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Sunday 30 August 2015

Treatable Chiari 1 “brain hernia” present in 7% of Autism












Today’s post is again prompted by a reader’s comment.

Regular readers will be accustomed to learning here about “rare”, often treatable, disorders that may cause, or just aggravate autism; add Chiari 1 to that list.
  
The Chiari 1 brain hernia occurs when part of the brain is forced downwards into the spinal column.  It is supposedly very rare, occurring in only one person per thousand.  It is generally not life-threatening and can be surgically repaired.  The symptoms of Chiari 1 do rather overlap with those of autism.

You can diagnose Chiari 1 using an MRI scan.  Very few people with autism ever receive any diagnostic follow up, be it genetic testing, metabolic testing or a scan of their brain.

There have been anecdotal reports associating Chiari with autism, and indeed of the corrective surgery greatly improving autism symptoms.  This goes back to the day of Bernie Rimland (Autism Research Institute and DAN).


Finally we have some genuine data:-




Abstract
OBJECT:
Patients with symptomatic Chiari malformation Type I (CM-I) frequently present with headaches, neck pain, difficulty swallowing, and balance disturbances. In children with autism spectrum disorder (ASD), diagnosing CM-I can be a challenging task. Moreover, even if symptomatic, some patients do not undergo further evaluation or management, as their presentations are attributed to autism and its myriad symptoms. Therefore, cranial MRI findings were reviewed after evaluating and treating patients with coexisting ASD and CM-I. In this paper, the authors report on 5 children with ASD and symptomatic CM-I, including their clinical presentation, imaging studies, management, and outcomes, and discuss the likely under recognized coexistence of these conditions.
METHODS:
All pediatric patients with ASD and cranial MRI conducted for any reason in the period from 1999 to 2013 were considered for analysis. All cases with concomitant symptomatic CM-I were eligible for this retrospective analysis.
RESULTS:
One hundred twenty-five pediatric patients diagnosed with ASD had undergone MRI, and 9 of them had evidence of cerebellar tonsillar herniation. Five patients were symptomatic and underwent suboccipital craniectomy, a C-1 or a C-1 and C-2 laminectomy, and duraplasty with bovine pericardium or Type I collagen allograft. There were no intraoperative complications. All patients showed symptom improvement and/or resolution of presenting symptoms, which included headache, dysphasia, speech, and irritability.
CONCLUSIONS:
There is no identified cause of autism. Children with ASD can be difficult to assess specifically in a neurological examination. Thus, cranial MRI considered when completing a comprehensive diagnostic evaluation. While cranial MRI is not a routine part of ASD evaluation, this study demonstrates that CM-I and ASD may coexist and be underrecognized. The study reinforces the importance of a comprehensive medical evaluation designed to elucidate neurological findings in children with impaired communication abilities and suggests the judicious use of neuroimaging.
KEYWORDS:
ASD = autism spectrum disorder; CM-I = Chiari malformation Type I; Chiari malformation I; autism; autism spectrum disorder; suboccipital craniectomy



Conjecture

We know that in many cases of classic autism there is accelerated brain growth until the age of five (Courchesne, UC San Diego) and frequently this is associated with large heads (Macrocephaly).

As usual in autism, both extremes exist and so Microcephaly (small brains/heads) is also present.  The result is that in studies the average head size is meaningless.  Just as with many other possible markers, like cholesterol levels.  The same is true with signaling pathways like mTOR, Wnt, ERK and BDNF; both hypo function and hyper function exist and both can lead to “autism”.
   


Data from a series of 126 autistic children ages 2-16 years and referred to an Autism Diagnosis Unit in South-West France were examined. Macrocephaly (head circumference > 97th centile) was observed in 16.7% of the sample, a significantly higher proportion than that expected. Macrocephaly was more frequent among older subjects but was otherwise not associated with gender, developmental level, the presence of epilepsy or of medical disorders, or severity of autistic symptomatology. Microcephaly (head circumference < 3rd centile) was also significantly raised and found in 15.1% of the sample. Microcephaly was significantly associated with the presence of medical disorders. Results support those from recent studies suggesting a raised rate of macrocephaly in autism which, pooling published data, can be estimated to be 20%. It is argued that the raised incidence of microcephaly among low-functioning autistic subjects with medical disorders might have contributed to delay the recognition of an increased head circumference among a minority of subjects with idiopathic autism.


It is not hard to imagine what might happen if the brain is expanding faster than the skull is growing.  It would be reasonable to think that, in some cases, autism might cause Chiari malformation I.

Most people consider Chiari malformation I to be genetic.  In people with no underlying cause(s) of autism, the hernia itself may be the sole cause of the associated symptoms.

Since we know that autism is often caused by multiple “hits”, in some people the Chiari malformation might just be one of those handful of hits/triggers.  Oxidative stress and inflammation are both key drivers and consequences of autism; clearly hernia(s) growing in the spinal column are going to aggravate this.


To Treat or Not?

Surprisingly, some neurologists/neurosurgeons are unwilling to repair Chiari malformation I in children with autism.

If you recall my recent post on the history of autism, the reason becomes clearer.

Those neurologists/neurosurgeon hold the historical view that autism is untreatable and so how could surgery possible help?  It seems that in as many as 7% of autism cases, surgery might indeed help.  That is a surprise to me.

Fortunately, enough people with autism and Chiari 1 have been treated for it to be known that it does improve autism.

Since treatment involved a brain operation, it is not without risks.  Not treating the brain hernia likely also has risks.


Dr. Manuel Casanova on Chiari and Autism

Dr Casanova is a neurologist with a blog and an interest in autism. He is of the opinion that Chiari does not cause autism, but just makes it worse.

I am not a neurologist, but if you accept that autism, like cancer, is often caused by multiple hits, Chiari would seem like quite a dangerous hit, and perhaps more so than an immune over-reaction to childhood vaccines. In my recent autism history post we saw that for Hannah Poling the vaccine was enough to cause profound autism; she had two hits the first being a genetic mitochondrial dysfunction and the second an inflammatory reaction to the vaccines.

Over to Dr Casanova:-



"If you ever do a search through the internet you will find a lot of interest among multiple health boards on the possible correlation between the Chiari malformation and autism. Dr. Neil Felstein, Director of the Pediatric Neurosurgery Division of the Morgan Stanley Children’s Hospital, has seen many children with both conditions (http://abclocal.go.com/wabc/story?section=news/health&id=5251975 ). He believes that there is an association but can’t provide an explanation. Although a Chiari malformation is certainly not the cause of autism, it can aggravate the same. It may be worth noting that the Chiari malformation is seen as a comorbidity to both the Ehlers-Danlos and Marfan syndromes (Milhorat et al., 2007).  Both of these conditions manifest autistic symptomatology in a high percentage of cases (http://bit.ly/167eZuR )."



Head Circumference

Since data on head circumference is routinely collected during childhood, it would not be difficult to go back to the 125 cases studied by MRI in the research study, quoted at the start of this post.  You could then look for a correlations between head size, brain size and the Chiari hernia.

This might show that in autism the head was just not big enough at some critical point in time.



More links






Conclusion

It looks like you might want to add an MRI to those metabolic and genetic tests that most children with autism never receive, but perhaps should.

Or, as put in today’s study:-

“The study reinforces the importance of a comprehensive medical evaluation designed to elucidate neurological findings in children with impaired communication abilities and suggests the judicious use of neuroimaging.”








Thursday 27 August 2015

Cinnamon (Cinnamaldehyde), Mast Cells (Allergy) & Autism










A reader of the previous post on cinnamon left a helpful comment highlighting research that suggests yet another reason why Cinnamon might be an effective treatment for some types of autism.






Abstract
BACKGROUND:
Mast cells (MC) are main effector cells of allergic and other inflammatory reactions; however, only a few anti-MC agents are available for therapy. It has been reported that cinnamon extract (CE) attenuates allergic symptoms by affecting immune cells; however, its influence on MC was not studied so far. Here, we analyzed the effects of CE on human and rodent MC in vitro and in vivo.
METHODS:
Expression of MC-specific proteases was examined in vivo in duodenum of mice following oral administration of CE. Release of mediators and phosphorylation of signaling molecules were analyzed in vitro in human MC isolated from intestinal tissue (hiMC) or RBL-2H3 cells challenged with CE prior to stimulation by FcεRI cross-linking.
RESULTS:
Following oral treatment with CE, expression of the mast cell proteases MCP6 and MC-CPA was significantly decreased in mice. In hiMC, CE also caused a reduced expression of tryptase. Moreover, in hiMC stimulated by IgE cross-linking, the release of β-hexosaminidase was reduced to about 20% by CE. The de novo synthesis of cysteinyl leukotrienes, TNFα, CXCL8, CCL2, CCL3, and CCL4, was almost completely inhibited by CE. The attenuation of mast cell mediators by CE seems to be related to particular signaling pathways, because we found that activation of the MAP kinases ERK, JNK, and p38 as well as of Akt was strongly reduced by CE.
CONCLUSION:
CE decreases expression of mast cell-specific mediators in vitro and in vivo and thus is a new plant-originated candidate for anti-allergic therapy


In a later study by the same authors they identify Cinnamaldehyde as the main mediator of cinnamon extract in mast cell inhibition.



A chemistry note:

Cinnamon contains three major compounds (cinnamaldehyde, cinnamyl acetate and cinnamyl alcohol), which are converted into cinnamic acid by oxidation and hydrolysis, respectively. In the liver, this cinnamic acid is β-oxidized to benzoate that exists as sodium salt (sodium benzoate; NaB) or benzoyl-CoA.

As is often the case with natural substances with medicinal properties, it is unclear which constituent provides the benefit, or whether there is a synergistic benefit between them.

As I suggested in an earlier post, even though Sodium benzoate (NaB) has been shown to be the reason for some of cinnamon’s benefits and is widely available, I propose to use cinnamon itself.

The mast cell benefits of cinnamon come from cinnamaldehyde and may not be produced by the metabolite NaB.
  



Purpose

In terms of their involvement in allergic and inflammatory conditions, mast cells (MC) can be promising targets for medical agents in therapy. Because of their good compliance and effectiveness, phytochemicals are of great interest as new therapeutic tools in form of nutraceuticals. We found recently that cinnamon extract (CE) inhibits mast cell activation. Here, we analysed the effects of a major compound of CE, cinnamaldehyde (CA), on mast cell activation. 

Conclusions

CA decreases release and expression of pro-inflammatory mast cell mediators. This inhibitory action is similar to the effects observed for CE indicating CA as the main active compound in CE leading to its anti-allergic properties.



Conclusion

Today’s post gives a particular reason for people with autism, allergies and mast cell issues to trial cinnamon.

The only thing to be careful of is histamine intolerance.  This does affect several readers of this blog.

The main cause of histamine intolerance is an impaired histamine degradation caused by genetic or acquired impairment of the enzymatic function of DAO or HNMT.

One reader pointed out that the cheap 23andme genetic test includes the genes for histamine intolerance (this service is no longer available in all countries).

The sodium benzoate (NaB) produced by cinnamon is a DAO inhibitor and so will further impair histamine degradation in people with genetic impairment.  

In most people, even if they have allergies, a teaspoon of cinnamon will not affect their ability to degrade histamine.











Tuesday 25 August 2015

Vienna and some selected Autism History


  
Monty aged 12 with ASD, “You have been transformed into an Australopithecus afarensis, you walked upright more than 3 million years ago. Your picture is attached. This morphing-station is a co-production between Naturhistorisches Museum Vienna, Austria and the Smithsonian Natural History Museum in Washington”


We can never know if they had autism 3 million years ago, but it certainly is not a recent phenomenon.  Today’s post, prompted by a visit to Vienna, is a collection of historical episodes that I thought I should include in this blog, before I forget them.

Austria, as well as being home to an excellent natural history museum, where you can see what your children might have looked like had they been born 3 million years ago, is the home of autism. 

Both Hans Asperger and Leo Kanner were Austrian.  Kanner was later educated in Berlin and then, being Jewish, had the foresight to emigrate in 1924 to the US. In 1930 he developed the first child psychiatry service in an American pediatric hospital at Johns Hopkins Hospital.  He published his research on autism in 1943.  His narrowly defined type of autism became known as Kanner’s autism or classic autism; however if you read his actual case histories below you will see that they include quite high functioning people as well


                   
Kanner clearly made a valuable contribution, but he also had some odd ideas, like autism is just a childhood condition, so adults cannot have autism and that autism is extremely rare.  He thought that if a patient had epilepsy they could not be autistic. He also famously suggested that autism was caused by refrigerator mothers.

But unlike all the doctors who preceded him, at least he wrote down his findings and sought out public attention.

Hans Asperger, presumably not Jewish, eventually became chair of pediatrics at the University of Vienna.  In 1943 he published, in German, his paper on autism that focused on gifted children and what would become known as Asperger’s syndrome. 


The paper was finally rediscovered in 1991 and translated into English by Uta Frith.  Thereafter in the English speaking world, people could finally be diagnosed with Asperger’s Syndrome.  Personally I think it is a very useful/clear diagnosis: - no speech delay, no cognitive dysfunction, just the trademark differences of mild autism.

It later became known that while he may have published research on very high functioning people, he also had many patients who were low functioning.  The reason Asperger highlighted the gifted children was that during World War 2, the Nazis had a program called Aktion T4, which was set up to kill people with disabilities (unable to work).  People with Down syndrome, epilepsy, mental retardation etc. were removed from their residential institutions or homes and given a lethal injection or just carbon monoxide poisoning.  The family later received a letter that the child had sadly died of pneumonia.

At Schloss Hartheim, near Linz, two hours west on Vienna, about 30,000 people were killed, including those selected under Aktion T4.

So not surprisingly, Asperger did not write about those with autism without special gifts and talents.





Schloss Hartheim


Great Ormond Street Hospital, London 1877

Twenty years even before Johns Hopkins Hospital had been founded in Baltimore, children with epilepsy, “autism” and GI problems were being treated in London at Great Ormond Street Hospital, today of Europe's top children's hospitals.

They were using a very early drug to shift the excitatory/inhibitory balance of the neurotransmitter GABA.  It was Potassium Bromide, which is still used today in Germany to treat children with epilepsy.  Of course back in 1877 they did not know why it was effective.  Below is a link to a fascinating chapter of a book.




In 2015 this same hospital would tell you that autism is untreatable and that GI problems are not comorbid with autism.

At some point I will be writing a post all about Potassium Bromide and autism.


More History

For those of you who despair sometimes about the low level of knowledge and understanding regarding autism among healthcare providers and even supposed “experts”, I suggest you look back at the history.

As is often the case, history holds many of the answers.

Until relatively recently most children with disorders like Downs Syndrome or classic autism were sent from a very young age to live in so called “homes for the feeble minded”.  In recent times this occurs far less common and nobody uses terms like feeble-minded, but nonetheless difficult to control children are still put “into care”.

It really was a case of out sight being out of mind.

As we saw in the data on Down syndrome in the US, life expectancy was extremely short in these massive institutions where the kids lived in dormitories.  The average being only 10 years as recently as 1970.

As in Austria and Germany, in the US being sent to a home for the feeble minded was very often a death sentence, albeit a slower one.  The Germans even went as far as to financially justify their actions by quoting the cost of keeping a child in an institution for 10 years (the same life expectancy of Down's kids in the US, just 50 years ago).

Given this backdrop, not surprisingly everybody kept quiet about autism, almost nobody was interested in treating it and nobody would dream of using the word autism, for someone who was fully verbal and not mentally retarded.

So it is hardly surprising that there are/were very few older people with autism, or indeed Downs Syndrome.


Homes for the Feeble-Minded

There were numerous Homes for the Feeble-Minded in the US and across the world.  Here are some examples.





Maine School for the Feeble-Minded



Throughout its first 40 years, Belchertown operated mostly without scrutiny from outside sources. Author Benjamin Ricci (whose son lived at the school, and who later led a class-action lawsuit protesting the conditions there) referred to the conditions as "horrific", "medieval and "barbaric". Doctors at the school had little regard for patients' mental capacity, evidenced by this quote:

His method of evaluating me consisted of looking me over during the physical exam and deciding that since I couldn't talk and apparently couldn't understand what he was saying, I must be an imbecile. [...] Since I couldn't ask him to speak up or repeat what he said, he assumed I was a moron

The horrendous conditions at Belchertown were revealed in 1971 in a newspaper article entitled "The Tragedy of Belchertown". Parents sued the school, and when the state Attorney General toured the facility, he described it as "a hell hole".



In Michigan they even gave a special mention to those with epilepsy:

Michigan Home for the Feeble Minded and Epileptic



Why feeble minded?

Going back 110 years in the United Kingdom, you can see where terms like feeble minded came from:


They disallow the name of “Lunatic” and “Asylum” and classify the mentally defective as follows:-
·          Persons of unsound mind (who require care and control).
·          Persons mentally infirm (who are incapable of managing their own affairs)
·          Idiots. Defective in mind from birth.
·          Imbeciles. (Capable of guarding themselves against common physical dangers, but incapable of earning their own living).
·          Feeble-Minded. (Persons who may be capable of earning their own living under favourable conditions, but are incapable of competing with others or managing themselves).
·          Moral Imbeciles. (Persons who display some Mental Defect with vicious or criminal propensities on which punishment is no deterrent).
·          Epileptics.
·          Inebriates.  All of these three are considered Mentally Defective.
·          Deaf, Dumb and Blind.


Almost all such people were, in effect, locked up. In the UK at that time there were 149,628 such people deemed to be mentally defective.  That is 0.4% of the population at that time.




Modern Times

In rich western countries large “out of sight out of mind” institutions are a thing of the past.  They still exist in some other countries.

Now that at least some children with disabilities are educated in the community, or at least live at home many things began to change.  

The incentive to hide your disability was replaced by an incentive to promote it.  For each child with a diagnosis extra money is allocated to the school district (in the US) and in many countries families are entitled to weekly or monthly benefits payments.

Changes to diagnosis began to be made such that children with MR/ID were now diagnosed as having autism, boosting prevalence.

Then from the 1990s onwards came the boom in diagnosing Asperger’s in children and then later diagnosing Asperger’s in quite old adults.  

Finally, just to confuse everyone, in the US at least, Asperger’s has been merged into autism.

Once a rare condition, autism has become anything but; all over the period of 20 years. But it is not the same autism.

Even though the science is clearly indicating that within autism are numerous separate biological disorders and as many as 1,000 genes are involved, the US psychiatrists, with DSM5, have decided that it is all just “autism” and you are ranked on a scale of 1 to 3 for severity. I would have thought 1 to 300 might have been more reasonable.

The key discriminating factors like regressive or not, MR/ID or not, epilepsy or not, speech delay or not are not seen a relevant.

As a result the modern diagnosis of “autism” then just begs the question “what sort?”

Better to forget about “autism awareness”; much better to explain what autism really is and how certain types can be treated today based on existing hard science.



Dr Wakefield

Until Dr Wakefield published his paper in 1998, few people were familiar with autism, because nobody spoke about it.  Talk of the MMR vaccine and autism created fear among parents.

In the end Wakefield did a great deal of harm, even though much of what he said was actually true.  There is an unwritten rule that must not be challenged, “vaccines do no harm”.

As Martha Herbert pointed out, everything regarded as “Wakefield” became taboo, and research in those areas became un-fundable.  The link to GI problems is one area she highlighted and is still disputed by many, but not Boston Children’s Hospital, supposedly the number one Pediatric hospital in the world.   


Hannah Poling

As was shown in the legal case brought by US neurologist Dr Jon Poling, regarding his daughter Hannah, children with mitochondrial dysfunction can suffer an inflammatory response to multiple vaccines that can trigger mitochondrial damage leading to profound autism.  This doctor meticulously documented his case and was awarded compensation of $1.5 million plus $500,000 a year thereafter. 

It turns out that in the last 25 years the US government has paid out $3 billion dollars in compensation for childhood vaccinations (see table below).

It was expected that this case would act as a precedent to later cases, opening the flood gates so to speak.  It did not.

In this case Dr Poling was much more effective that Wakefield.  He made his point and kept his medical license.

But the public health interest in vaccination programs is immense.  Hundreds of millions of lives have been saved by vaccines and nothing is going to be let to get in the way of that.  Vaccines are effective once a critical mass of people have taken them, (Herd Immunity).  So in theory it would be fine for certain groups not to be vaccinated, like those with genetic mitochondrial dysfunctions.

As Dr Poling pointed out, quite a large minority of people with autism do have mitochondrial disorders; even Dr Kelley from Johns Hopkins has referred to this.
 




Herd Immunity

When a critical proportion of the population becomes immune, called the herd immunity threshold (HIT) or herd immunity level (HIL), the disease may no longer persist in the population





It should be noted that in about 2% of people vaccination may fail to provide immunity.   In the case of influenza you have to know which type of virus to protect against.


  
Here is Dr Poling’s response to the highly sceptical Dr Steven Novella, an American clinical neurologist and assistant professor at Yale University School of Medicine and a blogger. Novella is best known for his involvement in the skeptical movement. He had written about the Hannah Poling case on his blog.


Dear Dr. Novella,

Your assertion that the scientific question of Autism etiology belongs to the medical community rather than Hollywood Stars is correct.  I also agree that Hollywood opinions are more likely to be broadcast to millions because of their position in the media.  This heightened awareness is nothing but a positive thing for the million families struggling with this difficult, and all too common, disorder.  Jenny McCarthy is an Autism Mom looking for answers and rattling some cages—good for her.  Amanda Peet is a new mom who believes in the importance of vaccines to protect her baby—good for her too.  Don’t attack the moms, listen to them.   

These issues are very complex as we exchanged before and not amenable to soundbites.  Regarding your entry on Hannah’s case, your blog entry unfortunately propagates several of the mistakes from the media.

In criticizing the journalism of Mr. David Kirby, you wrote:

“He refers again to the Hannah Poling case, a girl with a mitochondrial disorder who developed a neurodegenerative disorder with “features of autism” after getting a fever from vaccines.”

Actually—Hannah has diagnoses of DSM-IV Autism (by JHU/KKI psychology) and mitochondrial disorder (by two metabolic experts).  The only ‘degeneration’ that occurred (along with 6mos of total growth failure) after 18mos of NORMAL development followed vaccination and nothing else! Of course, any ‘scientist’ can obviously point out that temporal correlation in a single case never proves causation. Rule number one of pediatrics though is “LISTEN TO THE MOM.”  Are 10s of thousands of autism moms over the last decade suffering from mass hysteria induced by Hollywood?  Not likely.

You also noted:

“This special case - which is not a case of autism being caused by toxins in vaccines - says nothing about the broader vaccine-autism debate.”

The only thing unique about my little girl’s case is the level of medical documentation—5 to 20% of patients with ASDs have mitochondrial dysfunction.  Many other cases where mitochondrial testing is WNL is because "we never looked" not because the testing would be "within normal limits."  Most mitochondrial experts will tell you that the dots of autism and mitochondrial disorders are strongly connected.
Finally, you say:

“The case was settled (not judged in Poling’s favor, but settled) because both sides realized it was a special case that could not be extrapolated to other vaccine-autism cases.”

The case was not settled, it was conceded by medical representatives of Sec HHS.  We are obviously pleased with the HHS decision to concede our case, but we had NOTHING to do with the concession.  This was a unilateral decision from HHS (recall that HHS is the respondent, rather than the vaccine maker, as manufacturers have blanket liability protection afforded by the Vaccine Injury Program established in 1986)  I will not speculate on the obvious question—why concede?   Hannah’s case was positioned to set precedent as a test case in the Omnibus Autism Proceedings for potentially thousands of other cases.
With regard to the science of Autism, I have no argument with the assertion that a single case does not prove causation of a generalized autism-vaccine link.  What the case does illustrate though is a more subtle point that many physicians cannot or do not want to comprehend (ostensibly because vaccines are too important to even question).  Autism is a heterogeneous disorder defined by behavioral criteria and having multiple causes.  Epidemiological studies which have not found a link between autism and aspects of vaccination do not consider the concept of autism subgroups.  Indeed, in a heterogeneous disorder like Autism, subgroups may indeed be ‘vaccine-injured’ but the effect is diluted out in the larger population (improperly powered study due to inability to calculate effect size with unknown susceptible subpopulation).   I think former NIH Director, Dr. Bernadine Healey explained it best in that population epidemiology studies are not “granular” enough to rule-out a susceptible subgroup. 

Furthermore, ‘science’ has not systematically studied the children who fell ill following vaccination to determine what the cause(s) for their adverse reaction was.  It would follow that if you never tried to understand why a single child developed encephalopathy following vaccination—you wouldn’t have the first clue as to what aspects of vaccination you could alter which could increase the relative risk of that adverse event (whether it be thimerosal, live virus, or ‘too many’). Could the susceptibility be a mitochondrial genetic haplogroup similar to Chloramphenicol toxicity—sure it could!  Why did a few Alzheimer’s patients die of fatal encephalitis following administration of the failed AN-1792 vaccine, but the majority had no ill effects (vaccine didn’t work though)? 

Definition:  Autism is a heterogeneous systemic disorder with primary neuropsychiatric manifestations due to complex genetic and gene-environmental interactions likely affecting synaptic plasticity early in childhood development.  This new theory of Autism is rapidly replacing the ‘old guard’ dictum that Autism is a genetically predetermined developmental brain disorder of synaptic formation/pruning that is set in motion prenatally.  By the ‘10 year rule of science,’ your time is about up! 

Until the biological basis of ASD subgroups are better understood, further epidemiological and genetic studies regarding “Autism” causation will be relatively meaningless.  We need good science to be able to address these complex issues which parallel nicely the emerging story of genetic and environmental influences in Parkinson’s disease.  Perhaps some Parkinson’s researchers want to take a crack at Autism?
Recommended SCIENCE reading for the evening:
 
Altered calcium homeostasis in autism-spectrum disorders: evidence from biochemical and genetic studies of the mitochondrial aspartate/glutamate carrier AGC1. Mol Psychiatry 2008 Jul 8.  (The discussion includes thimerosal as a potential toxin that could trigger further perturbations of calcium homeostasis leading to neuronal injury—and in a mainstream Nature publication no less)

Thank-you Dr. Novella and his band of skeptics for continuing the debate.

Dr. Jon Poling
Jon S. Poling MD PhD
Managing Partner, Athens Neurological Associates
Clinical Assistant Professor, Department of Neurology, Medical College of Georgia
Diplomate, American Association of Neuromuscular and Electrodiagnostic Medicine
ASN Certified in MRI and CT Neuroimaging
                               


In the US there is $0.75 levy on childhood vaccines to fund a compensation scheme.









By the 1980/90s almost all of the huge institutions for “feeble minded” children had been closed in the US and other Western countries.  The understanding of autism among medical practitioners did not really change.  Finally Asperger’s old papers were translated from German into English and in the 1990s large numbers of children started to get diagnosed with Asperger’s syndrome.  The stigma of such a diagnosis was no longer as it would have been a few decades before.




Conclusion

It is rather odd that many people’s points of reference regarding autism still date back to those two Austrians, Kanner and Asperger, from 1943.

Neuroscience has moved on a fair way since world war two, but in many ways autism has not.  In some ways it is now going backwards.

The main change is the surge of interest in Asperger’s, which is now, unhelpfully, being referred to simply as autism.  This does a great disservice to those with what used to be known as autism.  They generally cannot speak up for themselves and really do need customized medical treatment.

People with Asperger’s are more than capable enough to decide for themselves whether they want/need to treat their condition.

Fortunately researchers probably pay little attention to what is (mis)reported in the mass media regarding autism and the so those research papers will keep coming.

Drug firms have been struggling for decades to come up with new treatments for neurological disorders.  Apparently the disease likely to be first “overcome” is Parkinson’s.  Dr Poling did suggest in his commentary above that autism might benefit from some Parkinson’s researchers; maybe there will be some surplus ones sometime soon.

It is clear that no serious investigation of the type suggested by Dr Poling into the effect of vaccines on specific sub-types of autism will happen.  The link with mitochondrial disease and its treatment remains almost hushed up, even though the clinicians involved are at leading institutions (Johns Hopkins, Harvard etc.).  As one reader commented to me, “why is Dr Kelley’s work on mitochondrial disease and autism not published in the literature?”.

In reality, I expect that only a tiny percentage of autism can be traced back to vaccines, so there should be nothing for public health authorities to be fearful about.  Even Dr Poling remains pro-vaccines.

I am still shocked that in the US over $3 billion has already been paid out in compensation for damage caused by childhood vaccines.