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Like all preliminary studies, this one is... preliminary. In other words, it has not been replicated, and the findings may turn out to be misleading.

The upshot of these differences is that the columns in an autistic brain seem to be more connected than normal with their close neighbours, and less connected with their distant ones. Though it is an interpretative stretch, that pattern of connection might reduce a person’s ability to generalise (since disparate data are less easily integrated) and increase his ability to concentrate (by drawing together similar inputs).

Dr Snyder argues that savant skills are latent in everyone, but that access to them is inhibited in non-savants by other neurological processes. He is able to remove this inhibition using a technique called repetitive transcranial magnetic stimulation.

In 2006 your lab published a paper in Nature Neuroscience linking a mirror neuron dysfunction to autism. How might reduced mirror neuron activity explain the symptoms of autism?

Reduced mirror neuron activity obviously weakens the ability of these patients to experience immediately and effortlessly what other people are experiencing, thus making social interactions particularly difficult for these patients. Patients with autism have also often motor problems and language problems. It turns out that a deficit in mirror neurons can in principle explain also these other major symptoms. The motor deficits in autism can be easily explained because mirror neurons are just special types of premotor neurons, brain cells essential for planning and selecting actions. It has been also hypothesized that mirror neurons may be important in language evolution and language acquisition.

Thus, a deficit in mirror neurons can in principle account for three major symptoms of autism, the social, motor and language problems.

There is convincing behavioral evidence linking media violence with imitative violence. Mirror neurons provide a plausible neurobiological mechanism that explains why being exposed to media violence leads to imitative violence.

I think there are two key points to keep in mind. The first one is the one we started with: mirror neurons are brain cells specialized for actions. They are obviously critical cells for social interactions but they can’t explain non-social cognition. The second point to keep in mind is that every brain cell and every neural system does not operate in a vacuum. Everything in the brain is interconnected, so that the activity of each cell reflects the dynamic interactions with other brain cells and other neural systems.

Facilitated Communication therapy began in Australia with Rosemary Crossley. The center for FC in the United States is Syracuse University, which houses the Facilitated Communication Institute (FCI) in their School of Education.

A very damaging, detailed criticism was presented on PBS's "Frontline", October 19, 1993. The program was repeated December 17, 1996, and added that since the first showing, Syracuse University has claimed to have done three studies which verify the reality and effectiveness of FC, while thirty other studies done elsewhere have concluded just the opposite.

Furthermore, FC clients routinely use a flat board or keyboard, over which the facilitator holds their pointing finger. Even the most expert typist could not routinely hit correct letters without some reference as a starting point.

Facilitators routinely look at the keyboard; clients do not. The messages' basic coherence indicates that they most probably are produced by someone who is looking at the keyboard.

Anyone familiar with Helen Keller, Stephen Hawking or Christy Brown knows that blindness, deafness, cerebral palsy, multiple sclerosis, amyotrophic lateral sclerosis (ALS), or physical or neurological disorders, do not necessarily affect the intellect. There is no necessary connection between a physical handicap and a mental handicap. We also know that such people often require an assistant to facilitate their communication. But what facilitators do to help the likes of a Hawking or a Brown is a far cry from what those in the facilitated communication business are doing.

But the vast majority of FC clients apparently are mentally retarded or autistic. Their facilitators appear to be reporting their own thoughts, not their patient's thoughts. Interestingly, the facilitators are genuinely shocked when they discover that they are not really communicating their patient's thoughts. Their reaction is similar to that of dowsers and others with "special powers" who, when tested under controlled conditions, find they don't have any special powers at all.

It is interesting that the parents and other loved ones who have been bonding with the patient for years are unable to be facilitators with their own children.

And when the kind strangers and their patients are put to the test, they generally fail. We are told that is because the conditions made them nervous. These ad hoc excuses sound familiar; they sound like the complaints of parapsychologists.

Skeptics think the evidence is in and FC is a delusion for the most part. It is also a dangerous delusion. Critics have noted a similarity between FC therapy and repressed memory therapy: patients are accusing their parents and others of having sexually abused them. Facilitators are taught that something like 13% of their clients have been sexually abused. This information may unconsciously influence their work.

Another weakness of the study is that it was short term, only four weeks. It therefore did not test if the effect of hyperbaric treatment survives much beyond the treatment itself. Even if the effect in this study is real, it may represent only a temporary symptomatic benefit - not altering the course of autism itself. Therefore longer followup studies are needed as well.

It is not impossible that hyperbaric oxygen may have some benefit in some children with autism.

The biggest risk of the treatment now is that it is expensive - costing 150-900 dollars per treatment or 14-17 thousand dollars for a chamber.

But one thing is clear - any future studies should be very tightly controlled, or they will be counterproductive.

Einstein researchers contend that scientific evidence directly points to the locus coeruleus–noradrenergic (LC-NA) system as being involved in autism. “The LC-NA system is the only brain system involved both in producing fever and controlling behavior,” says co-author Dominick P. Purpura, M.D., dean emeritus and distinguished professor of neuroscience at Einstein.

The locus coeruleus has widespread connections to brain regions that process sensory information.

It is also involved in a variety of complex behaviors, such as attentional focusing (the ability to concentrate attention on environmental cues relevant to the task in hand, or to switch attention from one task to another).

“What is unique about the locus coeruleus is that it activates almost all higher-order brain centers that are involved in complex cognitive tasks,” says Dr. Mehler.

Drs. Purpura and Mehler hypothesize that in autism, the LC-NA system is dysregulated by the interplay of environment, genetic, and epigenetic factors (chemical substances both within as well as outside the genome that regulate the expression of genes). They believe that stress plays a central role in dysregulation of the LC-NA system, especially in the latter stages of prenatal development when the fetal brain is particularly vulnerable.

Drs. Purpura and Mehler believe that, in autistic children, fever stimulates the LC-NA system, temporarily restoring its normal regulatory function.

the future of autism treatment probably lies in drugs that selectively target certain types of noradrenergic brain receptors or, more likely, in epigenetic therapies targeting genes of the LC-NA system.

“You can’t take a complex neuropsychiatric disease that has escaped our understanding for 50 years and in one fell swoop have a therapy that is going to reverse it — that’s folly. On the other hand, we now have clues to the neurobiology, the genetics, and the epigenetics of autism. To move forward, we need to invest more money in basic science to look at the genome and the epigenome in a more focused way.”

This study documented that autistic children experience behavior changes during fever.

Einstein researchers contend that scientific evidence directly points to the locus coeruleus–noradrenergic (LC-NA) system as being involved in autism. "The LC-NA system is the only brain system involved both in producing fever and controlling behavior," says co-author Dominick P. Purpura, M.D., dean emeritus and distinguished professor of neuroscience at Einstein.

The locus coeruleus has widespread connections to brain regions that process sensory information. It secretes most of the brain's noradrenaline, a neurotransmitter that plays a key role in arousal mechanisms, such as the "fight or flight" response. It is also involved in a variety of complex behaviors, such as attentional focusing (the ability to concentrate attention on environmental cues relevant to the task in hand, or to switch attention from one task to another). Poor attentional focusing is a defining characteristic of autism.

"What is unique about the locus coeruleus is that it activates almost all higher-order brain centers that are involved in complex cognitive tasks," says Dr. Mehler.

autism, the LC-NA system is dysregulated by the interplay of environment, genetic, and epigenetic factors

They believe that stress plays a central role in dysregulation of the LC-NA system, especially in the latter stages of prenatal development when the fetal brain is particularly vulnerable.

a higher incidence of autism among children whose mothers had been exposed to hurricanes and tropical storms during pregnancy.

autistic children, fever stimulates the LC-NA system, temporarily restoring its normal regulatory function. "This could not happen if autism was caused by a lesion or some structural abnormality of the brain," says Dr. Purpura.

future of autism treatment probably lies in drugs that selectively target certain types of noradrenergic brain receptors or, more likely, in epigenetic therapies targeting genes of the LC-NA system.

If the locus coeruleus is impaired in autism, it is probably because tens or hundreds, maybe even thousands, of genes are dysregulated in subtle and complex ways," says Dr. Mehler. "The only way you can reverse this process is with epigenetic therapies, which, we are beginning to learn, have the ability to coordinate very large integrated gene networks."

"You can't take a complex neuropsychiatric disease that has escaped our understanding for 50 years and in one fell swoop have a therapy that is going to reverse it — that's folly. On the other hand, we now have clues to the neurobiology, the genetics, and the epigenetics of autism. To move forward, we need to invest more money in basic science to look at the genome and the epigenome in a more focused way."

Thompson (1993) describes facilitated communication as a classic example of the self-fulfilling prophecy. The facilitator wants to believe that the person with a severe cognitive and language disability is actually of normal to superior intellectual ability. Parents especially want to believe that a way has been found to finally unlock the door to their real son or daughter.

In short, people want facilitated communication to work.

Advocates of facilitated communication often respond to naysayers, "It can't hurt to try it." Biklen agrees, "It is not harmful to teach people to communicate through pointing." However, he qualifies his claim with the caveat that "it can be harmful if the facilitator over interprets, does not monitor the person's eyes, facilitates when the person is looking away, is not sensitive to the possibility of guiding the person, and asks leading rather than clarifying questions."

Some argue that "false communication" may distort beliefs, understanding, and rehabilitative approaches to persons with autism and other developmental disabilities.

Additionally, facilitated communication in the past few years has been the source of many contested abuse allegations, usually allegedly reported by an individual with very limited unassisted communication skills against a family caregiver or caregivers.

There are at least 50 legal cases in the U.S. involving allegations of sexual abuse produced through facilitated communication (Berger, 1994). Several such cases have already occurred in Australia, and some have arisen in Europe (Green, 1992).

With the exception of three empirical studies (Intellectual Disability Review Panel, 1989; Calculator and Singer, 1992; and Velazquez (in press)) which provide preliminary validation of facilitated communication, most of the support for the validity of facilitated communication is based on anecdotal reports.

Unfortunately, validity questions surround anecdotal reports of facilitated communication. In general, these reports lack the controls necessary to rule out experimenter biases, reliability concerns, and threats to validity (Cummins and Prior, 1992; Jacobsen, Eberlin, Mulick, Schwartz, Szempruch, and Wheeler, 1994).

Although Biklen (1990) admits that facilitator influence is a real possibility, facilitated communications are typically reported as though they are the words of the person with a disability.

Without exception, these empirical studies have questioned the authenticity of the communication as truly coming from the individual versus the facilitator.

Interdisciplinary Party Report (1988) and the Intellectual Disability Review Panel (1989) both of which examined the source of facilitated communications produced by persons in Australia, and found strong evidence that responses obtained through facilitation were influenced by the facilitator.

Gina Green, Director of Research for the New England Center for Autism and Associate Scientist for the E.K. Shriver Center for Mental Retardation, Inc., has reviewed over 150 cases where empirical testing was performed and cites 15 independent conduct evaluations involving 136 individuals with autism and/or mental retardatiion who were alleged to have been taught to communicate via facilitated communication. In none of the cases were investigators able to confirm facilitated communication by the 136 individuals.

Pervasive Developmental Disorders, including Autistic Disorder, Asperger Disorder, Pervasive Developmental Disorder Not Otherwise Specified, and Childhood Disintegrative Disorder.

For autistic disorder, Fombonne says: The correlation between prevalence and year of publication was statistically significant and studies with prevalenceover 7/10,000 were all published since 1987. These findings point towards an increase in prevalence estimates in the last 15-20 years.

recent autism surveys have consistently identified smaller numbers of children with AS than those with autism within the same survey.

How much lower is difficult to establish from existing data, but a ratio of 3 or 4 to 1 would appear an acceptable,

We therefore used for subsequent calculations an estimate of 6/10,000 for AS, recognizing the strong limitations of available data on AS.

Eight studies provided data on childhood disintegrative disorder (CDD). Prevalence estimates ranged from 0 to 9.2/100,000.

The upper-bound limit of the associated confidence interval (4.0/100,000) indicates that CDD is a very rare condition, with about 1 case to occur for every 103 cases of autistic disorder.

Current evidence does not strongly support the hypothesis of a secular increase in the incidence of autism but power todetect time trends is seriously limited in existing datasets.

Whilst it is clear that prevalence estimates have gone up over time, this increase most likely represents changes in the concepts, definitions, service availability and awareness of autistic-spectrum disorders in both the lay and professional public.

The possibility that a true change in the underlying incidence has contributed to higher prevalence figures remains, however, to be adequately tested.

The picture with autism in Somali children is a little murkier. It turns out that the incidence of autism is very high in children of Somali origin who were born in the US (several times higher than normal), while it appears to be very low in Somali children born in their native country. Again, vaccination has been identified as the likely cause by Somali parents and by many observers — but again, clamping follows placental delivery in Somalia, while the cord has been clamped without delay as a general practice in Minnesota, where a high incidence of autism in these children of Somali immigrants was first discovered.

It found several genetic variants commonly associated with ASD, all of them pointing two specific genes found on chromosome 5 which control production of proteins which help cells stick to each other, and make nervous connections.

One variant, linked to a gene called CDH10, was so common - present in over 65% of cases of autism - that the researchers calculated that fixing it would cut the number of autism cases by 15%.

They also linked ASD rather less strongly to a group of about 30 genes which produce proteins that play a key role in enabling brain cells to migrate to correct places, and to connect to neighbouring cells.

Professor Simon Baron-Cohen, an autism expert at the University of Cambridge, said 133 genes had now been linked to the condition, and much work was needed to piece together how they interacted with each other and the environment.

The National Autistic Society said the exact causes of autism were unknown. In a statement, the society said: "There is evidence to suggest that genetic factors are responsible for some forms of autism. "However, the difficulty of establishing gene involvement is compounded by the interaction of genes and by their interaction with environmental factors. "Various studies over many years have sought to identify candidate genes but so far inconclusively."

all the success stories related inside the pages of EPSS are accompanied by fortuitous exposure to various forms of structured material, clearly marking out the most promising path for autistic development and growth.

And of course these discussions fly in the face of the current clamor for early intervention in autism, where it would seem the goal is always to yank the autistic child away as early as possible from his or her preferred method of engaging the world, and substitute instead an intense bombardment of socially based indoctrination, hoping to turn the child around while there is still time for the “malleable” brain to be re-molded.

In my opinion, it is no mere coincidence that the very same elements that stand at the core of the Mottron team's affirmative description of autistic perception and cognition are also the very same elements that stand at the core of humanity’s sudden departure off the savannah and leap into the modern world.

Admittedly, a thorough discussion of such a topic would be much too large for inclusion in an academic research paper such as EPSS, but the fact that the Mottron team does not mention, or even hint at, the connection between the features of autistic perception and the features of human cognitive history leave it unclear whether the team has ever considered such a connection.

At this point in time, the Mottron team seems to be the only autism research team heading in a positive and enlightening direction—a direction that is constructive for autistic individuals everywhere—and I look forward to all their future contributions.