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AUTISM FIRST STEPS
AUTISM DAILY NEWSLETTER
Saturday, December. 1, 2001
INDEX:
* 'My daughters have lost their childhood'
* Autism parents need help to fend off bigotry
* State
considers mandatory chickenpox vaccine for schoolchildren
* Hundreds protest Mass. Legislature's mental
health budget cuts
* STUDY POINTS TO TREATMENT FOR FRAGILE X SYNDROME
* Seizure
Prediction Could Change Treatment Of Epilepsy
CHATS AND TRAINING:
* HALF-DAY PROGRAM FOR CHILDREN WITH AUTISM OR
OTHER
DEVELOPMENTAL DISABILITIES
* Michigan-Chat
******************************
FRIDAY NOVEMBER 30 2001
'My daughters have lost their
childhood'
BY OLIVER
WRIGHT
FOR Liz Chell, discovering that her two young daughters did not have epilepsy
was almost as bad as the moment that she was told that they did. Over the last
ten years she has had to watch them grow up on a cocktail of drugs which often
left them unable to walk or communicate, behind at school and depressed that
they would never be like their friends. Now, doctors say that Emerald, the
younger daughter, is autistic, and that her sister Rosie was more likely to
have been suffering from migraines. Twice a year Mrs Chell would take them to
Dr Holton, but the message would always be the same. Both girls had epilepsy
and to take them off their medication could only make them worse. Yesterday, as
she listened to the results of the independent inquiry into Dr Holton’s work,
Mrs Chell, 38, said she believed her daughters’ childhood had been stolen from
them. She has already begun legal action against the hospital. “It is really unbelievable
that for nearly ten years my daughters were wrongly diagnosed and nothing was
suspected,” she said. “I still find what they went through as a result very
hard to take.” Rosie, now 11, was first said to have epilepsy when she was ten
months old. “Rosie spent ten years of her life on five medications which caused
untold damage and now we discover all she needs are strong painkillers,” Mrs
Chell said. “I find that unbelievable. “While she is in a normal school she has
always been behind and I don’t know if we can ever make up for that.” Doctors
also say that Emerald, now 10, was in no need of the drugs prescribed. “I
remember when they were both young I had to get two wheelchairs for them,
because they simply could not walk on the medication they were on. At one stage
one of the drugs stopped Emerald sleeping. She was having to go to school with
just two hours sleep a night. “The doctors say there is no long-term damage
from the drugs, but that does not make up for the damage which has already been
done,” she said. “How can you make up for the lost education? How can you make
up for their lost childhood.”
http://www.thetimes.co.uk/article/0,,2-2001553549,00.html
******************************
FRIDAY NOVEMBER 30 2001
The Times
Christmas Appeal
Autism parents need help to
fend off bigotry
BY NIGEL
HAWKES, HEALTH EDITOR
TO HAVE a child with autism can be saddening enough. But in recent years
another hazard has been added to those that litter the path of parents seeking
help. Because of the publicity given to Munchausen by proxy, a disorder in
parents who use and sometimes injure their children to attract attention, the
parents of autistic children may be treated with suspicion by doctors. Forty
years ago, autism was wrongly seen as a failure of parenting, according to
Lorna Wing, a founder of the National Autistic Society, who has made a lifelong
study of the condition. Though that error has been corrected, parents are again
finding themselves under suspicion. “Terrible things do happen to children, but
some parents of autistic children are being unfairly blamed. It’s tragic,
because nobody is denying that there are abused children,” Dr Wing said. “But
we say that before making the diagnosis, the child should be seen by somebody
specialised in autism. The society is taking up the problem with the Department
of Health.” Dr Wing strongly backs this year’s Times Christmas Appeal,
which aims to raise funds for the society, in particular for its schools in
which autistic children are given the chance to lead a normal life. “If an
autistic child in late childhood decides to fit into the world, he will. If he
doesn’t, nothing you can do will make him. So doing the best we can when
children are young is really important.” In 1991 Dr Wing and her colleague
Judith Gould set up the Centre for Social and Communication Disorders, where
children can be properly assessed. “We bought an ordinary house in Bromley,
southeast London,” Dr Wing said. “A lot of autistic children won’t go near a
hospital, but they are very happy to come to us.” Each assessment takes most of
a morning. Parents are asked detailed questions about their children to
discover whether, for example, a baby responds to play, waves goodbye when
parents go away and babbles in an attempt to communicate. An autistic baby does
none of these. “Parents love it,” she said. “A lot of them say they have never
been asked any of these questions before. Then, in the afternoon, we get
together and explain the diagnosis, and discuss the needs the child will have,
both now and as an adult.” The diagnosis of autism has changed rapidly, in part
because of Dr Wing’s work. Once, children who failed to communicate were
regarded as mentally handicapped and spent their lives in asylums. In 1980 Dr
Wing and colleagues assessed 890 patients in a hospital for the mentally
handicapped in Dartford, Kent. “A third of them fell somewhere in the autistic
spectrum, and a quarter of those met the narrowest definition of autism. None
of them had been diagnosed as autistic before.” The range of symptoms is wide.
Autistic children can be completely uncommunicative or talk but remain naive in
social relations and become obsessively focused on their own interests. Such
symptoms were first described by the Austrian Hans Asperger. However, the idea
that Asperger’s syndrome was related to autism was not initially recognised, Dr
Wing said. She believes that the existence of the syndrome provides a clue to
why autism has persisted. The condition is genetic — as twin and family studies
have shown — but is not caused by a single gene. Only a combination of genes
can create the full condition. Having one or two of the genes can even be an
advantage, she said. Many sucessful people detach themselves from society to
concentrate on work.
http://www.thetimes.co.uk/article/0,,2-2001553413,00.html
******************************
State considers mandatory chickenpox vaccine for schoolchildren
By Associated Press, 11/30/2001 02:16 LEWISTON, Maine (AP) The state is considering making a
chickenpox vaccination mandatory for school children. Public health officials
say widespread use of varivax can prevent epidemics. ''Vaccines are the most
cost-effective health investment you can make,'' said Dora Mills, director of
the state's Bureau of Health. Children who catch chickenpox can develop serious
complications, including pneumonia and staph infections, Mills said, and
pregnant women exposed to the disease risk delivering a baby with birth
defects. A vaccine against chickenpox was developed about 25 years ago in Japan
and was licensed for use in the United States in 1995. The Centers for Disease
Control recommended the vaccine for those people who haven't had chickenpox and
children who at least 12 months old. The District of Columbia and 19 states now
require children to be vaccinated before they enter elementary school, the CDC
said. Mills said most children born in Maine since 1995 have been vaccinated.
But many physicians and public health officials believe it would be better if
the shot was required for all children entering school. ''There's no reason, as
far as I'm concerned as a physician, not to vaccinate a child,'' said David
Baker, a pediatrician at Central Maine Pediatrics in Lewiston. Baker said the
vaccine provides immunity for 70 to 90 percent of children who get the shots
and lessens the symptoms for those who contract chickenpox later in life. Those
who aren't immunized face a larger risk of exposure when they are older and are
likely to develop more serious complications, Baker said. Yet some parents are
leery of a vaccine that has only been approved for use in the country for six
years. ''My gut feeling is chickenpox isn't a bad thing. No one dies from it,''
said Lewiston resident Pam Leary, who has four school-age children. She said
she probably would not have had them immunized when they were babies if the
vaccine had been available. ''Just because it's so new,'' Leary said. ''I
wouldn't want them to be experimented on.'' There will be a public hearing on
mandatory chickenpox vaccinations Friday at 8:30 a.m. at the Burton Cross State
Office Building in Augusta.
http://www.boston.com/dailynews/334/region/State_considers_mandatory_chic:.shtml
******************************
Hundreds protest Mass. Legislature's mental health budget cuts
By Leslie Miller, Associated Press, 11/29/2001 17:16 BOSTON (AP) About 300 demonstrators marched
into the Statehouse Thursday to protest the Legislature's steep cuts in
services for the mentally ill outside acting Gov. Jane Swift's office. Beacon
Hill traffic stalled around noon as protesters waved signs, cheered and chanted
''Support mental health'' while state police tried to control the crowd.
Hundreds marched into the building, and police barred hundreds more from coming
inside. ''This is an emergency situation,'' said Dr. Bruce Cohen, president and
chief psychiatrist at McLean Hospital, who joined the protest. ''We won't be
able to get people out of the hospital when they're ready to leave.'' The
Legislature voted to cut at least $18 million from the Department of Mental
Health last week as part of its effort to close a $1.35 billion budget
shortfall. Swift, who cannot add to the budget, has said she will try to
restore at least $6 million in mental health funds as part of a supplemental
budget. ''She has already said there are some mental health cuts that we're
legally bound to fund,'' said administration spokesman Dominick Ianno. ''To
accommodate for the $500 to $600 million legally mandated underfunding by the
Legislature, the governor will have to use her veto pen,'' he said. House
Speaker Thomas Finneran said some money could be restored to human service
accounts if Swift vetoes enough money in other areas to keep the budget
balanced. Advocates for mentally ill children sued in U.S. District Court last
month, claiming the state is violating federal law by failing to provide
home-based care for them. Kim Holt, who has bipolar disorder, fears losing her
home, which is partially supported by the state. ''If I were to get sick and
can't support myself, I would have nowhere to go,'' she said. ''I'm two
paychecks away from becoming homeless.'' Toby Fisher, executive director of the
National Alliance for the Mentally Ill of Massachusetts, said 27,000 people
served by the Department of Mental Health will either lose services or see the
quality of their services decline. ''We are faced with extinction,'' said John
Simpson, who held a sign reading ''Please Fund Community Mental Health
Programs.'' Simpson is a member of the Cove Clubhouse in Harwich, which provides
meals and education to people with mental illness. ''They discharge you (from
the hospital) and say 'Here's your new home' a park bench,'' he said.
http://www.boston.com/dailynews/333/region/Hundreds_protest_Mass_Legislat:.shtml
******************************
University of Utah
30-Nov-01
Study Points to Treatment for
Fragile X Syndrome
Library: MED
Keywords: FRAGILE X SYNDROME MENTAL RETARDATION TREATMENT
Description: A University of Utah study apparently overturns the belief
that fragile X syndrome is too complex to be treated effectively. The findings
raise hope that existing drugs might be used within a few years to treat the
most common inherited form of mental retardation. (Cell, 30-Nov-2001)
UNIVERSITY OF UTAH MEDIA RELEASE
Embargoed by the journal Cell for release at 10 a.m. MST Thursday Nov. 29, 2001
Contacts:
-- Kendal Broadie, assistant professor of biology -- office (801) 585-9426, lab
(801) 585-9425, home (801) 359-1590, broadie@biology.utah.edu
-- Lee Siegel, science news specialist, University of Utah -- office (801)
581-8993, cell (801) 244-5399, leesiegel@ucomm.utah.edu
STUDY POINTS TO TREATMENT FOR FRAGILE X SYNDROME
Utah Biologists Pinpoint Defects in Common Form of Mental Retardation
Nov. 29, 2001 -- A new study by Utah and California biologists appears to
overturn the long-held belief that fragile X syndrome is too complex to be
treated effectively in the foreseeable future. The findings raise hope that
existing drugs might be used within a few years to treat the most common
inherited form of mental retardation.
The discovery, published in the Nov. 30 issue of the journal Cell, indicates
the disease's cause is much simpler than previously believed, resulting from
nerve defects caused by the interaction of only two genes.
Biologists Kendal Broadie at the University of Utah and Gerald M. Rubin at the
University of California, Berkeley, led the research.
The study involved the fruit fly version of the human fragile X gene. When the
fruit fly and human genes are mutated, each fails to produce a protein,
resulting in strikingly similar symptoms in both flies and in humans with
fragile X syndrome.
The researchers showed how the absence of the fragile X protein in fruit flies
causes over-activity of a second gene, resulting in excessive growth of
tube-like support structures named "microtubules" at the ends of
nerve cells. There, at places called synapses, nerve signals are transmitted
from one nerve cell to another.
The excessive growth of microtubules made nerve-signal transmission go haywire
in the flies. That suggests an almost identical process makes nerve-signal
transmission malfunction in humans to cause fragile X syndrome.
The scientists cured the flies by using genetic manipulation to eliminate the
excessive growth of microtubules. Because excessive microtubules can be broken
down with medications such as colchicine -- a drug now used to combat certain
cancers -- the discovery in fruit flies points directly to the possibility of
using colchicine or similar drugs to treat mental retardation and other fragile
X symptoms in people.
"Something like colchicine at very low doses -- much lower than you would
give to a cancer patient -- might serve to counteract the effects of fragile X
disease," said Broadie, chief author of the study and an assistant
professor of biology at the University of Utah.
Treatment "could be just a few years away," he said. "It depends
entirely on the side effects of drug treatments and the dosage of the drug
required to counteract the brain defects."
Treatment with colchicine could cause side effects because microtubules, in
normal amounts, are essential to help cells maintain their structure and
divide.
But "in fragile X, the mental retardation is so severe [with an IQ
averaging 35, or 65 points below normal], you might be willing to put up with
some side effects," Broadie said.
The new study was conducted in Broadie's Utah lab and in Rubin's lab at
Berkeley. Postdoctoral researchers Yong Zhang at Utah and Adina Bailey at
Berkeley conducted much of the work. Other coauthors were University of Utah
postdoctoral biologist Heinrich Matthies and graduate students Robert Renden,
Mark A. Smith and Sean Speese.
Fragile X syndrome -- which was identified and named in 1991 -- afflicts one of
every 2,000 male newborns and one in every 4,000 female newborns in the United
States, with an estimated 100,000 affected Americans. Severity of symptoms can
vary. It is the most common inherited form of mental retardation. Down syndrome
is more common, but is not inherited.
Other symptoms include elongated ears, a prominent chin, unusually flexible
fingers and loose joints, visual problems, flat feet, speech and emotional
delays, occasional heart valve abnormalities and, in boys, enlarged testicles
at puberty. Fragile X patients also often suffer anxiety, attention deficit and
hyperactivity, shyness, impaired social skills, hypersensitivity to sensory
stimulation, over-reaction to changes and behavior resembling autism, including
hand-flapping, avoidance of eye contact, and hand-biting.
While some symptoms can be treated by drugs and speech, occupational and
physical therapy, there has been no treatment for the syndrome, which is
detected through a blood test.
The genetic mutation that causes fragile X syndrome occurs in the X chromosome.
Every female has two X chromosomes. Every male has one X chromosome and one Y
chromosome. Fragile X syndrome is so named because the long arm of the X-shaped
X chromosome looks like it may break off. This is due to extra genetic material
-- a stuttering-like repeat of a sequence of nucleic acids within the
chromosome's long arm.
Boys with the mutant fragile X chromosome always have symptoms -- ranging from
mild to severe retardation -- because they have only one X chromosome. Girls
have two X chromosomes, so the normal X chromosome often compensates when the
other one is mutated. Thus, about one-third of fragile X girls suffer mental
retardation, another 20 percent have less severe learning problems, and other
have no symptoms.
One in 260 women carries the fragile X chromosome and has a 50-50 chance of
passing the defect to her children, male or female. About one in 800 men
carries the defect, but can pass it only to daughters, not to sons.
DETAILS OF THE STUDY:
Scientists already knew a human gene named FMR1 carries the code that makes
human cells produce a protein named FMRP. In people with fragile X syndrome,
the FMR1 gene is mutant, resulting in either reduced amounts or an absence of
the FMRP protein.
In the new study, Broadie and colleagues showed a gene named dfxr is the fruit
fly equivalent of the human fragile X gene FMR1. Then they "knocked
out" or disabled the dfxr gene in fruit flies, resulting in abnormalities
in the synapses where nerve signals are transmitted. Because of the
abnormalities, the fruit flies suffered impaired vision as well as
uncoordinated movements that made them fly poorly.
Broadie noted that people with fragile X syndrome also have visual problems and
trouble coordinating complex behaviors such as movement and learning.
In a series of experiments, Broadie and the other researchers showed exactly
why the nerve transmission abnormalities and resulting problems developed in
flies. They found that when the fruit fly fragile X gene dfxr was disabled,
there was a resulting increase in activity of another gene that produces a
protein named "futsch." The overproduction of futsch led to excessive
growth of microtubules at the synapses, impairing the structure of the synapses
and their ability to transmit nerve signals.
To confirm the finding, Broadie and colleagues created "double
knock-out" fruit flies in which both the dfxr gene and the futsch gene
were disabled. While the disabled dfxr gene led to abnormalities in the flies,
disabling the futsch gene prevented excessive growth of microtubules and reversed
the abnormalities. The double-knockout flies showed perfectly normal behavior
-- and normal synapse structure and nerve-signal transmission.
The equivalent of the fruit fly futsch gene in humans in named MAP1B, which
helps form microtubules in people. So Broadie and colleagues concluded that in
people, a crippled FMR1 gene causes over-activity of the MAP1B gene and
protein, resulting in excessive growth of microtubules, nerve synapse
abnormalities and symptoms of fragile X syndrome -- just as a crippled dfxr
gene in fruit flies led to futsch over-activity, excessive microtubule growth,
nerve signal abnormalities and fly symptoms analogous to fragile X syndrome.
Broadie said the human FMR1 and fruit fly dfxr genes each regulate formation of
hundreds of proteins. The new study's big surprise is that dfxr's influence on
only one protein -- futsch -- causes the fruit fly equivalent of fragile X
syndrome. That implies the disease also has a similar simple cause in humans:
the interaction of the FMR1 and MAP1B genes.
The new study is the second major fragile X paper published recently in Cell.
The Nov. 16 issue carried an Emory University/Rockefeller University study
showing the human fragile X protein, FMRP, normally interacts with a variety of
proteins in human brain cells.
Broadie said that even though his study was in fruit flies, it goes well beyond
the other study by showing the specific interaction between the dfxr gene and
futsch protein in fruit flies, thus implying human fragile X results solely from
FMR1's interaction with MAP1B.
Kendal Broadie's web site is at:
http://synapse.biology.utah.edu
The FRAXA Research Foundation web site is at:
http://www.fraxa.org
University of Utah Public Relations
201 S Presidents Circle, Room 308
Salt Lake City, Utah 84112-9017
801) 581-6773 fax: 585-3350
http://www.newswise.com/articles/2001/11/FRAGILEX.UUT.html
******************************
Seizure Prediction Could Change Treatment Of Epilepsy
Researchers at the University of Florida and the Malcom
Randall Veterans Affairs Medical Center have been granted a U.S. patent for a
seizure-prediction technique that one day may change the course of epilepsy
treatment.
With a new five-year, $4.4 million National Institutes of Health grant, the
research team is continuing efforts to refine the system, which involves
analyzing complex electrical activity in the brain to identify patterns that
reveal a seizure is developing-minutes to hours before it occurs.
"Basically our idea is to identify a pre-seizure transition phase. At that
point, one could inject a drug, or have a drug released, that would 'reset' the
brain in order to prevent the seizure from happening," said J. Chris
Sackellares, M.D., a VA neurologist and a UF professor of neurology, biomedical
engineering and neuroscience.
"Our goal would be to enable people with epilepsy to take less medicine
than they currently do, and to be able to use it only when it's necessary,
rather than having it constantly in their systems," said Sackellares, who
is affiliated with the Evelyn F. and William L. McKnight Brain Institute of UF.
"Down the road, we also may explore giving the brain a small electrical
stimulus to prevent seizures when they are beginning to form."
UF is negotiating with companies interested in licensing the technology to
develop commercial applications. Such products could include implantable
devices that can detect signs a seizure is approaching and then deliver
medication or other type of stimulus to prevent it.
The Epilepsy Foundation of America estimates that 2.3 million people in the
United States suffer from seizure disorders, which are grouped under the common
name of epilepsy. In 70 percent of the cases, there is no known cause; genetic
disorders, birth defects, head trauma, tumors, strokes, infections and poisons
are implicated in the others. Treatment typically consists of medicines, but
the drugs can cause side effects and often do not offer complete prevention of
seizures.
Sackellares and Leonidas D. Iasemidis, Ph.D., a former VA research engineer and
UF faculty member, began to suspect in 1988 that "chaos" science
would be able to shed light on epilepsy. Chaos theory suggests that through
sophisticated mathematical analysis, patterns sometimes can be observed in
events that previously had appeared to be random.
Early in the 1990s, Sackellares and Iasemidis, who is now at Arizona State
University, became the first to identify the existence of a pre-seizure
transition period. In the past several years, they have begun to develop
methods to detect the transition anywhere from minutes to many hours ahead of
time. They accomplish this through computer analysis of the brain's complex
electrical signals, which can be recorded by electroencephalograms, or EEGs.
With the new grant, a multidisciplinary team of researchers, including
scientists at Arizona State, will seek to improve the accuracy of the
seizure-prediction technique, in part by analyzing additional measures of
electrical activity in the brain and determining which sites to monitor with
electrodes to yield the most significant information about the potential for
seizures. They are conducting the research by analyzing brain electrical
activity in people and in mice.
"We need to look at the complex patterns involved in the transition to the
pre-seizure state. Like turbulence in the air, this occurs in a very complex
way, not always in the same place, and not the same size or length of time, so
it's not easy to identify," Sackellares said. "We're trying to
develop more sophisticated time-series analysis techniques to account for
this."
In addition to Sackellares, other key UF players in the research effort are
Jose Principe, Ph.D., John Harris, Ph.D., and Panos Pardalos, Ph.D., from the
College of Engineering; Paul Carney, M.D., Steven Roper, M.D., Johannes van
Oostrom, Ph.D., and Richard Melker, M.D., from the College of Medicine; and
Mark Yang, Ph.D., from the College of Liberal Arts and Sciences. - By Victoria
WhiteRelated website:
[Contact: Victoria White]
30-Nov-2001
http://unisci.com/stories/20014/1130012.htm
******************************
HALF-DAY PROGRAM FOR CHILDREN
WITH
AUTISM OR OTHER DEVELOPMENTAL DISABILITIES
OPENING IN GREENSBORO, NORTH CAROLINA
PROGRAM WILL PROVIDE ONE-ON-ONE INSTRUCTION FOR CHILDREN AGES 3-6 IN THE
FOLLOWING AREAS:
- INCLUSION OPPORTUNITIES IN A PRESCHOOL SETTING
- EMPHASIS ON DEVELOPMENTAL MILESTONES WITH A FOCUS ON
LANGUAGE DEVELOPMENT
- BEHAVIORAL INTERVENTIONS
- SUPPORT IN TRANSITIONING FROM ONE SETTING TO ANOTHER
**CAP AND MEDICAID CLIENTS ELIGIBLE
*PRIVATE AVAILABLE
FOR MORE INFORMATION PLEASE CONTACT:
EDUCATIONAL SOLUTIONS OF NC at ESNC1@aol.com
OR
TRIAD COORDINATED SERVICES at
TriadCoordinated@aol.com
******************************
Michigan-Chat
Date: Friday, November 30, 2001
Time: 9:00PM - 10:00PM EST (GMT-05:00)
Dear Michigan Parents, Advocates & Attorneys:
Come and chat with other Michigan special education parents,
advocates & attorneys.
Every Friday evening from 9:00PM-10:00ishPM, Eastern Standard
Time.
The webpage to access the chat is:
http://groups.yahoo.com/group/Chat-SpecialEdLawMichigan/chat
You must be a member of that listserv to enter the chatroom. You
may join at:
http://groups.yahoo.com/group/Chat-SpecialEdLawMichigan
The topic will always be Special Education Law, however, there
may be some weeks that there will be special guests at the
chats! Stay Tuned!
Thanks!
Your Hosts,
Kim and Bella
******************************
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