
meaning of the thoughts conveyed by those sentences.

Our knowledge of the contributions of the right cerebral hemisphere to


communication is, as yet, incomplete. It is, however, clear from the study of
patients with acquired right hemisphere lesions that communication skills can
be impaired following right hemisphere damage. Such patients seem to have
an abnormal cognitive style which reflects an inability to integrate multimodal
perceptual information. This cognitive difficulty reveals itself in their
communication, which tends to be fluent and grammatical, but irrelevant, with
stereotyped utterances and over-literal interpretations.

Their difficulties lie in comprehending the deeper realms of meaning, and in


making use of paralinguistic features. Gardner's description (Gardner, 1975,
p.296) of the abnormal cognitive style of patients with acquired right
hemisphere lesions could be a description of semantic-pragmatic disorder:

the patient appears unconcerned about his message; insensitive to his


situation, or to the environment; resembling a language machine, a talking
computer that decodes literally, gives the most immediate response -

25
insensitive to the ideas behind the questions or to the implications of the
questions.

Myers (1984) concludes that this disruption in cognitive style, the inability to
use visual imagery, the inability to understand figurative language, the altered
affect and the abnormal sense of humour together influence the way patients
look at the world, the way they integrate what they see and hear, and the way
they respond.

Conclusion:

Though it is reported that the autistic children have some abnormalities in


their cortical asymmetry in the brain, still the researchers need to study the
causes of autism. With more research, scientists hope to learn precisely how
differences in the structures and processes of the brain contribute DLD and
autism , and how these differences might be treated or prevented.

Temple Grandin: “As a person with autism I want to emphasize the


importance of developing the child’s talents. Skills are often uneven in autism,
and a child may be good at one thing and poor at another. I had talents in
drawing, and these talents later developed into a career in designing cattle
handling systems for major beef companies. Too often there is too much
emphasis on the deficits and not enough emphasis on the talents. Abilities in
children with autism will vary greatly, and many individuals will function at a
lower level than me. However, developing talents and improving skills will
benefit all. If a child becomes fixated on trains, then use the great motivation
of that fixation to motivate learning other skills. For example, use a book

26
about trains to teach reading, use calculating the speed of a train to teach
math, and encourage an interest in history by studying the history of the
railroads.”

Autism is not resulted from cursing rather they are called GIFTED. So each
and everyone of the society should take care of them and show the
INDIFFERENT respect to them.

----THANK YOU----

References:

Oxford Journal : A journal of neurology; Brain Vol. 128 No. 1


Guarantors of Brain 2004.

Links used : http://www.universaltheory.org/QuantumBrain.html


http://www.learner.org/discoveringpsychology/06/e0
6expand.html
http://www.waiting.com/brainfunction.html#anchor31
8669
http://www.childdevelopmentinfo.com/development/
piaget.shtml
http://www.sagepub.com/garrettbb2study/animation
s/9.23.htm
http://www.autismspeaks.org/science/research/initiat
ives/white_matter_story.php

Psychology and Language: Clark. Herbert. H and Clark. Eve. V.

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