A Shade Of Grey

Joining the Wellsphere Health Bloggers Network

2008-07-04T02:17:00.006-04:00

A couple of weeks ago I received an offer on my blog email (which I must confess I don't check very regularly) inviting me to join the Wellsphere Health Bloggers Network. I thought about it and decided to join up. You're thinking "So?"

The reason I decided to accept was that this offers a potential opportunity to discuss autism with a wider group of readers outside of the autism community. When I first started this blog, I expected that most readers would be from the community of those touched by autism. While there is a wide spectrum of opinions within this community, there is - to really stretch a point - at least some common basis of knowledge and understanding about ASD. Outside of this community, this probably does not exist.

Unfortunately for the Bear, she lives in a society that not only does not understand her, but one that is often exposed to extremely negative perceptions about ASD and therefore - by implication - her. What society often sees is snippets of information - often inaccurate or incomplete - that suggests ideas such as 'autism is worse than cancer' or that autistics lack some of the features that make us human (um, then what does that make them?), or - my personal favourite - that "Without treatment, kids like this are usually institutionalized by the time they're adolescents. They're living in restraints, living in diapers. They have to have their teeth removed because they bite." That last one was actually written in a major Canadian newspaper by a respected columnist, quoting someone from F.E.A.T of BC, and accepted without question or critical comment.

Even within those who work with autistics and would hopefully know better, misunderstandings and misperceptions are not exactly uncommon. As an example, in the case of Carly Fleischman, I was disappointed by the amount of surprise, and especialy the amount of initial skepticism and/or disbelief of some who worked with her. I'm also disapointed by the unwillingness of some who should know better to consider that if Carly is an isolated case, then this may be due to lack of opportunity rather than lack of potential. I'm a believer that expectations influence results, and low expectations will often be met.

To be clear, I'm not suggesting that society should be sheltered from the trials and tribulations of ASD. I also understand - although I strongly disagree with - some of the excesses spoken by 'autism advocates' to paint a bleak picture to gain support for autism services. But how does this negative advocacy help society to accept my bubbly, smiling, happy little girl for whom she really is and is in the process of becoming?

As I wrote elsewhere,

"I believe that one of the things we need to work towards is ensuring that autistics are ‘just another group’ towards whom tolerance and acceptance is extended, accepting autistics for who they are now and for whom they will become. Regardless of whether one takes a neurodiversity perspective, a ‘cure’ perspective, or is within the great swath of opinion in between, we all have an interest in having society accept autistics, and accept and endorse the right of accommodation where required."

To my mind, the way that we will get there is through a greater understanding of ASD and autistics. As such, I decided to take the opportunity to potentially reach a wider audience, and to offer a more balanced point of view. I know that many within our community do not share all (or any?) of my views, and I am no more than one voice among many. I will be clear that I am not a spokesperson for autism, but instead am offering an opinion. But I will take this opportunity, for the sake of my daughter and others like her. And if you disagree with my posts, well, that's what comments are for.

Normal Female

2008-06-10T19:36:00.000-04:00

As part of the process and follow-up we went through to secure the Bear’s ASD diagnosis, we were eventually offered access to genetic testing. My first post was about autism and genetics, in which I suggested that while ASD has clear genetic links, there is evidence from MZ twin studies that more than just genetics or epigenetics is required to explain a significant proportion of ASD cases. As such, I was interested in what such testing might find.

I’ve also previously written some thoughts here on pre-natal genetic testing, if anyone is interested. But at this point, genetic testing of the Bear was presumably past most of the potential moral hazard issues. As such, I figured, why not? If any issues were to be detected then at least we would know and could plan for them.

So, last summer the Bear and I met with a Doctor who specializes in genetics and apparently ASD too, and went through all of the family history. The Doctor explained what they were looking for - in some cases particular alleles, in other cases duplications or omissions of genetic material – and how the testing would be done, and we agreed to go ahead. Some of the testing was to be done in the U.S., so we also had to fill out a form to get OHIP to cover this out of country work. It was approved, and we could proceed.

We waited until September to get the blood work done, as we wanted to combine it with a couple of other tests (regular stuff – nothing fancy). Let’s just leave it at saying that pinning the Bear down to draw blood is not an easy feat (she is quite strong! And feisty!), so we prefer to do this as infrequently as possible. We managed to get the blood with most limbs still intact (ours, not hers – she was fine), and off went the samples to various locations in Canada and the US for the genetic testing.

Four months after the blood draw the Hospital for Sick Children in Toronto (AKA Sick Kids) had announced another one of those
‘breakthrough autism tests’. We thought that we had probably missed this one, but this test too was performed.

It took several months for all of the results to come back, and last month I went in for a meeting with the Doctor to discuss the results. The test interpretation read:

"Microarray analysis of 622 loci using 1887 BAC clones for the subtelomeres, pericentromeric regions and known genetic syndromes (see attached list) detected no abnormalities in the DNA of this specimen. Thus, this is a normal microarray result showing no alterations of the loci tested."

All tests were negative. The Doctor told us that further research was being conducted, and that we should come back in about five years to try again. I wasn’t surprised at the results, but I was a bit relieved. Future tests may ultimately detect a genetic variation that caused the Bear’s autism, but I would not be surprised if the result instead is the identification of a genetic vulnerability rather than a genetic cause. Personally, I lean to immune/auto-immune causation in her case, but we’ll see.

The relief came from the fact that – at least so far – genetics has not proven to equate to destiny. Some may seize upon that statement as indicating that I’m a ‘curebie’. While I don’t disagree with those who are seeking a cure, this is not what I mean. FWIW, the Bear has been autistic for such a formulative period in her life that it has shaped her development, and I believe it will always be a part of her. But autistic thought and outlook to my mind is not the same thing as some of the difficulties associated with autism, and to the extent that these difficulties are not genetically based, they may be open to amelioration.

For those who need an example, the Bear constantly touches objects as she passes them, not in an investigative manner, but in what appears to be an attempt to generate location-related sensory input to be able to understand herself in relation to her surroundings. If so, then this suggests that she has sensory integration issues related to physical self-awareness within her environment, which - if anyone has read my 'ASD as a Developmental Disorder - A Suggested Neurological Underpinning' post – may ultimately result in significant further consequences related to her interoceptive capabilities. If so, then ‘fixing’ this particular SI issue could ultimately lead to the potential enhancement of other neurological capabilities (sorry, but you have to read that post to understand this – it is far too involved to fully explain here). It wouldn’t change who she is, but it could potentially add to her capabilities. And if I’m wrong on this, ‘fixing’ this issue would still enable the Bear to more capably and comfortably understand and maneuver within her environment, which presumably is a goal to which no one would object.

Anyway, I went away with a copy of the tests, and sat down that night to read them in detail. On the cover of the results was an explanation page, and in the space next to ‘Result:’ were the words ‘Normal Female’. This pretty much sums it up for me. The Bear is not neurotypical, and for a while we had some issues accepting this. I'd say that today we are much further along that path. We work hard to help the Bear become the best and most capable Bear that she can be. But along with this is an acceptance of who she is - our adorable and happy little girl. She is our everyday normal daughter.

Feeling A Little Optimistic

2008-05-01T20:28:00.000-04:00

From my last post, one might conclude that I’m feeling a bit pessimistic these days. Instead, I’m actually feeling a little optimistic. The reason is related to the Bear’s education.

Just to get the point out of the way, if anyone has an issue with IBI, my thoughts on the Bear’s program are here. Read this before you raise points about all the negative IBI practices that I’ve previously stated that our IBI provider does not follow.

Longer term, I’m still more than a little worried about the Bear’s education. The powers that be will probably try to boot her out of her IBI program when she reaches Grade One. IBI support does not automatically expire at this point, but rumour has it that the criteria become more stringent, as the intent is to hand over responsibility to the school boards. I’m also more than a little concerned with the possible direction that the School Board may want to take. They may want to move her to an ASD program in a different school. Our preference is to keep her local and part of the community, but that also depends on the local resources that are available (will there be an EA for the full day? One-on-one or shared?) and whether the educational opportunities will be better at another location. As well, what happens in the summer? Does the school have a program? If not, is funding available for other programs, or do we have to pay?

But for the short term, things are actually looking okay. I just had the regular IEP meeting with the IBI provider, and the Bear is making some progress. This year she rated on ABBLLS-R in nearly half the categories, vs. last year’s assessment, when she did not show up on the grid. She is also showing improvement in self-help skills, responding, some imitation, requesting, gross and fine motor skills, and social interaction. She can also match on identical and non-identical objects, pictures, and colours when she chooses to. So far so good. But the real optimism comes from the progress to date and the goals for the Bear’s communication abilities.

The Bear is non-verbal. She does make a variety of sounds, a couple of which have meaning, but they appear to be more mood related than specific words that are used to communicate with us. Despite the absence of speech, she does a reasonable job of letting us know what she wants, often by taking our hand and walking us to whatever she wants. including walking us over to sit down and play with her. She is also able to make choices when we present her with two or more options, e.g. juice vs. ‘(rice) milk’, or different DVDs to watch.

The Bear had also demonstrated an ability to use PECS to communicate. We used to use this at home, with a few different pictures. We stopped when the Bear destroyed the pictures through twisting, folding, and chewing them. Both JK and IBI were also using a small range of pictures, but with no formal program in place.

I started pressing earlier this year for the Bear to start learning the alphabet and numbers, so that we could start to teach her to read. I also expressed a desire to move towards acquiring a Communications device, so that we could begin to teach her how to communicate vocally/electronically. Unfortunately, you can’t just buy a device and put it in front of her (well you can, but….), or we would have done that long ago. She also needs to know how to use it, which requires some specialized teaching. Our issue was that we no longer had access to an SLP, having slipped between the gap between the 0 – pre-JK years (under the auspices of the local ASD support agency) and Grade One and up (the school board). We discussed it with our IBI provider, but they appeared interested but non-committal at the time, given the issues the Bear appeared to be having with matching (capable but no consistency). For obvious reasons, matching could be considered a pre-requisite for PECS Stage 3 (discriminating between pictures) and above. I knew that the Bear could match, having seen this skill demonstrated regularly, but she also needed to be consistent.

What a difference a couple of months have made. The IBI program altered their teaching slightly, and it turned out that the Bear’s ‘errors’ were in fact non-attempts and getting side-tracked in manipulating the pictures or objects rather than applying them. When motivated, she is quite capable of matching at will. IBI also increased their use of PECS after a bit of a hiatus, and the Bear showed that she was quite capable of communicating this way.

The other difference was Carly Fleischman. For those who have not heard of her, Carly is a 13 year old non-verbal girl with autism who has learned to communicate by typing words into a laptop that the machine then ‘speaks’. Just as importantly, Carly has demonstrated that you can’t judge the potential of autistics only by the capabilities and behaviours that can be readily seen. To my mind her major contribution has been to change perceptions – at least among those who are open minded - of what autistics are potentially capable of, given the right support, environment, and assistance. I have long thought of the Bear as another ‘Carly’ in the making, even before I knew that Carly existed. But Carly’s very public demonstration of the ability of autistics to think, understand, show emotion, and communicate (all of which should have been apparent - or at least not easily dismissed – by those who were paying attention) reinforced both my desire to push harder for a communications strategy for the Bear, and made it much easier to make the case to others – if they weren’t already starting to move in this direction in response to Carly’s example.

The net result is that a major part of the Bear’s learning is now focusing on communications. The IBI school has bought a Talk Board (pictures that ‘speak’ when pressed) to enable them to teach her how to use this. They are also working on strengthening the Bear’s PECS skills, and she is doing quite well. On Tuesday, in over 600 communications with multiple cards requiring discrimination she required only two prompts – both were related to the Bear wanting to turn on a video without first using the PECS card to request this. Given that she never had to use the card in the past, this was understandable, and once she knew the card was required, she adapted to that as well. Since then she has been progressing very quickly, traveling to communicate and communicating with the correct person in changing situations. The next step is to make a PECS binder that she will keep with her in JK and home, as well as at IBI. As this is mastered the Bear will be taught to use the Talk Board, and when she is ready we can transition to other technologies and a keyboard. In the meantime there will also be more emphasis on teaching her the alphabet and other skills to get her ready for this.

JK is also very much in alignment with using PECS. The Bear’s EA has had PECS training in the past, and has asked to visit the IBI school to see how they are using PECS with the Bear, in order to use the same techniques in JK. She is now enthusiastically waiting for the binder to start using it, as are we to use it at home.

Finally, another cause for optimism is how well the Bear is fitting in at school. For a while she was off on her own with the EAs for significant periods of time, duplicating a lot of the work that the IBI program was doing in the morning, and reducing her interaction with the other children in her class. The IBI program head did a site visit to the school, and recommended that the Bear be more fully integrated with the rest of the class, and the teacher and EAs agreed. The Bear is now more involved, and even has a couple of girls who are friendly and interact with her. When she is at the computer many of the other children apparently gravitate over to watch and take an interest in what she is doing. She has been well received by the school as a whole, and when the IBI head did her site visit she was very impressed with how much the rest of the school knew and regarded her – “They just love [the Bear]”. At different times she interacts with children from other grades in various activities, and everyone apparently knows and likes her. This to me is more good news, as one of the goals of having the Bear enrolled in JK was that she would fit in early and be accepted, rather than join the school later and potentially be perceived as an outsider.

So, there appears to be progress, we have a clear direction to follow and alignment among all concerned, and the Bear is already adapting well to the new focus. As such, I am feeling a bit more optimistic these days.

So Where Did That Parker Clown Go?

2008-04-08T19:29:00.002-04:00

Yes, it has been a while since I last posted: 131 days, to be precise. Unfortunately I’ve been busy, and haven’t been able to find any time to post, although I have a few in my head that I want to write. FWIW, I still consider this blog an ongoing concern, and I miss writing it. I miss the idea of crafting a good post, and while I’ve been waiting for my first one I’ve also enjoyed writing the stuff I’ve posted so far.

The following isn’t about autism, but it does explain my absence.

First, someone at my work decided that I should take on a new project - the same project that I haven’t had time to take on in the past couple of years. That person just happened to convince the company President and COO that this was a good idea, and that was that. Of course, new projects require project charters, which include details like business requirements (why are we doing this?) – too bad no one had any, so I had to make them up. The ironic thing was that there was an ongoing effort to get me out of my day job (which was the result of a past project that I was supposed to hand off – but the people I handed it off to screwed up and it landed back on my plate) to do something that the business really needed. But while no one could find a way to get me out of that role, they could somehow manage to find time for me to do a project for which no one could really answer ‘why are we doing this’?.

Timelines are also important. The part I liked best was when one Department said we need it by Date X. Isn’t it amazing how the amount of work required magically fit the required timelines – oops, not possible. My boss (on the org chart I reported to the Chief Marketing Officer, or CMO, but in reality I reported to the CFO – for the record I’m in neither Marketing nor Finance) kept telling me that the project timelines could reflect the amount of work involved and that he would convince the COO of this. But he seemed to give a slightly different message to the COO. So I wrote up the charter, with the full timelines, and it sat before the Management Board while they took months to approve it. Meanwhile, time was slipping away and the deadline wasn't and I was trying to move the project forward AND do my day job.

Then the owning company fired the COO, CMO, and CFO (surprise!), and their chief representative became the new President and COO. Everyone who reported to the CFO now reported to the COO – except me. That little detail about me reporting in theory to the CMO ensured that I now reported to his replacement, who held the position of head of a combined Marketing and Sales department. Did I mention that this was the person who said we needed the project completed by Date X?

Anyway, on to reason two (I’ll come back to reason one again). During this time, over Chrismas, my FIL died – theoretically of cancer, but in actual fact of starvation. He originally had felt uncomfortable after coming back from vacation nearly two years ago, and went to the doctor. The diagnosis – hepatitis. So he, my MIL and my BIL got their hepatitis shots, and wouldn’t you know it, but the diagnosis changed. Instead, there was a mass on his pancreatic duct (so how the #$%^ did they come up with hepatitis?).

He went in to the hospital to get a stent put in to allow him to eat while they figured out what to do next, and delayed things for a couple of weeks – all the while he couldn’t keep any significant amount of food down. Net result – he lost some weight. Then they decided to open him up and take out the mass. A three hour operation turned into six hours for a ‘whipple procedure’, in which they pretty much rebuilt his upper GI tract. But they thought they had got all of what turned out to be cancer. And guess what – he lost more weight. All through the winter and following summer he continued to slowly lose and gain weight (more loss than gain), and one of the biggest (he was a farm boy growing up – "strong like bull") and most vital people I knew was slowly wasting away. It wasn’t the chemo – he tolerated that very well – but he just couldn’t eat that much (no room and little stomach acid to digest what he could eat). But by the fall he was stable. He went off to Montreal for a big social event, and while there they got the phone call.

The cancer was back, and he was brought in for more chemo. And again he had trouble eating. It turned out that there was a constricting pressure on his ‘new’ GI tract that made it difficult for food to pass through (again). Since he wasn’t able to eat he began to lose weight more quickly.

He was brought into the hospital, supposedly to get a stent put in. He went in on Wednesday night for a Thursday procedure that was delayed. So he had to stay overnight again. And that was when they overdosed him on morphine.

His chart (we found out later) had him down for palliative care, rather than for the stent. And while he was in no pain, and told the nurse not to give him morphine (witnesses in the room clearly heard this) the nurse gave it to him anyway, saying that this way she would not have to come back later that night and give it to him then. She overdosed him, and he almost died. It took the weekend for him to (barely) recover, but he was not in any condition for the surgery for the first couple of days afterward. Meanwhile, he still wasn’t eating, and the most they would give him was a ‘fat pack’ on an IV.

It took over two weeks for the hospital to get round to putting in a stent. They kept dithering, not sure whether to do it or not, waiting for a cat scan, then more dithering. Should we put in a feeding tube? Well, that might enable cancer cells to spread into his stomach. Should we put him on chemo to kill the cancer cells? Well, no, because he wasn’t eating. Should we put in the stent? Well, it might not work and he needed the chemo. Meanwhile, he still wasn’t eating, and they weren’t giving him anything. He was literally starving.

My MIL and I ended up going to the hospital ombudsperson to get things moving, but apparently even that wasn’t enough. He was delayed again by the need for another cat scan (held up by that Chalk River incident), and when they got him in it didn't work because he was still full of barium from the last test (meanwhile the scarce isotopes that could have helped someone else were also wasted). Eventually they put in the stent, but by then he was really weak (remember, he had already been losing weight over the last year), and it didn’t work. He was still starving, and we had to keep insisting that he at least get a ‘fat pack’ IV. When he had this he was perfectly lucid and in no pain (other than from hunger). When they took him off of it he was barely there (probably without enough energy to power his brain).

The hospital called for a family meeting with his 'team' (sic). My SIL flew in from abroad with her 15 yo daughter (my niece), so she was there. My BIL, who was at school out of town, was also there, and I went in place of Momma Bear (she thought I’d have a better idea of what to do, and someone had to be available to look after the Bear). In the meeting they let us know he was at stage four. So why weren’t we told this earlier? My MIL would have taken him down to the Mayo Clinic had she have known, but by then it was too late. Did he want to go home? He murmured yes, but then the staff talked him and my MIL out of it, instead trying to push him into the palliative care wing of the hospital (where there was no space - he never made it), but in the meantime suggesting that they would give him better care than he could get at home. The doctor also told my MIL that if she didn’t like his care then she should get another doctor. This wasn’t the first time he told them this, but this time he told them in front of several hospital staff, as well as the family.

We also argued for IV feeding, to which the hospital grudgingly agreed – for five days! Apparently one’s veins cannot support a large IV for more than about five days (so they couldn’t find another vein?? Does he only have one?). This wasn’t “The Protocol” – and starvation was? – but they reluctantly did this. That night he was on an IV feed. The next day he became fully lucid again, and but didn’t remember the previous day’s meeting (for which he had no 'food').

Meanwhile, conditions got worse at the hospital. No one on the staff looked after him, and my MIL, SIL and BIL ended up doing shifts to make sure there was always someone with him, since the nurses rarely responded to the call button or offered any care. Momma Bear did overnight weekend shifts, as I was working and someone had to be home to meet the Bear out of school. If Momma Bear went down to the hospital she could only be there for a couple of hours at most, otherwise she might not be home in time for the school bus (and missing the bus was VERBOTEN). And we have no one where we live who could look after her as backup.

I won’t go into too much detail about the rest, but conditions were horrible at the hospital. Example – he had a fluid buildup that had to be drained every couple of days. My MIL noticed that one of the doctor’s was doing it differently and called him on it. Too bad. The end result was that he leaked fluid for the next couple of hours and soaked the bed. No one came to change the bed, so the family had to get him up and do it with the clean sheets that weren't provided. Another time they nearly overdosed him again. A nurse came in to give him his morphine and didn’t write it down. Ten minutes later another nurse came in and tried to give it to him again, but my BIL stopped her. The family had to bathe him, as the nurses didn’t. And then there’s the IV line. They finally agreed to put in a PIC (sp)?, which is a line into a major artery (or vein?) so they could give him a proper feeding tube. So they gave him the surgery to put in the PIC (painful and then uncomfortable), and then only rarely gave him a feeding bag. All the while he was still starving.

By mid December my work schedule was relaxing a bit (no boss and no organization to speak of as everyone tried to figure out what was going on with the new organization), so I could give more help looking after the Bear. So I worked at home until noon, then went into the office and came home around 7 PM. Momma Bear would head off to the hospital, come home around 4 AM, and would sleep until noon when the cycle began again. We did this until close to Christmas, when I was home and things relaxed a bit – although Momma Bear still had the same shift, and I took the Bear and pitched in with maintenance and shoveling at my MILs house. I took the Bear over to my mother’s for a very quiet Christmas (we normally spent it with my monther, FIL and MIL, and family), as Momma Bear’s family were in no mood to do anything (and they were all still doing shifts at the hospital). A few days later my FIL died. Did I mention that one of the last acts was for the doctor to prescribe him a suppository for his pain? But no one was there to administer it, so my SIL’s friend (a nurse) had to do it. What kind of place expects you to self-administer your own suppository in your last few hours on your deathbed?

And then there was the family BS that went along with all of this. A friend of mine said “What’s the definition of a dysfunctional family? One with two or more members.” My BIL and SIL both went after Momma Bear for not doing what they considered to be her share. Neither of them had any responsibilities other than for themselves (oh, and for a fifteen year old who could get her own food and hung out with my SIL’s nurse friend’s daughter). Meanwhile, I was still working and we had to tag team to look after the Bear, who requires significantly more care than a toilet trained 15 yo who knows how to get her own food and wipe her own bum (sorry, but I’m a bit peeved). A few minutes after my FIL died, my wife went over to the bed to be with him. My SIL came over and said “He’s dead now. Why are you still here?” My SIL’s nurse friend very quickly dragged my SIL away before Momma Bear could react (good thing, too).

BTW, did I mention that in the past Momma Bear quit her job and looked after my MIL’s mother (her Grandmother) for TEN years, while the rest of the family did close to nothing? The grandmother was a lot of work and had attitude (that's an understatement), and my wife did everything for her (bills, doctors, shopping, cleaning, outings, everything). No one else would help as the grandmother was more than just a bit of a handful. In the last year and a half of her life after we moved out of town my MIL and BIL finally pitched in. But Momma Bear didn’t do her share? Momma Bear also has some health issues of her own and is now quite worn out.

Anyway, back to the office. By the new year the new President and COO started to find out what I could do and what my experience was in my past life (meant not in a Shirley MacLean sense, but in former jobs at other companies), and assigned me to head his pet project. So now I was reporting half of the time to him - unofficially - and the other half to the CM&SO, with two big projects. And wouldn’t it figure that my role on the COO’s project led me into the opposite side of a series of major decisions with the CM&SO. Fun times for all! Eventually (two weeks ago), my reporting relationship landed in one place (the COO). The first project was put on hold (no, it hasn’t vanished - that's what summers are for), and now I only have one big project, plus a new role, plus the CM&SO indicating that things aren’t moving fast enough on work he wants from me, and I’m still responsible for my old role as I’m trying to train up two other people to take it over.

So I’ve been busy, Momma Bear is worn out and needs more support, and I’m only now beginning to find some time to post to my blog. As I said above, I have a few posts in my head that I want to write, and hopefully I can find the time to do so soon. But I’ve been a little busy.

Just A Small First (But a Big One for Me)

2007-11-29T18:05:00.000-05:00

We used to have a big white cat. Every day when I got home from work he would come to the door to greet me and 'stripe' me (as big, white, shedding cats are prone to do as they rub past your leg). Eventually he got old and difficult to care for, and a few months after the Bear was born, Momma Bear said it was time for him to go. I protested, and amongst other things used this daily greeting as an example (one among many) of something that I would really miss. Momma Bear promised that soon enough the Bear would be greeting me at the door, and that this would also make my day. So off went the cat - to the outlaws, where he lived quite happily for another year or so - and I waited for the day when the Bear would start coming to the door to greet me.

But the Bear, despite being very affectionate with me at other times, never came. She will often give a big smile, and sometimes get up to greet me after IBI, where she's waiting on the couch by the door when I come in. This alone is special - the couch there is a big comfy magnet for her, and she doesn't willingly jump off of it for just anyone - but she never did this at home.

Yesterday I got home from work as usual. Normally I go in, and after getting stuff put away and settled I go and find the Bear and spend some time with her. Not yesterday though.

After bringing in the groceries I started taking my boots off, and Momma Bear called out, as she sometimes does, "[Bear], Daddy's home! Daddy's at the front door." I heard the Bear bouncing on the mini-trampoline (she loves to bounce on it on her butt) in the living room (yes, living room - where do you keep your mini-trampoline?), but then the noise stopped, and I heard the pitter patter of tiny footsteps down the hall. The Bear peeked round the corner, looked at me, gave me a big smile and quickly came over to greet me. I went down on one knee, and she came over and sat on my lap and leaned into me (a 'Bear' hug). This was the first time that she had ever come to greet me at the front door.

I told her how nice it was that she came to see me, thanked her, told her I loved her and missed her all afternoon (I do the shuttle between IBI and Junior Kindergarten, so I see her at lunch), and picked her up for a big hug and a spin. Daddy is a big amusement park full of assorted rides and spins, and the Bear loves all of them.

Hopefully she will come to the door to greet me again soon. But regardless, this first was special, and easily the best greeting I've ever had. I still sometimes miss the cat, but I now have the prospect of other special welcomes to look forward to.

‘Autistic’ vs. ‘Has Autism’

2007-11-22T20:20:00.000-05:00

One of the many points of contention in the world of those touched by autism is the way in which one who has a diagnosis is labeled: ‘autistic’ or ‘has autism’. While I don’t think about this too much, I was watching a movie on Sunday in which someone referred to a child as ‘autistic’, and the parent deliberately corrected the person with the statement ‘has autism’. That started me thinking about the divide.

I tend to use the term ‘autistic’, in part because it is a term that appears to be favoured by those with the diagnosis who have an opinion on the subject – e.g. see Jim Sinclair here. But I’m not particularly fussed by the use of ‘has autism’, and (if anyone cares) I find this description to be not offensive (unless one wants to be offended), but merely incomplete in its descriptiveness.

Not everyone feels this way. A researcher who replied by e-mail to my ‘ASD as a Developmental Disorder - A Suggested Neurological Underpinning’ post (no, I will not say who it was, and I quote this strictly to show another POV, not to challenge the researcher) wrote the following:

"A minor point, but I have always been told that it is impolite to use the word 'autistics' as a noun. I tend to write 'people with autism' or 'autistic children' instead. I realize opinions differ widely on this type of 'political correctness', but many journals now ban the term 'autistics' and I find it grates when I read it."

While I don’t agree (and I wrote back to explain my use of the term and to forward a link to Jim Sinclair’s above-mentioned post), I think I do understand why people might feel this way. Not to link the person above to Jenny McCarthy, but I also recall hearing the other parent who did the road show with her clearly make the distinction between the two terms, favouring ‘has’.

The dividing line between the two terms of reference – the difference between ‘is’ and ‘has’ - seems to be in related in part to one’s view of ‘cause’ and ‘cure’. If one believes that autism is a disorder/disease, and therefore as a negative, then it is presumably something that happens to a person rather than being part of them. As such, it would not define the person (i.e. ‘is’), but is instead an affliction that someone ‘has’, and which may therefore be potentially subject to elimination (i.e. the person ‘does not have’ autism after being cured). After autism has been removed, the person presumably still ‘is’, even though they ‘no longer have’.

A related point is that some use ‘has’ because they want to convey that the autistic person is more than just autistic, such that autism alone does not define them, but is only part of the story. Also, if autism is seen as a negative, then that is a further reason to distance the person from the disorder. ‘Has’ suggests that this negative is not a core part of the person but an add-on that does not define them as much as modify them. It enables the speaker to distance the person from the negative, in that the negative does not define them but instead moves them off course from the person that they truly are (or would be if they were not autistic). I would suggest that many who do not believe in the current possibility of a cure still see autism as such and use the ‘has’ descriptor.

If, conversely, one believes that autism is an inseparable part of a person, it is therefore an ‘is’, and part of their ‘being’, rather than a ‘has’. Many who hold this view are anti-cure, suggesting that a cure would change who the autistic person ‘is’, to the point that the original person would no longer exist. Further, I’d suggest that while those who see autism as an ‘is’ would agree that it brings definite challenges, they would not see it as a negative as much as an ‘other’, a natural variation that has its positives and negatives. As such, one of the fault lines in autism runs along the ‘is’/’has’ divide, not just between cure vs. anti-cure, but also between natural variation and a disorder/disease model.

From my perspective, I’m probably on the wrong side of line. I see autism as a disorder with potentially many causes, but one that occurs in those who have a pre-existing and underlying natural variation that makes them vulnerable to autistic disabilities. My issue as such is not with autism per se, but with autistic disabilities. The distinction is too complex an argument to present here (it is embedded in a fairly complex forty-plus page post here), but in a highly summarized form I would suggest that autism is the result of a different developmental path that is strongly impacted by underlying neurological issues manifested in the anterior cingulate cortex and especially in the anterior insula (AI). There is considerable evidence about the role of the anterior insula in general, and it is in this area of the brain that I would suggest the major autistic sensory integration issues are derived. If this hypothesis is correct, then ‘curing’ autistic AI issues would significantly increase the SI capabilities of autistics and open additional developmental pathways, but this would not immediately change who they are. Instead, it would open other potential future paths that would be equally as authentic and true to the person as their existing developmental pathways, but without compromising existing development. As such, the resulting new capabilities would be additive rather than displacing or superseding the existing set.

Despite the above, I still feel that the ‘is’ term is appropriate. To my mind autism really is both profound and pervasive in its role in the lives of those who qualify for a diagnosis, regardless of whether one ultimately believes in the possibility of a cure. I see the term as being explanatory rather than negative or pejorative, and as such it is nothing to distance my daughter from. If a ‘cure’ is found (from the above, my definition of ‘cure’ – ‘the addition of neurologically-based capabilities’, rather than ‘becoming NT’ - is probably different than that of most people), I would then say that my daughter ‘was autistic’ if as a result the diagnosis no longer applied.

Having said that, I do not feel that using ‘autistic’ indicates or suggests that autism is the sum total of the person. The Bear, for example, has a ‘severe’ diagnosis, and yet does not share several of the characteristics that many expect of autistics (as an example, she has no issues with spontaneity or changes in routine – except perhaps when there is not enough of either). Other autistic children I know also each have characteristics that don’t conform to stereotypical expectations. They each differ widely enough that one of my current expressions is "If you’ve met one autistic, you’ve met one autistic." (as opposed to “you’ve met them all”). In the Bear’s case, autism no more totally defines her or sums up her existence than ‘Canadian’ or ‘female’ do, yet she ‘is’ both of these too.

I find it interesting that people who insist on ‘has autism’ would probably use the terms ‘paraplegic’ and ’quadriplegic’ without a second thought, rather than using ‘has paraplegia’ or ‘has quadriplegia’. To be clear, I am not comparing autism with either of those conditions in any way other than their potentially profound and pervasive impact on those so identified, and I am not suggesting that any of the three terms limits or completely defines the people so identified. Instead, the comparison is intended to highlight the discrepancy in the terminology used in each case. Why would one term be unacceptable while the others are not?

I am comfortable with the term ‘autistic’. If others are not, I believe that I understand why, but I will politely disagree. They are free to do the same.

Call off the Search Parties

2007-11-22T20:03:00.000-05:00

Just a quick post to let anyone know who is wondering what happened to Ian that he and his family have been found safe and sound, somewhere in Ontario. Unfortunately Ian has been quite busy with various activities, preoccupations, duties, chores, perseverations, etc. over the past ten weeks (has it really been that long?), but promises to do his best to continue to maintain this blog as a going concern. This is not an abandoned blog (Honestly!). Several posts are currently percolating, but finding the time to complete them is an ongoing issue. Ian may even try at some point to post a picture of the Bear dressed as a giraffe for Halloween (it is much cuter than it sounds) if it is not too late to do so.

For those who were not wondering about Ian’s extended absence, why are you still here reading this?

Encouraging Tolerance and Acceptance in Public Schools

2007-09-14T17:28:00.000-04:00

(No, this is not the ‘Acceptance’ post that I keep saying I’m going to write. But I have started it…)

I’ve been thinking about tolerance and acceptance for a while now, and with the Bear’s entry into Kindergarten the subject is very top of mind. Recently (at least in ‘Ian time’) Kristina posted What is your dream autism school? over at AutismVox. One of the comments particularly struck me:

"The public school’s sole responsibility is to educate children. It is not the public school’s responsibility to dictate sociological norms, ethical norms, and religious norms. The public schools have repeatedly displayed time and time again that they will never be able to adequately parent a child. The society that expects a public school to parent to the children they teach is always weakened by that expectation."

To which I responded:

"Other than on the last one (religious norms) and softening the word ‘dictate’ (I would suggest something between disseminate and encourage) I would disagree. Part of educating children is teaching them about the rights and responsibilities that come with being part of society. Building ‘good citizens’ has been an implicit - where not explicit - part of the public school agenda since the beginning of universal public education, in the U.S. and much of the world. In the Western world the rise of the nation-state and the introduction of universal public education went hand in hand. This is not the same thing as ‘parenting’.

Teaching tolerance and acceptance of diversity is a legitimate social goal, especially as societies themselves become increasingly diverse. At least in my daughter’s school this is stated as one of the benefits - for the entire student population - of inclusion."

What amazed me in the back and forth that followed was that there should even be any debate about this. (What didn’t surprise me was the typical practice of responding to ‘what I want to say you wrote’ rather than what I actually did write.) Regardless of whether public schools ARE teaching tolerance and acceptance – which is a different, although related issue - do people not feel that teaching tolerance and acceptance of others is one of the school system’s responsibilities?

To those who argue that the school’s responsibility is to educate, do they not feel that social education is also part of this? Children do not sit isolated in cubicles but are part of a classroom and a school, and ultimately of a community and a society. Are schools not responsible – along with parents - for teaching students how to behave, interact, and treat others in that classroom, school, community and society?

To be clear, I'm not arguing against educating autistic children in separate classrooms or separate schools (or private schools), where appropriate, required, or desired by the family. Instead, I am stating what I believe is the responsibility of the public education system to all students and to society.

In the Bear’s first ‘Friday file’ (the school batches up a lot of communication into a folder that is sent home every Friday, to be read and initialed by parents for return on Monday morning) was a pamphlet entitled “Safe and caring schools”. In this the School Board stressed the importance of school safety, and that this is a shared responsibility between the school, the student, and parents. The Board indicated that:

"We work with parents and the community to help children and teens develop social skills and appropriate behaviours as they learn and grow. We teach all children about safety, healthy choices and positive values and behaviour."

Further, the pamphlet indicated that it is the school's responsibility to (among other items):

”- teach positive behaviour and good citizenship"

" - teach acceptance of and respect for others”

and that it is the student’s responsibility to (among other items):

" - be courteous to fellow students and staff"

" - show respect for the rights and feelings of others"

Parents also have the responsibility to look for ways to reinforce the same messages at home.

The School Board further indicated that "We do not tolerate violence, harassment, racism, verbal and physical abuse, bullying, fighting… intimidation… or any other dangerous, detrimental or inappropriate behaviour" and also that "there are clear consequences for inappropriate behaviour". At a minimum, the School Board has at least accepted and taken ownership of this responsibility.

Some might say that this is just a pamphlet, paying lip service to concepts that are quickly forgotten. But at least in the Bear’s school, this appears not to be the case. In various ongoing talks with the principal and the ASD coordinator, they both have specifically indicated that the school takes a very inclusive approach, where possible, and that one of the benefits of this was that of teaching tolerance and acceptance to all of the children. They also indicated that they ‘buddy-up’ special needs children with peers and older children to help them fit in and find support within the wider school environment. The policy is not one of forced inclusion (there are other options available besides mainstreaming, where appropriate), but of accommodation and support within the school and community environment.

My neighbour’s children previously attended the same school (the youngest finished her last year there in June, before moving on to the next school level this September). I had earlier asked them about whether there were any autistic children at the school, how they were treated, etc., and specifically asked about bullying. The younger child was a ‘buddy’ to one of the autistic children, and indicated that the child was an accepted part of the group and was fun to play with. She considered him a friend. She and the rest of her family also indicated that bullying was not tolerated, and that it was not an issue at the school or in the community.

Since the Bear is new to the school, I can’t say how well the school system will ultimately live up to these ideals in her case. But what I can say is that these principles are an accepted part of school policy and appear to be part of the school and community culture. Today when I dropped the Bear off I talked to the EA about how she was doing, and how well she was interacting with the other children. One of my questions was ‘How well are the other children accepting her?’ So far so good. I indicated that I thought it was just as important that the other children learn to accept the Bear as it was for her to interact with them, and the EA strongly indicated her agreement.

In Ontario, we’re now in the middle of a provincial election campaign. One of the big issues is public school funding, and whether it should be extended to religious schools. I’m not going to dive into the issue, but what I would say is that all three major parties are committed to the idea of Ontario schools being a place of social integration. The party supporting the extension of funding to religious schools is discussing the issue at least in part in terms of bringing them into the public system, teaching the standard curriculum and adhering to provincial guidelines. The parties opposed to this reject the move in part as being counter to the objective of integrating various cultures and religions within the public school system. What is interesting is that all parties appear to see schools as a method of integrating various cultures within a multicultural society, not via conformity but through tolerance and acceptance of differences and diversity.

This is not to say that we don’t have problems, or that everything works here. There are major issues connected with public education in this province (including funding), as well as social issues that need to be addressed. But I would suggest that the idea of the school system being an agent of societal integration, with a mandate to encourage tolerance and acceptance, is a very mainstream idea in this province.

I believe that one of the things we need to work towards is ensuring that autistics are ‘just another group’ towards whom tolerance and acceptance is extended, accepting autistics for who they are now and for whom they will become. Regardless of whether one takes a neurodiversity perspective, a ‘cure’ perspective, or is within the great swath of opinion in between, we all have an interest in having society accept autistics, and accept and endorse the right of accommodation where required. This is one of the areas in which presumably the whole community of those touched by autism could agree? For those who take a neurodiversity perspective I’d suggest that this is probably obvious, but even for those pursuing a cure, presumably the rights of autistic children to acceptance and accommodation as autistics should be accepted and respected until their cure is achieved?

Social change can sometimes happen quickly, but some changes take time to permeate through society. The public school system is probably the most universal of all social programs (the Ministry of Transportation / DMV probably comes close, but it would be difficult to teach acceptance of diversity as part of a driving test). If we do not expect – and where necessary, demand – that the school systems take ownership of their responsibility to teach tolerance and acceptance to the next generation, and ingrain this within society - and hold them accountable for doing so - then who instead do we expect to do this?

Maybe Oprah?

Again, I fail to see why this is controversial.

Ch.. Ch.. Ch.. Ch.. Changes

2007-09-05T20:21:00.000-04:00

Today marked the transition of the Bear from pre-schooler to student. She bravely marched into her combined Jr and Sr Kindergarten class, head held high, backpack on, and, well, a little tearful. But her day went well.

Everyone accidentally overslept this morning, and despite the previous night's preparations for the Bear’s first day at school, of course everything went wrong. Wrong snacks, wrong clothes, no 'first day artwork’ done, etc., and no time to make everything right.

I also missed taking the Bear’s ‘first day of school’ picture. Momma Bear has a picture of her first day at school, taken on the driveway before heading out, and I thought it might be a good tradition to follow. But with the rush and a big outburst of tears I thought that this might not be a Kodak moment. Without a picture we can let glossy memories fill the void.

I drove the Bear to school, as we do not have bus service ‘there’. We couldn’t arrange transport between the Bear’s IBI program – which is ‘out of area’ - and school, and the bus pickup time was unworkable unless we could teleport the Bear home. Once there I put her backpack on her and walked her across the parking lot to the Kindergarten door, and her EA came out to meet her. The Bear was a bit tearful, but walked in, and I had a very brief chat with the EA regarding the contents of her backpack, etc.

“What do we do if she cries?” the EA asked. “Well, give us a call and I guess I’ll come and pick her up”, I answered, thinking with my overprotective pre-school hat. The EA gave me a look and I realized that no, that was no longer an appropriate answer, if it ever was. “How do you calm her down?” came back a second question. I gave a lame answer and then it was time to go. I mentioned that I would be back at 3:00 PM, just in case there was an issue with the Bear taking the bus for the first time - feeling like the overprotective Dad that I told myself I would not be - kissed her goodbye, and left.

When I came back just before 3:00 PM, the buses were lined up, and three short buses were parked nearby. I went up to the drivers and asked if any of them had the Bear on their list. One did, and I introduced myself. I also asked if the bus driver had the same understanding I did (from the ASD coordinator) that the bus would come up our driveway. Nope.

I went back over to the school, met a couple of other ‘first day’ parents, and then the EA - who was helping with bus duty - came out. She said that the Bear had a GREAT first day. She was interested, looked all around the classroom, taking everything in, and went up to the other children and tapped or gently poked them - a cross between “Hello” and a curious “Who are you?” She ate her snack, only one diaper change, and she was now sitting in the Gym with the rest of the school, lined up in their bus routes. Would I like to go in and take a look?

I went in and was quite impressed with the efficiency with which everyone was being organized for the trip home. And in her line of two was the Bear, sitting and lounging back on the backpack she was wearing, smiling, and quite content to take it all in. Eventually she sat up and started crying. The EA went over to comfort her, while I deliberately stayed away and went outside.

Soon enough the kids came out and got on their assigned buses. The Bear came out and was still crying, until the EA took off her backpack. The tears stopped immediately. Dad kicked himself that he did not acclimatize the Bear to the backpack over the summer like he was supposed to have done. The backpack was fine, as long as someone else carried it. I think the Bear is destined for management.

She was supposed to get on her bus, but the EA first checked her seat and noticed that there was no child seat for her. She called over the bus coordinator and (nicely) called on him to make the obvious decision that it was not safe for her. So the Bear went home with me, while the EA indicated that she would immediately get the process started to get a seat installed for the Bear. Another issue, but I was impressed that the EA was conscientious enough to catch this and deal with it. On the way back to the car I noticed that the other two small buses had lots of children on them, which was also a relief. The ‘short bus’ was normal transportation here, rather than a source of stigma.

So, all round it was a slightly mixed up day with a few issues, but the Bear had a good first start, which is the most important thing. She is no longer a pre-schooler, but a public school veteran. Tomorrow she has her first full day, with IBI in the morning and Kindergarten in the afternoon, so we’ll see how that goes. But given how well the first day went, I think that the Bear might adapt to Kindergarten just fine.

Another BM Post (Sorry...)

2007-08-16T18:17:00.000-04:00

I started this blog because my daughter is autistic, but these days autism is definitely a secondary consideration - dare I say a luxury? Life is now about bowel movements – the Bear’s, not mine. In an earlier post I promised to do my best not to write about this subject again. So instead, let’s just say that this post is about GI tract issues.

The Bear’s constipation issues are now always with us to some degree or another, but fairly recently we seemed to be on top of things (figuratively speaking), getting her down to two to three days between BMs. But nothing lasts forever.

For those who have any doubts as to my position on autism and GI tract issues, my working hypothesis these days is that while GI issues may not directly cause autism, there is definitely room for a relationship between the two – i.e. a comorbidity. As I noted in the ‘Kitchen Sink’ section of my ‘ASD as a Developmental Disorder’ post (in which I suggested that there is evidence that the Anterior Cingulate Cortex (ACC) and Anterior Insula may play a major role in autism), Devinsky et al (1995) noted a potential link between ACC seizures and muscle tone. Further, Ming et al (2007) identified hypotonia as the most common motor symptom (51%) in a study of children with ASD. I would suggest that given the ACC’s role in autonomic functions, including digestion, plus its potential link to hypotonia (which presumably can also affect the muscles of the intestines), that low GI tract motility, like ASD, could potentially be related to ACC issues. If not, GI motility and hypotonia could still be related. To be clear, I’m not suggesting that GI issues are universal in those on the spectrum. But I would suggest that in some cases the two could at least be comorbid. I also could be wrong. Regardless, I don’t expect any protest directed towards my call to 'Cure Low-Motility Now'.

We know that the Bear has motility issues, given the length of time it takes certain foods to transit the length of the GI tract. This is not the only cause of her constipation. We also know that she ‘holds’. Given some of her BMs (the word ‘brick’ comes to mind), I can understand why. And unfortunately it is difficult to reason with her (I try, I really do) that ‘holding’ makes BMs more difficult, while ‘going’ will lessen the issues over the long term. Our regimen so far has been Lansoyl (the sole contribution of our GI Specialist), kiwi fruit (seems to help a bit), and suppositories, as required. Suppositories are a last resort, when the Bear ‘stances’ (yes, this has gone on long enough for us to have developed our own terminology) – sitting, leaning back, stomach tightened, arms flapping, legs extended and pointing, as she tries to ‘hold’ – on and off over an extended period (usually at least a couple of hours, often several). Unfortunately, this last resort seems to be invoked about half the time, although we recently saw a reduction in the need to intervene.

On Sunday a couple of weeks ago the Bear had a BM after a five day hiatus. We didn’t think it was quite ‘enough’ (it is hard to tell - is there a standard for this?), but we expected another BM on Monday or Tuesday. No luck. And no ‘stances’. Perhaps we were wrong about the volume? By Wednesday afternoon she seemed a bit reluctant to drink her (rice) milk – normally it is almost the Bear's mission in life to grab us by the hand and lead us to the fridge to request this - but only slightly. And she seemed in good spirits. We took her to Canada’s Wonderland for the evening, and she had a good time, despite the oppressive heat and humidity. But Thursday at music therapy she was totally uninterested in her milk, pushing it away. This was very strange indeed, since she usually requests milk at least a couple of times during the 45 minute session. But she still seemed okay. Getting her to eat her dinner took some effort (a video, a book to read, parental singing and dancing – yes, dinner sometimes becomes ‘dinner theatre’) but she ate it. And we were still at day four, so no alarm bells were going off yet.

Supper was a different story. The Bear drank her evening milk very slowly. Momma Bear then gave her a bath, in which she drank a lot of bath water (from the tap as she was ‘showered’). By supper time she was very reluctant to eat, but the entertainment prevailed and we got some food in her.

Suddenly, everything came out - milk, food, and bath water - but from the wrong end and with considerable velocity. Everywhere. Momma Bear threw her in the bath to clean her up while I mopped up. We checked her temperature (no fever), and then put her to bed for the night.

The next morning we checked her temperature again (no fever), and felt her belly. I noted a reasonably firm spot below her navel (but not being a doctor, I wasn’t really sure what I was looking for), and we discussed taking her to the doctor. I wanted to take her in, but she was eating (reduced portions to go easy on her) and drinking again, and seemed in good spirits, although a little subdued. Momma Bear thought that maybe she picked up a bug from the amusement park, or maybe wasn’t agreeing with the heat, or drank too much water during her bath. So we agreed to hold off for a day, and upped the Lansoyl dose. Still no BM.

Saturday we again debated taking her in to the doctor. The Bear was a bit sluggish, but still seemed in good spirits. We waited for any stances (none). We were supposed to go over to my outlaws’ that afternoon/evening for a farewell gathering of family and friends for my sister-in-law and her family. They were in town for the summer, but heading back home to another hemisphere in a couple of days. We went reluctantly that evening, taking the potty and bath tub, just in case. We figured that we could take the Bear to the local children’s hospital if need be, as it was not too too far from the outlaws’ house.

At the outlaws the Bear was very sluggish. She cuddled up with her grandfather, which was not unusual, but later, rather than wanting to wander and explore she just wanted to curl up on the couch and be cuddled by various family memebers. She did request her milk though, so we thought maybe she was starting to feel better. But we did discuss taking her to the doctor the next day.

I crashed on the living room floor and the Bear came over and curled up beside me. Everything seemed okay, but then she sat up, and everything came up again – everywhere (including drenching me), and again with considerable velocity.

This time there was no debate. After getting a change of clothes (my father-in-law is much bigger than me, so there was actually some humour in this - somewhere) I put the Bear in the car and headed for the children's hospital. I figured that we’d have a better chance of finding someone there who understood both pediatric GI issues and autism than we would at a local hospital. Since it was late, Momma Bear stayed at the outlaws to get some sleep, so that she would be rested enough to take over the next morning. The expectation was that the Bear and I would be at the hospital until the wee hours of the morning.

We checked in at midnight, had a quick triage assessment, and then sat in the waiting room. Another girl, probably around 10 or so, was there with her father and kept throwing up into a bed pan. The Bear found this fascinating, and walked over to look at her several times. I explained that the Bear was probably interested in the fact that the girl had the same issue as she did, and the girl and her father were quite good natured about this.

Other than that though the Bear was still sluggish, and was quite content to curl up in my lap and sit. Not sleep. Just quietly sit. Normally she would have taken me by the hand and pulled me around exploring. Not this time. Other than visiting the other girl a few times, we did only a couple of tours of the waiting room and hallways. Eventually we had a second triage assessment (1 AM), in which I was given some pedialyte and an oral syringe (with not much luck giving this to the Bear), and were able to register (about 2 AM). The only commotion of the night was about 15 minutes of tears from the Bear when they put the hospital wrist band on her. Once she calmed down it was back to quiet waiting.

The waiting room was rather full, with people trying to lay flat across groups of chairs. We were able to get two chairs, and I sprawled awkwardly across them with the Bear curled up on me (I would have given her both chairs to sleep, but then I would not have been able to be near her, and I was worried that she would fall off onto the floor). And we waited. Other than people getting called out to register before returning, no one moved until 6:00 AM (when a nurse came around with apple juice). The ER examination rooms were occupied, and the whole system was backed up (an appropriate metaphor).

At 6:30 AM a couple of families moved out into examination rooms, and that left a three chair combination open, which I grabbed, again with the Bear sleeping on top of me. Ah, luxury. By 7:30 AM we were given an examination room, which was cold. But I was at least able to put the Bear on a flat surface and cover her with a sweat shirt.

At 8:00 AM we saw the first doctor, who was ‘new’ as she put it. I gave her the Bear’s history, and then the Bear was thrilled to be woken up, and sat passively (yes, this part is fiction) while she was poked and prodded and had her temperature taken. We finally had to wrestle her down so that the doctor could feel her belly, but with all the wriggling the doctor was unable to feel anything. I mentioned that I had felt a firm spot on Friday, and the doctor said she would consult with her supervisor. The Bear fell asleep again, and when the senior doctor came in he was able to feel her belly without any resistance. Yes, there was a ‘lump’. The doctor indicated that Lansoyl was not going to move it, and we ended up with a prescription for a pediatric dose of the same product that is used to clear intestines prior to a colonoscopy.

By 9:30 AM we were out of there (yes, only 9.5 hours), and went back to my outlaws. We let the Bear sleep while I went to the pharmacy to get the prescription (which turned out to be an ‘over the counter’ medication) and some pedialyte to replace the Bear’s lost fluids and electrolytes. Back at the outlaws it turned out that everyone knew about the meds, including other relatives from out of town who had stayed over. I think my wife and I were the only people in the house who had never had a camera shoved up our … (Does everyone get this? Maybe it’s a Canadian thing). Anyway, everyone loved the product and commented on how well it had worked for them (thanks to all for sharing).

We woke the Bear around noon and gave her the meds and required liquids, and got the potty ready with a big pot underneath. Within about three hours she showed signs of movement, and we put her on the potty. Whoosh. No more blockage, and one very relieved and happy (but tired) Bear. But it still didn’t seem like enough came out.

Of course, that wasn’t the end of things. For the next week we kept waiting – in vain - for some action. We held off giving her Lansoyl for the first couple of days, since it slows absorption, and she had eaten and kept down a lot less food than usual over the earlier period. But by mid week we started again, and the doses kept increasing. Finally, by Saturday morning (day six again) we moved on to lactulose, which the hospital had recommended if Lansoyl wasn’t working. Saturday night we were rewarded. Another dose brought a similar reward on Sunday. Monday and Tuesday’s doses did not pay out (panic rising) and by Wednesday we were wondering if even the lactulose was going to fail us. But Wednesday night saw further success, albeit after a prodding with a suppository. This morning we skipped the lactulose (the doctor indicated that it does not cause dependence, but the label on the bottle disagreed), but will maybe try it every second or third day as (if) required. At least we have another option. And there is always the colon cleaner as a fallback.

Now with this out of the way, all we have to do is get through the adventure of Friday’s MRI (that's another post).

So what was that autism thing again?

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On an (hopefully) unrelated note, my site meter indicates that I've recently crossed the ten thousand mark. My biggest readers are probably Google, Yahoo, and Microsoft (i.e. search engines), but to the rest of you who have stopped by, thank you for visiting. I know that 10,000 is a drop in the bucket compared to some blogs, but considering that I'm unaffiliated, I'll take the compliment.

Interestingly, I had more weekly visitors during my nearly four month hiatus while I researched and wrote the 'ASD as a Developmental Disorder’ post than I do now. With a few more posts like this one, maybe next year I'll be celebrating my 11,000th visit.

People Make The Difference

2007-07-31T19:55:00.000-04:00

This year will see some significant changes in the life of the Bear. She will be entering Junior Kindergarten in September, and June saw some activity associated with preparation for that event. The same month also saw the Bear reach the top of the waiting list for IBI funding from the provincial government. Either of these events could have gone well or not so well. But fortunately, good people have made a difference.

I'm looking forward to the Bear starting JK in September. The school has been good so far. The Bear and I had a meeting in early June with the principal and ASD coordinator. She didn’t get her own EA (there are two other ASD children and two EAs already - a lot for a small school that only goes up to grade 5), but they had arranged to front-load the other two children with EA-assisted activities in the morning and more inclusive activities in the afternoon, so that one of the EAs should always be available to work with her. I actually quite like this solution, as it reduces the risk that she becomes too dependent on one person. The principal and ASD coordinator also both later indicated - I asked - that responsibility for educating the Bear resided with the teacher, rather than the EAs, who are there to assist. This reduces the risk that the teacher and EAs each think it is the job of the other to educate my daughter. The Bear’s Kindergarten teacher is a former SpecEd teacher, so this too bodes well.

Plus, the school takes a very inclusive approach, where possible. As well as favouring integration in the classroom, when appropriate, they buddy-up special needs children with peers and older children. My neighbour’s children used to attend the school - the youngest one just finished there in June. She had earlier told me about this, saying that she played with one of the other ASD kids at recess, etc. The ASD coordinator was quite clear in describing the buddying-up that in selecting the children they were not looking for ‘little mothers’. Instead, they wanted to help the ASD children to fit in and find support.

After the meeting the ASD coordinator took the Bear and I for a tour of the school. At one point we walked into a Kindergarten class, and stood at the back. The teacher and children were in a circle on the floor, reading and acting out scenes from a book. The Bear took a quick look around, and then walked over and sat down in the circle with the other kids. I knew she was in the right place.

In the week following our visit the ASD coordinator conducted a workshop for the Kindergarten teacher and EAs. Afterwards the teacher called me to introduce herself and asked for permission for her and then the two EAs to visit the Bear at her IBI program, to see what she was doing there and to establish a connection with the IBI school. I thought this was pretty cool (no, actually I was flabbergasted - they actually approached the principal and volunteered to do this). They even sent the IBI program a thank-you card afterward.

The Bear handled her Kindergarten Orientation quite well too, despite it being considerably more lively than the classroom that we had visited earlier. One of the other parents came over during the orientation and noted that the Bear was handling the class and the noise very well. "Um, yes. (pause) Er, do you know that she has autism?" I asked. It turned out that the parent was an OT. Unfortunately, her son will be in the morning session – the Bear will be in the afternoon – so they won't be together until Grade 1. Still, a child with a parent who 'gets it' is not a bad thing. The OT parent also went over and spent some time with the Bear, which was nice. The other parents also seemed okay. A couple of parents said hi in the parking lot afterward, and no one appeared to act 'funny' about having an ASD kid in their child's class. I was (am) a bit worried that some parents might fear that the Bear will be disruptive, or that any negativity on the parents’ part might rub off on their kids, but I didn't perceive any issues.

The ASD coordinator and principal have also continued to try to help out. As well as conducting the workshop, they're trying to get the school bus to pick the Bear up at IBI (which would save me about two hours of traveling each day, going from work to IBI to home/school and back to work). So far they're having no luck with this (officially, the IBI school is "out of area"), but they're still trying, and they volunteered to do this - I didn't ask. They also made the Bear an orientation video welcoming her to the school (which unfortunately is locked up until mid-August, since the school had closed for the summer about half hour before I could pick it up, and the remaining teacher and caretaker could not find it).

Overall, while we (parents) are still a bit nervous, we’re quite looking forward to the start of the school year.

The other big news for us is that we now have IBI funding from the provincial government. That saves us a lot (I mean a lot) of money per year, and also adds some hours to the IBI program each week (now officially 21, vs. 15 before). The Bear will continue with IBI in the morning, attending Kindergarten in the afternoon. Both are supposed to be 'fun' (our IBI is not doctrinaire ABA), so hopefully she'll be able to handle the hours (6+ per day in total, plus traveling time). We'll have to monitor this carefully, but the Bear has a great disposition and actually likes/craves novelty and stimulation, so hopefully she'll be able to handle both.

What was especially nice was that the staff at the Ministry of Children and Youth Services (MCYS) went out of their way to be helpful. In an earlier post I lamented that funding required either the Direct Service Option (DSO), which was totally funded, but required the Bear had to be available from 9 to 5 every day, i.e. forgoing Kindergarten, or the Direct Funding Option (DFO), in which we received funding at the rate of $36 per hour (now $39) to select our own IBI provider, but the result would be a balance of approximately $20,000 per year that we would still have to pay ourselves. I explained this to the Program Supervisor from the MCYS while we were discussing the options. I indicated that we would probably prefer the DFO option because we wanted the Bear to go to Kindergarten, but that in effect this turned (public) Kindergarten into private school, since we had to pay a significant amount for the privilege of sending her there.

Later the same afternoon I phoned the Program Supervisor back with a couple of questions. She indicated that she and some of the others at the Ministry had been discussing our case, and that they would see what they could do. What they ultimately did was to negotiate changes with the current DSO provider, another local ASD support agency, and our IBI provider to get us both full coverage and the ability to send the Bear to Kindergarten. On their own initiative, without any prompting from me, the people at the MCYS ‘made it happen’, and probably at less cost than that had we selected the original DSO option.

Obviously we have been very lucky with the way that both Kindergarten and funding have worked out so far, and are also very appreciative. In both cases we have been fortunate to have dealt with people who have gone out of their way to help. I’ve read of many difficult encounters that parents of children with ASD have faced with school boards and securing government funding. In two recent examples, Shawn wrote about bullying by school administrators, and Wade Rankin wrote about the issues another family faced with their school district over a communications device. Some of these issues may be bureaucratic in origin, but even in bureaucracies - in the most pejorative sense of that word - people can sometimes find some room for discretion and maneuver, if they really search for it. Sometimes there is also an ability to cause changes to the rules if they cannot.

In our case it is good people who have made the difference.

ASD as a Developmental Disorder - A Suggested Neurological Underpinning

2007-06-17T01:00:00.000-04:00

(This post is available in MS Word. To request a copy, please e-mail me - see sidebar for address.)

In a previous post – Autism, Genius, and Minicolumns – I wrote about a research paper by Dr Casanova et al comparing the brains of three prominent neuroscientists vs. controls. One of the findings in this paper was a similarity (and differences) between the minicolumnar structures of the neuroscientists and those with ASD. I speculated based on the results that one of the differences between the neuroscientists and those with ASD might have been related to spindle cells (VENs). Since then the monkeys have been busy typing, and have another post ready. This post will explore the potential links between VENs, the Anterior Cingulate Cortex (ACC), Anterior Insular Cortex (AI), the frontopolar cortex, and autism. I will suggest that together they may explain the developmental origins of ASD.

Von Economo Neuron Morphology and Connectivity

Von Economo neurons (VENs) are large, bipolar neurons located in layer V of Brodmann Area 24 of the anterior cingulate cortex (ACC), and anterior insular cortex (AI) (Watson et al, 2006). A key difference between VENs and pyramidal neurons is that the former have only a single large basal dendrite (vs. an array of smaller basal dendrites in pyramidal cells). VENs have been found in the ACC of humans and all of the great apes, and in the AI of humans and some other apes. They were not found in any other primate species, nor in 30 non-primate mammalian species examined by Nimchinsky et al (1999). VENs have also recently been reported in the brains of several marine mammal species (humpback whales, fin whales, killer whales and sperm whales) in both the ACC and the AI, plus – unlike humans and apes – in the frontopolar cortex, as well as being sparsely distributed in other areas.

VENs are significantly more numerous in humans than in other apes. In the human ACC they occur most often in clusters of three to six neurons, are located in layer Vb, and are conspicuous because of an otherwise low cellular density in this layer. They account for 5.6% of the number of pyramidal cells in layer V of the ACC (Nimchinsky et al, 1999).

Although their function has not been definitively established, VEN morphology and location offer definite clues. The VENs in the ACC and AI appear to be a single population of cells - i.e. undifferentiated by region – (Watson et al, 2006), potentially suggesting a common origin (see VEN Development below). Unlike pyramidal cells, with relatively sparse apical dendrites and highly branched basal dendrites, VENs have long, narrow radial arborization, with similar profiles in their apical and basal dendrites in terms of 'branchiness' and length (Watson et al, 2006). Cell morphology is significant in that neuronal shape is directly related to the computations performed by the cells. Both spines and branches of neurons can operate as computational compartments, and VENs have fewer of both compared with layer V pyramidal cells.

Narrow arborization also impacts VEN connectivity. Minicolumnar structure tends to result in input into a column being relayed rapidly in a vertical direction, but not on a horizontal dimension. The narrow VEN dendritic trees suggest that they usually receive neurotransmission only within their individual minicolumns. Watson et al (2006) suggests that VENs could be a specialization that facilitates rapid output of minicolumnar processing.

This role is also suggested by the size of VENs. Their somas (cell bodies) are on average 4.6 times larger than layer V pyramidal cells, suggesting that they possess large and rapidly conducting axons. From Allman et al (2001), "Because cell body size is probably related to the size of the axonal arborization, the axonal arborization of the spindle cells may be extensive and on a scale with encephalization. This observation suggests that the spindle cells may have widespread connections with other parts of the brain". Allman et al (2005) postulated that the function of the VENs may be to provide a rapid relay to other parts of the brain of a simple signal derived from information processed within the AI and ACC. While it has not yet been firmly established where VENs project, their connections with the rest of the brain may be substantial.

VEN Development

VENs appear relatively late in human development. They first appear in very small numbers in the 35th week of gestation. At birth only about 15% of the final postnatal population are present, with potentially 95% of the total VEN population being present by four years of age (see Fig 1). The source of VENs is still unknown, but they could arise either from differentiation of a pre-existing cell type, or via migration, potentially from the ventricles. In human infants they often appear in pairs and sometimes in vertical chains of three or four neurons, suggesting that they may be following an anatomical or chemical path. Sometimes in infants they have long, undulating leading and trailing processes that resemble flagella, which also suggests migration.

Fig. 1 – Source: Allman et al, 2005

Regardless of migration vs. differentiation, VEN emergence may be vulnerable to disruption during post-natal development, resulting in ‘dysfunctional’ consequences related to neuropsychiatric disorders (Allman et al, 2005). In great apes and humans, VENs are approximately 30% more numerous in the AI in the right hemisphere (rAI) than the left. But they are only about 6% more numerous in the rAI over the left in newborns, so this right hemisphere predominance emerges postnatally, and may be related to the right hemispheric specialization for social emotions. The fact that this 30% right preference is so consistent across post-natal humans and apes suggests that it is important for normal functioning, and that deviations could be dysfunctional. In MRI comparisons of left and right hemispheres in a large population of normal subjects, the cortical grey matter volume was also greater in the rAI, consistent with the rightward predominance of VENs in this area (Allman et al, 2005).

Further support for the possibility of disruption of VEN development can be extrapolated from the known potential for disruption of other postnatally generated neurons. Allman et al (2001) refers to the example of postnatally generated neurons in the dentate gyrus of the hippocampus as being vulnerable to many stress-related events, and the survival of these cells can be enhanced by enriched environments. As well, the survival of postnatally generated neurons in the olfactory bulb is dependent on olfactory stimulation and the presence of brain-derived neurotrophic factor (BDNF), which in rat pups is enhanced by maternal care. It is thus conceivable that environmental stimulation, stress, and quality of parental care could affect the survival and development of VENs during infancy, ultimately influencing adult confidence or dysfunction in emotional self-control and problem solving.

Anterior Cingulate Cortex

The role of VENs is probably best considered in relation to their location. The ACC is the frontal part of the cingulate cortex (so named because it resembles a ‘collar’ around the corpus callosum), and includes both the ventral and dorsal areas of the cingulate cortex. Dr Maclean, in his triune brain model, theorized that the mammalian brain evolved in a series of concentric layers. The underlying reptilian core is comprised of the brain stem and cerebellum. Next is the limbic system, associated with emotions, motivation, and the association of emotions with memory, followed by the neocortex in mammals. In this view the ACC was considered part of the brain’s reptilian core.

More recent studies have found that the mammalian brain is homologous with the dorsal part of the forebrain in non-mammalian vertebrates, and was thus a specialization that evolved from this area. This specialization involved the segregation of the cortex into layers with distinct inputs and outputs. The ACC is distinct from much of the neocortex, in that it lacks layer IV, which is one of several layers that receive input from the thalamus. But it has a well developed layer V, and is similar in this laminar specialization to the motor areas of the neocortex, which lie adjacent to it. This, combined with findings discussed below, suggest that the anterior cingulate cortex is a specialized area of the neocortex devoted to the regulation of emotional and cognitive behavior (Allman et al, 2001).

Devinsky et al (1995) described the ACC as the mechanism by which affect and intellect can be joined, stating that it can be viewed as "both an amplifier and a filter, interconnecting the emotional and cognitive components of the mind." It plays a crucial role in initiation, motivation, and goal directed behaviours, and is part of a larger matrix of structures engaged in similar functions, described as a rostral limbic system, including the amygdala, periaqueductal grey, ventral striatum, orbitofrontal and anterior insular cortices. The system formed by these interconnected structures assesses the motivational content of internal and external stimuli and regulates context-dependent behaviours (Devinsky et al, 1995). Another feature of the ACC is its diverse thalamic afferents and resulting ability to sample a wider range of thalamic input than any other cortical region, which is significant, given its contribution to response selection. The ACC is also connected with the prefrontal cortex and parietal cortex as well as the motor system and frontal eye fields, making it a central station for processing top-down and bottom-up stimuli and assigning control as appropriate to other areas of the brain.

The ACC can be divided into a ventral/rostral affect region and a dorsal/caudal cognition region. The affect division is involved in conditioned emotional learning, vocalizations associated with expressing internal states, assessment of motivational content, and assigning emotional importance to internal and external stimuli, and maternal-infant interactions. The cognitive division contributes to skeletomotor control and is involved in nociception and pain response. A key role is in response selection associated with skeletomotor activity and responses to noxious stimuli. While the cognitive area may be related to some affective processes, evidence suggests that its role in affect is secondary to its role in cognitive processes, such as response selection, that do not require affect (Devinsky et al, 1995). Evidence of the division can be seen from electrical stimulation of the ACC. Stimulation of the ventral part of the ACC produces intense fear or pleasure in conscious patients, while stimulation of the dorsal part of the ACC produces a sense of anticipation of movement, supporting a disassociation between avoidance behaviour and affect (Allman et al, 2001; Devinsky et al, 1995)

Fig. 2 – Centers of activation of the ACC from brain imaging studies. Note the overlap between areas activated by cognitive and emotional tasks. The cortex containing VENs is indicated by purple shading, with the gradient in shading indicating anterior to posterior VEN density. From Allman et al, 2002.

Evidence of the affective / cognitive split can be seen by fMRI during different Stroop tasks. Stroop tasks require subjects to respond in the presence of conflicting or confounding information. In a cognitive version, a person could be asked to report the number of words on a screen, with the words being numbers such as ‘three’ written four times. In the emotional version, the words are emotionally charged, such as ‘murder’ written four times. The cognitive stroop version activates the dorsal part of the ACC, while the emotional stroop activates the ventral part. Although the areas of activation in these types of tests are largely separated, there is an overlap, suggesting that the dorsal and ventral parts of the ACC are probably interconnected (Allman et al, 2001).

The affective region plays a role in a wide variety of autonomic functions, such as the regulation of blood pressure, heart rate, respiration, and visceral responses to stimulation can include nausea, vomiting, epigastric sensation, salivation, and bowel or bladder evacuation. It is also involved in vocalization associated with internal states (Devinsky et al,1995). Activation is also associated with the experience of intense emotion, such as anger, love, and lust, and states of intense behavioral drive such as pain, hunger, thirst and breathlessness are also linked to strong activity. It is the affective region that receives a strong projection from the amygdala (Devinsky et al, 1995), which probably relays negative, fear-related information (Allman et al, 2001). There is also evidence that discrimination of emotion in faces – which is related to social awareness - activates the affective region (Devinsky et al, 1995), as well as evidence of increased ACC functioning in individuals with higher levels of social awareness (Allman et al, 2002).

The dorsal (cognitive) part of the ACC is strongly activated during focused problem solving and the performance of cognitively demanding tasks, with activation increasing with increases in task difficulty, and the same area is activated during the experience of intense drives such as love or lust. The commonality is that both types of activity involve intense mental focus (Allman et al, 2002). Studies suggest that the ACC is involved in response selection when novel choices are required, rather than during practiced responses, and that more demanding tasks increase ACC activation, while less demanding tasks reduce activation (Devinsky et al, 1995). The ACC is engaged in early premotor events that require cognitive information processing and correct response selection where a movement may be needed, including the determination of whether movement is actually required. The common feature in these functions is that they occur well before movement occurs, and the ACC may play an essential role in the transition from premotor to behavioural states. Devinsky et al (1995) indicate that this is one of the primary contributions of the ACC to human behaviour.

The cognitive region of the ACC is also involved in the perception of pain. Frith and Frith (2003) indicate that first order representation of pain occurs in the caudal ACC, but that the subjective perception of pain is located in the rostral ACC. Devinsky et al (1995) suggest the ACC role in pain sensation may be a) to determine its emotional affect, b) to select a motor response (i.e. initiate behaviour to escape the pain) and c) to learn how to predict and avoid pain in the future – i.e. learning. Of note, ACC lesions in animal studies retarded acquisition of discriminative avoidance learning. Other evidence of an ACC role – along with other brain regions - in learning and memory is evidenced by the ACC's role (mentioned above) in response selection when novel choices are required, rather than during practiced responses.

Both AI and ACC activation also increase with the degree of uncertainty, and they may be involved in both adaptive decision-making and response and cognitive flexibility. There is also a link between ACC signal output and the recognition of errors, resulting in a change in ACC electrical output called ‘error-related negativity’. Studies involving monkeys have shown that ACC neuron activation is related to the expectation of reward, supporting the concept that the ACC is continuously monitoring changes in feedback from interactions with the environment that affect survival and reproduction, and initiating behavioral responses to maintain or improve these conditions. These findings indicate that the ACC's error recognition and correction functions predate the appearance of VENs (Allman et al, 2002).

The ACC also appears to play a role in social interactions. Structural or functional changes in the ACC can cause significant changes in social behaviour. Studies have noted changes such as blunted affect, apathy, impulsivity, disinhibition, aggressive behaviour with minimal or no provocation, psychosis, sexually deviant behaviour, disabling obsessions and compulsions, and impaired social judgment. (To be very clear, given that this post is ultimately about ASD, I am NOT suggesting that those with ASD manifest the above behaviours).

One case in particular, reported by Eslinger and Damasio (1985), followed a previously successful accountant who – following bilateral ACC and orbito-frontal damage after a tumour resection, was unable to maintain his job, marriage, and finances despite preserved ‘intelligence and memory’. His ability to interpret social cues and adapt to social situations were severely impaired. He could recall normal patterns of social behaviour in hypothetical situations, but was unable to execute correct actions in real life. Of interest, follow-up research (Damasio et al, 1990) determined that there was a disconnection between his intellectual understanding of affect and the autonomic expression of same (measured by skin conduction during exposure to emotionally charged visual images). Devinsky et al (1995) speculated that the lack of physiological emotional cues may contribute to the patient’s ability to appreciate the emotional significance of stimuli. Of note too, area 24 lesions in infant monkeys impairs the separation cry when the infant is removed from the mother, and disrupts the mother’s ability to attend to the infant. (see Anterior Insular Cortex below for a discussion of interoception).

The ACC may also have a role in speech. ACC blood flow is elevated during the processing of words, suggesting a role in word and sentence selection. Devinsky et al (1995) suggest this is part of a broader response selection function rather than a specific language function or a linking of words to emotion, as this processing occurs in the dorsal (cognitive) division of the ACC. Other evidence of an ACC role in speech comes from akinetic mutism, which is most often associated with bilateral ACC lesions. One patient reported by Damasio and Van Hoesen (1983), who recovered from a left ACC stroke, initially had no spontaneous speech but was able to repeat. "She commented that ‘she did not talk because she had nothing to say. Her mind was ‘empty’. ‘Nothing mattered.’" During her initial illness she could follow the doctors’ conversations but ‘felt no will to reply’ to questions. This was interpreted by the authors as indicating that such lesions cause a ‘profound behavioural disturbance', preventing the normal expression and experience of affect. As mentioned by Allman et al (2001), patients with lesions in the ACC show reduced levels of spontaneous behaviour and willingness to act. Another recent paper (Chiung-Chih Chang et al, 2007) reported two cases of right ACC stroke that resulted in speech initiation problems. The authors suggest that in some cases, speech initiation requires the participation of the right ACC in addition to the language network in the left hemisphere. This too is probably more related to response selection than language function.

Overall, the ACC appears to play a crucial role in the brain, linking emotion, cognition, and response selection, and coordinating these capabilities with the rest of the brain. VENs may enhance the ability of the ACC to relay information to other parts of the brain. Layer V neurons typically relay the output of cortical processing to other cortical areas and subcortical structures, and the ACC has particularly large layer V pyramidal neurons (Devinsky et al, 1995). VENs may enhance the projection capabilities of the ACC, further enabling it to connect to the larger human brain. Allman et al (2001) indicated that VEN size across humans and great apes varies as a function of relative brain size - unlike pyramidal neurons in layer V and fusiform cells in layer VI of the ACC. VEN size and number are therefore probably an evolutionary response to the requirements of encephalization, responding to both increasing distance and increasing connectivity requirements.

ACC and the Development of Executive Awareness and Function

The ACC has also been linked to executive processes. Executive function is traditionally an umbrella term covering functions such as planning, working memory, impulse control, inhibition and mental flexibility, as well as the initiation and monitoring of action (Hill, 2004a). Frith and Frith (2003) indicate that many kinds of executive tasks are known to activate the ACC. They refer to a meta-analysis of executive tasks conducted by Duncan & Owen (2000), placing the peak activation of most of these tasks in the rostral cingulate zone (the same area activated by Stroop-like tasks). While Frith and Frith (2003) indicate that executive function is located separately in the brain from the mentalizing or theory of mind region, Hill (2004b) notes that studies indicate that executive function predicts performance on ToM tests, but not vise versa, suggesting that there is a complex relationship between the two (discussed further below).

It has been proposed by Posner and Rothbart (1998), that the ACC is involved in the maturation of self-control and executive function as the individual progresses from infancy to childhood to adulthood. The ACC is involved in evaluating pain, from a distress rather than a sensory perspective. Posner and Rothbart indicate that negative affect may be controlled by attention (e.g. distraction, as recognized by anyone trying to comfort an infant by attempting to focus their attention on other stimuli), suggesting that the ACC’s direction of attention develops as a means of coping with or controlling feelings of distress. They state that "amygdala-cingulate interaction might be a reasonable candidate for the earliest form of self-regulation in the infant". Initially this control of orienting is at least partially externally (e.g. care-giver) driven, but over time more direct control of attention shifts from care-givers to infants themselves, and infants become more involved in attempting to solicit adult attention.

Posner and Rothbart go on to state that "It seems likely that the same mechanisms used to cope with self-regulation of emotion are then transferred to issues of control of cognition during later infancy and childhood." From executive attention follows the early development of behavioural and emotional control. The authors demonstrate a developmental flow – supported by experimental results - from visual conflict resolution related to eye position (e.g. a transition from reaching requiring line of sight) to the generalization of this capability. Conflict resolution may further develop into error monitoring and voluntary inhibitory control over behaviour - including error correction - commensurate with ACC development.

As Posner and Rothbart (1998) wrote:

"The effort to develop ways of controlling distress provides a locus of control in the cingulate which may, step-by-step, generalize to other situations where conflicting demands must be resolved. Many years are devoted to development of systems of self-regulation. Indeed it seems likely that this development continues into adolescence and may be open to change in adult life."

This hypothesis is supported by the steady increase in the metabolic activity of the ACC from childhood to young adulthood, as well as studies linking ACC size in children and the ability to perform tasks requiring focal attention control.

Anterior Insular Cortex

The anterior insular cortex – the other area in the brain containing VENs – is known, along with the ACC, to have an important role in interoception, i.e. the subjective awareness of inner feelings. As Bud Craig (Craig, 2004) wrote, "The concept of ‘interoception’ was classically restricted to visceral sensations, but recent neuroanatomical and neurophysiological results indicate that sensations related to the ongoing physiological condition of all organs of the body – muscles, joints, teeth, and skin as well as the viscera – are processed together." These inputs are ultimately relayed from the thalamus to the insular cortex, and give rise to feelings such as pain, temperature, itch, muscle burn, visceral sensations, hunger, thirst, taste, and even sensual touch. Craig indicates that these feelings represent ‘the material me’, and the somatic-marker hypothesis of consciousness (proposed by A.R. Damasio) suggests that the sensory representation of the body is the basis for the mental representation of the sentient self, allowing the brain to distinguish the inner world from the outer world. In this theory, individual differences in emotional awareness are directly related to differences in the capacity for interoceptive feelings.

Research has demonstrated that right anterior insular cortex (rAI) activation and size are uniquely correlated with the subjective awareness of internal feelings of human beings. Sensory representation of the physiological condition of the body is initially on a same-side basis, and is then remapped to the rAI through the corpus callosum, supporting a role of the rAI in subjective feelings and the awareness of the physical self as a feeling entity, while thalamic inputs to the ACC produce behavioural drive (Singer et al, 2004). The rAI and rACC also appear to play a role in the integration of information about oneself linked to the process of visual self-recognition (Devue et al, 2007). Given rAI activation (selectively or in conjunction with the ACC) during many emotions, including anger, happiness, sadness, disgust, and lust, as well as by music, this supports the somatic-marker hypothesis and the link between interoception and "the emotional feelings that characterize human sentience" (Craig, 2004). The implication is that individual differences in subjective interoceptive awareness, and by extension emotional depth and complexity, might be expressed in part by the degree of expansion of the rAI.

Further, the rAI appears to be co-activated with the ACC when subjects experience social emotions (which as Craig (2004) pointed out, can be linked to physiological changes) such as guilt, embarrassment, violation of social norms, distress resulting from social exclusion, and humour, as well as when engaging in deception (Watson et al, 2006; Singer et al, 2004). Singer indicates that this may involve a simultaneous generation of both a feeling and an emotional motivation, along with its associated autonomic effects. I would suggest that this would be self-reinforcing, as the autonomic effects would feed back into interoceptive awareness. Both areas are activated when subjects view an image of a loved one compared with an acquaintance, suggesting that these structures may be involved in bonding (Allman et al, 2005). Further evidence for a role in bonding is provided by the presence of vasopressin 1a receptors in the VENs in these areas (see below). Further, Singer et al (2004) also found that the AI (bilateral but with peak activation in the rAI) and ACC (along with the brainstem and cerebellum) were activated not only when a subject receives pain, but also by a signal that a loved one experiences pain.

This indicates first a differentiation within the neural systems between the actual sensory experience of pain and its subjective experience and interpretation. But further, given the link of the ACC and rAI to the experience of a wide range of emotions, it also supports their role – independent of internal and external sensory inputs - as the neural basis of understanding both our own feelings and the feelings of others. Further evidence of the role of the AI and ACC in interpreting the emotion of others comes from Wicker et al (2003). In an fMRI study they found that observing the emotional facial expression of disgust in others activated the same sites in the AI and to a lesser extent in the ACC as activated by one’s own experience of disgust. Thus the authors suggested that observing an emotion in others activates the same neural representation of that emotion in us. Singer et al (2004) suggests that the ability to understand the feelings of others and to empathize evolved out of our own ability to subjectively represent our internal body states. Further, this capability is a necessary part of our ability to mentalize, i.e. to understand the thoughts, beliefs and intentions of others.

Given the existence of the capability for self-understanding, it is logical (in hindsight) that any evolved ability to understand others would be based on utilizing the same existing capability used to understand ourselves, rather than creating the functionality anew elsewhere in the brain.

Frontopolar Cortex

The frontopolar cortex is another area of specialization in hominoids, especially humans. Brodmann Area 10 is large and well developed in humans, less so in great apes, and is much smaller in gibbons and monkeys. Within hominoids it declines in size in the same order as the decline in density of VENs (Allman et al, 2002). The lateral part of area 10 appears to be involved in episodic (related to specific events) as opposed to semantic (general knowledge) memory, and part of area 10 below this area is activated in the choice between smaller but more probable rewards vs. larger but more uncertain rewards, as is the ACC (i.e. response selection). The medial part of area 10 is activated when subjects are presented with emotionally charged moral dilemmas requiring choices that affect the lives of others. The medial and anterior areas are activated when subjects develop a successful decision-making strategy related to rewards. This activation may be related to the recollection of the outcome of recent attempts (episodic memory), the assessment of reward probability, and the choice of a strategy for the next attempt (Allman et al, 2002).

Strange et al (2001) indicates that the frontopolar cortex is activated during complex cognitive tasks, especially (along with multiple other regions) reasoning tasks, as demonstrated during the Wisconsin Card Sorting Test (WCST), the Tower of London task, inductive and probabilistic reasoning tasks, probabilistic classification, and the Raven’s progressive matrices test. There is evidence that it is involved in intentional or explicit rule induction - including generating and testing hypotheses about relationships between stimuli - when abstract structures or rules are needed, but that once a rule is learned then other areas are involved in its application. Damage to the frontopolar cortex can produce greater WCST sorting category switching impairments than damage to the dorsolateral prefrontal cortex (DLPFC), another key WCST-activated area, with frontopolar cortex activation and dysfunction linked to rule changes and learning and DLPFC activation and dysfunction linked to rule application. This is in line with another study cited by Strange et al (White and Wise, 1999) that the dorsal, ventral, and dorsolateral prefrontal cortices are involved in guiding behaviour according to previously learned rules. The frontopolar cortex may also mediate switching between different executive processes (Strange et al, 2001) .

The frontopolar cortex is also involved during working memory tasks, including when working memory requirements approach and exceed people’s short term memory limits, or when memory is split between tasks, as well as in ‘branching’ (a process in which an overall goal must be maintained while working on sub-goals), and the evaluation of retrieved episodic memories (Strange et al, 2001). The authors suggest that frontopolar cortex activation occurs in high level tasks that involve planning and executive control of cognitive functions, in particular those tasks that require a strategy or evaluative process to be applied to information held in short term or working memory, for example to test hypotheses on multiple items during rule induction. Decety and Jackson (2004) also suggested a potential frontopolar cortex role in the evaluation of self-generated responses, including when a task requires monitoring and manipulation of internally generated information.

Area 10 may also have a wider role along with the ACC in executive function and the behavioural maturation of self-control (discussed above). Strange et al (2001) saw a wider frontopolar cortex role in switching between different executive processes, a role which Posner and Rothbart indicates is also linked to the ACC. Both areas are activated when engaging in tasks requiring episodic memory – specifically in post-retrieval analysis (Strange et al, 2001) - and Allman et al (2002) suggest that an important part of the process of developing self-control and behavioural maturation is the ability to use past experience as a guide in responding to current events. Given ACC activation in these tasks, Allman et al (2002) suggest a functional linkage between the two areas, in which the ACC monitors the current state of reward and punishment and signals the need for behavioural adaptation, while area 10 compares the current state with past experience and - linking this to the consideration of the well-being of others (as per activation during emotionally charge moral dilemmas affecting others) - makes choices governing future behaviour. Based on Strange et al (2001)’s findings and White and Wise (1999)’s interpretation of the role of the prefrontal cortex, it may be possible to expand this to include a frontopolar cortex role in learning, with this knowledge then being passed on to the rest of the prefrontal cortex for continued execution.

Area 10 may also have a role in joint attention. Williams et al (2005) developed a video stimuli that, when watched by a subject, stimulated an experience of joint attention that could be monitored in an fMRI environment. The result was activation of the ventromedial frontal cortex, the left superior frontal gyrus (area 10), cingulate cortex, and caudate nuclei. The authors indicated that the VMFC has consistently shown activation during tasks involving the attribution of mental state. They further suggest that area 10 may serve a cognitive integration function, which in joint attention seems to utilize a perception-action matching process. The authors see the links between the areas above as evidence that the areas engaged in joint attention also serve a mentalizing function.

Allman et al (2002) indicates that the size of the dendritic arborization and the number of synapses of pyramidal neurons in area 10 is greater than in any other cortical area, suggesting an integrative role of this area fitting with that suggested by Williams et al (2005) above, and also by Strange et al (2001). This enhanced connectivity would presumably increase the impact of the ACC’s links to area 10 through subsequent activation of other areas. Interestingly enough, the finding of VENs in the frontopolar cortex of certain large marine mammals (see above) may also support Allman et al (2002) hypothesis of an evolutionary linkage between area 10 and the ACC, with potentially the same chemical signaling of VEN proliferation in the human brain being extended in the brains of the marine mammals in question.

The Role of VEN Neurotransmitter Receptors

The role of VENs may also be deduced from their neurotransmitter receptors (see Allman et al, 2005), which suggest that they are involved in the formation of social bonds and the anticipation of reward and punishment in uncertain conditions. They are part of a limited set of AI and ACC neurons in layer V that possess the vasopressin 1a receptor, which in rodent studies is strongly linked to the formation of social bonds. They are rich in dopamine D3 receptors, a high affinity dopamine receptor that has been proposed to signal the expectation of reward under uncertain conditions. AI and ACC activation increases with the degree of uncertainty, and the suggestion is that these areas are involved in adaptive decision-making and cognitive flexibility.

The serotonin 2b receptor is also strongly expressed in VENs. While it is rarely expressed elsewhere in the central nervous system, this receptor is also strongly expressed in the human stomach and intestines, where it promotes contractions of the smooth muscles responsible for peristalsis. Serotonin might serve as an antagonistic signal to dopamine, with serotonin signaling punishment and dopamine signaling reward. Activation of the serotonin 2b receptor on VENs might be related to the capacity of the activity in the GI tract to signal impending danger or punishment (literally ‘gut feelings’) and thus might be an opponent to the dopamine D3 signal of reward expectation. The result of these processes could be an evaluation by VENs of the relative likelihood of punishment vs. reward and a role in ‘gut level’ or intuitive decision-making in a given behavioral context.

Given the ACC and AI role in interoception discussed above, the presence of serotonin 2b receptors on the VENs that are otherwise rare in the brain, but common in the viscera, suggests an extension of the concept that the ACC and AI are monitoring activity in the gut. Allman et al (2005), suggests that these receptors might represent a transposition of this function from the gut into the brain, which would enable the organism to react more quickly to threatening circumstances than if it depended solely on monitoring sensations arising from the gut.

VENs and Intuition

Allman et al (2005) proposed a role for VENs in intuition. They wrote that:

"Intuition is a form of cognition in which many variables are rapidly evaluated to yield a fast decision. Typically we are unaware of the logical steps or assumptions underlying the process although intuition is based on experience-based probabilistic models. We experience the intuitive process at a visceral level. Intuitive decisionmaking enables us to react quickly in situations that involve a high degree of uncertainty which commonly involve social interactions. Frequently we do not have the luxury of sufficient time to perform deliberative cost-benefit analyses to determine the most appropriate course of action, but instead must rely on rapid intuitive judgments."

The ACC and AI are both active when individuals make decisions under a high degree of uncertainty. They are also involved in the subjective experience of pain, which is magnified by uncertainty, plus when subjects experience guilt, embarrassment, and engage in deception. They are also active in humour, trust, empathy, and the discrimination of the mental states of others. All of these social emotions are influenced by the degree of uncertainty involved. Allman et al (2005) hypothesize that "VENs and related structures integrate the probability of reward and punishment derived from many inputs and enable individuals to make quick, intuitive decisions that enable them to adapt to rapidly changing conditions". They would also be involved in relaying this output to other brain structures. As such, VENs would be an adaptation supporting the increased complexity of hominid - and especially human - social networks.

Minicolumns – Setting the Stage

Research by Casanova et al has indicated that those with ASD have a higher number of minicolumns than average, but that those minicolumns are of a narrower than average width, with smaller neurons but the same average number of neurons per minicolumn. The net result is a brain structure that skews in favour of processing stimuli that require discrimination, potentially at the expense of generalizing the salience of a particular stimulus. Smaller and more densely packed minicolumns could also allow for more complex information processing.

These attributes come at a potential cost. The reduction in width is a result of a reduction in the minicolumn’s peripheral zone of inhibitory and disinhibitory activity. The inhibitory fibers act to keep stimuli within individual minicolumns, and the reduction in this space increases the chance of stimuli overflowing to adjacent minicolumns, providing an amplifier effect and potential hypersensitivity. Narrower minicolumns may also result in an increased number of minicolumns per macrocolumn, which can also result in an amplification of thalamic input, and as each minicolumn’s response to thalamic input is modulated by the activity of neighbouring columns, a reduction in GABAergic inhibitory activity could also result in a loss of inhibition and greater amplification. Stimuli ‘spill’ and greater amplification could result in the increased incidence of seizures in autistics.

An additional factor is the reduction in neuron size, which reduces the ability of neurons to sustain connections over distances. Smaller neurons result in a metabolic bias favouring shorter connections at the expense of both longer distance and inter-hemispheral connectivity. The result is that autistic brains have a bias towards local (intra-regional) over global (inter-regional) connectivity and processing. Short intra-regional processing functions include mathematical calculations and visual processing. Cognitive functions that require inter-regional processing would be less metabolically efficient, including language, face recognition, and joint attention (Casanova - Abnormalities Of Cortical Circuitry In The Brains Of Autistic Individuals). Given the high metabolic cost of the brain (2.5% of our body weight but 22% of our resting metabolism - Leonard and Robertson 1992, p 186), smaller neurons may be a response to resource constraints.

Of note, while reduced minicolumnar width appears to be a prerequisite for ASD, the reported minicolumnar widths found within autistic brains are still within the normal distribution of minicolumnar width, albeit at the tail end (Casanova, 2006). In other words, people with narrow minicolumnar widths – i.e. a pre-autistic brain - are not necessarily on the ASD spectrum, but instead, minicolumnar width is part of normal human variation (neurodiversity). Something further is required to cause ASD.

VENs and ASD

Given the roles of the ACC, AI, and VENs discussed above, any disruptions in VENs in the autistic brain could potentially be expected to have an impact on the functions performed by the ACC and AI. And disruptions appear to exist.

Allman et al (2005) noted a study demonstrating the portion of the ACC in the right hemisphere containing VENs was reduced in volume in individuals with ASD compared with matched controls. A diffusion tensor imaging (DTI) study found that long distance fibre connections in the white matter adjacent to the ACC, including the area which in normal subjects carries the axons of VENs, was disordered in ASD subjects. Postmortem analysis of ASD brains by Kemper and Bauman (1993) found that the ACC was poorly laminated. Another study found isolated pockets of neurons in the white matter of the frontal cortex of ASD subjects, suggesting a defect in neuronal migration (which might also impact VENs). Further, Allman et al (2005) makes reference to unpublished data (also Allman et al) from autopsies of a 9 year old boy and 9 year old girl with ASD which found heavy concentrations of VENs in the white matter and extending through layer VI into layer V in the AI. VENs in these subjects were also located medially to their normal AI location.

Functional imaging data also suggests a connection between the AI and ASD. A study asking high functioning autistics and controls to identify the mental state of photographed individuals found rAI activation in controls but not in those with ASD. Allman et al (2005) also noted reports of reductions in measurements of embarrassment and empathy (both of which activate the AI and ACC) in autistic subjects, although they also noted that there is a considerable overlap between autistic and normal subjects.

Allman et al (2005) hypothesizes that the social disabilities in ASD are partially due to abnormal VEN development. The authors state that:

"our hypothesis is that the VENs and related structures integrate the probability of reward and punishment derived from many inputs and enable individuals to make quick, intuitive decisions that enable them to adapt to rapidly changing conditions. Because social emotions by their very nature involve considerable uncertainty, and because social interactions are often of a rapidly changing nature, an impairment of the VEN system would be predicted to compromise social functioning. The lack of quick social intuitions is a key deficit in autism spectrum disorders."

Allman et al (2005) also link the possibility of a reduction in ability to quickly process uncertainty with the desire for sameness and routine in ASD. "In short, we believe that the VEN system for rapid, intuitive responses in situations involving considerable uncertainty is impaired in autism spectrum disorders." They are clear that they are not proposing that VENs are related to Theory of Mind, but rather, that VENs might serve as input into the neural system that creates mental models of the thinking of others.

A recent paper by Kennedy et al (2007) also explored VENs in ASD, originally hypothesizing a reduction in the number of VENs in the ASD brain. They sampled and extrapolated the number of VENs in 4 ASD brains (three lAI and one rAI) vs. five controls (two lAI, one rAI and two with both hemispheres). But rather than finding a reduction in VENs in ASD brains, they found similar overall numbers, once the ASD outlier (lAI) was omitted. While the low sample sizes render any comparisons anecdotal, I did note that the VEN counts in the ASD 3 year old (lAI) were quite high compared with most of the controls, and the ASD outlier count was 27% higher than the next highest (control) count and 63% higher than the average adult control count (three left and two right hemispheres). I also noted that the VEN numbers found (even considering most counts are for a single hemisphere) are substantially lower than the equivalent AI counts for both hemispheres indicated by Allman et al (2005) (see Figure 1 above), despite the fact that both sets of numbers were generated through stereological counts. Even so, the common methodology used for all samples in the Kennedy et al (2007) paper could allow for a valid comparison between samples. The authors also noted that they observed no qualitative difference in the size of VENs in control and ASD samples at either the younger or older ages.

My takeaway from the paper, regarding ASD and the AI, is that there may be issues regarding VEN quantity, migration, and ‘pruning’ that require further investigation. I would also note, as did the authors, that their findings are not necessarily applicable to the ACC.

Going Further – Implicating VENs, ACC, AI, Frontopolar Cortex and ASD

When approaching the subject of ASD, one of the benefits of being a parent rather than a neuroscientist is one can speculate without risk of damaging one’s professional reputation. So here goes. I would suggest that there is a link between VENs, the ACC, AI, frontopolar cortex, the narrower minicolumn hypothesis, potentially the cerebellum, and ASD.

As mentioned above, the major period of VEN proliferation is during the post-natal period, and these cells are found in the ACC and AI. I would speculate that some of the major deficits in ASD may result from disruption of VEN development and/or development of the ACC and AI. VEN development issues may precede or follow ACC/AI disruptions, but evidence (e.g. as per Allman et al, 2005) suggests that VEN development may be impacted, and the results may be significant.

VEN Variations

VENs may be the class of neurons that compensate for the bias inherent in smaller pyramidal neurons in the reduced minicolumnar width pre-autistic brain. Because of their size and projection capabilities, VENs may enable the ACC and AI to adequately connect to and influence the development of the brain despite the bias of smaller pyramidal neurons against more global connectivity (as per the minicolumn hypothesis). Belmonte and Carpenter (1998) noted findings by Bauman and Kemper (1985) of small, closely packed cells in the ACC of autistic brains, presumably including the pyramidal neurons in layer V. I would suggest that this is in keeping with Dr Casanova’s minicolumn findings discussed above. A functional population of VENs could presumably compensate for the bias in favour of shorter connections in these smaller cells. But disruption in the network of VEN cells would reduce this compensatory effect.

To be clear, I’m not suggesting an ‘all or nothing’ impact from variations in VENs in ASD. Instead, I would suggest that variations in VEN location and numbers could result in variations in connectivity and development. Three thoughts come to mind. First, a higher or lower number of VENs could result in ‘over-connectivity’ or ‘under-connectivity’, but dysfunctional connectivity nonetheless. As per Allman et al (2005):

"This right hemisphere VEN predominance [in the AI] may be related to the right hemispheric specialization for the social emotions. The fact that this 30% right preference is so tightly regulated and consistent across postnatal humans and apes suggests that it is important for normal functioning and that deviations from this ratio could be dysfunctional."

In addition, as mentioned in Allman et al (2002), neuron death is also necessary for normal development, and Allman et al speculated that excessive VEN survival could contribute to psychiatric disorders associated with over-activity of the ACC, such as OCD, which is characterized by excessively active vigilance and error-correcting behaviour. Higher VEN counts in ASD might also have an impact. In contrast, VENs are noted to be particularly vulnerable to degeneration in Alzheimer’s disease, with a loss of 60% of VEN neurons noted by Nimchinsky et al (1999).

Second, altered migration could result in dysfunctional connectivity. As mentioned above, Allman et al found heavy concentrations of VENs in the white matter and extending through layer VI into layer V in the AI, and noted that VENs were located medially to their normal location. Given the expectation that neurons will connect and function or perish, mislocated pockets of VENs would presumably still be functional, leading to the possibility of arbitrary and errant connectivity, with potentially disruptive consequences.

Third, variations in ASD may result from different ‘autisms’ – i.e. different etiologies and vulnerabilities mixing with variations in environmental factors (‘environment’ being defined broadly) - and result in variations in presentation. For example (this is pure speculation), higher levels of BDNF in ASD may signal an increase in VEN birth and/or survival, at the expense of necessary ‘pruning’. Various autism etiologies may lead to variations in VEN proliferation, brain connectivity, and – ultimately – ASD presentation.

Other impacts

The cerebellum may also play a role in ACC and AI issues. Brain imaging studies have shown that the cerebellum plays an important role in selective attention (i.e. the focusing on a specific aspect of a scene while ignoring other aspects - Wikipedia). Belmonte and Carper (1998) indicate that purkinje cells of the cerebellar cortex are the sole inhibitory input to the deep cerebellar nuclei. Loss of appropriate inhibition could produce activation of the deep nuclei and result in nonspecific activation of the cerebral cortex, resulting in impairment of attentional functions. Purkinje cell counts are known to be reduced in those with ASD. In contrast, Bischoff-Grethe et al (2002) suggests that the cerebellum is involved in response reassignment downstream, based in part on input from the ACC. Ravizza and Ivry (2001) also suggest that attentional deficits regarded as being due to cerebellar dysfunction may be at least in part due to issues related to coordinating successive responses.

Regardless of the cerebellum’s position in the attentional loop, any impairment in cerebellar function relating to attention shifting – input and/or output related - would presumably negatively affect the ‘success’ of the ACC in ultimately directing attention, and could result in significant developmental consequences. From a VEN perspective, the developmental and/or migratory stimuli and pathways are as yet unknown, but one could reasonably suggest that alterations in connectivity between the cerebellum, AI and ACC might potentially affect the chemical messaging required for VEN development.

Key Assumptions

Implicit (and sometimes explicit) in the discussion below are four assumptions. The first assumption, which is presumably fairly widely held, is that cognitive evolution has historically been driven by tests of social fitness. Big brains are metabolically very expensive, and intelligence – presumably inherent in a larger brain - is a luxury that is too expensive for most species. To be flippant, the test of evolutionary fitness that the human ‘big brain’ passed on the African savannah was not the ability to do calculus, but the ability to successfully function in social groups that multiplied the effectiveness of individual human capabilities through social interaction. The fact that this evolution in social cognition also left most humans capable of higher cognitive thought has obviously very recently (in evolutionary terms) had great impact, but through most of our history the value of a big brain to homo sapiens was in enabling us to work with, provide for, and understand (well, sort of) our fellow human beings.

The second assumption, which I would suggest is reasonably obvious only in hindsight, is that the most logical method of evolving the neurological capability to understand others is based on using ourselves - and therefore the neurological processes that we use to operate ourselves - as a model and a base. It is presumably far easier to evolve and adapt the capability to use our own neural network to model the behaviour of others than to build an entirely new and independent neurological network to do the same job. In addition, our existing neurology presumably works reasonably well at explaining human behaviour (at least for a sample of one). An entirely new and independent system using a different neurological construct might not be as accurate in predicting the outcomes that are generated by the original system.

Third, human development and maturation is a process in which certain steps lay the foundation for further development, and altered and/or dysfunctional development in one area may have downstream consequences in other areas, even when those areas may not be closely linked after maturation.

Fourth, while the discussion below describes various facets of autism, there is no implication intended that there is one ‘autism’ or that all autistics have the same set of capabilities, issues or symptoms. I have often seen attempted refutations of autism findings or hypotheses on the basis that they are not ‘universal’ or that other disorders also share some of the same characteristics. In the discussion below I fully acknowledge that there are both variations and exceptions in autistic capabilities. Admittedly my exposure to the scientific literature is limited, as is my personal experience with autistic children, but I am a proponent of the concept of multiple etiologies (one that I believe is fairly widely shared), “where multiple pathways funnel through final common pathways, while one or a few mechanisms lead to multiple consequences” (Herbert, 2005). As such, I do not see the absence of ‘universality’ as necessarily implying anything other than that variations in impact on certain neurological systems exist due to variations in etiology and developmental environment, among other factors.

Hypothesis – ACC and AI Dysfunction and ASD

Belmonte and Carper (1998) wrote that:

"the effect of a lesion in a developing brain often is more severe than or is distinct from the effect of a similar lesion in a mature brain, because brain systems downstream from the lesion may depend on correct input for their proper maturation."

I would hypothesize that ASD results from early ACC and AI dysfunction in a susceptible pre-autistic brain. A common thread in ASD is sensory integration issues (see below). Building on Posner and Rothbart’s hypothesis, a disruption in the brain’s ability to integrate sensory input and integrate autonomic functions with interoception could impact the development of executive functions, as well as corresponding development within the frontopolar cortex and VMPFC, and ultimately have far reaching developmental consequences, including emotional and social development, and result in dysfunction within the mentalizing and mirror neuron systems.

This disruption may be the result of dysfunctional ACC and AI input, VEN dysfunction, or both (altered ACC and AI functioning might affect the VEN developmental and migrational pathways). ACC and AI dysfunction could also be totally unrelated to VEN issues and still have the same result. But given Allman et al (2005)’s findings of VEN issues in ASD, and the roles of the ACC and AI in neurological development and functioning, VENs are a common thread linking these areas together and a logical candidate for involvement.

The result, given the roles of the ACC, AI and frontopolar cortex discussed above, could be the development of ASD in an otherwise pre-autistic but susceptible brain.

Sensory Issues, Interoception and Attention

Sensory integration issues in ASD are widely (anecdotally) reported but (as far as I can tell) largely unquantified. An exception is Kern et al (2007), which examined the relationship between auditory, visual, touch, and oral sensory dysfunction in autism in 104 children and adults. The authors indicated that findings suggested that all main sensory systems and multi-sensory processing appear to be affected; that sensory processing dysfunction in autism is global in nature; and that sensory processing problems need to be considered part of the disorder. Among other results, the authors also found that sensory disturbance correlates with severity of autism in children, but not adolescents and adults.

Interestingly, another paper by Williams et al (2006) found a more pronounced impairment in sensory perceptual abilities in childhood in autism vs. controls, but that these impairments become attenuated, such that no significant differences were detected between autistics and controls in later adolescence and adulthood. The suggestion was that this attenuation may reflect sensory system developmental amelioration over time. The authors stated that greater sensory disturbance in children would be consistent with the findings reported in the small sensory literature of the prominence of sensory symptoms in children, plus the frequent use of sensory interventions in children for calming.

Belmonte and Carper (1998) noted studies that autistic children are universally dyspraxic (Jones and Prior, 1985), have disturbances in gait (Vilensky et al, 1981), that can persist into adulthood (Hallett et al, 1993), and motor anomalies clear enough that blind raters could identify autistic from normal children based on mobility and other factors seen in home movies from before autism was suspected (Adrien et al, 1992).

A more direct account of autistic sensory issues is that of Chandima Rajapatirana, an autistic writer, from Time magazine's cover story on Autism (May 15th, 2006 issue, written by Claudia Wallis):

"[The] knack of knowing where my body is does not come easy for me. Interestingly I do not know if I am sitting or standing. I am not aware of my body unless it is touching something... Your hand on mine lets me know where my hand is. Jarring my legs by walking tells me I am alive."

Chandima Rajapatirana's account may not be typical, but it is illustrative of the extent to which sensory issues may impact some autistics. But these issues are not part of the DSM-IV, and this potentially affects the amount of attention that they receive in studies of ASD.

The minicolumn hypothesis already suggests the potential for an increased number of minicolumns per macrocolumn, which could result in an amplification of thalamic input to the ACC and AI. In addition, smaller neurons, especially in Layer V, would reduce the potential for longer distance connectivity. Factor in the potential for VEN dysfunction (potentially linked to a variety of reasons) and/or increased cerebellar input and the result of sensory integration issues could be a significant impact on ACC and AI functional development.

VENs were previously thought to appear around the fourth month after birth (Allman et al, 2001). While current findings indicate that they first appear in very small numbers in the 35th week of gestation and that about 15% of the final postnatal population are present at birth, the previous fourth month estimate suggests that VEN counts start to increase significantly about that time. Given their location, it is a logical assumption that they begin to play an increasingly significant role in AI and ACC functionality at this time, which coincides with the infant’s capacity to hold its head steady, smile spontaneously, track an object visually, and reach for that object. Allman et al (2001) suggest that VENs may participate in the neural circuitry responsible for these functions, which are related to focused attention and emotional expression. Further, some of the VENs present in four to eight month olds bear indications of potential migration, suggesting that this is an active period for VEN proliferation. It is also a period in which infants develop increasing control of their senses and bodies.

I would suggest that proper sensory integration development is required for the development of interoception, and that interoception issues would hinder efforts to control and regulate attention. As per Singer’s indication that joint ACC-AI activation may involve a simultaneous generation of both a feeling and an emotional motivation, along with its associated autonomic effects (see Anterior Insular Cortex, above) any dysfunction in this functionality in a developing infant could presumably weaken the link between emotion and associated motivations. If this link is self-reinforcing via autonomic responses feeding back into interoception, or if alterations in autonomic responses connected with emotional shifts are dysfunctional, then disruption of autonomic responses would also have an additional impact on the regulation of emotional states.

Posner and Rothbart (1998) suggest that early infant life is concerned with the regulation of state, including distress, and that attention appears to be important in developing this form of control. They state that prior to three months, holding and rocking are usually the main means of quieting an infant, but at about three months, many care-givers attempt to distract their infants by bringing their attention to other stimuli. As infants attend, they are often quieted and their distress appears to diminish. I would suggest that if this process is interrupted – via a reduction in the infant’s developing ability to subjectively recognize distress and other emotional states, or by a weakening of the distress-regulating impact of attention (e.g. reduced autonomic feedback or reduced ability to perceive the feedback via interoception) - then the link between attention and comfort would be compromised. Variations in AI or ACC development that alter the infant’s ability to either feel or indicate distress could result in a slower or weaker development of attention as a means of control. Also, disruption of the development of interoception and/or attention could also impact development of the infant’s attempts to gain more direct control of attention and become more involved in attempting to solicit adult attention, i.e. interact with the world.

This dysfunction in autistics may also partially account for the prevalence of stimming and repetitive motions in ASD. A.R. Damasio's somatic-marker hypothesis of consciousness suggests that the sensory representation of the body is the basis for the mental representation of the sentient self, allowing the brain to distinguish the inner world from the outer world. As such, stimming and repetitive motions may be an attempt to generate sensory input, to increase AI functionality and enable autistics to help make sense of their internal and external environment.

One route for the impact of interoception issues via VENs may be through the vasopressin 1a receptors. Vasopressin has a role in promoting social bonding, and any disruption in V1a receptors in the AI or ACC could have an impact. In mice, V1a receptor knockout mice have a profound deficit in social recognition (Bielsky et al, 2004). A hypothesis is that vasopressin may play a role in the formation of social bonds between caregivers and infants, and that a disruption in these bonds, combined with a weakening in the development of attention, may impede the development of joint looking and gaze following, which would have implications for the development of joint social attention (see below).

Note that this impairment would be neurologically driven – this is not the refrigerator mother hypothesis, but a more profound neurological disruption. I am also NOT suggesting that autistic children do not show attachment to their caregivers. In a meta-analysis of sixteen studies of autism and attachment by Rutgers et al (2004), a majority of studies found evidence for attachment behaviours in autistic children, although children with autism were significantly less securely attached to their parents than comparison children, and that there was a link between level of mental development and security of attachment.

A further thought on interoception is that the development of subjective self-awareness of self is presumably required before one can project this capability to the analysis of others. As such, sensory integration and interoception issues that delay development of subjective self-awareness would presumably impact the extension of this capability to others. Schultz et al (2003) cite Gusnard et al (2001) as suggesting that the medial prefrontal cortex (MPFC) is involved in any kind of thought that uses the self as a referent. And Frith and Frith (2003) indicate that the MPFC is activated when we attend to our own mental state as well as the mental state of others. If this MPFC role in subjective awareness and understanding is developmental in origin, then issues related to interoception and self-awareness could presumably impact the development of mentalizing capabilities (more below).

ACC – Amygdala Interaction

Posner and Rothbart (1998) suggested that “amygdala-cingulate interaction might be a reasonable candidate for the earliest form of self-regulation in the infant”. Evidence of dysfunction in this relationship can be extrapolated from analysis of the amygdala in those with ASD. Schumann and Amaral (2006) indicated that in typical development the amygdala undergoes a prolonged postnatal increase in volume, reaching adult size in adolescence. In ASD, the amygdala is larger in young children and reaches adult size by about 8 years old due to faster growth, but then ultimately declines in size and has fewer neurons than age-matched controls. One hypothesis is that the amygdala has a normal or even increased number of neurons in early postnatal life, but that due to stress overload and the resulting overproduction of cortisol, over time this heightened response could have damaging effects leading to the loss of neurons and a smaller amygdala. The authors indicate that anxiety is a common comorbid feature of autism. I would suggest that this is due at least in part to the reduced ability of the ACC to mediate distress.

Executive Functions

As mentioned above, the frontopolar cortex is activated by executive functions, and overlaps with the ventromedial prefrontal cortex (VMPFC - areas 25, ventral 24, 32 and medial 10, 11 and 12), which is also implicated in some executive function tasks. Building on Posner and Rothbart (1998)’s hypothesis that executive function and control development is linked to the ACC, and Allman et al (2002)’s hypothesis of an evolutionary linkage between the ACC and area 10, a disruption in ACC and/or its links with the prefrontal cortex could impact the ability of the brain to develop the capability to direct attention, disrupting the development of follow-on capabilities, including self regulation of emotion, conflict resolution, error monitoring and correction, etc. This disruption may further carry over to impact mentalizing capabilities (see below), as performance on tests of executive function predict performance on theory of mind tests (Hill, 2004b). There may be an overlap in the areas of the brain activated by each function.

Hill (2004a) and Hill (2004b) give a good overview of executive dysfunction in autism. Autistics are not impaired on all executive function tasks. One area of impairment appears to be that of mental flexibility (Hill 2004a). Reduced mental flexibility is illustrated by perseverative, stereotyped behaviour and difficulties in the regulation and modulation of motor acts. Mental flexibility presumably activates the frontopolar cortex (Decety and Jackson, 2004), given this area’s engagement during intentional or explicit rule induction, as well as its suggested roll in mediating switching between different executive processes (Strange et al, 2001). In the WCST task, which is known to activate the frontopolar cortex, autistics usually (but not universally – Hill 2004b) experience difficulty in adapting to shifts in sorting by a new rule due to perseverative responses (Hill 2004a).

Autistics also have difficulties with some aspects of inhibition, specifically including the ability to inhibit prepotent response (Hill 2004b). A study by Stieben et al (2007) linked inhibitory control to dorsal ACC and error-related negativity (ERN) EEG activity in control children. Allman et al (2002) notes that while the error recognition and correcting function of the ACC evolved in our ancestors prior to VENs, that "spindle cells may serve to augment and relay the error-correcting information to other parts of the brain." This may include the frontopolar cortex, which also appears to play a significant role in inhibition (Decety and Jackson, 2004). One researcher (J Russell) suggested that autistic inhibitory issues may be related to the apparent arbitrary nature of the rules involved in the tests (Hill 2004b). Given that the frontopolar cortex is implicated in rule induction, dysfunctional ACC – frontopolar cortex interaction could be implicated in difficulties in deciphering arbitrary rules. Further evidence of a more direct inhibitory role of the frontopolar cortex is cited by Decety and Jackson (2004), in which several studies identified the frontopolar cortex in being involved in inhibitory or regulating processing (discussed further below).

Interestingly, Posner and Rothbart (1998) linked both the ACC’s role in error recognition and the role of inhibitory control in an experiment similar to the ‘Simon Says’ game. Children aged 40 – 48 months were asked to execute a response when given a command by a toy bear, but inhibit it when given a command by a toy elephant. Children up to 42 months scored no better than chance, but by 46 months they were virtually perfect, as inhibitory (physical) control developed. But the children who scored at chance levels apparently recognized they were not supposed to respond, as demonstrated by both slower incorrect response times and slowed responses to trials following errors. If inhibitory control is a frontopolar cortex function (discussed further, below) and error recognition is an ACC function, then this test demonstrates both the link between the two executive functions, and presumably the existence of a developmental link between the ACC and frontopolar cortex.

As per the key assumptions stated above, I would suggest that while area 10 is involved in rule induction and learning, that this is originally a socially-linked involvement, and that potentially the original ‘rules’ that train this area of the brain are both social in nature and are linked to experience-based development. In addition to area 10’s activation during emotionally charged moral dilemmas (mentioned above), further evidence supporting this involvement may come from Greene et al (2001), in which fMRIs were conducted on subjects being asked to make choices regarding moral-personal, moral-impersonal, and non-moral conditions. The medial portions of areas 9 and 10 (among other areas) showed significantly more activation during the moral-personal choices. I would suggest that this is because the role of area 10 is at least in part to decipher the social ‘rules of the game’, which may be among the most complicated and arbitrary rules in human existence. This role fits well with Allman et al (2002)’s hypothesis of a link between the ACC and area 10, the role of VEN neurotransmitter receptors in reward (dopamine) and punishment (serotonin), and Allman et al (2005)’s suggestion of one of the roles of VENs as being linked to intuition, with dysfunction in this role being a key deficit in ASD.

As suggested by Allman et al (2002), the role of the ACC may be to monitor the current state of reward and punishment and signal the need for behavioural adaptation, including to the frontopolar cortex. As such, a dysfunctional linkage between the two might impact the development of mental flexibility. Given the evidence that the frontopolar cortex is linked to rule changes and learning, while the dorsal, ventral, and dorsolateral prefrontal cortices are involved in guiding behaviour according to previously learned rules, dysfunctional ACC – frontopolar cortex connectivity could therefore have at least four major consequences: i) less frontopolar cortex experience-based development of the capacity to make adaptive responses to changing conditions, ii) greater reliance on existing learned strategies in a given situation due to reduced or altered frontopolar cortex activation, iii) a reduced ‘learned-experience’ set to call upon in a given situation, and iv) a resulting alteration in prefrontal cortex development, including potentially altered and/or dysfunctional development.

Frontopolar cortex developmental issues might therefore impact the frontal cortex as a whole. Bechara (2002) notes that impairments of emotional and social behaviour are often observed after damage to the VMPFC. "Previously well-adapted individuals become unable to observe social conventions and decide advantageously on personal matters. Their ability to express emotion and to experience feelings in appropriate social situations becomes compromised." Studies determined that theses deficits were the result of impaired ‘judgment and decision-making’. If VMPFC damage impacts the application of social knowledge, then presumably a frontopolar developmental impact on the VMFPC could be felt as an impaired ability to acquire this knowledge. Elsinger et al (2004) builds upon the notion of prefrontal cortex dysfunction from a developmental perspective, suggesting that age, experience, and an ‘altered integration and interplay of cognitive, emotional, self-regulatory, and executive/meta-cognitive deficits’ contribute to differences in behavioural outcomes.

Eye Contact and Face Processing

Averted gaze (i.e. avoiding eye contact) is a defining feature of autism. A reasonable assumption is that lack of eye contact can have an impact on the ability of autistics to decipher emotion in others. Autistics have also been reported to show less activation in the ‘fusiform face area’ (FFA) in the right fusiform gyrus (FG). This area is implicated in face perception in non-autistics (Schultz et al, 2003). Ashwin et al (2007) indicated that there is much evidence showing that autistics use a different cognitive style than controls for face processing, and found differences in brain activation during perception of fearful faces. Sasson et al (2007) identified that when processing emotional information in social scenes, individuals with ASD fixate on faces less than controls, and fail to orient to faces rapidly when facial information is available. But as Gernsbacher and Frymiare et al (2005) wrote, "It is not too surprising that autistics are less likely to activate the putative face processing area; autistics are less likely to look at faces." They indicated that autistics have described eye contact as threatening, painful, or draining. I would hypothesize that variations in gaze and face processing in those with ASD can be ultimately linked back to issues in the ACC and AI.

According to Decety and Jackson (2004), when reading emotions on the face of another one activates the same facial muscles at a sub-threshold level, triggering the same expressions on one’s own face, even in the absence of conscious recognition of the stimulus. Evidence further suggests that this results in autonomic changes, and is associated with a subjective experience of the corresponding emotion. As stated above, Singer et al (2004) suggests that the ability to understand the feelings of others and to empathize evolved out of our own ability to subjectively represent our internal body states. If so, then impairment in interoception (AI) or in the ability to generate the appropriate autonomic response (ACC) could render face emotion processing more difficult for those with ASD. In this case the face could be a less useful tool in eliciting information regarding the emotional state of others. As well, changes in gaze are presumably linked to attentional shifting and mental flexibility, which are also indicated (above) to be issues in autism, and will be explored further below (in Joint Attention).

Further, the left amygdala (among other regions) is activated during the discernment of gaze direction, and the right amygdala is activated when another individual’s gaze is directed at oneself, suggesting that the amygdala plays a role in reading social signals from the face (Kawashima et al, 1999). In much of the animal kingdom, direct gaze indicates threat. As Frith and Blakemore (2004) indicate, this is clearly not the case in humans, who use eye gaze to indicate a wide variety of positive and negative emotions and intentions. From an evolutionary perspective it makes sense that the neurological mechanisms that interpret direct gaze as a threat would continue to exist, but would be mediated by the social brain. M.A. Williams et al (2005) indicated that emotional facial expressions - especially expressions that convey potential threat - increase amygdala activation, even when the face is masked from awareness. Ashwin et al (2007) also confirmed activation of the social brain network in face processing in controls.

An amygdala subjected to less social brain mediation would presumably play an increased role in face perception, and the result might be more ‘discomfort’ in face processing, with eye gaze avoidance being an adaptive response. One source of this reduced mediation might be attention related. As mentioned above, dysfunctional ACC attentional development could have an impact on ACC regulation of the amygdala. Over time, the impact of altered ‘social brain’ development would also have an impact. Dalton et al (2005) reported that in autistic subjects, the amygdala is activated to an abnormal extent during a direct gaze upon a non-threatening face. As Richard Davidson (one of the researchers in Dalton et al, 2005) pointed out, it is over-aroused amygdalas that make autistic children want to look away: "Imagine walking through the world and interpreting every face that looks at you as a threat, even the face of your own mother." Evidence of a heightened response to direct gaze was also indicated by Kylliainen et al (2006). In measurements of skin conductance responses (SCR) to another person's gaze, ASD children showed greater SCR to straight gaze over averted gaze (i.e. a variation in autonomic response and discomfort), versus no difference in controls, indicating enhanced arousal to eye contact in those with ASD. Given the potential for both a reduced ability to read facial emotions and heightened discomfort when looking at faces, eye gaze avoidance in autistic children as an adaptive response should not be surprising.

Face processing is an emergent and developmental skill that is heavily mediated by early experience with faces (Sasson, 2006). As such, it is not unreasonable to expect differences in eye gaze behaviour to lead to differences in face processing between autistics and controls. But recent research suggests that the differences in FFA processing are not as great as once thought, while other variations in processing exist in the social brain network. Hadjikhani et al (2004) found that individuals with ASD activated the FFA and other brain areas normally involved in face processing when they viewed faces as compared to non-face stimuli. This suggests that ASD face-processing deficits are not due to a simple FFA dysfunction, but rather to more complex anomalies in the areas of the brain involved in social perception and cognition. Hadjikhani et al (2007) replicated the original findings of significant activation of face identity-processing areas (FFA and inferior occipital gyrus, IOG) in ASD, but also found activation to faces in this broader ‘social brain’ network. They identified hypoactivation in the more widely distributed network of brain areas involved in face processing, including the right amygdala, inferior frontal cortex (IFC), superior temporal sulcus (STS), and face-related somatosensory and premotor cortex, with atypical patterns of activation in the IFC and STS, suggesting that areas belonging to the mirror neuron system are involved in the face-processing disturbances in ASD.

Pierce et al (2004) looked at responses in adult autistics to both personally meaningful faces as well as to those of strangers. They also found significant FFA activity in autistic subjects, as well as greater FFA activity in response to familiar over stranger faces, plus right hemisphere dominance in response to both face types. The authors suggest that the study design may have contributed in part to the greater than expected activation to the faces of strangers, in that the use of familiar faces may have heightened the overall level of interest. They suggested that FFA activation may be related in part to neural systems related to social drive and motivation or cognitive and attentional engagement, reflecting (as above) that atypical FFA results in ASD may be related to the systems that modulate FFA activity.

A further interpretation of FFA activation is discussed in Schultz et al (2003). This paper noted Gauthier’s finding that the FFA responds preferentially to any class of object for which a person is perceptually an expert, which suggests that the FFA is organized by experience. Further, an experience bias normally indicates that it is important to discriminate faces by identity, biasing the FFA toward individual identification. The FG also encodes semantic information for category identification (including anything that helps identify faces as a category), and Schultz et al (2003) suggested that social information would also be stored, since the social retrieval of faces and social judgment is a repeated perceptual experience. The suggestion is that the middle FG area would store general information about people or a meta-representation of ‘peopleness’, including facial information during social events (i.e. facial affect), in an area overlapping with the FFA. Schultz et al (2003) also indicated that the FFA is activated as part of the social network, contributing to the identification of social events and emotions related to faces. The implication was that deficits in FFA processing in ASD would also impact social cognition. But if the FFA is activated in ASD then potentially this FFA social expression recognition functionality may also be active too.

Another area preferentially but not consistently linked to face processing is the superior temporal sulcus (STS). The STS is activated when observing the behaviour and also when retrieving information about the behaviour of living things, and perhaps with any complex behaviour. This area is also part of the mentalizing network of the brain (Frith & Frith, 2003). Hoffman and Haxby (2000) indicate that the STS has a role in the perception of eye and mouth movement and the changeable aspects of faces (e.g. expression), as well as in determination of eye gaze direction (see Joint Attention below). Blair (2003) indicates that the FFA is probably more associated with facial recognition, while the STS is more involved in processing social communications, presumably including recognition of affect. Even so, both the STS and FFA have a greater response to emotional over neutral expressions, and tasks requiring increased attention to emotional expressions result in a greater activation of both. Blair (2003) indicated that social expressions activated both the FFA and STS, and also indicated that STS can be further activated during recognition of emotion after preliminary activation, possibly as a consequence of amygdala activity. In effect, this subsequent activation may be an interpretive activity as part of this area’s role in the social brain network.

Clear evidence exists that autistics can recognize emotional states. Back et al (2007), for example, found that autistics were able to infer mental states from dynamic and static facial stimuli at a better than chance rate (but less accurately than controls). Autistics were also as successful as controls in recognizing mental states when eyes were presented in isolation or in the context of the whole face (presumably a function of STS processing). While studies have reported that autistic children have difficulty recognizing the emotional expression of others, Blair (2003) indicates that these studies have failed to match children on mental age. When appropriately matched, he states that autistic children have usually been found to be unimpaired in facial affect recognition. Further, several studies have found the emotion processing impairment to be pronounced only in complex cognitive emotions such as surprise or embarrassment. The issue in autism may not be an inability to recognize affect (when the autistic is looking at the face to be ‘read’). The evidence above indicates that autistics can use the FFA and STS for face processing and recognition of affect. Instead, the difficulty for the autistic, given reduced activation of the social brain network, would be in processing the emotion and (as per Blair, 2003) representing the emoter’s intent (see Emotion and Empathy, below). This is how I would interpret the findings of Hadjikhani et al (2007) of a hypoactivation (as distinct from lack of activation) in the more widely distributed network of brain areas involved in face processing, including the STS.

Interestingly, Pierce et al (2004) also noted significant amygdala activation in both controls and autistics, unlike Hadjikhani et al (2007)’s finding of reduced ASD activation. Given the conflicting amygdala results, I would interpret amygdala activity as changing over time. As noted above, Dalton et al (2005) showed heightened amygdala activity in children, while Hadjikhani et al (2007) and Pierce et al (2004) both examined older autistics. In addition, Pierce et al (2004) included a significant number of familiar faces, which could have motivated a higher emotional response among autistics vs. Hadjikhani et al (2007). As noted in Schumann and Amaral (2006) above, the amygdala in autistics reaches adult size by 8 years old and then ultimately declines in size. I would suggest a) that over time the role of the amygdala changes with autistic neural development, and b) the later development of some social brain capabilities may impact key developmental windows of other functions, reducing some downstream capabilities. As an example, the later development of theory of mind capabilities may miss the developmental window that allows for effortless social brain mediation of amygdala reactions to faces.

Emotion and Empathy

A significant consequence of interoception issues may be the inability to fully understand one’s own emotional state, and the emotional state of others, which could manifest as a difficulty in developing empathy.

Decety and Jackson (2004) defines empathy as "a complex form of psychological inference in which observation, memory, knowledge, and reasoning are combined to yield insights into the thoughts and feelings of others". Three primary components are involved: a) an affective response to another person - often but not always including sharing their emotional state – based on perception-action coupling (see below) that leads to shared representations of behaviour, b) self-other awareness, separating temporary identification with the other from emotional contagion, and c) the mental flexibility to adopt the subjective perspective of the other but subject to self-regulation (Decety and Jackson, 2004).

Shared representations between self and others is based on the concept that the perception of emotion in another automatically activates the neural mechanisms that are responsible for generating emotions in us, leading to our own representation of that behaviour. The underlying theory is that perception and action are linked – perception is a means to action and action is a means to perception – and that this is hardwired into our nervous system. In this hypothesis, the recognition of emotion in others (especially the intuitive recognition of same) stems from at least partially recreating the bodily and motor components of that emotion in ourselves. This is supported in part by the finding in lesion studies of paired deficits between emotional production and emotion recognition. In this view, some developmental psychologists propose that the understanding of others is ‘primarily a form of embodied practice’. "Humans develop and maintain their self-concept through the process of taking action and then reflecting on what they have done – that is, the sensory consequences of their actions – and later in life, what others tell about what they have done." From this, "the understanding of the other person emerges in part from being ‘like them’ in action, through imitation, and that this provides the basic mechanisms for empathy." (Decety and Jackson, 2004)

Carr et al (2003) indicated that the AI plays a fundamental role in the recognition of emotion in others, relaying action representation information to areas processing emotional content. They demonstrated that both the observation and imitation of emotional facial expressions in others activated overlapping neural networks. This included the pre-supplementary motor area and the rostral cingulate zone (RCZp, part of the ACC), causing a robust pre-motor response, supporting the concept that recognition of emotion in others is linked to sub-threshold action representation and subsequent interpretation within the self as per Decety and Jackson (2004), and Singer et al (2004). But if interoception issues impact the effective subjective understanding of oneself, then reading a representation of others within ourselves would also be problematic.

Self-awareness and other-awareness are also potentially linked in another key manner. It has been suggested that both develop in close synchrony during the 2nd year because both types of cognition are based on a capacity for secondary representation. Self-awareness is based on secondary representation because the self as an object of knowledge is a secondary representation. Other-awareness requires a secondary representation as it implies taking the perspective of another person into account. The development of this capability may be the driver of significant increases in social-cognitive competence during this period (Decety and Jackson, 2004), e.g. triadic joint attention, theory of mind, empathy, etc.

This development may be linked to executive function. Carlson and Moses (2001) demonstrated that inhibitory control was strongly related ToM performance in preschool age children. A conflict task, requiring a novel response in the face of a conflicting prepotent response, was significantly related to ToM. The authors indicate that the findings suggest that inhibitory control may be a crucial enabling factor for ToM development, possibly affecting both the emergence and the expression of mental state knowledge. Kelly et al (2004) conditionally linked inhibitory control to the frontopolar cortex.

Decety and Jackson (2004) links empathy to perspective taking, i.e. the ability to more or less consciously adopt the subjective point of view of another. They stated that perspective taking develops gradually, and that it is around 18 months that children demonstrate an emerging awareness of the subjectivity of other people’s emotions. They also note that realizing that others can have a perspective that differs from one’s own does not mean that one is able to adopt the other’s perspective. People are fundamentally egocentric and their predictions of the feelings of others tend to be largely based on their predictions of how they would feel in the same situation. This is compatible with simulation theory, in which one is assumed to predict the behavior and mental state of others by simulating it as if we were in the same situation. Children especially often have to judge situations from a first-person perspective, and one study found that they were better at predicting what another would see if they had actually been in that situation themselves first. As such, self-perspective is the default mode of the mind.

Mental flexibility and self-regulation are therefore important parts of empathy in that they enable one to regulate one’s own perspective, recognizing that the other is like the self but while maintaining a clear separation between self and other. In this Decety and Jackson (2004) suggested that evidence from clinical neuropsychology and neuroscience points to the frontopolar cortex as being chiefly involved in inhibitory or regulating processing. Evidence suggests that damage to this area results in individuals taking an excessively egocentric perspective in moral dilemmas, revealing a lack of inhibition (or modulation) of self-perspective at the conceptual level. Decety and Jackson (2004) also cited neuroimaging studies of perspective taking supporting the hypothesis of an inhibitory role of the frontopolar cortex for adopting the subjective viewpoint of others, whether the shared activated representations are motor, conceptual, or emotional in nature. Further support for this role was provided by fMRI studies in which involvement of the right lateral prefrontal cortex was detected when participants inhibited a prepotent response in a sensory motor task and also in a deductive-reasoning task.

As such, Decety and Jackson (2004) argues that the inhibitory component of the frontopolar cortex is required to regulate and tone down self-perspective to allow for the evaluation of the other-perspective. The authors indicate that this is required because the automatic link between perception and action renders the self-perspective as the default mode and prepotent response. Regulation of this prepotent response (potentially an executive function impairment in autism, as discussed above) allows for cognitive and affective flexibility. I would suggest that dysfunction in ACC-frontopolar cortex linkages, potentially related to issues of VEN functionality, may drive the impairment in inhibitory control in ASD.

The above is not to say autistics have universal impairment in empathy (see Key Assumption 4, above). Gernsbacher (2006) discusses the example of Walker Hughes, an autistic who clearly demonstrates a capacity for empathy. I would also suggest that difficulties in the ability of autistics to empathize may too often be inaccurately linked in the minds of others to a lack of desire to empathize or emotionally bond with others. Difficulty in understanding others does not automatically equate to a lack of desire for understanding or a lack of desire to try. But that is another post.

Joint Attention

Joint attention can be defined as the interaction between two people about a third object (Frith and Blakemore, 2004). But as per Frith and Frith (2003), joint attention can be defined according to strict or lenient criteria. If joint looking or gaze following is required, then this can occur relatively early. From approximately 12 months, infants tend to automatically look at a target that an adult is looking at. But this only happens when the target is already within the infant’s point of view. Strictly defined, joint attention indicates an implicit awareness that others can pay attention to different things than oneself, and that others’ attention can be directed to coincide with one’s own interests. This level of joint attention emerges around 18 months, and indicates an implicit ability to mentalize (Frith and Frith, 2003). Joint attention issues are probably universal in autism (Hill, 2004a). I would suggest though that joint attention difficulties are a follow-on consequence of some of the issues discussed above.

Infants can reflexively use movement of gaze as a priming cue for own eye movement at three months. But as Frith and Frith (2003) indicate, this is probably both innate and rests on an entirely different set of neural capabilities than those demonstrated by joint attention. Voluntary gaze following is first seen around 12 months, and suggests a primitive understanding that gaze involves a relation between a person and the object of their gaze. Note that this is not the same as joint attention, strictly defined, and this voluntary gaze following occurs only when the target object is within the infant’s line of vision (Frith and Frith, 2003). Another similar activity is ‘social referencing’, which starts at around 8 to 10 months, and involves an active attempt by infants to obtain emotional cues from others to assist in their assessment of uncertain or ambiguous objects or situations (Decety and Jackson, 2004; Blair, 2003). Both cases require the infant to actively focus attention on another, and I would suggest that both could be an issue for infants who will later be diagnosed with ASD.

One could speculate, as per the discussion in Eye Contact and Face Processing above, that if children with ASD have difficulty in looking at the eyes of others then gaze following could also potentially be impacted. One of the areas linked to gaze following is the superior temporal sulcus (STS). In a test of congruent vs. non-congruent eye gaze, Pelphrey et al (2005) found that both controls and autistics activated the STS region in response to shifts in eye gaze. But only controls showed STS activity that differentiated congruent vs. incongruent gaze shifts. In autistics they reported that the only reliable changes linked with incongruent gaze was activity in the insular cortex and inferior frontal gyrus. In controls, greater STS activity was associated with violation of expectations and a need for revision of expectations. In autistics, incongruent activity did trigger a response, so recognition of incongruent activity did occur. But the response did not involve activation of the social network as per the controls. From this one could suggest that ASD issues with joint attention are related not to gaze identification (which is presumably a precondition of same) but to 'attention' and the subsequent analysis of the gaze intention of others, i.e. mentalizing.

According to Carpenter et al (2002), typical infant development follows a reliable sequence. Infants first share others’ attention (alternating gaze between an object and an adult), then follow others’ attention and then behaviour (imitation), and then they direct others’ attention (declarative gestures) and then behaviour (imperative gestures). Autistic children tend to follow the typical pattern of sharing, then following, then directing, but with attention following rather than leading behaviour – i.e. follow behaviour, share attention, direct behaviour, follow attention, and then direct attention (Carpenter et al, 2002).

This makes sense if one considers that autistics may have an early difficulty in the development of an understanding of others, due to both attentional issues and difficulties in interoception and the development of self-understanding. Hobson and Hobson (2007) suggest that “the propensity to adopt the bodily anchored psychological stance of another person is essential to certain forms of joint attention and imitation, and that a weak tendency to identify with others is pivotal for the developmental psychopathology of autism”. But if the understanding of others is ‘primarily a form of embodied practice’ (Decety and Jackson, 2004), then how does one accomplish this in the right order if one has difficulty with interoception and in embodying one’s own persona?

Identification with others could be also potentially be impacted via issues in the detection of external agency. Blair et al (2002) indicated that there is some evidence of a reduced sensitivity to agency cues in ASD, especially related to movement. Evidence suggests that the inferior parietal cortex plays a role in the elaboration of the image of the body in space and time, and that the right inferior parietal cortex in conjunction with the prefrontal areas may be critical in distinguishing self from others (Decety and Jackson, 2004). In a shared representation framework, an efficient body schema may be necessary not only for recognizing one’s own actions but also for subjectively understanding the actions of others. Decety and Jackson (2004) suggests that the inferior parietal cortex in conjunction with the prefrontal cortex plays a pivotal role in the sense of self by comparing the source of sensory signals, crucial in maintaining a distinction between the self and the other and keeping track of the origin of feelings.

Farrer and Frith (2002) suggested an AI role in this process, concerned with the integration of input associated with voluntary movements, while the inferior parietal cortex represents movements that can be applied to the actions of others as well as oneself. Being aware of causing an action was associated with activation in the AI, while being aware of not causing the action and attributing it to another was associated with activation in the inferior parietal cortex. Farrer et al (2003) took this further, suggesting that the sense of agency is based on a continuous mechanism, with greater correspondence of input indicating a greater sense of agency and greater insula activity, and weaker correspondence resulting in higher levels of activity in the right inferior parietal lobe. I would suggest that AI-based interoception issues would have a significant impact on this mechanism: if one has difficulty in detecting and determining the origin of one's own sensory input, then how can the brain use this information to determine the degree of correspondence of input required to attribute agency?

To the extent that inferior parietal lobe development depends on AI functioning and connectivity, inferior parietal lobe functionality could be impacted by AI dysfunction. I would suggest that Pelphrey et al (2005)’s finding of insular cortex activity but not further activity in the mentalizing system in those with ASD in incongruent gaze detection is a demonstration of the inability of the AI-inferior parietal cortex agency determination mechanism. I would suggest that information processing could not get past the agency determination 'gate' to activate the mentalizing system. As such, AI issues could explain issues related to social referencing and gaze following, both of which presumably require a functional sense of agency attribution. To the extent that they are developmentally related, they could also impact joint attention, the development of which also presumably requires the ability to assign agency.

As mentioned previously, the frontopolar cortex and cingulate cortex are involved in joint attention, along with the ventromedial frontal cortex (Williams et al, 2005). Dysfunctional connectivity between the ACC and frontopolar cortex could presumably impact the development of the frontopolar cortex and any related functionality. Strange et al (2001) suggested that the dorsal, ventral, and dorsolateral prefrontal cortices are involved in guiding behaviour according to previously learned rules. Given the suggested role of the frontopolar cortex in deciphering ‘the rules’ for later application by other areas of the prefrontal cortex, any frontopolar cortex issues would presumably have a knock on effect on development on those areas.

Given the role of the frontopolar cortex in inhibitory control (discussed above), which - as per Decety and Jackson (2004) - appears to be required to regulate and tone down self-perspective to allow for the evaluation of the other-perspective, a deficit in the development of inhibitory control may impact attention shifting required for social referencing, joint gaze, and the development of joint attention, above and beyond a weak tendency to identify with others. It may also impact the ability to develop a capacity for secondary representation that is required for both self-awareness and other awareness (i.e. the ability to see both self and other as an object of knowledge), given that this requires the development of inhibitory control.

Mirror Neuron System

One of the theories of autism is the ‘broken mirrors’ hypothesis. As stated by Hamilton (in press), "At its simplest, the broken mirror hypothesis claims that children with autism have a dysfunction of the mirror neuron system, and that this is the primary cause of their social disability (Dapretto et al., 2006; Iacoboni & Dapretto, 2006; Ramachandran & Oberman, 2006; Williams et al., 2001)." To examine this hypothesis, it is necessary first to define the mirror neuron system (MNS).

The core of the MNS is the inferior parietal lobule (IPL) and inferior frontal gyrus (IFG), which respond when hand actions are performed, imagined, planned, and imitated, and are widely assumed to contain ‘mirror neurons’ similar to those studied in equivalent regions of the macaque brain. Associated with this area is a region stretching from he lateral occipital sulcus through the middle temporal gyrus to the STS, labeled by Hamilton for simplicity as the MTG, which is robustly engaged in action observation tasks and modulated by motor performance (Hamilton, in press).

First, one of my own biases (that may reflect my lack of knowledge) is that I don’t believe that there are ‘mirror neurons’ in humans, but rather neurons that are activated as part of the MNS. To the best of my knowledge, no one has been able to clearly identify a ‘mirror neuron’ as a unique cell type, but instead, a ‘mirror neuron’ appears to be a neuron invoked during both self and ‘other’ representation. Second, as Hamilton (in press) identifies, the MNS is part of the motor system, and is an essential part of the neurological control of our own actions, in addition to its activation during imitation and action observation tasks. As per my stated assumptions (earlier), in hindsight it makes sense that rather than recreate a new system to explain others, it is more feasible that evolution has endowed humans with the ability to explain others using the same neurology that is used to operate and explain ourselves. Thus, if autistics have a dysfunctional MNS then the result should be impairment in all cognitive tasks that utilize this system, i.e. performing goal directed actions, imitating others, and understanding the goals of others (Hamilton, in press).

Frith and Frith (2003) identified the principle of rationality. Between 9 and 12 months, infants develop the expectation that agents will approach a goal in the most economical way, and are surprised if an agent does not do so, but – for example – jumps over an invisible hurdle. This demonstrates that infants can separately represent the goals of agents and the means used to reach the goal, both of which the authors indicate are likely to be important prerequisites of the ability to represent intentions. Carpenter et al (2001) studied the understanding of others’ intentions in 2.5 – 5 year old autistics vs. controls with other developmental delays using a test of others’ unfulfilled intentions in an imitation context. They found no significant between-group differences on any measure involving the understanding of others’ intentions. They suggested that those with ASD may have a slightly less complex understanding of others’ intentions than do other children (I would suggest that this might be experience-related) but was clear that any deficits in this area were not as marked as those found in ToM tests.

Hamilton et al (2007) also tested ASD children vs. controls with the same verbal mental age on four action representation tasks, as well as a series of ToM tests. ASD children demonstrated the same tendency as controls to imitate an examiner’s goals, imitate hand-goals in mirror fashion, and imitate grasps in a motor planning task, and on a gesture recognition task outperformed the controls, despite impairment on the ToM tasks. The authors concluded that autistic children have no difficulties understanding the meaning of an action or imitating the goal of an action, demonstrating clear evidence against a general imitation impairment or global MNS deficit, and therefore refuting the ‘broken mirror’ hypothesis. Instead, Hamilton (in press) identifies that where imitation errors do occur in ASD, they tend to be tasks requiring mimicry of style or meaningless actions. These types of tasks tend to require copying the low level kinematic features of an action. In contrast, goal oriented emulation tasks require the understanding the goal, from whence one can, if one chooses, plan or reconstruct the action by one’s own means, and this capability is intact in autistics.

The differences in capabilities relate to differences in the three components of the MNS, and the information flow between them. The MTG provides a visual representation of the low level, kinematic parameters of the observed action, the IPL provides a more abstract representation of the goal of the observed action, and the IFG provides a motor representation of the observed kinematic parameters, in preparation for imitating the action. Together the three nodes enable humans to plan and perform complex visually guided hand actions, to imitate another person’s action, and to understand the meaning of that action (Hamilton, in press).

In addition, the pathways between the three nodes explains differences in processing (Hamilton, in press). The primary MNS route is the EP route, in which imitation occurs in two stages. First, in the E route the visual representation of the observed action in MTG is used to infer the goal or meaning of the action in IPL. Once the goal representation is obtained, the P route between the IPL and IFG is used to plan an action based on that goal, with the planned action represented in the IFG in terms of its motor parameters. The result is a separation between action understanding and action planning. Together they become goal-emulation. Hamilton (in press) indicates however that there is evidence of another pathway, the M route between MTG and IFG that allows for the mimicking of the low level kinematic features of observed actions without requiring the prior understanding of a goal.

In typical individuals Hamilton (in press) suggests that both routes may be used separately or often together, but in ASD the suggestion is that the EP route is functional while M route may be compromised. The result is that ASD children can emulate an observed action if they understand the goal, but the ability to spontaneously imitate a meaningless gesture or facial expression may be reduced.

Hamilton (in press) raises the further hypothesis that the dysfunction is not with the M route, which may in fact be intact, but with modulating the route and deciding who and when to mimic, with this impairment being driven by dysfunction in the mentalizing network of the brain. As such, dysfunction in the ‘theory of mind network’ would be a cause rather than a consequence of abnormalities in the direct M route. I will discuss mentalizing further in the following section.

I would also suggest that this dysfunction may be related to an issue in the detection of agency. To use the EP-M model, for the person’s own system to become a mirror system it would first need the capability to detect agency, both externally (recognizing others as actors) and internally (i.e. recognizing whether represented actions are ‘self’ or ‘other’ generated). From an external perspective, children with ASD have the ability to detect agency in external actors and thus according to the EP model can use mirror neuron system capabilities to determine and emulate goal linked behaviour, assuming that attention is directed towards the ‘other’.

For the M route though, detection of external agency may not be enough, especially as some mimicry behaviour is not consciously directed, and some behaviour is ignored. As Kilner et al (2006) "everyday we are in situations in which we observe many people moving simultaneously and it seems highly unlikely that the ‘mirror system’ is activated equally by all the observed movements." Their study determined that modulation of parietal-occipital α-frequency range oscillations (which are attenuated during action observations) varied depending on whether the observed actor was facing towards or away from the subject. Given that the STS detects biological motion, the authors suggested that input to the ‘mirror system’ is filtered by modulating visuospatial attention, and that social relevance might modulate information entering the ‘mirror system’.

The M route is a direct route between observation and motor kinetics. Given the perception-action link, the M route could be assumed to require the ability to separate representation of self vs. other actions, i.e. to determine the agency associated with the internal representation of action. As per the discussion in Joint Attention (above), Frith and Frith (2002) indicated AI involvement along with the inferior parietal cortex in determining a sense of agency. Farrer et al (2003)’s suggestion that the sense of agency is based on a continuous mechanism - greater correspondence of input indicating a greater sense of agency and greater insula activity, and weaker correspondence resulting in higher levels of activity in the right inferior parietal lobe – further suggests that AI interoception issues would impact the ability to determine agency. I would suggest that this determination of agency would be an essential precondition or gate for the activation of the motor system, and thus the inability to internally determine agency would result in the exclusion of ‘other’ representations from the M route. I would go further and suggest that inability to determine agency may also impact self generated attempts to activate the motor systems and may therefore partially explain bodily control and movement issues in some with ASD. But that is another post.

Mentalizing (Theory of Mind)

Frith and Frith (2003) indicate that the mentalizing system of the brain is probably operational from about 18 months, allowing the implicit attribution of intentions and other mental states. Another major leap in development occurs between ages 4 and 6, during which explicit mentalizing becomes possible, which includes a full and explicit awareness of others’ mental states and their role in the explanation and prediction of their behaviour.

"Tentatively, we can conclude that an implicit version of the intentional stance emerges first, concerned with desires, goals and intentions. This is usually dated at around 18 months. At 18–24 months there is a convergence of several important developmental milestones, including a true understanding of joint attention, deliberate imitation and the ability to track a speaker’s intention while learning words. There is also evidence for the ability to understand knowing and seeing at an implicit level, and possibly even an implicit understanding of false belief." (Frith and Frith, 2003)

Mentalizing capabilities are widely accepted as being impaired in those with ASD. To be clear, I fully accept that those with ASD can be fully capable of performing tasks requiring explicit mentalizing (and even that degree of waffle is due only to my inability to state that ALL autistics have this capability, any more than I can state that all people have ANY particular capability). Frith (2004) references Happe (1994) as indicating that children with autism who have sufficient verbal ability to follow mentalizing tests show a delay in this area of about five years. What those with ASD appear to lack is the ability to intuitively process the intent of others. As Frith and Blakemore (2004) indicate, the slow acquisition of an explicit theory of mind does not replace the missing intuitive capabilities, and even very capable adults with Asperger syndrome demonstrate slow and error prone responses during mentalizing tasks.

Mentalizing appears to be based on three consistently activated areas of the brain – the medial prefrontal cortex (MPFC); temporal poles, bilaterally, with greater activation on the left; and posterior STS, bilaterally, with greater activation on the right (Frith and Frith, 2003). The STS is activated by biological motion and the behaviour of living things, including gaze detection. As discussed above (Joint Attention), autistics can detect gaze direction and incongruent gazes, and anyone who has spent any time with an autistic knows that they can detect biological agency. Presumably this means that the STS is functional in autism.

The temporal poles are activated in studies of language and semantics (left), semantics, autobiographical memory, and the recognition of familiar faces. Frith and Frith (2003) suggest that the region generates a wider semantic and emotional context for material being processed, on the basis of past experience, which would aid in interpretation. Included in this is the generation and retrieval of scripts, which capture the actions and goals in a particular activity or setting and time, and are built through experience. Identifying the appropriate script for a situation helps in predicting the actions of others, and provides a framework in which mentalizing can operate. Further, mentalizing may be required to understand deviations from scripts. Given that autistics can apply scripts – indeed, it may be when life deviates from scripts that autistics encounter difficulties – one could speculate that temporal pole functionality may be relatively intact in those with ASD.

Which brings us to the MPFC. In a comparison of 12 mentalizing tasks analyzed via fMRI, Frith and Frith (2003) reported that all twelve tasks activated the MPFC. The mentalizing area in question includes the most anterior part of the paracingulate cortex (BA 32) and overlaps with (depending on the nomenclature used) the anterior rostral cingulate zone and the emotional division of the ACC. BA 32 is described as a cingulo-frontal transition area that is anatomically and potentially functionally distinct from the ACC (Devinsky et al, 1995, Frith and Frith, 2003). In two of the mentalizing tasks compared above (an economic game of mutual cooperation and ‘Stone-Paper-Scissors), the MPFC was the only region differentially activated when subjects thought they were playing another person rather than a computer. This suggests that the temporal poles and STS are more concerned with the sensory signals that initiate the mentalizing process, while the MPFC is engaged by attending to the mental state of the self and others (Frith and Frith, 2003).

As with emotion and empathy and the mirror neuron system, it appears that the capacity for mentalizing about others arises from the activation of the same area of our brain that is activated in mentalizing tasks in which the subject is oneself. While the AI appears to contain the subjective representation of our body state, the MPFC contains the subjective representation of our mental state. The ability to understand oneself relies on the ability to generate a second-order or subjective representation. The first-order representation is the actual physical stimulus, while second-order representation is the mental attitudes that we take towards the stimulus. As Frith and Frith (2003) wrote, these second-order representations are decoupled from the physical world, and are no longer subject to normal input-output relationships - e.g. a change in stimulus does not necessarily correspond to a change in one’s perception of an event.

Activity in the MPFC is linked to the creation of decoupled representations of beliefs about the world that may or may not correspond with the actual state of the world. Thoughts, feelings and beliefs need not be accurate representations of reality. And as Frith and Frith (2003) indicate, mentalizing is not only about representing our own mental states as distinct from reality, but also about representing the mental states of others. Schultz et al 2003 quotes Gusnard et al. (2001) as suggesting that the dorsal MPFC is involved in any kind of thought that uses the self as a referent, e.g. theorizing about others’ minds but with explicit reference to the participant’s own frame of reference as to how they would feel in a similar situation. Decety and Jackson (2004) also indicates that the MPFC is involved in both self-perspective and other-perspective. Interestingly, self-perspectives also activated the AI and secondary somatosensory areas, while the adopting of other-perspectives also activated the frontopolar cortex and posterior cingulate.

The role of the frontopolar cortex may be of critical importance in mentalizing. As mentioned above, Carlson and Moses (2001) demonstrated that inhibitory control was strongly related ToM performance in preschool age children, and suggested that inhibitory control may be a crucial enabling factor for ToM development, possibly affecting both the emergence and the expression of mental state knowledge. Kelly et al (2004) and Decety and Jackson (2004) both linked inhibitory control to the frontopolar cortex.

Given that self-awareness and other-awareness both activate the MPFC, as per Decety and Jackson (2004), there is a requirement for regulation and inhibitory control to be able to separate the self from the other. As per above (Emotion and Empathy), this is required to regulate and tone down self-perspective to allow for the evaluation of the other-perspective. They argue that this is required because the automatic link between perception and action renders the self-perspective as the default mode and prepotent response. While the authors were considering this requirement in relation to emotion and empathy, logically it should apply to any representation that could have a self or external origin. As such, I would suggest that the same frontopolar based inhibitory control mechanism that enables one to take an ‘other-perspective’ from an emotional standpoint is also required to do the same from a cognitive perspective. As above, I would suggest that dysfunction in ACC-frontopolar cortex linkages, potentially related to issues of VEN functionality, may drive the impairment in inhibitory control in ASD. This would also impact the intuitive ability to mentalize.

Given that much of learning is both experiential and socially based, difficulties in acquiring the ability to interpret and understand the thoughts of others would have profound consequences for overall development in autistic children. Lack of understanding of others could significantly impair the development of social competencies, as well as impact the ability to learn from others. This could account for many of the criteria that lead to a diagnosis of autism, as well as secondary (non-DSM IV) criteria such as lower IQ, which in many cases may be related more to perceptual issues and the ability to learn from others than a reflection of any underlying cognitive deficits.

Language acquisition may be another area that is impacted. Frith (2001) referred to an Baron-Cohen et al (1997)’s use of the discrepant looking paradigm, in which the speaker and listener attend to different objects while the speaker utters a new word. Controls mapped the word to the object the speaker was looking at, while children with ASD erroneously mapped the word to the object that they were looking at. Frith and Frith (2003) suggest that the rapid learning of language from around 18 months may result from a child’s ability to track a speaker’s intentions when they utter a word. Carpenter et al (2002) suggested that autistic children instead used imitation (imitative learning – i.e. goal directed learning) to acquire language prior to the development of joint attention, which could account for some of the atypical features of the language of autistic children.

Mentalizing difficulties would especially impact role reversal imitation. The ability to reverse roles may require a holistic understanding of a shared interaction, with each person’s role being interchangeable, i.e. a second-order representation. Carpenter et al (2005) indicate that this ability may be a prerequisite for the learning of bidirectional communicative symbols, e.g. the understanding and use of pronouns. The authors indicate that children see themselves and others as interchangeable (I am like them and they are like me) and actively use this understanding, learning from others (self-self role reversal – e.g. you touch your hand, I touch mine), reciprocating (other-other role reversal – e.g. you pat my head, I pat yours) and engaging in collaboration through object-mediated role reversals (e.g. I hold a basket, you put items into it, then reverse). These reversal imitations become acts of cultural learning and participation. Carpenter et al (2005) suggest that the difficulties that autistic children have with role reversal at each level has a cascading detrimental impact on their cultural involvement.

The Kitchen Sink

In a post that has probably unwisely included everything but the kitchen sink, here goes. One of the points that caught my attention while reading Devinsky et al (1995) was related to a link between ACC seizures and muscle tone. Anecdotally speaking, I’ve heard a lot of reports of hypotonia in autistic children, and Ming et al (2007) identified this as the most common motor symptom (51%) in a study of 154 children with ASD. Other conditions found included motor apraxia (34%), and gross motor delay (9%). The authors noted that all of these conditions appeared to improve over time. While I don’t have corresponding data for the general population, I will speculate that these numbers are significantly higher than normally found, and thus may be more than comorbidities.

Given Devinsky et al (1995)’s linking of the ACC to early premotor processing, I would speculate that ACC issues may contribute to the difficulties some autistic children have with motor impairment, and that this may be worthy of further research.

Conclusion (Finally)

Based on the evidence suggested above, I believe that there are reasonable grounds for suggesting that the major neurological and behavioural issues related to ASD may be the result of developmental consequences linked to ACC and AI dysfunction, with follow-on consequences related to ACC-frontopolar cortex connectivity and development. Further, these issues may be linked to a dysfunction in VEN development. VEN issues are not ‘required’ to account for the ACC and AI dysfunction suggested above, but I would suggest – assuming that there is some validity in this analysis – that it may be more than circumstantial that these three ‘final common pathways’ are all linked through either the presence of VENs or potentially via VEN connectivity (assuming ACC – frontopolar cortex links as per Allman et al (2002)). If VEN issues do exist then they may be a result rather than the primary cause of ACC, AI and frontopolar dysfunction, e.g. prior issues may impact VEN migration and development. Regardless, given the potentially significant role of VENs human neurology, any VEN disruption may have significant follow-on consequences.

I would suggest, based on the above, that the ACC, AI, frontopolar cortex and VENs are worthy of significantly more research by those seeking to understand the causes and consequences of ASD.

Further, if this analysis has some validity then I would suggest that it may require some rethinking about the nature of ASD. For a start, it would link ASD’s current DSM-IV behavioural criteria to a neurological foundation and a potential chain of developmental events. It would also call into question some of the more pejorative historical assumptions about ASD and those who qualify for the diagnosis. I will explore these issues in a follow-on post related to ‘Acceptance’.

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Williams JH, Waiter GD, Perra O, Perrett DI, Whitten A (2005) "An fMRI study of joint attention experience" Neuroimage 2005 Mar; 25(1):133-40 (Link)

Williams MA, McGlone F, Abbott DF, Mattingley JB (2005) "Differential amygdala responses to happy and fearful facial expressions depend on selective attention" Neuroimage. 2005 Jan 15;24(2):417-25 (Link)

My Next Post

2007-06-15T22:24:00.000-04:00

Okay, after a very long hiatus I'm back.

I've been working on a post that has nearly morphed into a research paper, and it is finally time to post it.

First, a warning. The paper is verrryyyy long. My recommendation, for anyone who is interested in reading it, is that you break it into smaller sections and read a little at a time. This approach has worked well for someone who had an earlier draft copy. The paper is already divided into sections that may make for convenient break-points.

For those who are asking why I have not broken the paper up for you, my answers are that a) after spending so long writing this I just want to get it out there (and so do not want to delay posting even further to take the time to burst it), b) that anyone who is interested in reading it can probably judge how large a 'chunk' is digestible for them at a time, c) that any criticism should probably be based on having a full copy of the paper to skewer, rather than picking at parts, d) that the blogging community is no longer the only audience that I'm trying to reach with this post and e) writer's fatigue. (E is probably the most honest answer.)

For those who are interested, the paper is also available in MS Word. Just drop me an email if you want a Word copy (see the link in the side bar for an email address, if you don't have my real email).

My overall hypothesis is that the disorders called ASD can be explained through a developmental interaction of the Anterior Cingulate Cortex (ACC), Anterior Insula (AI), and Frontopolar Cortex. From the developmental interaction of these regions I think that one can link sensory issues, executive functions, eye contact and face processing, emotion and empathy, joint attention, the mirror neuron system, and mentalizing (theory of mind) in an overall explanation of ASD. I have not tried to account for every facet of ASD (the paper is already long enough, thank you - I had to come to a stop somewhere), but I believe that many of the omissions can also be explained in light of the material presented. If pressed hard enough I might try to do so.

One key omission is that of speech (although I touch upon language acquisition in places). I would suggest that speech issues can ultimately be linked to a variety of causes, primary and secondary, including sensory and motor integration and developmental issues, but that this is a topic worthy of its own post. I could not do the subject justice by cramming it into this post, but invite you to write your own if you feel so inclined.

Not all of you will like the explanation that I am proposing. Oh well. The real test is whether it ultimately holds water, not whether anyone in particular likes it.

To be clear, I do not propose an answer as to WHY the issues that I describe have occurred. My view is that there are probably multiple etiologies behind what is ultimately called ASD. What I am suggesting though is that various causation models ultimately result in ACC and AI dysfunction to a greater or lesser degree, and that the developmental impact of this dysfunction results in various presentations of ASD. If I am wrong then so be it. I still have my job as a used car salesman to fall back on (kidding!). At a minimum there is probably some interesting learning for those who are willing to do some reading, and the references (with links, where available) at the end of the post make for a pretty good reading list.

I would also like to point out that I am solely responsible for any factual errors or misinterpretations of existing work found in this post. Having said that, I am grateful to the person (a fellow blogger) who has been reading through the material and has let me know that there may actually be something here that is worth reading. I'm not going to reveal who that person is, only because I don't want to unfairly saddle them with any responsibility (or - in the ASD blogging world - blame) for the content. But I am grateful for this person's efforts (you know who you are - Thank You).

So, I'll post the paper in the next day or so. I'm up for an interesting discussion on this, if anyone is willing. All I ask is that any debate remain civil and courteous, and be based on what is written (or not written but that legitimately challenges the hypothesis), rather than what anyone wants to pretend that I have written.

Finally, I plan on following up the post with the 'Acceptance' post that I have been threatening to write for a while. After this I finally feel that I have enough written that I can clearly state what it is that I do and do not 'accept'.

Yes, I'm Still Here

2007-04-23T17:55:00.000-04:00

Hi All,

Just a quick post to let you know that I'm still here. I haven't stopped blogging (although it may certainly look that way, given the dearth of recent posts), but instead have been caught up in researching what I think will be a very interesting (but long) post. Of course, I'm biased on this (on the 'interesting' part - you can trust me on the 'long' part). I've been working on it for a while now, and each time I dig a bit deeper I find something even more interesting, to the extent that it has become quite the perseveration. Anyway, just in case anyone noticed, that's why my head's been down for the past few weeks, on both my blog and on others' blogs too.

During this time it appears that I missed my one year blogiversary (March 31st). I've turned off the comments on this post, because I didn't raise the point to solicit comments. I've had enough kind words from people both here and on other blogs, and links to here from other sites, to know that you can at least interest some of the people some of the time. For those who don't like what I have to say, well, that's fine too. As I said in my 'About Me', I learn the most from those I don't agree with, and I plan on giving you more opportunities agree or disagree in the future. I think that I'm usually pretty open to a reasonable discussion.

Instead, I'd like to take this opportunity to thank everyone who has dropped by over the past year, either commenting or lurking. I've enjoyed the blogging experience so far - both here and on other blogs - and met some nice people, and hope to resume the dialog soon. (I'm aiming for the end of the week, but - sigh - 'end of the week' has been my target for a couple of weeks now.) I hope that you've enjoyed visting too - or at a minimum have found at least one of the posts to be thought-provoking - and will find interesting 'food for thought' here in the future.

Thanks,

Ian

A Bear Update

2007-02-23T19:59:00.000-05:00

I haven’t written a post about the Bear in a couple of months, so I figure that now is a good time for an update.

One of the things we’re interested in for the Bear is music therapy. I still don’t know much about it, but another parent at our IBI school told me of a program that her son was in, how much he enjoyed it, and how she thought that it was really beneficial. I have to admit that music therapy was not previously high on my ‘should do’ list, but she gave the program a good review. Momma Bear and I gave it a quick bit of thought and came to the conclusion that this might be a good option to try. So I gave the therapist a call, and while there was no space available, we did secure a spot at the top of the waiting list. We didn’t expect to start the program until the summer.

The Bear LOVES musical interaction. I’ve never noticed her exhibiting any particular attraction to songs on her videos, but whenever my wife or I sing to her she absolutely loves it. She constantly gestures for me to sing to her (I never said she had good taste ;-) ) and Momma Bear can get her to positively beam with delight when she sings. The Bear does not seem overly interested in making music herself, although she does occasionally enjoy playing with the piano at my outlaws’ house, and will sometimes play with a keyboard at home. She also has some toys that play songs, and sometimes will press the button to play a few repetitions of certain songs.

Last week I received a call from the music therapist telling me that one of her clients was out of town for three weeks, so there was an opening if we wanted to take it. I said I’d take the first one and we’d see how it went, with the expectation but not a firm commitment to take the other two. (I offered to pay for the other two if we bowed out, but she said there was no need.) So the Bear went to her first session on Saturday morning. I sat at the back of the room and watched.

What a great experience! The therapist allowed the Bear to get acclimatized, which she did by doing a quick exploration of the room, and then the therapist sat in front of the Bear and started playing guitar and singing. The Bear loved it, and was hooked. When the therapist put down the guitar and started singing and playing a shaker, the Bear crawled up into her lap to participate. Over the course of the 45 minute session the therapist played different instruments, banged on various drums, shook tambourines and bells, sang, played a keyboard, and physically interacted with the Bear to determine how to gain her interest. She also gave the Bear various instruments to play. She encouraged her to explore, to play, to imitate, and was even able to get her to play her bells as part of some of the songs. With the exception of a couple of trips over to Dad to get her ‘milk’ and a couple of quick sessions on a rocking chair (to which the therapist added some music), the Bear maintained her interest and focus on the session and the therapist for pretty much the entire time, and was smiling and grinning throughout.

At the end, the therapist asked if we would be returning for the other two sessions. Very definitely. What was also interesting to me was that the therapist said afterwards that she was surprised by the Bear’s level of exploration and interaction, especially for a first session. I had previously told her that the Bear was assessed as ‘autism at the severe end of the spectrum’. While she said that she was not a doctor and did not ‘do’ diagnoses, from her experience the Bear was much more interactive than she would have expected. That was very heartening to hear.

The Bear is also doing well at school. Among other programs, she’s mastering or mastered shape shorting, shape puzzles, matching 3D objects (and as an added surprise stacked blocks up to 5 high), 2D objects, matching on colour, and among other tasks is working on matching quantities (e.g. moving three objects to match the number 3) and matching object categories (e.g. matching different cars to a cars category, or different dogs to a dog category). Her fine motor skills are improving with various exercises. She also appears to know her primary colours. When as a lark I tested her one day with various colours in assorted combinations – e.g. “which one is the red ring” - she got the first ten correct before she became bored and stopped me. Until then I had no idea she knew her colours by name.

We also expose her a lot to numbers and the alphabet, not in any particularly structured way, but instead to familiarize her with them and see what at this point she can pick up implicitly. We’ve noticed that she prefers complicated over simple visuals (e.g. she prefers the back of her video cases to the front, will spend a lot of time analyzing detailed and complicated pictures, and loves to get hold of my Economists and flip through them), which suggests to me that she is potentially analyzing and interpreting the complexity that she sees.

She has also very recently learned to drink with a straw. I consider this a big deal, as we can now use this as part of OT. I’ve come across a couple of OT exercises that use sucking and blowing through straws to encourage mouth control and coordination, which the Bear may have issues with. The evil Dad that I am, I’m also trying to teach her to stick out her tongue (and greatly look forward to the day when she does so (in)appropriately). She tries to imitate me, but she either twists it or makes a U shape. Again, helping improve her ability to use her mouth effectively may also help her to produce more sounds and ultimately learn how to speak.

The Bear also dances with us. Nothing too fancy, but she will sway from side to side and foot to foot to follow our lead, usually alternating her focus between our faces and our feet while trying to match our sway. Her IBI program can also get her to spin while dancing, and I’ve been able to get her to do this myself at times.

So, overall I’m quite pleased with how things are going. Whether one wants to credit her progress to IBI, our efforts, or just natural development (my money is on a combination of the three), the fact is that she is progressing, and we are seeing learning and growth. I fully believe that she is more capable than we know, but what we can see suggests considerable and even accelerating gains.

I wrote the above not to boast, as obviously there are children who are progressing both faster, slower, and on alternate paths to the Bear. There are also things that are clearly a challenge to her that we feel she ultimately needs to learn and overcome. Instead, the point I’m trying to make is that there is learning, and there is progress. All too often autism is presented entirely negatively, and with a bleak prognosis. At least in our case, we can also see good reasons for optimism and hope.

Some Thoughts On Blogging

2007-02-20T19:52:00.000-05:00

Phew, a narrow escape. I was worried that if I was hit by a bus and 'lost' that the previous post would have been left on my blog forever. Not that I regret the post. The way the comment that started it all was worded, it appeared that I was part of the 'mercury militia', so I felt the need to defend myself. Having said that, it was not my proudest moment. And FWIW, I accept Bazooka Joe’s overall explanation about what he meant (as opposed to what he originally wrote), even though I disagree that this blog is used by EoHers as evidence that an environmental trigger is responsible for autism. From my perspective there are no hard feelings.

Anyway, I’ve been thinking for a little bit now about why I’m blogging. Memory can sometimes be a bit self-serving, but I believe that I originally started for two reasons. First, as stated in my first post, I thought that in light of the increasing polarization of the ‘debate’, and as the “challenge to the more contentious bio-med practices is morphing into a more direct challenge against even mainstream accepted methods of investigating and potentially treating autism” that it was time for more moderates to join the debate. And second, I thought of the blog as a record of my thoughts and views for my daughter, the Bear. When she’s older she can read it, if she chooses, to understand the evolution of my thinking.

Very quickly, when I saw someone’s Demeaning Words I added a third reason – advocacy of understanding and (my view of) acceptance. I have intended to write a post specifically about ‘Acceptance’ for a while now, but I keep holding off. There is always one more post that I want to write first, to build my views upon. I don’t feel I can do the subject justice until I can point to what it is that I actually ‘accept’.

Also, because of the tone of the ‘debate’, I expect to get ‘lawyered’, which - no disrespect intended to my friend in the legal profession - is a shorthand I use for being exposed to a rigorous and hostile cross-examination. I’ve gone through these before, and witnessed a lot of others facing them too (on both ‘sides’). I also notice that sometimes when people can’t find an opening in something that was said that they then proceed to attribute both statements and motives to people that happen to be non-existent. The best defence is to have material to which to link, to clearly substantiate one’s views.

Since then I’ve added another reason for blogging, which is to draw attention to some of the science in autism that I think is both important and interesting (and that I understand). At either end of the debate a lot of time is spent using science - and in some cases what loosely passes as 'science' - as a weapon, or to explain what ‘isn’t’. I’m trying to use it to explain hypotheses of ‘what may be’. So far I’ve focused on minicolumns, but there are also other subjects that I find of interest that I am also digging into. I also like to go after ToM, at this point anecdotally, to demonstrate where I think some of the accepted scientific beliefs – especially those that underestimate the Bear - may go a bit too far. I hope to back this up with more scientific evidence in the future. If nothing else, this aspect of the blog has been very educational for me, since I like to have a clue about what I’m writing about. In this regard, blogging is probably a good excuse for following my own perseverations. And on this note, I’ll point out that I’m very much looking forward to María Luján’s upcoming posts.

What I try to avoid is joining in some of the more vigorous causation debates. They already have enough participants. I do not see it as wrong to defend one’s POV in these debates, and I do support efforts to keep the discussions both scientifically honest and grounded in respect for those who are autistic. But I do believe that some (and by no means all) debaters can a) over-interpret some scientific evidence, b) support their positions using ‘bogus’ science, c) sometimes go beyond arguing the ‘science’ to arguing an agenda that is at this point still hypothetical, anecdotal, and/or unsupported, and d) have turned the debates into blood-sport and/or an opportunity to throw out gratuitous insults. There is an awful lot about autism that is still unknown at this point. Some argue as if all the evidence they need to support their opinion is already in. Maybe to them it is. Personally, I’m still waiting for some answers, and I don’t think that they will ultimately support either extreme. But that too is just an opinion.

Which brings me in a long-winded way to the final thought of this post. What I find more than a little sad is that last week’s post resulted in the highest readership that this blog has ever had. Not by a huge amount, but it was quite noticeable. I don't worry too much about readership stats, but I would have liked the Minicolumns, Genius, and Autism post to hold the top spot, because it - the subject, not the post - was about something potentially important to our understanding of autism. I’d like to think that this week's blip in readers occurred because over time a blog can build up a group of people who find it interesting, like to stop by to see what one has to say, and possibly to engage in some reasoned discussion of the material posted. Unfortunately, I don’t think that this is the case. I’m the one who is at fault here, as I am the one responsible for the blog’s content. But the post in question is not the direction in which I want this blog to go - I’m not interested in hosting one more autism battlefield. My next post will get back to more reasonable territory.

Okay, maybe I do regret my last post a little bit.

Unmasked At Last

2007-02-12T17:55:00.000-05:00

I knew it couldn’t last. No matter how hard I tried to disguise myself, someone would eventually discover that I’m part of the ‘Mercury Militia’. I tried all kinds of subterfuge to remain hidden, but alas, to no avail. A cunning sleuth has discovered my deception and 'outed' me.

(That was sarcasm, BTW)

The first comment on Prometheus’s post What You Want is What You Get was by Bazooka Joe (sorry, no link), who linked me and my blog to the ‘Mercury Militia’, and inferred a couple of other points. The comment has now been deleted from Prometheus’s blog, as has my reply below:

-----------------

Hi Prometheus,

Since you permitted Bazooka Joe’s comment, I hope that you will allow me the courtesy of a reply.

"They [linked to Generation Rescue et al, with the clear implication that ‘they’ refers to the ‘Mercury Militia’] have started blogs; here's a list:
…
Ian's blog, ashadeofgrey, has focused on reprinting Manny Cassanova's minicolumn research, including grant proposals and unpublished data.
…
So you see, it's no wonder that people like Kirby use the term, blogger, with derision. Effective blogging is not what the mercury militia do well."

The implication is that I am part of the mercury militia? Um, Bazooka Joe, can you show me any evidence where I’ve stated that mercury and/or thimerosal and/or vaccines cause autism? For the record, I’m Ian Parker, not the ‘Ian’ who sometimes comments on Kev’s blog (and maybe elsewhere), if that helps refine the search.

Regarding ‘reprinting’ Dr Casanova’s research, if you read his research you’ll find that I’ve added interpretations that go beyond what he has written, after first explaining his hypotheses from a body of work regarding minicolumns covering the period from 2002 to 2006. As for referencing the grant proposal (it sounds like you consider this pejorative), why not? I’d suggest that Dr Casanova’s reputation is as much on the line in his proposal (which has been widely distributed) as it is in his peer-reviewed published work. Besides, it included some cool illustrations.

As for ‘unpublished data’ (two papers), I know of other researchers (as in other than Dr C) who have also reviewed the same information, and the latter paper will be published shortly. FWIW, Dr Casanova forwarded me the papers because we correspond, and he knows of my high level of interest in such matters. I asked permission before I used them in my posts. The first paper is a hypothesis work, and fully referenced. The latter is now in review. The fact that some of this paper’s findings are now in circulation linked to his name (sans refutation) conveys a certain level of trust. When the paper is published, you are free to read it and compare it to my post to see how much original thought and interpretation, if any, that I have added.

I also write about subjects other than the three minicolumn posts, including some posts about ToM, autism and evolution (I waited for Prometheus to write this one, but…), and a variety of other subjects, including my daughter. If you’re interested (I somehow doubt it – if you were I doubt that I would be writing this) you can find them under ‘Blog Archive’ by clicking on the little triangular buttons on the right of the window and then following the links.

Regarding "Effective blogging is not what the mercury militia do well", while temporarily suspending disbelief that I’m part of the mercury militia, I’ll leave it to the people who read my blog to determine that. If they don’t like it then presumably they won’t come back.

As a final thought, I find it interesting that ‘we members of the mercury militia’ are often accused of ignoring peer-reviewed science, and yet my posting about peer-reviewed research is being used to indict me?

Curious.

-----------------

María Luján and Wade Rankin, were also mentioned - among others - in Bazooka Joe’s comment, and both tried to reply. Eventually Prometheus deleted both of our comments and added his own thoughts as follows:

"Bazooka Joe,

I think you and Ian Parker should take your discussion off this blog, since it seems to be related to your personal differences of opinion. You're both welcome to post comments here, but only if you stay a bit closer to the subject."

And following:

"Wade Rankin,

I realize now that approving Bazooka Joe's comment was a mistake, which is why I allowed Ian Parker to have a go. I do not intend to allow every aggrieved party a chance to vent their spleen at Bazooka Joe (or to allow him to reply to all of them in turn).

I have removed both Bazooka Joe's original comment and Ian Parker's reply. I suggest that anyone who feels a need for "satisfaction" find a more suitable venue (how about http://www.mudwrestling.blogspot.com ?)."

So, based on Prometheus’s comment, apparently Bazooka Joe seems to feel that this is unresolved. Meanwhile, I am curious as to why I was included in this ‘drive-by shooting’? I’ll leave aside the 'reprint' reference to my three of 23 posts that discuss the work of Dr Casanova, as I think I answered that sufficiently above, at least until someone takes another shot. As for the quality of my blog, as bad and/or ineffective as it is, if you're reading this then I've sucked you in one more time. And I'll resist the temptation to go pejorative and make comments about 'reading comprehension'.

Anyway, I’m presuming that being a member of the ‘Mercury Militia’ requires something more of me than walking upright and drawing breath (I do both, BTW). My assumption is that the term ‘Mercury Militia’ refers to those who believe that ‘thimerosal’ or ‘mercury’ injected during vaccinations has ‘caused’ their child’s autism. This definition could probably be extended to include the MMR causation hypothesis as well. I would suggest that a further qualification would be that one would not only believe the above but also be relatively active and adamant in discussing the matter, but for now let's take the more relaxed definition. If anyone wants to propose another definition, feel free.

I did a quick search on my blog, looking for some key words. I mention ‘mercury’ (excluding NotMercury, the blogger) in four posts. In the Respect Meme I indicated the following:

"A related issue is that some ‘wrap themselves in the flag’. On one side, some autistics view a disagreement with their ideas as a challenge or an attack on all of those who are autistic. "If you disagree with me then you don’t respect autistics". The mirror image on the 'all autism=mercury poisoning' side is "If you don’t agree with me then you are abusing children". Er, no, on both counts."

And

"Respect is very relevant to the autism discussion. I would suggest that from the point of view of the neurodiversity community, respect – and the perception (and in a lot of cases the reality) of the absence of respect - is one of the driving reasons behind their participation in the debate. I would suggest that the ‘autism = mercury’ parents also see the debate – in their case with the government and with many in the scientific community – as a respect issue, and also lack respect for the ND point of view as well as for many of its proponents. And for the majority of parents and caregivers, the respect issue revolves around government and support agencies not providing the amount of care and support that is required to improve the quality of life and accommodation of those touched by autism (i.e. not respecting what they see as the conditions required to respect the right to proper and adequate support)."

In Moderate Does Not Mean Neutral, I wrote:

"Having said that, I also oppose poorly conducted science, which I believe does not serve anyone well. Exploring a reasonable hypothesis that does not have mainstream support is not poor science. Exploring hypotheses without using the scientific method and without having the goal of arriving at replicable results that can withstand peer review is poor science. Some on the treatment side have conducted poor science, and I believe that the result has been an overstatement of results and a damaging loss of credibility that may slow the ultimate search for answers. I also think that the ‘all autism = mercury’ approach has hampered other research that may find other causes, and I disagree with those that take this one-size-fits-all approach to autism research."

(You may want to pay particular attention to that last sentence.)

And

"We do not chelate our child, and to be honest, the process scares me. For the record, my daughter has some potential heavy metal issues (not mercury) that showed up on a mainstream test (discovered by accident – we were testing for essential minerals and ticked the toxic panel as an afterthought). Our approach has been to monitor this and try to naturally rebuild the Bear's detox system rather than use chelation. But I do not oppose others using chelation as long as they have clearly dealt with other bio-medical issues first, have tested their child and found the presence of heavy metals, and are careful to conduct chelation under qualified and experienced supervision and with regular testing/monitoring performed by reputable labs to ensure that no harm is being done."

(I think this is one of only two spots where I mention chelation, BTW)

And

"There is a history of extremes targeting moderates to turn situations into a clear black vs. white, ‘us’ vs. ’them’ issues, eliminating any room for diversity of viewpoints or compromise. It is easy to caricature or ridicule an extremist opponent (e.g. ‘all autism = mercury’ is downright silly), but it is harder to ridicule a moderate interventionist approach backed by replicable medical tests and following a moderate educational approach based on what many would consider common sense."

In Demeaning Words I wrote:

"Second, it is not intended as a personal attack on JB Handley or his objectives. One may agree or disagree with his views (I personally do not agree with his view - if I perceive it correctly - that all autism is the result of mercury poisoning), but that is not the subject of this post."

And finally, in Autism – It’s Not Always A Natural Variation, I wrote:

"This logic does not support the conclusion that no autism is purely genetic (75% could still theoretically be purely genetic - or more if the 60% concordance rate is too low). In fact, it supports the conclusion that autism in a significant number of cases involves at a minimum a degree of genetic susceptibility. It does not prove or disprove that the 'second hit' is thimerosal or mercury. It does not argue for or against chelation. It does not suggest that autism originates either in the womb or after birth. It does not suggest or refute the possibility that autism is curable, or that a cure is or is not desirable."

This paragraph also contains my only reference to thimerosal.

Finally, I use vaccines once:

"But I also see a discussion that is increasingly polarizing, in which accepting that others have different views is giving way to an advocacy that rejects other viewpoints as unenlightened, wrong, or not yet at their level of "awakening". This used to be a hallmark of the more activist element within the anti-vaccine crowd, but is also becoming increasingly apparent in the "autism is natural variation" crowd too. It is one thing to oppose some of the more contentious attempts to cure autism, e.g. chelation, or lupron (which IMHO is just nuts), or to reject the concept of treatment for oneself. But as this challenge to the more contentious bio-med practices is morphing into a more direct challenge against even mainstream accepted methods of investigating and potentially treating autism, I think it is time for more moderates to join the debate."

(The other spot where 'chelation' is mentioned)

So, based on the above, what exactly is it again that marks me as being part of the Mercury Militia?

Minicolumns, Genius, and Autism

2007-02-01T10:32:00.000-05:00

In earlier posts I wrote about Autism and Minicolumns and Autism and the Evolution of the Brain, based on research by Dr. Casanova et al. Minicolumns are the basic organizational unit of the cortex, and are vertical arrays of pyramidal cells (neurons). The underlying argument in these posts was that those with ASD have a higher number of minicolumns than average, but that those minicolumns are of a narrower than average width, with smaller neurons but the same average number of neurons per minicolumn. The net result is a brain structure that skews in favour of processing stimuli that require discrimination, potentially at the expense of generalizing the salience of a particular stimulus. Smaller and more densely packed minicolumns could also allow for more complex information processing.

These attributes come at a potential cost. The reduction in width is a result of a reduction in the minicolumn’s peripheral zone of inhibitory and disinhibitory activity. The inhibitory fibers act to keep stimuli within individual minicolumns, and the reduction in this space increases the chance of stimuli overflowing to adjacent minicolumns, providing an amplifier effect and potential hypersensitivity. Narrower minicolumns may also result in an increased number of minicolumns per macrocolumn, which can also result in an amplification of thalamic input, and as each minicolumn’s response to thalamic input is modulated by the activity of neighbouring columns, a reduction in GABAergic inhibitory activity could also result in a loss of inhibition and greater amplification. Stimuli ‘spill’ and greater amplification could result in the increased incidence of seizures in autistics.

An additional factor is the reduction in neuron size, which reduces the ability of neurons to sustain connections over distances. Smaller neurons result in a metabolic bias favouring shorter connections at the expense of both longer distance and inter-hemispheral connectivity. The result is that autistic brains have a bias towards local (intra-regional) over global (inter-regional) connectivity and processing. Short intra-regional processing functions include mathematical calculations and visual processing. Cognitive functions that require inter-regional processing would be less metabolically efficient, including language, face recognition, and joint attention (Casanova - Abnormalities Of Cortical Circuitry In The Brains Of Autistic Individuals). Given the high metabolic cost of the brain (2.5% of our body weight but 22% of our resting metabolism - Leonard and Robertson 1992, p 186), smaller neurons may be a response to resource constraints.

Of note, while reduced minicolumnar width appears to be a prerequisite for ASD, the reported minicolumn widths found within autistic brains are still within the normal distribution of minicolumnar width, albeit at the tail end (Casanova, 2006). In other words, people with narrow minicolumnar widths are not necessarily on the ASD spectrum.

Narrower Minicolumns Without ASD

Confirmation of this is suggested in "Comparison of the Minicolumnar Morphometry of Three Distinguished Neuroscientists and Controls", a new research paper by Dr. Casanova et al, currently in review. The research in question involved analyzing and comparing the minicolumns of three distinguished neuroscientists ("supernormals") and six normative controls. The ‘supernormals’ are described as:

"researchers of high distinction within the neurosciences. Although personal history and interviews with those who knew these neuroscientists emphasize their wide range of knowledge (polymaths) and divergent thinking no claim is made regarding their intelligence or creativity."

That being said, the descriptions of the three individuals in question clearly suggest that they were very intelligent, focused, productive, and intellectually self-assured.

The research found the following:

"Overall, there were significant differences (p < 0.001) between the comparison groups in both minicolumnar width (cw) and mean cell spacing (mcs). Although our supernormals did not exhibit deficits in communication or interpersonal skills the resultant minicolumnar phenotype bears similarity to that described for both autism and Asperger’s syndrome."

The findings in this paper are fascinating (at least to me) in that they clearly indicate both similarities and differences between the brains of autistics and those of the three neuroscientists, suggesting some answers and raising some interesting questions. The major reported similarity is the finding of narrow minicolumnar widths. As stated in the paper, "A minicolumnar phenotype that provides for discrimination and/or focused attention may help explain the savant abilities observed in the intellectually gifted." It is unknown at this point whether two other characteristics linked to narrower width minicolumns in autistics – i.e. smaller neurons and a higher number of minicolumns – also occurred in these neuroscientists’ brains, but it is a logical assumption that these characteristics were present too. Smaller neurons are hypothesized by Dr. Casanova to be a requirement for the existence of narrower width minicolumns, based on laws of conservation for brain grows and evolution (from personal correspondence, with permission).

Differences

There were also significant minicolumnar differences between the neuroscientist brains and ASD brains. First, the neuroscientists had a lower mean cell spacing (MCS) – i.e. a smaller average distance between neurons - than the controls. In other words, their neurons were closer together than in typical minicolumns with large mean cell spacing. Previously analyzed ASD brains had ‘normal’ or typical mean cell spacing. Unfortunately, no direct numerical comparisons of MCS between this research and previous analyses are possible due to the difference in age between the neuroscientists (58, 84, and 89) and the autistic patients (average age being 12 years).

Second, the neuroscientists differ from those with ASD in terms of the horizontal spacing between neurons (relative dispersion of cells). The neuroscientist minicolumns were similar to typical minicolumns in that they had a small relative dispersion, i.e. cells tended to be clustered closer to the axis of the column. Those with ASD have a large relative dispersion, with cells distributed more uniformly within the minicolumn core.

Figure 1 (below, based on Fig 2 from the research paper) is a hypothetical representation of both mean cell spacing and relative dispersion in minicolumns, (after disregarding both neuroscientist and ASD reduced minicolumnar width). The neuroscientist and typical minicolumns have a smaller relative dispersion than the ASD minicolumn (i.e. tighter clustering toward the column axis vs. more uniform distribution). The neuroscientist column also has a smaller mean cell spacing, with cells being closer to each other than in the other two minicolumnar types, regardless of their distribution around the minicolumn axis.

I would speculate that the differences between the neuroscientist and ASD minicolumns would have a significant - but incomplete - explanatory role in accounting for the differences between the two groups. In both groups, narrower width would increase the risk of ‘spill’ between minicolumns. But the reduced mean cell spacing in the neuroscientists would presumably result in greater integrity of processing within the column (as well as potentially an increase in speed), while the tighter grouping of neurons around the axis would increase the distance between the neurons and those in adjacent columns, maximizing the zone of interneuronal inhibitory activity between the adjacent vertical arrays of pyramidal cells. This is significant, in that this maximized inhibitory zone could at least partially compensate for any reductions due to the narrower column width.

In contrast, the higher ASD MCS could result in comparatively lower signal intensity and - along with a more uniform horizontal dispersion – result in a higher risk that neurons in adjacent columns might in fact be closer in distance than neurons within the same column, increasing the risk of ‘spill’. Plus, the more uniform horizontal dispersion would result in more neurons being found towards the outer periphery of the column, with an even smaller zone of inhibitory activity between these outer neurons and adjacent minicolumns.

More Questions

This still leaves some significant questions for further research regarding differences between the neuroscientist and ASD minicolumns. For one, as the paper suggests:

"the widespread morphometric changes in our scientists suggest that any brain-related ability they may have possessed (e.g., cross-discipline learning, abstracting, dimensional thinking) involved multiple cortical regions. In developing these abilities the various association cortices acted as nodes or epicenters, binding multimodal information, within a neural network (Mesulam 1994; 1998). Contrary to earlier formulations, modern observations suggest that higher cognitive processes are encoded in flexible distributed networks rather than rigid convergent ones (Mesulam, 1994; 1998)."

As such, the neuroscientists had brains capable of exceptional thinking, combining deep focus and discrimination, but linked to distributed (global) processing. If the neuroscientist neurons were smaller, biasing against global connectivity, then was there a compensatory effect? Spindle neurons serve to connect more distant, non-neighbouring regions of the brain (Casanova - Big Brains Manuscript, in preparation for submission). From Wikipedia:

"Spindle cells appear to play a central role in the development of intelligent behavior and adaptive response to changing conditions and cognitive dissonance. They emerge postnatally [emphasis added] and eventually become widely connected with diverse parts of the brain, evidencing their essential contributions to the superior capacity of hominids to focus on difficult problems."

Spindle neurons are known to be found in reduced numbers in those with ASD. Perhaps they helped the neuroscientists compensate for – and even exploit the benefits of – the bias towards local processing inherent in reduced width minicolumns?

Another potential difference between the two groups might be found within their corpus callosi, the structure that connects the left and right cerebral hemispheres, which have consistently shown to be smaller in autistics. The research paper suggested that "the fact that the left hemisphere lags in development behind the right hemisphere may offer an alternate explanation to savant skills (Geschwind & Galaburda, 1986)." Examining the corpus callosi of the neuroscientists might also provide some insights regarding similarities and differences in connectivity between them and those with ASD.

Evolutionary Benefit and Risk

The neuroscientist finding also potentially answers some evolutionary questions. In my Autism, Genetics, and Evolution post, I suggested that the alleles that cause autism could have been with humanity for at least 40,000 years.

"Assuming 30 to 35 years per generation (which is conservative), there have been 1100 to 1300 generations since the two populations diverged. This presumably should have been enough time to eliminate the various alleles that cause autism from the gene pool, if they are in fact deleterious.

Obviously this has not occurred. This means that the individual alleles that in combination cause autism must individually or in lesser combinations have had a beneficial effect to compensate for the reduced reproductive rates of autistics."

As the neuroscientist paper indicates, the same narrower width minicolumnar structure found in ASD may be a competitive advantage in the case of the neuroscientists. If the same alleles that contribute to ASD can result in a competitive advantage in other circumstances through (intellectual) fitness, this would easily explain the continued existence of ASD over time. The research paper quotes T.G West from In the Mind’s Eye (1997):

"One of the most important lessons to be learned from the genetic study of many diseases in recent years has been that the paradoxically high frequency of certain conditions is explained by the fact that important advantages conferred on those who carry the predisposition to these conditions may outweigh the obvious dramatic disadvantages."

My Autism and Minicolumns post suggested that a) ASD has a minicolumnar underpinning, b) this underpinning is required (i.e. no narrow minicolumns means no ASD), c) it originates in the first 40 days of fetal development (i.e. it is not itself acquired post-natally), d) that this difference falls within the normal range (i.e. that having it does not ‘cause’ a diagnosis, although it may very well result in diversity of thought and cognition, i.e. neurodiversity), e) that something else is therefore required (with no significant speculation as to what that something else may be, other than to generically label it as a ‘second hit’), and f) that research needs to prove or exclude causality among the population of the vulnerable, i.e. proving that something does not cause ASD in those who are invulnerable does not prove that it does not cause ASD in those who are vulnerable.

I would suggest that the Neuroscientist research lends significant credence to the above, especially to point d, and suggests that the differences between the neuroscientists and those with ASD may point to the ‘something else required’ that follows.

Talking About 'Crap' and GI Issues

2007-01-17T19:59:00.000-05:00

There seems to be a bit of a stir lately in the community of those linked by autism. The subject? 'Crap', AKA bowel movements.

Kim Stagliano recently posted The Crappy Life of the Autism Mom on The Huffington Post. In this post she suggested that there were different severities of autism, that some levels of severity justify efforts aimed at ‘recovery’, and used a particularly graphic description of a “crapisode” to illustrate a “taste” of what autism looks like in her household, to justify the intervention.

As well as the ‘tell it like it is’ support that Ms Stagliano’s post drew, it also drew a lot of fire. A good mix of views of those opposing the post can be found in this post and comments on Do’C’s Autism Street blog. Objections included attempting to separate out the neurodiversity proponents from the ‘severe’ kids (the implication being that the first group can’t speak for the second), that this viewpoint is all about the parents rather than the kids, that some are attempting to divide the world into HFA and LFA based on toileting abilities, that raising the issue does nothing for autistics’ sense of self-value but instead demeans them, and that such issues affect only a small group of autistic children. Wade Rankin's Injecting Sense blog also raised the Stagliano post and the reaction to it here as an example of the divisions with the community of those linked by autism.

For what it’s worth, my daughter is a paid up member of the ‘Problem Poo’ club, as I described here. Since that post, not only has the issue not been resolved, but it has worsened. I will state that aside from the occasional hand in the wrong place at the wrong time, the Bear does not ‘smear’, ‘play’ with the problem or exacerbate it in any way. And FWIW, I’m now quite familiar with the procedures for using a suppository and renting a rug shampooer (not necessarily connected). Having said that, we’re working through it. Obviously the biggest sufferer is the Bear. It tears my heart out to watch her struggling in pain. But my pain is emotional – hers is physical and it is worse.

Anyway, the following are a few thoughts on the 'poo' issue, GI issues, and comorbidities in general.

First, we don’t know the degree to which autism and various comorbidites are linked, in part because there hasn’t exactly been a wealth of large scale peer-reviewed studies. Anecdotal evidence abounds (e.g. the OT at the local autism support agency – and neither she nor the organization subscribe to any particular causation philosophy – suggests that in her experience the issue is quite common), but the evidence is just that – anecdotal. Counter-anecdotal evidence also abounds – "My autistic child doesn’t have these issues" is also anecdotal, BTW. There are probably a wide variety of ‘causes’ of autism(s), and one person’s lack of affect cannot be assumed to imply a universal lack of affect, any more than the fact that my child has issues (that may or may not be related to autism) indicates that all autistic children have similar issues.

We need to determine whether there are subgroups of autism in which comorbidities may occur and/or potentially affect overall autistic presentation, and the way to do that is through peer-reviewed research. The CHARGE study being conducted by the M.I.N.D. Institute at UCDavis is a good start.

Second, I agree with Do’C’s statement - other than the 'very small portion' part, which I would suggest is unknown - from his post that:

"I won’t claim that feces is fun to clean up, it’s not. But complaining about this not-necessarily permanent aspect of only a very small portion of autistic children is probably not going to instill any sense of 'value as people'. To the contrary, it’s probably more likely to demonize autistic children as 'inconvenient.'"

There is evidence that "the human disgust emotion may be an evolved response to objects in the environment that represent threats of infectious disease." As such, it should not be a total surprise that those who endure ‘shitstorms’ are not particularly fond of them and regard them as more than just a minor inconvenience. Of note, the research suggests that this response diminishes with age. The issue is how we deal with this ‘disgust’. I personally have no issues with raising BM and related issues, as long as it is done for the right reasons. From Leila’s comment on Do’C’s post:

"If we want to keep discussion honest, we also have to talk about how hard it is to deal with the difficulties that autism brings, both for the autistic individuals and their parents and siblings. If it was all positive, we wouldn’t all be so eager to exchange information and support through the blogosphere, in order to try to make sense of all what happened to our lives."

I would also agree though that raising the issue to differentiate between 'degrees of severity' to justify who can and cannot speak about autism, or in some other way to exploit the issue, is wrong.

Third, I would suggest that toilet training is potentially more difficult for autistic children. Not in all cases, but definitely for some, and maybe for more than just ‘some’. I would suggest that there are overlapping ranges on this one. As an example, men are - on average – faster runners than women. But the top few percentiles of women runners could leave most men in the dust. Many children, whether NT or autistic, have toilet issues. But – on average – there are fewer communications issues with NT children, which makes the job of teaching NT children – on average – easier. Obviously there are exceptions. Further, autistic children are more likely to have sensory issues that inhibit their perception and understanding of bodily functions and their ability to control them. This too can make toilet training more difficult.

Fourth, while I may be wrong on this, I do detect more than a subtle undercurrent of opposition to raising GI issues, in that somehow they may link to the idea of 'causation' or 'treatment'. FWIW, I do not believe that solving the Bear’s GI issues will render her ‘normal’, and ‘normal’ is not our goal, but I do believe that these issues may have an impact on the severity of her autism. A detailed explanation why is beyond the scope of this post, but you can read more here and here if interested. The following is a quick summary.

There is considerable evidence that the autistic brain has some unique characteristics. Findings by Dr Casanova and others discussed here indicate that the autistic brain has a higher number of minicolumns than average, but with a ‘normal’ number of neurons per minicolumn. While autistic minicolumns are of narrower width and autistic neurons tend to be smaller, the net result is that autistic brains have a larger total number of neurons.

Studies have also shown a postnatal acceleration in brain growth in autistics, resulting in increased brain volume in autistic children vs. controls (e.g. Redcay and Courchesne, 2005, Aylward et al, 2002, among others). As per Hazlett et al, 2006:

"Significant enlargement was detected in cerebral cortical volumes but not cerebellar volumes in individuals with autism. Enlargement was present in both white and gray matter, and it was generalized throughout the cerebral cortex. Head circumference appears normal at birth, with a significantly increased rate of HC growth appearing to begin around 12 months of age. CONCLUSIONS: Generalized enlargement of gray and white matter cerebral volumes, but not cerebellar volumes, are present at 2 years of age in autism. Indirect evidence suggests that this increased rate of brain growth in autism may have its onset postnatally in the latter part of the first year of life."

On their Centre for Autism Research website , Courchesne and Pierce indicate that:

"...children with ASD showed an extremely abnormal pattern of growth: mean head circumference jumped from the 25th percentile at birth to the 84th percentile by 6 to 14 months. And among those at the more severe end of the autism spectrum, 59% showed growth at least 2 standard deviations greater than normal, and 71% showed growth at least 1.5 standard deviations greater. In comparison, only 6% of the normally developing children in the Fels [Fels Longitudinal Study] data showed growth at least 2 standard deviations greater than normal, and 9% showed growth at least 1.5 standard deviations greater."

Thus the autistic brain appears to have more minicolumns, more neurons generally, and appears to grow faster than NT brains.

A normal brain constitutes 2.5% of body mass and accounts for 22% of basal metabolic energy requirements, or BMR (Leonard and Robertson 1992, p 186). The energy required by the brain is even higher in infants and small children. There is considerable evidence that the high cost of brain growth has stretched human metabolic capabilities, resulted in fundamental physical adaptation (e.g. the 'efficient tissue hypothesis' - Aiello and Wheeler, 1995) and resulted in delayed maturation (Foley and Lee, 1991) to meet the high cost of supporting a large brain. In addition, there is evidence that our current brains have actually decreased in size compared with human brains of 35,000 to 10,000 years ago (Ruff, Trinkaus, and Holliday, 1997), as a direct result of dietary limitations. If current human brains are already smaller as a result of nutritional limitations, how much more taxing would a larger and faster growing brain tax be?

Regardless of where one sits on the 'neurodiversity' to 'cure' spectrum, if one believes the (peer reviewed and generally accepted) scientific evidence regarding autistic brain growth, then it is a logical conclusion that the autistic brain requires more resources than average to both sustain itself and to fuel the documented growth spurt. As such, the nutritional requirements and proper metabolic functioning of all children – but especially autistic children - should be of great concern to all sides. The nutrients to fuel autistic brain growth cannot be spontaneously generated – they need to be eaten and absorbed through the GI tract. Bowel issues, as indicative of GI tract issues, should therefore be a primary concern, as should issues of malabsorption, dietary limitations due to sensory preferences, etc., regardless of what percentage of autistic children appear to have them. Rather than being a point of division between the various sides - are these issues causative, comorbid, or coincidental? - I would suggest that this is one area in which we could all agree, even if we get there via different goals and agendas (e.g. ‘cure’ vs. ‘optimal functioning of a naturally different brain’).

Regardless of one’s beliefs, we presumably all want healthy children who are able to function according to their potential, and there are reasonable grounds to hypothesize that autistic metabolic requirements may be different (i.e. higher), based on exceptional brain growth if nothing else. We should all be pushing for more research in this area, and in the meantime it is reasonable for everyone - regardless of beliefs regarding cure vs. neurodiversity - to pay more attention to nutritional and GI issues. When one believes that these issues are being raised in an exploitative manner it is legitimate to 'call' people on this. But in most circumstances, this issue should not belong to only one side.

Those Funding Blues

2007-01-12T19:56:00.000-05:00

Recently the Ontario government (Ministry of Children and Youth Services) commissioned a survey of those families waiting for intensive behavioural intervention services. The Bear has been on the list as of March 2005 (note that ‘on the list since’ means that she is still ‘on the list’ - 22 months and counting), so we received the survey. One of the questions was "If IBI services were to become available, which service option do you prefer?"

Direct funding option (DFO)?
Direct service option (DSO)?

Under the DSO option, the local service provider agency is assigned to the child, and is responsible for administering the child’s program, providing the Senior and Instructor therapists, and providing ongoing clinical supervision of the child’s IBI program. There is no cost to the family associated with the DSO choice.

Under the DFO option, the parents/guardians are responsible for administering the child’s program by purchasing the services of private IBI providers. The government designated agency’s contact is with the family, not the IBI provider. The family assumes all the responsibilities of an employer, although the service provider must be approved by the designated agency, in accordance with ministry guidelines, and the agency provides financial assistance to defray the cost associated with the purchase of private IBI services, at the current rate of $31 per hour. All paperwork and account reconciliations associated with the DFO option must be completed by the family on an ongoing basis. Also, funding is for IBI only, and does not cover other associated costs (e.g. training, travel, supplies, photocopying, etc).

There was a number provided for more information, and in an attempt to be a diligent parent I called it. At this time I learned the ‘other’ rules.

It turns out that the program mandates 21 hours per week of IBI under both DFO and DSO. This 21 hours is mandatory. We cannot opt in for 15, 20, or any other variation below 21 hours per week. Under the DSO option, the child must be available for instruction between the hours of 9AM and 4PM each day (um, this is significantly more than 21 hours per week, isn't it?).

I raised the point that the Bear, currently 3yrs and almost 7 months old, is supposed to start K1 in September 2007 (for the uninitiated, K1 and K2 are the new terms for Junior and Senior Kindergarten). How would she do this if she had to be available during the above-mentioned hours? The answer – parents need to make a choice as to whether to participate in the IBI program OR enroll in Kindergarten.

What?

The local agency also runs the preschool speech and language instruction in our area, and the Bear participated in a 10 week group PECS session as part of this. She thrived in these sessions. While she didn’t seem to pay any attention to the other children, she seemed to grasp many of the group concepts very well, in fact, much better than the other children. This leads me to believe that she may actually benefit considerably from mixing with other children and participating in kindergarten.

In addition, we live in a rural community, and the local school seems to be quite good. I met with the principal and the local autism coordinator last summer, and I was pleasantly surprised by how well they handle certain things. As an example, the older children are tasked with the responsibility for keeping an eye out for special needs children, and making sure that they are safe, can participate, have ‘buddies’ during recess, etc. I asked my neighbour's children about this (the youngest is currently in her last year at this school, and the eldest attended until recently), and they both confirmed this practice and that there was definitely a sense of community, acceptance and watching out and helping those children with special needs. The youngest stated that she currently spends some of her recesses playing with a younger autistic boy, and that they both enjoy this time.

The other factor is that if the Bear starts K1 with the other children then she will be part of that year’s intake. She will be no more the 'new kid' than anyone else. By Grade 1 she would be familiar with the other children and them with her - part of the scenery. If she starts Grade 1 after missing K1 and K2 she will be the 'new kid’, and may have a tougher time being accepted by those who have already known each other for two years and have previously established friendships, groups, etc. Autism may make this even more difficult. My preference is therefore that she starts K1 on day one, just like everyone else.

So, DFO seems a natural choice, right?

But, there are issues here too. The first is that requirement of 21 hours. Is it just me, or does 21 hours not divide evenly into five days (assuming that four hours and 12 minutes is not considered ‘even’)? Second, K1 and K2 are either in the morning (9 – 11:30) or afternoon (1- 3:30). Neither of those blocks of time allow for an easy integration of 21 hours of IBI, although the morning Kindergarten sessions are a better fit. Neither option fits well with a 9 to 5 work day with a lunch break. Again, 15 hours works out much better, but that is not an option if one wants to access funding. Or, one can choose to forgo Kindergarten. Or maybe play hooky one day per week?

Then comes the additional issue of costs. At a rough calc of per hour charges, 21 hours of IBI at current rates is nearly $51K per year. The DFO funding will cover nearly $30K of that, leaving a shortfall of $21K to be covered by the family (although it is less than we are currently paying for 15 hours - Wow, we get to pay less!). For many families that is still a prohibitively expensive cost, removing the DFO option from the table. This funding does not cover psychological services costs, which I’ve heard are a mandatory part of the DFO process but are not a billable part of the $31 per hour coverage. So the $21K is probably an under-estimate.

So let’s get creative here. Assuming one can afford DFO, or can negotiate with the DSO provider, can the IBI be delivered at school? That would certainly solve some of the scheduling issues for either approach. But, no, the school boards do not allow IBI or any outside agency to deliver services on school property. These are the same school boards, by the way, that may also provide zero, part time, or shared EA support instead of the full time support that may be required for a child. I can partially understand why (e.g. liability), but surely someone could find a way to cover off the issues?

So where does that leave us? If we want the DSO option (or if it is all we can afford) then we have to choose to forgo Kindergarten, resulting in missed learning, socializing and bonding opportunities that may also have consequences in Grade 1 and subsequent years. If we want the DFO option then we either forgo Kindergarten or still have significant scheduling issues, plus we have a shortfall of $21K or more per year.

I know that some out there are not fans of IBI, and will recommend forgoing it. My reply to this is that we have found IBI helpful for the Bear. I can raise the same points again about her instruction: the lack of aversives or any negative conditioning, that no attempt is made to eliminate her stims, that no attempt is made (or desired) to enable her to ‘pass as NT’, that the goal is to teach her skills to enable her to better and more independently function in the world, that part of the program involves following her lead, etc., but these points are already made here and tangentially here. I could also mention that IBI is one of the methods used to educate the Bear (we’re also fans of the ‘More than Words' approach by The Hanen Centre, which we practice at home, and Dr. Gernsbacher’s thoughts here are quite familiar to us through earlier papers and her website - I especially recommend the videos here).

But regardless of these points, we find that IBI has been helpful to the Bear and would like to continue it as part of her educational program. We have a provincial government that is theoretically committed to helping the Bear through programs that they both authorize and fund, a local support agency that recognizes the issues but has to work within the rules handed down, and a school board that may or may not fund an EA but won't let anyone else lend assistance on school property.

Why is this so difficult?

Apocalyptic Advocacy

2006-12-15T16:41:00.000-05:00

One of the things I’ve noticed in the discussions and debates regarding autism is the regular use of 'impending doom' (cue ominous music) by advocates to make their case. This use is not limited to one particular ‘side’ of the autism debate – it can be seen at both ends of the viewpoint ‘spectrum’. And while I can see why some may feel that appeals to otherwise 'impending doom' (cue thunder) may strengthen their case, in the end I think it harms all of us. There are enough legitimate points to be made in autism discussions without having to unduly exaggerate or fabricate. And misinformation - especially misinformation that casts autistics in a damaging light – can outweigh the benefits that advocates are seeking to achieve.

One of the recent examples that comes to mind - courtesy of a post in Michelle Dawson’s blog - is the article Autism needs hope, written by Margaret Wente in the Globe and Mail on Nov 21, 2006.

From the article:

"My son is in a mainstream class. He goes to other kids' birthday parties," says Jean Lewis. She is the mother of an autistic 12-year-old and also a director of a B.C. parents' lobby group. Where would her son be without treatment? "He wouldn't be living at home," she says. "Without treatment, kids like this are usually institutionalized by the time they're adolescents. They're living in restraints, living in diapers. They have to have their teeth removed because they bite."

Um, excuse me?

The BC parents lobby group in question is F.E.A.T. of B.C. (F.E.A.T. stands for Families for Early Autism Treatment). A major goal of F.E.A.T. of BC, as per its official petition, is to "amend the Canada Health Act and corresponding Regulations to include IBI/ABA therapy for children with autism as a medically necessary treatment and require that all Provinces provide or fund this essential treatment for autism".

My daughter (3yrs 6mos old) is in an IBI program five mornings per week. While she was diagnosed as ‘autism, at the severe end of the spectrum’, and is approved and on the waiting list for IBI funding (currently running 'neck and neck' with university acceptance in terms of timing), we currently pay for her treatment privately. We pay a lot – a lot more than 50% of the figure quoted in the article. And for the moment, we feel that it is worth it. As such, groups like FEAT should theoretically be natural allies, or at least fellow travelers.

(BTW, for those who want to criticize us for using IBI, you may want to read here and here first to find out what we’re actually doing and believe. As an example, the Bear is not in IBI to teach her to pass for 'normal'. I’m sure that there is plenty of scope to criticize us for what we ARE doing without having to make things up that we DO NOT DO or support.)

But to me a central issue for lobbying groups and advocates is how they portray autistics. One might suggest that the quote above was an isolated statement. But from a story about ABA in 2005 referring to Ms Lewis’s son:

"Now in grade five in a regular classroom, the boy is a busy 11-year-old. He bikes, skis, swims and even plays clarinet in his school orchestra. He's also, "an active participant in family life," says Mr Lewis, who also serves as the President of the Autism Society of British Columbia. "Whatever we do, he's part of it."

But…

"But if his son's treatment was stopped, Mr Lewis is convinced the child would need to be institutionalized, possibly immediately. "If not now, then shortly," he says."

And from an Autism Fact Sheet on FEAT BC’s website:

"Without treatment, autism is a lifelong affliction that results in 90% of afflicted individuals placed in institutions and residential facilities, facing an unfulfilling and bleak existence for both the individual and family members."

Clearly the view being promoted is that autistics are dependent on ABA to avoid an 'unfulfilling and bleak' life of institutionalization (without teeth?). So much for Floortime, RDI, and other therapies, or implicit learning. (sarcasm) I guess THOSE parents should start saving for institutionalization now... (/sarcasm)

Ms Wente’s article also mentioned the ‘Autism Every Day’ video, including the ‘in another life, I’d love to go out for a bagel.' quote, and "For a glimpse of a day in the life of autism parents" it refers readers to a link to the video.

Personally, I support government funding (and not just limited to IBI - I favour a multi-disciplinary approach) for the support and education of autistic children, as well as required support for autistic adults. In this, organizations such as F.E.A.T. of B.C. should theoretically have my support. But I object to their methods, which clearly involve portraying autistics in a negative light through the dissemination of obviously incorrect information. It should not be necessary to denigrate my daughter to secure funding. Nor should appeals for funding be reduced to 'pay up now or I'll cost you more later'. What about the intrinsic right to an education and equality of opportunity?

As I wrote previously about the ‘Autism Every Day’ video:

"I quite like the idea of a video to explain our lives to others. But I'd prefer that it didn't make my child (by association) look like a ‘nightmare’ inflicted on us (and potentially on others when they come in contact with her). As a parent, autism is hard and painful at times to deal with, but there is also a joy that we can feel from our children, and one that our children can feel, even if we cannot always see it - and I think that much of the time I can see it, written on my daughter’s face. I don't want people to shy away from the Bear, to be afraid of the disruption that they fear she may cause, or to pity her, but rather, I want them to understand her and accept her.

Asking for acceptance does not mean that I'm not going to work like hell to fix her SI, immune, GI, etc. issues. I have no problem with autistic thought per se, but with autistic 'issues' - it is these that I'm working to help her overcome, and I believe there is a link between her medical symptoms and these ‘issues’. Asking for acceptance also does not mean that I won’t try through IBI or other teaching methods to teach or enable her to learn the skills she needs to make her way in the world. Instead, acceptance means recognizing her as a human being worthy of the same respect and rights as anyone else. Implying that she is a nightmare to deal with is not only untrue, but does nothing to further this goal."

In the same way, I believe that the message (as distinct from the goal of funding) propagated by FEAT of BC also does nothing to further the goal of acceptance of my daughter as a human being with full rights and worthy of respect.

I wrote to Ms Wente, pointing out my issues with her article, and closing with the following:

"While it is too late to change your article, might I suggest that you take a second look at this issue, as time permits? I (and probably most parents of autistic children) definitely appreciate anyone speaking on our children’s behalf, but what I’m asking is that you do so in a way that more accurately reflects our children’s reality – good and bad - and ultimately the reality of the autistic adults that they will become. I’m definitely not suggesting that you sugar coat the presentation. The reality is what it is, and should be presented rather than hidden away. But I would also ask that you recognize that our children are human beings, worthy of an accurate portrayal."

I will update this post with any reply, providing due consideration for Ms Wente’s privacy. In the meantime, if anyone else wants to contact her to offer their opinions, her e-mail - posted at the bottom of the autism article - is mwente@globeandmail.com. If you do so, please play nicely. "You can catch more flies with honey..."

In the meantime, I'll start saving for dentures for the Bear. After all, what is a bear without teeth?

The Sneaky Bear - Another Example of 'Theory of Mind'?

2006-11-20T18:21:00.000-05:00

As I wrote in a previous post, I would suggest that the Bear is at least occasionally demonstrating Theory of Mind, despite some expert opinions that ToM in autistics is impaired, deficient, or non-existent (especially at such a young age). Recently we had another interesting (to me at least) potential example.

From Wikipedia, Theory of Mind is generally described as:

“a specific cognitive capacity: the ability to understand that others have beliefs, desires and intentions that are different from one's own.”

Further:

“This theory of mind covers two separate concepts:

1. Gaining the understanding that others also have minds, with different and separate beliefs, desires, mental states, and intentions

2. Being able to form operational hypotheses (theories), or mental models, with a degree of accuracy, as to what those beliefs, desires, mental states, and intentions are.“

Based on the the Sally-Ann test, 'normal' children below the age of four and most autistic children (of all ages) do not demonstrate this capability. (The link and also a comment by Camille on the previous ToM post discuss some of the issues with this test.)

A week or so ago, the Bear (who is 3 yrs, 5 mos old) was working with her IBI instructor, and her snack (chopped up pear chunks) was sitting in her bowl, nearby but out of immediate reach. At one point the instructor had to leave the room for a moment. While she was gone, the Bear reached over into the bowl to grab and eat some pear chunks, something that she would never have done while the instructor was present. What was more interesting though is that as the Bear realized that the instructor was returning, she quickly sat back and put her hands down in front of her with a 'butter wouldn't melt in her mouth' look, hiding the fact that she had been reaching into the bowl. It was the gestural equivalent of "I didn't do nuthin'!" To be clear, she didn't merely stop when she sensed that the instructor was returning, but acted in such a way to actually hide her previous actions.

Given the two conditions above, the implication is that:

a) the Bear understood (albeit incorrectly) that the instructor did not know that she had taken some of her snack (i.e. different and separate beliefs and intentions), and

b) that she formed an operational hypothesis that concealment of her actions was a possibility, i.e. that she had knowledge that her instructor might not have and that she might be able to maintain this state of differential knowledge.

As in the previous ToM post, I would suggest - if my interpretation of the Bear's actions is correct - that she is demonstrating that a child diagnostically labeled as ‘autism, at the severe end of the spectrum’ is capable of Theory of Mind, and at a young age. Again, maybe the 'experts' aren't totally correct on this one?

The Bear Goes Trick or Treating

2006-11-14T22:02:00.000-05:00

This was the first Halloween for the Bear. We dressed her as a Hawaiian hula girl, complete with a lei (double wrapped) around her neck, another lei around her waist, a grass skirt, and a garland of flowers on her ankle. Given that this is Canada, the outdoor version also included leotards and a heavy top (both very non-Hawaiian), plus a coat to hide it all. We would have also liked to put a garland on top of her head, but it would have had the same life expectancy as any hat that is not tied down.

The Bear’s IBI program put on a Halloween event for the kids, providing loot bags, and practicing trick or treating. The Bear is GFCF, so I made the ultimate sacrifice, and afterwards replaced the treats with fruit. The Bear seemed to be quite accepting of her costume, and was very interested in the fact that everyone else was wearing one too.

Momma Bear and I talked about whether we should take her out trick or treating. We live in an area that is not exactly urban. The nearest driveway is nearly 300m away from the foot of our driveway, and that doesn’t include the distance to walk up to each house and back (often a 100m or more). Unless we wanted to drive to an urban area, any trick or treating would have to be via a car. Instead, Momma Bear thought that Halloween would be a good opportunity to introduce the Bear to the X’s.

The X’s are a couple (with older children, I believe in University) who live across the street and a couple of properties down. Mr X was in politics for many years. I won’t say any more since it will a) identify the X’s (I’d like to respect their privacy) and b) more closely identify us. We often see them riding their horses along the street and wave to them, and they say hi when they see us out and about. Mr X drops a bottle of wine off every Christmas on behalf of the local riding club. We have also been to their house for a neighbourhood gathering, plus to see the start of a one of the local hunts. But they had never met the Bear. Given that she is part of the neighbourhood (and also a potential flight risk), Momma Bear thought we should let them meet her so that they would know who she was.

So we dressed the Bear up and I drove her (with instructions to just stop by quickly, say hi, and come back) down the street and up their driveway. I walked the Bear to the door and knocked. Mrs X and the family dog came to the door, and she was surprised to see a trick or treater. Given the neighbourhood distances, we were probably the first to come by in a decade. I reminded her who we were (never taking it for granted that anyone who doesn’t see me often will remember exactly who I am), and said I just dropped by to quickly introduce my daughter to them.

Mrs X said hi to the Bear, complimented her on her costume, and seemed to immediately take to her. I mentioned at that point (since the Bear wasn’t saying anything) that she did not yet speak. This interested Mrs X. She had recently finished writing a book with a character that was ‘selectively mute’ and had done some research on this subject. I mentioned that the Bear was autistic, and she said that she had done some reading about autism too, and hinted that the character was on the spectrum.

Mrs X said that she would go and get a treat for the Bear, at which point I said that there was no need. She was on a selective diet, and I had just brought her over to introduce her, so that when they saw her they’d know who she was. Mr X was not home to meet the Bear, but Mrs X really seemed to take a shine to her. She wouldn’t take no for an answer on the treat, and asked what she could give her. After listing a few things (no, no, no...) she suggested a box of raisins, which I said would be okay. She invited us inside while she went to get them. Her voice seemed to be searching for something else, and then she asked if the Bear liked rocking horses? I said I thought so, so she said that they had one and she would pull it out.

Meanwhile, the Bear decided to go walking. Before I could grab her, she walked off into the darkened house. Crap. I’m inside the doorway in my shoes, the Bear has just walked off into their house, and Mrs X is down the hall off the kitchen trying to pull out the rocking horse. Something had to give, so I apologized and walked in. Meanwhile, the Bear had circled the front hallway and came into the kitchen from the opposite side. I came up the other side, helped Mrs X pull out a large fur and wood rocking horse, and finally everyone was in the same place, including the dog, (who also took a friendly interest in the Bear).

We put the Bear on the horse, and she seemed to enjoy it. I wish that I had a camera with me, since the opportunity to get a picture of my daughter in Hawaiian winter dress on a rocking horse does not come along that often. I mentioned that she was quite the daredevil and liked amusement rides, going on them at the local park where we had season’s passes.

Mrs X appeared to be quite interested in the Bear, and seemed to want to do more. “Does she like horses?” I’m not really sure, I answered. “Well, I have to feed and water the horses later anyway, so would she like to see the barn?” Er, okay? I said that we’d only popped by to say hi and introduce the Bear, and didn’t want to be any trouble, but Mrs X ducked the opportunity to politely shoo us off. So off we went to the barn. I carried the Bear as the path was a bit mucky, and continued to carry her though the barn and stables.

The barn was quite large, with about 20 horses (both theirs and boarders). Mrs X took us round and introduced each horse and its history, one by one, including a mother with a new colt. The Bear did not smile much, but she was clearly interested. She watched and took everything in, and was quite content to be carried around the barn. She patted a couple of the horses (hand over hand) and bopped a couple of horses that appeared too interested in tasting her lei and her grass skirt. Mrs X remarked on several occasions that she looked quite observant and also quite intelligent (which is a good way to make her Dad feel proud). Mrs X knew someone else in the neighbourhood (largely defined) who had an autistic son, and talked about him and his experiences.

We had a good chat about a lot of things, including but not limited to the Bear, got a good tour of the barn and the indoor riding area, looked (unsuccessfully) for the barn cat, and watched Mrs X give hay and water to each of the horses. Again, she seemed quite taken with the Bear, and ducked the opportunities I gave her to politely usher us on our way.

After the tour, she walked us back to our vehicle, and said that we could come by any time. I mentioned that my wife and I were not horse people (we’re probably the only ones in the neighbourhood who are not, although Momma Bear has ridden before), so that this was all new to us. Mrs X then mentioned teaching the Bear to ride, and I’m pretty sure that she actually offered to teach her. I’m not sure if I heard that correctly, and I’m not going to push the point. Mrs X did also mention that riding was probably good for autistic children. Living in horse country at least gives the Bear more of an opportunity, but on that we will have to see if she is interested.

Anyway, to make a long story short, Mrs X was the perfect host, and we really appreciated the time and the kindness that she provided. After I thanked her and drove off, I realized that we had been there for an hour and a half. All in all it was a good Halloween. The Bear had a nice experience, and made a new friend.

We need more Halloweens.

(FYI, a) the picture is in mid-swing (I'm quite impressed with the camera), b) the slant on the background is real - it is a hill behind her, and c) given Canadian weather this time of year, this is a reasonably realistic representation of what her costume looked like after coats, etc. were added)

Respect Meme

2006-11-03T20:41:00.000-05:00

Jonathan and María Luján started a ‘Respect Meme’ a couple of weeks ago, and NotMercury joined in. Their versions are here, here, and here respectively. I thought that I would join the stampede and give it a go.

1. What is respect for others?

I quite like and agree with NotMercury’s answer to this:

"Respect for others comes when we recognize our differences and make an effort to treat others the way we wish to be treated in spite of our differences"

I also like María Luján’s point about empathy being the root of a true understanding. A lot of people confuse empathy with agreement, but agreement is not required. To me, empathy is an understanding – or at least a reasonable attempt at understanding – of the position of another. Understanding another’s views does not require agreeing with them, or even liking them. But it does require listening rather than ‘selective listening’ or prejudging.

There will undoubtedly be disagreements, and it is legitimate to raise and discuss them. But disagreements over ideas, concepts, and even 'facts' and their interpretations (some forget that even 'facts' can be open to interpretation, especially when it comes to their meaning, importance, and implications) should not be treated as an excuse to attack the person with whom one disagrees. Even in the case of disagreement over conduct, one should still attempt to confine oneself to commenting on the behaviour, not the person. People make mistakes, and an error in judgment or action does not automatically render one a person unworthy of respect.

Having said that, I do not think that everyone is deserving of respect. I would suggest that one should always give the other person the benefit of the doubt, i.e. treat people as deserving of respect until they clearly demonstrate otherwise. But some people do clearly demonstrate otherwise. And then one has to choose how to respond. More on this in Question 4.

2. What are things that appear to respect issues, but are not?

I agree with Jonathan that some cannot separate the argument from their personhood, and thus incorrectly see a challenge to their ideas as a personal challenge. Confining one’s challenge to the idea itself and not the person behind can help to minimize this, but this will still be an issue at times.

A related issue is that some ‘wrap themselves in the flag’. On one side, some autistics view a disagreement with their ideas as a challenge or an attack on all of those who are autistic. "If you disagree with me then you don’t respect autistics". The mirror image on the 'all autism=mercury poisoning' side is "If you don’t agree with me then you are abusing children". Er, no, on both counts.

Another point I would agree with is that of NotMercury, who answered this with "When intentions are offered as justification for irresponsible actions." Good intentions do not automatically make one right or excuse negative actions, and should not shield those negative actions from comment or judgment. And legitimately questioning those actions can also be accomplished in such a way as to not disparage the intentions behind them (assuming that the intentions are good).

3. Is this relevant to the autism discussion and why?

Respect is very relevant to the autism discussion. I would suggest that from the point of view of the neurodiversity community, respect – and the perception (and in a lot of cases the reality) of the absence of respect - is one of the driving reasons behind their participation in the debate. I would suggest that the ‘autism = mercury’ parents also see the debate – in their case with the government and with many in the scientific community – as a respect issue, and also lack respect for the ND point of view as well as for many of its proponents. And for the majority of parents and caregivers, the respect issue revolves around government and support agencies not providing the amount of care and support that is required to improve the quality of life and accommodation of those touched by autism (i.e. not respecting what they see as the conditions required to respect the right to proper and adequate support).

I would suggest that the actions of many in response to the lack of respect that they feel they should be accorded are negatively affecting the wellbeing of all. But of course, "They started it!", so they will rail against and wait for the ‘other’ to fix the issues rather than seeking to build consensus around points on which they can agree. I would only half jokingly suggest that all involved need a course in ‘Interest Group Accommodation’. As a hint, more success can often be had by sitting at the table where the decisions are being made than by banging on the door outside. The goal is to get to the table, not to impotently make noise. Has anyone ever heard of the politics of entryism?

Some may argue that ‘rights’ are not items to be negotiated. But that is not what I am saying. Instead, I’ll use the analogy of the U.S. and the Soviet Union during the Cold War. Neither side was particularly accommodating of the other, nor were they willing to cede their rights where interests clashed. And at least in the Soviet case the expectation was not of long term co-existence but of an eventual ‘inevitable’ victory of communism and elimination of the other side (in its existing political form) as an opponent. Yet the two sides were still able to find common ground and agreement on more than a few issues that they shared in common, to mutual gain, while still remaining true to their long term goals.

4. What can we do to help resolve these issues?

Regardless of whether the other person deserves respect, one's own conduct is a separate issue. As María Luján quoted me on her blog:

"The real test of moral conduct is how one acts in the face of provocation. Someone else's bad behaviour towards me gives me the right to respond and to defend myself, but it does not give me carte blanche to respond in kind."

That is not an easy statement to live up to, and I would not even begin to suggest that I am successful in doing so in life. But one has to start somewhere. If my moral code goes out the window whenever someone challenges me, then what is it worth? To me, the correct response to clearly improper and sustained conduct is to point out the behavioural failings while remaining civil and true to one’s own code of civil conduct. Easier said than done. But if I bring myself down to the level of behaviour that I am objecting to then what have I gained?

To me, it all boils down to ‘Why are we participating in this *debate*?’ I am here to learn, possibly to contribute something back, and to act as a representative for my daughter until she is ready to take on this role for herself. I stand a better chance of accomplishing these goals if others are willing to engage in a dialogue. I am not here to make enemies - this is counterproductive. Some may be angered by my opposition to their viewpoints. That cannot be helped. But I can try my best to ensure that no one has as an excuse to shut down dialogue that I have personally and maliciously attacked them.

So, on to my point. Regardless of whether I respect someone, I owe it to them (usually), myself (definitely) and my daughter (definitely) to conduct myself in a civil manner, to remain true to my own ideals and code of conduct. I would suggest that – ultimately – this is the more powerful response. To be clear, I’m not suggesting that one should not defend oneself, or refrain from criticizing the arguments of others. Far from it, and I believe that I am quite vigorous in defending myself. But I am suggesting that there is a big difference between defending oneself and sinking to the level of one’s opponent.

5. How well do you think this will be accomplished?

On a personal level, I will try my best to be respectful of others, and at a minimum remain civil. At times I will fail (and should be called on this), but this is not an excuse to not try.

From an autism community standpoint, my expectations are low in the short term. It doesn't take long to find posts that have descended into slanging matches, or even posts that started at that level. Longer term, I think that answers provided by science, combined with the fact that the current generation of autistic children will one day become adults and influence the debate - probably in ways that will surprise all ‘sides’ - will be positive developments.

One of the keys to altering the tone of the debate is 'understanding' (again, this is distinct from 'agreement'), which is currently in short supply. I believe that as we learn more about autism we will find more items on which we can agree. But that will be a very long process.

As a final note, the above should not be construed as suggestive of anyone in particular. I would say that I have no issues with anyone who has commented on my blog to date (not just because they have commented here, but because we have ultimately been able to engage in a reasonable dialogue over time, even when we disagree). While I have had run-ins with some in the past, I have tried not to let it get personal, and I have found that one can (at least so far) eventually get to engage in a reasonable dialogue. I hope that others have found the same with me. As suggested on my ‘About Me’, we don't need to agree: I learn the most from those I don't agree with. And I would like to keep the discussion going.

Autism and the Evolution of the Brain

2006-10-13T20:22:00.000-04:00

In an earlier post I approached the subject of Autism, Genetics, and Evolution from the perspective of the requirements imposed by alleles and the theory of evolution. This post is an attempt to approach the subject from a different perspective, i.e. the evolution of the brain. My last post discussed autism and minicolumns, suggesting that a) ASD has a minicolumnar underpinning, b) this underpinning is required (i.e. no narrow minicolumns means no ASD), c) it originates in the first 40 days of fetal development (i.e. it is not itself acquired post-natally), d) that this difference falls within the normal range (i.e. that having it does not ‘cause’ a diagnosis, although it may very well result in diversity of thought and cognition, i.e. neurodiversity), e) that something else is therefore required (with no significant speculation as to what that something else may be, other than to generically label it as a ‘second hit’), and f) that research needs to prove or exclude causality among the population of the vulnerable, i.e. proving that something does not cause ASD in those who are invulnerable does not prove that it does not cause ASD in those who are vulnerable. This post builds upon the minicolumn post.

Dr Casanova also provided me with a copy of a work in progress on brain evolution and minicolumns (Casanova - Big Brains Manuscript, in preparation for submission), which has some interesting implications for autism, and prompted me to do some further reading. The same caveat applies as in my last post: I’m attempting to post about some of his work and add what I consider to be some of the implications. As before, bear in mind that I am not a neuroscientist, and as such there is the definite possibility that I have misinterpreted some of the ideas and findings. As such, any errors are mine. In addition, any implications beyond those explicitly stated in Dr Casanova’s research papers should not be attributed to Dr Casanova unless specifically noted.

Brain Size and Structure

A logical starting point in evaluating brain evolution is encephalization, or brain size. Statistical models have been built that compare body vs. brain size across species, from which one can derive an ‘expected’ brain mass based on body size. The actual brain mass divided by the expected brain mass yields an encephalization quotient (EQ). A result higher than one indicates a larger than expected brain mass, while a result less than one indicates a smaller than expected brain mass.

EQ is important as it allows for comparisons of brain sizes across species by automatically adjusting for body size. Larger animals would be expected to have larger brains, and elephants and some whales do have larger brains than humans. But after adjusting for body size, humans have much larger brains than other species. Using an EQ measure based on encephalization of insectivorous primates, humans have an EQ of 28.8, and there is a large gap between modern humans and all non-human primates, including the great apes (our closest relatives). This large gap is filled by the increasing encephalization of prehistoric hominid ancestors.

Encephalization has not affected all parts of the brain equally. The neocortex has been the primary beneficiary of this trend:

"The enlargement of the brain is not proportional; that is, all parts do not develop at the same rate. The neocortex is by far the most progressive structure and therefore used to evaluate evolutionary progress" (Stephan, 1972, p 174)

And Dr Casanova writes (Casanova - Big Brains Manuscript):

"It is the areal expansion of the isocortex and its connections that is ultimately responsible for primate encephalization. Ultimately, the simple addition of minicolumns is sufficient to explain cortical expansion, increased gyrification, and the subsequent parcellation and re-optimization of functional neural networks."

As brain size increases, connectivity requirements also change. Increases in cognitive capabilities may not result simply from increasing brain size or adding minicolumns, but rather, may be a function of brain connectivity. A key requirement for the brain is to generate a network of connections allowing for stable information processing while minimizing conduction and wiring costs. Connectivity is ‘expensive’ in terms of energy required to build and maintain connections. Bigger brains require both more connections and the interconnection of distant locations. Longer connections can result in signal delay/attenuation, and increase the probability of something going wrong. Increasing physical distance also raises the costs of connectivity, as the amount of energy required to maintain connections over longer distances is significant.

The answer to this connectivity issue appears to be at least threefold: modularization, gyrification, and parcellation.

By arranging neurons into minicolumns and driving connectivity between minicolumns, connectivity costs are reduced. Further organization of minicolumns into macrocolumns and then parcellation into functionally differentiated cortical regions also reduces overall connectivity requirements. The net effect is to allow a large number of cells to be connected by fewer axons and in more short-range connections.

Gyrification, i.e. the ‘folding’ of the cortex, reduces the physical distance between different areas and therefore the length of interconnecting fibers. Think of a piece of paper with two dots on it. The absolute distance between the two dots decreases as the paper is folded and the two dimensional surface in effect becomes three dimensional. Only one third of the human cortex is exposed to the surface, with the rest being found within sulci. Increased gyrification also increases the ratio of short range versus long rang connections within the brain.

Encephalization also results in an increase in parcellation of the brain into functionally differentiated cortical regions. Connectivity does not scale absolutely with brain size. As Dr Casanova writes: "increasing numbers of minicolumns impose a connectivity constraint, as non-adjacent or near-neighboring minicolumns become isolated by physical distance. Increasing distance limits connectivity as the amount of energy required to generate and maintain long-distance connections is substantial." Parcellation reduces the need for long distance connectivity by concentrating functions within locations. As encephalization increases, so does the amount of white matter dedicated to local connections. The result is a brain that is "not as equally densely connected relative to a smaller brain."

Within primates the corpus callosum, which connects the right and left hemispheres, generally becomes relatively smaller as isocortex size increases. As Dr Casanova writes, "Interestingly, at a gross anatomical level, perhaps the most obvious manifestation of increased parcellation is that the two cerebral hemispheres tend to be less densely interconnected and more independent." Connections between more distant regions are still required, and these may be maintained through specialized neurons, e.g. spindle neurons. As encephalization increases parcellation and decreases and/or channels connectivity into communication between larger units, there appears to be a corresponding increase in the number of spindle neurons to maintain functional communications.

The Costs of Encephalization

The human brain is expensive to build and maintain from an energy and nutritional standpoint. Kleiber’s law expresses the relationship between body mass and body metabolic requirements, i.e. resting metabolic energy requirements (RMR), also known as basal metabolic energy requirements (BMR). The equation is:

RMR = 70 * (W^0.75)

where RMR is measured in kcal/day, and weight (w) is measured in kg.

Mammalian brain size also scales with body mass, according to the formula:

E = 1.77 * (W^0.76)

where E is brain mass in grams. The similarity in the two exponential scaling coefficients is significant, implying that brain size and RMR are related, and a further inference is that the size of an individual’s brain is closely linked to the amount of energy available to sustain it (Foley and Lee, 1991).

While the brain is about 2.5% of our body weight, it accounts for 22% of our resting metabolism (Leonard and Robertson 1992, p 186). This is in sharp contrast to anthropoid primates using approximately 8% of resting metabolism for the brain, and other mammals using 3-4%. In contrast though, total human resting metabolism does not differ significantly from that of other mammals. So the question is, where does the metabolic energy to grow and sustain the human brain come from?

The answer is the ‘Expensive Tissue Hypothesis’, posited by Aiello and Wheeler, 1995. Aiello and Wheeler analyzed the ‘expensive’ (in terms of metabolic energy) organs in the body - the heart, kidneys, liver and GI tract – noting that together with the brain they accounted for the major share of total body BMR. Comparing the expected vs. actual size of these organs for an average 65 kg human, they found that there were significant differences in actual vs. expected size for both the brain and the gut.

They wrote (Aiello and Wheeler 1995, p 203-205):

"Although the human heart and kidneys are both close to the size expected for a 65-kg primate, the mass of the splanchnic [abdominal/gut] organs is approximately 900g less than expected. Almost all of this shortfall is due to a reduction in the gastrointestinal tract, the total mass of which is only about 60% of that expected for a similar-sized primate. Therefore, the increase in mass of the human brain appears to be balanced by an almost identical reduction in the size of the gastrointestinal tract…

"Consequently, the energetic saving attributable to the reduction in the gastrointestinal tract is approximately the same as the additional cost of the larger brain. "

Since the heart, kidneys and liver cannot be significantly reduced in size, due to their critical functions, to keep BMR at the expected level the higher energy costs of encephalization must be met by the gut. The implication for humans is that there had to have been an increase in dietary quality – e.g. more easily digested food, and the liberation of more energy/nutrients per unit of expended digestive energy - to allow for both a smaller gut and the reallocation of energy to encephalization.

Further evidence for the link between diet and brain size comes from the recent (in evolutionary terms) decrease in brain size in humans. Ruff, Trinkaus, and Holliday (1997) found that the human EQ reached its peak approximately 90,000 years ago, and has since remained fairly constant. But, absolute brain size has decreased by 11% since 35,000 years ago, with most of this decrease (8%) coming in the last 10,000 years. EQ has remained relatively constant because of an equivalent decrease in body size during the same timeframe.

So, what happened? The most plausible interpretation is that EQ is a genetically governed trait, and should not have changed materially in the last 10,000 years. This period has also seen the greatest social/cultural progress in human history, suggesting that the change is not the result of evolutionary selective pressure. Instead, the most likely change has been one of a shortfall in meeting nutritional requirements, in the form of one or more limiting factors preventing the body and brain from achieving their maximum potential development. The most obvious change in this period was the introduction of agriculture (i.e. the agricultural revolution), accompanied by a large rise in grain consumption and a significant drop in animal consumption (from perhaps 50% of diet to 10% in some cases).

The issue is presumably not caloric. Instead, the most plausible current hypothesis is that the decrease in animal consumption resulted in a consequent shortfall in consumption of preformed long-chain fatty acids (Eaton and Eaton 1998). For optimal growth the brain is dependent on the fatty acids DHA (docosahexaenoic acid), DTA (docosatetraenoic acid), and AA (arachidonic acid), which constitute over 94% of all HUFA (highly unsaturated fatty acids) in human and mammalian gray matter (Eaton et al 1998). Neuronal membranes are composed of a thin double-layer of fatty acid molecules. Loss in DHA concentrations in brain cell membranes correlates to a decline in structural and functional integrity of this tissue (source).

There is some evidence that humans are not able to synthesize sufficient levels of EPA (eicosapentaenoic acid – another omega-3 fatty acid) or DHA from precursor alpha-linolenic acid (LNA), and thus must get these EFAs from their diet. An impaired ability to synthesize EPA or DHA would increase the dietary dependence. All of the above are far more plentiful in animal foods than plants. Analysis of likely EFA intake during prehistoric times under a wide range of assumptions suggests that levels of EFA would have been sufficient (0.9g/1000kcal) to allow brain expansion and evolution (Eaton et al 1998). As the human diet changed, our access to these essential fatty acids declined.

Eaton et al 1998 discuss the differences in Paleolithic vs. current dietary EFA consumption, comparing a composite ‘diet of evolutionary adaptedness’ or DEA to current EFA intakes. Prior to the agricultural revolution, human consumption of DHA is estimated at 270 mg/day, while AA consumption is estimated at 1810 mg/day. Current estimates for Western diets are 80 mg/day and 100-1000 mg/day respectively, and the discrepancy for DTA is assumed to be similar. Paleolithic C18 PUFA consumption is estimated at nearly 21.5 g/day, with LA (linoleic acid) at 8.84 g/day and LNA (linolenic acid) at 12.61 g/day, with an overall omega 6:3 ratio of 0.70 in the C18 category. Current Western consumption is LA at 22.5 g/day and LNA at 1.2 g/day, with a total omega 6:3 ratio of 16.74. The result is a massive variation from EFA consumption during the period of peak human brain size, and may result in a shortfall in availability of key EFAs. Why does this shortfall matter?

As Cordain et al, 2001 explains, all mammalian brain tissue appears to have an invariant requirement for DHA and AA, without which normal neural function cannot occur: "Limitations to the supply of either one of these fatty acids will determine limitations to brain growth." They also indicate that the supply of these EFAs is constrained by the limited ability of the liver as well as other tissue to synthesize these fatty acids from their dietary precursors (LNA and LA). As such, we must consume the EFAs we need to build brain tissue. As the authors state: "Encephalization quotients decrease with increasing body size because there literally may be insufficient long chain fatty acid product (AA and DHA) to build more brain tissue."

To add a further note, while the researchers above have concentrated on the implications of EFA changes in our diets, it is also reasonable to assume that the changes in diet with the agricultural revolution would also impact access to other key nutrients, minerals, and even essential and conditionally essential amino acids, as discussed here. Access to zinc, iron, taurine, natural Vitamin A (as distinct from beta carotene) and B12 are some of the nutrients that would have been significantly impacted by the change in diet, although these changes have not been explored to nearly the same extent as the EFA issue. This is not to comment on the implications of these changes or to suggest any consequences or causality, other than to note that they exist and may have implications beyond those discussed in this post.

The increased cost of encephalization has also had another consequence for human development – delayed maturity. As part of their analysis, Foley and Lee, 1991 compare the development of human and chimpanzee brain growth patterns. Chimpanzees are born with a brain mass that is 47% of adult brain mass, and adult size is reached by four years of age. Humans, in contrast are born with brain masses that are 25% of adult brain mass, and by four years old have reached only 84.1% of adult mass. Despite a slower maturation, human daily brain energy costs start at twice those of chimpanzees, and by age five are 3.3 times higher. Growth costs are also commensurately higher.

Foley and Lee suggested that “Mothers from a variety of primate (and other mammalian species) have a goal of weaning infants at an optimal mass, ensuring those infants’ survival, and themselves producing again.” They theorize that the reason for delayed maturity in humans was an inability to sustain both higher brain energy costs and high rates of brain growth, leading to evolutionary selection for the energetically less demanding strategy of increasing the duration of human growth and maturity. Despite a higher DQ and increased foraging efficiency (through increased socialization and cooperation over time), human brain energy costs were sufficiently high to force a slowdown in the rate of growth, despite the cost of reducing female lifetime reproductive rates. Larger brains forced slower growth rates and delayed human maturation.

Brain Evolution and Autism

The evolutionary factors described above have some implications for autism. First, as I stated in the prior post, analysis has determined that minicolumns in the brains of autistic individuals tend to be smaller in size, although with the same total number of cells per column (Casanova et al, 2002a and Casanova et al 2002b). Given that autistic brains tend to be larger than average, the results indicate that autistics also have a higher number of minicolumns. In addition, the neurons within these individual minicolumns tend to be reduced in size. Reduced minicolumn width appears to be a prerequisite for autism. But, the reported minicolumn widths found within autistic brains are still within the normal distribution of minicolumnar width, albeit at the tail end (Casanova 2006). For lack of a better term, I’ll refer to this as a ‘pre-autistic brain’, i.e. meeting the structural requirements for idiopathic autism but not qualifying for an ASD diagnosis (perhaps the broader autism phenotype or BAP?). I’ll also assume that the pre-autistic brain neurons are also of reduced size, for reasons that I will discuss below.

Studies have also shown a postnatal acceleration in brain growth in autistics, resulting in increased brain volume in autistic children vs. controls (e.g. Redcay and Courchesne, 2005), Aylward et al 2002, among others). As per Hazlett et al, 2006, "Significant enlargement was detected in cerebral cortical volumes but not cerebellar volumes in individuals with autism. Enlargement was present in both white and gray matter, and it was generalized throughout the cerebral cortex. Head circumference appears normal at birth, with a significantly increased rate of HC growth appearing to begin around 12 months of age. CONCLUSIONS: Generalized enlargement of gray and white matter cerebral volumes, but not cerebellar volumes, are present at 2 years of age in autism. Indirect evidence suggests that this increased rate of brain growth in autism may have its onset postnatally in the latter part of the first year of life." Thus the autistic brain appears to have more minicolumns, more neurons generally, and appears to grow faster than NT brains.

Given that encephalization appears to result from the addition of more minicolumns, with a resulting increase in gyrification and parcellation, could a more densely packed autistic or pre-autistic brain be a continuation of this evolutionary trend? If so, then the adaptations related to encephalization would also be expected to increase, e.g. increased gyrification and altered parcellation. This appears to be the case. Hardan et al 2004 reported an increase in left frontal gyrification in autistic children and adolescents compared with controls. Herbert et al 2004 reported differences in the parcellation of white matter (Casanova - Big Brains Manuscript), as well as increases in cerebral white matter (Herbert et al, 2003). More minicolumns require more connectivity, requiring more white matter, increasing total brain size, and increasing the bias toward local over global connectivity. The smaller neuronal size within the autistic brain would further reinforce this local connectivity bias.

It may also be noteworthy that the larger than average brains of autistic individuals have consistently shown smaller corpus callosi. Basically, a 'pre-autistic' brain is potentially a more cell-dense brain that may have advantages but is less robust. The addition of more minicolumns could explain the larger brain, increased gyrification, and some variations in parcellation, all within the normal range (albeit at the tail end of the distribution curve), and all of the above would help explain an increased preference of this brain for local over global processing (continuing the encephalization-linked trend), even without any further impact that would tip this still non-autistic brain into ASD (hence the term 'pre-autistic').

I would hypothesize that this pre-autistic brain is another variation along the path of increased encephalization, created by genetic lottery to either survive and reproduce - if this 'model' ultimately has an absolute advantage or niche advantage - or wither if it does not. Could more minicolumns - but of narrower width - and more neurons but of reduced size be a 'normal' tradeoff related in part to metabolism and limits in connectivity and skull size? Larger neurons would have higher metabolic requirements, so smaller neurons might be a response to a resource constraint (i.e. they might have been larger if the resources to grow and sustain them were available). If the same number of minicolumns and neurons were of 'normal' size then this might also unduly strain connectivity and metabolic demands (connectivity over increasing distance results in increased metabolic requirements) and skull size past any reasonable limits (e.g. an increase in minicolumn width from 44.3 um to 67.8 um as per Figure 1 below would be a 53% increase). In this light, the pre-autistic brain can be viewed as an evolutionary attempt to increase the size of the brain within existing resource constraints.

(Figure 1 Source – TMS Research proposal in preparation for submission, pg 2, with permission)

I would suggest that another reasonable hypothesis is that the pre-autistic brain could strain the nutritional capabilities of the body. If a normal brain constitutes 2.5% of body mass and accounts for 22% of BMR, (Wikipedia suggests that the developing infant brain consumes around 60% of the energy used by the body), then how much more would a larger and faster growing brain tax the metabolic system? Presumably a smaller neuron would require less energy or nutrition than a larger neuron, but I would suggest that the relationship is not linear, e.g. a neuron twice as large would require less than double the resources (in the case of the BMR, the exponential coefficient is 0.75, and it might be reasonable to expect something similar at a cellular level).

To the best of my knowledge it is an open question as to whether a pre-autistic brain also grows faster than average. A hypothesis is that the difference between the autistic and pre-autistic brain is the difference in growth rates. As stated in Courchesne, Redcay, and Kennedy 2004, “Head circumference, an accurate indicator of brain size in children, was reported to jump from normal or below normal size in the first postnatal months in autistic infants to the 84 th percentile by about 1 year of age; this abnormally accelerated growth was concluded by 2 years of age. Infants with extreme head (and therefore brain) growth fell into the severe end of the clinical spectrum and had more extreme neuroanatomical abnormalities.” Could increases in severity be a consequence of brain growth outstripping the required resources?

If autistic children have an increased rate of brain growth in the first few years of life then presumably this imposes a metabolic strain over and above the brain growth of NT children. Since no growth is ‘free’, this metabolic strain (energy and nutrients) must be somehow accounted for, either via an increased BMR, a reallocation of resources within the body, substitution (e.g. a deficiency in omega 3 EFA is compensated for by omega 6 EFAs, but at a functional cost), or through structural or operational deficiency. From Cordain et al, 2001 Fig. 2. “(Log-to-log chart of the resting metabolic rate of 20 anthropoids (new and old world monkey, apes and humans) relative to the predicted relationship based upon the Klieber equation)”, it is apparent that the actual to predicted BMR relationship is very close. I would suggest that BMR is a measure of efficiency that has been very tightly honed as a measure of evolutionary fitness (too low a BMR would result in energy constraints, while too high a BMR would increase the risk of starvation), and there is no reason to presume that autistics would vary significantly from non-autistics in adhering to expected results. But all of the other options result in potential downstream consequences in either the brain or other tissue.

If a shortfall in EFAs has potentially resulted in a decrease in size of the human brain by 11%, then what effect would the shortfall have on a pre-autistic brain with more minicolumns and an equivalent number of neurons per minicolumn – i.e. a brain with more neurons? Further, the increased rate of growth of the autistic (and pre-autistic?) brain in early childhood would increase even further the strain imposed by a shortage of EFAs. Smaller neurons, with a corresponding reduction in cell membranes and reduced metabolic demands might be a compensatory measure, gaining in metabolic efficiency and enhancing processing speed, the ability to process stimuli that require discrimination, and allowing for more complex information processing via local processing, but at a cost of reduced global processing and a reduction in ‘robustness’.

This tradeoff could still potentially have other consequences. Even with reduced neuronal size, the pre-autistic/autistic brain should presumably still require more energy and more nutrients than an NT brain, especially during the period of early childhood brain growth. If autistics adhere to the efficient tissue hypothesis then the logical tradeoff to satisfy this increased demand is with the GI system. And I would further speculate that another tradeoff may potentially occur with the liver.

Let’s be clear that I’m not suggesting at this point that the all autistic or pre-autistic children have GI or liver issues. What I am suggesting though is the following: a) that the increased brain costs must be met somehow, since no growth is ‘free’, b) that the GI system (and liver) are the logical organs to endure reductions to meet increased brain requirements, and c) that there in some cases may be consequences to this tradeoff in terms of the functional capabilities of these organs and potentially for overall health. In the case of the GI tract, some of these consequences could conceivably result in downstream issues (e.g. immune issues, impaired enzyme production, reduced metabolic efficiency, reduced nutrient and mineral absorption, etc.) that could have other systemic consequences, including consequences for the brain. Note that these issues would not ‘cause’ the brain to become ‘pre-autistic’, but they might have consequences for the pre-autistic brain that might result in an ASD diagnosis. Liver issues too could hypothetically have downstream consequences via a reduction in detox capabilities.

Further, if an NT brain is already facing resource constraints resulting in diminished size vs. potential (i.e. that 11% decrease in size), how much more critical would a GI 'issue' be for a pre-autistic brain? Even if the pre-autistic brain did not result in GI issues, comorbid GI issues might provide an additional resource constraint for a pre-autistic brain that could have a substantial impact on outcome. In this case it is not required that pre-autistic/autistic children have more GI issues than NT children, but rather, that given the increased metabolic demands of a pre-autistic/autistic brain, that the consequences of GI issues might be significantly greater on a larger and more demanding but less robust brain. The rates of comorbidity may be the same (although the efficient tissue hypothesis potentially suggests otherwise) but the consequences might not.

A further implication of the above goes back to the delayed maturity required of human offspring to allow for the management of the higher energy costs of encephalization. Since the autistic (and possibly the pre-autistic) brain is larger than an NT brain during the first few years of life and experiences a higher rate of growth, could delayed maturity be a further adaptive mechanism? Although much of this early growth is driven by connectivity, the increased number of neurons and minicolumns suggests that there is a lot more in the pre-autistic/autistic brain to connect, requiring substantial resources and energy. While this white matter growth is higher in autistics than NTs, it might still be a reduced rate of growth compared to what would be required to maintain an equivalent level of maturation in this larger brain as found in NT children.

Regardless of one’s beliefs regarding autism etiology, I would suggest that there are some serious implications regarding the nutritional status of autistics that flow from this analysis. The evolutionary and nutritional science referred to above is both mainstream and peer reviewed - no DAN! practitioners in sight. While the analysis has some similarities to Children With Starving Brains, the analysis, conclusions and hypotheses presented were arrived at from a different direction. I would suggest that it is a reasonable proposition that the autistic brain, if it is larger in childhood and goes through the growth spurt that mainstream research has detected, would have to face the same resource and energy constraints of NT brains, but with even higher requirements needing to be met. As such, one does not have to believe that addressing autistic nutritional requirements will result in a ‘cure’ to buy into the concept that autism brings with it some increased nutritional requirements, and that autistic brain ‘performance’ might be enhanced by compensatory nutritional intervention. Notice that I have ducked the entire issue of whether some autistic children with compromised diets due to sensory or tactile issues are further compounding any nutritional issues.

Finally, just to throw a hat into the discussion (see the last post’s comments regarding “The Meaning of Life” and hats for context), the above discussion may also offer a hypothesis to explain the ‘epidemic’, i.e. the perceived increase in the number of autistics in the past couple of decades. As mentioned above, absolute brain size has decreased by 11% since 35,000 years ago, with most of this decrease (8%) coming in the last 10,000 years. EQ has remained relatively constant because of an equivalent decrease in body size during the same timeframe. But in the post-WWII period human height has been increasing in the Western world and Asia. If EQ is genetically driven, then as stature increases, is brain size also on the rise? If resource constraints are lessening (perhaps with more variety in the diet, more access to protein, more access to EFAs?), then might constraints on pre-autistic brain size be diminishing along with constraints on human stature in general? Human stature can take at least two generations to recover (your grandmother’s dietary deficits affected your mother and the resources that she could bring to bear during your gestation). What if nutritional quality gains over the past two or more generations are now removing some of the nutritional constraints on pre-autistic brain development and size (i.e. more resources could allow for higher numbers of minicolumns to be generated during that first 40 days)? This might increase the pool of pre-autistic brains, i.e. the brains described above as being vulnerable to ASD.

Just something to think about.

Autism and Minicolumns

2006-09-05T11:19:00.000-04:00

As a parent of an autistic child (and potentially as an Aspie myself) a subject I find very interesting - and let’s distinguish up front between interest and comprehension or understanding - is ASD and brain research. To my mind, some of the more interesting work is being conducted by Dr. Manuel Casanova, at the University of Louisville, especially in the area of minicolumns. I have read some of Dr Casanova’s research and have written to him, and he has been gracious in replying and even forwarding other papers. I thought that I would make an attempt at a post about his findings and add what I consider to be some of the implications. Bear in mind that I am not a neuroscientist (no, really!) and as such there is the definite possibility that I have misinterpreted some of the ideas and findings. As such, any errors are mine. In addition, any implications beyond those explicitly stated in Dr Casanova’s research papers should not be attributed to Dr Casanova unless specifically noted.

I believe that autism has been ‘discovered’ in the wrong order. Autistic thought, loosely labeled as the broader autism phenotype (BAP), is a perfectly normal and reasonable example of neurodiversity, within the normal range of human thought. I see autistic disabilities as being driven by sensory integration issues to which those who fall within the BAP are more vulnerable. In this paradigm it is reasonable to expect the medical and psychiatric professions to ‘discover’ ASD in reverse order of severity, i.e. defining first the more severe disabilities, then lesser disabling cases, and then the population out of which these cases arise. It is also reasonable that the disabling ‘comorbidities’ of the BAP are therefore not essential features of this neurology, but rather, that they may be medical conditions worthy of amelioration, and that ameliorating these conditions would not change the underlying BAP way of thinking, but instead would allow it to flourish.

Minicolumns and The Brain

The neocortex (also known as the isocortex) is the 2 to 4mm tick top layer of the cerebral hemispheres and outer layer of the cerebral cortex. This layer is responsible for higher functions such as sensory perception, generation of motor commands, spatial reasoning, conscious thought, and language. The neocortex itself is divided into six layers, although there are no borders between these layers, and neuron dendrites and axons cross multiple layers.

The basic anatomical and physiological unit of the neocortex is the minicolumn. (Casanova 2006) As its name suggests, a minicolumn is a vertically aligned collection of cells and their projected connections. It is the smallest unit capable of information processing in the brain - resembling a mini-processor in function - receiving stimuli from elsewhere, processing information, and providing the capability of a response. Information is transmitted through the core of the minicolumn and is prevented from activating neighboring minicolumns by surrounding inhibitory fibers (interneuronal projections).

Pyramidal cells make up approximately 80% of the neurons of the cortex, and are the heart of the information processing capability of the minicolumn. Pyramidal cell somata (cell bodies) in layers III, V and VI are vertically oriented. Their dendrites and axon trees cross at least three layers, and in many cases all of the layers of the neocortex. They release glutamate as their neurotransmitter, and are the major excitatory component of the cortex.

Another component of minicolumns are various types of GABAergic inhibitory interneurons (i.e. neurons that produce GABA as their neurotransmitter), which tend to be aligned one on top of the other and modulate the activity of minicolumn pyramidal cells. Double bouquet cells are present in all layers, but are most dense in layers II and III. The axon bundles (long projections that conduct electrical impulses away from the cell body) of these cells are projected deep into the cortex from layer II to layer V, terminating on pyramidal cells as well as other inhibitory interneurons. They create a narrow vertical stream of inhibition through the cortex, as well as a vertically directed disinhibition of those pyramidal cells upon which the other inhibitory interneurons project. Other interneurons include Chandelier cells, which synapse directly onto the axon hillock (base of the axon projection from the cell body) of pyramidal cells, modulating cell output and participating in intra-columnar inhibition, and basket cells, which contacts the soma and dendrites of pyramidal cells, modulating input to these cells. Although these interneurons make up a small fraction of the total number of minicolumn cells, they play a significant role in finely tuning cortical information processing. A simplified representation of a minicolumn is thus of a processing core surrounded by a GABAergic interneuron circumferential zone of inhibitory and disinhibitory activity.

(Figure 2 Source – TMS Research Proposal in preparation for submission, pg 2, with permission)

(Figure 3 Source – TMS Research proposal in preparation for submission, pg 3, with permission)

Minicolumns are the basic organizational unit of the cortex. It is an increase in the number of minicolumns, expanding the area covered by the isocortex, that is responsible for the historical process of encephalization, i.e. the increase in size of the brain to a degree greater than that expected based on body size (in modern humans, brain size is three to five times greater than expected when comparing to mammals of equal body mass) (Casanova - Big Brains Manuscript, in preparation for submission). A variable number of minicolumns are dynamically clustered with neighbouring minicolumns into macrocolumns, and from there in networks of macrocolumns and regions of functional differentiation within the brain. The minicolumn-macrocolumn relationship may be linked in part to both the termination of projections from the thalamus, which span a fixed distance and may serve to link together minicolumns that receive input from the same thalamocortical fibers, and by the effects of serotonin, changing columnar development in the cortex during brain development (Casanova 2006).

This minicolumn organizational structure conveys certain advantages. Through limiting connectivity within the brain (connectivity requires a significant amount of energy), the result is a reduction in metabolic expenditure. Instead of connecting every cell within the cortex to different brain regions, projections are organized into modules. Single cells project to target sites, and information gained or transmitted is transferred to other neurons within the same modules. Another advantage is plasticity, or the ability of the brain to naturally reorganize connections. Similarities between minicolumns suggest that they are capable of performing similar transformations on incoming information, allowing them to replace each other in case of injury or to adapt to changing requirements. This is not to suggest that all minicolumns are identical. There are variations within different regions, but these may arise from variations in input, output targets, interconnectivity, and inhibition (Casanova - Big Brains Manuscript, in preparation for submission).

So, what does this have to do with autism?

Analysis has determined that minicolumns in the brains of autistic individuals tend to be smaller in size, although with the same total number of cells per column (Casanova et al, 2002a and Casanova et al 2002b). Given that autistic brains tend to be larger than average, the results indicate that autistics also have a higher number of minicolumns. In addition, the neurons within these individual minicolumns tend to be reduced in size.

(Figure 1 Source – TMS Research proposal in preparation for submission, pg 2, with permission)

Smaller minicolumns would skew information processing (noise/signal) in favour of signal, potentially enhancing the ability to process stimuli that require discrimination, but also potentially at the expense of generalizing the salience of a particular stimulus. Smaller and more densely packed minicolumns could also allow for more complex information processing. As an example, the smaller minicolumns in the visual cortex may support added functionality, e.g. depth or color perception. This may be due to the overlap of neuronal projections allowed for when neuronal dendrites and axons remain the same size but the distance to neighbouring minicolumns is reduced (Casanova - Abnormalities Of Cortical Circuitry In The Brains Of Autistic Individuals).

These enhancements come at a cost. In autism, minicolumn size reductions result primarily from reductions in the peripheral zone of inhibitory and disinhibitory activity. The inhibitory fibers act to keep the stimuli within individual minicolumns, and the reduction in this space results in stimuli no longer being contained. Instead, they can overflow to adjacent minicolumns, providing an amplifier effect, which may explain hypersensitivity in some autistics. Thalamic input may also be amplified if thalamic terminal fields remain the same size and therefore result in more minicolumns per stimulated macrocolumn. Each minicolumn’s response to thalamic input is also modulated by the activity of neighbouring columns to a greater or lesser degree, allowing for gradations of response, so a reduction in GABAergic inhibitory activity could also result in a loss of inhibition and greater amplification (see Figure 1). Stimuli ‘spill’ and amplification could result in increased incidence of seizures in autistics.

(Casanova 2006, pg 3, with permission)

An additional cost is that imposed by a reduction in neuron size. The ability of a neuron to sustain a connection over distance is related to the size of its cell body. Smaller neurons result in a metabolic bias favouring shorter connections at the expense of both longer distance and inter-hemispheral connectivity. The result is that autistic brains have a bias towards local (intra-regional) over global (inter-regional) connectivity and processing. Short intra-regional processing functions include mathematical calculations and visual processing. Cognitive functions that require inter-regional processing would be less metabolically efficient, including language, face recognition, and joint attention (Casanova - Abnormalities Of Cortical Circuitry In The Brains Of Autistic Individuals).

The total number of minicolumns in the human brain is defined during the first forty days of fetal development. Symmetrical divisions of germinal cells determine the total number of minicolumns, and a second phase of asymmetrical divisions provides for cell migration into the cortex, with successive divisions determining the number of cells in each minicolumn. This is a complex process, defined by a large number of genes interacting with the environment. The result is that a higher number of minicolumns is not something that someone can ‘acquire’ or be vulnerable to within the post-natal period. It is possible for disruptions during the narrow window of fetal development (e.g. rubella, thalidomide, tuberous sclerosis) to also result in an increase in the number of minicolumns, by influencing this process (Casanova - Abnormalities Of Cortical Circuitry In The Brains Of Autistic Individuals; Casanova 2006).

One point that is important to make is that while narrower minicolumns is a factor in autism, evidence suggests that it is not related to mental retardation. In Down Syndrome, as an example, minicolumn width is normal, despite the smaller brain sizes of Down Syndrome patients.

Implications

Reduced minicolumn width appears to be a prerequisite for autism. But, the reported minicolumn widths found within autistic brains are still within the normal distribution of minicolumnar width, albeit at the tail end (Casanova 2006). This suggests to me that the existence of narrow minicolumns is not enough by itself to result in an ASD diagnosis. The key instead appears to be a reduction in inhibition within minicolumns, rather than width alone. Reduced width increases the consequences of reduced inhibition, but does not automatically cause it. In effect, a brain with narrower minicolumns may be less robust, and therefore more vulnerable to the complications that could come with deviation from the narrow tolerances within which the brain functions. In a brain with wider minicolumns, a loss of inhibition would not have as significant an impact, as minicolumnar width (and therefore distance between minicolumn information processing cores) would still exist to reduce intercolumnal spill, and thalamic projections would result in fewer minicolumns per macrocolumn to be affected.

It is a logical assumption that minicolumn development in MZ twins would be similar (same alleles, very minimal epigenetic differences during the early weeks of fetal development). But MZ twins do not always share the same ASD diagnosis. In cases in which one twin has an ASD diagnosis, the chance of the second twin also having an ASD diagnosis (not necessarily of the same severity) is 60%, and the chance of the second twin being within the broader autism phenotype is 92%. While ASD clearly has an inheritable component (the prevalence of ASD in the population is 0.6%, but within families with an ASD child, the chance of subsequent children being ASD is up to 10%), genetics alone is not sufficient to explain a diagnosis in all cases. This, combined with the fact that reduced autism minicolumn widths still fall within the normal range suggests to me that the issue in autism relates to loss of inhibition, to which autistics are more vulnerable than average, i.e. reduced minicolumnar width is a precondition for autism but a 'second hit' is still required. If that second hit were purely genetic, as distinct from epigenetic or environmental, then presumably both MZ twins should be similarly affected. This is clearly not the case a significant percentage of the time.

Support for this may come from studies of the brains of MZ twins discordant for autism. In Kates et al 2003, a comparison of MZ twins discordant for autism indicated that both the autistic and non-autistic (broader autism phenotype) twins showed no significant differences in cerebral gray matter. This suggests a structural similarity in MZ twins, and the possibility of a requirement for a ‘second hit’ to explain the discordant outcomes.

We can speculate on what that ‘second hit’ may be, and indeed the speculation as to a) whether a second hit exists and b) the causes, if any, are among the most controversial subjects of debate within the community of those linked by autism. I will look a bit more closely in this direction in a post in the near future.

What is clear from above though is that if narrow minicolumnar width is a) a precondition for ASD and b) not sufficient by itself to cause ASD, then this should have an impact on ASD research. If narrow minicolumns creates a vulnerability that wider minicolumns do not, then demonstrating lack of effect in those who are invulnerable does not demonstrate lack of effect in those who may be vulnerable. In many cases the correct population in causation analyses (e.g. epidemiological studies?) would not be the wider population, but instead the sub-section of the population who are actually vulnerable. And in looking for causes of autistic disability, we may want to look more closely at those events and/or stimuli that may reduce inhibition within the brain and/or further discourage global connectivity.

It is also a reasonable proposition is that a ‘cure’ for autism would not alter the underlying narrow minicolumnar structure of the brain. Instead, it would allow this structure to function more effectively, maintaining its strengths while reducing or eliminating the more disabling features of ASD. A cure would not change who one is, which is one of the fears of the neurodiversity community. Instead, it would allow autistic thought to function without the disabling comorbidities, serving to maintain neurodiversity and allowing it to flourish.

Update - Related post:

Autism and the Evolution of the Brain (Oct 13, 2006)

The Agony of Waiting for Poo

2006-08-29T11:40:00.000-04:00

Yes, dear reader, this post is about poo (bowel movements in adult speak), or more accurately, the absence of same. And please note that the ‘No Sarcasm’ sign has been turned off for the duration of this post.

Fortunately, it has been revealed by some in the neurodiversity camp that there are no proven links between any comorbidities and the causes of autism (other than - potentially - seizures). As such, I can therefore hold my head high and treat the Bear’s medical issues without any fear that I could be accused of trying to ameliorate her autism. Her biggest set of remaining medical issues - yes, there are others that now appear to have been ameliorated - are GI related, including alternating and sometimes concurrent chronic constipation and diarrhea, and absorption problems (e.g. low levels of many essential trace minerals and iron – as confirmed by Ontario government medical lab tests, for those whose thoughts veer off in rebuttal in the direction of quack labs - despite supplementation).

The latest bout (note that 'latest' is not synonymous with 'first') started on Friday at around 2:00 PM. The Bear, who had not had a bowel movement in three days, had what we affectionately call a 'shart', i.e. a small leak of gas and liquid stool. Momma Bear cleaned her up and waited for ‘the big one’ which usually follows. Instead, the Bear had another shart. Same cleanup, same wait. And another. Same cleanup, same wait. The Bear usually has a bath after a bowel movement (like night usually follows day - to us it is not a BM but a BM&B) and is fine. This time she did not, and the combination of wipes, rubbing, and irritation from the sharts left her rectum sore and red. Now comes the really fun part.

The Bear began to try harder and harder to have a bowel movement. It obviously hurt, and she started to cry. She strained harder, and cried more. And then she relaxed, calmed down, and looked just plain uncomfortable. A half hour later, the same thing, but with louder crying, screaming, and more tears. Crying is unfortunately ‘normal’ on these occasions, but this time it was worse, and the crying and straining continued on and off with increasing frequency for a few hours. Eventually she passed a small brick (yes, it was about that hard), with much crying, obvious pain, and discomfort. Momma Bear had a very hard time cleaning her up, because by this point the Bear was quite sore and resisting any and all efforts. She then had her bath, I came home from post-work grocery shopping, and we thought this was over for the evening.

But it wasn’t. Within a half an hour, she started sharting again. And pushing, and straining, and crying, and yelling. We kept checking, and trying to clean and wipe her and load on the protective barrier. Because she was so sore she kept resisting. Obviously more was coming, and the frequency of sharts was too much to put her in the bath. Faced with the choice of leaving her and allowing her to become more inflamed, or wrestling with her to clean her, we chose the second option. For some reason, the fact that we kept explaining what we were doing and saying that we were trying to help her didn’t seem to matter to her very much. And Wow! - residual hypotonia notwithstanding, is she ever strong! The frequency of attempts increased to about every ten minutes and went on for hours. We talked about taking her to the ER to see if we could get an enema (my choice), but figured that she would probably sit in the waiting room for a few hours with the same issue and no easy way for us to keep her clean, which would lead to further irritation (Momma Bear’s thoughts).

By about 3:00 AM she fell asleep, exhausted. For about ten minutes. Then she woke up, crying and whimpering as she strained, and fell back asleep. This continued all night. By about 8:00 AM, when the Bear woke up for good, Momma Bear and I were at wits end. When we checked her diaper, sure enough she had had more sharts during the night. More cleanup, more wrestling. Of course, we were handling this like the mature (and well rested) adults that we are (if you believe this…), which was helping the situation immensely. We compromised on phoning the provincial Telehealth service, where we could speak to an RN.

The RN walked us through the emergency list (still breathing - from constipation??? - and no fever, which was good), and ensured the Bear was properly hydrated (she was). She asked about her diet, which contained all the right foods, etc., and we mentioned that a) the diet was worked out by a PhD in Nutrition and b) that the Bear was in the process of coming under the care of a GI specialist at a local children’s hospital (thankfully, as a corollary of free medical care everything works at lighting speed). She suggested monitoring the situation (our first choice too for a distressed child who is regularly screaming out in pain) and bringing her to the Doctor if it didn’t clear up by the next day. She gave us a list of preferred foods (pretty much all of which the Bear already eats). She also asked if we had tried a suppository. "Er, no?" Given my experience with such things, she explained how to use one – “You want me to do what?” – and off I went to the Pharmacist to buy some.

Back home, we went through another cycle of pushing, and then we cleaned the Bear up and tried the suppository. (Of note, this is the first ‘supplement’ that I’ve tried on her that I haven’t tried on myself first). Of course, the Bear graciously cooperated through this. We put a diaper on and waited. Within five minutes she gave a mighty strain, complete with screaming and tears, and there it was – ‘Brick, the Sequel’, complete with an embedded and undissolved suppository. We were overjoyed. By early afternoon the Bear was cleaned up again, bathed, fed, and she was happy. Much happier than anyone with no real sleep the night before had any right to be. She ran around giggling, wanted to play, wrestle, was in great spirits, and still actually liked us (I’m still expecting PTSD to kick in within a few days). Now all we had to worry about was the two jars of prunes and the spoonfuls of Lansoyl. We didn’t want any more action for at least 24 hours so that the cream and time could have their healing effect.

Sunday morning, and all was still quiet. Then the strains and crying started again. And the pushing. And the sharts. She also started toe-walking, something that she had stopped doing nearly a year ago. Here we go again. This time though, we had the suppositories. We waited about half an hour to see if the Bear could resolve the problem. Momma Bear wanted to wait a few minutes more, but not this time. In went the suppository (again, with the Bear’s complete and total cooperation), and within five minutes, out came Brick #3. After the cleanup and bath, peace and order was restored. For now.

So far, everything is okay. The GI specialist has moved much higher up our priority list, and we’re trying to figure out just how many prunes one little girl can eat. But thankfully I can rest assured that – despite a lack of research (only now is the UC at Davis starting to look seriously and systematically at the issue of comorbidities) – like all of the Bear’s many medical conditions that we have cleared up (commensurate – totally coincidentally - with some of her most significant gains), this has nothing whatsoever to do with her autism. What a relief!

The ‘No Sarcasm’ sign has now been turned back on.

---

Update – Yesterday the prunes and Lansoyl caught up. The Bear had three 'normal' (for her) mushy wet BM&Bs, without a lot of upset. We’re now back to the other end of the BM spectrum, until the pendulum swings back to constipation. Note also that I promise to do my best not to write about this issue again.

A Couple of Bear Updates

2006-08-18T17:35:00.000-04:00

Sometimes you lose, and sometimes you win.

On Wednesday the Bear had another PECS session. She was doing so well at home, demonstrating that she understood which card to use to request ‘milk’, or her soother, or the swing, and she was also showing signs that she was starting to understand other cards as well (for various videos and games we play with her).

So at the PECS session, I set up her binder with three cards on it (nose, spoon, and ‘milk’). She selected the milk card and handed it to me. I held it up to show her, said ‘milk’, and then handed her the cup with a couple of ounces of milk in it. While she drank the 'milk' I put the binder out again with the soother card. When she finished, she handed me the cup, looked over, grabbed the soother card, and handed it to me. I again showed her the card, said ‘soother’ and gave it to her. So far so good.

The therapist then said, what would happen if you gave her a choice of milk or soother, and then had her choose the right item after giving me the card? I was confident that she would get this right. We put both cards on the binder, and she pulled the milk card. I then showed her the card and identified it, and put both options in front of her. She scooped up the soother and walked away.

We repeated this three times, and each time she selected the milk card and then took the soother. Apparently ‘milk’ is the first card to choose in any situation, followed by soother, and then by something else.

We’ll keep working on this one. At least she can distinguish between the cards. Now we just have to link them to the correct object/action.

---

When the Bear goes to IBI we always pack her a snack. Today was sliced organic strawberries and kiwi. The goal is to get her to use a pincer grasp to pick up the fruit and eat it. If they put the food in her hand she will put it in her mouth, but getting her to pick it up herself is not easy, and a pincer grasp is harder still. Most of the time she will grab the tutor’s hand and guide it to the bowl to signal that she wants them to pick up the food for her and put it in her hand. We and they also put food on her spoon and try to get her (guided) to put it in her mouth. She has never attempted to do this by herself.

Today, totally unprompted, she reached over by herself and picked up the spoon, which had a piece of fruit on it, and put it in her mouth, as if she had been doing it for years. Her school is closed for vacation for the next two weeks. In the meantime, you can bet that she will have lots of access to a bowl of sliced fruit and a spoon.

Sometimes you get a win, and sometimes you don’t. I’ll put this week in the win column. Tonight we’re off to Canada’s Wonderland to celebrate.

Five Weird Things

2006-08-12T14:47:00.000-04:00

As part of the meme going around the bloggosphere, Wade ‘tagged’ me to identify five weird things about myself. Narrowing down the list was hard – e.g. do the giant one-eyed white cat (now deceased), and the constant presence of Lithuanians in my life count? Where is Lithuania, anyway? (Don’t worry, I know exactly where it is!) But here goes:

1. I can’t swim. Yes, I know Canada is cold at least one month of the year, but it does have a lot of lakes, ocean shoreline, swimming pools, etc., plus the colony of Florida, so the opportunity is there. Despite repeated attempts to learn, I cannot master the breathing technique involved. I love the water, I love to canoe (and am quite fast), I’ve done more than a little portaging and whitewater, and can finally make my way across the length of a small backyard pool. But that is my limit. Fortunately, Momma Bear has every lifeguard designation imaginable. The Bear loves the water, so we’ll see who’s genes she has inherited.

2. I like to travel on my own. While I also enjoy vacations with others, and have gone away with family, large groups, small groups, girlfriends, and now Momma Bear (not yet with the Bear, but soon), I’m quite comfortable going on my own. I went to Israel by myself and worked on a kibbutz for four months (not a southern kibbutz where one hangs out with other non-Israelis, but a smaller northern kibbutz where I was at times the only volunteer). I’ve also backpacked and EurRailed around Europe by myself, from Norway and Finland to Greece and Italy, including through what was once East Germany and Yugoslavia. I also studied abroad with a girlfriend, and when we broke up I again went off traveling by myself for a bit. Whenever I wanted company it was never an issue to meet people and temporarily travel with them, but when it was time to move on, so be it. I would feel quite comfortable doing the same today, but confess that I would much rather go with the Bear and Momma Bear.

3. I love cartoons. I’ll date myself by mentioning The Flintstones, The Jetsons, Tom & Jerry, Bugs Bunny (for which I will drop almost anything), Tweety & Sylvester, Yosemite Sam, the Roadrunner & Wile E Coyote, etc. I’m not so big on the more up-to-date stuff, but I will confess to having to be dragged out of Entertainment departments in stores when 'Ice Age' or 'Monsters, Inc' have been playing.

4. I designed our house. I don’t mean rough sketches, but a proper blueprint-ready design. When we were ready to trade up, my wife and I hunted on weekends for a house that we liked. She also went looking during the week. For two years she scoured our region (we had the gas bills and mileage to prove it). When we couldn’t find anything, she switched to looking for land so that we could build to our own design. Once we found land, we went looking for a design, but again couldn’t find anything that was ‘just right’, so I got a couple of good books on design, figured out how to do it (including sizing – e.g. size rooms to match construction material sizing to keep costs in line), and drew up my own design (obviously with input and approval from Momma Bear). When done, we found a contractor to build it, and he turned it into final blueprints first. He didn’t have to change a thing.

My only regret is that the master bedroom is downstairs, while the rest of the bedrooms are upstairs. The theory was that the kids would be five and under for five years and teenagers for seven. I’m paying for that now.

5. I won a weight loss contest, losing 46 lbs in 77 days. We had a contest at work to see who could lose the largest percentage of their starting body weight. The contest ran from early January to end of March. Everyone put in $100 each, and the person who won took the pot, with second and third place getting their money back. There were twelve of us. I weighed in at 197 lbs (I’m 6 feet tall). It was during the time that we were building the house, and I wanted to use the money to pay for a Jaccuzi. I’m also way too cheap to give away $100. So I dieted (proper nutrition in small quantities and vitamins), exercised (at one point I was walking up 100 floors per day – yes, 100 floors), and the weight melted away. I had no idea how the others were doing except during the two early weigh-ins (in which a couple of others were close), so I just kept going. By the end of the contest I was down to 151 lbs, which in perspective is four pounds less than I weighed in undergrad. No one else was even close. Yes, I can be a bit competitive.

I used the money to buy a two person Jaccuzi (well, the contest paid for most of it). We’ve used the Jacuzzi three times in five years (all in the first two months). Today it holds the Bear’s bath tub, where my wife baths her. I now weigh around 180 lbs, having put most of the weight back on within three months.

So, now it’s my turn to tag three people. I tag:

María Luján (I’ll guest host if you want, but I see no reason that you should escape this)

Kristina

Shawn

Sorry all.

And Wade, starting a new meme tradition, in retaliation I just signed you up for the Lithuanian Wine of the Month club. ;-)

Thoughts on Prenatal Genetic Testing

2006-07-25T19:51:00.000-04:00

One of the latest controversies within the community of those touched by autism is that of prenatal genetic testing. Some fear that this testing will lead to the termination of pregnancies of ASD fetuses, with the result being in effect the elimination of future generations of potentially ASD children. As such, they oppose the development of such tests, and are campaigning to oppose their use. I am not opposed to such tests, or any prenatal genetic testing, for a number of reasons.

When ‘we’ were pregnant, as part of the routine ultrasound process we had a nuchal translucency test, plus the fetal nose scan. The results were negative. We also had the AFP/Triple Screen test. The results came back positive. We received the call to come in for counseling.

During the counseling process we were informed that the results of the AFP/Triple Screen indicated that our baby had an elevated risk of having Down Syndrome. The risk was not ‘through the roof’, but it was definitely there. The next step would be to conduct an amniocentesis, i.e. the definitive test. We were informed that the reported risk of this test was fetal death in up to 1% of cases. How did we want to proceed?

Over the next week, we did some research on Down Syndrome and discussed the risks and issues, and came to the conclusion that we did not want any further testing. The Bear was originally a twin, and we had already lost the other baby at around 11 weeks. We did not want to risk losing her too. We had learned enough about Down Syndrome – on our own, not from counseling - to know that we would also be happy with a Down Syndrome child, and that was the end of the matter. Admittedly, there was a bit of nervousness around delivery time (‘acceptance’ does not necessarily equate to ‘preference’), but my wife delivered a healthy baby who was perfect in every way.

For what it is worth, I am not comfortable with abortion. I can’t say that I would never opt for this choice, but I can say that whenever the possibility of having to make the choice has been anticipated the answer has always been ‘no’. And when the potential existed for having a Down Syndrome child, we rejected the choice, and would do the same for the possibility of having an autistic child.

But, the fact that I am not comfortable with such a choice does not mean that I would deny it to others. I do believe that reproductive choice is a right (at least in the first trimester and possibly early in the second, cases of 'moral hazard', and in cases where the mother’s life is at risk), even if it is a right that I would not choose to exercise. Thank you, but I do not need comments on my lack of morality for feeling this way, if you hold a more anti-abortion viewpoint. From what I can gather, my views are solidly within the majority, regarding the rights of others to choose (although that is not why I hold them), and the purpose of this post is not to debate my views on abortion per se, but rather, to discuss prenatal genetic testing and its consequences.

If ‘choice’ is a right, then it is a right that exists regardless of how comfortable I am with how others choose to use it. The rights of others (e.g. reproductive choice, freedom of speech, freedom of assembly, freedom of worship, democratic rights) are not conditional upon my approval of how they are exercised, but only on the condition that they are exercised within the bounds of the law. I do not have to like how others exercise their rights, any more than others have to like how I choose to do so. But I am required to tolerate them.

Beyond reproductive choice, most prenatal testing has potential benefits that are often overlooked. Testing can lead to increased medical intervention during the prenatal period, better preparedness (e.g. learning) on the part of parents and caregivers, plus time to come to terms with one’s feelings and learn acceptance. As one mother wrote in an Epinion that I highly recommend reading,

"I would ask you to at least consider the benefits of prenatal testing. Knowledge is indeed power. By knowing about potential problems, you give your child the best chance at a safe and healthy delivery and start in life."

In the case of autism there may or may not be any interventions that one can take – depending on beliefs - to lessen the risks or severity, but preparedness and adjustment are both valuable in their own right, as is the knowledge to plan early intervention, increased stimuli and interaction, etc.

Some would argue that this early ‘knowing’ can be postponed until the post-natal period (specifically to rule out eugenic abortion), but if genetic testing is available at all then it will be available on a prenatal basis. Arguing that it should only be available on a post-natal basis is an unrealistic and unrealizable limitation. And the delay pushes acceptance and preparedness into this same period, delaying what for many will be a necessary period of adjustment (even if we don’t always want to admit that adjustment is often required).

Another reason I do not oppose prenatal genetic testing is that I think that testing is inseparable from genetic research. Once science understands the genetic basis for an outcome, I don’t believe that there is any way to prevent the development of a genetic test, even if such a test was not the primary goal of research. And an understanding of the genetics of autism is valuable in its own right, leading to greater understanding, better and earlier diagnosis and intervention, and amelioration of the negative consequences of autism (e.g. communications issues). Some have argued that autism may be a social construct, but some of its disabilities are very real, as may be some medical consequences (i.e. the suggested co-morbidities). To the extent that they are not a required part of autistic thought (and since not all with ASD have them, presumably they are not ‘required’) then they are legitimate targets for intervention and amelioration.

Finally, I’m not sure that a definitive genetic test for autism will ever exist. As I discussed in an earlier post, in MZ twins, if one is ASD then the chance of the other also being ASD is 60% (92% for the broader autism phenotype). The fact that the concordance rate is not 100% suggests that some other factor or factors may also be involved. Thus, even a positive result on a genetic test does not mean that autism is a foregone conclusion. This is another reason to continue genetic research, to discover the limits of genetic (and epigenetic) predictability.

Instead of attempting to ban prenatal genetic testing, I would recommend that it should instead be regulated - not in terms of availability, but rather in terms of requiring the availability of counseling and support. As I mentioned above, when we had to choose, we researched the issue ourselves. Our counseling was along the lines of ‘you have x number of days to decide’, rather than ‘here’s what the future may hold’. I would recommend that genetic testing should include the option of counseling as a matter of course, not just on prenatal options, but also on the joys, trials and tribulations of raising special needs children, letting people know that a) life goes on and b) can be very rewarding. We would have found this information helpful. Probably one of the biggest issues parents encounter is fear of the unknown. Good counseling can help mitigate some of that fear.

One of the arguments used against testing is that after the development of a Down Syndrome test, 90% of detected Down Syndrome fetuses are aborted. The fear is that the same would happen with an autism test. To me this is a defeatist argument. Through education of society, counseling of parents, progress in terms of interventions to mitigate the negative consequences of autism, improved teaching methods and methodologies to help autistic children learn, and proof of better outcomes, we should be able to change that number. Rather than attempting to deny parents a test that is coming anyway, or deny them their legal right to choose because we don’t like how they may exercise it, a more worthy goal is to provide them with hope and the likelihood of a better outcome.

But this is just one person’s opinion.

Is The Bear Exhibiting 'Theory of Mind'?

2006-06-30T16:20:00.000-04:00

The other day, the Bear, Momma Bear and I were watching a video together – Baby Einstein’s Baby da Vinci™. In one scene there is an owl, located in front of some trees, who hoots a couple of times. A second owl comes up within the trees, unseen by the first owl. The second owl hoots, and then ducks and hides, while the first owl turns towards the sound, looking for its source. The second owl appears in a different location - again unseen by the first owl - watches the first owl for a couple of seconds, and hoot and hides again. This occurs a third time, and then while the first owl is looking in the last place he heard the hoot, the second owl 'walks' up behind him, taps him on the shoulder, and they both giggle. Fade to black.

The Bear thinks this is absolutely hysterical. She giggles away, gets excited, flaps, climbs up on the table we put in front of the TV to keep her from sitting too close to the screen (sigh), giggles and flaps again, and then climbs down and walks over to Momma Bear or myself to either pull our hand or even hand us the remote to rewind the scene so that she can see the whole thing again. This is repeated over and over until she tires of it.

A subsequent scene involves two hippos. The first hippo yawns. The second hippo begins a yawn, and appears to produce a noise like an elephant’s trumpeting. Both hippos are startled. Again the first hippo yawns. The second hippo yawns, with the same elephant sound as a result, and the same sense of surprise. Then the second hippo yawns first, and yawns normally. The first hippo yawns and produces the same elephant sound. Both hippos look at each other, shake their heads, and walk away. Once they are gone, up pops an elephant, giggling and trumpeting away, pleased with its joke. Fade to black.

In this example too the Bear cracks up, and while she is not as insistent on getting us to rewind this segment to watch it again, we end up repeating the scene a few times.

I’ve also described in a previous post an example of playing peek-a-boo with the Bear, in which she clearly outsmarted me (not that you have to get up too early in the morning to accomplish this) by turning the tables and sneaking up on me.

It struck me that the common thread between these three occasions was that the Bear was able to understand the difference in perception between the various characters (in the latter case the characters being the Bear and me), i.e. that each saw the world differently, and drew humour from the differences in perception. Then it occurred to me, are these not demonstrations of Theory of Mind?

From Wikipedia, Theory of Mind is generally described as:

“a specific cognitive capacity: the ability to understand that others have beliefs, desires and intentions that are different from one's own.”

Further:

“This theory of mind covers two separate concepts:
1. Gaining the understanding that others also have minds, with different and separate beliefs, desires, mental states, and intentions
2. Being able to form operational hypotheses (theories), or mental models, with a degree of accuracy, as to what those beliefs, desires, mental states, and intentions are.“

The Bear has very recently turned three (Happy Birthday Bear!), so I should not be surprised if she did not yet demonstrate Theory of Mind.

A common ToM test is the Sally-Ann test:

"The experimenter uses two dolls, "Sally" and "Anne." Sally has a basket; Anne has a box. Experimenters show their subjects (usually children) a simple skit, in which Sally puts a marble in her basket and then leaves the scene. While Sally is away, Anne takes the marble out of Sally's basket and puts it into her box. Sally then returns and the children are asked where they think she will look for her marble. A child is said to "pass" the test if he realizes that Sally will first look inside her basket before realizing that her marble isn't there. This is based upon their developing the notion that she "cannot watch..."

"Normal children under the age of four (emphasis added), and most autistic children (of all ages), will cheerfully and confidently answer "Anne's box"-- they do not conclude that Sally cannot know that her marble has been moved."

"Children who pass the test (presumably) understand that there are two different sets of beliefs:
• their own beliefs, based on what they have personally seen, heard, remembered, imagined, reasoned, etc., and
• the beliefs of others, based on what they have seen, heard, etc.."

Those who fail the test are said by some psychologists to lack a ‘theory of other people’s minds’, although there are problems with the test (discussed in the link) that may call this interpretation into question.

In the three examples above, does the Bear exhibit an understanding that the various characters see the world differently?

In the owl example, while she has a clear sense of excitement and anticipation, she does not react when the first owl hoots. She also does not react when the second owl repeatedly appears. It is only when the second owl hoots and hides that she really starts to laugh, suggesting – to me at least - that she clearly understands that the joke is the deception of the first owl by the second owl. She is also amused when the joke is revealed, but not as much as when the prank is being executed. To understand this scene, I’d suggest that she has to understand that the first owl has a different perception of the world than either the second owl or the viewer.

In the second example, she gets excited when the hippos appear to produce the elephant sound, and when the elephant appears, but she does not appear to have a particularly strong reaction when the elephant trumpets triumphantly (i.e. I don't think it is the elephant trumpet itself that she is reacting to). This example is a more open to question, in that she may be reacting to the incongruity of the elephant sound emanating from the hippo, but I really think she is getting the joke, that the elephant is deceiving the hippos (to whom the joke is never ultimately revealed) and that therefore the two sets of protagonists see the world quite differently.

In the third example, I’d suggest that the Bear understands that I am visibly ‘sneaking up’ on her, and by surreptitiously sneaking up on me she understands that she and I do not perceive the world in the same way. Otherwise, there would be no point in sneaking up on me because I would know that this is occurring.

So, am I overanalyzing, or is the Bear demonstrating Theory of Mind, based on the notion of ‘cannot watch’ mentioned above? If she is, then this demonstrates that a child diagnostically labeled as ‘autism, at the severe end of the spectrum’ is capable of Theory of Mind, and at a young age. Given that 'normal' children don’t usually pass the Sally-Anne test until four (which may be an issue with the test as much as with their cognitive abilities), this would be an interesting result.

If she is not yet demonstrating Theory of Mind in these examples, I would not interpret this as meaning that she is not capable of this ability and/or would not be capable of demonstrating it in the future. Any issues she, and other autistics, demonstrate in this area could presumably be related to sensory integration issues as much or more than due to cognitive weaknesses. If one has difficulty processing incoming stimuli, especially input from other peoples’ faces, then it stands to reason that the ability to analyze the expressions of others - as cues to their state of mind - may be impacted long before this ability fails at a cognitive hurdle.

Those are my thoughts. I’m interested in hearing yours.

Moderate Does Not Mean Neutral

2006-06-13T19:48:00.000-04:00

There have been occasional comments on and off from the neurodiversity side that refer negatively to some bloggers and/or commenters as being moderate or neutral. This is the latest one to catch my attention:

Some people don’t believe in “rocking the boat,” they want to give themselves the superficial sheen of “neutrality” and portray themselves as being on the moral high-ground by staking out their imaginary “middle ground.” I think they are part of the problem, myself.

I’m guessing that they are not aimed at me personally – I recognize that my profile is not high enough to gain enough notice (that’s not a lament, just a statement) – but regardless, I thought I’d reply on behalf of at least this one moderate bio-med parent.

So, let’s start with a couple of definitions.

First – Neutral:
1. Not aligned with, supporting, or favoring either side in a war, dispute, or contest.
2. Belonging to neither side in a controversy: on neutral ground.
3. Belonging to neither kind; not one thing or the other.

Second - Moderate:

As an adjective:
1. Being within reasonable limits; not excessive or extreme: a moderate price.
2. Not violent or subject to extremes; mild or calm; temperate: a moderate climate.
3. Opposed to radical or extreme views or measures, especially in politics or religion.

As a noun:

One who holds or champions moderate views or opinions, especially in politics or religion.

So, let’s note the difference: neutral means not aligned with, belonging to neither side in a controversy. Moderate means being within reasonable limits, not subject to extremes. To be clear, moderate does not mean neutral, and I am definitely not neutral.

For the record, I consider myself a moderate bio-med. I draw a distinction between autistic thought and autistic disabilities or ‘issues’. I do not believe that there is anything wrong with autistic thought per se, and I am not seeking to cure my daughter of this type of thought. In this I believe I am in broad agreement with those holding a neurodiversity point of view. For the record, I myself am probably part of the broader autism phenotype (BAP), and share more than a few characteristics with my daughter. These traits, including an ability to see the world a little differently than most, have served me well. The difference between us is that I do not seem to have incurred any significant disability (aside from an occasional social cluelessness) to go along with these traits. But my daughter has, and I am seeking to ‘cure’ her of her communications and sensory integration difficulties, believing that they drive her autistic disabilities. In this I am much closer to the mainstream and ‘cure’ side of the autism debate.

As to etiology, I believe that there is more than one cause for autism, and that autism is probably more than one ‘disorder’. My previous posts demonstrate that I clearly believe that there is an underlying genetic vulnerability, but I also believe that there is evidence that ‘something more’ is often required. In the Bear’s case I believe that the ‘something more’ is likely immune/auto-immune related (these issues are in the family), but I am also open to the possibility that it is environmental (defined broadly). I strongly support research efforts to find the causes of autism, and consider myself in opposition to those who do not support this search.

Having said that, I also oppose poorly conducted science, which I believe does not serve anyone well. Exploring a reasonable hypothesis that does not have mainstream support is not poor science. Exploring hypotheses without using the scientific method and without having the goal of arriving at replicable results that can withstand peer review is poor science. Some on the treatment side have conducted poor science, and I believe that the result has been an overstatement of results and a damaging loss of credibility that may slow the ultimate search for answers. I also think that the ‘all autism = mercury’ approach has hampered other research that may find other causes, and I disagree with those that take this one-size-fits-all approach to autism research.

As for treatment, I am definitely on the bio-med side of the debate. We have tested our daughter, using Ontario government health system labs and the Kennedy Krieger Institute, and have found clear medical and nutritional issues that are obvious to mainstream medicine (and for which our very mainstream pediatrician has referred us to specialists). One of the things I am grateful to Kev for is a statement he wrote in 2005 (and I’m paraphrasing) that if an issue is real then it should be detectable by a reputable mainstream lab. We have followed this approach, and mainstream testing has identified – among other things - serious nutritional issues related in part to absorption deficiencies in my daughter. We have worked to correct these issues, using diet and supplements (under the care of a PhD in nutrition) in dosages that take into account RDA limits, and have been successful in controlling and even eliminating some medical issues. We have also seen increased development in our daughter during this time, but I cannot guarantee that the bio-med treatments are the sole source of this improvement.

We do not chelate our child, and to be honest, the process scares me. For the record, my daughter has some potential heavy metal issues (not mercury) that showed up on a mainstream test (discovered by accident – we were testing for essential minerals and ticked the toxic panel as an afterthought). Our approach has been to monitor this and try to naturally rebuild the Bear's detox system rather than use chelation. But I do not oppose others using chelation as long as they have clearly dealt with other bio-medical issues first, have tested their child and found the presence of heavy metals, and are careful to conduct chelation under qualified and experienced supervision and with regular testing/monitoring performed by reputable labs to ensure that no harm is being done.

I am also on the interventionist side in terms of education. My daughter is in an IBI program five mornings per week. As I posted previously, “The goal of her program is not to get her to ‘pass as NT’ - before she was enrolled, the program head very clearly told us that the IBI program would not make her ‘normal’. Instead, it is to teach her skills that will enable her to better and more independently function in the world. Absolutely no effort is expended to get her to act ‘normal’. Instead, she is developing her gross and fine motor skills (e.g. learning how to walk up and down stairs or turn a doorknob), looking at books, learning to communicate through PECS, etc.”

Further, we don’t use IBI to stop her from stimming, since ” we view her stims as a method of communication, self-orientation, and comfort. Her IBI program feels the same way. Instead of trying to make my daughter look NT, they’re trying to teach her the skills that will help her as a human being, regardless of her neuro-orientation.” And as part of the program, ”IBI taught my daughter the first two stages of PECS, as well as helping her to understand the purpose and value of gesturing to communicate. When she gestures, they follow her lead, and they believe that it is important to encourage this. She can now take someone by the hand and lead them a considerable distance to the object of her desire and then communicate to them what she wants, despite being unable to form a single word. As she learns to discriminate between the PECS cards her communications abilities will improve further. Note that none of this is making her any less autistic, but all of it is enabling her to better interact with those around her, make her needs known, and get them met – including her need to socialize and have fun.”

We also have access to a speech and language program, that we’re currently using to teach the Bear stage three of PECS (discrimination), which she is picking up very quickly. Since she cannot talk, we figure that we need to find her another way to communicate, and through both PECS and gesturing she can usually make herself quite well understood. We also had access to OT services, but this access is petering out now that she is nearly three years old. We do have a couple of follow-up sessions due to the generosity of our OT provider, but would welcome more OT support if we can access it.

As for some of the public issues regarding autism, e.g. demonizing autism, the Autism Speaks video or the murder of Katie McCarron, again I am clearly not neutral. My daughter has every right to the same degree of respect and security of person as anyone else, and I oppose any effort to demean, belittle, disrespect, or threaten her because she is autistic. While I do not condone the use of tragedy to falsely label others or to support ideological goals (sorry, but supporting an interventionist or even cure approach to autism does not equate with condoning or justifying murder, and it is insulting to attempt to make or insinuate this link), I will stand with those who respect my daughter and support her rights, and speak out against those who do not.

So, overall we are firmly on the interventionist side of the autism debate, although moderate in application, and - we believe - respectful of our daughter. We are not intervening to ‘cure’ autism, but to treat and hopefully ameliorate the issues that some believe are co-morbidities and some (including us) suspect are the drivers of autistic disabilities. We firmly believe that if we can achieve this our daughter will still be autistic in thought, part of the BAP, and we have absolutely no issue with this – again, our issue is with autistic disabilities, not autistic thought. If our daughter retains her ‘severe autism’ diagnosis then we will accept that too. Our joy is not the Joy of Autism, but the Joy of the Bear, and she will continue to be our joy regardless of her outcome.

What I find interesting is that moderation (not necessarily my moderation, but moderation in general) seems to be threatening to some. My guess is that moderation is probably a greater threat to the ideological poles than their polar opponents. There is a history of extremes targeting moderates to turn situations into a clear black vs. white, ‘us’ vs. ’them’ issues, eliminating any room for diversity of viewpoints or compromise. It is easy to caricature or ridicule an extremist opponent (e.g. ‘all autism = mercury’ is downright silly), but it is harder to ridicule a moderate interventionist approach backed by replicable medical tests and following a moderate educational approach based on what many would consider common sense. In this, moderates could therefore be considered the greater threat.

I’m not saying that my approach is necessarily correct, or that others should follow it. What I am saying though is that it is a reasonable attempt, backed by mainstream derived evidence, to follow a common sense path to help my daughter grow into the person that she is in the process of becoming, and we have a right to follow it. I’m not saying that everyone has to agree, but I have the right to hold my opinions, they are no threat to anyone else, and they do not make people like me ‘part of the problem’.

I’m not neutral. I’m on the side of the Bear.

Contrasting Two Presentations of Autism

2006-05-30T18:28:00.000-04:00

My wife and I and my outlaws (they’re great, but this is still my handle for them – my only ‘in-laws’ joke) took the Bear to Black Creek Pioneer Village on Sunday for an outing. We all had a good time, and the Bear, true to form, wandered everywhere to see everything, but didn’t seem to be focusing much on anything in particular. We stopped in a yard outside one of the houses and hung out under the shade of the trees, and the outlaws played with the Bear.

“She might not look like she’s paying attention, but she’s taking everything in.” said my father-in-law. “She understands a lot more than we know.” My jaw dropped. Then I clued in, and that reminded me to mention to my mother-in-law that we now had a copy of the Time magazine with the cover story on Autism (May 15th, 2006 issue, written by Claudia Wallis). “Oh, we forgot to bring it”, she said, but it didn’t matter. We had all missed that edition on the newstand. Relatives in Michigan had a copy and sent it to my outlaws for them and then us to read. “Did you read it?” I asked. Both answered yes and that they had found it very interesting, and helpful in understanding autism. They’ve always been good with the Bear, but their comments on Sunday showed that they ‘got it’, at least as much as one could from the Time write-up. They knew that what they could see was not indicative of what the Bear was thinking or understanding or capable of. It was one thing for us to say it, but now it was in print too, so it must be true.

The outlaws then proved that they didn’t ‘get’ everything when they asked about the Bear’s school. They forgot that she goes to IBI five mornings a week, and were still under the impression that the government must be paying for her IBI since the government had ‘approved’ her for funding. We obviously must be doing something wrong (because there surely couldn’t be a waiting list for something so important?). Why didn’t we just demand that they pay? But that’s another story.

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I found the Time write-up to be surprisingly good. Among other points, it talked about previously unrecognized (by non-ASD people) capabilities of those with ASD, autistic brain structure (raising the surprisingly sophisticated question of how much is the cause vs. the result of autism), autism subtypes, the view that ASD may be a combination of genetic vulnerabilities and environmental triggers, and the potential of the immune system to play a role. It also included an article on ABA and Floortime/DIR (developmental, individual-difference, relationship based) teaching, showing that teaching is not just possible, but very achievable. The write-up also mentioned some of the negatives, but did not dwell on them to the exclusion of the positives or of progress and hope. It was surprisingly balanced in its overall approach.

My favorite part was the following bullet-point under “Among the surprises:”

”Many classic symptoms of autism – spinning, head banging, endlessly repeating phrases – appear to be coping mechanisms rather than hard-wired behavior. Other classic symptoms – a lack of emotion, an inability to love – can now largely be dismissed as artifacts of impaired communication. The same may be true of the supposedly high incidence of mental retardation.”

This one quote highlights the most important take-away from the Time articles that I want everyone who meets the Bear to know. If they remember nothing else, I want them to remember this. For this alone I am grateful to Time and the author.

Contrast this with “Autism Every Day”.

I was quite taken aback by the video itself. I feel sympathy for the families involved, but I also have some major issues. To me this was a ‘train wreck’ video, and while autism is obviously difficult, I don’t feel that families touched by autism are well served by disaster movies. A more honest video would have showed the difficulties, but also the good times, and that it is possible to cope, learn, and improve the quality of life of our children, and for that matter for ourselves as parents, siblings, etc. The video asked for understanding, but it appeared to me to be understanding for the parents in having to deal with their children, rather than understanding for both children and parents.

I quite like the idea of a video to explain our lives to others. But I'd prefer that it didn't make my child (by association) look like a ‘nightmare’ inflicted on us (and potentially on others when they come in contact with her). As a parent, autism is hard and painful at times to deal with, but there is also a joy that we can feel from our children, and one that our children can feel, even if we cannot always see it - and I think that much of the time I can see it, written on my daughter’s face. I don't want people to shy away from the Bear, to be afraid of the disruption that they fear she may cause, or to pity her, but rather, I want them to understand her and accept her.

Asking for acceptance does not mean that I'm not going to work like hell to fix her SI, immune, GI, etc. issues. I have no problem with autistic thought per se, but with autistic 'issues' - it is these that I'm working to help her overcome, and I believe there is a link between her medical symptoms and these ‘issues’. Asking for acceptance also does not mean that I won’t try through IBI or other teaching methods to teach or enable her to learn the skills she needs to make her way in the world. Instead, acceptance means recognizing her as a human being worthy of the same respect and rights as anyone else. Implying that she is a nightmare to deal with is not only untrue, but does nothing to further this goal.

I'm also angry at some of the comments of the parents. I believe that my daughter is capable of understanding far more than I can see (and I often get confirmation of this, at the most surprising times). I would never say in front of my child (or behind her back, for that matter) that I was contemplating driving off a bridge with her in the car, or that she will never get married, or that hopefully medical science will find a cure before her sister has children, the implication being so that the sister does not have to deal with a child like her. What about medical science ameliorating her autistic daughter's difficulties, or enabling her to lead a rich life through learning and inclusion too? More than one of the parents sounded like they viewed their kids as 'write-offs', and did so right in front of them. That made me cringe.

A major point left out of both the Time write-up and the video is that learning and assistance for parents is definitely needed and in short supply. This is needed so that parents can better understand autism (not that I do yet, either), how to help their children, and what their children are - and can become capable of - achieving. The lack of understanding of the powers that be (especially including front line and even some 'expert' medical people, but also government and some in the various support services) is short-changing everyone involved. Both missed this point.

The words and actions of the parents may be related in part to this lack of knowledge. Given that my daughter is not yet three, I'm also very conscious of 'there but for the grace of God go I', so I don't want to judge too harshly, or publicly condemn them (although I guess I just did). My daughter is 'severe' (or was last summer), but I have no idea what she will be like when she is five, 10, 15, 20, etc. I think she is becoming significantly more capable and will surprise us all. But even if she doesn't lose the 'severe' diagnosis, I hope that I will never look at her as I perceived that the parents in the video looked at their children. To me, that would be a tragedy.

Overall, the Time article is one that I wish that everyone coming in contact with the Bear could read. I hope that it helps them gain a better understanding of what autism is, accept the Bear’s strengths and challenges for what they are, and see her as filled with potential.

In contrast, I hope that no one who meets the Bear has seen ‘Autism Every Day’. I hope that any who have can recognize that the video is not a true reflection of life with the Bear, and I definitely do not want them to judge her based on what they’ve seen. Getting people to understand and accept the Bear will be hard enough, without her having to deal with the ‘own-goal’ called Autism Every Day. The Bear is not a nightmare to be endured. She is my daughter, she is a great kid, recognized as such by all who meet her, and she deserves better than the video. The Time article is a good place to start.

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On a bright note, the Bear ate with her hands for the first time today. Previously, all food came from a spoon or a sippy-cup. We recently got her to allow us to put banana from our hands into her mouth. But today, for the first time, she ate strawberries with her own hands. Small steps, but a big leap in independence. Go Bear!

The Murder of Katherine McCarron

2006-05-25T20:12:00.000-04:00

Like many in the community of people linked by autism, I am deeply saddened and troubled by the murder of Katherine ‘Katie’ McCarron. Some have suggested as a mitigating factor the view that autism can be difficult to deal with (using the “Autism Every Day” video as an example of the difficulties of being an autistic parent), some have blamed the video for its one-sided portrayal of autism as a 'nightmare' to be endured, some have blamed bio-meds, etc. Personally, I’m just going to stick to the basics.

Children are not objects, possessions, or property. They are fellow human beings, temporarily entrusted to us for care, nurturing, protection, support, and growth, and especially for love.

Their life was ours to give, but it is not ours to take away. No parent has the right to murder their child. Period.

I’m not going to say that this murder was worse because Katie was autistic. The murder of any child, especially by a parent, is equally horrific. And to be clear, we do not yet even know the mother’s motives, but are only surmising that autism may be part of this, because Katie was autistic and her parents may have been following an 'amelioration' approach. But what does makes this case worse is that some – possibly including the mother - may believe that the fact that Katie was autistic somehow partially justifies the act, lessens the severity of the crime, or is somehow a mitigating or explanatory factor.

There are no gradations of humanity, no ‘part’ humans, no ‘people, but’. Autistics may face communications and other issues, but these issues in no way render someone any less human and deserving of life, security, and respect. Whatever autism ‘is’ to anyone – a diversity to be celebrated, something to be cured, something to be understood, something to be lived with, something to ‘be’ – it is not is an excuse or justification for murder.