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Showing posts with label cognitive enhancement. Show all posts
Showing posts with label cognitive enhancement. Show all posts

Friday 4 March 2016

Cognitive Impairment in Schizophrenia, Bipolar & Autism


Neurological/neuropsychiatric disorders are often poorly described and poorly treated, but adult-onset conditions have historically been taken much more seriously and so the research is more advanced .  I find myself quite often looking at research on schizophrenia and bipolar; many of the same genes and metabolic dysfunctions common in autism show up in those conditions.

Many people really dislike the term Mental Retardation (MR), which is actually a very accurate descriptive term, meaning that someone is cognitively behind their peers.  Most lay people have no idea what Intellectual Disability (ID) means.

It is interesting that about 90% of people with schizophrenia and 50% of people with bipolar are cognitively behind their peers.  I suspect the figure for autism would also be about 90%, if someone measured it.  Most people with Asperger’s are not top of the class.

Only in extreme cases of being cognitively behind their peers, when their IQ is less than 70, does a person get diagnosed with MR/ID.

So the clinical diagnosis of MR/ID is just an arbitrary cut-off point.  The idea that if IQ is greater than 70 there is no cognitive deficit is entirely flawed.

It seems than in autism, as in schizophrenia and bipolar we should assume that cognitive dysfunction is present; the only question is how much and what to do about it.

Having treated the cognitive dysfunction(s), the person is then in a better place to compensate for the other dysfunctions they might have.

Even though the psychiatrists and psychologists will tell you that autism is all about the triad of impairments, I think they are missing the most important element, which is cognitive dysfunction.




As people with autism age, many find their symptoms associated with the above “triad of impairments” mellow.  The substantial minority who experience untreated flare-ups driven by inflammation caused by things like allergy, GI problems and even juvenile arthritis may not be so lucky.

I imagine that cognitive function in adulthood remains at the level it reached as a teenager.



Cognitive Function as the Therapeutic Target

Since many children with autism do eventually overcome many of their challenges in childhood, perhaps cognitive function really should be given a higher priority in treatment and research.

Many caregivers and educators are mainly focused on minimizing bad/disruptive behaviors (and bruises) rather than the emergence of good behaviors and learning.  This is sad but true.

As the child matures, in many cases these bad/disruptive behaviors may fade without any clever interventions.

So an intervention that stops stereotypy in a toddler, which was blocking learning, may have very much less impact in an adolescent.  Or at least the impact may be much less obvious.

I remember reading about a parent with two children with Fragile-X who was very upset when the Arbaclofen trials were halted, since her kids had responded well.  But two years later in another article it was clear that things were going fine without Arbaclofen.  The son whose violence towards his mother had been controlled by Arbaclofen, was no longer aggressive.  He continued to suffer cognitively, being a male with Fragile-X, the sister was much less affected  (females with fragile X syndrome have two X chromosomes and only one of the chromosomes usually have an abnormal gene, so usually females are less affected).   

The advantage of using cognitive function as a target is that it is much easier to measure than subjective behavioral deficits.  For the majority of people it is likely to be the most important factor in their future success and well-being.

In the substantial minority of cases where there are seizures and/or factors causing autism flare-ups, the behavioral deficits may remain undiminished into adulthood.  These people would also benefit from maximized cognitive function.



Cognitive Deficit in Schizophrenia & Bipolar (BPD)


To most lay people schizophrenia is characterized by abnormal social behavior and failure to recognize what is real. Common symptoms include false beliefs, unclear or confused thinking, hearing voices, reduced social engagement and emotional expression, and a lack of motivation. People often have additional mental health problems such as major depression, anxiety disorders, or substance use disorder. Symptoms typically come on gradually, begin in early adulthood, and last a long time.


Cognitive impairments and psychopathological parameters in patients of the schizophrenic spectrum.

  

Abstract

Cognitive impairment is a core feature of schizophrenia and it is considered by many researchers as one of the dimensional components of the disorder. Cognitive dysfunction occurs in 85% of schizophrenic patients and it is negatively associated with the outcome of the disorder, the psychosocial functioning of the patients, and non-compliance with treatment. Many different cognitive domains are impaired in schizophrenia, such as attention, memory, executive functions and speech. Nowadays, it is argued that apart from clinical heterogeneity of schizophrenia, there is probable heterogeneity in the accompanying neurocognitive dysfunction. Recent studies for cognitive dysfunction in schizophrenia employ computerized assessment batteries of cognitive tests, designed to assess specific cognitive impairments. Computerized cognitive testing permits for more detailed data collection (e.g. precise timing scores of responses), eliminates researcher's measurement errors and bias, assists the manipulation of data collected, and improves reliability of measurements through standardized data collection methods. The aims of the present study are: the comparison of cognitive performance of our sample of patients and that of healthy controls, on different specific cognitive tests, and the testing for possible association between patients' psychopathological symptoms and specific cognitive impairments, using the Cogtest computerized cognitive assessment battery. 71 male inpatients diagnosed with schizophrenia or other psychotic spectrum disorders (mean = 30.23 ± 7.71 years of age), admitted in a psychiatric unit of the First Department of Psychiatry, Athens University Medical School, Eginition Hospital (continuous admissions) were studied. Patients were excluded from the study if they suffered from severe neurological conditions, severe visual or hearing impairment, mental retardation, or if they abused alcohol or drugs.


Bipolar disorder, also known as bipolar affective disorder or manic depression, is a mental disorder characterized by periods of depression and periods of elevated mood. The elevated mood is significant and is known as mania or hypomania depending on the severity or whether symptoms of psychosis are present. During mania an individual feels or acts abnormally happy, energetic, or irritable. They often make poorly thought out decisions with little regard to the consequences. The need for sleep is usually reduced. During periods of depression there may be crying, poor eye contact with others, and a negative outlook on life


It also turns out that cognitive deficit is generally present in bipolar disorder (BPD).



  
“One area that Dr. Burdick is exploring is the frequency of neurocognitive impairment in BPD. Research shows that approximately 90 percent of schizophrenic patients suffer from cognitive deficits compared to only 40 to 60 percent of BPD patients. Understanding why certain patients develop significant cognitive difficulties while others do not is critical in optimizing patients’ quality of life, she says.”



Bipolar is probably not something you would connect with autism.  Being an observational diagnosis you would not tend to look at the biological underpinnings. The biological basis of both bipolar and schizophrenia are far better studied than autism and do significantly overlap with it.

In a recent post I looked at epigenetics and autism, when it comes to schizophrenia and bipolar the role of epigenetics is far more in the mainstream.

There is an approved epigenetic therapy (the HDAC inhibitor Valproate) for Bipolar mania and there is a clinical trial to improve cognitive function in schizophrenia using ather epigenetic therapy (the HDAC inhibitor Sodium Butyrate.)

Butyrate is also showed promise in a mouse model (D-AMPH) of Bipolar.


Epigenetic mechanisms in schizophrenia



Effects of sodium butyrate on oxidative stress and behavioral changes induced by administration of D-AMPH





Conclusion

I think people should be more open to discuss cognitive deficits and not hide behind politically correct terminology.

It seems that in both bipolar and schizophrenia cognitive deficits are recognized to be at the core of the disorder, even though 99% will not have an IQ<70 and so not be labelled with MR/ID.

Autism therapies which clearly improve cognitive function, like Bumetanide and low-dose Clonazepam, should be promoted as such.  Clinical trials should measure the cognitive improvement separately from autism measures.  As the person ages I think the benefit will often be more noticeable/measurable cognitively than behaviorally.












Tuesday 31 March 2015

Reassessing Cognitive Impairment in Autism – Improving the Prognosis




When Monty, now aged 11 with ASD, was diagnosed aged three and a half we were told that he had autism and “this may be indicative of the presence of an associated learning disability, but it is impossible at this stage to give a prognosis as to his future difficulties” and also “he is not yet able to take part in formal assessments of his cognitive ability. When his skills and ability to share interests with adults and to follow direction/instruction develop, it will be possible to formally assess his cognitive skills using standard measures.”

Off the record, we were also told that he might develop epilepsy.

We never measured his IQ and he has never had a seizure.

With hindsight, it is interesting what they said about it being pointless to try and measure his IQ.  Apparently it is not uncommon to do just that.


Improving Cognitive Function

This post is about cognitive improvement, so do not be put off by the introduction to MR/ID.  Several regular readers who are using some of the suggested drugs discussed in this blog are now also commenting on the resulting cognitive improvement, so it really is not just a case of N=1.

Nobody here is measuring the change in their child’s IQ, so these remain anecdotes.


To start on a happy note

Monty, aged 11 and diagnosed with classic autism, has been learning the piano for three years.  At the start he was not very cooperative with his teacher and after a few months the lessons stopped.  

27 months ago he started on bumetanide, the first part of his autism Polypill.  After years of ABA, slow but solid development appeared to have reached a plateau; but then he began to accelerate.  We restarted piano lessons again, with a new teacher.  Having added Atorvastatin, from the very next day he began to practice daily, playing without his teacher.  He has had two 40 minutes lessons most weeks since.  Two years later this is the result:-



 Click the image to play, turn up the volume (video may not work on Apples)

  
  
So there is no doubt that Monty got smarter.  When I heard him playing this piece, I thought it was the piano teacher, but she was recording Monty on her phone.

Big brother also did not believe little brother was playing this, until he saw the full video (with moving fingers).

Reading, writing, and numeracy have all improved and are now at a similar level to those of many of his NT classmates (who are 2 to 3 years younger than him).  Rather unexpectedly, he was recently the only one in class who understood how to multiply fractions; this was never taught at home.   

Prior to starting the Polypill drugs, I had spent three years, on and off, trying to teach Monty prepositions, without much progress.  This is almost always a difficult area for those with classic autism.  In the end he figured it all out by himself, with a little help from Bumetanide.

Recently yet another cognitive step forward seems to have have occurred, which appears to be the result of PAK 1 inhibiting propolis and/or the tangeretin flavonoid.  Monty's assistant in school was today proudly showing me his latest school test result, "73% and it was all his own work".  She thinks it is the tangeretin.

In earlier years school was for “socialization”, not learning.  This is fine as long as the learning takes place at home, otherwise inclusion means no education.



Cognitive Function, IQ, MR/ID

I prefer to talk about cognitive function, and its improvement or enhancement.  Drugs that achieve this are usually called Nootropic.

I think that many people remain skeptical about Nootropics.

Psychiatrists, Pediatricians and Psychologists prefer to think about IQ, MR/ID.

People affected do not like the old term of Mental Retardation (MR) and so quite recently, in English speaking countries, it was replaced by the term Intellectual Disability (ID).  The World Health Organization still use the old term, as does almost everybody else.

Somebody is diagnosed with MR or ID if their IQ is below 70.  In a typical group of 100 people, two people (2.2%) would be expected to fall into that category.  The average IQ (mean, median and mode) is 100.




In theory as you progress through childhood and into adulthood your IQ is expected to stay the same.  So the tests used adjust for your age.  There are special non-verbal tests.

If you acquire new skills at a lower rate than typical, your IQ would appear to fall over time.  This does not mean that you have lost skills just that you are acquiring new skills at a slower rate than your peers.  This explains why parents of kids with ASD, who do have their IQ tested, often find their score goes down as they get older.


Measuring IQ in Autism

I think it is generally a bad idea to measure IQ in people with autism.

There is anecdotal evidence to show that the results are often not valid, because the test is based on the assumption of compliance and that the child is actually doing his/her best.  Not surprisingly, the experts have found that children undergoing an ABA program improve their measured IQ by 10s.  After a few months of ABA the previously unfocused child has been trained to sit down, sit still, pay attention and work.  Of course they then get a higher score, but are they now more intelligent?

One reason put forward for not measuring IQ, is that while people will go a long way to help a child with autism to learn, once you add a diagnosis of MR/ID, some people will try much less hard.

Nonetheless people do measure IQ in autism and it is worth a quick look at what is known.

Some people are saying that 50% of people with autism have MR/ID.  I always found that odd, and what exactly do they mean by autism?

Using the previous US DSM definitions, Asperger’s was a part of the autistic spectrum but had the precondition that there was no MR/ID and no language delay.  Then you had the middle group with the odd name of PDD-NOS    (Pervasive Developmental Disorder Not Otherwise Specified).  This groups the people with more issues than Asperger’s, but without many of the problems experienced by those diagnosed with Autism.

So in the old US system there were 3 main categories, plus 2 minor ones:-

1.     Asperger’s
2.     PDD-NOS
3.     Autism
4.     Retts Syndrome
5.     Childhood Disintegrative Disorder (CDD)

Very few people have Retts or CDD.

The Autistic Spectrum was, in effect, also called PDD (Pervasive Developmental Disorder) just to confuse people a little more.  PDD = ASD = the above five conditions.

The latest version DSM5 went several steps backwards.  Everybody affected in the US is now just ASD, all five categories were merged.  

Hopefully nobody else in the world will pay any attention.

Unfortunately being Psychiatrists, they again have to muddy the water and all the future data/statistics.  A portion of people formerly diagnosed with PDD-NOS, will now get diagnosed with SCD (Social Communication Disorder) which is set outside the new definition of ASD.

“Congratulations you are off the Spectrum” 


I really do wonder about the IQ of these Psychiatrists.


Reliable Data on ASD

I do like to have some reliable data.  The quality of data in the field of autism is usually very poor and incompatible (i.e. rubbish).  Most data, like that from the CDC in the US, is unreliable.  It seems that richer “Ethnic European” parents push to get an autism diagnosis much harder than poorer “Hispanic” and “African American” parents.  Perhaps hard to believe as an outsider, but in the US poverty equals low diagnosis of autism and wealth equals high diagnosis.  Incidence does not equal diagnosis.  CDC data is just who got diagnosed; in the US many poorer people do not get diagnosed.  If you live in a country with free socialized healthcare, as in Europe, this will look strange.

I have chosen a highly regarded, and very highly cited, Canadian source for my data.

Éric Fombonne  is a French psychiatrist and epidemiologist based at McGill University in Montreal.  He co-authored a pair of studies in 2001 and 2005 with Suniti Chakrabarti, that examined the entire preschool and early school population of one large area of the United Kingdom (falling under the South Staffordshire Health Authority).

There is a stable population of indigenous British people with a small (1.4%), mostly Asian, immigrant population. The total population living in the area was 320 000 people.



The studies are:-







All children from 2.5 to 6.5 years old were screened, a total of 15,500 children in total 97 children (79.4% male)  were found to have a PDD (i.e. be somewhere on the autistic spectrum)

Of the 97 children, 29 (29.9%) had no functional use of language defined as the daily spontaneous use of 3-word phrases. The proportion of children without functional language was however strongly associated with diagnostic subtype (AD, 69.2%; Asperger syndrome, 0%; PDD-NOS, 16.1%).

Of the 97 children, 37 children underwent Merrill-Palmer testing and 56, Wechsler Preschool and Primary Scale of Intelligence testing. Four children could not be tested for practical reasons. Overall, 24 (25.8%) of 93 children had some degree of mental retardation. The 2 children with childhood disintegrative disorder and Retts syndrome scored in the moderate range of mental retardation.








Side-note about shoddy research

To show those of you still unconvinced that published, and moderately highly cited, autism research can be rubbish, the authoritative sounding paper written by a Professor of Psychology below also reviewed the above research data.


The author commented:-

Recent epidemiological surveys have shown that the prevalence rates of MR in children with autism is between 40% and 55% (e.g., Chakrabarti & Fombonne, 2001), much lower than the typical rates cited in the literature.”

The Chakrabarti & Fombonne 2001 paper clearly shows 69% of people with the narrow diagnosis of “autism” had MR whereas 25.8% of those with the broader diagnosis of ASD/PDD.

More than 100 other papers now cite the author’s incorrect readings of the original research.

I do not know what IQ you need to have to be a Professor of Psychology, but it clearly needs to be increased.



Back to the Fombonne studies

Four years later they repeated the same study on the next cohort of English school children:-

The rate of mental retardation in the autistic disorder group was 66.7%, compared to 12.0% in the group with pervasive developmental disorder not otherwise specified and 0.0% in the Asperger's disorder group


So I will take the average of the two studies

            Autism                       68% with MR/ID
            PD-NOS                     10% with MR/ID
            Asperger’s                    0% with MR/ID


What surprised me was the breakdown of the children by PDD.  Most kids (>50%) were PD-NOS, I did not expect that.

  Autism                        31%
            PD-NOS                     52%
            Asperger’s                  16%
            CDD/Retts                    1%

So the percentage all PDD (i.e. all ASD) with MR was 27%



Combining this as a graphic:-  






  

So now when people tell me that 50% of kids with autism have MR/ID, at least I know the likely reality.  It is either more, or less, depending on what you mean by “autism”; but is not 50%.



Conclusion

Most people think you cannot change your IQ.

The reality is that testing a young child with severer ASD is highly likely to underestimate their IQ, since the test assumes that the child will comply with the tester.  Most young children with autism do not comply with their parents, let alone an IQ tester.

ABA will improve compliance and hence improve an IQ test result.

Long term ABA use will, in many cases, gradually improve the child’s ability to learn and hence boost cognitive function and by implication an IQ test result.  You will find references to people saying ABA raised their kids IQ score by one or two dozen.

Correcting the biological dysfunctions underlying autism undermines the whole shaky DSM system.

PDD-NOS is, in effect, milder classic autism without the stereotypy .
Take some N-acetyl cysteine pills, you lower oxidative stress and you can stop the stereotypy.  So then your “expert” diagnosis would change from classic autism to PDD-NOS?

Take a few more pills and instead being in the 68%, with an IQ of less than 70, you can move up to 85 and, who knows, maybe much higher.

But it has to be said that the concept of IQ is something many people think they understand.

If one day, I were to make a clinical trial of my autism Polypill, I would definitely include a before and after measurement of IQ, alongside all the usual behavioral measures that most people would not understand.

And then …

“Wonder drug rescues people with autism from mental retardation”

In the meantime, we can continue correcting the remaining biological dysfunctions underlying autism and thus improving cognitive function.






Note the rocket, for those with classic autism doing just this and changing their prognosis.








Friday 8 August 2014

Cognitive Function Restored, with Bumetanide

Regular readers will know that every summer Monty, aged 11 with ASD, has a “flare-up” in his autism.  Behaviour gets very much worse and now we notice that also cognitive function is impaired.

In my last post I repeated how the aggression and SIB (self-injurious behaviour) was very effectively suppressed by Verapamil and I was pondering how to solve the, now visible, cognitive decline.

I suppose some readers may be thinking all this sounds fanciful.  Once a child with autism is verbal and has got as far as basic maths, it is very easy to measure cognitive function.  For years I have asked Monty what he had for lunch at school that day, to check how “switched-on” he was.  Now, I just need to ask him something like “what is five times five”.

Ted, Monty’s older brother, has also noticed these changes and has recently delighted in showing how his brother does not know six times six, or even twelve plus five.  He would ask him questions when we are all in the car, and then I would have to start making excuses for his brother.  Well with Verapamil, at least Ted is not going to get punched by Monty, as they sit in the back of the car.

We know that for most of the year Monty knows the right answer to all these questions, but from July to early October he may get them wrong, or does not answer.  This was all traced back to the effect of a mild pollen allergy.

Rather than look for something new, I decided that as a first step I would just increase the dose of one of his existing Polypill ingredients and “hey presto” the problem was solved.  A nice surprise, indeed.

I increased the Bumetanide dose from 1mg once a day, to 1mg twice a day.

Every time since that I ask Monty five times five, or six times four he gets the right answer, even if he is in the middle of doing something else, like jumping into the swimming pool.  That is proof enough for me.  Even Ted has noticed.

In previous posts I did complain about the effectiveness of autism rating scales and suggested that measuring academic performance (in older kids) might be more reliable.   In the case of Bumetanide this really is the case.

As to the relationship between bumetanide and allergy, there are various possibilities.  I did yesterday highlight this impact to the French researchers currently working to get Bumetanide approved officially as drug for autism, since it could be useful for them to know.


Conclusion

So, the current summertime allergy solution is:-

Aggression and SIB – Verapamil three times a day

Cognitive impairment – Bumetanide one extra daily dose of 1mg

All that is left of the “autism flare-up” is a very occasional rapid mood swing from happy to sad.

Compared to last summer, the difference is profound and now the difference between behaviour in summer and winter is very small.




  

Monday 4 August 2014

Allergies, Autism and Cognitive Impairment

Previous posts showed how pollen allergies can lead to summertime flare-ups in autism; most noticeable are violent/aggressive behaviours, but there is actually much more going on.

I established that Verapamil, the calcium channel blocker, and surprisingly also a mast cell stabilizer, can very effectively extinguish the aggression, but without really solving the usual allergy symptoms like itchy eyes.  As a result, you need to use a convention anti-allergy treatment as well.


Asthma/Pollen Hot Spots

Any asthma suffer will be able to tell you about the places that make them feel worse and the places that places that reduce their symptoms.  It seems that pine forests high in the mountains and on certain coastlines are best.

Forested areas around cities are not good for asthma, Berlin being an example. So you can easily check if you live in an asthma hot spot, or in a better place.


Cognitive Impairment

We just spent two weeks under the olive trees beside the sea in Greece, which I would classify as a low pollen location.  Having returned home to a big city and a house directly opposite a forest, we could see the effect of an asthma/pollen hot spot.

Monty, aged 11 with ASD, mild pollen allergy and mild asthma, did change his behaviour almost immediately.

The Verapamil does continue to block aggressive behaviour, but what changed was an immediate return of mild atopic dermatitis (red patches behind knees) and what Monty’s brother Ted, aged 14, described as Monty became “more stupid”.  It is not a nice way to describe it, but when you look closely, it is there.  The allergy has effectively lowered his cognitive function.  It is very easy to check, just ask some simple maths questions or memory questions (what did you have for breakfast?).  It is as if he is very mildly intoxicated (drunk), he is not staggering around, but he is not as sharp as he was in Greece, or at home in the spring.

Faced with an aggressive child, the last thing you would bother about is how good he is at mental maths, and so you would probably never notice it.  But having solved the aggression we are left with the observation that the allergy causes some temporary cognitive impairment.  I say temporary, because if you take away the allergens, everything improves and returns to where it was.


What is going on?

We know that allergens cause mast cell degranulation, which releases histamine, IL-6, and other pro-inflammatory substances in a chain reaction.  We know that these cross the BBB (blood brain barrier) where there are several types of histamine receptor.  The body has at least 4 types: - H1, H2, H3 and H4, and maybe more not yet identified.

Typical anti-histamines only block H1, and the newer ones are specifically designed not to cross the BBB, so as not to make you drowsy.  We later discovered that most H1 anti-histamines have moderate mast cell stabilizing properties, meaning they do reduce the release of histamine itself.

Calcium channel signaling is known to be disturbed in autism and there is excess physical calcium found in the autistic brain.  This did suggest that modifying calcium channel behaviour might be of benefit.  A known genetic variation in autism does affect the L-type calcium channels.  This suggested that blocking the L-channels might be helpful.  This was shown to be true in Timothy syndrome and I showed it to be true in Monty.

Other research has shown that Verapamil is an effective mast cell stabilizer, which did come as a surprise.

Now we come back to the effect of the allergy.  If untreated, it will “dumb down” the child and also lead to extreme behaviours like aggression, but also even odd physical tics, like moving the head forwards and backwards like a pigeon.

Perhaps there is a two stage process going on, which ultimately leads to the aberrant signaling of the L-type calcium channels and aggression.  Or is it just a progression from mild to severe?

Is it a coincidence that a calcium channel blocker can stabilize mast cells?  I think it unlikely.


Autism as an Allergy of the Brain

The idea put forward by Professor Theoharides, that autism is, at least in part, an allergy of the brain, looks more and more valid.  It was the subject of an earlier post.


I do wonder how much mental retardation (MR) / cognitive impairment is also caused by the same mechanism.  Depending on how you define “autism” and whose figures you use, between 20% and 50% of people with autism have MR.  MR is defined as an IQ of 70 or less.

·        Mild retardation: Mild retardation: IQ level 50-55 to approximately 70 (85% of people with mental retardation are in this category)
·        Moderate retardation: IQ level 35-40 to 50-55 (10% of people with mental retardation)
·        Severe retardation: IQ level 20-25 to 35-40 (3 - 4% of people with mental retardation)
·        Profound retardation: IQ level below 20 or 25 (1 - 2% of people with mental retardation)

I would suggest that many people with autism might be “cognitively impaired” by allergies, be they caused by pollen, cats, dust, food, detergents, pollution or anything else.  Maybe they just dropped from a potential IQ of 120 to 110, or maybe they dropped from 80 to 35 and are now known as severely retarded.


Verapamil treats more than aggression and SIB

Based on my sample of one, it would be conceivable that Verapamil merely treats aggression and self-injurious behaviour (SIB), and that allergies are a side issue.  But thanks to the feedback on this blog, it is clear that Verapamil is treating the allergy.  One reader gave very extensive feedback showing how Verapamil greatly reduced her child’s GI problems (caused by food intolerance/allergies) and improved behaviour.  So based on a sample of two, Verapamil’s effect does seem to be related to mast cell degranulation and allergies.


Conclusion

I am very happy to have discovered the benefits of Verapamil, but I will continue to look into how further to reduce the “brain allergy effect”.  Perhaps the allergy is somehow affecting the excitatory/inhibitory balance of the Neurotransmitter GABA, I say this because Monty’s behaviour somehow resembles life without Bumetanide.  

Bumetanide’s role in autism is to lower brain Cl- concentration and to switch GABA to be inhibitory.  A recent comment on one of my Bumetanide posts was from somebody highlighting a paper that questioned whether enough Bumetanide crosses into the brain to switch GABA to be inhibitory.  

Note that a recently published comprehensive review on the use of bumetanide in the treatment of neonatal seizures indicates that theres is no evidence to support the use of this drug in the treatment of central nervous system disorders via the NKCC1-dependent mechanism described above, as at the very low doses that are given to infants and children bumetanide does not reach sufficient levels in the brain.

direct link to the original review:
http://onlinelibrary.wiley.com/doi/10.1111/epi.12620/pdf

It is conceivable that allergies affect the blood brain barrier (BBB), although you might expect allergies to weaken the BBB, rather than strengthen it; but the body does plenty of strange things.  So a second daily dose of Bumetanide just might help.  In France, the autism researchers working with Bumetanide do give it twice a day.

The simplest method to reduce the “brain allergy effect” would be to just avoid the allergen(s).  In the case of Monty, this would be to go and live in a low pollen environment, and perhaps even avoid cats.

Since 30+% of people with autism apparently suffer from asthma, then 30% of people with autism might also find behavioral relief by avoiding pollen.  Those suffering from aggression and SIB would very likely benefit dramatically from Verapamil.

This might also suggest that residential facilities for people with severe autism should be in low pollen areas.

Incidentally, our local special needs school used to be surrounded by a rampant overgrowth of ragweed/ambrosia.  This is one of the most notorious plants for causing allergies in humans.  The current number 1 in the ATP world tennis rankings then gave them some money to tidy up the grounds.  Coincidentally, like many of the “inmates”, he also favors a gluten free diet.






Thursday 12 June 2014

Cognitive Enhancement, Classic Autism and School


The school year is coming to an end and now we get the results of assessment week, the end of year tests.


Personally I never liked exams, or rather revising for them, but for teachers, assessment is a big part of what they do.  I used to be asked at the start of the school year for a list of benchmarks to measure my son Monty’s progress during the year, since the usual benchmarks were seen not as applicable.  Then we would spend lots of time discussing the list.

Typical kids just follow the standard curriculum and get their standardized progress tests.  If you follow an ABA program, you are constantly measuring performance and you only progress when you master a skill, so it is like continuous assessment.

Monty, aged 10 with ASD, goes to a very small international school.  So there is no special needs teacher, no IEP (individual educational plan), just a nice friendly environment.  This works very well because it means you can build your own educational system, not restricted by any rigid rules.

From the age of about four years old till seven or eight, in effect, Monty’s curriculum was the ABBLS (Assessment of Basic Language and Learning Skills), which is a rather intimidating list of 544 skills from 25 skill areas including language, social interaction, self-help, academic and motor skills that most typically developing children acquire prior to entering kindergarten.  These are very basic skills, that we never had to teach to Ted, Monty’s big brother, but without these skills you really cannot do much. They are the basic skills on which everything else is built.  It includes things like toilet training, stacking coloured blocks in order and, at the intellectual end, involves ultra-basic speech, being about to count and being able to read.

When your child has just a handful of these 544 skills, it appears that you have a mountain to climb; indeed you do.

Fortunately for us, Monty’s then Assistant and best pal, Irena, took on much of this daunting task.  He did become verbal, he did learn to read, he learned how to write and yes, finally, got to grips with numeracy.  (All without any help from drugs)  

This all occurred in parallel with going to "school".  The learning all occurred at home, school was just for practice.

Back then, the end of year report did not really have much importance.

At some point you do hope that school will actually be a place for learning.

It does appear that in many cases of “inclusion”, school is little more than daycare.  Some special schools are brilliant, but even if you live near one, they tend to be hugely expensive and access is highly restricted.

My observation of the limited number of people with autism I am familiar with, is that they tend not to get on with each other; they actually like to be around nice friendly neurotypical kids.  Until you get to secondary school, many kids are nice to special needs kids.  After that, most really are not nice at all, and any idea of going to school for “socialization” becomes nonsense, because the “normal” kids openly seem to ignore, provoke and even hate the kids with HFA/Asperger’s.  Sad, but true.


What is Normal for Kids with Classic Autism?

Most kids with classic autism end up in a special school, or a special needs unit attached to a mainstream school.

One of our former 1:1 assistants was a trainee at the local special school and later became a teacher at another one.  We discussed what went on there and I did visit a few the school a few times.  It was much better than I expected, but was more about keeping the kids calm and under control, than academic advancement.  There were 6 kids per member of staff and the kids had very mixed ability, they were just grouped by age.

I took a look at Treehouse, the leading autism school in London, to see what is in their curriculum.

In the US there are many such schools.  In Europe, Treehouse is quite well known, because it seems to be unique.  One of our former ABA consultants from the US used to work at Treehouse and another former one is on the Board of Governors.  Our current ABA consultant was doing her PhD in Behavioral Science in the US, when the founders of Treehouse visited the leading US autism schools for inspiration many years ago.  A small world indeed.

In fact the Treehouse curriculum bears little resemblance to what goes on in mainstream schools.

I really do not understand what kids with classic autism can achieve in big mainstream schools, even with an assistant.  I just discussed this with Monty’s teacher, how can you “include” a child who has no understanding of what you are teaching the other kids?

Two year ago I agreed with our school to hold Monty back by two years, to be at his academic level, so he is two years older than most of his classmates.  There is no rush to get to secondary/high school.

The question I have had for a long time is whether Monty will be able to learn at school.  To date he has had thousands of hours of 1:1 learning at home, following his home program, which now combines ABA-based learning of things like social skills, conversation etc., with academic work like numeracy and verbal comprehension.


School for Learning?

My plan, when I realized that drug interventions do really cognitively improve autism, was to retain my model of school in the morning and 1:1 learning at home in the afternoon and aim for a time when school could genuinely be for learning.

The good news is that we really do seem to have reached that point.

I had the end of year meeting with Monty’s class teacher and it was almost as if we were discussing a regular kid.  For a start, we were discussing results from standard tests for science, maths and English provided by Cambridge University for international schools following their primary curriculum, so much less scope for the usual “sympathy grading”.

Lots of kids do get extra time in tests, for example if they have dyslexia.  Why not for autism?    The Asperger’s boy in Monty’s brother’s class gets an easier English test and extra time.

In Monty’s case, I did not want extra time; anyway he does not need it.  If he does not understand what to do, extra time is no help.  The question was whether his assistant should give him any “hints” as to what the questions mean, when she knows he really does know the answer. (e.g. when asked verbally by the teacher, so not in writing,  "what is the next factor of 5, after 30")

We had this debate and we agreed; no help of any kind.  That way at least the test tells us something useful.  If the test is based on prompting/help, how big was the prompt?  Better to see the real result and then we can do the “oh, but he really can do that”.

So this year was the first time we have the same tests as the other kids and definitely no help.  This is the result:-


Speaking and Listening        C+
Reading                                 B+
Writing                                   B+
Mathematics                          C+
Science                                  A-
ICT                                         A+
Music                                      A
Art                                           A


Well the results show Monty ended Year 3 ahead of anyone’s expectations, including the teacher.

I think the art teacher was probably being over generous, which is what tends to happen (sympathy grading).  ICT (Information and Communication Technology) is pretty basic at this level, but Monty can do it all.  When it comes to music, Monty is in his element; he can read music, plays his piano and has started to sing.

So the grades seem to be genuine, and he was not at the bottom of the class in any subject. That might not be a common educational benchmark, but I think it is a pretty good one to see if “inclusion” is really working.

As I said to his present teacher, only two years ago he was hitting his then class teacher, assistant and even, on rare occasions, his classmates.  Back then there was very little learning going on at school and not much social interaction either.


Cognitive Enhancement

Along with greatly improved social skills, simple conversation with peers, and even some sporting ability, has come cognitive enhancement.  He still is not “normal”, but it is a remarkable transition nonetheless.

How far he can get following the mainstream curriculum is an open question, but it is far further than anyone could have dreamed of, until he started his drug therapy.

I continue to be amazed, but the gains are almost entirely reversed if he stops taking his drugs.