that way confusion lies

Whichever way you look at it and whatever you think causes it, autism is a complex phenomenon. So it isn’t surprising that different researchers have different conceptual models of how autistic characteristics and their causes are related. Different conceptual models might confuse the public, but researchers are generally well aware of what other researchers think and why. But confusion can arise when conceptual models appear similar but are subtly different.

Here’s Mary Coleman in an interview with Adam Feinstein: “I came to realize that autism is like mental retardation – it’s a final common pathway in the brain affected by many different underlying causes, many different disease entities.” (p.147).

Feinstein says Coleman is ‘convinced that autism will eventually be found to consist of dozens – possibly hundreds – of different subtypes, each the result of a specific medical condition. She told me: “I’m not talking about co-morbidity. I’m talking about the basic disease which causes the autistic symptoms.”’ (p.194)

Now Isabelle Rapin, also interviewed by Feinstein:

Autism is a behavioural, not a medical diagnosis…I agree entirely with the concept of autism as a disorder of the developing brain. What I emphasize is that autism is defined behaviourally, in the same sense that dementia is behaviourally defined…but is, of course, medically caused. There… is no single cause, but many. I disagree with the idea that autism is a ‘disease’ – in the sense that it has one defined cause. I have always believed it reflects dysfunction of particular circuitry in the brain, whatever the biological cause of the dysfunction.” (p 194)

Thomas Kemper, who with Margaret Bauman carried out some pioneering studies of brain development in autism, says;

I still think there’s a unifying feature or group of features about children with autism: the way they use language, the way they interact socially, their play skills. There is a key group of features. I accept that it is a spectrum. But we should still be hunting for what is similar, the unifying characteristic. Even if Mary Coleman refers to 70 different kinds of autism, she’s still calling it autism. There may be different ways of getting there, but I’m not ready to give up on the hunt for some core, unifying feature of the brains of children with autism.” (p. 210)

fan-in/fan-out model

It seems to me that each of the above researchers subscribes to essentially the same ‘fan-in/fan-out’ model; that many different biological causes can produce impairments in a final common pathway that varies widely in its manifestations. Each has a different but important emphasis. Coleman emphasises the differences between the causal disease entities; Rapin the distinction between behavioural characteristics and their biological causes; and Kemper the similarities in behaviour between children.

The term ‘autism’ is a construct that refers to a triad of types of symptom. Whether that maps on to a single ‘thing’ in the real word remains to be seen, but it’s not safe to assume that it does. Jon Brock has addressed this point elegantly in his blog here.

What I find intriguing is that each of these researchers subscribes to the idea of a ‘final common pathway’, ‘dysfunction of a particular circuitry in the brain’, ‘some core, unifying feature of the brains of children with autism’. What, if anything, all people diagnosed with autism have in common is a moot point. The issue of what it is they actually have in common is dealt with explicitly by John Morton and Uta Frith in their work on causal modelling. I plan to examine this in more detail in a later post, but for the moment I’ll concentrate on the confusion in conceptual models.

That way confusion lies

It’s bad enough having to take into account subtle differences in the same conceptual model. It gets even more confusing when the same terminology has different meanings. I’ve noted some terms that are each used in different ways in the autism literature.

1. autism

can refer to either;

autistic characteristics – impairments in social interaction, communication and flexible behaviour


a medical condition assumed to cause autistic characteristics.

Using the same label for both is like diagnosing patients with a sore throat, rash and fever as having ‘sore-throat-rash-and-fever disorder’. It’s an accurate and valid label – all patients with those symptoms definitely have them – but using that term for both cause and effect wouldn’t make it clear whether you were talking about the symptoms or what causes them. It also implies that all patients have the same cause for their symptoms, when we know that there are many different causes for sore throats, rashes and fevers. In the case of autism the jury is still out on the links between cause and effect, so it’s not safe to assume, implicitly or explicitly, that there is only one underlying cause.

2. disease, illness, disorder, condition

are often used interchangeably.

As far as I can ascertain, the usual technical meanings of these terms are as follows;

disease – an infection that impairs normal function

illness – the patient feels unwell. Patients can have impaired function but not be ill, or be ill but not have impaired function.

disorder – a disruption in normal functioning. Normality is an interesting concept and one I plan to discuss in a later post.

condition – the patient’s state from a medical perspective. The patient doesn’t necessarily have a disease, illness or disorder.

The term ‘autistic spectrum condition’ (ASC) is sometimes used in place of ‘autistic spectrum disorder’ (ASD) because ‘condition’ doesn’t imply there is anything ‘abnormal’ about the person.

3. autism is a disorder with a heterogeneous aetiology

can mean either;

different things cause autistic characteristics in different people


different things cause autistic characteristics in an individual.

This phrase is often found in the introductory sections of research papers, but it’s not always clear what it means. One theory for the origins of autism is that autistic characteristics are triggered by environmental factors if a relevant genetic predisposition is present. It’s possible that several genes might be involved. So the causes of autism within an individual can be heterogeneous. Researchers using the phrase might be saying that different people probably have different causes for their autistic characteristics or might be assuming that every person diagnosed with autism has the same heterogeneous aetiology for their symptoms.

Enough of conceptual models for the moment. Bearing in mind the ambiguities in conceptual models and terminology, I next want to turn my attention to theories about the causes of autism.


Feinstein, A (2010). A History of Autism. Wiley Blackwell.


dual diagnosis: autism and other medical conditions

Many theories have been advanced for the causes of autism. Before looking at them in more detail, I want to examine a broader issue; the association between known medical disorders and autistic characteristics.

In their book The biology of the autistic syndromes, Christopher Gillberg and Mary Coleman devote an entire section (six chapters) to medical conditions associated with a formal diagnosis of autism. (My copy is of the 2nd edition published in 1992; the 1st edition came out in 1985, the 3rd in 2000 and the 4th, entitled The Autisms was published in 2012.) The authors don’t speculate on how the medical conditions they list might be related to autism, but it’s clear from this and later works that they are of the view that there are ‘autisms’, rather than a single disorder with different manifestations. From the preface of The Autisms;

Although Kanner, who first accurately described autism in 1943, likely assumed it was a single disease entity…over time it became clear that this was not so, as multiple studies… were published. Instead autism was found to be a specific set of symptoms found in a conglomeration of different diseases some of which overlapped with the intellectual disability/mental retardation syndromes.” (p.xi)

I think Gillberg and Coleman are suggesting that autistic characteristics (which by definition form a syndrome) arise as a consequence of a range of medical conditions, implying that the causes for autistic characteristics are probably different in different patients – hence the authors referring to ‘autisms’ in the plural. In 1974 Coleman had studied a group of 78 autistic children. In an interview with Adam Feinstein for A History of Autism, she says;

As a result of this [1974] study, I came to realize that autism is like mental retardation – it’s a final common pathway in the brain affected by many different underlying causes, many different disease entities.” (p.147)

I’ve summarised below the ‘disease entities’ listed by Gillberg and Coleman as associated with autism. (The list is from the 1992 edition; later research has expanded on it.)

Gillberg & Coleman's disease entities associated with autism

Gillberg and Coleman are by no means the only authors to identify an association between autistic characteristics and other medical disorders. Here are the ‘organic conditions’ reported by Wing and Gould (1979) in children who met Kanner’s criteria in their Camberwell study:

maternal rubella
infantile spasms
severe perinatal complications
multiple congenital abnormalities
unconfirmed viral illness under 1 year
gastroenteritis under 1 year
unconfirmed head injury under 1 year
operation for cleft palate under 1 year.

Michael Rutter and Eric Schopler (1988) comment:

The last issue concerns the question of etiological heterogeneity within the field of autism syndromes. We have already noted that there is undoubted heterogeneity. The very fact that the clinical picture of autism can arise from diseases as diverse as congenital rubella, tuberous sclerosis, encephalopathy, infantile spasms with hypsarrhythmia, cerebral lipoidosis and neurofibromatosis makes that clear.” [references omitted](p.28)

Patterns of association

Because autistic characteristics involve high-level processes, the relationships between autistic disorder and other medical disorders are likely to be complex and varied. However, the relationships between autistic characteristics, somatic symptoms and underlying causes will fall into one of four basic patterns, as shown below.

relationship between autistic characteristics, somatic symptoms and underlying causes

The section on other medical conditions in Gillberg and Coleman’s book was originally entitled “Disease entities that have a subgroup of patients with autistic symptoms” – in other words, not all children diagnosed with a particular disease entity were autistic, suggesting that for each disease entity:


the sub-group of children with autistic symptoms had a distinct second disorder (an autistic syndrome)


the sub-group of children with autistic symptoms had a predisposition to develop those symptoms and that they have been triggered by the disease entity.

Patterns of association and diagnosis

Depending on how strong the association is between autistic characteristics and a particular medical disorder, diagnosis is likely to proceed as follows;

A. If a medical disorder (e.g. disorder A) is frequently associated with autistic symptoms, it’s likely that the medical disorder will be assumed to account for the autistic symptoms and the child will get a single diagnosis of disorder A.

B. If a medical disorder (e.g. disorder B) is only occasionally associated with autistic symptoms, it’s likely that the medical disorder will be assumed not to account for the autistic symptoms and the child will get a dual diagnosis of disorder B and autistic disorder.

C. If the child has somatic symptoms that don’t fit the criteria for any known medical disorder, unless severe, those symptoms are likely to be overlooked and the child will get a diagnosis relating only to their behaviour – autistic disorder.

Each of these options is problematic if the cause of the child’s symptoms is to be identified, because in each group – A, B or C – the autistic characteristics might or might not be caused by whatever causes the somatic symptoms. The only ways to find out would be either to investigate all the symptoms shown by each individual, or to look at the differences between individuals who are autistic and those who aren’t, in respect of each of the other medical disorders.

What isn’t helpful is to assume that everybody’s autism has the same cause.

Coleman, M & Gillberg, C. (2012) The Autisms (4th edn). Oxford University Press.
Feinstein, A. (2010). A History of Autism. Wiley-Blackwell.
Gillberg, C. & Coleman, M. (1992) The Biology of the Autistic Syndromes (2nd edition). Mac Keith Press.
Rutter, M. & Schopler, E. (1988). Concepts and diagnostic issues in E. Schopler & G.B. Mesibov (eds.) Diagnosis and assessment in autism. Springer.
Wing, L. & Gould, J. (1979). Severe impairments of social interaction and associated abnormalities in children: Epidemiology and classification, Journal of Autism and Childhood Schizophrenia, 9, 11-29.

autism and its co-morbidities

In the previous post I looked at the different levels of complexity involved in classifying things, including behaviour. I want to apply this idea to the behaviours involved in autism.

Classifying autistic behaviours

Autism is defined in terms of impairments in three types of behaviour; social interaction, communication and flexibility (people diagnosed with autism show ‘restricted, repetitive and stereotyped patterns of behaviour’). The definition is at a high level of complexity – each type of behaviour involved is the equivalent of a class in the Linnaean system. Many behaviours come under the heading ‘communication’, an even larger number under ‘social interaction’ and ‘restricted, repetitive and stereotyped patterns of behaviour’ could refer to almost anything. It’s true that the DSM narrows things down a bit by listing certain aspects of impairments in these behavioural classes, but there’s still a lot of scope for variation between individuals. Even the specific behaviours mentioned, such as impaired eye-to-eye gaze, delayed speech or persistent preoccupation with parts of objects could have different causes in different people. Jon Brock has calculated the number of possible combinations of the 12 types of behaviour listed in the DSM criteria here; the figure would be much higher if individual variations in these were taken into account.

I’ve illustrated the complexity of the behavioural classes by mapping out the relationship between a low-level behaviour that would qualify as an impairment in the class of behaviours that we call ‘communication’. I’ve chosen one of the behaviours noted by Kanner – ‘pronominal reversal’ (reversal of pronouns). Pronoun errors are common in young children. Very young children often don’t use them at all – ‘Harry do it’ – or sometimes use only one as a default – everyone is referred to as ‘he’. ‘Pronoun error’ is ambiguous because it could mean several different things, but it’s very clear what’s meant by pronoun reversal. Ironically, despite listing ‘pronomial reversal’ as one of the essential common characteristics of his syndrome, in five of the six cases where Kanner records pronoun errors, the children don’t consistently reverse pronouns. The reversals appear to be due to the use of echolalia e.g. ‘you want candy’ instead of ‘I want candy’ or ‘want me to draw a spider’ for ‘I want you to draw a spider’. Jon Brock expands on this point in his blog.)

classification of pronoun reversal

My classification of this behaviour is not exhaustive or authoritative. Nor does it show all the linkages between levels; it simply illustrates the levels of complexity between communication in general and pronoun reversal in particular. Note also that the diagram illustrates the way pronoun reversal could be classified – it doesn’t reflect the way children actually develop language. As I pointed out in the previous post, each level of complexity is equally valid; pronoun reversal could accurately be described as an impairment of pronoun use, or of pragmatics, syntax, language, verbal communication or communication in general. But even if a description at each level of complexity is equally valid, it doesn’t mean each level of complexity is equally useful for all purposes.

Here’s the same diagram again, but this time showing the impairments in communication a doctor diagnosing autism would be looking for. One feature would need to be observed.

diagnostic criteria for impairments in communication

Levels of complexity and autism

Although the diagnostic criteria listed in the DSM appear at first glance to be precise, when mapped onto a diagrammatic representation of the set of behaviours involved in communication, it’s clear that the criteria are at quite a high level of complexity, so the impairments might manifest themselves in different ways and there might be more than one possible cause for each impairment.

A key problem with the definition of autism, as I see it, is that it is framed at too high a level of complexity to be useful in determining what’s causing an individual’s developmental impairments. There is no doubt that a child diagnosed with autistic disorder has impairments in social interaction, communication and flexible behaviour, because that’s how autistic disorder is defined. But because those classes of behaviour encompass so many low-level behaviours, people with totally different impairments to each other can all end up with a diagnosis of autistic disorder. And the atypicalities of people with autism aren’t confined to behaviours; some somatic (bodily) symptoms frequently occur alongside autism. They are referred to as co-morbidities.

Autism and its co-morbidities

When diagnosing a somatic disorder, doctors tend to look at a patient’s low-level symptoms – the type of breathing difficulty, cough, pain or rash. Many diagnostic tests are at an even lower level – the shape of cells or presence of specific molecules. The reason for this is that many somatic disorders have very similar symptoms, so it’s important to identify exactly what symptoms each patient has. In the case of autism the diagnostic process is different. A doctor might first rule out any medical conditions known to cause autistic characteristics (e.g. Fragile X) and might note all the patient’s symptoms, but what’s seen as important is not all the patient’s symptoms, but whether or not the patient’s behaviour fits the criteria for autistic disorder.

Because autistic disorder is defined in terms of behaviour, and because autistic behaviours are often the most obvious of a child’s symptoms, autistic disorder frequently becomes the primary diagnosis and any minor somatic symptoms associated with autism are relegated to the category of ‘co-morbidities’. (Also see Paul Whiteley’s blog on this topic). So sensory atypicalities, epilepsy, sleep disorders, hypermobile joints, growth abnormalities, dietary intolerances, digestive problems and allergies, unless serious, are seen as features that might or might not be caused by whatever causes the autistic characteristics. But because these somatic features aren’t typical of everyone diagnosed with autism, they don’t qualify as part of the autistic syndrome.

That’s fair enough if what you want to do is refine the definition of autism. But if you want to find out what might be causing an individual child’s developmental abnormalities, you need to look at all the child’s symptoms, autism being only one of them.

Harry and Sam

To illustrate this point, I want to look at the symptoms shown by Harry and Sam. Harry’s intelligent and has an excellent grasp of language and abstract ideas. He loves maths and science and has a photographic memory. But he can’t discriminate between some speech sounds or between some letters. He can’t keep track of what people are saying in noisy environments or unless they speak slowly and clearly, and his own speech is hesitant and mumbled. High-pitched sounds, such as children screaming, hurt his ears. He loses track of things that move quickly, like balls or other children, and his motor co-ordination is poor. If he puts his head back he feels sick and dizzy and sometimes blacks out. He finds light touch unbearably tickly but has a high pain threshold. He has a persistent dry cough, can fold his legs behind his head and often gets pain in his legs and chest when walking. He’s a fussy eater, is extremely skinny and his chest is sunken. Certain foods give him diarrhoea, and a casein-free diet has improved his energy levels considerably. Not surprisingly, Harry struggles with conversation, avoids social interaction if he can, and, because he finds almost everything he tries to do difficult, sticks to things he can do best and with least discomfort, like reading, lego, computer games or watching tv. But Harry’s diagnosis is ‘autistic disorder’; his specific problems with receptive and expressive speech, visual discrimination and tracking, auditory hyperacusis, motor and vestibular function, pain, joint mobility, growth and dietary issues just don’t come into the picture. There’s a group of children like Harry with almost identical symptoms at the ‘high-functioning’ end of the autistic spectrum. Their symptoms aren’t just behavioural, but involve sensory processing, motor function, skeletal development and digestion as well. Because the children have symptoms that are so similar (unlike the wide variation seen in ‘autistic disorder’) it’s quite possible that this group of children all have the same cause for their symptoms.

There are other groups with distinctive symptoms on the autistic spectrum too, such as ‘low-functioning’ children like Sam. Sam has little speech, intellectual impairment and poor motor control. He’s big for his age, has epilepsy, pica, is doubly incontinent and smears faeces. He often has tantrums, is aggressive to others, beats his head and throws himself against the walls and furniture. Sam also has a diagnosis of autistic disorder. Do Harry and Sam have the same medical condition? Unlikely, I’d say.

Note that I’m not saying the autistic spectrum can be divided into two sub-groups – ‘high-functioning’ and ‘low-functioning’. There are children across the autistic spectrum who have different symptoms to both Harry and Sam. I’ve just described patterns of symptoms that I’m most familiar with. I also want to emphasise that neither group, Harry’s or Sam’s, would form a sub-group of ‘autism’ because autism is only one of their symptoms. They have symptoms other than behavioural ones, but these are currently classified as ‘co-morbidities’ of autism, rather than being seen as symptoms in their own right.

Biological markers for genetic variations

There’s been a great deal of interest in recent years in the genetics of autism. The Autism Genome Project identified a number of genetic ‘rare variants’ associated with autistic disorders. What geneticists are keen to identify are biological markers that indicate the endophenotype that results from a specific genetic variation. A major problem with this approach is that because the diagnostic criteria for autistic disorder lump together everyone who has autism as one of their symptoms, scientists often aren’t looking for the biological markers for genetic variations in a specific individual, but for the biological markers for genetic variations in everybody diagnosed with autism. And only for the markers associated with autism, not with the other symptoms that individuals might have. It’s quite possible that these much sought-after biological markers are actually in plain sight in the form of co-morbidities, but are being ignored because autistic disorder is seen as the primary diagnosis and is framed only in terms of behaviours.

Next, I want to look at some of the possible causes of autism and its co-morbidities.

only connect: how everything is linked to everything else

My teenage son keeps reminding me that everything is subject to the laws of physics. That idea is often disputed, but since there’s general agreement that autistic characteristics are caused by something in the physical world, I want to have a go at explaining how the laws of physics tie together everything in the physical world – including autism. How we believe everything is tied together affects how we categorise or classify things – including autistic behaviour.

The way human knowledge is organised by educational institutions, libraries and encyclopedias, you could be forgiven for thinking that the laws of physics might apply to the behaviour of solids, liquids and gases, but aren’t relevant to things like art, literature or human emotion. People don’t behave like subatomic particles, so thinking of them in terms of subatomic particles is often dismissed as reductionist, because it ignores the complexity and subtlety of thought and behaviour – there must be something qualitatively different about living organisms, especially humans beings.

Levels of complexity

The reason my son says everything is subject to the laws of physics is because subatomic particles (I’ll stick with ‘particles’ for simplicity) behave in consistent ways that we describe as ‘laws’. Everything in the physical world consists of subatomic particles in different configurations of varying complexity. Subatomic particles interact to form atoms. Different configurations result in different kinds of atoms – chemical elements. Atoms form molecules, ranging from simple chemical compounds to highly complex organic molecules. Organic molecules make up living organisms, and some of those organisms can paint, write and express their emotions.

Each different configuration of particles opens up some possibilities for change but closes down others. If a set of particles has formed an atom of gold, for example, its configuration is very stable, so there’s not much likelihood of it changing. That’s why we can dig gold out of the ground. An atom of sodium on the other hand, is in an unstable configuration, so there’s a lot of potential for change. Sodium readily combines with other elements to form salts – sodium chloride, carbonate and bicarbonate etc. Which is why don’t find chunks of sodium lying around underground – any pure sodium would have combined with other elements.

molecular structure of sodium chloride

Opportunities that a specific configuration opens up are called affordances, and opportunities that those configurations close down are called constraints. At different levels of complexity, different affordances and constraints come into play. Subatomic particles can form hydrogen, release vast amounts of energy and hold the universe together. Sodium atoms can’t do those things, but they can form chemical compounds, which single subatomic particles can’t. Human beings can’t transport oxygen between cells (not without a lot of equipment anyway); haemoglobin can, but it can’t paint a picture or write a book.

Because everything in the physical world is connected in this way, anything – from a physical object to the most sophisticated human activity – can be construed any level of complexity you care to choose. A bit like zooming up and down on Google Earth. Writing a novel, for example, can be seen at the level of the author’s ideas, emotions and experiences. Or at the level of the physical activities involved; muscle movements, using a keyboard or making notes. If you felt so inclined you could even analyse novel-writing in terms of the rearrangement of subatomic particles. An important point about looking at a phenomenon at different levels of complexity is that each level of complexity is equally valid. Novel-writing is about the author’s ideas, emotions and experiences. At the same time, it’s also about muscle movement and using a keyboard, and about the configuration of subatomic particles. But not all levels of complexity are equally useful for all purposes.

The way we organize knowledge

Levels of complexity have an important role in the way we organize our knowledge. Organizing knowledge is important because it reduces the amount of effort we have to put into thinking – our cognitive load. Instead of having to think about thousands of individual examples, we group things into categories and label the categories; ‘tigers’, ‘furniture’, ‘criminals’, ‘unacceptable behaviour’. For some entities we use informal ‘folk’ classifications that are loosely structured and often involve differences of opinion, such as the different types of criminal behaviour or which activities are acceptable and which are not. Sometimes there is general agreement on how to classify things and we develop formal, consistent classification systems – like the periodic table or the Linnaean taxonomy of biological organisms.

Carl Linnaeus’ classification of biological organisms has been in use for nearly 300 years. It’s stood the test of time because Linnaeus based it on the morphology (form) of organisms, rather than on their colour, habitat or uses, criteria that some previous classification systems had used. The form of organisms is very stable compared to their colour, habitat or what uses people make of them, which makes Linnaeus’ system highly reliable. His system has several levels of complexity called ‘ranks’, such as species, genus, family and class. The lowest rank is the species – organisms that are essentially identical in form. The higher the rank the more organisms are included in it. A genus might include only two species, whereas a class (e.g. mammals) might include thousands.

Levels of complexity are also referred to as levels of abstraction. That’s because each level has key defining features that can be abstracted out. The class ‘mammals’ for example, is defined by features such as the ability to regulate body temperature internally, having hair, mammary glands and a distinctive inner ear structure. On the face of it, abstracting key features appears to simplify matters because it tells you only about what all the members of the class have in common. But the class Mammalia includes thousands of species that possess many variations of the key features and lots of other features that aren’t common to all mammals, so although the shared features might be simple, a class could encompass a huge number of individual differences. A vet, called to treat an exotic species of squirrel, would find it useful to know that a squirrel is a mammal, but information about the squirrel’s species and about the individual squirrel’s medical history would be even more helpful.

Classifying behaviour

What has all this got to do with autism? Classification is important to autism because anything can be classified; chemical elements, biological organisms or human behaviour. Autism is defined in terms of behaviour – or more accurately, behavioural impairments. As far as I’m aware, although some people have devised classifications of behaviour for specific purposes, no one has produced the equivalent of a behavioural periodic table or Linnaean taxonomy. That’s because chemical elements and biological organisms are relatively stable things but behaviour isn’t. Although we can identify common behavioural patterns (eating, walking) and behavioural traits (neuroticism, aggression), behaviour tends to be very variable. Because of its variability there’s often disagreement about what constitutes a particular behaviour, so devising a formal, universally accepted classification system is problematic.

But behaviours can be classified, and at different levels of complexity, too. Take ‘feeding’ for example. Feeding is a label we attach to a set of behaviours that includes suckling, eating, drinking and foraging. ‘Eating’ can be broken down into more simple, lower level behaviours; opening the mouth, putting in food, masticating and swallowing. Each of these behaviours could be broken down even further if necessary, into the way specific muscles function, for example, or right down to the level of molecules or the ubiquitous subatomic particles. Which level of complexity we use to describe ‘eating’ will depend on why we are referring to that particular behaviour; a restaurant manager and physiotherapist will be interested in different levels.

The behaviours that are impaired in autistic disorder are social interaction, communication and behavioural flexibility – people diagnosed with autism show ‘restricted, repetitive and stereotyped patterns of behavior interests and activities’. There’s no doubt that those are features common to a large group of people. But each of those areas is a very large class of behaviours – it’s at a high level of complexity. This means that although two people might have totally different behavioural impairments, they can both qualify for a diagnosis of autism. It’s those individual differences I want to look at next.

gold image: Rob Lavinsky, – CC-BY-SA-3.0