Channelopathies in Autism - treating Cav1.2 with Verapamil

 

In December 2013 I wrote about a leading Italian researcher and clinician called Professor Antonio Persico and gave a link to an excellent presentation he gave in the US, about his views on the underlying biological process behind autism.

Excess Calcium and Calcium Signaling in the Autistic Brain

  

He had a nice graphic in which he depicted the puzzle that is autism.

  

One of his findings was that in the autistic brain there is an excess of both physical calcium and calcium signaling (via ion channels). He did not draw any therapeutic conclusions, which as I said was a pity.

In fact, Persico is far from the first scientist to point the finger at calcium channelopathies.

A few months before this, I had decided I would apply myself to see if there were any safe, practical therapies that could be applied, based on all the scientific research about calcium ion channels; incomplete as it might be.

After a few hours, or so, of reading about the biology of calcium channels, the available drugs and the existing research in their use in conditions other than autism, I came to the conclusion that Verapamil looked a very likely candidate.

Verapamil is a so-called L-type calcium channel blocker (L representing long-lasting length of activation); it particularly affects a type of voltage-gated calcium channel called Cav1.2.  For various reasons, I had deduced that these Cav1.2 channels were possible open more often than they should be in the brain of Monty, aged 10 with ASD.  I proposed that over activation of these channels resulted in extreme agitation that leads to aggression and self-injurious behavior in autism.

Back in September 2013, Monty was still having behavioral problems, apparently brought about by summertime pollen allergies.  I did write extensively about this and how I had narrowed the problem down to mast cell degranulation and histamine.  Treating the allergy did a lot of good, but was never a complete solution, since the standard allergy drugs worked for only a couple of hours, rather than the 24 hours they claimed.

So I had Monty in a state of near explosion by mid-afternoon most days, with a red face and letting us all know he was not feeling good.  He would say things including “be nice”, “I want to be nice”, “to hit your head” or even, on a good day, “to hit your head and see birdies”.  By then, he was also having Rupatadine, a mast cell stabilizer, which did seem to help.  The eruptions were far less often and less severe than in July, but it was clear that more could be done.

One afternoon, I decided to give a very small dose (20mg) of Verapamil, and before my eyes, the anger and agitation began to fade and was replaced by calm.  It was the most amazing experiment that I have witnessed and within 20 minutes there was complete calm.

In the following weeks, I would still hear Monty say “be nice”, but this was no longer followed by any aggressive behaviour.  The trigger was still there to energize these channels, but they had blocked by Verapamil.  It was like firing a gun, but with no ammunition; there was a “click”, but no “bang”.

This is the reason that Verapamil is in the PolyPill, in case anyone has wondered.

Before you start googling, there is absolutely no published research to support the use of Verapamil in autism.  This is part of the reason I did not to write about it at the time.

Verapamil is also a blocker of certain voltage-gated potassium channels and has the effect of raising potassium levels in the blood.  We have seen in earlier posts that potassium channel dysfunction is also present in autism and that raising potassium levels helps reduce sensory overload.  One effect of bumetanide is that it lowers levels of potassium, so bumetanide and verapamil are in that way very complementary.

Subsequently, I have read that mutation of the CACNA1C gene is associated with schizophrenia, which is like adult-onset autism.  The calcium channel produced from the CACNA1C gene is Cav1.2.  So this might be a case of what helps in autism might help in schizophrenia.

The bipolar disorder risk allele at CACNA1C also confers risk of recurrent major depression and of schizophrenia.

 If you are interested in why I decided to test Verapamil, read on.

 

Observations

Anger & SIB

Anger, leading to violence against others and to yourself are behaviours that arise in many people with autism.  There are undoubtedly many causes, and many are behavioral.  If a non-verbal person cannot express what he wants, or a partially verbal child has some pain (e.g. toothache) and does not understand it, things are likely to get out of control.

But there are other times, when for no apparent reason, nasty behaviour can occur, so I presumed that there might be a biological explanation.  If there was one, then I would think about a biological intervention.

My wife always asked Monty if his head was hurting when these kinds of behaviors popped up.  He would usually say “yes”, but it could well have been to avoid any other questions.  But why not consider it as possible that there is a pain prior to SIB.

Fever Effect

Then we have the recurring observation about autistic behaviours changing when the person has a high temperature; the fever effect.  This has now been studied by literally warming people up in hot water and then carrying out behavioural test.

Hyperthermia and the Amelioration of AutismSymptoms

As usual in autism, this effect applies much more to some people than to others.  Monty is moderately affected, but some people are dramatically improved.

Headaches

Headaches are very common, but some people do seem to get far more than their fair share.  Migraines are particular nasty and so is another type, the cluster headache.

Cluster headaches are severe headaches that are clustered together.

Cluster headaches are occasionally referred to as "alarm clock headaches" because of the regularity of their timing and they may awaken individuals from sleep. Both individual attacks and the cluster grouping can have a metronomic regularity; attacks striking at a precise time of day each morning or night is typical. This has prompted researchers to speculate involvement, or dysfunction of the brain's hypothalamus, which controls the body's "biological clock" and circadian rhythm.

Now I have noted that in some literature it is claimed that parents of children with autism often have a history of headaches (and I do not mean caused by dealing with their child’s autism).  

Note that most younger people with autism have a “faulty” biological clock, so they have trouble sleeping through the night.

 

Febrile seizures

Seizures and autism are closely related.  Febrile seizures occur in some children when they have a temperature greater than 38 °C (100.4 °F).  They are twice as common in Japanese children than they are in Western children, occurring in up to 9% of children and mainly in boys.

It is not agreed exactly what causes febrile seizures, Japanese research points to voltage-gated sodium channels, which does not really support my theory.  However, rather than delete this part of the post, I did a little more digging and found a paper in the Journal of Neuroscience that does neatly fit by theory.

Temperature-sensitive Cav1.2 calcium channels support intrinsic firing of pyramidal neurons andprovide a target for the treatment of febrile seizures.

Comorbidities

It is well documented that poor cardiac health is associated with autism.  I have commented before that it is not entirely by coincidence that some drugs that help autism were actually developed as drugs for heart problems.  By treating the autism, a side benefit is that you may also be treating (and perhaps avoiding) the heart disease that would otherwise likely to develop at quite a young age.

So, while giving statins and calcium channel blockers to a healthy young person would be irresponsible, the same may not true for people with autism.  In the same way that people with type 1 diabetes have been recognized as being at high risk of heart disease and are put on preventative drugs at a much younger age than the wider public. Patients with type 1 diabetes are 10 times more at risk from heart disease than other healthy patients.  They are recommended statins, aspirin therapy and an ACE inhibitor.  An ACE inhibitor reduces blood pressure in a different way to how Verapamil also lowers blood pressure.

Due to the severity of neurological/behavioral problems of autism, medical practitioners are not really worrying about cardiac health.

Too Much Calcium

There are opposing views about the role of vitamin D in autism; in other words, too much or too little.  There have been some interesting thoughts about milk and autism, and not about whether or not it is fortified with extra vitamin D; the point was the role played by calcium.

Then there is the mother who found that supplementing her autistic child with calcium had some frightening consequences, producing profound regression.

Basic Biology

If you want to read about the basic biology of calcium channels, here are links to Wikipedia;-

Calcium Channels

L-type Calcium Channels

Calcium Channel Blockers

Connections with the biology

One of the things that drew my attention was the fact that the behaviour of some calcium channels is temperature dependent.  There are other ion channels that are also temperature dependent.  The Cav1.2 channels are known to behave differently according to their temperature.

Connections within the literature

Timothy syndrome

I have covered Timothy syndrome previously in this blog.

This is a, thankfully, extremely rare condition in which the most people do not survive to childhood; those few that do are likely to have autistic-like symptoms.

The syndrome is caused by severe mutations of the CACNA1C gene.  As a result it is also associated with severe heart problems, since this gene expresses the Cav1.2 channel that is found in the heart and the brain.

The Timothy syndrome mutation differentially affects voltage- and calcium-dependent inactivation of CaV1.2 L-type calcium channels

In the following article, Dr Ricardo Dolmetsch used an experimental L-type calcium channel blocker, called Roscovitine, to “successfully” treat his model of Timothy Syndrome.

Scientists identify defect in brain cell channel that may cause autism-like syndrome 

Dolmetsch is now Head of Neuroscience at the Novartis Institute for Biomedical Research.  I did write to him once, when he was still at Stanford, to ask if he was interested in discussing some of my ideas – no answer, I guess he was busy curing autism.

Headaches

It has been known for many years that some L-type calcium channel blockers are effective in treating both migraine headaches and cluster headaches.

Individualizing treatment with verapamil for cluster headache patients

 

CONCLUSIONS:

Providing the dosage for each individual is adequate, preventing CH with verapamil is highly effective, taken three (occasionally with higher doses, four) times a day. In the majority (94%) with episodic CH steady dose increase under supervision, totally suppressed attacks. However in the chronic variety only 55% were completely relieved, 69% men, but only 20% women. In both groups, for those with partial attack suppression, additional prophylactic drugs or acute treatment was necessary.

This study found that some people required 5 times higher dose than others and doses were up to 960mg per day.

Verapamil in prophylactic therapy of migraine

We conducted a double-blind, placebo-controlled crossover study of verapamil HCI in the prophylaxis of chronic migraine headaches. Verapamil significantly reduced both headache frequency and duration with few side effects. The drug may be useful for a segment of the migraine population refractory to other prophylactic agents or for those who cannot tolerate the side effects of other drugs

Mice and SIB (Self Injurious Behaviour)

Lots of people do not like the idea of being compared to mice, or even worse rats.  Nonetheless, this following paper is indeed very relevant, it showed that it you active the L type calcium channels in mice they will engage in self injurious behaviour.

Calcium channel activation and self-biting in mice

The L type calcium channel agonist Bay K 8644 has been reported to cause characteristic motor abnormalities in adult mice. The current study shows that administration of this drug can also cause the unusual phenomenon of self-injurious biting, particularly when given to young mice.

The self-biting provoked by Bay K 8644 can be inhibited by pretreating the mice with dihydropyridine L type calcium channel antagonists such as nifedipine, nimodipine, or nitrendipine.

However, self-biting is not inhibited by nondihydropyridine antagonists including diltiazem, flunarizine, or verapamil.

If Monty was a mouse, verapamil would therefore likely not work and I would probably have had to use nimodipine.

Genes

I do not claim to be an expert in Genetics, but I can uses genes to support my case.

In 2013 a paper was published in the Lancet that looked for genetic links between a range of neurological disorders.

Identification of risk loci with shared effects on five major psychiatric disorders: a genome-wide analysis

In this paper you can find out many things, including:-

•  Gain-of-function mutations in CACNA1C causes Timothy syndrome

•  CACNA1C is a susceptibility gene for bipolar disorder, schizophrenia, and major depressive disorder

• neuroimaging studies have documented effects of CACNA1C variants on a range of structural and functional brain phenotypes, including circuitry involved in emotion processing, executive function, attention, and memory

• Mutation in the CACNB2 gene are associated with Brugada syndrome, autism, attention deficit-hyperactivity disorder (ADHD), bipolar disorder, major depressive disorder, and schizophrenia

• CACNB2 encodes an auxiliary voltage-gated calcium-channel subunit that interacts with L-type calcium-channel subunits (including CACNA1C, CACNA1D, and CACNA1S) to promote their trafficking to the plasma membrane, increase their function, and regulate their modulation by other signaling proteins and molecules

Now “my” Calcium channel, also known as Cav1.2, is encoded by the very same CACNA1C gene.

In a similar paper, autism also gets a mention 

“Genetic variation in CACNA1C have also been associated with depression, schizophrenia, autism spectrum disorders”

CACNA1C (Cav1.2) in the pathophysiology of psychiatric disease

So all in all the genetic analysis also point to Cav1.2 as a good candidate for some intervention.

Epilepsy

Verapamil is being investigated to treat various forms of epilepsy and seizure.  This is interesting, since seizures are highly comorbid with autism.

Seizures tend to develop in early puberty in many cases of autism.  It appears possible (maybe not probable) that if you can avoid the onset of epilepsy during this time of hormonal change, you may be free of it for life.  The science has shown that the first seizure makes a biological change occur;  the same is indeed true with asthma.  If you can identify the at risk group (i.e. people with autism for epilepsy and atopic dermatitis for asthma) you may indeed be able to avoid it.

I was not aware of this until after Monty, aged 10 with ASD, had developed asthma, but I am well aware of it now.  I am actively taking steps to avoid epilepsy.

The other useful aspect of this research is that they are all clinical trials of Verapamil in children.  This is important from the safety perspective.

Study suggests Verapamil could be used to fight refractory epilepsies

Verapamil as Therapy for Children and Young Adults With Dravet Syndrome

Addition of verapamil in the treatment of severe myoclonic epilepsy in infancy

Calcium channel blocker Verapamil Administration in Prolonged and Refractory Status Epilepticus

Choice of Channel Blocker

In medicine, calcium channel blockers were developed to treat heart conditions.  A common problem in treating autism is the need for drugs to freely cross the blood barrier (BBB); most do not.

Other issues include the half-life of the drug and most importantly the safety of the drug.

Given these considerations, and the fact that I know precisely which calcium channel I want to block, this led to me to Verapamil.

It is very widely used, and is available very cheaply as a generic in sizes down to 40mg.  Adult and indeed child dosages go all the way up to 400+mg a day.

Since the idea is to subtly affect the brain and not dilate blood vessels in the heart, which increases the supply of blood and oxygen; a small dose was envisaged, 20 mg.

On paper, Nimodipine, also looks a very interesting candidate, but it is rarely used in children.  It would be useful to trial it on adults with autism.  It works better than verapamil in mice with SIB.

Conclusion

I must admit that some of my “evidence” was gathered after I had proved my theory was valid, like the mice with SIB after their L-type channels were activated.

Given all of the “evidence” it does amaze me that it did not occur to anyone to try a drug like Verapamil in children with autism.

Clearly all drugs carry a risk, but so does violence and self-injury.

P.S.  Note that magnesium is also a calcium channel blocker

Schizophrenia rather than Fragile-X and Retts Syndrome, as a Reference for ASD

You may, like me, have wondered why so much autism research seems to mention Fragile-X syndrome and Retts syndrome.  

Both Fragile-X and Retts are caused by the mutation of single genes, FMR1 and MECP2 respectively.  Autism can be caused by very many, seemingly unrelated things, both genetic and environmental.

When you look at it objectively, there is a much closer comparison for autism, it is schizophrenia.  

I know from the research I am reading that in fact autism and schizophrenia are intertwined and there is no boundary were one stops and the other starts.  Most likely some of the individual biological dysfunctions in autism are present in a greater/lesser degree in schizophrenia and vice versa.  This will be developed in later posts.

For those interested in learning more about schizophrenia here is a nice PowerPoint presentation.

https://files.itslearning.com/data/1512/469/SCHIZO%20PP.pptx

Here are some excerpts:-

·        A biological disorder of the brain which causes disturbances in thinking, speech, perception of reality, emotion (mood), and behavior.

·        Approximately 1% of the population develops schizophrenia during their lifetime.

·        Although schizophrenia affects men and women with equal frequency, the disorder often appears early in men (usually late teens), than women (generally late twenties/early thirties).

The most ASD-like sub-type is called disorganized schizophrenia; and it principal features are:-

•      Confusion and Incoherence

•      Severe deterioration of adaptive behavior

–     Lack of social skills

–     Poor personal hygiene & self-care

•      Behavior appears silly and/or child-like

•      Highly  inappropriate emotional responses

It is not hard to see the potential overlap between ASD and Disorganized Schizophrenia.

We even have a researcher suggesting a very similar strategy for Schizophrenia, to that I am proposing/developing for autism.

Phenotype of schizophrenia: a review and formulation

The discovery of the pathophysiology(ies) for schizophrenia is necessary to direct rational treatment directions for this brain disorder. Firm knowledge about this illness is limited to areas of phenomenology, clinical electrophysiology, and genetic risk; some aspects of dopamine pharmacology, cognitive symptoms, and risk genes are known. Basic questions remain about diagnostic heterogeneity, tissue neurochemistry, and in vivo brain function. It is an illness ripe for molecular characterization using a rational approach with a confirmatory strategy; drug discovery based on knowledge is the only way to advance fully effective treatments. This paper reviews the status of general knowledge in this area and proposes an approach to discovery, including identifying brain regions of dysfunction and subsequent localized, hypothesis-driven molecular screening.

For psychiatrists, the main difference between autism and schizophrenia seems to be when is the onset of symptoms.  Autism strikes at the age of two or three, whereas schizophrenia occurs much older.  Whether in fact some of the same biological mechanisms might be at work does not seem to be relevant to psychiatrists.  Not surprisingly, they have not made much progress treating either condition.

In the days before the autism was so widely diagnosed, there were many more cases of childhood schizophrenia reported, now it is very rarely diagnosed condition, it became autism.

I did look for some statistics that included autism and schizophrenia, but those clever psychiatrists seem to have separated them, so autism is with developmental disabilities and schizophrenia is not.

But I did find some interesting statistics about developmental disabilities.

When you look at the US statistics (1997 – 2008), based on parent-reported developmental disabilities.

Source:  http://pediatrics.aappublications.org/content/early/2011/05/19/peds.2010-2989.full.pdf+html

You can see that about 15% of kids have some kind of developmental disability.  Cases of autism increase from 0.2% to  0.7% over the ten years, but those with a learning disability is pretty flat at around 7% and mental retardation (MR) / intellectual disability is also pretty flat at 0.7%.

You also see that the incidence of seizures remains flat at about 0.7%.

According to the medical research, about 30% of people with autism will also have seizures; you would expect to see a seizure “epidemic’, if there had been an autism “epidemic”.  Whereas diagnosing autism is highly subjective, recognizing most types of seizure is not.

So clearly the numbers do not add up.  Perhaps now only 10% of people with autism have seizures?  Or perhaps only 30% of people with autism, really have it?   

The same is true with the incidence of mental retardation (intellectual disability) it remains flat at 0.7%.  According to the WHO, 50% of people with autism also have MR.  So, if there had been a big increase in new people with autism, you would expect an increase in MR.  If the level of MR remains flat it would seem that some people with MR have just been given an additional diagnosis of autism.  Either that, or the 50% figure is now much lower in the US, (which is what I expect is the reality).

With even the most basic figures not adding up, is it really surprising how little progress has been made in the hard part – actually finding treatments?

Autism has changed and now means entirely different things, to different people.  In particular, comparisons across countries are completely meaningless.

Schizophrenia

Schizophrenia has also changed and is now considered as a family or spectrum of disorders.

Like autism, nobody really knows what causes schizophrenia and most likely many things do, like autism.  There is no single gene, like with Fragile-X or Retts, and there is no cure.

When researchers compared the mixture of genetic dysfunctions in schizophrenia and autism, they found a clear overlap.  This is interesting and perhaps should not have come as a surprise.

In some ways Fragile-X and Retts are actually the opposite of autism.  For example in the case of Retts, the very important substance, Nerve Growth Factor (NGF), is almost at zero, whereas in autism levels tend to be elevated.

Just as we can learn from the comorbidities of autism, I think we can learn a thing or two from the existing research in Schizophrenia.  Indeed I already have.

MR

If anyone was seriously researching treating Mental Retardation (MR), in physically “normal” people, who have not suffered from a brain infection, toxic exposure, malnutrition or any kind of pre-natal or natal problem, we would have another great resource.  It would probably show that, in some cases, MR is caused by a partially-reversible imbalance in the actions of various neurotransmitters, ion channels, hormones etc.  Some of these imbalances will also exist in numerous cases of autism.

According to the well-known expert, Professor Howlin, only about 20% of people with ASD have an IQ in the normal range (i.e. above 70) and 50% have moderate or greater MR (i.e. IQ less than 50).  It would seem that the missing 30% must have mild MR (i.e. an IQ 50 to 70).

I suspect that the cognitive improvement found by treating some types of autism could be replicated in some cases of MR, without ASD.  If there were any clever therapies for treating MR, I would think they would likely be beneficial in autism.  In most countries, as many children have MR as have ASD, so it is strange nobody is looking how to treat it.  They assume the “defects” are hard-wired into the brain; I looks to me that some are not.

Clinical Trials

Even though ASD is a lifelong condition, nearly all the clinical trials are in children, and most often, in quite young children.  Assessing such people is doubly difficult.  Working with adults should be much easier and provide better quality data.

Other neurological conditions like schizophrenia and bi-polar disorder are regarded as adult conditions, so hopefully the quality of the research data is better.  We will see.

Plenty of adults have ASD and the ones with Asperger’s will have no difficulty articulating the effects of any intervention, so it is a pity they are rarely involved in research. 

   

Conclusion

On a happier note, I believe that if you can tune the autistic brain to its optimal performance, you will see a marked improvement in cognitive ability and, by implication, in measured IQ.  

I have no doubt that a well executed, intensive ABA program, over a few years, could also show a marked improvement in measured IQ, in many cases.  ABA is also a kind of retuning of the brain, but it has to be done right to be effective.

Biological tuning plus ABA should yield the best results.

As for schizophrenia, the biological "overlap" with autism does indeed exist. Two such areas are dysfunctional calcium channels and indeed the glutamate receptor mGluR5.  This will be developed later.

When Less is More - Tuning the Autistic Brain with Clonazepam

   

I cannot say whether there will ever be a “cure” for autism, but this blog has shown that certain types of autism can be treated today.  Actually, it is becoming much more like tuning.

Tucked away in the scientific literature, you can find that some receptors in the brain respond very differently to small stimuli than to large ones, I found this intriguing but thought little more of it.  Then, in the recent post on Glutamate receptors, I saw a chart from the MIT researcher that showed how using drugs you could increase/decrease protein synthesis in the brain, to optimize neural performance.  Rather like tuning the ignition timing on your car, some people were a little ahead of where they should be (Fragile X) and others were a little behind (Rett’s).  By using the right dose of either a positive or a negative modulator (of the mGluR5 receptor) you could tune the brain for optimal performance.

Source: Contributions of metabotropic glutamate receptors to the Pathophysiology of Autism

In the case of a recently investigated GABA dysfunction in autism, the drug is Clonazepam.  Tiny doses of this drug improve the performance of the neurotransmitter GABA, apparently by affecting the Na_v1.1 ion channel.

In the research (on mice) it was shown that, within a tight dosage range, there was a measurable improvement in cognitive behaviour.  Too much, or too little of the drug and this benefit was lost.  So you would have to tune the dosing very carefully to get any effect.

It appears in humans things are more complicated than in mice, the small band of dosage where positive effects are seen does exist also in humans, but at slightly higher doses the effect turns negative before disappearing.

Source: Peter research

  

 This means that you have to get the dosage and timing just right to get the good effect.  Unlike tuning your car, where the effect is immediate, Clonazepam has a half-life of 30 hours.  This means that the concentration in the blood is made up of several doses from the last few days.

This made me realize what a challenge this would be to get right in other people.

I should point out that the same issue applies with TRH.  At the effective (also tiny) dosage you get a nice positive effect, but go too far and you get instant anger.  An Italian-Swiss researcher is using another analogue of TRH to treat some of the effects of aging.  He clearly had the same problem;  too much ended up having a bad effect.  Now he cycles one month on the drug and the next month with none.  TRH has numerous effects in different parts of the body, it has now been suggested that falling levels in middle age triggers hair to start to go grey.

With Clonazepam, along with some cognitive improvement, you also get very good mood, but at slightly higher concentrations happiness is replaced by anxiety. 

The effective Clonazepam dosage seems to fall over time; this is a very good thing, but further complicates getting things just right.  In high standard doses, the effect of Clonazepam normally reduces over time and patients need more of it.  The drug is normally used in doses 20 to 150 times higher to treat anxiety and seizures.

A further complication is that the optimal dose is 8% of the smallest available tablet.  The tablets do not dissolve nicely in water, you get a lumpy suspension.  As a result the dosage is always going to be a bit “hit or miss”

Conclusion

It looks to me that future autism treatment will include “tuning” specific dysfunctions with tiny amounts of drugs.

The good news is that tiny doses are far safer and less likely to have any secondary effects, than large doses.

The bad news is who is going to do the tuning?

People with Asperger’s, some of whom read this blog, will able to tune themselves; for others it will not be so easy.

In the case of Glutamate (mGluR5), the drugs required are still experimental.  In the case of GABA, they already exist.

A Surprise at the Dentist

The dentist is probably the worst place you can imagine to have to take a child with autism.  The same is true with many typical kids and even some adults.

If you talk to older people about their childhood experience at the dentist, before high speed drills and the like, it was more like torture.  Times have changed, it is not just better equipment, but (some) attitudes have changed.

For someone with autism, going to the dentist should not have to be a terrifying experience; people with autism actually have a high pain threshold.  True they have lots of sensory issues, but it seems to be the fact that they do not understand what is going on, that is the real problem.

A better way

There exist some very child-friendly dentists who are more than a match for a child with autism.  They can achieve what seems impossible, a calm and cooperative dental patient, who will sit back and let the dentist do his work.

One such dentist has even made a training program for other dentists to show how to achieve this.  In effect, it is a very practical ABA lesson for dentists.  The dentist is called Dr Tesini and his program is called D-Termined and he is indeed determined to succeed.

Here is clip from Youtube.

 Dr Tesini even teamed up with an autism charity to make a DVD of his method.  It used to be free but now costs $13.

Here is a link to the foundation that funded the program.

I acquired the DVD 6 years ago, but could not find any local dentist interested to apply the method.

The method is great because once the child has got used to the nice friendly Dr Tesini and gone through all the steps, he is apparently then able to “tolerate” the less friendly regular dentists, for future dental visits.

In some special schools they have a dental chair for the kids to practice on, which as another great idea.

 

Monty at the Dentist Five years ago

We have a nice friendly dentist, but I think he felt from the start that working on a child with ASD was going to be too much.  We made a few very brief visits when Monty was four and five years old and even brought along the Dr Tesini D-Termined DVD,  but this really just showed how difficult a task lay ahead if any actual drilling and filling was required.

It was never really clear whether Monty had toothache or not, since he could not verbalize the problem.  So sometimes if he was behaving aggressively, we might think that he had tooth problems.  Later things would calm down and we would forget about teeth and dentists.

In the end I had to find a practical solution.  Were we live there seemed to be no good solutions;  generally people with ASD just have rotten teeth.  A State hospital clinic did in theory offer dentistry under full anesthetic, but it looks like the hospital block of a gulag and there was a three month wait anyway.  Private dentists are not allowed to give sedation or full anesthetic, for safety reasons, just local anesthetic.

Eventually I found a solution in a neighboring country where you could have dental work under general anesthetic, in surroundings that did not look like a prisoner of war camp. Aged five, Monty had his four fillings and one extraction under full anesthetic with a German dentist and a Hungarian anesthetist.  The first part involves an injection into a vein in the arm, even this little step involved a great deal of kicking and screaming (Monty and his Mum).

So as not to repeat this unpleasant, and very expensive, experience too often, I stopped Monty drinking so much fruit juice and came up with a special tooth brushing regime.

One of Monty’s first words, aged about 40 months was “juice” and so pleased were people to hear him use any word, that juice is what he got.  In fact when he said “juice” he really just meant he was thirsty, water would have been just fine.  The acidity of fruit juice rots milk teeth.  Also, at the start of an ABA program, or even PECS program, there are a lot of edible reinforcers (candies) involved; great for speech, but not your teeth.

The teeth brushing regime involved brushing first with a manual brush and then again with an electric tooth brush.  This way there is more chance of not missing anything.

Monty at the Dentist Five Years On

Having not had any dental work for five years and still not having found a dentist who wanted to learn how to treat a child with autism, I was faced again with the undesirable option of full anesthetic.  I hoped that in the subsequent five years there might be some options closer to home.

While it seems that only hospitals can give full anesthetic, one of the small private medical clinics that also do minor surgery, has started to offer dentistry.  So I thought that if they have an anesthetist available for the minor surgery, why can’t the dentist use him?

A few phone calls later, it did indeed seem to be possible.  It clearly was not something they usually did, but the dentist did not think it was a crazy idea.

So last week Monty, myself and his assistant, who teaches him at home in the afternoon, turned up at the clinic.  Expecting to see an older male dentist with a serious face, I was very surprised to see a small slim female dentist and her smiling assistant.  It was as if we had stepped in to Dr Tesini’s training video.

All happy, smiling and fun, the dentist let Monty play with all the buttons and bits of equipment.  She made balloons out of surgical gloves and generally made friends with her new patient.

Her attitude was “why would I need anesthetic to treat such a nice boy”.  She gave him an examination, with Monty being surprisingly compliant.  She concluded that his toothache was caused by his four rear permanent that have yet to emerge.  One of the five year old fillings in his milk teeth looks a bit poor, but the X-ray showed that it is far from the pulp of the tooth.  The tooth should fall out before the filling fails.

In fact the only intervention is protective fissure sealant on four permanent teeth and ultrasonic de-scaling his front teeth.

I say “only”, but this still needs him to keep still with a drill inside his mouth and not bite the dentist or her to cut his tongue.

So far so good

After six visits, three teeth have their fissure sealant and one more visit remains.

Monty is friends with the dentist and is dancing to the music in the waiting room as he leaves for home.

Who could have imagined such a surprise at the dentist?