Brain's disfunction in autism and DLD

8/9/2019 Brain's disfunction in autism and DLD

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Abstract:

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

The search for the brain basis of autism started out as a hunt for a particularplace in the brain where the problem could be located. Though the limbic system,cerebellum and other structures showed abnormalities in some studies, thesefindings were not always consistent or explanatory. Rather than any onestructure being affected, researchers now think that the defect may lie within theneural circuitry, the way the brain is wired together. One critical link betweenbrain circuitry may be the increasingly replicated finding of larger brain size inautism 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 increasedwhite matter in autism and developmental language disorder.

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Introduction

Language is a system of communication in which ideas and feelings are encodedinto signals of sounds, gestures, signs, or marks that convey meaning within agroup or community.

Language consists of two components words and grammar. A word is anarbitrary association between a signal and a meaning. Grammar is a system thatspecifies how words can be combined and how the meaning of a combination ofwords can be determined.

Language Acquisition in Children

Humans are born with the ability to perceive the full range of phonemes (thesmallest unit of speech sound). Babies make language-like sounds at 5-7months, 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, theydiscriminate only phonemes used by their parents. By age one, babies can beginto comprehend words and have a 30-50 word vocabulary. By age three, childrenspeak in full sentences and have a rich vocabulary, but still have difficulty withgrammar. Older children build up understanding of grammatical structure, ratherthan simply imitating the speech of others. By age 6, children comprehend about13,000 words, and high school graduates know 60,000 words.Language development in children led Noam Chomsky to hypothesize in the late1950s that the human brain has evolved an innate neural circuitry dedicated tothe acquisition of language. Some psychologists and linguists disagree, believingthat the capacity for language is one expression of a general cognitive ability to

learn patterns, rather than a specific system for language. Whichever view iscorrect, 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 animalkingdom. The lack of animal models for language has limited our ability tounderstand the neural basis of language. Consequently, most of our knowledgeabout which brain regions are involved inlanguage processing and how they function derives from the description oflanguage disorders, or aphasias, caused by focal brain lesions, most frequentlystroke or head injury.

Specific brain structures and their functions:

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

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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 wemake about what occurs in our daily activities. Controls our emotionalresponse. Controls our expressive language. Assigns meaning to thewords 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 spontaneityin interacting with others. Loss of flexibility in thinking. Persistence of asingle 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 anobject (Anomia). Inability to locate the words for writing (Agraphia).Problems with reading (Alexia). Difficulty with drawing objects. Difficulty indistinguishing 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. Inabilityto 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 inenvironment. Difficulty with identifying colors (Color Agnosia). Productionof hallucinations Visual illusions - inaccurately seeing objects. Word

blindness - inability to recognize words. Difficulty in recognizing drawnobjects. Inability to recognize the movement of an object (MovementAgnosia).

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

Increased aggressive behavior.

Relation between language and brain:

Currently there is more work and less agreement in neurolinguistics. The resultsof neuropsychophysiological research investigations are often contradictory. Tomake a comparison of these studies which generally lack uniformity is anexacting task.The studies differ in terms of the variables under examination, experimentaltasks, methodological procedures, criteria for subject selection, measuresemployed for testing, scoring and analysis, etc. Occasionally even with uniformityin 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. Experimentalcontrol is very easily exercised, in comparison, on environmental variables.Accordingly, in spite of vast and intensive research and consequent variedevidence, it is still very difficult to conclude as to what part of the brain controlsand to what extent, a certain human behaviour such as language.Also this non-agreement on the morphology of the cortical structures and thefunctions subserved by them is an indication of the very complexity of the humanbehaviour, 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 isrepresented in brain. Research in science, however, does not stop at theseuncertainties and it should go on, with empirical data and systematic explorationtowards controlled generalizable interpretations, with the hope that at one time inthe 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 ofthe central nervous system focusing on the ontogeny of speech and language.Language is said to be lateralized to one of the hemispheres and, morecommonly, to the left than to the right hemisphere.Various tests are availed to determine the dominant hemisphere for languageprocessing. Some of them include reaction time studies, dichotic listening tests,tachistoscopic viewing technique, the wada technique, etc. Averaged evokedpotential techniques have also been added to the repertory. Biochemical,electrophysiological and morphological criteria are all availed of to drawinterpretations concerning the neuropsychophysiology of language.

Language Components and Human Brain:

It is generally observed that the different levels or components of language aredifferentially distributed in brain with respect to their structure and function(Whitaker 1978).Various localizationistic and functional models of brain have proposed. Therecent view is indicative of a combined approach. It has been found that differentparts of the brain, each small in area, subserve a particular function and thatdamage to certain areas of the brain result in certain deficits in language

functioning.The different cortical structures contribute differently to total languageperformance. Whitaker (1978) terms it as "performance grammar", thecomponents of which are differentially distributed in the brain. A small area in thebrain subserves several functions and a single function is contributed by anumber of such small areas.This simple observation would indicate the intricacy and the complexity of thebrain mechanism in relation to human behavior.Small areas in frontal, parietal, temporal and occipital lobes are responsibletogether for language function and most part of the cortex does not contribute toperformance grammar. The classical zones like Broca's and Wernicke's areas,supramarginal gyrus, angular gyrus and other motor and sensory corticalstructures are responsible for functions like speech, audition, reading, writing,etc.The evidence for differential distribution of language components comes fromstudies on individuals with brain damage who exhibit a dissociated linguisticdisability. Some present a linguistic picture of deficient performance at thesyntactic 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 dependingon some crucial factors.Any modality or language skill among the four important ones could be disturbedat the central level. Even within the modalities, there might be a differentialpicture of the two languages of a bilingual. For instance, within the broad

category of writing, an individual can present a dissociated disability between thephonetically based writing systems and visually based one thus indicating adifferential localization of the two writing systems (Sasanuma, 1975).There are cerebral Lateralization measures that suggest that asymmetry inhemispheric dominance could be brought about by language-specific factors.Particularly strong is the evidence that different orthographic system (Syllabic oralphabetic versus ideographic) left to right versus right to left may enhancedifferent cerebral organization (Albert and Obler 1978).

Left versus right hemisphere:

The left hemisphere, rather than the right, is considered dominant for languagefunctions in majority of right handed humans, Schnitzer (1978) asserts that theleft hemisphere, rather than the right hemisphere, is endowed from birth with agreater 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 inhundred adult brains. In addition, the neuroanatomical evidence for prenatal andparanatal asymmetry has also been reported.

Wada, Clarke and Hamm (1975) find evidence of morphological asymmetry ofboth the temporal planum and the frontal operculum (adjacent to Broca's area) inthe twenty-ninth week of gestation, when those of the left hemisphere are foundto be larger than those of right hemisphere in 90% of the adults and fetuses. Thishas been supported by many, thus erasing the notion that Lateralization is afunction of language or that there is a strict cause and effect relationship betweenthe two.

In addition to such neuroanatomical asymmetry, behavioral asymmetry hasalso been widely reported. Dennis and Whitaker (1976) studied the linguistic

abilities of 10 year old children with complete hemisphererctomy prior to 4 months of age. The isolated normal left hemispheres and the isolated normalright hemisphere of matched groups were compared along various phonological,semantic and syntactic tasks. Syntax seemed to be the most affected in lefthemispherectonized individuals. On the basis of the findings it was concludedthat the right hemisphere was deficient in the following abilities:

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1. Understanding language auditorily especially when meaning wasconveyed 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 missingpronoun, and

7. Judging the relationships among words in sentences.

It was noted that the right hemisphere was less endowed hierarchical abilitiesrather 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 independentwhere 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 languagestructure as other linguistic aspects. This was in view of the finding that whilechildren learn or acquire language(s), they do so without a foreign accentwhereas most of the adults learning a second language would retain their mothertongue accent in the newly acquired language. Schnitzer (1978) is also of theopinion that, of all the linguistic components, phonology can be mastered by theright hemisphere to a relatively comparable level as the left hemisphere. One caninfer 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 betweenpatients language deficits and the brain areas that had been damaged,determined by an autopsy at the time of death. These studies led to thediscovery that most language processing goes on in one hemisphere, called thedominant hemisphere. In over 90% of people (98% in right-handed people andabout 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 byGeshwind and Levitsky (1968), who discovered that about 60% of human brainsdisplay anatomical differences between the two hemispheres in the posteriortemporal lobe (the region which encompasses Wernickes area). In line withthese 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 documentedbetween the two cerebral hemispheres.The study of split-brained subjects in the late 20th century provided a great dealof 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 longercommunicate with each other and there is no transfer of auditory, visual, orsensory information from one hemisphere to the other. Commissurotomy issometimes the only treatment available for patients with intractable epilepsy. Theprocedure can diminish the number and severity of the patients seizures.

The corpus collosum is essential for melding the actions of each hemisphere intoa unitary whole. Once the collosum is bisected, the hemispheres appear to actindependently. The study of this phenomenon has led to some surprising findingsin 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 patients left or right visual field (LVF or RVF,respectively). Information about an image presented to the LVF of a split-brainsubject only reaches the RIGHT cerebral hemisphere, and vice versa. When theimage of an object is projected onto the RVF, the subject can easily name theobject because the information is accessible to the left, dominant, languagehemisphere. When the image is projected onto the LVF, the subject cannotverbally identify it and may even deny ever seeing it - the language areas of theleft hemisphere are unaware of the image. However, the patient can readilyidentify the object non-verbally, such as pointing to it with the left hand, or usingtactile cues to distinguish it from several other unseen objects. This suggests thatwhile the right hemisphere cannot talk, it is able to perceive, learn, remember,

and issue commands for motor tasks, even when the subject is not consciouslyaware of these processes.

In another set of experiments, the split-brained patients ability to identify writtenwords was examined. Words presented to the RVF were easily read out loud. Onthe other hand, the patients were unable to pronounce the word if it waspresented to the LVF. Interestingly, some patients could write words projectedonto 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 requirenon-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 alanguage that requires a certain level of cortical maturation and hemisphericLateralization, which in itself is an on going process. A biological barrier iserected guiding the quality of language acquisition before and after the criticalperiod in specific ways.

Penfield and Roberts (1959) and Lenneberg (1967) conceived of Lateralizationas 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 aspecific period. The process of Lateralization and the critical period wereconsidered 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 andRoberts 1959). However, this has been widely refuted.

Lenneberg (1967) asserted that language Lateralization was complete by 11-14years. Krashen (1973) cited evidence that language Lateralization was completeby 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 thatlanguage Lateralization occurred early, be it to the left or right, and that both thehemispheres participated in language processing before the Lateralization wascomplete.

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

Critical Period:

Critical period was viewed as the congenial period for language acquisition whenthe child's brain is highly receptive and plastic. However, this traditional idea ofthe critical period is undergoing a radical change with the advent of recentstudies 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 foracquisition of certain functions.

The new interpretation (Seliger, 1978) given to the Lateralization and criticalperiod 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 ofplasticity in various parts of the brain for different functions over most of one's lifetime. In this light, Lateralization effects are those of both intra andinterhemispheric nature. The evidence for Seliger's (Seliger 1978), multiplecritical period hypothesis stemmed from age dependent aphasia and universalsecond language inabilities which were taken to be indicative of both the state oflocalization process and the gradual loss of plasticity.

Plasticity

According to Schnitzer (1978), although upto some point of development, thebrain is "plastic" and "transfer" from left hemisphere to the right hemisphere is notdone as proficiently as it is done by the intact left hemisphere. Schnitzer furtherremarked that although the brain is lateralized for language functions from beforebirth, it is relatively "plastic" for the first 5 years of life so that language could beshifted to the contralateral hemisphere in the event of neuropathology during thisperiod. 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 arepresent prior to or at birth and that the brain is more plastic in the first few yearsof life than later to the extent that cortical structures can change and assume afunction different from the originally intended ones in the event of pathology tothe predetermined areas in the cortex and perform well, though not to the sameextent managed by left hemisphere. Disuse of certain areas for a long time wouldnaturally preclude the revival of the functions to the original extent. Thus,probably, the previously uncommitted or differently committed right hemispherecould be less capacitated to start all over again with a new function. However, wenotice in normal right hemisphere dominant individuals from birth that there isnormal performance equivalent to the left hemisphere functioning.

Literacy Skills

Literacy (reading and writing) skills are said to enhance left hemispheredominance. Even in an adult second language learner the left hemisphere mightplay a major role although in the initial stages the right hemisphere mayparticipate. 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 secondlanguage learning (Galloway 1981).

A controlled comparison of child and adult second language performances wouldyield some information on the strategies adopted and the cerebral organization in

second language performance. A comparison of matched groups with andwithout current formal schooling (where reading and writing skills areemphasized) would also help in this venture to understand the extent ofcontribution of literacy factor in hemispheric Lateralization.

The Wernicke-Geschwind model of language comprehensionand speech production

The other major discovery revealed by study of patients with aphasias was that

two cerebral cortical areas Brocas area in the lateral frontal lobe andWernickes area in the posterior superior temporal lobe are major neuralsubstrates of language. A useful, if somewhat simplified, model for understandinghow the two language areas interact is the Wernicke-Geschwind model. Thismodel has been quite successful in predicting the effects of damage in severalbrain regions and how visual information is processed in naming an object.

The model posits that Brocas area, which is connected to regions of motorcortex that control the face and tongue, is involved in planning the motorexecution of speech, and that Wernickes area, which is connected to auditorycortex, is involved in recognizing and representing the sound pattern of words.Within this model, the arcuate fasciculus is a unidirectional pathway that bringsinformation from Wernickes area to Brocas area.

According to the Wernicke-Geschwind model, there is a clear, linear flow ofinformation through these two cortical areas for the recognition and production ofspeech. Wernickes area contains the auditory codes for words - what they soundlike Brocas area contains the articulatory codes for words - the motor commandsthat tell the mouth and larynx how to articulate each word. The behavior ofrepeating a spoken word exemplifies how the Wernicke-Geschwind modelunderstand language processing. When a spoken word is heard, the sound isprocessed in auditory cortex and then transmitted to Wernicke's area.

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There the sound is matched to its auditory code, and its meaning can beinterpreted by other association areas of the cerebral cortex. The auditory codeis transmitted to Broca's area through the arcuate fasciculus, where thearticulatory code for the word is activated and sent to motor cortex for speechproduction.

Reading comprehension also requires Wernickes area in the Wernicke-Geschwind model. Visual information is sent to the angular gyrus whichtranslates the visual code to a form accessible by Wernickes area. Wernickesarea then matches the word to its auditory code, as for spoken speech. Thus,according to this model, reading requires the phonological recoding of words inWernickes area.

The Wernicke-Geschwind model provided a framework for understanding theneural mechanisms of the aphasias. Patients with damage to Brocas areascannot produce speech, but they can still comprehend speech becauseWernicke's area is intact. Damage to Wernicke's area, on the other hand,

produces no problems in speech production because Brocaa area is unaffected,but the meaning of the speech of others is improperly understood, and thepatients own speech has virtually no meaning.

Other brain areas and pathways involved in language

Despite its success predicting clinical outcomes, the Wernicke-Geschwind modelhas significant limitations. New lesion studies, research in neuropsychology and

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linguistics, functional imaging (PET, fMRI), and direct neural recordingtechniques (event-related electrical potentials, direct intraoperative recordingsfrom human cerebral cortex) have better defined the brain areas and pathwaysinvolved in language processing.

It is now clear that there is a direct connection between the parieto-occipito-temporal association cortices and Brocas area. These pathways are involved inthe understanding and repetition of written language (i.e., visual recognition).Thus, read words do not need to be transformed into auditory representations.Instead, Brocas area and other higher order association areas can handle thisinformation directly.In addition, while Brocas and Wernickes areas are important structures forlanguage, they do not operate independently for language production andcomprehension to the extent hypothesized in the Wernicke-Geschwind model.The arcuate fasciculus is in fact a bidirectional pathway that connects Brocasand Wernickes areas to many other regions of cortex in the dominant

hemisphere. The prefrontal, premotor, and supplementary motor cortices in thefrontal lobes are necessary for higher order aspects of speech planning andproduction, and for proper syntax of language comprehension and production.Some areas of insular cortex are also related to speech articulation.Wernickes area has reciprocal connections with the supramarginal and angulargyri of the parietal lobe as well as with areas in the temporal lobe in the dominanthemisphere. These regions are important for language comprehension, and alsoparticipate in the mapping of the sounds of words to their meanings. The angulargyrus in the language dominant hemisphere contributes to the understanding ofwritten language. Finally, several sub-cortical structures, such as the thalamusand basal ganglia of the dominant hemisphere, are also critical for language

processing.

The non-dominant language hemisphere is also involved in many aspects oflanguage. Lesion studies and studies in split-brain patients reveal that the non-dominant hemisphere can understand many words and can take on responsibilityfor many aspects of language in children with damage to the dominanthemisphere. In normal function, the non-dominant language hemisphereparticipates 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-dominanthemisphere codes information in a more general way, representing the overallstructure of a stimulus.

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FIG: Pathways involved in language

For instance, the right hemisphere is involved in determining if a statement isfunny, which involves analyzing the content of that statement as a whole ratherthan the individual words.

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WHAT IS AUTISM?

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

Autism typically is diagnosed during a childs second year and is lifelong,although symptoms may lessen over time. There is no cure for autism, butappropriate treatments can help a child develop life skills to function more

independently.

Autism and developmental language disorder (DLD) are both behaviorallydefined disorders that emerge in early childhood. Both involve languageimpairment, and autism additionally involves impaired social reciprocity as wellas 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 worldwhere they are unable to successfully communicate and interact with others.Children with autism may have difficulty developing language skills andunderstanding what others say to them. They also may have difficultycommunicating nonverbally, such as through hand gestures, eye contact, andfacial expressions.

Not every child with an autism spectrum disorder will have a language problem.A childs 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 ingreat detail. Most children with autism have little or no problem pronouncingwords. The majority, however, have difficulty using language effectively,especially when they talk to other people. Many have problems with the meaningand rhythm of words and sentences. They also may be unable to understandbody language and the nuances of vocal tones.

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

Repetitive or rigid language: Often, children with autism who can speakwill 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 fiverepeatedly. Or a child may continuously repeat words he or she hasheard, a condition called echolalia. Immediate echolalia occurs when thechild repeats words someone has just said. For example, the child mayrespond 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 Doyou want something to drink? whenever he or she asks for a drink.

Some children with autism speak in a high-pitched or singsong voice oruse robot-like speech. Other children with autism may use stock phrasesto 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 whatthey hear on television programs or commercials.

Narrow interests and exceptional abilities: Some children may be ableto 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 conversationabout the same topic. Others have musical talents or an advanced abilityto count and do math calculations. Approximately 10 percent of childrenwith autism show savant skills, or extremely high abilities in such ascalendar 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, andtheir progress is usually uneven. For example, they may develop a strongvocabulary in a particular area of interest very quickly. Many children havegood memories for information just heard or seen. Some children may beable to read words before 5 years of age, but they may not comprehendwhat they have read. They often do not respond to the speech of othersand may not respond to their own names . As a result, children with autismsometimes are mistakenly thought to have a hearing problem.

Poor nonverbal conversation skills: Children with autism often areunable to use gesturessuch as pointing to an objectto give meaning to

their speech. They often avoid eye contact, which can make them seemrude, uninterested, or inattentive. Without meaningful gestures or thelanguage to communicate, many children with autism become frustrated intheir attempts to make their feelings and needs known. They may act outtheir frustrations through vocal outbursts or other inappropriate behaviors.

In autism there is increasing evidence that the disorder is associated with atendency towards large brain volume in childhood (Bailey et al., 1998;

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

In DLD, brain investigations have largely focused on language regions of thebrain, 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 andDLD has identified multiple similarities between these two groups, though withmodest differences in degree: both share a pervasive morphometric anomaly-notably, larger than normal brain and white matter volumes- but it is morepronounced in autism (Herbert et al,. 2004). The white matter enlargement isnon uniformly disturbed, involving sub cortical radiate white matter butsparing the corpus collosum (Herbert et al,. 2004). Thus, the volumecomprising intrahemispheric connection is disproportionately enlarged

compared to intrahemispheric white matter, and this may have an impact onbrain asymmetry.

Data are drawn from a comprehensive researched study of a segmentation oftheentire brainand a parcellation of the cerebral cortex, allowinganalyses atmultiple nested anatomical levels. First, they examinedlarge-scale patterns ofasymmetry in the hemispheres, in the principal grey and white matterstructures of the brain, in the cerebral lobular partitions and in aggregatedcortical parcellationunits (PUs). Secondly, because they parcellated the entirecortex, they were able to explore asymmetries in groupings of PUs

approximating

the primary sensorimotor cortex, unimodal association cortexand higher-order association cortex. It has been proposed that more complexprocessing is impaired in autism (Minshew et al., 1997), and that rapidprocessing is impaired in DLD (Benasichand Tallal, 2002). Association cortexmay provide an anatomical correlate for complex or rapid processingimpairments in these disorders. The hypothesis is that because corticalcomponents of neural systems with greater interconnectivity are likely to bepreferentially affected by abnormalities of whitematter,one should therefore

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see greater differences from controls in volume asymmetry in higher-orderassociation cortex. In addition, because language impairments are found inboth autism and DLD, they also looked for differences among groups in asubset of association cortex PUs that are considered to be involved inlanguage functions. Since these brains are the products of atypical

development,

it may be that functional divisions will differ from controls

inunknown ways, or that anatomical underpinnings of abnormalitiesin complexprocessing (including language) may involve widely distributed circuit-disrupting abnormalities. They therefore performed a comparison ofasymmetry patterns across the entire cerebral cortex, and hypothesized thatthese three groups would differfrom each other at this level. This study is thusthe first comprehensive whole-brain survey of volume asymmetry in high-functioningautism and DLD.

Result:

To determine whether differences in asymmetry between autistic,

DLD andcontrol boys were specific to PU involved in associationalprocessing, the PUwere classified according to general functional type. Based on previouslypublished PU classifications (Rademacher et al., 1992), researchers wereable to classify 40 of the PUs as beingpredominantly (i) primary sensory ormotor cortex (six PUs),(ii) unimodal association cortex (17 PUs) or (iii) higher-order association cortex (17 PUs). The remaining eight PUs could not beclearly classified because of overlapping functions within the definedboundaries 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 oftotal brain volume (cerebral cortex, cerebral white matter, cerebellum,caudate, globus pallidusputamen,diencephalon, brainstem), (iii) lobes of thecerebral cortex(derived by grouping cortical PUs according to lobe) and (iv)individual cortical PUs for the entire cerebral cortex. A symmetry index wascalculated for anatomical units at each of these levels. To classify eachstructure as being significantly left- or right-asymmetrical, one-sampleStudent's ttests were used to assess the probability that the mean SI for eachsegmented 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 indexdetermined classification as left-asymmetrical or right-asymmetrical.Structures or PUs for which the one-sample t-test was not significant wereclassifiedas being symmetrical.

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Fig. Asymmetries of segmented structures. The xaxis indicates percentage asymmetry tothe left or the right. *Asymmetry is significantly different from zero.

A GLM-CD (General linear models for correlated data) showed significantoverall differences between autistic, DLD and control boys regarding

asymmetry in language-relatedcortical 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-functioningboyswith autism and DLD, the main findings are that patterns of cerebral symmetryare closely similar in the brains of autisticchildren and children with DLD, butdiffer substantially frombrains of controls. Thus, in neither autism nor DLD is

thereasymmetry at the levels of major grey and white regions or thecerebralcortical lobes. However, nested within their overall and lobar cortical lack ofasymmetry, in both autistic and DLDsamples we see a substantial increasecompared with controlsin the aggregate amount of cortical PU asymmetry. Inparticular, right-asymmetrical cortex is substantially increased in autism andDLD; 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

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autistic brains. This leadsto a similar reversal of the right : left cerebral cortexasymmetryratio 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 PUsappear to drive the differences atthe level of unimodal associationcortex, while higher-order association cortexdifferences are more robust, showing differences beyond those PUsconsidered to be related to language function. They also found that in theirpatterns of significant asymmetry throughout the cerebral cortex,children withautism or DLD differed from controls but were verysimilar to each other.

These findings invite several observations. First, researchers see an intriguingdisconnection in the asymmetry findings between the different levels ofanalysis, asymmetries being increasingly masked as the size of the units of

analysis increases. Secondly,

while the increase in rightward asymmetry is inkeeping with prior reported findings, the increase in total asymmetry ofaggregated cortical PUs is different from the loss of asymmetrythat has beencommonly reported and that we have found at our larger-unit levels ofanalysis. Finally, the differences fromcontrols are not only more pronouncedin higher-order associationareas but also for the most part the same in bothautism and DLD groups. If the widespread atypical asymmetries found inthese two disorders were not so similar, the perturbations outside of languageareas might be dismissed as random, or as fluctuating asymmetry(Rasmuson, 2002). That the two samples are so similar not only implies arelationship between these disorders, but also suggests that these changes

reflect systematic and

similar alterations in neural systems. The widelydistributedsignificant asymmetry shifts in these two groups of brains mayalsoindicate that meaningful asymmetries are widespread inthe cerebral cortex.

The loss of overall asymmetry of total cerebral cortex in autism and DLD, asmeasured by greywhite segmentation, may in fact be consistent with thegain in aggregate asymmetry of thecerebral cortex when it is subdivided intoPUs. The autism and DLD brains showed an increase in the number (andvolume) ofcortical PUs with rightward asymmetry, but at the same time theyshowed either no loss (autism) or only a small loss (DLD)in the number (andvolume) of cortical PUs with leftward asymmetry. The combined effectappears to be that the increase in rightwardcortical asymmetry in autism andDLD has cancelled out the leftwardasymmetry, so that the cortex taken as awhole (in the segmentationmeasure) appears symmetrical.

Resting regional cerebral blood flow asymmetry was shifted frompredominantly left to predominantly right in both an autistic (Chiron et al.,1995) and a dysphasic(childhood speechdisorder) group (Chironet al., 1999).However, this ratio shift had a different origin in each group. In the autism

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group this reversal of the right: left ratio was driven by regional cerebral bloodflow thatwas no different from controls on the right but diminished onthe left,while in the dysphasia group the left regional cerebralblood flow was largelyunchanged while the right was increased. There thus appears to be lessoverall 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 volumeasymmetry is driven wholly in autism and predominantly in DLD by anincrease in aggregate volume of asymmetrical PUs on theright. If the volumeasymmetries similar to the ones we reporthere were present in subjects fromboth groups in the studies by Chiron, this would suggest that volume andmetabolic rateshave a different relationship in dysphasia than in autism.

Widespread abnormalities in white matter, connectivity and asymmetry mayrelate to the functional abnormalities in autism and DLD,but because they donot understand the mechanisms by which these anatomical changes mayexert their functional impacts, researchers donot assume that there is a direct

correlation between the magnitude

of anatomical changes and the magnitudeof functional impact. In DLD, where asymmetry in language regions hasreceived greater study, the existence or magnitude of asymmetry has notcorrelatedconsistently with diagnosis (Gaugeret al., 1997; Preis et al.,1998).In the face of more widespread asymmetry abnormalities that go beyondregions associated with the deficits specificallycharacterizing either disorder,formulating the possible significance of such widespread changes wouldminimally require systematic correlation with behavioural data that goesbeyond the scopeof this paper. However, researchers would argue that it alsoand more fundamentally requires going beneath the defining behavioralfeatures of the disorders.

From a cognitive neuroscience vantage point, the behavioursand deficits thatdefine autism and DLD may be surface manifestations of underlyingprocessing abnormalities (Morton and Frith, 1995; Belmonte et al., 2004). Ithas been proposed that the features of the autistic behavioural phenotypeemerge from an underlyingdeficit that can be characterized as weak centralcoherence (Shah and Frith, 1993) or a generalized impairment in complexprocessing (Minshew et al., 1997), and that thelanguage as well as the wide-ranging though subtle non-languageimpairments (Bishop, 2002; Kail, 1994) inDLD may arise froman underlying pervasive processing disorder (Kail, 1994;Johnstonet al., 1997). While the presence of language abnormalities in bothdisorders and the behavioral and social interaction impairments additionallyfound in autism (American Psychiatric Association, 1994 Rapin and Dunn,2003; Rapin et al., 2003) have invited a search for underlying focal brainabnormalities,the regional anatomical abnormalities that have been reportedare not consistently replicated, while increased brain volume,which has beenfound frequently, challenges modular approaches to structurefunctioncorrelation (Herbert, in press). It may be that volume and white matterincreases are anatomical correlates of underlying processing abnormalities.

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The tissueabnormalities leading to increased white matter volume couldleadto suboptimal connectivity, and this could in turn lead to poor coordinationamong individual components of neural circuits, resulting in pervasiveprocessing abnormalities (Just et al ., 2004). Because higher-orderassociational activity involvesgreater integration than unimodal associational

processing,

areas with greater interconnections would, in this model, haveheightened vulnerability to connectivity abnormalities.

Cortical areas related to language function are embedded in the unimodal andhigher-order association areas that showed significant differences in theiranalysis. It may thus be thecase that language functions are not specificallytargeted by the underlying pathogenesis in either disorder, but rather areprominently affected because they are so highly reliant on associationalprocessing (Mesulam, 1998). It may also be the case that the functions ofsocial interaction and behaviour additionally impaired in autism are similarlyvulnerable because of their dependence on complex associational

processing. If this is the case, then

since the behavioural abnormalities wouldeventuate from systems perturbations rather than only from focaldisturbances, the magnitude of asymmetries in individual PUs may be lesssalientregarding functional significance.

There is a further temporal component of vulnerability: the brain and whitematter enlargement found in both groups appears to occur substantiallypostnatal. This postnatal growth pattern has been documented for autism(Lainhart et al., 1997; Courchesne et al., 2003), and it may be inferred forDLD as well, since in both the autism and DLD samples, white matterenlargement is not only present (Herbert et al., 2003a, b) but is greater in

areas that myelinate later (Herbert et al., 2004). These

abnormal volumes andgrowth trajectories may create pressures towards asymmetry that amplifyover time.

Thus, while the increased number of cortical regions with rightwardasymmetry may have significant consequences in terms of alteredfunctionality, this phenomenon may not be primary in terms ofpathogenesis.Altered cortical asymmetries may instead emergeas a response or adaptationto an abnormal brain and white matter growth trajectory. While increasedvolume and its associated dysfunctional connectivity may together lead togreater lateralization, the increased and aberrant lateralization may thenfurther degrade the functioning of the cortical networks that already, due towhite matter abnormalities, have suboptimal connectivity.

The asymmetry alterations researchers report, seen in the context of thevolume changes they accompany, may thus be the consequence of a positivefeedback loop: increased volume results from white matter tissue changesthat may impair connectivity, favoring lateralization and local processing.Moreover, the volume increase itself may on its own create a bias towards

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lateralization. These two dynamics may in turn combine to promote aprogressive divergence from the norm regarding functions requiringassociational activity. Such divergence may lead to processing andlocalizationthat are dysfunctional, and that in turn feed back into and amplifythe 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 cannotaddress.

While researchers' multivariate analysis found that differences among thegroups were most robust in higher-order association areas, their analysisprovided a lens into the pervasiveness of theasymmetry alterations, both inshowing that they are widelysimilar between autism and DLD, and in showingthat they go beyond our initial functional classifications. These widespreadalterations in anatomical asymmetry suggest that neural systemsdisruption inthese disorders is pervasive, rather than limited to functionally relevantcircuits. In this light, the instancesof atypical functional localization that have

been documented,

such as in autism where the fusiform face area may(Hadjikhaniet al., 2004) or may not (Schultz et al., 2000; Pierce et al.,2001)activate normally for face processing, may actually be parts of morewidespread but largely not yet identified neural systems abnormalities(Belmonte and Yurgelun-Todd, 2003; Hadjikhani et al., 2004; Herbert et al.,2004). The variable but commonpresence of additional non-language-basedneurological and processingabnormalities such as clumsiness (Trauneret al.,2000; Hill,2001; Hardan et al., 2003; Herbert et al., 2003a, b; RubensteinandMerzenich, 2003), often seen in these two groups, may be furtherconsequences of these widespread abnormalities, andin that light not purelycoincidental. Given these anatomical and processing abnormalities, one

would predict that functional

imaging or electrophysiological measuressensitive to altered timing would find reduced coordination among regions.This hasbeen addressed theoretically (Brock et al., 2002) and documentedina 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 corticalasymmetries have been the subject of an increasing body of research, butthese studies have mainly focused on language regions, wheredifferences incytoarchitectural organization appear to be related to asymmetries in corticalprocessing capacities (Anderson et al., 1999; Hutsler, 2003; Hutsler andGaluske, 2003). Researchers' findings demonstrate asymmetries in corticalPUs that are not only widely but also similarly (and hence probablysystematically) distributedthroughout the brain in two separate samples. Thismay suggest functionally meaningful hemispheric differences in corticalmicrostructure in brain regions other than those that are associated withlanguage. Even though these increased and shifted asymmetries could alsobe dysfunctional (Escalante-Mead et al., 2003), their apparent systematicdistribution remains of interest.

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cognitive abnormalities, many of which resemble mild forms of autisticfeatures (Bishop & Rosenbloom, 1987). Abnormal patterns of hemisphericalasymmetry have been suspected in autism, and early work hypothesized lefthemisphere dysfunction due to the language deficits involved. However, as insemantic-pragmatic disorder, it is delay in language development and

abnormal use of language that characterize communication in autism, and thecondition can be found in the presence of relatively intact language form.Autistic children show deficits in the areas of prosody, the social use oflanguage and the ability to read emotional expression in language. To theextent to which these functions are lateralized in normal adults, it is the righthemisphere, 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 manyof the characteristic social-affective abnormalities can more plausibly belinked with right hemisphere deficits. Goodman (1989) considered the relativecontribution of the two cerebral hemispheres to the features of autism and

Asperger's syndrome, noting that language in such individuals is deviant inthe domains of pragmatics and prosody. He suggests that innate deficits inthe expression and comprehension of non-verbal communication couldunderpin 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 andinterpersonal difficulties, shyness, visuospatial difficulties, and inadequateparalinguistic communicative abilities. These patients lack eye contact and do

not use normal prosody or gesture. They perform worse on aurally presentedstory recall tests than on paired associative learning tasks (Weintraub &Mesulam, 1983; Voeller, 1986). Weintraub and Mesulam (1983, p.468) feelthat:

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

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

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'hyperlexia', where tests such as the Neale Analysis of Reading Ability (Neale,1958) reveal their good scores for reading accuracy, accompanied by poorscores for reading comprehension. The autistic children had no decodingproblem, 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 fielddependent) had been noted in other cognitive tasks (Shah & Frith, 1983) andseemed to be a general characteristic of their behaviour. Their failure inreading for meaning could be seen as related to their failure in making use ofredundancy (Hermelin & O'Connor, 1970; Hermelin & Frith, 1971), yet thereseemed 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 toexplain many of the handicaps of autistic children (Aurnhammer-Frith, 1969;Hermelin & Frith, 1971). This notion of use of redundancy relates closely tonotions of use of context in perception and especially in reading (Frith &

Snowling, 1983).

Sperber and Wilson (1986) proposed the theory of relevance, which has beenused to explain the communication difficulties of autism. The communicationdifficulties displayed by both some patients with acquired right hemispherelesions and children with semantic-pragmatic language disorder indicate afailure to understand the processes of inference. These patients can copewith the encoding and decoding aspects of communication, and can extractmeaning from the basic sound (or letter) patterns of speech (or writing), butthey are unable to deduce the speaker's informative intention so as to bridgethe 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 tocommunication is, as yet, incomplete. It is, however, clear from the study ofpatients with acquired right hemisphere lesions that communication skills canbe impaired following right hemisphere damage. Such patients seem to havean abnormal cognitive style which reflects an inability to integrate multimodalperceptual information. This cognitive difficulty reveals itself in theircommunication, which tends to be fluent and grammatical, but irrelevant, withstereotyped utterances and over-literal interpretations.

Their difficulties lie in comprehending the deeper realms of meaning, and inmaking use of paralinguistic features. Gardner's description (Gardner, 1975,p.296) of the abnormal cognitive style of patients with acquired righthemisphere lesions could be a description of semantic-pragmatic disorder:

the patient appears unconcerned about his message; insensitive to hissituation, or to the environment; resembling a language machine, a talkingcomputer that decodes literally, gives the most immediate response -

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

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

Conclusion:

Though it is reported that the autistic children have some abnormalities intheir cortical asymmetry in the brain, still the researchers need to study thecauses of autism. With more research, scientists hope to learn precisely howdifferences in the structures and processes of the brain contribute DLD andautism , and how these differences might be treated or prevented.

Temple Grandin: As a person with autism I want to emphasize theimportance of developing the childs talents. Skills are often uneven in autism,

and a child may be good at one thing and poor at another. I had talents indrawing, and these talents later developed into a career in designing cattlehandling systems for major beef companies. Too often there is too muchemphasis on the deficits and not enough emphasis on the talents. Abilities inchildren with autism will vary greatly, and many individuals will function at alower level than me. However, developing talents and improving skills willbenefit all. If a child becomes fixated on trains, then use the great motivationof that fixation to motivate learning other skills. For example, use a book

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about trains to teach reading, use calculating the speed of a train to teachmath, and encourage an interest in history by studying the history of therailroads.

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 theINDIFFERENTrespect to them.

----THANK YOU----

References:

Oxford Journal :A journal of neurology; Brain Vol. 128 No. 1Guarantors of Brain 2004.

Links used : http://www.universaltheory.org/QuantumBrain.htmlhttp://www.learner.org/discoveringpsychology/06/e06expand.htmlhttp://www.waiting.com/brainfunction.html#anchor318669http://www.childdevelopmentinfo.com/development/piaget.shtmlhttp://www.sagepub.com/garrettbb2study/animations/9.23.htmhttp://www.autismspeaks.org/science/research/initiatives/white_matter_story.php

Psychology and Language: Clark. Herbert. H and Clark. Eve. V.
http://brain.oxfordjournals.org/misc/terms.shtmlhttp://brain.oxfordjournals.org/misc/terms.shtmlhttp://brain.oxfordjournals.org/misc/terms.shtmlhttp://brain.oxfordjournals.org/misc/terms.shtml

Brain's disfunction in autism and DLD

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