Tuesday, October 30, 2007

Millennial Opportunities: Managing developmental progress in children/adults -the new guidelines

Global Strategic Enterprises, Inc for Peace and Prosperity- www.globalbelai4u.blogspot.com; GSE4P&P

Re: Managing developmental progress in Children/Adults- The Autism Spectrum and the New Guidelines!

It is now common knowledge that our cognitive and social development is a work in progress.

We all need enriching relationships!

At some level, we are all developing and adapting to our new environment in a continuous basis be it growing, aging, or just keeping up with technological and social development progress that is taking place at home, school, work both in the local and global community. This is creating a new type of existence in several levels at the real, cyber, and the most hidden in our own subconscious where vision, dream and passion are so mixed up, some times we cannot differentiate one from the other.

Nurturing partnerships/networking!

By and large it is safe to say that some of us need parenting, others mentoring or some form of buddy groups and even competitive partnerships to help us succeed in our respective communities. It is always critical to connect with people who share similar interests, life styles or cultural diversity. In some sense, almost all of us need some level of nurturing and partnership through out our lives.

Competitive and reckless life styles!

The challenge of this millennium is that the competitive environment is creating hostile environments not only for adults,seniors and those with disabilities but even those so called harmony driven religious communities are becoming so competitive they are consuming the most vulnerable members of our community, the future of our children. Child abuse and exposure to toxic life styles begins as early as conception, where the toxic lifestyle is challenging even developing embryos as revealed in this story.

Positive Parenting/Nurturing!

In effect, parenting and Child development is managing the impact of both nature and nurture at its best. As such, parenting is the most neglected human activity in modern world. The impact of this early child or embryo abuse is now manifesting as the new epidemic of ASD and ADD with substantial impact of the future. Disorders that were not common some 25 years or even ten years are becoming common practice today.

Social Networking Vs Scientific and technological advances!

As we excel in social and scientific advances, our most important task on earth: that of procreation and nurturing of our offsprings to normal productive adults; is taking the back seat in almost all communities, with potential serious negative consequences. Our scientific and technological advances need to be matched with comparable nurturing social networking skills and ecology.

Modern children need more guidance than what is available!

In some child communities, abuse has taken new roles that includes child suicide bombings; in others, the way we over medicate our children instead of providing them with a nurturing environment, is creating the new challenges of dealing with abused children growing up to taking on the reign of unprepared role of precarious adulthood and potentially abusing us all as we grow old too. This is fast becoming a new reality in certain communities.

Technologically savvy and socially naive youths become delinquent adults!

Child development is being challenged by new disorders such ASD (Autism Spectrum Disorder and ADD (Attention Deficit Disorders), etc which are becoming new pediatric diagnosis that was not common 50 years ago, and even ten years ago. Technological savvy but socially naive children are turning into delinquent adults too soon.

Awareness leads to Passionate transformation!

The new information about ASD: Autism Spectrum Disorder that is becoming a new epidemic and even pandemic is partly due to the result of self abusing young adults with toxic lifestyles. Some lead such risky and dangerous life styles and do manage to procreate and conceive children while in those toxic states, negatively impacting the genetic coding of their embryos, with resultant chromosomal abnormalities of deletion, transferring etc, and negatively impacting the early neurodevelopmental stages of our children. Here comes ASD in all its spectrum of modern children and youth!

The pandemics of rare conditions such as ASD & ADD across the globe!

One cannot be far from the truth, that the epidemics of ASD and ADD in the modern family is so great that we might need to screen not only children but young adults too, if we want to impact positively our respective communities, hopefully reducing the damage of living with highly violent communities across the world.

All the same, here is an interesting story about the evolution of the new ASD epidemic and how the scientific and family community is likely to deal with it.

Managing a violent home and global community!

The recent wave of violence among youths and subsequent pandemics of terror and violence in almost all communities across the world, can eventually come down to ( Poor Procreation and Parenting skills) or in our incompetence of the basic functions of life, that of procreation and nurturing our offspring to productive adult life. This is not rocket science but some of these ASD cohorts are making their ways to the highest offices of the land and may be even the planet with all sorts of repercussions.

The current level of violence can be due to poor parenting!

Imagine a series of war lords and gorilla leaders, prime ministers and presidents with untreated ASD and ADD. Perhaps that is what is happening today around the world. We need to screen some of these people and the new technology and tools are available to do so. One might think this is far fetched, but if you read your news carefully, the behavior of some of these Holy Wood and Boly Wood Stars and Governors and Presidents around the world cannot be explained in any other sane way.

The Sacred institution of procreation and parenting is being defiled!

Imagine, if most children are conceived under the influence of substance abuse be it alcohol, drugs, hashish or some mood altering drugs to facilitate the scene, it is very easy to visualize the ecology of the embryo that has to survive in a hostile environment of conception early development. Add to this the chaotic childhood environment at home and the community these cohorts of ASD have very little chance of success or even bare survival.

Making Poor Parenting History!

The current trend of parenting and even the practice of pediatrics is so inadequate around the world, this story is a very critical social development with highly negative impact that we need to be aware of the social dynamics that sacrifices the future of our children. The attached information provides a wealth of information that future scientists, policy makers and most of all future parents should seriously consider. Making Poor Parenting History! Creative Parenting! Passionate for Good Parenting could be some of the slogans of the future generation!

Paying attention to the ASD and ADD Pandemics!

Here is the story of ASD and its impact on our respective communities around the world. Awareness is the beginning of transformation. Accessing the latest information on child and adult development is perhaps the beginning of understanding the series of anti-social behaviors that is evolving in the world stage and if not challenged early, it will feed into the man made violence infernos that we now witness taking place in the Middle East and the Horn of Africa.

Prevention is and Proactive parenting!

The secret is to be pre-emptive and have the necessary knowledge and tools to modify behaviors and talents before it is too late. Here is the recent development in our understanding of anti-social behaviors, attention deficit and the autism spectrum disorders that is becoming a new challenge and threat to future generations.

Dr B

Guidance for Parents From an Expert on Autism
By Nancy Shute
Posted October 29, 2007

The earlier parents and doctors realize that a child has autism, the earlier that child gets help.

The American Academy of Pediatrics today issued new guidelines aimed at making it easier for children with autism to be diagnosed earlier and get appropriate therapy sooner.

Related News

Pediatricians' Group Issues New Autism Guidelines

Kids' Vaccine Ingredient Not Likely Linked to Neurological Problems (Sep. 26)

Resource Launches for Families Affected By Autism (May 14)

Video: Autism Diagnoses On the Rise

Chris Plauché Johnson, a clinical professor of pediatrics at the University of Texas Health Science Center at San Antonio and coauthor of the new clinical reports, spoke with U.S.News & World Report about the tools available to parents and pediatricians.

The American Academy of Pediatrics issued guidelines on diagnosing autism not very long ago. What's new?

Early screening! at 18 and 24 months visits!

What's brand-new is that we're asking pediatricians to screen all children for autism at the 18-month and 24-month well-baby visits—not just children with speech delays and children of parents who have a concern.

Social and language defects!

We're also telling pediatricians to ask parents about social and language deficits that may be present in very young children.

The reason is that we know a lot more about what autism looks like in young children than we did seven years ago.

Over 100 tools on screening for disabilities!

And we have developed a tool kit that is a step-by-step plan on how a pediatrician can conduct surveillance and screening at a well-baby visit, with over 100 tools (from formal methods of screening for disabilities to the simple "point test," to see if a baby follows a person's point and gaze) for identifying these children and managing their disability.

Waiting- room observation tools!

In a very brief office visit, the biggest barrier for pediatricians is, when do I find time to do this? The technique we have suggested for surveillance and screening is a lot of waiting-room stuff.

Scoring parent's questionnaires!

Once parents check in, they'll be given questionnaires, and the office staff can score it. Then the pediatrician can look at it. If it's negative, fine. If it's positive, they can deal with it on the spot. The screening is done minutes before the patients see the pediatrician.

No more wait and see policy!

In the past, pediatricians often told parents who were worried about their baby to wait and see how the child does as a toddler.

Early intervention is the key!

That's exactly what we're trying to eliminate, the let's-wait-and-see. Early intervention is crucial to effective treatment. When parents do have a concern, most of the time there is something. It may be a speech delay, but it's good to know. We don't want the pediatrician to say, I'm going to refer you to a specialist, then wait six to 13 months.

Send them to specialists early!

The key point is: Don't wait to send them to early intervention. Those intervention people are good. They will tailor the intervention to the child. They don't need a diagnosis to get started and help the child, even if the intervention is for a simple speech delay.

Autism what is it?

All parents seem to worry that their baby may have autism. What can parents do to allay those fears before they see the pediatrician?

Autism Speaks web site in Florida! Check First Signs Inc.

There is a wonderful website that has just gone up from Autism Speaks, Florida State University, and First Signs Inc. It lists signs and symptoms of autism and shows them in video clips comparing a normal baby with a baby later diagnosed with autism.

Comparing children with standard normal!

When parents see videos like that, isn't there a risk that they'll be convinced their baby has autism when he's fine?

Differentiating delay from autism!

That's the concern. We're already seeing that with all the media attention about autism in general over the past five years. I've been in the business for 30 years. In the past, parents would come in with concerns about speech. It's totally different now. Parents come in saying, "I'm worried my child has autism," where it's only a little speech problem.

Treating over anxious parents!

There is a danger that these videos can make a parent overanxious. But on the other hand, when parents go to the doctor they will bring it up, and it clicks into the screening. Screening helps eliminate the false concerns or the overanxious concerns. The screening process can help allay fears as much as identify kids who do have autism.

Treating autism!

If a child is diagnosed with autism, what treatment choices do parents have?
Pediatricians have an important role to play in managing autism spectrum disorders.

Intensive intervention at least 25 hours per week!

The academy also has published a new report evaluating the many treatments available for autism, which include intensive intervention of at least 25 hours a week, pharmacological and nonpharmacologic intervention for medical conditions that often accompany autism, and use of complementary and alternative treatments.

Supporting and educating parents!

The goal is not only to help pediatricians provide medical care to children on the autism spectrum but to support and educate families, and guide them to empirically supported interventions for their children.

The Autism Spectrum!

The two new American Academy of Pediatrics reports, "Identification and Evaluation of Children With Autism Spectrum Disorders" and "Management of Children With Autism Spectrum Disorders," are available at www.aap.org.

Resources Sharing!


Obsessively stacking or lining up objects may indicate autism.

ICD-10 F84.0
ICD-9 299.0
OMIM 209850
DiseasesDB 1142
MedlinePlus 001526
eMedicine med/3202 ped/180
MeSH D001321

What is Autism?

Autism is a brain development disorder characterized by impairments in social interaction and communication, and restricted and repetitive behavior, all exhibited before a child is three years old. These characteristics distinguish autism from milder autism spectrum disorders (ASD).

Heritability of Autism?

Heritability contributes a large fraction of the risk of a child's developing the disorder, although the genetics of autism are complex, and it is generally unclear which genes are responsible.[1]

Associated with birth defects!

In rare cases, autism is strongly associated with agents that cause birth defects.[2] Other proposed causes, such as the exposure of children to vaccines, are controversial and the vaccine hypotheses are unsupported by convincing scientific evidence.[3]

Prevalence: 1-2 cases per 1,000; 4.3;1 Male-to-female ratio!

Most recent reviews estimate a prevalence of one to two cases per 1,000 people for autism, and about six per 1,000 for ASD, with ASD averaging a 4.3:1 male-to-female ratio.

Changes in prevalence: Diagnostic tools or epidemiology?

The number of people known to have autism has increased dramatically since the 1980s, at least partly due to changes in diagnostic practice; the question of whether prevalence has increased is unresolved.[4]

Brain the main target of pathology!

Autism affects many parts of the brain; how this occurs is poorly understood. Parents usually notice signs in the first year or two of their child's life.

No cure but Early intervention for self care and social skills!

Early intervention may help children gain self-care and social skills, although few of these interventions are supported by scientific studies. There is no cure.[5] With severe autism, independent living is unlikely; with milder autism, there are some success stories for adults,[6] and an autistic culture has developed, with some seeking a cure and others believing that autism is a condition rather than a disorder.[7]

Contents [hide]
1 Classification
2 Characteristics
2.1 Social development
2.2 Communication
2.3 Repetitive behavior
2.4 Other symptoms
3 Causes
4 Mechanism
4.1 Pathophysiology
4.2 Neuropsychology
5 Screening
6 Diagnosis
7 Treatment
8 Prognosis
9 Epidemiology
10 History
11 References
12 External links


Hans Asperger described a form of ASD in the 1940s that later became known as Asperger syndrome.

Autism is a developmental disorder of the human brain that first shows signs during infancy or childhood and follows a steady course without remission or relapse.[8] Impairments result from maturation-related changes in various systems of the brain.

Autism spectrum disorders (ASD)

[9] Autism is one of the five pervasive developmental disorders (PDD) or autism spectrum disorders (ASD), which are characterized by widespread abnormalities of social interactions and communication, and severely restricted interests and highly repetitive behavior.[8]Of the other four autism spectrum disorders, Asperger syndrome is closest to autism in signs and likely causes; Rett syndrome and childhood disintegrative disorder share several signs with autism, but may have unrelated causes; PDD not otherwise specified (PDD-NOS) is diagnosed when the criteria are not met for a more specific disorder.[10]

Asperger's has no speech delay!

Unlike autism, Asperger's has no substantial delay in language development.[11] The terminology of autism can be bewildering, with autism, Asperger's and PDD-NOS sometimes called the autistic disorders,[1] whereas autism itself is often called autistic disorder, childhood autism, or infantile autism.

BAP - Autism Phenotype!

In this article, autism refers to the classic autistic disorder, while other sources sometimes use autism or the autisms to refer to autistic disorders or even ASD.[12] ASD, in turn, is a subset of the broader autism phenotype (BAP), which describes individuals who may not have ASD but do have autistic-like traits, such as avoiding eye contact.[13]

Wide spectrum manifestations!

The manifestations of autism cover a wide spectrum, ranging from individuals with severe impairments—who may be silent, mentally disabled, and locked into hand flapping and rocking—to less impaired individuals who may have active but distinctly odd social approaches, narrowly focused interests, and verbose, pedantic communication.[14]

Hierarchies of functions!

Sometimes the syndrome is divided into low-, medium- and high-functioning autism (LFA, MFA, and HFA), based on IQ thresholds,[15] or on how much support the individual requires in daily life; these subdivisions are not standardized and are controversial.

Syndromal and non Syndromal associations!

Autism can also be divided into syndromal and non-syndromal autism, where the former is associated with severe or profound mental retardation or a congenital syndrome with physical symptoms, such as tuberous sclerosis.[16] Although individuals with Asperger's tend to perform better cognitively than those with autism, the extent of the overlap between Asperger's, HFA, and non-syndromal autism is unclear.[17]

Progress rather than loss of language and social skills!

Some studies have reported diagnoses of autism in children due to a loss of language or social skills, as opposed to a failure to make progress. Several terms are used for this phenomenon, including regressive autism, setback autism, and developmental stagnation. The validity of this distinction remains controversial; it is possible that regressive autism is a specific subtype.[18][19]


Pattern of symptoms!

Autism is distinguished by a pattern of symptoms rather than one single symptom. The main characteristics are impairments in social interaction, impairments in communication, restricted interests and repetitive behavior. Other aspects, such as atypical eating, are also common but are not essential for diagnosis.[20] Individual symptoms of autism occur in the general population and appear not to associate highly, without a sharp line separating pathological severity from common traits.[21]

Social development

People with autism have social impairments and often lack the intuition about others that many people take for granted. Noted autistic Temple Grandin described her inability to understand the social communication of neurotypicals as leaving her feeling "like an anthropologist on Mars".[22]

Social impairments become apparent early in childhood and continue through adulthood. Autistic infants show less attention to social stimuli, smile and look at others less often, and respond less to their own name. Autistic toddlers have more striking social deviance; for example, they have less eye contact and anticipatory postures and are less likely to use another person's hand or body as a tool.[19]

Face and Emotion recognition!

Three- to five-year-old autistic children are less likely to exhibit social understanding, approach others spontaneously, imitate and respond to emotions, communicate nonverbally, and take turns with others. However, they do form attachments to their primary caregivers.[23] They display moderately less attachment security than usual, although this feature disappears in children with higher mental development or less severe ASD.[24] Older children and adults with ASD perform worse on tests of face and emotion recognition.[25]

Friendship and loneliness (Quality more than quantity is critical!)

Contrary to common belief, autistic children do not prefer to be alone. Making and maintaining friendships often proves to be difficult for those with autism. For them, the quality of friendships, not the number of friends, predicts how lonely they are.[26]

Agression and violence symptomatic!

There are many anecdotal reports, but few systematic studies, of aggression and violence in individuals with ASD. The limited data suggest that in children with mental retardation, autism is associated with aggression, destruction of property, and tantrums. Dominick et al. interviewed the parents of 67 children with ASD and reported that about two-thirds of the children had periods of severe tantrums and about one third had a history of aggression, with tantrums significantly more common than in children with a history of language impairment.[27]


About a third to a half of individuals with autism do not develop enough natural speech to meet their daily communication needs.[28] Differences in communication may be present from the first year of life, and may include delayed onset of babbling, unusual gestures, diminished responsiveness, and the desynchronization of vocal patterns with the caregiver.

Echolalia (repeat other's words)

In the second and third years, autistic children have less frequent and less diverse babbling, consonants, words, and word combinations; their gestures are less often integrated with words. Autistic children are less likely to make requests or share experiences, and are more likely to simply repeat others' words (echolalia)[18][29] or reverse pronouns.[30]

Challenges with imaginative play!

Autistic children may have difficulty with imaginative play and with developing symbols into language.[18][29] They are more likely to have problems understanding pointing; for example, they may look at a pointing hand instead of the pointed-at object.[19][29]

Level os communication performance!

In a pair of studies, high-functioning autistic children aged 8–15 performed equally well, and adults better than individually matched controls at basic language tasks involving vocabulary and spelling. Both autistic groups performed worse than controls at complex language tasks such as figurative language, comprehension and inference.

As people are often sized up initially from their basic language skills, these studies suggest that people speaking to autistic individuals are more likely to overestimate what their audience comprehends.[31]

Repetitive behavior

A young boy with autism, and the precise line of toys he madeAutistic individuals display many forms of repetitive or restricted behavior, which the Repetitive Behavior Scale-Revised (RBS-R) categorizes as follows.

Stereotypy is apparently purposeless movement, such as hand flapping, head rolling, body rocking, or spinning a plate.

Compulsive behavior is intended and appears to follow rules, such as arranging objects in a certain way.

Sameness is resistance to change; for example, insisting that the furniture not be moved or refusing to be interrupted.

Ritualistic behavior involves the performance of daily activities the same way each time, such as an unvarying menu or dressing ritual.

Restricted behavior is limited in focus, interest, or activity, such as preoccupation with a single television program.

Self-injury includes movements that injure or can injure the person, such as biting oneself. Dominick et al. reported that self-injury at some point affected about 30% of children with ASD.[27]

No single repetitive behavior seems to be specific to autism, but only autism appears to have an elevated pattern of occurrence and severity of these behaviors.[32]

Other symptoms

Autistic individuals may have symptoms that are independent of the diagnosis, but that can affect the individual or the family.[20] A small fraction of individuals with ASD show unusual abilities, ranging from splinter skills such as the memorization of trivia to the extraordinarily rare talents of prodigious autistic savants.[33]

Impaired tactile perception!

Unusual responses to sensory stimuli are more common and prominent in autistic children, although there is no good evidence that sensory symptoms differentiate autism from other developmental disorders.[34] The responses may be more common in children: a pair of studies found that autistic children had impaired tactile perception while autistic adults did not.

Problem with Complex memory and reasoning sills!

The same two studies also found that autistic individuals had more problems with complex memory and reasoning tasks such as Twenty Questions; these problems were somewhat more marked among adults.[31] Several studies have reported associated motor problems that include poor muscle tone, poor motor planning, and toe walking; ASD is not associated with severe motor disturbances.[35]

Atypical eating behavior!

Atypical eating behavior occurs in about three-quarters of children with ASD, to the extent that it was formerly a diagnostic indicator. Selectivity is the most common problem, although eating rituals and food refusal also occur;[27] this does not appear to result in malnutrition. Some children with autism also have gastrointestinal (GI) symptoms, but there is a lack of published rigorous data to support the theory that autistic children have more or different GI symptoms than usual.[36]

Sleep problems common!

Sleep problems are known to be more common in children with developmental disabilities, and there is some evidence that children with ASD are more likely to have even more sleep problems than those with other developmental disabilities; autistic children may experience problems including difficulty in falling asleep, frequent nocturnal awakenings, and early morning awakenings. Dominick et al. found that about two-thirds of children with ASD had a history of sleep problems.[27]

Causes: Main article: Causes of autism

Although many genetic and environmental causes of autism have been proposed, its theory of causation is still incomplete.[37] Some researchers argue this is because autism is not a single disorder, but rather a triad of core aspects (social impairment, communication difficulties, and repetitive behaviors) that have distinct causes but often co-occur.[38]

More than 90% heritability!

Genetic factors are the most significant cause for autism spectrum disorders. Early studies of twins estimated heritability to be more than 90%; in other words, that genetics explains more than 90% of autism cases.[1] This may be an overestimate; new twin data and models with structural genetic variation are needed.[39] When only one identical twin is autistic, the other often has learning or social disabilities. For adult siblings, the risk of having one or more features of the broader autism phenotype might be as high as 30%,[40] much higher than the risk in controls.[41]

Complex gentics!

The genetics of autism is complex.[1] Genetic linkage analysis has been inconclusive; many association analyses have had inadequate power.[39] For each autistic individual, mutations in more than one gene may be implicated. Mutations in different sets of genes may be involved in different autistic individuals. There may be significant interactions among mutations in several genes, or between the environment and mutated genes.

Neural development protein encoding problem!

By identifying genetic markers inherited with autism in family studies, numerous candidate genes have been located, most of which encode proteins involved in neural development and function.[42] However, for most of the candidate genes, the actual mutations that increase the risk for autism have not been identified. Typically, autism cannot be traced to a Mendelian (single-gene) mutation or to single chromosome abnormalities such as fragile X syndrome or 22q13 deletion syndrome.[16][43]

Chromosomal deletion, duplication and inversion are the suspects!

Deletion (1), duplication (2) and inversion (3) are all chromosome abnormalities that have been implicated in autism.[44]The large number of autistic individuals with unaffected family members may result from copy number variations (CNVs)—spontaneous alterations in the genetic material during meiosis that delete or duplicate genetic material.

Array comparative genomic hygridization studies!

Sporadic (non-inherited) cases have been examined to identify candidate genetic loci involved in autism. Using array comparative genomic hybridization (array CGH), a technique for detecting CNVs, one study found them in 10% of families with one affected child.[45] Some of the altered loci had been identified in previous studies of inherited autism; many were unique to the sporadic cases examined in this study.

Autism may be highly heritable but not inherited! Contradictions?

Hence, a substantial fraction of autism may be highly heritable but not inherited: that is, the mutation that causes the autism is not present in the parental genome. Although the fraction of autism traceable to a genetic cause may grow to 30–40% as the resolution of array CGH improves,[44] several results in this area have been described incautiously, possibly misleading the public into thinking that a large proportion of autism is caused by CNVs and is detectable via array CGH, or that detecting CNVs is tantamount to a genetic diagnosis.[46]

The Autism Genome Project- every human chromosome may be involved?

The Autism Genome Project database contains genetic linkage and CNV data that connect autism to genetic loci and suggest that every human chromosome may be involved.[47]

Suspected teratogens: thalidomide, valproic acid, misoprostol, rubella

Teratogens (agents that cause birth defects) related to the risk of autism include exposure of the embryo to thalidomide, valproic acid, or misoprostol, or to rubella infection in the mother. These cases are rare.[48]

First 8 weeks teratogen exposure!

All known teratogens appear to act during the first eight weeks from conception, and though this does not exclude the possibility that autism can be initiated or affected later, it is strong evidence that autism arises very early in development.[2] Although extensive searches are underway for other environmental causes,[48] evidence for them is anecdotal and has not been confirmed by reliable studies.[3]

Mothers lifestyle and exposure to toxins!

Several other pre- or post-natal environmental factors have been claimed to contribute to autism or exacerbate its symptoms, or may be important to consider in future research. They include certain foods,[49] infectious disease, heavy metals, solvents, diesel exhaust, PCBs, phthalates and phenols used in plastic products, pesticides, brominated flame retardants, alcohol, smoking, illicit drugs, and vaccines.[4]

MMR Preservative thiomersal could be one of the toxins?

Although parents may first become aware of autistic symptoms in their child around the time of a routine vaccination, and parental concern about vaccines has led to a decreasing uptake of childhood immunizations and an increasing likelihood of measles outbreaks, there is overwhelming scientific evidence showing no causal association between the measles-mumps-rubella vaccine and autism, and there is no convincing evidence that the vaccine preservative thiomersal helps cause autism.[50][51]

Mechanism: ? Neuropsychological linkages between brain structues!

Despite extensive investigation, how autism occurs is not well understood. Its mechanism can be divided into two areas: the pathophysiology of brain structures and processes associated with autism, and the neuropsychological linkages between brain structures and behaviors.[9] The behaviors appear to have multiple pathophysiologies.[21]


Early alteration in brain development almost after conception!

Autism affects many parts of the brain.Autism appears to result from developmental factors that affect many or all functional brain systems.[43] Neuroanatomical studies and the associations with teratogens strongly suggest that autism's mechanism includes alteration of brain development soon after conception.[2] This localized anomaly appears to start a cascade of pathological events in the brain that are significantly influenced by environmental factors.[52]

The cortex, cerebellum, inferior olives and reduction in Purkinje cells!

Poorly regulated growth of neurons increase in brain weight and volume!

Many major structures of the human brain have been implicated. Consistent abnormalities have been found in the development of the cerebral cortex; and in the cerebellum and related inferior olive, which have a significant decrease in the number of Purkinje cells. Brain weight and volume and head circumference tend to be greater in autistic children; the effects of these are unknown.[53] It may be due to poorly regulated growth of neurons.[9]

Balanced immune response and successful neurodevelopment!

Interactions between the immune system and the nervous system begin early during embryogenesis, and successful neurodevelopment depends on a balanced immune response. Several symptoms consistent with a poorly regulated immune response have been reported in autistic children.

Aberrant immune activity during critical periods of neurodevelopment

It is possible that aberrant immune activity during critical periods of neurodevelopment is part of the mechanism of some forms of ASD.[54] As autoantibodies have not been associated with pathology, are found in diseases other than ASD, and are not always present in ASD,[55] it is still hard to draw conclusions about the role of immune factors in autism.[56]

Increased serum serotonin!

Several neurotransmitter abnormalities have been detected in autism, notably increased blood levels of serotonin. Whether these lead to structural or behavioral abnormalities is unclear.[9]

The Mirror Neuron System (MNS) theory!

The mirror neuron system (MNS) theory of autism hypothesizes that distortion in the development of the MNS interferes with imitation and leads to autism's core features of social impairment and communication difficulties.

The MNS operates when an animal performs an action or observes another animal of the same species perform the same action. The MNS may contribute to an individual's understanding of other people by enabling the modeling of their behavior via embodied simulation of their actions, intentions, and emotions.[57]

Reduced MSN activity- delay in the activationof the core circuit for imitation!

Several studies have tested this hypothesis by demonstrating structural abnormalities in MNS regions of individuals with ASD, delay in the activation in the core circuit for imitation in individuals with Asperger's, and a correlation between reduced MNS activity and severity of the syndrome in children with ASD.[58]

Underconnectivity theory! high level neural connections and synchronizations!

Functional magnetic resonance imaging provides some evidence for the underconnectivity theory of autism.The underconnectivity theory of autism hypothesizes that autism is marked by underfunctioning high-level neural connections and synchronization, along with an excess of low-level processes.[59]

cortical local overconnectivity & weak functional connections with the frontal lobe!

ASD a disease of the associaton cortex between the two hemispheres?

Evidence for this theory has been found in functional neuroimaging studies on autistic individuals[31] and by a brain wave study that suggested that adults with ASD have local overconnectivity in the cortex and weak functional connections between the frontal lobe and the rest of the cortex.[60] Other evidence suggests the underconnectivity is mainly within each hemisphere of the cortex and that autism is a disorder of the association cortex.[61]


Two major categories of cognitive theories have been proposed about the links between autistic brains and behavior.

A. Deficits in social cognition!

The first category focuses on deficits in social cognition. Hyper-systemizing hypothesizes that autistic individuals can systematize—that is, they can develop internal rules of operation to handle internal events—but are less effective at empathizing by handling events generated by other agents.[15]

Extreme male theory: systemizing than empathizing!

It extends the extreme male brain theory, which hypothesizes that autism is an extreme case of the male brain, defined psychometrically as individuals in whom systemizing is better than empathizing.[62] This in turn is related to the earlier theory of mind, which hypothesizes that autistic behavior arises from an inability to ascribe mental states to oneself and others.

Support by Sally-Anne test for reasoning!

The theory of mind is supported by autistic children's atypical responses to the Sally-Anne test for reasoning about others' motivations,[63] and is mapped well from the mirror neuron system theory of autism.[58]

Executive Dysfunctional Hypothesis!

Narrow interests: deficits in flexibility, planning,and executive functions!

The second category focuses on nonsocial or general processing. Executive dysfunction hypothesizes that autistic behavior results in part from deficits in flexibility, planning, and other forms of executive function. A strength of the theory is predicting stereotyped behavior and narrow interests;[64] a weakness is that executive function deficits are not found in young autistic children.[25]

Limited ability to see the big picture!

Weak central coherence theory hypothesizes that a limited ability to see the big picture underlies the central disturbance in autism. One strength of this theory is predicting special talents and peaks in performance in autistic people.[65] A related theory—enhanced perceptual functioning—focuses more on the superiority of locally oriented and perceptual operations in autistic individuals.[66] These theories map well from the underconnectivity theory of autism.

Combining the Social Cognitive and Neuropsychological theories?

Neither category is satisfactory on its own; social cognition theories poorly address autism's rigid and repetitive behaviors, while the nonsocial theories have difficulty explaining social impairment and communication difficulties.[38] A combined theory based on multiple deficits may prove to be more useful.[7]


Parents are usually the first to notice unusual behaviors in their child.[67] As postponing treatment may affect long-term outcome, any of the following signs is reason to have a child evaluated by a specialist without delay:

No babbling by 12 months.
No gesturing (pointing, waving goodbye, etc.) by 12 months.
No single words by 16 months.
No two-word spontaneous phrases (not including echolalia) by 24 months.
Any loss of any language or social skills, at any age.[20]

Screening for ASD in the General Population!

The American Academy of Pediatrics recommends that all children be screened for ASD at the 18- and 24-month well-child doctor visits, using autism-specific formal screening tests.[68]

In contrast, the UK National Screening Committee recommends against screening for ASD in the general population, because screening tools have not been fully validated and interventions lack sufficient evidence for effectiveness.[69]

Genetic screening is too hot now (political and ethical correctness!)

Genetic screening for autism is generally still impractical. As genetic tests are developed several ethical, legal, and social issues will emerge. Commercial availability of tests may precede adequate understanding of how to use test results, given the complexity of autism's genetics.[70]


Behavior based diagnosis Vs DSM-IV-TR!

Diagnosis is based on behavior, not cause or mechanism.[21] Autism is defined in the DSM-IV-TR as exhibiting at least six symptoms total, including at least two symptoms of qualitative impairment in social interaction, at least one symptom of qualitative impairment in communication, and at least one symptom of restricted and repetitive behavior.

Lack of social and emotional reciprocity!

Sample symptoms include:

1. lack of social or emotional reciprocity,

2. stereotyped and repetitive use of language or idiosyncratic language,and

3. persistent preoccupation with parts of objects.

4. Onset must be prior to age three years, with delays or abnormal functioning in either social interaction, language as used in social communication, or symbolic or imaginative play.

5. The disturbance must not be better accounted for by Rett syndrome or childhood disintegrative disorder.[71]

ICD-10 uses essentially the same definition.[8]

Diagnostic instruments

Several diagnostic instruments are available. Two are commonly used in autism research:

1. the Autism Diagnostic Interview-Revised (ADI-R) is a semistructured parent interview, and the Autism Diagnostic Observation Schedule (ADOS) uses observation and interaction with the child.

2. The Childhood Autism Rating Scale (CARS) is used widely in clinical environments to assess severity of autism based on observation of children.[19]

Developmental history and physical examination!

A pediatrician commonly performs a preliminary investigation by taking developmental history and physically examining the child.

ASD Specialists: cognitive, communication and family factors

If warranted, diagnosis and evaluations are conducted with help from ASD specialists, observing and assessing cognitive, communication, family, and other factors using standardized tools, and taking into account any associated medical conditions.

A differential diagnosis for ASD at this stage might also consider mental retardation, hearing impairment, and a specific language impairment[72] such as Landau-Kleffner syndrome.[73]

Early diagnosis by 14, 48 months and 61 months

In the UK the National Autism Plan for Children recommends at most 30 weeks from first concern to completed diagnosis and assessment, though few cases are handled that quickly in practice.[72] ASD can sometimes be diagnosed by age 14 months,[74] but a 2006 U.S. study found the average age of first evaluation by a qualified professional was 48 months and of formal ASD diagnosis was 61 months, reflecting an average 13-month delay, all far above recommendations.[75]

Changes in diagnostic practices for under and over diagnosis!

Underdiagnosis and overdiagnosis are problems in marginal cases, and much of the recent increase in the number of reported ASD cases is likely due to changes in diagnostic practices. The increasing popularity of drug treatment options and the expansion of benefits has given providers incentives to diagnose ASD, resulting in some overdiagnosis of children with uncertain symptoms. Conversely, the cost of screening and diagnosis and the challenge of obtaining payment can inhibit or delay diagnosis.[76]

Autistic symptoms overlap with common blindeness syndrome!

It is particularly hard to diagnose autism among the visually impaired, partly because some of its diagnostic criteria depend on vision, and partly because autistic symptoms overlap with those of common blindness syndromes.[77]

Retrospective diagnosis for adults!

The symptoms of autism and ASD begin early in childhood but are occasionally missed. Adults may seek retrospective diagnoses to help them or their friends and family understand themselves, to help their employers make adjustments, or in some locations to claim disability living allowances or other benefits.[78]

Treatment: Main article: Autism therapies

Child's needs based treatment!

The goal of treatment is to manage and improve symptoms and functioning. No single treatment is best and treatment is typically tailored to the child's needs.

intenstive, sustained special education programs!

Intensive, sustained special education programs and behavior therapy early in life can help children acquire self-care, social, and job skills;[79][80] claims that intervention by age 2–3 years is crucial are not substantiated.[81]

Applied behavior analysis (ABA): One-on-one task teaching!

Among the available approaches, applied behavior analysis (ABA) has demonstrated efficacy in promoting social and language development and in reducing behaviors that interfere with learning and cognitive functioning;[80] ABA focuses on teaching tasks one-on-one using the behaviorist principles of stimulus, response and reward.[82]

TEACH: Structuring the physical environment and using visual support

Several programs are based on ABA. Some focus on discrete trial teaching; more-comprehensive ones use multiple assessment and intervention methods individually and dynamically.[83] Cognitive therapies based on comprehensive programs in treatment centers are a common alternative: for example, TEACCH focuses on structuring the physical environment and using visual supports for language development tasks.[80]

Home-based early intensive behavior intervention is best!

A 2005 California study found that early intensive behavior analytic treatment, a form of ABA, was substantially more effective for preschool children with autism than the mixture of methods provided in many programs,[82] but a 2007 British study found that home-based early intensive behavioral interventions, another ABA form, was no more effective than nursery-based eclectic programs.[84] The limited research on the effectiveness of adult residential programs shows mixed results.[85]

Anti-depressants, stimulants and anti-pschotics?

Medications are often used to treat problems associated with ASD. More than half of U.S. children diagnosed with ASD are prescribed psychoactive drugs or anticonvulsants, with the most common drug classes being antidepressants, stimulants, and antipsychotics.[86]

Risperodine- anti psyhotic for symptomatic irritability! for 5-16 years!

In the United States, the antipsychotic risperidone is approved for treating symptomatic irritability in autistic children aged 5–16 years.[87]

Serotoning inhibitors and Dopamine blockers for maladoptive behaviors!

Other drugs are prescribed off-label, which means they have not been approved for treating ASD. For example, some selective serotonin reuptake inhibitors and dopamine blockers can reduce some maladaptive behaviors associated with ASD.[88] However, there is scant reliable research about the effectiveness or safety of drug treatments for adolescents and adults with ASD.[89]

Effectiveness and Safety are concerns!

A person with ASD may respond atypically to medications, the medications can have adverse side effects, and no known medication relieves autism's core symptoms of social and communication impairments.[67][90]

Therapeutic interventions!

Many other therapies and interventions are available. Few are supported by scientific studies.[5][25][91][92] Treatment approaches lack empirical support in quality-of-life contexts, and many programs focus on success measures that lack predictive validity and real-world relevance.[26]

Watch out for program marketeers!

Scientific evidence appears to matter less to service providers than program marketing, training availability, and parent requests.[93] Even if they do not help, conservative treatments such as changes in diet are probably harmless aside from their bother and cost.[49] Dubious invasive treatments are a much more serious matter: for example, in 2005, botched chelation therapy killed a 5-year-old autistic boy.[50]

ASD is a costly disorder!

Treatment is expensive;[94] indirect costs are more so. A U.S. study estimated the average additional lifetime cost due exclusively to autism to be $3.2 million in 2003 U.S. dollars for an autistic individual born in 2000, with about 10% medical care, 30% nonmedical care such as child care and education, and 60% the lost economic productivity of individuals and their parents.[95]

An average lifetime cost of @.4 Million Pounds!

A British study estimated an average lifetime cost of ₤2.4 million in 1997–1998 British pounds.[96] Legal rights to treatment are complex, vary with location and age, and require advocacy by caregivers.[92] Publicly supported programs are often inadequate or inappropriate for a given child, and unreimbursed out-of-pocket medical or therapy expenses are associated with likelihood of family financial problems.[97]

Long term care: residential care, job training, sexuality & social skills!

After childhood, key treatment issues include residential care, job training and placement, sexuality, social skills, and estate planning.[92]


There is no cure.[5] Most children with autism lack social support, meaningful relationships, future employment opportunities or self-determination.[26] Although core difficulties remain, symptoms often become less severe in later childhood.[81]

Few high-quality studies address long-term prognosis. Some adults show modest improvement in some symptoms, but some decline; no study has focused on autism after midlife.[98] Acquiring language before age 6, having IQ above 50, and having a marketable skill all predict better outcomes; independent living is unlikely with severe autism.[99]

A 2004 British study of 68 adults who were diagnosed before 1980 as autistic children with IQ above 50 found that 12% achieved a high level of independence as adults, 10% had some friends and were generally in work but required some support, 19% had some independence but were generally living at home and needed considerable support and supervision in daily living, 46% needed specialist residential provision from facilities specializing in ASD with a high level of support and very limited autonomy, and 12% needed high-level hospital care.[6]

A 2005 Swedish study of 78 adults that did not exclude low IQ found worse prognosis; for example, only 4% achieved independence.[100] Changes in diagnostic practice and increased availability of effective early intervention make it unclear whether these findings can be generalized to recently diagnosed children.[4]


Further information: Conditions comorbid to autism spectrum disorders
Estimates of the prevalence of autism vary widely depending on diagnostic criteria, age of children screened, and geographical location.[101]

Most recent reviews tend to estimate a prevalence of 1–2 per 1,000 for autism and close to 6 per 1,000 for ASD;[4]

PDD-NOS is the vast majority of ASD, Asperger's is about 0.3 per 1,000 and the atypical forms childhood disintegrative disorder and Rett syndrome are much rarer.[102]

A 2006 study of nearly 57,000 British nine- and ten-year-olds reported a prevalence of 3.89 per 1,000 for autism and 11.61 per 1,000 for ASD; these higher figures could be associated with broadening diagnostic criteria.[103]

The risk of autism is associated with several prenatal and perinatal risk factors. A 2007 review of risk factors found associated parental characteristics that included advanced maternal age, advanced paternal age, and maternal place of birth outside Europe or North America, and also found associated obstetric conditions that included low birth weight and gestation duration, and hypoxia during childbirth.[104]

About 10–15% of autism cases have an identifiable Mendelian (single-gene) condition, chromosome abnormality, or other genetic syndrome,[40] and ASD is associated with several genetic disorders.[105]

Autism is associated with mental retardation: a 2001 British study of 26 autistic children found about 30% with intelligence in the normal range (IQ above 70), 50% with mild to moderate retardation, and about 20% with severe to profound retardation (IQ below 35).

For ASD other than autism the association is much weaker: the same study reported about 94% of 65 children with PDD-NOS or Asperger's had normal intelligence.[106] ASD is also associated with epilepsy, with variations in risk of epilepsy due to age, cognitive level, and type of language disorder.[107] Boys are at higher risk for autism than girls.

The ASD sex ratio averages 4.3:1 and is greatly modified by cognitive impairment: it may be close to 2:1 with mental retardation and more than 5.5:1 without. Recent studies have found no association with socioeconomic status, and have reported inconsistent results about associations with race or ethnicity.[4] Phobias, depression and other psychopathological disorders have often been described along with ASD but this has not been assessed systematically.[108]

Autism's incidence, despite its advantages for assessing risk, is less useful in autism epidemiology, as the disorder starts long before it is diagnosed, and the gap between initiation and diagnosis is influenced by many factors unrelated to risk.

Attention is focused mostly on whether prevalence is increasing with time. Earlier prevalence estimates were lower, centering at about 0.5 per 1,000 for autism during the 1960s and 1970s and about 1 per 1,000 in the 1980s, as opposed to today's 1–2 per 1,000.[4]

Reports of autism cases grew dramatically in the U.S. in 1996–2005. It is unknown how much, if any, growth came from changes in autism's prevalence.The number of reported cases of autism increased dramatically in the 1990s and early 2000s.

This increase is largely attributable to changes in diagnostic practices, referral patterns, availability of services, age at diagnosis, and public awareness,[109] though as-yet-unidentified contributing environmental risk factors cannot be ruled out.[3]

A widely cited 2002 pilot study concluded that the observed increase in autism in California cannot be explained by changes in diagnostic criteria,[110] but a 2006 analysis found that special education data poorly measured prevalence because so many cases were undiagnosed, and that the 1994–2003 U.S. increase was associated with declines in other diagnostic categories, indicating that diagnostic substitution had occurred.[111]

It is unknown whether autism's prevalence increased during the same period. An increase in prevalence would suggest directing more attention and funding toward changing environmental factors instead of continuing to focus on genetics.[48]


A few examples of autistic symptoms and treatments were described long before autism was named. The Table Talk of Martin Luther contains a story of a 12-year-old boy who may have been severely autistic.[112]

According to Luther's notetaker Mathesius, Luther thought the boy was a soulless mass of flesh possessed by the devil, and suggested that he be suffocated.[113] Victor of Aveyron, a feral child caught in 1798, showed several signs of autism; the medical student Jean Itard treated him with a behavioral program designed to help him form social attachments and to induce speech via imitation.[114]

The New Latin word autismus (English translation autism) was coined by the Swiss psychiatrist Eugen Bleuler in 1910 as he was defining symptoms of schizophrenia. He derived it from the Greek word autos (αὐτός, meaning self), and used it to mean morbid self-admiration, referring to "autistic withdrawal of the patient to his fantasies, against which any influence from outside becomes an intolerable disturbance."[115]

Leo Kanner introduced the label early infantile autism in 1943.The word autism first took its modern sense in 1938 when the Viennese pediatrician Hans Asperger adopted Bleuler's terminology "autistic psychopaths" in a lecture in German about child psychology.[116]

Asperger was investigating a form of ASD now known as Asperger syndrome, though for various reasons it was not widely recognized as a separate diagnosis until 1981.[114]

Leo Kanner of the Johns Hopkins Hospital first used autism in its modern sense in English when he introduced the label early infantile autism in a 1943 report of 11 children with striking behavioral similarities.[30] Almost all the characteristics described in Kanner's first paper on the subject, notably "autistic aloneness" and "insistence on sameness", are still regarded as typical of the autistic spectrum of disorders.[38] It is not known whether Kanner derived the term independently of Asperger.[117]

Kanner's reuse of autism led to decades of confused terminology like "infantile schizophrenia", and child psychiatry's focus on maternal deprivation during the mid-1900s led to misconceptions of autism as an infant's response to "refrigerator mothers".

Starting in the late 1960s autism was established as a separate syndrome by demonstrating that it is lifelong, distinguishing it from mental retardation and schizophrenia and from other developmental disorders, and demonstrating the benefits of involving parents in active programs of therapy.[118] As late as the mid-1970s there was little evidence of a genetic role in autism; now it is thought to be one of the most heritable of all psychiatric conditions.[119] The rise of parent organizations and the destigmatization of childhood ASD have deeply affected how we view ASD, its boundaries, and its treatments.[114]

The Internet has helped autistic individuals bypass nonverbal cues and emotional sharing that they find so hard to deal with, and has given them a way to form online communities and work remotely.[120] Sociological and cultural aspects of autism have developed: some in the community seek a cure, while others believe that autism is simply another way of being.[7][121]


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^ Lack of research on drug treatments:
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^ Lack of support for interventions:
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^ Prevalence estimates vary:
Fombonne E (2007). "Epidemiological surveys of pervasive developmental disorders", in Volkmar FR: Autism and Pervasive Developmental Disorders, 2nd ed, Cambridge University Press, 33–68. ISBN 0521549574.

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^ Changes in diagnostic practices:
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