SCHAFER AUTISM REPORT "Healing Autism:

No Finer a Cause on the Planet"

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Friday, October 11, 2002 Promote Your Event - Free! - Send a

CALENDAR LISTING: EVENTS@doitnow.com

TREATMENT

* New Tool To Predict Social Competence In Autistic People

RESEARCH

* Subjects with Asperger's Syndrome have Abnormalities In Prefrontal Lobe

* Melatonin and Epilepsy

* Glutamic Acid Reduced with Autism

* Autistic Symptoms Following Herpes Encephalitis

* Childhood Disintegrative Disorder Re-examination of the Current Concept

* Contingent Shock Researched as Treatment for Self-Injurous Behavior

* Using Picture Exchange Communication System (PECS) with ASD Kids

* New Study Shows Efficacy Of Gene Therapy for Parkinson's Disease

* Taking a Clinical Look at Human Emotions

EDUCATION

* 9th Circuit: IDEA Due Process Needn't Exhaust

State Complaint System

PUBLIC HEALTH

* Separate MMR Jabs At New Clinics in UK

FUNDRAISING

* Walk F.A.R. for NAAR Raises Nearly $2 million in First Four Fall Events

LETTERS

* On the 'B.C. Must Pay For Autism Treatment' Ruling

* "My Cbild is Autistic" is Bothersome

* Readers' Posts

TREATMENT

New Tool To Predict Social Competence In Autistic People

By observing the way people with autism watched a classic 1960s movie, US investigators believe they may have found a way of predicting the social competence of people with the disorder.

Psychiatrists from Yale University, Connecticut, looked at the way 15 autistic men with IQs in the normal range focused on the characters in the film of the Edward Albee play “Who’s Afraid of Virginia Woolf?” and compared the findings with those from 15 controls.

The film was chosen because it contains a high number of scenes involving intense verbal and nonverbal exchanges between the protagonists in an environment where there are few distractions.

Dr Ami Klin, associate professor of child psychology and psychiatry at the university’s Child Study Center, and colleagues found an association between the time spent focusing on the film characters’ mouths and the autistic subjects’ social competence.

Dr Klin says the findings came as a surprise because they had predicted that autistic people would follow the normal pattern, in which focusing on eyes suggests social competence.

However, she says that their results suggest that individuals with autism not only focus less on people’s eyes but when they do they fail to glean much information.

The researchers suggest that individuals with autism and normal IQs miss the “very important” non-verbal cues conveyed in social interaction through the eyes including instances of irony and sarcasm.

The team also found that the more individuals focused on objects contained in the film, rather than people, the less socially competent they were.

They say that their findings could provide an opportunity to predict how children with autism will develop and provide an opportunity to improve their prognosis.

Social skills, such as looking preferentially at eyes rather than mouths, emerge in the first few months of life, which means that a vulnerability to autism could be detected at a very early stage, say Dr Klin and colleagues.

“This is the first time in autism research that we have results on an experimental measure to actually predict level of social competence in real life,” she says.

Reference: Klin et al, Archives of General Psychiatry 2002;59:809-816

© HMG Worldwide 2002

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Subjects with Asperger's Syndrome have Abnormalities In Prefrontal Lobe 'Asperger syndrome: a proton magnetic resonance spectroscopy study of brain.'

ds=12365875&dopt=Abstract

Murphy DG, Critchley HD, Schmitz N, McAlonan G, Van Amelsvoort T, Robertson D, Daly E, Rowe A, Russell A, Simmons A, Murphy KC, Howlin P. P050 Institute of Psychiatry, De Crespigny Park, Camberwell, London SE5 8AF, England. sphadgm@iop.kcl.ac.uk

BACKGROUND: Asperger syndrome (AS; an autistic disorder) is associated with impaired social skills and obsessional/repetitive behavior. Patients with autism have significant abnormalities in the frontal lobe and frontoparietal connectivity. Nobody has examined the relationship between abnormalities in the frontal and parietal lobes and clinical symptoms in people with AS.

METHODS: We used in vivo proton magnetic resonance spectroscopy to examine neuronal integrity of the medial prefrontal and parietal lobes in 14 non-learning-disabled adults with AS and 18 control subjects (of similar sex, age, and IQ). We obtained measures of the prefrontal lobe in 11, the parietal lobe in 13, and both lobes in 10 subjects with AS. We measured concentrations and ratios of N-acetylaspartate (NAA), creatine and phosphocreatine (Cr + PCr), and choline (Cho). Levels of NAA, Cr + PCr, and Cho are indicators of neuronal density and mitochondrial metabolism, phosphate metabolism, and membrane turnover. Frontal metabolite levels were correlated with scores on the Yale-Brown Obsessive Compulsive Scale and the Autism Diagnostic Interview. RESULTS: Subjects with AS had a significantly higher prefrontal lobe concentration of NAA (z = -3.1; P =.002), Cr + PCr (z = -2.2; P =.03), and Cho (z = -2.9; P =.003). Increased prefrontal NAA concentration was significantly correlated with obsessional behavior (tau = 0.67; P =.005); increased prefrontal concentration of Cho, with social function (tau = 0.72; P =.02). We found no significant differences in parietal lobe metabolite concentrations. CONCLUSION: Subjects with AS have abnormalities in neuronal integrity of the prefrontal lobe, which is related to severity of clinical symptoms.

PMID: 12365875 [PubMed - in process]

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ds=12373656&dopt=Abstract [Article in Spanish] Rufo Campos M. Hospital Universitario Virgen del Rocio, Sevilla, Espa.

OBJECTIVE. This review has been prepared in response to the increasing interest shown in understanding the part played by melatonin in the body, which has led to the search for new uses of it in cerebral disorders, such as sleep disorders including insomnia, irritability, depression, behaviour disorders and even the treatment of autism, since sleep disorders also occur in this condition. We pay particular attention to studies involving epilepsy.

DEVELOPMENT. We show that interest in melatonin is rapidly increasing and new discoveries are being made of the part it plays in the biological regulation of circadian rhythm, sleep, mood, ageing, tumour growth and reproduction. Perhaps these processes between them have led to its use in the treatment of many current problems such as neuroprotection, migraine and the control of epileptic seizures.

CONCLUSIONS. It has been shown that in both children and adults melatonin is of low toxicity and may be used in high risk persons. In this paper we make a careful analysis of recent publications in the medical literature dealing with the use of melatonin in the control of epileptic seizures and discuss its advantages and disadvantages. However, as with other types of treatment, further study, both experimental and otherwise, is necessary for confirmation.

PMID: 12373656 [PubMed - in process]

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Glutamic Acid Reduced with Autism

ds=12372652&dopt=Abstract Fatemi S, Halt A, Stary J, Kanodia R, Schulz S, Realmuto G. Division of Neuroscience Research (SHF, ARH, JMS, RK), University of Minnesota Medical School, Minneapolis, Minnesota, USA

A limited number of reports have demonstrated abnormalities involving the glutamate and gamma amino butyric acid systems in blood and platelets of subjects with autism.

To further investigate these studies, brain levels of rate limiting enzyme, glutamic acid decarboxylase, which is responsible for normal conversion of glutamate to gamma amino butyric acid in the brain, were investigated.Postmortem cerebellar and parietal cortices of age (mean +/- SD for controls 23 +/- 4.2, autistic 25.2 +/- 5.2 cerebellum; controls 23.5 +/- 4.8, autistic 21.6 +/- 3.8 parietal cortex), gender and postmortem interval-matched autistic and control subjects (n = 8 control, n = 5 autism, cerebellum; n = 4 control, n = 5 autism, parietal cortex) were subjected to SDS-PAGE and western blotting.

Brain levels of glutamic acid decarboxylase proteins of 65 and 67 kDa and beta-actin were determined.Glutamic acid decarboxylase protein of 65 kDa was reduced by 48% and 50% in parietal and cerebellar (p <.02) areas of autistic brains versus controls respectively.

By the same token, glutamic acid decarboxylase protein of 67 kDa was reduced by 61% and 51% in parietal (p <.03) and cerebellar areas of autistic brains versus controls respectively. Brain levels of beta-actin were essentially similar in both groups.The observed reductions in glutamic acid decarboxylase 65 and 67 kDa levels may account for reported increases of glutamate in blood and platelets of autistic subjects. Glutamic acid decarboxylase deficiency may be due to or associated with abnormalities in levels of glutamate/gamma amino butyric acid, or transporter/receptor density in autistic brain.

PMID: 12372652 [PubMed - in process]

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Autistic Symptoms Following Herpes Encephalitis

ds=12369775&dopt=Abstract Ghaziuddin M, Al-Khouri I, Ghaziuddin N.

Division of Child and Adolescent Psychiatry, University of Michigan Medical Center, Ann Arbor 48109-0390, USA. mghaziud@umich.edu Autism is a childhood onset neurodevelopmental disorder characterized by reciprocal social deficits, communication impairment, and rigid ritualistic interests, with the onset almost always before three years of age.

Although the etiology of the disorder is strongly influenced by genes, environmental factors are also important. In this context, several reports have described its association with known medical conditions, including infections affecting the central nervous system. In this report, we describe an 11-year-old Asian youngster who developed the symptoms of autism following an episode of herpes encephalitis. In contrast to previous similar reports, imaging studies suggested a predominant involvement of the frontal lobes.

At follow-up after three years, he continued to show the core deficits of autism. This case further supports the role of environmental factors, such as infections, in the etiology of autism, and suggests that in a minority of cases, autistic symptoms can develop in later childhood.

PMID: 12369775 [PubMed - in process]

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Childhood Disintegrative Disorder Re-examination of the Current Concept

ds=12369769&dopt=Abstract Malhotra S, Gupta N.

Department of Psychiatry, Postgraduate Institute of Medical Education & Research, Chandigarh, India. savitam@sancharnet.in Childhood disintegrative disorder (CDD), which is classified as a sub-type of pervasive developmental disorder (PDD), has been recognised for many years. Research data on CDD, however, is sparse and it primarily describes the clinical parameters. In this research report clinical data on 12 cases of CDD and 21 cases of typical autism, seen during a specified period, are compared and critically evaluated in reference to the diagnostic criteria in ICD-10 for these disorders.

While the findings support the clinical validity of CDD, these also highlight the limitations of the current criteria (ICD-10) particularly the age of onset in CDD and the conceptual confusion in labelling it as a 'PDD'. Need for more research in the areas of the biology, course and outcome of CDD is emphasised.

PMID: 12369769 [PubMed - in process]

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Contingent Shock Researched as Treatment for Self-Injurous Behavior 'Effects of single and repeated shock on perceived pain and startle response in healthy volunteers.'

ds=12365852&dopt=Abstract

Duker PC, Douwenga H, Joosten S, Franken T.

Psychology Laboratory, University of Nijmegen and Plurijn Foundation, Netherlands. p.duker@ped.kun.nl

Contingent shock (CS) has been used in a number of studies to suppress health-threatening self-injurious behavior of individuals with mental retardation and autism. As sustained suppression is an issue of concern, research into procedural variables of CS is needed.

In this study, clinical evidence was used to infer a variable that might be of relevance for the application of clinical contingent shock, that is, to assess the effect of single versus repeated shock at a specific location on the body.

With pain intensity and startle response as dependent variables, shocks were administered to 48 healthy volunteers. Electric shocks were identical to those that used in clinical practice.

The second shock in succession to the same location of the body produced higher pain intensity ratings than the first shock and that the third shock in succession to the same location of the body produced higher pain intensity ratings than the second shock in succession. Startle responses, however, failed to be affected in this direction. The latter result is consistent with a previous study. Our data suggest that repeated shock to the same location is likely to be more effective to establish suppression than repeated shock to different locations.

PMID: 12365852 [PubMed - in process]

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Using Picture Exchange Communication System (PECS) with ASD Kids Assessment of PECS acquisition, speech, social-communicative behavior, and problem behavior.

ds=12365736&dopt=Abstract Charlop-Christy MH, Carpenter M, Le L, LeBlanc LA, Kellet K. Claremont McKenna College, USA.

The picture exchange communication system (PECS) is an augmentative communication system frequently used with children with autism (Bondy & Frost, 1994; Siegel, 2000; Yamall, 2000). Despite its common clinical use, no well-controlled empirical investigations have been conducted to test the effectiveness of PECS.

Using a multiple baseline design, the present study examined the acquisition of PECS with 3 children with autism. In addition, the study examined the effects of PECS training on the emergence of speech in play and academic settings.

Ancillary measures of social-communicative behaviors and problem behaviors were recorded. Results indicated that all 3 children met the learning criterion for PECS and showed concomitant increases in verbal speech. Ancillary gains were associated with increases in social-communicative behaviors and decreases in problem behaviors. The results are discussed in terms of the provision of empirical support for PECS as well as the concomitant positive side effects of its use.

PMID: 12365736 [PubMed - in process]

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New Study Shows Efficacy Of Gene Therapy for Parkinson's Disease First-ever clinical trials using gene therapy for Parkinson's disease anticipated to begin by end of year

Auckland, New Zealand and New York, NY: In a study published today in the journal Science, scientists from the University of Auckland and Weill Cornell Medical College reported on the effectiveness of a new gene therapy approach to Parkinson's Disease, and the potential for this therapy to affect the overall progression of the disease itself. Based on this study and other data, the U.S. Food and Drug Administration (FDA) has given its approval to begin testing this therapy in a small Phase I clinical trial. This will be the first time in the world that gene therapy will be used in patients with Parkinson's Disease.

The Science publication is authored by lead investigator, Dr. Matthew J.

During, Professor of Molecular Medicine at the University of Auckland, first author Dr. Jia Luo, and co-investigator Dr. Michael G. Kaplitt, Director of Stereotactic and Functional Neurosurgery and Asst. Professor at Weill Cornell Medical College. Dr. During and Dr. Kaplitt are also co-principal investigators on the upcoming clinical trial of this therapy.

"We are using gene therapy to "re-set" a specific group of cells that have become overactive in an affected part of the brain, causing the impaired movement and other symptoms associated with Parkinson's Disease," said Dr.

During. "We are very encouraged that in addition to the affect this therapy has on quieting symptoms, we present evidence that suggests it may arrest or delay disease progression."

People with Parkinson's Disease have a profound loss of a specific group of nerve cells deep in the brain which make dopamine, a signaling molecule. The loss of dopamine leads to a disturbance in the brain's network activity controlling movement. In the center of this network is a region called the subthalamic nucleus (STN), which in Parkinson's Disease is extremely overactive, and if silenced leads to a dramatic reduction in the symptoms.

Targeting the overactive cells, researchers inserted the "GAD" gene into a viral vector (adeno-associated virus or AAV) to allow it to be efficiently delivered into the affected region of the brain. GAD is responsible for making a small molecule called GABA, which is released by nerve cells to inhibit, or dampen activity. After this gene therapy is introduced, the overactive cells are "re-set" and brain network activity controlling movement returns towards more normal function. In 1994, Dr. Kaplitt and Dr.

During were the first to demonstrate that AAV could be a safe and effective vehicle for gene therapy in the brain. Since that time, AAV has been used safely in a variety of clinical gene therapy trials, and the virus has never been associated with any human disease.

Although medical therapy is usually effective for most symptoms of Parkinson's, over time many patients become resistant to treatment or develop disabling side effects. "Current surgical therapies for such patients attempt to interrupt this network abnormality by destroying overactive brain areas or placing DBS (deep brain stimulation) electrodes to quiet these areas. Both of these treatments, however, have certain limitations and side effects," said Dr. Kaplitt. "Our approach is based on a similar rationale, but we use gene therapy to adjust the chemical signaling of these brain areas to a more normal setting. This exploits the best parts of current therapy but makes it more powerful, less invasive and potentially safer."

The Science paper reports on testing of this theory using a combination of techniques to measure brain function in rodents that were made Parkinsonian.

Five tests were conducted. These tests showed the GAD gene was present and producing GABA as anticipated. Several behavior tests were also conducted in the rodents to show they had retained more normal function and did not develop further signs of Parkinson's as did the control rats. In add ition to work in rodents, primate studies demonstrated that the therapy was safe and there were no toxicities associated with the treatment.

Based upon the recent FDA approval, the first Phase I trial of this treatment is anticipated to begin within the next few months. Selected patients will undergo surgical gene therapy at The New York Presbyterian Hospital/Weill Medical College of Cornell University by Dr. Kaplitt. These patients will be recruited and followed by Drs. David Eidelberg and Andrew Feigin at the North Shore Hospital Long Island Jewish Movement Disorder Clinic. The initial trial will be limited to 12 patients with severe Parkinson's Disease, of at least five years duration, for whom current therapies are no longer effective.

"The Science report and our team's translation of this approach to treatment of human disease represent the culmination of over a decade of research in this area," said Dr. During. "Our primary objective has been to stress patient safety above all else, and the NIH (National Institutes of

Health) and FDA have helped us design a clinical intervention which has exciting efficacy potential and attempts to minimize in any way possible risks of adverse events to patients in the study. It is our hope that with this approach, our trial will help demonstrate that gene therapy in the brain can be both safe and effective."

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Taking a Clinical Look at Human Emotions

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On a recent balmy evening, Dr. Joseph LeDoux, a professor of neuroscience at New York University, strode to the stage of the Cornelia Street Cafe in Greenwich Village and read from his latest book, "The Synaptic Self: How Our Brains Become Who We Are."

Astonishingly, the audience — graduate students, publishing executives and scientists — greeted Dr. LeDoux's performance with enthusiasm usually reserved for rock stars.

In the world of the brain sciences, Dr. LeDoux, 52, is a star of high wattage. Through his research and writings, he has been a major force in changing approaches to human brain research. Previously, brain studies tended to bypass phenomena that are difficult to measure, like emotions and the unconscious. Dr. LeDoux, in his laboratory, began finding ways to study how the brain processes emotions.

Rather than treat emotion as an experience, he looked at it as a process. And in doing this, he uncovered a path into the territory that is the human mind. "I'm studying the quantifiable aspects of the mind," Dr. LeDoux said over coffee on a morning not long after his cafe performance. "I'm saying, `Here's how you can quantify certain aspects of it and make some progress.' "

Q. In "The Synaptic Self," you say, "We are our synapses." Why do you say that the key to humanness is to be found in the microscopic spaces between two nerve cells?

A. Synapses are the spaces between brain cells. But more importantly, they are the channels of communication between cells that make possible all brain functions, including perception, memory, emotion and thinking.

It's practically a truism to say the synapses underlie personality since synapses underlie everything the brain does. More important yet: synapses are the sites of storage of information, including information that is encoded by our genes and also by our experiences — our memories.

When it comes to personality, genes and experience are just two ways of doing the same thing — wiring synapses. That's why I say, To the extent that we are a product of our genes and experiences, we are our synapses.

This doesn't mean that the essence of who you are is encoded at a particular synapse. It means that your self is a very complex pattern of synaptic connectivity in your brain.

Q. Why is this a breakthrough?

A. In science, it's often important to define a problem in a practical way before you can make progress on it. Psychological conceptions of the self have tended to be framed in terms not compatible with what we know about the brain. It would be hard, for instance, to track down the neural basis of concepts like superego, narcissism, esteem or actualization.

To solve this, I've long felt that scientists needed to come up with a new way of thinking about the self. I do it by attacking it from two angles. One is bottom up. Given that synapses are important to both genetic and experiential aspects of the self, studies of synapses give us a neural anchor to understand how these psychological constructs work.

The other is top down. Given that memory is so important to maintenance of the self, and that much is known about the mechanisms of memory, we can use it as a way in to understanding the synaptic basis of the self.

Q. What have you done to help us gain this knowledge?

A. My work has been focused on the brain mechanisms of emotional memory, a form of unconscious memory formed in a region of the brain called the amygdala. Through studies of fearful or traumatic experiences in rats, my colleagues and I have been able to identify specific synapses that participate in the formation of the memory. Studies of humans have confirmed that the same basic circuits are involved.

Q. One area you've specialized in is the biology of emotions. Was there, until recently, a kind of bias among experts against looking at this?

A. Oh yes. For years, you couldn't study the mind. At first, the problem was the behaviorists who said, "no, no, no, no" to any mind studies because they felt that observable behavior was the only legitimate psychological topic.

What I feel is that we now need is more of a mind science because cognition is about cognition and emotion is about emotion. The mind is about both things.

Q. Marvin Minsky, the M.I.T. computer scientist who has written about the mind, believes, to simplify, that we are basically a mass of chemicals and switches. Do you agree?

A. That's what the brain is: just a piece of meat that has chemicals and electrical charges. The mind, of course, is a special version of that. And we may not know in our lifetime all about how the brain works to make the mind. What we know about the brain is that it's got neurons that communicate across synapses by releasing a neurotransmitter and that generates electrical impulses and the receiving neuron that then talks to its neighbors the same way. If the mind depends on the brain, then all aspects of the mind are going to depend on these simple electrical, chemical processes.

Q. Speaking of meat, is it true you come from a family of butchers?

A. Yes, my father was a butcher. As a young person, it was my job to clean the membranes off the brains we sold in the shop. The most vivid image I retain from that time is pulling the bullets out of cows' brains. The way animals were killed was by being shot. And so I'd pull the bullets in order to clean the brain. Often while I was doing it, I wondered what being shot could mean for the cow's mind.

Q. How then did you find your way into neuroscience.

A. I haven't been a scientist all my adult life. I have two degrees in marketing. I had studied marketing because my parents, small-town people from Louisiana, wanted me to. I was totally uninterested in business and ended up taking a master's in marketing and consumer psychology. As part of that, I took at course at L.S.U. with the late Robert Thompson. So I worked in his lab and we published a few papers, and he endeavored to get me into graduate school at SUNY Stony Brook in New York. That was the beginning.

Q. As a student of both the brain and the mind, do you sometimes try to visualize your own brain at work?

A. Sometimes, yes. Especially if I'm afraid of something. Let's say I'm walking in the woods and suddenly I see something on the ground. I pause and I imagine my amygdala being driven by that curved shape on the ground. Then I realize that the object is a stick and not a snake and I move along. Yes, I can visualize the whole process.

Q. Is being a brain scientist something like becoming an astronaut? You are always entering into completely new areas of discovery?

A. No. It's more like a deep sea explorer. When you're studying the brain, it doesn't feel like you are going into open space — more like into a confined space. It feels like you are getting into a ship that can take you down to find those little creatures in the dark depths of the sea. Interestingly, I never find brain studies confining. Every time you discover something and you try to understand it, you know that you've only scratched the surface.

Q. In the last few years, we've seen a lot of big-name physicists and even geneticists, take up the brain sciences. Why all this cross-disciplinary migration?

A. Brain science has been a favorite one for this kind of migration because the mysteries of the brain are so attractive. So people like Gerald Edelman and Francis Crick have turned to solving problems of the brain. These are smart people. The more the merrier.

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EDUCATION

9th Circuit: IDEA Due Process Needn't Exhaust State Complaint System Porter v Board of Trustees of Manhattan Beach Unified Sch. Dist.

Plaintiffs, autistic child and his parents, suing under Individuals with Disabilities Education Act for district's failure to implement directives of order issued as result of IDEA due process hearing were not required to exhaust California's complaint resolution process before suit.

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PUBLIC HEALTH

Separate MMR Jabs At New Clinics in UK

Four new clinics in East Anglia will be offering single vaccines to replace the controversial mumps, measles and rubella (MMR) innoculation. Children are given the triple MMR vaccine from the age of 13 months but some parents fear a possible link with autism. Families can pay for single vaccines, but only at specialist centres.

18 months plus

Later this year a private firm, Healthchoice UK, is opening clinics offering separate immunisation with three vaccines at Cambridge and Peterborough in Cambridgeshire, Ipswich in Suffolk and Chelmsford in Essex.

The MMR three-in-one vaccine is offered free of charge on the National Health Service. Each single vaccine costs £80 and is only available to children over 18 months old.

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FUNDRAISING

Walk F.A.R. for NAAR Raises Nearly $2 million in First Four Fall Events Nearly 20,000 Walkers Make Strides to Support Autism Research

Upcoming Events include Northern New Jersey & Southern Florida Events

[From a NAAR press release.]

Princeton, NJ – Never underestimate what can be accomplished when taking a walk. Nearly 20,000 individuals and corporations in four communities made big strides for autism research at the National Alliance for Autism Research’s (NAAR) first fall WALK F.A.R. for NAAR events, raising nearly $2 million for autism research. NAAR’s first Walk events this fall included, Long Island (Sept. 28); New England (Sept. 29); Buffalo (Sept. 29) and Central New Jersey (Oct. 6). So far this year, Walk F.A.R. for NAAR has raised more than $3.2 million for autism research. “We are thrilled that our first fall Walk events have been so successful in raising money for autism research and promoting autism awareness,” said Prisca Chen Marvin, NAAR president. “We thank everyone who took part in these events and applaud the remarkable efforts of our extraordinary walk chairs and committee members, who invested their time and talents to help make these events so special.”

Long Island Walk F.A.R. for NAAR - Sept. 28 at Eisenhower Park, East Meadow, NY. Chair: Karen Cerise. Approximately 7,000 walkers and an estimated $800,000 raised.

New England Walk F.A.R. for NAAR – Sept. 29 at MDC Artesani Park, Brighton, MA. Chairs: Margie Pascetta, Dolores Rezendes, Karen Bodamer. Approximately 7,000 walkers and an estimated $750,000 raised.

Buffalo Walk F.A.R. for NAAR – Sept. 29 at Delaware Park, Buffalo, NY.

Chairs: Monica Moshenko and Anita Brenon-Bickert. Approximately 3,000 walkers and an estimated $100,000 raised.

Central New Jersey Walk F.A.R. for NAAR – Oct. 6 at Mercer County Park, West Windsor, NJ. Chair: Jim Brady. Approximately 2,500 walkers and an estimated $275,000 raised. (more)

Upcoming Walk F.A.R. for NAAR events include: Northern New Jersey Walk F.A.R. for NAAR on Oct. 19 at Giants Stadium, East Rutherford, NJ. Call

Palm Beach Walk F.A.R. for NAAR on Nov. 17 at John Prince Park, Lake

NAAR kicked off the 2002 Walk season with Walk F.A.R. for NAAR events in Pittsburgh, PA, Purchase, NY, Pennsauken, NJ, Seattle, WA and Des Moines, IA, raising $1.3 million for autism research

_______________________________________________________

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LETTERS

B.C. Attorney General Geoff Plant said the government is examining the impact of the ruling but said the province is in fact already funding early-intervention treatment.

"We have a program in place for that purpose," he said. "So we'll be studying the reasons for judgment and deciding what implications they have for us in the days a weeks to come."

The REASON Mr. Plant obviously has missed, and yet the ruling clearly states, there is to be NO age cut off for treatment. The program now in place is only for birth to 6 years old. Usually, we are so late in getting our children diagnosed here as ASD (typically age 5 here), the wait list prevents them from ever getting treatment.

Mr. Plant also forgot to mention that the program he is refering to actually only started one year ago for that age group. Prior to then there were no services available for children with autism. So now we will have to see how they handle the lifting of the age restriction!

-Kerry Ayotte

"My Child is Autistic" is Bothersome

Being a parent of a child with Autism, I find that it is bothersome to hear people say that my child is Autistic. My child is a person not a disability. Her disability is just her passport to receive services. I believe that people should say that she is a child with Autism instead of an Autistic child. But then again autism is just a word, not what my daughter is.

I can't believe that you would discredit the people that you are doing the newsletter for. I commend you on your beliefs and to say that is all it is, a belief. If we lived in a perfect world then we wouldn't need the term person-first language. Regardless of how information is put across, I am one parent that has more than one child with a disability that knows the information that you provide is great whether or not it is person-first language.

Thank you for doing such a great job educating us parents and for allowing for the opportunity for there to be a little debate every once in a while. Sincerely, what's the big deal?

- Mikebelind@cs.com

Well, that is the point. The issue is symbolic and supported mostly by blustery assertion and pointed examples – both can be met with counter-assertion and counter-examples. There is not sufficient evidence to support the contention that non-person or non-people first usage is disrespectful or harmful. So round-and-around we go. Pressing the issue itself is harmful in that it creates needless divisions amongst people who otherwise share common goals -- and thus should be opposed as counterproductive, if for that reason alone. There is something to be said for picking one's battles carefully. –LS

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Readers' Posts

My son, 15, has Aspergers, ADHD and an anxiety disorder. Psychiatrist prescribed Trileptal 2 weeks ago for aggressive thoughts and actions. It helped much, but 2 days ago, he started hallucinating. He stopped Trileptal, but still hallucinates. Doctor said Trileptal shouldn't cause hallucinations, but may in combination with Ritalin. My son hallucinated when he was 11 and 12. Once when he took Wellbutrin, and once from a cold pill which interfered with his Ritalin. Have other readers had experience with hallucinations? If Trileptal is the problem, do you know other medications that control aggression? Sharri at: semarcin@aol.com

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What is carnosine and where can you find it? Lester Starnes bstarnes@texoma.net

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Are there any support groups in the San Gabriel Valley area in Southern

Calif.- from Diamond Bar to Rancho Cucamonga area? Loretta Puuwali@adelphia.net

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This month's issue of Exceptional Parent magazine (October/2002) has a series of articles on Autism. They also have committed to a series of articles through 2003 and will further be exploring the causes, effects and treatment of Autism. Carolyn

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Does anyone have an Asperger's child who does not sleep? What do you do for your child? I need help. Clonidine is no longer working at a safe dose. Christina ecsalsman@excite.com

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