Once again, I’m returning to my readings in the Philosophy of Science, a field of knowledge that few scientists acquaint themselves with, though more really should. I’m browsing through a text I’d previously read, Kuhn’s The Structure of Scientific Revolutions, and am reviewing some of my notes. Chapter 8, The Response to Crisis, is particularly relevant to my own field of study, autism, in which many fascinating findings are published almost on a daily basis and yet we still don’t quite know what to make of them. As Kuhn states,
Copernicus complained that in his day astronomers were so ‘inconsistent in these [astronomical] investigations . . . that they cannot even explain or observe the constant length of the seasonal year.’ ‘With them,’ he continued, ‘it is as though an artist were to gather the hands, feet, head and other members for his images from diverse models, each part excellently drawn, but not related to a single body, and since they in no way match each other, the result would be monster rather than man'” (p. 83).
For now, it seems, the many scientific factions studying autism have created a Frankenstein-ian monster of mismatched parts, all eagerly following individual lines of evidence but never capable of seeing the body as a whole. Autism research is left as some sort of exquisite corpse, a jumbled mess of hodge podge parts, with each laboratory tracking down its own pet theories. And I am no exception to the current state.
An example of an Exquisite Corpse, a multi-artist rendering in which each artist is blind to the others’ works until completion. It is a parlor game that was refined by the French Surrealists such as André Breton.
Though we have attempted to define and redefine autism at the behavioral level, we still lack a concrete definition of its biology, with the exception of vague notions of excitatory-inhibitory imbalance, long-range underconnectivity/short-range overconnectivity, or– my personal favorite due both to its amorphous nature conjoined with the theory’s surprising popularity– “synaptic dysfunction”.
In contrast, the field of cancer research is much more unidirectional– though still maintaining many subfields of study– in that it can claim a basic biologic model of cancer. While there may not be full agreement on the variables that drive cancer risk and development, nevertheless any student of the discipline can describe the basic process of oncogenesis at the tissue and cellular levels– and in fact, a surprising number of laypeople could probably also do the same. But not even scientists could tell you with true certainty what autism is. I certainly don’t know what it is and how it differs, other than symptomologically, from other neurodevelopmental conditions.
In this regard, the field of autism research lacks a basic model. And as such, our research wanders rather aimlessly without that compass with which to check ourselves. Kuhn says,
” . . . all crises close in one of three ways. Sometimes normal science ultimately proves able to handle the crisis-provoking problem despite the despair of those who have seen it as the end of an existing paradigm. On the other occasions the problem resists even apparently radical new approaches. Then scientists may conclude that no solution will be forthcoming in the present state of their field. The problem is labelled and set aside for a future generation with more developed tools. Or, finally, the case that will most concern us here, a crisis may end with the emergence of a new candidate for paradigm and with the ensuing battle over its acceptance (p. 84).
I’m not exactly certain what stage we’re at in the field at the moment, whether we’re on the cusp waiting for a new paradigm to emerge that will make most or all of the pieces finally fall into place, or whether we are too methologically limited and must wait for future generations to attack the problem with a new set of tools. Given that time is important for those needing help now, I hope we’re rapidly moving towards a new paradigm that will finally allow us to define autism with greater precision and move forward with our research.
I’m sure that etiological heterogeneity has provided many of the hurdles in our quest to understand the condition. It’s difficult to define something when, in fact, you are studying many “somethings”. Sometimes I wonder, however, whether our attachment to labels– this one being “autism”– has blinded us in seeing what’s before our eyes. Are we so set in our ways that we expect to see the Old Crone when in fact we should be looking for the Young Lady?
Speaking as one professional who has worked with people have symptoms of autism since 1968, I feel that I must say that professionals must avoid getting stuck with one perspective. So moving away from a behavioral perspective was so difficult that even when it was obvious that a sensory treatment worked on a particular case, my colleagues “morphed” it into behaviorism by saying that the concept was, in fact, behavioral. That was back in 1978. The issue is that professionals often paint themselves into a corner, without realizing that they can step on wet paint to get out. Nothing is fixed/static when it comes to autism. There may be so many subtypes that we will never have a single treatment format.
For me personally, I am curious whether there isn’t some root commonality that leads to overlapping symptoms across the different conditions. Working with the genetics side of things, I can see that, for instance, a child with Fragile X has a different syndrome than, say, one with CHARGE syndrome, even though both may frequently present with symptoms of autism. They’re both autistic syndromes and yet they’re not.
However, what behavioral commonalities they can have, I wonder if there isn’t a common physiology that underlies it– especially the repetitive/restricted routines aspect of autism. Does it have links with the excitatory/inhibitory imbalance idea? And if so, what structures/systems in the brain are affected that lead to the core symptomology? Just a few questions I continue to ask myself.
Cancer has a much better handle on the pathopysiology than autism, in autism there is no biologically-based method of diagnosis as exists in cancer.. Too much specialization in my view on research into autism. Too many silos and especially lack of co operation between groups. For example, the excitatory/inhibitory imbalance in autism is also being researched in schizophrenia and are finding similar findings as seen in autism as far as excitatory/inhibitory imbalances is concerned.
I couldn’t agree more, Robert. The way research is set up here and in other countries, it’s a large community made up of solo PI’s, occasionally collaborating, but also largely competing with one another. While it’s a reflection of human nature, it’s certainly the dregs of the barrel. The system is not built to promote people to achieve as a whole but instead for the few to achieve at the expense of the many and, in this case, at the expense of the population they study. Very very sad. I can’t help but wonder if we would see the better side of human nature arise more often in the science community if the state of things (e.g., financially) weren’t so cut-throat.