For those of you who haven’t been following the discussion about
the theories that underpin RDI, the discussion takes part in the previous two
blogposts and the comments on those blogposts.
First – an apology. Sorry
it has taken me an absolute age to respond – time is extremely tight for me in
term time.
Emotional regulation – I agree that emotions can fluctuate
and clearly there are functional reasons for that…we need to be able to express
happiness, anger etc but I do think we need to come back to an equilibrium and
would suggest that its unhealthy (both for mind and body) to remain in a state
of heightened emotion if that emotion is a negative one. For example, frustration increases stress
hormones. Stress hormones depress the
immune system and we become more vulnerable to toxins and infections. The way I read it, this is what Bowlby
means….that whatever our natural fluctuations in emotions, we need to come back
to a level equilibrium.
Re derailment from the typical developmental pathway - I
never said that difficulties managing uncertainty and change (lack of dynamic
intelligence) is the only cause of anxiety.
I agree that heightened functioning of the amygdala would
result in anxiety but I would question why the amygdala is functioning in a
heightened fashion. It might be because
a person is being chased by a bear….in which case, the amygdala is doing its
job and triggering the fight or flight response. It might be due to sensory overload or
sensory processing difficulty. But the
amygdala may also be operating in a heightened fashion because the person (due
to derailment of the typical developmental process, which has resulted in lack
of DI) is unable to recruit the pre-frontal cortex to over-ride the amygdala
when confronted with uncertainty. Most
of the anxiety I see as an educator in children with autism is due to
difficulties managing uncertainty and change.
There is some anxiety resulting from sensory problems but much more, in
my experience, results from difficulties managing uncertainty. That said, I don’t currently work with
children who have huge sensory problems, so if I was in a different
environment, I might have a different experience.
Regarding episodic memory – if my topographical agnosia was
so overwhelming that it stopped me from travelling then I would want to be able
to work on it so that it no longer disabled me.
I would hope that I could access therapy that would allow me to get to a
point where I had enough positive episodic memories of success in my resilience
repository to be able to tap into them in order to manage my condition.
I agree that some children with autism experience
overwhelming sensory experiences which prevent them from accessing everyday
activities. In RDI we would advocate
that a sensory obstacle was worked on via sensory integration before beginning
to address weaknesses in dynamic intelligence.
Re humans being hard wired to be social and your suggestion
that no evidence has been presented for this.
I am happy with the evidence that I have cited. Plus it fits into a theory of evolutionary
psychology, which makes sense to me.
Looked at through the lens of evolutionary psychology, advances in
humans and other animals serves a purpose.
The purpose of being hard wired to be social is the potential for
developing dynamic intelligence that this confers. Dynamic intelligence doesn’t
develop any other way. We can’t teach
it, it is something that unfolds naturally during the interpersonal engagement
that is Peter Hobson’s ‘Cradle of Thought’. That is why humans are the dominant species on
the plant. I guess we will just have to
agree to differ on that one.
I never suggested that the social model of child development
explains delays in other milestones that are often found in autism. My blog contains posts (link) from guest
bloggers that look at theories behind delays in fine motor skills and sensory
impairment.
The theory I am proposing (which underpins the RDI model) is
a theory that explains the weaknesses in DI in children with autism – nothing
more.
Sue it has been an interesting journey! I wish I had more time to continue with these
discussions but I’m afraid this will be the last time I can participate in this
dialogue due to family and work commitments.
If you are interested in discussing these and other similar issues
further, I would recommend you have a look at the facebook group AutismGuide. There you will find over 500
parents and RDI Consultants - some of whom are also parents as well as qualified
in professional fields such as sensory integration, child development, speech and
language therapy.
Hi Zoe
ReplyDeleteThanks for coming back on this. Response in two parts.
1/2
We appear to be in agreement that sustained negative emotions are undesirable, but when it comes to emotional regulation...
If I've understood Bowlby correctly, what he's saying is this: If an organism is adapted to its environment, its behaviour will fall within certain limits, which suggests that a homeostatic control mechanism is in operation. (This is different to Freud's concept of inertia, which is more like the idea of a level equilibrium.) The organism appraises its environment and a physiological response occurs. 'Feelings' are a part that we are aware of, of physiological processes, and we react in response to them. So 'feelings' have a role in the homeostatic mechanism that controls behaviour. Bowlby explicitly talks about 'feelings', not 'emotions', because feelings cover things like hunger, fatigue etc and make sense in terms of a biological mechanism for appraising and responding to the environment.
The idea of emotional regulation appears to be a much more recent concept and it isn't always clear what people mean by it. You use it, for example, to mean maintaining an equilibrium, whereas some other writers mean emotional management, which is a broader definition. There's also the knotty problem of how we know whether it's the emotion or the display of emotion that's being regulated. The idea of emotional regulation is certainly derived from Bowlby's work, but from what he says about emotion, I think he would have had problems with it.
Derailment from the typical developmental pathway: The only reason I mentioned other causes of anxiety in autism is because you appeared to be saying there was only one cause. I might be mistaken, but you seem to be doing the same regarding pre-frontal cortex. What you've suggested about not being able to recruit pre-frontal cortex is certainly a possibility. Another is that failure to develop pre-frontal cortex functionality (for whole host of possible reasons) is the reason why development hasn't followed a typical trajectory.
2/2
ReplyDeleteI've emphasised the importance of sensory functioning because that's how we get all our information about the outside world (and the inside one for that matter). That includes information about what's going to happen next. Impaired sensory functioning, especially if it consists of delayed or fluctuating processing of sensory information would result in major problems dealing with uncertainty and change. Some autistic children experience high levels of anxiety even in stable, non-uncertain situations, which kind of suggests a physiological problem, rather than an executive function one. And it isn't necessarily a sensory *integration* problem, there might be a primary sensory processing issue - if the signals from the sense organ to the brain aren't up to the job, no amount of sensory integration is likely to help.
Episodic memory - I'd want to be able to work at a disabling issue so that it no longer disabled me too. And I'd hope, too, that I could access therapy. Unfortunately, memory doesn't always respond to wanting and hoping - or therapy for that matter.
Social hardwiring: I do understand that you are happy that hardwiring explains the evidence. I'm not happy with that explanation, because I can't see how the evidence you cited rules out alternative ones.
Evolutionary psychology: I think it's important to be cautious about 'purpose' in development and evolution. And about 'advances'. These concepts aren't supported by recent research in genetics and molecular biology. Life is a bit more haphazard than we originally thought.
Absence or delay in development: Sorry, I wasn't aware of the other posts. I'll have a look for them.
Overall, my main concern about the model of development in autism that you're proposing is this: That just because a model fits the data, it doesn't mean it's the only model that fits the data. And if it's a model involving a complex process, there are many points at which there could be alternative causes, explanations etc. When dealing with something as complex as development, it's obviously impossible to list all the alternatives. But I think it's important to flag up the fact that you're aware that there are alternatives, otherwise people like me (mistakenly) could come away with the idea that you see only one explanation as fitting the facts. I would agree with you about many of your observations about development in autism, but not necessarily with what you think is causing the things you've observed.
Sorry you're not able to discuss this further, but thank you for taking the time to respond.
Sue