 |
Main Menu |
|
|
 Home Community Members options Search Web
|
|
|
|
|
Survey |
|
|
How many children are on the spectrum in your family?
|
|
|
|
|
News
|
Research : Autism as a cognitive disorder
|
|
|
Posted by Sylvia on Saturday, January 27, 2007 (10:37:19)
UPI
January 2007
By LIDIA WASOWICZ
SAN FRANCISCO - Based on recent brain research, some scientists are calling for a redrawing of the current picture of autism as a primarily behavioral condition.
"It's time to understand autism as a cognitive disorder, not a behavioral disorder," said Steven Gutstein.
He is a psychologist, autism specialist, researcher, child, marital and family therapist and co-director of The Connections Center for Family and Personal Development and of the Relationship Development Research Institute in Houston.
Gutstein also is the author of "Autism Aspergers: Solving the Relationship Puzzle" (Future Horizons Inc., 2000), which explains the technique he developed for teaching social skills to people affected by the condition.
"The challenge of people with autism is integrative thinking, using several parts of the brain at once -- that's when they fall apart," Gutstein said in an interview.
Other studies are unveiling alterations in brain areas governing meaning and emotion.
This field of research attempts to get to the heart of one of the most confounding and devastating pieces of the autism puzzle: why children with the disorder so often appear to lack the natural inclination to forge social ties, specialists said.
Such ties are so fundamental to human nature, even a newborn turns his head toward the sound of his mother's voice and melds his tiny body into hers when picked up from the cradle, scientists said.
At its harshest, autism cuts the connections, repelling the magnetic pull of relationships, they said.
In his classic 1943 work, which described the first documented cases of the disorder, Johns Hopkins University psychiatrist Dr. Leo Kanner recounted his incredulous observations of a group of remarkable children disinterested in their parents and, as they grew older, in people in general -- but inexorably drawn to objects.
Upon entering his office, without exception, they would head for the toys and blocks, paying no more heed to any person present than to the desk, bookshelf or filing cabinet.
Over the intervening decades, such seeming apathy toward interpersonal interaction has frustrated generations of researchers and therapists whose primary treatment approaches depend largely on communication, specialists said.
Of late, however, investigators have begun to make a dent in the disorder's once impenetrable armor.
Using state-of-the-art tools that track eye movements and provide three-dimensional, color-coded images of the brain, scientists are parting the curtains of secrecy enough for glimmers of hope to start bursting through.
Scientific explorers navigating the brain's immensely intricate landscape have come across certain signposts that appear to point to biological underpinnings of the social-deficit domain of symptoms.
They began the journey on the premise that given the primary importance of human connections, special mechanisms must have evolved in our species for perceiving faces, a skill pivotal to social engagement.
If that were the case, perhaps some alteration in that apparatus lies at the heart of the aloneness that characterizes perhaps the only disorder that puts a damper on the innate inclination to gaze at and interpret a face, they surmised.
Over the past 30 years, key differences have started to emerge.
Experiments have shown, for example, that in sharp contrast to people without the disorder, those with autism see objects and faces with the same speed, suggesting that, just as Kanner noted, for them, the latter inspire no more interest than do boxes, dishes or pebbles, researchers said.
Armed with finely tuned instruments only recently made available, a Yale University team has probed this phenomenon more deeply.
Using a special eye-tracking technology that permits investigators to precisely monitor the direction of a person's gaze at any given moment, the investigators found that in watching a passionate scene between Richard Burton and Elizabeth Taylor in the 1966 Mike Nichols film, "Who's Afraid of Virginia Woolf?," the non-autistic study subjects tended to zero in on the actors' eyes.
In contrast, viewers with the disorder settled, in many instances, on peripheral objects, such as a light switch on a wall behind the paramours.
Despite such conspicuous differences in behavior, neuroscientists said they have found it surprisingly difficult to nail the responsible mechanisms. Through the years, they said, theories have come and gone, with only a handful withstanding the test of time.
|
|
|
|
|
|
|
comments? |   |
|
|
|
|
Research : Scientists link paternal gene, autism
|
|
|
Posted by Sylvia on Saturday, January 27, 2007 (10:24:30)
Monsters and Critics
January 2007
KOLKATA, India (UPI) - A study of autism in India has found that a gene passed on by fathers may be at least a contributing factor.
Scientists at the Manovikas Biomedical Research and Diagnostic Centre in Kolkata, the former Calcutta, called their findings 'a possible paternal effect.' But they warned their work is based on a small sample of autistic children.
Autism is a brain disorder marked by difficulties in communication and problems with language and social skills.
'We`re seeking clues to unravel the cause of autism -- this is important for science and for parents with autistic children,' Swagata Sinha, a psychiatrist and member of the research team told The Telegraph. 'Every parent wants to know the exact cause. And, at the moment, we have no answer to give them.'
The findings were published in the American Journal of Medical Genetics: Neuropsychiatric Genetics.
|
|
|
|
|
|
|
comments? | |
|
|
|
|
Research : By Age 2 Autistic Children's Brains Grow Larger, Why Is Not Clear
|
|
|
Posted by sylvia on Saturday, March 25, 2006 (16:29:37)
Medical News Today
By age 2, children with the often-devastating neurological condition physicians call autism show a generalized enlargement of their brains, a new University of North Carolina at Chapel Hill and Duke University medical schools study concludes.
Exactly why this roughly 5 percent greater brain growth occurs and what it means are not yet clear, scientists said. Indirect evidence suggested that the increased brain growth probably began during the later months of the children's first year of life.
A report on the finding appears in the December issue of the Archives of General Psychiatry. UNC authors are Dr. Heather Cody Hazlett, assistant professor of psychiatry; Dr. Michele Poe, a statistician with the FPG Child Development Institute; Dr. Guido Gerig, professor of computer science; imaging technician Rachel Gimpel Smith; and Drs. John Gilmore and Joseph Piven, professors of psychiatry.
At UNC, Piven, the senior author, directs both its Study to Advance Autism Research and Treatment (STAART) Center and its Neurodevelopmental Disorders Research Center. Duke authors are Drs. James Provenzale and Allison Ross, professor of radiology and associate professor of anesthesiology, respectively.
"Our team conducted brain magnetic resonance imaging scans on 51 autistic and 25 control children at age 2, making it the largest study of two-year-olds with autism," Cody Hazlett said. "Analysis of brain tissue volumes showed significant enlargement, across all regions in both gray and white tissue, in the cerebral cortex of the autistic children.
"While we saw the greatest volume increases in the temporal lobe, an area of the brain involved in language, we concluded that at this age, tissue enlargement is present throughout the cortex."
In the same paper, the team reported on the largest retrospective study of head circumference in autism reported to date, comparing head circumference measurements on 113 autistic children to 190 other youngsters who served as controls. Measurements took place periodically from birth to age 3.
"Our head circumference data suggest that enlarged head size is not present at birth and that the onset of enlarged head size in autistic children begins, on average, at around 12 months," Cody Hazlett said. "These findings, together with our brain volume data, give us reason to believe that a period of brain overgrowth in autism may occur between 12 months and 2 years of age.
"We do not know whether this brain enlargement plays a primary role in autism, or is a downstream effect of another process," she said. "Further studies of very early brain development may help us better understand the timing and nature of this brain overgrowth."
About four times as many male children suffer from autism as females, Cody Hazlett said. The disorder varies in severity, but affected patients often face mental retardation, poorly developed language skills and difficulty developing social relationships.
Grant support for the study, which builds on earlier work, came from the National Institutes of Health's mental health and child and human development institutes (NIMH and HICHD). Assistance also came from the Treatment and Education of Autistic and Related Communication Handicapped Children (TEACCH) centers and the Neurodevelopmental Disorders Research Center Autism Subjects Registry.
|
|
|
|
|
|
|
comments? | |
|
|
|
|
Research : UCLA imaging study of children with autism finds broken mirror neuron system
|
|
|
Posted by sylvia on Saturday, March 25, 2006 (16:17:25)
Eurekalert
New imaging research at UCLA detailed Dec. 4 as an advance online publication of the journal Nature Neuroscience shows children with autism have virtually no activity in a key part of the brain's mirror neuron system while imitating and observing emotions.
Mirror neurons fire when a person performs a goal-directed action and while he or she observes the same action performed by others. Neuroscientists believe this observation-execution matching system provides a neural mechanism by which others' actions, intentions and emotions can be understood automatically.
Symptoms of autism include difficulties with social interaction -- including verbal and nonverbal communication -- imitation and empathy. The new findings dramatically bolster a growing body of evidence pointing to a breakdown of the brain's mirror neuron system as the mechanism behind these autism symptoms.
"Our findings suggest that a dysfunctional mirror neuron system may underlie the social deficits observed in autism," said Mirella Dapretto, lead author and assistant professor in residence of psychiatry and biobehavioral sciences at the Semel Institute for Neuroscience and Human Behavior at UCLA and the David Geffen School of Medicine at UCLA.
"Together with other recent data, our results provide strong support for a mirror neuron theory of autism. This is exciting because we finally have an account that can explain all core symptoms of this disorder."
Conducted at the Semel Institute's Ahmanson-Lovelace Brain Mapping Center, the research used functional magnetic resonance imaging (fMRI) to measure brain activity in 10 high-functioning children with autism while they imitated and observed 80 photos depicting different emotions such as anger, fear, happiness or sadness. In addition, the brain activity of 10 typically developing children was studied while performing the same tasks.
Separately, symptom severity of each child with autism was tested using two independent measures (the Autism Diagnostic Observation Schedule -- Generic, and the Autism Diagnostic Interview).
The study shows that unlike typically developing children, children with autism have virtually no activity in the pars opercularis of the inferior frontal gyrus, identified by previous research as a key part of the mirror neuron system. Importantly, the level of mirror neuron activity seen in children with autism was inversely related to symptom severity in the social domain.
Children with autism also showed reduced activity in the emotion centers of the brain, consistent with the hypothesis that this mirroring mechanism may play a crucial role for understanding how others feel and for empathizing with them.
All of the children rehearsed the tasks prior to the fMRI scans to assure researchers they could perform the tasks. Both groups performed equally well. Normal brain activity in areas of the brain involving sight and facial movements indicated that the children with autism remained on task during the fMRI scans.
|
|
|
|
|
|
|
comments? | |
|
|
|
|
Research : Families share traits of autistic children
|
|
|
Posted by sylvia on Saturday, March 25, 2006 (09:14:49)
New Scientist
By Helen Phillips
Some relatives of people with autism also display behaviours and brain differences associated with the condition, even though they themselves do not have it. This could make it easier to spot families at risk of having an autistic child. It could also help in the quest to identify the genetic and environmental triggers for the condition, though it seems these triggers might vary from country to country.
Eric Peterson of the University of Colorado in Denver had compared an MRI study of the brains of 40 parents with autistic children to that of 40 age-matched controls. And he told the Society for Neuroscience annual meeting in Washington DC that the parents who had an autistic child shared several differences in brain structure with their offspring.
Looking at the group averages, the differences in parents of the autistic children included an unexpected increase in the size of the motor cortex and basal ganglia, areas important for movement planning and imitation. The somatosensory cortex, neighbouring the motor cortex, by contrast, was smaller than average. This region is important for understanding social information such as facial expressions - one key skill that autistic people often lack. These parents also had reductions in the cerebellum, important for coordinating movement, and in a frontal region thought to be responsible for understanding the intentions and feelings of others - the so-called theory of mind area.
In another study, Brendon Nacewicz of the University of Wisconsin-Madison Medical School and colleagues tested whether brothers of autistic children would avoid eye contact with others, a common feature of autism. While the parents seemed normal in this respect, brothers avoided eye contact just as strongly as their autistic sibling. He is now planning to test sisters too. Nacewicz also showed that the amygdala, a region important for processing emotions, particularly fear, was shrunken in the brothers too, just as it is in autistic people.
One theory laid to rest by these findings, says Nacewicz, is the idea that autism somehow falls on the far end of a shyness spectrum. The siblings showed no signs of autism or shyness, despite avoiding eye contact with others. Although gaze avoidance is accompanied by differences in the biology of the brain, he says, other brain areas must somehow compensate for the differences. Peterson agrees. This suggests that several core brain differences have to be present for someone to show the symptoms of autism, he says.
A further complexity in the underlying biology of autism was reported by Antonio Persico from the University of Rome. He found certain genetic variations linked with autism in North America were not present in autistic families in Italy. It is possible that there are regional differences in the environmental factors that interact with different genes to trigger autism, he suggests.
The differences were in a gene that makes an enzyme called paraoxonase. In North American populations, families with autistic members seemed to share a variant of the gene that makes a less active form of the enzyme. In Italian families with autism, however, that variant was no more common than in families without. One job of the enzyme is to inactivate organophosphates, which are often used in American homes as insecticides. In Italy, they are rarely found in the home. So one possible explanation, claims Persico, is that Americans with the less active enzyme use more of it to clear the pesticide, leaving less free to do another important job in helping neurons migrate to their right places during brain development.
In Italian families, the interaction between environment and genes may be different. For instance, an environmental effect may interact with the gene reelin, which also guides neurons to the right place, and has been linked to autism. "The important thing is that I am not trying to prove that organophosphates are bad," says Persico. These children may become sick anyway. The point is that there may be different genetic risk factors and different environmental interactions which lead to autism, he adds.
Dan Geschwind, an autism expert from the University of California, Los Angeles, who chaired the session on brain differences, is yet to be convinced about the claims of environmental triggers, however. "There is no evidence for one," he says, "but we can't rule it out."
|
|
|
|
|
|
|
comments? | |
|
|
|
|
|
Latest: 
New Today: 0
New Yesterday: 0
Overall: 11466
Members: 0
Visitors: 11
Total: 11
1: