F.E.A.T. - Chattanooga NEWSLETTER PO Box 23731 Volume I
Upcoming Meetings: February 8, 2000 -
Meeting Time and
Place *Parking Directions
(see our Group Information Page)
Thanks to all
of the members who were able to sell tickets for the tree giveaway. We raised
over $500 for FEAT. A special thank you to the Hixson Target store for donating
the tree and decorations.
On December
10th members of F.E.A.T. of Chattanooga celebrated the holidays with a
The committee asks that each FEAT member think of potential sponsors for the event. The best target sponsors are probably individuals or business people that we know and/or work with. The sponsorship levels will remain at $100, $250, and $500. Please call the FEAT number at 296-0092 with the sponsor information.
We need your information for the
newsletter. Please fax, email or mail your submission to Fax: 778-6837
Welcome Packets are available at
all meetings. If you have not received yours yet and are unable to attend the
next meeting, please call our FEAT-Chattanooga phone number and leave your name
and mailing address and we will send one to you.
A free Basic Rights workshop, provided by STEP (Support and Training for Exceptional Parents) will be held on Thursday January 13 from 6pm to 9pm. This workshop is designed for parents of children receiving special education, and parents of children who might need special education. If you have previously attended a Basic Law Workshop, you may want to attend this one, as it will cover the recent IDEA regulations. You will receive a copy of the new IDEA regulations, the 1997 IDEA Amendments, the new IEP forms and instructions for their use, and information on new components of the law. Come and learn about Special Education rights so that you can be an informed, prepared participant in the development of your child's IEP. To register or for more information,
We will
see you in Washington, DC next year!
A The Massoud
Pediatric Building now locks electronically at 6:00 p.m. The gravel lot (number
3) where several people parked is now closed. You should now park in the Erlanger
Parking Garage and enter
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In an effort
to ensure that more parents can attend our FEAT-Chattanooga monthly meetings, If you
would like to utilize this free assistance, prior to the meeting, bring your
child and their necessary items (diapers, juice, books, etc.) to the Children's
Therapy Services room on the first floor of the Massoud Pediatric Building.
(The first door on your right as you enter from the Erlanger parking garage
level 1). We will post signs for your assistance. From FEAT DAILY ONLINE NEWSLETTER http://www.feat.org/ New Theories Help Explain Mysteries
of Autism Tuesday, December 28, 1999 Inspired by new findings on the way animal brains develop before and after birth, scientists are developing provocative new theories to explain autism, a mysterious brain abnormality that prevents human infants from developing normal social and cognitive skills. By studying the anatomy of autistic
brains, researchers are trying to figure out when in development and where in
the brain the complex interaction of genes and environment causes things In autism, an entire brain circuit has been compromised, said Dr. David G. Amaral, a neuroscientist at the University of California at Davis. Researchers have only begun to study how different brain regions interact dynamically to give rise to such circuits, he said, which puts autism at the frontier of modern neuroscience. Autism undermines many aspects of
human behavior, including movement, attention, learning, memory, language, mood
and social interaction. It can be detected in the movements of babies who roll
over, sit up, crawl and walk in oddly uncoordinated ways. The symptoms of autism range from mild to severe, making the true incidence of the disorder difficult to assess, said Dr. Marie Bristol-Power, who coordinates autism research at the National Institute of Child Health and Human Development in Bethesda, Md. Classical autism in its more severe form, which results in mental retardation, occurs in about 1 in every 1,000 births, she said. When milder forms of autism like Aspberger's syndrome are included, the incidence is 1 in 500. The common feature among all children with autism is a lack of social relatedness. Some states are reporting what appear to be significant increases in cases of autism, Dr. Bristol-Power said. But it is not yet clear if the reports reflect higher incidence of the condition or better diagnosis and the availability of better treatment. Fifty years ago, researchers believed that autism was caused by cold "refrigerator" mothers and weak, absent fathers. Today they are zeroing in on genes. In identical twins, if one has autism, 90 percent of the time the second will also have it. At least five or six genes contribute to autism, said Dr. Bennett Leventhal, director of child and adolescent psychiatry at the University of Chicago. Studies thus far of autistic siblings suggest that these genes are on Chromosomes 7, 13 and 15. What these genes are doing is still anybody's guess. Studies of developing animal brains have found numerous growth factors and proteins that guide fetal brain cells into making proper connections. Other genes make factors that act as master switches, turning yet other genes on and off at particular points in development. Some genes suppress cellular activity while others ramp it up, setting the correct balance of chemicals involved in transmitting brain signals. After birth, different genes begin to nurse connections while others cause cells to die off in a dynamic dance of growth and pruning. But the growth and elaboration of the nervous system is a continuous process and if something goes seriously wrong early on, all subsequent development may be disturbed. The question is, how early and where. Dr. Patricia M. Rodier, an embryologist
at the University of Rochester School of Medicine, believes that the brain glitch
in autism occurs between Days 20 and 24 of gestation, before a woman knows she
is pregnant. She has evidence that genes involved in laying down basic body
and brain structures, called Dr. Margaret L. Bauman, a neurologist at Harvard Medical School, believes that the defect may occur before the middle of the second trimester of pregnancy. She bases this theory on her extensive knowledge of how and when certain circuits are wired. Some cells can be "missing" only if the defect occurs midway in fetal development, she said. But Dr. Eric Courchesne, a neuroscientist at the University of California at San Diego, said that the problem could just as easily occur after a baby is born and as the brain continues to develop. In October, researchers identified the precise genetic defect in a disorder, Rett's Syndrome, that was once commonly misdiagnosed as autism. Babies are born and develop normally until about the age of 6 to 24 months, when a gene that represses other genes fails to shut down as it should. As a result, the other genes do not swing into action and children stop growing, wring their hands and become mentally retarded. Dr. Courchesne and other researchers believe a similar process may be at work in autism. Like other brain researchers, scientists who study autism were startled by recent discoveries that the human brain continues to make new brain cells -- not just new connections, as was previously thought -- well into adulthood. One scientist even has evidence that the number of neurons in the human brain doubles between birth and 6 years. If this is true, Dr. Courchesne said, the child's brain would be undergoing a huge amount of construction created by the interplay of genes and environment. It might be, he said, that disturbances in this construction give rise to autism. This theory is supported, some researchers say, by the fact that a quarter of autistic children appear normal until age 14 to 22 months and then experience the sudden onset of autistic symptoms, said Dr. Nancy J. Minshew, a psychiatrist at the University of Pittsburgh. The onset may be caused by a malfunction in one or more genes, she said. Or it could be set off by something in the environment interacting with a genetically vulnerable child. Since 1983, Dr. Bauman and her colleagues have been studying brain tissue obtained in autopsies from autistic children and adults. While large areas of the 11 brains they studied look normal, she said, the brains are generally bigger and heavier than most. Most important, there are abnormalities in three major regions that help control social behavior. Parts of the frontal lobes, which enable decision-making and planning, are thicker than normal. Cells in the limbic system, where emotions are processed, are a third smaller than normal and are found in excessive numbers. The cells are also immature, with stunted connections. Cells in the cerebellum -- a structure that helps in making predictions about what will happen next in terms of movements, thoughts and emotions -- are reduced by 30 percent to 50 percent. Symptoms of autism can be traced to problems in each of these regions, said Dr. Amaral, the neuroscientist at U.C. Davis. For example, neurons in the amygdala respond to faces and the angle of gaze. Autistic children tend to ignore facial expressions, or at least do not seem to read them well. Experiments show that autistic children can use their cerebellums to shift attention when they are not paying attention to a particular task. But when they are asked make a conscious decision about changing attention, a task that activates their frontal lobes, they can no longer to do the task, presumably because a larger circuit is engaged. Animal studies also shed light on the biology of social behavior relevant to autism, Dr. Amaral said. For example, monkeys have brain cells that respond to moving hands and faces but not other moving things. They have cells called mirror neurons that fire not only when the monkey performs an action, like gripping a handlebar, but also when the monkey observes another monkey performing the same action. They have cells that are activated by sights and sounds generated by others but not by the same sights and sounds when they are self-generated. Perhaps the human equivalent of these specialized cells are not functioning properly in autism. Experiments conducted on human autistic children suggest that very specific elements of social behavior are abnormal. For example, autistic children can use sabotage, but not deception, to prevent another person from attaining a goal. They can use communicative gestures, like "come here," to affect another person's behavior but not expressive gestures, like "well done," to affect another's mental state. They can feel the basic pleasure in mastering a task but not the pride, said Dr. Chris Frith, a neuroscientist at University College London. An emotion like pride requires taking into account other people's expectations, he said. Another set of recent but not yet published experiments shows that that autistic children are bombarded by their own nervous systems, making them more sensitive to stimuli, not less, said Portia Iverson, the founder of Cure Autism Now, a parent group based in Los Angeles, who is an expert on the disorder. "If you hook a normal person up to a device that measures arousal and make direct eye contact," she said, "you'd see maybe four spikes a minute. In the same setting, the autistic child has a dozen or more spikes per minute, plus the peaks are extremely high and low, more severe and erratic. It's like you or I would feel during an earthquake, but they feel that way all day long." In normal learning and memory, Ms. Iverson said, people encode new information about 30 seconds after getting an arousal peak. "But what if you have six times too many peaks?" she asked. "You might encode enormous amounts of highly irrelevant information, focusing on details that don't matter to the rest of us." Autism researchers agree that it will take many years before the genetics and neurochemistry of the disorder are understood. In the meantime, intensive one-on-one therapies that teach children how control their movements and interact socially succeed in 30 percent to 50 percent of treated children, provided they start early, ideally by age 2 or 3. The goal is to intercept the miswiring of the autistic brain and, as the brain is developing, help it grow the connections it needs. Still, for a great many autistic children, the disorder is not diagnosed until age 5 or 6, when they start school, Dr. Bristol-Power said. Most pediatricians and family doctors still believe autism is a relatively rare disorder and are not trained to pick up symptoms, she said. Any child that is not speaking in short phrases by age 2 should be evaluated. Ms. Iverson said: "The fact that children's brains are dynamic and resilient is our greatest hope. The very essence of a human being is his or her interaction with the environment. If it's not done right the first time, we can make it up with restorative and regenerative therapies for the brain. We may not make kids completely normal but we can change the course of the illness."
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