Slow-Motion Miracle: One Boy's Journey Out of Autism's Grasp

[Guest guest]

{Words like Chelation, Autism Research Institute, and supplements do not

appear in this article. The NYT's one-sided, propagandistic approach to

pseudo-journalism continues. -}

Slow-Motion Miracle: One Boy's Journey Out of Autism's Grasp

By JOHN O'NEIL

http://www.nytimes.com/2004/12/29/education/29autism.html

O'Neil/The New York Times

{caption} when he was 2 years old. A bubbling child, he grew

increasingly withdrawn, repeating meaningless phrases, lying on the

floor squinting or crying at loud noises.

ix years ago, my son fell down a well, and he's still climbing out.

has autism. He is one of 150,000 or more American children

classified in the last decade as having the once-rare disorder,

including 25,000 in 2003. Half a century ago, polio epidemics left

perhaps 5,000 children a year with some degree of disability, and the

sight of children stricken overnight galvanized the nation. But autism's

arrival, and the response to it, has not been so dramatic.

In 's case, a bubbling 2-year-old who loved " mashed totatoes " and

sword-fighting faded away. In his place was a nearly silent, unhappy

child who repeated meaningless phrases, lay on the floor squinting or

pulled cowboy boots on and off until his feet were raw. Every day he

fell a little further out of the world.

But one recent afternoon sat at our kitchen table with his best

friend, Larry, goofing off instead of doing homework. They made dumb

jokes and gossiped about their " girlfriends " at their school, just up

the street.

It's hard for me to explain how many dreams-come-true are reflected in

that one sentence.

's journey is by no means over. He still has significant problems

with reading comprehension, math, attention and social skills. He gets

stuck on favorite subjects - though this year, the Yankees, thankfully,

replaced the War of 1812. He can sound as if he is speaking a second

language, with the halts and mangling of idioms that implies. With his

peers, he hovers at the border of acceptance.

But even that list of problems is a sign of how far he has come. Six

years ago, he couldn't engage with the world around him.

Scientists know little about autism. What they have learned has

underscored the complexity of its genetics and anatomical abnormalities,

which begin developing soon after conception. They do know a lot,

however, about what to do about autism, enough that a federal panel has

set a 10-year target of preventing 25 percent of new cases. The panel's

plan faces huge obstacles, starting with an absence of additional funds

to carry it out. But the hardest part, panel members said, is making use

of what we already can do.

In that sense, 's progress has a sadder side: that he has been such

an exception. Not everybody who gets the treatment he did progresses so

far, although some go further. But only a relative handful of children

with autism are thought to receive even the minimum standard of care, a

pattern reflected in an increase in requests for institutional

placements as the leading edge of last decade's cases reaches adolescence.

The other key to improved outcomes is early detection. Most cases are

caught much later than they could have been, and in that sense was

no exception. Had we any idea what to look for, we could have known in

's first year of life, I think.

was an easy baby. But looking back, part of the easiness was a

lack of intensity in his connection to us. There was some difficulty in

meeting our gaze, and a lack of curiosity about things pointed out to

him - both hallmarks of autism, and red flags on formal developmental

screenings. never got one, perhaps because his sunny disposition

obscured such flaws, and because we were never worried enough to raise

any concerns with his pediatrician.

When he was 2½, we moved to northern New Jersey six weeks after our

youngest son, Miles, was born. When 's behavior started to become a

bit odd, we just figured he was overwhelmed.

It took a third party to force us to focus on him. The director of

's new preschool took my wife, Marcia, aside one day. " He just

seems a little off to me, " Maureen, the director, said. " Sometimes he

seems not to hear me. "

We know now that she was worried about more than his hearing. In the

first of many strokes of luck, she was familiar with autism, having

taught in a local specialty school. She suggested that we contact the

local school district for an evaluation. was fine, I thought, but

why not?

As the evaluation process wound on toward his third birthday and 's

behavior became more difficult, it became clear that he was not fine.

When Maureen called Marcia into her office again, to give a name to our

fears - " I think is a little bit autistic " - it made all too much

sense.

Good News, Bad News

A library grew on our bedside table, bearing a message that seemed a

sort of good news, bad news joke. The bad news: autism has no cure. The

good news: there can be effective treatment. The bad news: it's

incredibly expensive, difficult and time-consuming - and nobody wants

your child to have it.

So we were pleasantly surprised when we sat down with the school's team

and learned the district had recently begun a preschool autism program

using the treatment the books recommended, applied behavioral analysis,

or A.B.A.

We had some questions. For one thing, he would be getting 10 hours of

one-on-one therapy a week, instead of the 30 to 40 hours a week called

for. We were told that quality was what counted, not quantity. We also

knew we had few options.

On the way home, Marcia, a physician, seethed. " Do you think I prescribe

half the appropriate dose of antibiotics? " she demanded. But

needed help, and the clock was ticking.

To get more help, Marcia took him to a private speech therapist.

She learned something about A.B.A. that day, but also about how little

we knew about what was going on inside his head. She learned, for

instance, that had forgotten his name.

" What's your name? " asked the therapist, Kathy Rooney.

Silence.

" What's your NAA-aaame, " she chanted in a singsong. " JAMES o-NEEE-il. "

After a few more times, she repeated the question. After a pause, he

answered, and Kathy showered him with praise.

The " analysis " in A.B.A. means figuring out what a child needs to learn,

the best way to teach it - and whether it's actually learned. The

behavioral part means rewarding desired behavior.

In some ways, that sounded like a more rigorous version of ordinary

parental tasks, and Marcia began to introduce bits of it, like giving

milk only when he said " milk " instead of just pointing. I was

taking him to the pool a lot, mostly to wear him out, since he had

trouble sleeping. loved to jump in, and I tried taking advantage

of that desire to perform what I'd later learn was " discrete trial

instruction. " I held up one finger and said, " How many? One! " If

said " one, " splash! By the end of the week, he was up to three, unprompted.

We began to discover that is, for a child with his problems, a

quick learner when taught in the right way. And not everything had been

lost. Shown a hard yellow plastic hat, he answered, slowly but surely,

" con-struc-tion hel-met. "

But as Marcia began to learn more, her enthusiasm about the happy notes

coming home with began to dim. His teachers seemed to have a hard

time motivating him. Most important, he just didn't seem to be learning

much.

We contacted the parents of the other children in the program, and found

they were also concerned. Together, we went to the district's special

education director, asking her to let an outside expert make

suggestions. But as the director talked about the many costs the

districts was facing, the tears trickling down one mother's cheeks dried

up. We all got the message: They may be your children, but this is our

program.

Home Program, Tiny Steps

That's how we came to find ourselves sitting in our basement on a

stifling July day with strangers who were about to become the most

important people in our lives.

When Marcia had first read about " home programs, " her reaction had been

succinct: " Not for us! " Creating a school for one from scratch seemed

insane, even without the lawsuit it would obviously require.

But she had given up her full-time position and done it. Our greatest

stroke of luck was finding someone to get us started: Hampel of the

Rutgers Autism Program, whom we had contacted when we thought the

district might like an expert's help.

He had high hopes, which he expressed in an unsettling way. " is

the kind of kid who is the scariest to work with, " he said, " because you

never know if you're going fast enough to keep up with his potential. "

What followed was an isolating time for , at a little table for up

to eight hours a day, doing work most children would find tedious in the

extreme. Skills normally acquired in a blended rush were introduced in

the tiniest of steps. An instructor would place two blocks side by side,

one flat, one vertical, say " Do this, " and hand them to . Or touch

her nose - " do this " - then her cheek, eyes, brow.

But after a few tantrums it became clear that liked to work. Not

just for the hugs and shiny stickers. He liked being connected. And it

was only under this kind of bare, intense focus that he could connect.

Data is the lifeblood of A.B.A.; it is the only way to spot your

mistakes. But along with charts of 's trial-by-trial performance,

his instructors kept a log of " spontaneous language. " On the program's

first day there is only one entry: " I want cheese crackers. " In August,

that starts to creep up, to a half a dozen or so. In late September

there is an explosion: " I want a big tickle. " " I want the Play-Doh. "

Another one also jumps out: " Where is ? "

A 4-year-old whose family had just arrived from Poland, came

with her mother several times a week to visit our neighbor. She knew no

English and had nothing to do - except try to get to play. Such a

determined child! was used to a language barrier and was

tireless in her efforts to get into a game, even as simple a one

as rolling toy cars down the steps. " Jems. Jems! JEMS!!!! "

And it worked. For brief snatches could play along. could play!

What was new wasn't just , of course. was waking up,

thanks to his work at the table. New skills were creating a new interest

in the world - which were making other new skills possible.

Now we tried to use our time to extend his learning. I enlisted his

brothers, Miles and to teach simple play scripts, like saying,

" Tickets, please! " when the chairs were lined up to make a train. We

worked on the countdown for a rocket ride. extended the script:

" To the moon! To the stars! AAAAAHHHH!!! WE CRASHED!!! "

But every so often there was a fresh bucket of cold water to remind us

of how far he had to go - and that time was passing. Like this blunt

assessment from a speech pathologist when he turned 4: " Unless his

language really picks up, he's not going to make it. "

Making it meant placement in a mainstream kindergarten - a crucial

sorting point. We went home scared, and Marcia made changes.

For six weeks, the instructors focused almost entirely on getting

to talk, a lot. One technique was simple. Usually got treats as a

reward for doing well at his programs. For now, all he needed to get

them was simply to ask for them.

And it worked. The data the instructors took on requests per hour crept

up and up, but in truth we didn't need it. He wouldn't shut up. The

intensive effort had jump-started some slumbering connection in the

brain. And over months we began to see flashes of a new kind of language

- talking that goes back and forth, that changes with each thing that is

said.

Then this, from the logbook for April 7, 2000:

Jeanette: I like to eat chicken.

: I like to eat breakfast.

Jeanette: I like waffles for breakfast.

: I like cereal for breakfast.

A conversation.

On the Road to Real School

Also that spring, returned to the district preschool program we

had withdrawn him from the year before. He hadn't been ready for it

then; now he was. And so were we: we had reached a settlement in the

lawsuit we had filed charging that the district had failed to provide

him with an education appropriate to his needs.

That yearlong migraine had drained us of time, emotion and money at a

time when we had little enough to spare. But we also felt that if we let

the district pound on our child without hitting back, the pounding would

never stop. In the end, the court sided with the first family to go to

trial in our district. The creation of district-run autism programs

clearly needs to be encouraged, the judge wrote, " but it cannot be at

the expense of a little boy. "

For the next year we were on the on-ramp to real school in a blur of

preparation. But kindergarten turned out to be an anticlimax. He was

accompanied by one of his home instructors, acting as a " shadow, " and

yes, things went well, and yes, his problems there were the same ones he

had at home, like staying on task and following directions.

What was big in kindergarten was something we hadn't prepared for: Larry.

Sometime during preschool, children had stopped being ghosts for .

But we gradually realized what was developing here was a friendship -

the hardest thing for a person with autism at any age.

Larry Pan is enthusiasm with a crew cut. What attracted Larry to ?

Perhaps it was 's sense of humor (think diaper jokes). Or maybe

they just were drawn to each others' big hearts.

After our rocky start with our district, elementary school has been

remarkably smooth. There was one dreadful time in first grade when

suddenly began hitting his aide, raising the prospect that perhaps he

could not continue where he was.

The solution turned out to be simple. A swap of aides was arranged, and

Jeanette, who had known since was 3, came in as a backup shadow.

She gave him a look and the nonsense stopped. But Marcia and I felt as

if we had been swept back to the cliff's edge. When a child falls out of

the mainstream, it is hard to return. Unable to sleep, I wondered if

this was what post-traumatic stress disorder felt like.

Knowing He Is Different

Nothing like that has happened again. There are still plenty of problems

- his progress, in some ways, consists of moving up to a better class of

problems. At camp this summer, didn't know how to handle a boy who

was mean; in years past he wouldn't have recognized the hostility.

used to be unnaturally compliant: now his favorite song begins, " You're

not the boss of me now... "

And then there's the most painful progress of all: right now is

wrestling with the knowledge that he has autism.

Over the last year, it has become slowly apparent to that he is

different from other children, or at least he is thinking about it. He

recently asked Miles, who is now in first grade, why Miles doesn't go to

a resource room.

But why tell him?

Giving him a name for the difference he is beginning to grasp means

letting him begin coping with the issues that will remain after his

intervention fades away. It's strange to be thinking of the path to

adulthood for a fan of " Ed, Edd n Eddy, " the silliest cartoon on TV. But

that's where this road leads.

In my glummer moments, I think about as a boy who fell off a train

and is running to get back on. Time and again he reaches it - but the

train, too, is accelerating. Will the running never end?

We used a more upbeat image to tell where he is now: he had

rounded third and was getting ready to slide home.

Still, raged and cried and insisted that he didn't have autism,

that other children he knew did.

But he also had a lot of good questions. He knows that Larry gets

tutoring in reading. Why doesn't that mean that he has autism? and

I had looked at an article about a kindergartner with cerebral palsy.

Could that boy get better? Which was worse?

And he kept on thinking. Earlier this month, at the end of a day spent

on a research study, he was offered a T-shirt with a picture of a brain.

He angrily refused it. " I don't want to wear that to school, " he said.

" Nobody else in my class has autism. "

In the car, he wept, asking " Why doesn't anybody else have autism? " The

next night, during a sleepover, he told Larry about the incident - about

how his brain was different, about how he used to have big problems.

What did Larry say? I asked . " That the only thing I know about is

peanut butter! " he said, and laughed.

He had taken a chance and learned a lesson: Larry cares about him, not

his label.

It made me realize: from now on who turns out to be is going to be

shaped more by him than by the work being done for him. will be

his own intervention.

O'Neil is deputy editor of special sections at The Times.

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[Guest guest]

On another list, a parent raised important concerns about my comment

regarding today's NYTimes article. The parent offered:

This seems to be a story written by the father - maybe they

don't know about chelation and biomedical intervention. Or maybe they

do, and have chosen not to try it. Is your point that the NYT shouldn't

publish stories about autism that don't mention alternative treatments?

We're doing just about everything with our son BUT ABA. He's

made some improvements, but I really don't know if they are due to the

interventions or the natural course of his autism. I'm really wondering

lately if we're missing by the boat by not also doing ABA or VB.

Here is my response:

My jibe at NYT today is because virtually all their articles don't

mention therapies other than training, thus today's article reinforces

yesterday's, which was far more blatant by bashing non-mainstream

approaches. Even Bernie Rimland says that intensive training asap is

beneficial. Many parents report that ABA effects were minimal until

augmented by biomed evals and child-specific treatments. CSB delineates

4 main categories of response to biomed treatments, from wonderful, to

really nice, to just something or other, to nothing at all. Several

challenges attend the child who hasn't improved. For instance, some

fetal and neonatal neurologic impairment may be permanent, eg,

disruption of synaptic development during critical developmental periods

has long been known to be capable of inducing lasting effects. Also,

the current vogue of lab-test arrays seems designed to be helpful for

most kids but not for all kids. Hugh Fudenberg's 1995-6 panels were far

more thorough (4). Today's panels seem to have some categories Hugh

didn't use. Every day I wonder, how many of the non-responders to

CSB-like protocols could be helped this year if an expanded lab array

had been purchased. And at this point the cost of lab arrays becomes

crucial. A more thorough array costs more and would identify treatable

pathologies in only a small percentage of additional kids.

I find myself wondering: among the non-responders, how many kids have

been evaluated for the antibodies Connolly describes (1)? For

intra-monocyte pathogens whose atypical presence (2) could contribute to

the BBB antibodies Connolly et al described? These two questions point

towards lab tests most docs don't recommend, towards lab assays

described in clinical-research articles but virtually unavailable to the

general public, and towards potentially treatable pathways in small

subgroups of autistic kids. Of course, only the very wealthy can afford

extensively more thorough lab arrays.

A 1979 book was remarkably prescient in describing the small subgroup of

autistic kids who got better (3). At one of my mini-DAN! presentations,

I offered quotes from the book (including the 1979 got-better rate) and

compared that rate with today's rates of improvement (eg, via IMFAR

chelation abstract of Holmes, Cave, El-Dahr) and asked if the new biomed

therapies are helping more kids than got better in 1979. The answer

appears to be Yes, even though not all kids get better enuff to attend

NT schools w/o aides, and some kids improve hardly at all.

A parallel to today's NYTimes article is found in cancer literature.

Spontaneous remissions are described, even in folks who refuse

treatment. The bodies of such individuals found ways to fight back

against the cancer and did so w/o chemotherapeutic intervention. A

question today's NYT article doesn't seem to ask is: Was the child a

sick child (go to NYTimes, see his picture) who for various reasons akin

to spontaneous remission got well, and, as this occurred, was having ABA

therapy?

For some parents, a non-responder to biomed evals and treatments faces a

dilemma - expand the array of lab data? Bail out? There's no eary

answer here. Each parent must choose. I recommend the DeMyer book for

parents and physicians wanting an eye-opening glimpse of autism circa

1979, when (even then) some sick kids who qualified for an autism dx

recovered.

Today, 53 copies were available vir http://www.Bookfinder.com, many

quite reasonably priced.

1: J Pediatr. 1999 May;134(5):607-13.

Serum autoantibodies to brain in Landau-Kleffner variant, autism, and other

neurologic disorders.

Connolly AM, Chez MG, Pestronk A, Arnold ST, Mehta S, Deuel RK.

Departments of Neurology and Pediatrics, Washington University, St. Louis

Children's Hospital, St Louis, Missouri, USA.

OBJECTIVE: Etiologically unexplained disorders of language and social

development have often been reported to improve in patients treated with

immune-modulating regimens. Here we determined the frequency of autoantibodies

to brain among such children. DESIGN: We collected sera from a cohort of

children with (1) pure Landau-Kleffner syndrome (n = 2), (2) Landau-Kleffner

syndrome variant (LKSV, n = 11), and (3) autistic spectrum disorder (ASD, n =

11). None had received immune-modulating treatment before the serum sample was

obtained. Control sera (n = 71) were from 29 healthy children, 22 with

non-neurologic illnesses (NNIs), and 20 children with other neurologic disorders

(ONDs). We identified brain autoantibodies by immunostaining of human temporal

cortex and antinuclear autoantibodies using commercially available kits.

RESULTS: IgG anti-brain autoantibodies were present in 45% of sera from children

with LKSV, 27% with ASD, and 10% with ONDs compared with 2% from healthy

children and control children with NNIs. IgM autoantibodies were present in 36%

of sera from children with ASD, 9% with LKSV, and 15% with ONDs compared with 0%

of control sera. Labeling studies identified one antigenic target to be

endothelial cells. Antinuclear antibodies with titers >/=1:80 were more common

in children with ASD and control children with ONDs. CONCLUSION: Children with

LKSV and ASD have a greater frequency of serum antibodies to brain endothelial

cells and to nuclei than children with NNIs or healthy children. The presence of

these antibodies raises the possibility that autoimmunity plays a role in the

pathogenesis of language and social developmental abnormalities in a subset of

children with these disorders.

PMID: 10228297 [PubMed - indexed for MEDLINE]

2: Med Hypotheses. 2001 Apr;56(4):523-31.

Intra-monocyte pathogens delineate autism subgroups.

Binstock T.

Immune panels of many autism-spectrum children reveal signs of atypical

infections and shifted cell counts. In conjunction with trait-related cerebral

hypometabolism and hypoperfusion, these findings suggest a hypothesis: Several

autism-spectrum subgroups derive from intra-monocyte pathogens such as measles

virus, cytomegalovirus, human herpesvirus 6, and Yersinia enterocolitica.

Furthermore, with much inter-child variation, their effects manifest as

diminished hematopoiesis, impaired peripheral immunity, and altered blood-brain

barrier function often accompanied by demyelination. In some such children, one

or more of these pathogens persists as a chronic-active, seemingly subclinical

infection etiologically significant to the child's autistic traits. Within these

subgroups, immune impairments and atypical infections may be treatable.

Copyright 2001 Harcourt Publishers Ltd.

PMID: 11339860 [PubMed - indexed for MEDLINE]

3. n K. DeMyer. Parents and children in autism.

4: Biotherapy. 1996;9(1-3):143-7.

Dialysable lymphocyte extract (DLyE) in infantile onset autism: a pilot study.

Fudenberg HH.

Neurolmmuno Therapeutics Research Foundation Spartanburg, S.C., USA.

40 infantile autistic patients were studied. They ranged from 6 years to 15

years of age at entry. 22 were cases of classical infantile autism; whereas 18

lacked one or more clinical defects associated with infantile autism

( " pseudo-autism " ). Of the 22 with classic autism, 21 responded to transfer

factor (TF) treatment by gaining at least 2 points in symptoms severity score

average (SSSA); and 10 became normal in that they were main-streamed in school

and clinical characteristics were fully normalized. Of the 18 remaining, 4

responded to TF, some to other therapies. After cessation of TF therapy, 5 in

the autistic group and 3 of the pseudo-autistic group regressed, but they did

not drop as low as baseline levels.

Publication Types:

Clinical Trial

PMID: 8993773 [PubMed - indexed for MEDLINE]

>

>

>

>

>

> {Words like Chelation, Autism Research Institute, and supplements do

> not appear in this article. The NYT's one-sided, propagandistic

> approach to pseudo-journalism continues. -}

>

> Slow-Motion Miracle: One Boy's Journey Out of Autism's Grasp

> By JOHN O'NEIL

> http://www.nytimes.com/2004/12/29/education/29autism.html

[Guest guest]

You need to do verbal behavior. You can use a skittle, crush it and

get about 10 pieces of candy out of one skittle. Hold out a full

skittle to your child and have them sign eat, or candy or say it if

they can. You really should be doing mand training, if skittles are

not reenforcing to your child try something else. My son does very

well w/ verbal behavior but probably would not have done well years

ago before chelation.

nne

> On another list, a parent raised important concerns about my

comment

> regarding today's NYTimes article. The parent offered:

> This seems to be a story written by the father - maybe

they

> don't know about chelation and biomedical intervention. Or maybe

they

> do, and have chosen not to try it. Is your point that the NYT

shouldn't

> publish stories about autism that don't mention alternative

treatments?

> We're doing just about everything with our son BUT ABA.

He's

> made some improvements, but I really don't know if they are due to

the

> interventions or the natural course of his autism. I'm really

wondering

> lately if we're missing by the boat by not also doing ABA or VB.

>

> Here is my response:

>

> My jibe at NYT today is because virtually all their articles don't

> mention therapies other than training, thus today's article

reinforces

> yesterday's, which was far more blatant by bashing non-mainstream

> approaches. Even Bernie Rimland says that intensive training asap

is

> beneficial. Many parents report that ABA effects were minimal

until

> augmented by biomed evals and child-specific treatments. CSB

delineates

> 4 main categories of response to biomed treatments, from

wonderful, to

> really nice, to just something or other, to nothing at all.

Several

> challenges attend the child who hasn't improved. For instance,

some

> fetal and neonatal neurologic impairment may be permanent, eg,

> disruption of synaptic development during critical developmental

periods

> has long been known to be capable of inducing lasting effects.

Also,

> the current vogue of lab-test arrays seems designed to be helpful

for

> most kids but not for all kids. Hugh Fudenberg's 1995-6 panels

were far

> more thorough (4). Today's panels seem to have some categories

Hugh

> didn't use. Every day I wonder, how many of the non-responders to

> CSB-like protocols could be helped this year if an expanded lab

array

> had been purchased. And at this point the cost of lab arrays

becomes

> crucial. A more thorough array costs more and would identify

treatable

> pathologies in only a small percentage of additional kids.

>

> I find myself wondering: among the non-responders, how many kids

have

> been evaluated for the antibodies Connolly describes (1)? For

> intra-monocyte pathogens whose atypical presence (2) could

contribute to

> the BBB antibodies Connolly et al described? These two questions

point

> towards lab tests most docs don't recommend, towards lab assays

> described in clinical-research articles but virtually unavailable

to the

> general public, and towards potentially treatable pathways in

small

> subgroups of autistic kids. Of course, only the very wealthy can

afford

> extensively more thorough lab arrays.

>

> A 1979 book was remarkably prescient in describing the small

subgroup of

> autistic kids who got better (3). At one of my mini-DAN!

presentations,

> I offered quotes from the book (including the 1979 got-better

rate) and

> compared that rate with today's rates of improvement (eg, via

IMFAR

> chelation abstract of Holmes, Cave, El-Dahr) and asked if the new

biomed

> therapies are helping more kids than got better in 1979. The

answer

> appears to be Yes, even though not all kids get better enuff to

attend

> NT schools w/o aides, and some kids improve hardly at all.

>

> A parallel to today's NYTimes article is found in cancer

literature.

> Spontaneous remissions are described, even in folks who refuse

> treatment. The bodies of such individuals found ways to fight

back

> against the cancer and did so w/o chemotherapeutic intervention.

A

> question today's NYT article doesn't seem to ask is: Was the child

a

> sick child (go to NYTimes, see his picture) who for various

reasons akin

> to spontaneous remission got well, and, as this occurred, was

having ABA

> therapy?

>

> For some parents, a non-responder to biomed evals and treatments

faces a

> dilemma - expand the array of lab data? Bail out? There's no eary

> answer here. Each parent must choose. I recommend the DeMyer book

for

> parents and physicians wanting an eye-opening glimpse of autism

circa

> 1979, when (even then) some sick kids who qualified for an autism

dx

> recovered.

>

> Today, 53 copies were available vir http://www.Bookfinder.com,

many

> quite reasonably priced.

>

>

>

> 1: J Pediatr. 1999 May;134(5):607-13.

>

> Serum autoantibodies to brain in Landau-Kleffner variant, autism,

and other

> neurologic disorders.

>

> Connolly AM, Chez MG, Pestronk A, Arnold ST, Mehta S, Deuel RK.

>

> Departments of Neurology and Pediatrics, Washington University,

St. Louis

> Children's Hospital, St Louis, Missouri, USA.

>

> OBJECTIVE: Etiologically unexplained disorders of language and

social

> development have often been reported to improve in patients

treated with

> immune-modulating regimens. Here we determined the frequency of

autoantibodies

> to brain among such children. DESIGN: We collected sera from a

cohort of

> children with (1) pure Landau-Kleffner syndrome (n = 2), (2)

Landau-Kleffner

> syndrome variant (LKSV, n = 11), and (3) autistic spectrum

disorder (ASD, n =

> 11). None had received immune-modulating treatment before the

serum sample was

> obtained. Control sera (n = 71) were from 29 healthy children, 22

with

> non-neurologic illnesses (NNIs), and 20 children with other

neurologic disorders

> (ONDs). We identified brain autoantibodies by immunostaining of

human temporal

> cortex and antinuclear autoantibodies using commercially available

kits.

> RESULTS: IgG anti-brain autoantibodies were present in 45% of sera

from children

> with LKSV, 27% with ASD, and 10% with ONDs compared with 2% from

healthy

> children and control children with NNIs. IgM autoantibodies were

present in 36%

> of sera from children with ASD, 9% with LKSV, and 15% with ONDs

compared with 0%

> of control sera. Labeling studies identified one antigenic target

to be

> endothelial cells. Antinuclear antibodies with titers >/=1:80 were

more common

> in children with ASD and control children with ONDs. CONCLUSION:

Children with

> LKSV and ASD have a greater frequency of serum antibodies to brain

endothelial

> cells and to nuclei than children with NNIs or healthy children.

The presence of

> these antibodies raises the possibility that autoimmunity plays a

role in the

> pathogenesis of language and social developmental abnormalities in

a subset of

> children with these disorders.

>

> PMID: 10228297 [PubMed - indexed for MEDLINE]

>

>

> 2: Med Hypotheses. 2001 Apr;56(4):523-31.

>

> Intra-monocyte pathogens delineate autism subgroups.

>

> Binstock T.

>

>

> Immune panels of many autism-spectrum children reveal signs of

atypical

> infections and shifted cell counts. In conjunction with trait-

related cerebral

> hypometabolism and hypoperfusion, these findings suggest a

hypothesis: Several

> autism-spectrum subgroups derive from intra-monocyte pathogens

such as measles

> virus, cytomegalovirus, human herpesvirus 6, and Yersinia

enterocolitica.

> Furthermore, with much inter-child variation, their effects

manifest as

> diminished hematopoiesis, impaired peripheral immunity, and

altered blood-brain

> barrier function often accompanied by demyelination. In some such

children, one

> or more of these pathogens persists as a chronic-active, seemingly

subclinical

> infection etiologically significant to the child's autistic

traits. Within these

> subgroups, immune impairments and atypical infections may be

treatable.

> Copyright 2001 Harcourt Publishers Ltd.

>

> PMID: 11339860 [PubMed - indexed for MEDLINE]

>

>

> 3. n K. DeMyer. Parents and children in autism.

>

> 4: Biotherapy. 1996;9(1-3):143-7.

>

> Dialysable lymphocyte extract (DLyE) in infantile onset autism: a

pilot study.

>

> Fudenberg HH.

>

> Neurolmmuno Therapeutics Research Foundation Spartanburg, S.C.,

USA.

>

> 40 infantile autistic patients were studied. They ranged from 6

years to 15

> years of age at entry. 22 were cases of classical infantile

autism; whereas 18

> lacked one or more clinical defects associated with infantile

autism

> ( " pseudo-autism " ). Of the 22 with classic autism, 21 responded to

transfer

> factor (TF) treatment by gaining at least 2 points in symptoms

severity score

> average (SSSA); and 10 became normal in that they were main-

streamed in school

> and clinical characteristics were fully normalized. Of the 18

remaining, 4

> responded to TF, some to other therapies. After cessation of TF

therapy, 5 in

> the autistic group and 3 of the pseudo-autistic group regressed,

but they did

> not drop as low as baseline levels.

>

> Publication Types:

> Clinical Trial

>

> PMID: 8993773 [PubMed - indexed for MEDLINE]

>

>

> >

> >

> >

> >

> >

> > {Words like Chelation, Autism Research Institute, and

supplements do

> > not appear in this article. The NYT's one-sided, propagandistic

> > approach to pseudo-journalism continues. -}

> >

> > Slow-Motion Miracle: One Boy's Journey Out of Autism's Grasp

> > By JOHN O'NEIL

> > http://www.nytimes.com/2004/12/29/education/29autism.html

>

>

>

>