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"Although these are early days, we think this difference in stress hormone levels could be really significant in explaining why children with AS are less able to react and cope with unexpected change,"

If these Asperger symptoms are caused primarily by stress, caregivers could learn to steer children away from situations that would add to anxiety, the researchers said.

"This study suggests that children with AS may not adjust normally to the challenge of a new environment on waking,"

The researchers, whose findings were published in the journal Psychoneuroendocrinology, will next study if this lack of cortisol upon waking also occurs in children with other types of autism.

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.

Why change an age-old practice invited by Mother Nature or the Creator of the Universe, when it is so obviously a product of 80 million years of natural selection?! Why race to get that clamp on the umbilical cord well before blood flow in the cord stopped on its own?

Interestingly, the obstetrics profession itself seems to be questioning the adoption of use of early-clamping procedures, as several important meta-analyses have now shown that late cord clamping (after the umbilical flow has stopped on its own = Nature’s Way) is (big surprise) beneficial to the newborn, with significant positive benefits for late (more natural) cord clamping recorded (in ferritin, which translates to hemoglobin which translates to oxygenation) up to 6 months later (e.g., see Hutton & Hassan, JAMA 297:1241).

It shall be interesting to see whether or not changes in these practices back to the “old way” results in a reduction in autism incidence. Stay tuned — because it looks like the experiment is now underway!

A groundbreaking study suggests people with autism-spectrum disorders such as Asperger’s do not lack empathy—rather they feel others’ emotions too intensely to cope.

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.