autism: syndrome under suspicion

This is the last post about syndromes. Promise. The reason I keep referring to syndromes is this: In recent years ‘autism’ as a label for a set of symptoms has become confused with ‘autism’ as a label for an underlying medical condition assumed to cause those symptoms. This confusion, in my view, has placed a major obstacle in the path of autism research. In this post, I round up what we know about syndromes, imagine being a doctor in the heyday of syndromes a century ago, and then expand on the two different uses of the word ‘autism’.

What we know about syndromes

Emil Kraepelin classified mental disorders in terms of syndromes. This approach makes perfect sense because:

1. A syndrome consists of signs and symptoms that tend to co-occur. (Technically, a sign is something someone else can detect, and a symptom is what the patient reports, but for the sake of brevity, I’ll refer to both as symptoms).

2. Symptoms that tend to co-occur are more likely to be causally linked than symptoms that don’t, so identifying a syndrome can provide an important clue as to what’s causing the symptoms.


3. The fact that symptoms tend to co-occur doesn’t guarantee that they are causally linked. Correlation doesn’t indicate causality.

4. The symptoms could all share the same cause; some symptoms could be causally linked, but not others; the causal links could be complex; or the symptoms could co-occur by chance.

Dr Smith’s syndrome

To illustrate the advantages and disadvantages of classifying symptoms in terms of syndromes, I’m going to imagine a doctor – Dr Smith – who has a successful medical practice in a large country town and tries to keep up to date with advances in medicine. It’s 1912. During the last month, Dr Smith has seen over a hundred patients with the same symptoms; breathing difficulties, a persistent cough and chest pain. His experience tells him that the sudden onset of such symptoms in a large number of patients living in the same geographical area indicates that the cause is likely to be a contagious disease. The course of the illness in the first few cases allows Dr Smith to reassure his patients that if they rest, keep warm and take plenty of nourishing broth they will probably be as right as rain within a week or two.

Like any diligent doctor, Dr Smith keeps notes on his patients’ progress. After the first half-dozen cases, he stops listing all the symptoms and writes ‘respiratory disorder’ as shorthand for breathing difficulties, cough and chest pain. If patients have other symptoms besides the three main ones, he makes a note of that. If patients don’t have all the core symptoms, he notes that too. The core symptoms Dr Smith has observed are so common that he wouldn’t dream of claiming that he’d found a new syndrome, but his ‘respiratory disorder’ is a syndrome nonetheless, and he would refer to it as such. It consists of core symptoms that tend to co-occur, but the severity of the symptoms varies between patients and some patients have additional symptoms.

Dr Smith is aware that although most patients with the syndrome ‘respiratory disorder’ will recover quickly because their symptoms are caused by a mild infection, the core symptoms of ‘respiratory disorder’ can also be caused by more serious illnesses such as pneumonia, tuberculosis or an allergic reaction to dust, so he keeps a careful eye on how his patients’ symptoms change. His patients have every confidence in him – but what does Dr Smith’s syndrome have to do with autism?

Autism as a descriptive term

The syndrome labelled ‘autistic disorder’ in DSM-IV has three core symptoms – impairments in social interaction and communication, together with restricted, repetitive behaviours. As far as the process of diagnosis is concerned, ‘autistic disorder’ is an exact parallel to Dr Smith’s ‘respiratory disorder’ – except of course that the causes, core symptoms and outcomes are different. Dr Smith used the term ‘respiratory disorder’ to describe the core symptoms of a syndrome, but he knew that there could be several causes for those symptoms. For many years, ‘autism’ and ‘autistic’ were also used descriptively. Bleuler, Kanner, Asperger, Eisenberg, Wing, Gould and a host of other medical practitioners between 1911 and 1979 used ‘autism’ to describe symptoms. DSM-IV also uses ‘autistic’ descriptively; autistic disorder is a disorder characterised by autistic features, ‘autistic’ being an adjective that describes behaviour, just as ‘excitable’ or ‘lethargic’ do.

Autism as a medical condition

Since 1979, a different use of the word ‘autism’ has crept into general use, and even into specialized use. It’s now used to refer to an underlying medical condition that is assumed to cause autistic behaviour. Why does that matter? It matters because what has also crept in is the assumption that if people meet the diagnostic criteria for autistic disorder, that means they have the underlying medical condition that causes autistic behaviiour – that everybody’s autistic characteristics must have the same cause.

That assumption is of crucial importance, because even if you find a genuine syndrome – a group of symptoms that do reliably co-occur – it doesn’t follow that all those symptoms are causally related, something that our fictitious Dr Smith was well aware of. Kanner was aware of it too; he refers to his syndrome as ‘unique’. This wasn’t any old group of symptoms that happened to crop up in eleven children but overlapped here and there in other children; his syndrome consisted of twenty (count ’em) essential common characteristics – how likely was that to happen by chance? Furthermore, Kanner also thought he’d found the cause of all those symptoms; what tied them together was a disturbance of affective contact. That explained everything, including the children’s abnormalities in feeding, speech and motor movement. But Kanner’s causal link between symptoms – a disruption of the social instinct – was based on an assumption made by psychodynamic theory. Not only does later research suggest that there’s little evidence for the existence of a social instinct, it also shows that Kanner was wrong about the symptoms he observed making up a syndrome.

As the number of children diagnosed with his syndrome increased, Kanner found he had to omit some of the symptoms because many children didn’t show them. He also had to group the remaining symptoms under five headings, because not all the children showed all the ones that were left. What Wing and Gould found in their epidemiological study was that although some children did meet the criteria for Kanner’s syndrome, there were no clear-cut differences between them and the rest of the socially impaired group. Wing and Gould pointed out that although social impairment was reliably associated with two other symptoms – i.e. it was part of a syndrome – that syndrome wasn’t clearly differentiable from social impairments in general. Indeed its symptoms formed a spectrum because they varied considerably in severity and blurred into each other.

Despite what Wing and Gould’s conclusions, a common current perception of autism is not that it’s a descriptive term for a rather vague group of symptoms that might have lots of different causes, but that it is a single medical condition that manifests itself in different ways in different individuals. The DSM and ICD, although technically using the word ‘autistic’ or ‘autism’ descriptively (the ICD equivalent of ‘autistic disorder’ is ‘childhood autism’), reinforce that idea in respect of autism and many other so-called mental disorders. That’s because they are both arranged in the form of labels for syndromes followed by a list of their symptoms, giving the impression that we know that these disorders exist, and we know what their symptoms are. All that remains is to find those elusive and complex causes.

Diagnostic criteria: the effect on research

This way of thinking about autistic characteristics in particular and mental disorders in general, poses a major problem for researchers. Many researchers are aware that we don’t actually know that the symptoms labeled ‘autistic disorder’ in the DSM (‘childhood autism’ in the ICD) are causally linked, and there might be different causes for the same symptoms in different cases, but the only way researchers can locate autistic research participants is by using the diagnostic criteria set out in the DSM or ICD. In many cases, for research purposes autistic participants are required to be diagnosed using specific standardized assessments. This process might look as if it ensures that all the autistic participants form a homogeneous group. They meet the same diagnostic criteria, certainly, but if those diagnostic criteria by definition put people with similar symptoms but different causes for those symptoms into the same basket, the researchers are in effect trying to find differences between a group of apples-and-oranges and a group of pears. Or more accurately, a group of apples-and-oranges and a group of mixed fruit. There will be some differences between the groups, but they are unlikely to shed any light on what causes apples to develop as apples, or what causes oranges to develop as oranges.

One by one, theories about the causes of autistic characteristics have been sidelined because none of them has explained the characteristics of everyone who meets the diagnostic criteria for autism. Studies investigating ‘refrigerator mothers’, sensory processing, theory of mind, executive function, central cognitive coherence, the extreme male brain, vaccines and dietary intolerances have all produced interesting and useful findings, but have all fallen by the wayside because those findings have also tended to be inconclusive and contradictory – not for the specific individuals involved but for people with autism in general. If everyone diagnosed with autistic disorder showed identical symptoms and we knew that all those people had the same cause for their symptoms, inconclusive and contradictory findings would indeed be frustrating and puzzling. But since autistic characteristics vary widely and we don’t know that all autistic people have the same causes for their symptoms, the most likely explanation for inconclusive and contradictory research findings is that there are several different causes for autistic characteristics (different causes in different people), but the diagnostic criteria lump them together regardless.

In the next post, I want to explore why that happens.

Illustration: this work by Phillip Martin is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License.


from syndrome to spectrum

Eagle-eyed readers will have spotted a big difference between Kanner’s 20 ‘essential common characteristics’ and the three characteristics of autistic disorder (impairments in social interaction and communication, and restricted and repetitive behaviour) outlined in fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) published in 1994. What happened to Kanner’s syndrome in those 50 intervening years?

To summarise the transformation of Kanner’s syndrome, I want to focus on two papers, one a review by Kanner and Leon Eisenberg in 1956 (I used a reprint of this paper from a book chapter), and the other by Lorna Wing and Judith Gould published in 1979 – the account of their famous Camberwell study. Comments from the authors in Adam Feinstein’s excellent resource A History of Autism shed further light on the changes that took place.

Reviewing Kanner’s syndrome

Kanner’s proposal that he’d found a new syndrome generated considerable interest, debate – and confusion. Similar syndromes with different names were puzzled over. There was much discussion about whether Kanner had found a new syndrome and whether (or in what way) it was related to schizophrenia. By 1956, Kanner’s syndrome had been diagnosed in over 120 children “with reasonable certainty”. Kanner and his new colleague at Johns Hopkins, Leon Eisenberg, reviewed the syndrome in their paper ‘Early infantile autism 1943-1955’ and tried to clarify the situation.

They first collapsed Kanner’s 20 essential common characteristics into five;

the five characteristics of early infantile autism

Several of the original 20 characteristics were omitted;

ability to speak
• physically normal
• food
• masturbatory orgiastic gratification
• from highly intelligent families.

The authors then identify two features as ‘pathognomonic’ (distinguishing characteristics); ‘extreme self-isolation’ and ‘obsessive insistence on the preservation of sameness’. An impairment in communication was no longer seen as a critical feature; “The vicissitudes of language development, often the most striking and challenging of the presenting phenomena, may be seen as derivatives of the basic disturbance in human relatedness.” (p.5). Adam Feinstein asked Leon Eisenberg why he and Kanner had left out the language impairment. Eisenberg said: “I was following Kanner’s lead. It wasn’t that we had extensive discussions.” (Feinstein, 2010; p.47)

Despite this attempt at clarification, the confusion over syndromes and symptoms continued. In 1958 the child psychotherapist E.J. Anthony observed wryly: “The cult of names added chaos to an already confused situation, since there did not seem to be a sufficiency of symptoms to share out among the various prospectors, without a good deal of overlap.” (Wing & Gould, 1979)

Kanner complained in 1965 about a “pseudo-diagnostic wastebasket into which an assortment of heterogeneous conditions were thrown indiscriminately. Infantile autism was stuffed into the basket along with everything else…Such looseness threw all curiosity about diagnostic criteria to the winds as irrelevant impediments on the road to therapy, which was applied to all-comers as if their problems were identical. The therapeutic cart was put before the diagnostic horse and, more often than not, the horse was left out altogether.” (Feinstein, 2010; p.41)

Carl Fenichel, who founded a treatment centre in New York thought differently. At the Leo Kanner Colloquium on Child Development, Deviations and Treatment in 1973 he said; “We scrapped these labels 18 years ago at our place….We found that all these labels are just meaningless… We learn more about these kids from working with them on a day-to-day basis. Too many people feel that sticking a label on them means that they now know what this kid needs. I think this is a dangerous, misleading and destructive process.” (Feinstein, 2010; p.53)

The Camberwell study

The situation was in desperate need of clarification. In 1977 Lorna Wing and Judith Gould, based at the Maudsley Hospital in London, began a study designed to sort out the classification of disorders of social interaction. In 1979 they published their findings. Their paper opens with list of syndromes similar to Kanner’s, which illustrates how confusing the picture was at the time;

dementia precoccissima
dementia precoccissima catatonia
primitive catatonic psychosis of idiocy
symbiotic psychosis
autistic psychopathy and
early infantile autism.

The symptoms of the syndromes tended to overlap, so rather than starting with the syndromes, Wing and Gould began with the children’s characteristics. They screened 914 children in the London Borough of Camberwell who were known to health, education or social services as having a physical or mental handicap or behaviour disturbance. They identified 132 who showed either the key features associated with impairments of social interaction in the literature (social interaction and verbal or nonverbal language and repetitive, stereotyped activities) or signs of severe retardation.

They found the children could be divided into two groups; the ‘sociable severely retarded’ group who showed social behaviour appropriate to their mental age, and the ‘socially impaired’ group, who didn’t. The only named syndrome that matched the characteristics of any of the children was Kanner’s early childhood autism, so the socially impaired group were sub-divided into autistic (according to Kanner’s criteria) and non-autistic children. (There were further sub-divisions that I’ll look at another time.) Two of Wing and Gould’s findings are especially relevant to a discussion about Kanner’s syndrome.

First, they found a cluster of abnormalities “consisting of impairment of social interaction, repetitive activities in place of imaginative symbolic interests, and impairment of language development”. This cluster became known as the Triad of Impairments. (Incidentally, if anyone knows when this term was first used, I’d be interested to know. My inquiries so far have drawn a blank.)

Secondly, although some children met the criteria for Kanner’s syndrome, the pattern of abnormalities Wing and Gould found within their socially impaired group wasn’t clear-cut; “Unlike the other named syndromes, the behavior pattern described by Kanner could be identified reliably, but the findings of the present study bring into question the usefulness of regarding childhood autism as a specific condition.” (p.27)

Wing and Gould concluded: “The distribution of the variables among the subgroups suggested that they formed a continuum of severity rather than discrete entities”. (p.26)

Later, the continuum became a spectrum. In an interview with Adam Feinstein, Judith Gould said; “we first called it the ‘autistic continuum’ and then we realized that the word continuum had an implication of discrete descriptions along a line, whereas that was not really what it was. It was not a question of moving in severity from very severe to mild… The concept is more like a spectrum of light, with blurring.” (Feinstein, 2010: p. 153.)

Wing and Gould were surprised by their findings. Lorna Wing commented:

“…Leo Kanner would have found it very difficult to accept the idea of an autistic spectrum, because he was so wedded to his idea of a unique syndrome. I myself started off quite convinced that Kanner was right. … meeting the children … showed me that the idea of a neat barrier between Kanner’s autism and the others was rubbish. And slowly, my view was changed. I had to accept the experience in front of my very eyes.” (Feinstein, 2010; p.151)

Wing and Gould’s findings showed that although some children did have the essential common characteristics described by Kanner (presumably Kanner and Eisenberg’s two pathognomonic features), they appeared to have those features by chance, rather than because they had a specific disorder with symptoms as described by Kanner.

What was also clear was that some children’s social skills were not commensurate with their mental age, that impaired social skills were associated with repetitive behaviours and impaired language, but that these impairments varied considerably between individuals. Wing and Gould’s findings have been supported by subsequent research and are reflected in the DSM-IV criteria for autistic disorder.

It’s interesting to note that as the number of children found to have impairments in social interaction went up, so the number of essential characteristics they had in common went down. Those common characteristics also became less specific. There’s a reason for that, which I’ll move on to in a later post.

What can we conclude about Kanner’s syndrome? I’ve suggested there’s little evidence to support what he thought was the cause of his syndrome (essentially a disruption of the social instinct), and Wing and Gould found little evidence to support the idea that childhood autism was a specific condition. Although we can probably reject Kanner’s hypothesis that he had found a unique syndrome, the children he described were clearly showing atypical development, so we’re still left with the question of why autistic disorder, as it’s now called, shows such a wide variation in symptoms and, of course, what causes them.

Before moving on to more recent theories about autism and its causes, at the risk of labouring the point, I next want to revisit the idea of the syndrome, a concept that still underpins the classification of mental disorders.


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

Kanner. L.. & Eisenberg, L. (1956). Early infantile autism 1943-1955, American Journal of Orthopsychiatry, 26, 55-65.

Reprinted as:

Eisenberg, L. & Kanner, L. (1958). Early infantile autism 1943-1955. In C. F. Reed, I. E. Alexander and S. S. Tomkins (eds.) Psychopathology: A Source Book, Harvard University Press.

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.

social instinct

BlaiseLaPsy on Twitter, in response to what I said about the Freudian concept of social instinct, raised an important point about the work of John Bowlby and Harry Harlow that appeared to provide evidence for the existence of a social instinct. I have reservations about the conclusions drawn from Bowlby’s and Harlow’s findings, and about how the term ‘instinct’ is used. First, a brief round-up of Bowlby and Harlow’s research.

Bowlby, who graduated in medicine and qualified as a psychoanalyst in the UK in the 1930s, was interested in the development of children with behavioural problems and those who had been separated from their parents due to being orphaned or hospitalized. Influenced by René Spitz’s work on orphans, Bowlby became an authority on the effects of maternal deprivation and developed Attachment theory. He concluded that for normal social development, children need a secure relationship with a primary caregiver (usually the mother). Mary Ainsworth later found in her ‘strange situation’ experiments that children showed one of four patterns of attachment to their primary carer.

Harlow qualified at the same time as Bowlby but had a very different academic background. He was an American psychologist; his PhD supervisor was Lewis Terman, who developed the Stanford-Binet IQ test. Prompted by Bowlby’s work, Harlow studied maternal deprivation in rhesus monkeys and macaques. His most famous experiment showed that rhesus monkey infants raised with substitute ‘mothers’ consisting of a wire frame covered/not covered with a terry cloth, preferred the cloth ‘mother’ and clung to it when frightened, even if it was only the wire mother that provided milk. The baby macaques were raised for varying lengths of time in isolation; Harlow looked at the effect on their development, which was invariably abnormal.

What the work by Spitz, Bowlby, Ainsworth and Harlow appears to show is that human and/or primate infants have a social instinct and that instinct triggers a typical pattern of social development. If an infant’s relationship with their primary carer is disrupted by lengthy separation, abnormal social development results. My main problem with these conclusions is the concept of ‘instinct’. Instinct is one of those constructs like ‘love’ or ‘education’ that everybody thinks they understand until they try to find out how it works, or until they discover that their concept of it is different to someone else’s.

We all know what we mean by ‘instinct’ – an automatic, unconscious behaviour. We know what Bowlby, Harlow and others mean by ‘social instinct’ – it’s an automatic, unconscious, typical pattern of social behaviour that appears to develop in the same way in everyone unless something stops it. But Bowlby, Harlow and their contemporaries faced three problems when it came to instinct.

First, as Blaise points out, conceptual models are influenced by cultural worldviews. At the time Spitz, Bowlby, Ainsworth, Harlow and Kanner were researching, human social behaviour was generally assumed to be governed by instincts. Darwin’s work on natural selection implied that many characteristics peculiar to a given species – physical features, physiology and behaviour patterns – were inherited. All male blackbirds have similar songs. Bowerbirds build and decorate complex bowers to attract mates. Ants live in complex colonies, dogs run in packs, cats tend to be solitary. Because human beings tend to behave socially in similar ways across cultures, there was no reason to suppose human social behaviour wasn’t as instinctive as that of blackbirds, bowerbirds, ants, cats or dogs. The main alternative to the psychodynamic framework at the time was Watson and Skinner’s behaviourism, which proposed that complex behaviours such as social interaction were learned. But behaviourism was widely treated with suspicion because it was seen as reductionist. (How can you reduce something as nuanced and complex as social interaction to something as basic as a rat’s tendency to run through tunnels or a pigeon’s tendency to peck?)

Secondly, no one working in child development prior to the 1960s knew much about how the brain worked. They were all guessing. Their guesses were often extremely well informed, but they were guesses nonetheless. Spitz, Bowlby, Ainsworth, Harlow and Kanner all came down on the ‘instinct’ side; Watson and Skinner on the ‘learned’ side, but none of them knew about the biochemical mechanism of learning in the brain.

Thirdly, none of the child development researchers needed to figure out how social instinct worked because the idea of ‘instinct’ itself explained their findings. It was a ‘black box’ concept. They didn’t know what was inside it and didn’t need to know; what they were interested in was what happened when the social instinct was disrupted.

People who did need to figure out how instinct worked and what was inside the black box, were ethologists studying the development of animal behaviour. In the 1950s, researchers such as Lorenz and Tinbergen began to look more closely at the difference between instinctive and learned behaviour. Most people are familiar with the famous pictures of Lorenz being followed by a column of baby geese. Because goslings and ducklings follow their mother from the moment they hatch, it was assumed that this was an instinctive behaviour. What Lorenz discovered was that the tendency to follow something was instinctive, but that what the goslings followed was learned – they followed the first moving object they saw after hatching. It might be their mother, a chicken foster-mother, the farm dog, a pair of boots (didn’t matter who was wearing them) or Konrad Lorenz.

There was a debate about instinct amongst ethologists in the 1960s because it had become clear that different researchers were using the term in different ways and so definitions got tightened up. Unfortunately, apart from Bowlby, many practitioners working in medicine or psychiatry wouldn’t have read the ethology literature – they weren’t (and often still aren’t) interested in the behaviour of goslings or wild macaques even if they had time to keep up to date with it. That’s a pity, or a tragedy depending on how you look at it, as far as instinct is concerned because what has emerged from animal behaviour research is a picture of instinct as an umbrella term that can be applied to a range of different concepts. Essentially, instinct refers to behaviours that are genetically determined, biologically controlled, automatic and unconscious. But it isn’t quite as simple as that.

Levels of instinctive behaviour

Starting at the lowest level, human physiology is genetically determined, biologically controlled, automatic and unconscious; circulation, respiration, digestion, growth and sexual development occur without any awareness or intervention on our part although we are aware of what happens as a result of them. We know a lot about how these autonomic functions work and that they are very similar in everybody. But we wouldn’t usually call autonomic functions ‘instinctive’ because instinct is about how organisms behave rather than how they function.

The most simple form of instinctive behaviour is the reflex – a simple, automatic motor response to specific stimulus. Reflexes – such as the rooting, palmar grasp, startle, swimming and stepping reflexes – are present from birth. Some have obvious survival value; others, like the stepping reflex, form the foundation for behaviours that emerge later – in this case, walking. We know a lot about how reflexes work and that they are very similar in everybody. Most people would classify reflexes as instinctive, I think.

More complex species-specific behaviours, like birds learning songs or building nests, often vary between individuals. Songbirds develop their own unique songs, bowerbirds make their bowers out of whatever materials are available. Although all human beings, regardless of culture, show similarities in social behaviour, the evidence to support the existence of a social instinct is pretty flimsy. We’d expect organisms with similar autonomic functions and similar reflexes to behave in similar ways, but that’s about as far as the evidence takes us. How people interact and communicate with each other and how frequently they do so varies much more than their autonomic functions or reflexes. Some people choose to live in tightly-knit highly interdependent groups, others to live in isolation. Some are highly gregarious, others prefer the company of cats, dogs, horses, the landscape or machines.

I’m a fan of Monkey Life, the TV documentary series about Monkey World, the primate sanctuary in Dorset, UK. A few years ago, Monkey World took in 88 capuchin monkeys from a lab in Chile. Some of them had been born in captivity, others had been captured from the wild. During their rehabilitation, Alison Cronin the sanctuary director commented that the wild-born capuchins instinctively knew how to eat their natural food but the cage-born capuchins didn’t – they had to learn to do that. Alison’s comment introduces a slightly different use of the word ‘instinct’, meaning a behaviour that happens automatically and unconsciously, but isn’t genetically determined and biologically controlled. The documentary also showed that chimps and orang-utans born in captivity tend to be poor mothers. You could argue, as the psychodynamic theorists would have done, that the capuchins’ feeding instinct and the chimps’ and orang-utans’ maternal instincts had been disrupted by their captivity and so hadn’t been allowed to develop normally. That’s one theory. What’s also possible is that the cage-born primates, or those captured in infancy, simply hadn’t had the opportunity to learn how to forage, peel fruit or rear babies.

Human social behaviour varies widely. That variation could be because the normal social instinct is disrupted by events in childhood. But because we don’t know exactly what ‘normal’ human behaviour looks like, and we have no idea how the social instinct works (in contrast to what we know about autonomic functions and reflexes), a more likely explanation is that some aspects of human social interaction are instinctive and others aren’t. Social behaviour is hugely complex, so the question is which bits of social behaviour are instinctive and which aren’t?

As I pointed out in the post about the social instinct and Kanner’s syndrome, the areas of the brain dealing with social behaviour handle complex information from many areas of the brain. From an information-processing perspective, social behaviour, far from being instinctive, results from an interaction between the way the body works, environmental factors such as nutrition, and experience. Most researchers in all areas of child development are aware of the importance of interaction between factors in development, but by necessity, they are usually focusing on one factor only, and tend to overlook anything outside their field of expertise.

Social or sensory deprivation?

A final observation about Harlow’s work. There’s no question that Harlow’s baby primates were socially deprived. But they also suffered sensory deprivation as well, and I don’t know if Harlow controlled for that. Given his conclusions I don’t get the impression he did. Some of the infant macaques, for example, were kept in total darkness for months. Light is essential for entraining circadian rhythms, so absence of light alone would have seriously messed up their physiological functions. Coincidentally, I was listening to Crossing Continents yesterday on BBC Radio 4. A former inmate of Louisiana State Penitentiary, who’d been in solitary confinement for 30 years, was describing his experiences. He highlighted, not so much the social isolation, as the sensory deprivation. He’d had a long time to think about what it was he missed; it would be all too easy to assume in the same situation we’d miss other human beings, when what we might actually miss is the complex sensory input we get from interactions with other people. I’m not trying to reduce social contact to sensory stimuli – social contact is clearly more than the sum of its parts – I’m just saying that it’s very difficult to make a distinction between social interaction and the sensory input that comes with it.

The benefits of hindsight

I’ve been quite critical of psychodynamic theorists, but I’m very aware that they were working with the knowledge that was available at the time. I think what we need to be wary of is assuming that knowledge develops in a straight line; that Freud, Bowlby, Harlow and Kanner were basically right but we now know more than they did. With the benefit of hindsight we can see which aspects of earlier theories are supported by later research and which aren’t. I don’t think there’s much evidence to support the idea of social instinct. What the evidence does suggest is that although instinctive behaviours are quite likely involved in social interaction they are only part of the story.

turning Kanner’s model of autism upside-down

Kanner’s model of autism should be turned on its head.
The idea that Kanner’s syndrome was caused by a fundamental impairment in social interaction has prevented us discovering the causes of autism.
Those are quite bold claims. In the next couple of posts I’ll explain why I made them.

Previously, I suggested that Kanner was using two theoretical frameworks to analyse the behaviour of the 11 children with his unique syndrome; Kraepelin’s classification of mental disorders and psychodynamic theory. Kanner’s comments imply that he interpreted abnormalities in feeding, speech and movement in social and sexual terms because of the psychodynamic framework. I want to look more closely at psychodynamic theory and explain my claim that viewing Kanner’s syndrome as caused by a fundamental impairment in social interaction has proved an obstacle to research into the causes of autism.

How the brain works: the psychodynamic model

As I pointed out earlier, three of the founders of psychodynamic theory, Freud, Jung and Adler, had neurological experience and would have known a fair amount about brain anatomy and about the specific functions of different parts of the brain. What they also would have known about was the patterns of electrical activity that had been observed in the brain. What was little understood at the time was how the brain worked, so the psychodynamic theorists had to make an educated guess based on their observations of people’s behaviour.

What Freud came up with was the idea that human behaviour is driven by life instincts such as the will to survive, to eat, to seek pleasure and sexual gratification. He eventually grouped these instincts together into a primary life instinct or ‘drive’ (Eros) that created flows of energy through the brain. The life drive was the origin of all behaviours that increased the chance of survival, such as an awareness of one’s surroundings and the ability to interact and communicate with others. (Freud later added a death drive (Thanatos) to explain aggression and destructive behaviour). In the light of what we now know about how the brain works, it’s clear that some aspects of Freud’s model were very insightful but others weren’t.

How the brain works: the information-processing model

Fifteen years after Kanner first described his syndrome, David Hubel and Torsten Wiesel began publishing their work on the visual cortex of the cat. Hubel and Wiesel’s research was significant, not just because it told us a lot about how cat vision develops, but because it provided some important insights into how brains in general process information – the mechanism that the psychodynamic theorists were trying to figure out.

Hubel and Wiesel’s research, and the work that followed it, revealed some key principles about how the human brain processes information.

1. All information about the outside world enters the brain via the senses.

2. Sensory information is processed in a hierarchical way, from simple to complex – broadly speaking, from the back to the front of the brain.

3. Different parts of the sense organs respond to different aspects of sensory information and that information is then integrated increasingly as it’s transmitted through the brain.

Say, for example, that I am looking at a table. Different cells in my retina respond to different properties of the pattern of light reflected off the table and entering my eye; some cells respond to the boundaries between light and dark areas, others to light of different wavelengths (colour). This very basic information about the pattern of light from the table is then integrated as it passes through my brain; first it’s chunked up to form a pattern that represents the table I’m looking at. This representation is then linked with stored representations of other images, such as other tables and chairs, and is then integrated with information from other sensory modalities such as what the word ‘table’ sounds like, what the written word ‘table’ looks like, what tables feel like and so on. This information ends up in the frontal area of the brain, which has been described as having an ‘executive function’ – it integrates information from all over the brain and makes decisions on the basis of that information. Except that information doesn’t actually ‘end up’ anywhere, because the brain has a complex series of feedback loops that send information from higher-level areas back to lower-level ones.

What does the way sensory information is processed have to do with Kanner’s syndrome?

Kanner concluded that the ‘…fundamental disorder is the children’s inability to relate themselves in the ordinary way to people and situations’ because he was working within the psychodynamic framework. He saw the children’s abnormal behaviours essentially as caused by a disruption in ‘the usual biologically provided affective contact’ – an instinct that emerged from the life drive. Kanner doesn’t use the terms ‘instinct’ or ‘life drive’ – he doesn’t need to because all his readers would be familiar with that framework – but he makes it clear that he sees affective contact as an innate, biologically-based ability that the children didn’t have.

I can understand where the psychodynamic idea of instincts came from. Most children develop skills like eating, walking, responding to the world around them, interacting with and communicating with other people, without any apparent effort on their part or any significant intervention from adults. Indeed, psychodynamic theorists felt that adult intervention often disrupted normal development. It made sense to assume that natural selection had ensured the ability to relate to people and situations developed instinctively – as automatically as growth or sexual development, or the way the heart, lungs and digestive system function.

I think Kanner’s conceptual model of his syndrome could be represented like this:

Kanner's conceptual model

But from what we now know about brain function, as far as the brain is concerned the ability to relate in the ordinary way to people and situations is exactly the opposite of a basic instinctive drive. There are areas of the brain that specialise in relating to people and situations; they are in the frontal lobes where information from many other brain areas is integrated. Relating to people and situations requires monitoring a constantly changing flow of complex information from a wide range of sources and constant feedback to other parts of the brain. The frontal lobes and their functions develop slowly and mature late – often not until early adulthood. Even after maturity, because of the plasticity of the brain, the frontal lobes continue to change in response to the environment.

Highly over-simplified schematic showing flow of sensory information to frontal lobes

We’re not usually aware of all this complex integration, monitoring and feedback of information; what we usually experience in ourselves, and observe in others, is that responses to the environment and to one another happen instinctively and automatically – that is, until something goes wrong. When we find we have too much or too little information, or that information is ambiguous, or we feel tired, hungry or anxious, then behaviours that most of the time feel and look instinctive and automatic, feel and look a bit less instinctive and automatic.

An impairment in processing any of the streams of information about people and situations would, to some extent, disrupt normal responses to people and situations. In the light of what we now know about the way the brain works, I propose that Kanner’s causal model should have looked more like this;

alternative model for Kanner's syndrome

What we now know about how the brain works suggests that Kanner’s conceptual model of his syndrome should actually be reversed; that relating to people and situations is the outcome of some very complex information-processing requiring input from many parts of the brain, rather than a basic, automatic instinct that drives other behaviours. The implication is that rather than a disturbance in affective contact causing problems with feeding, speech, body movements, social interaction and communication, what’s more likely is that problems with motor function, sensory processing, speech and language resulted in the children’s problems with relating to people and situations in the ordinary way; that Kanner’s model should be turned upside-down.

More on this later, but next I want to look again at Kraepelin’s classification system and find out what happened to Kanner’s syndrome after 1943.

a critical look at Kanner’s autism

In this post I want to take a close look at Leo Kanner’s ground-breaking paper ‘Autistic Disturbances of Affective Contact’ and explain why I consider Kanner’s analysis of the children featured in the paper to be critically flawed. I can understand why Kanner came to his conclusions; he was working in the light of knowledge that was available at the time. What concerns me is that his reasoning has been perpetuated in the diagnostic criteria for autism and in autism research. I suggest it’s because of this that 70 years later we are still scratching our heads about what causes autism.

In 1938, a five year-old boy named Don (later identified as Donald Triplett) was referred to Kanner’s clinic. Don’s was the first and most detailed of 11 case studies (eight boys and three girls) featured in Kanner’s paper published in the journal Nervous Child in 1943. Kanner claimed that he had identified a “unique ‘syndrome’, not heretofore reported” (p.242) consisting of “inborn autistic disturbances of affective contact” (p.250). He reviewed the children’s previous diagnoses and then outlined a list of “essential common characteristics” (p.242) that supported his hypothesis.

Previous diagnoses

Previous diagnoses included idiocy, imbecility, deafness or being hard of hearing, and schizophrenia. (At the time, ‘idiot’ and imbecile’ were technical terms; an imbecile was someone with an IQ score between 20 and 49, and an idiot had a score below 20. Anyone with an IQ between 50 and 69 was described as a ‘moron’). Kanner ruled out idiocy and imbecility because all the children had what he described as ‘good cognitive potentialities’ (p.247). He appears to have ruled out hearing difficulties on the grounds that another doctor had observed that one of the children (Virginia) “does not seem to be deaf from gross tests” (p.230). Kanner rejected the diagnosis of schizophrenia because the children had shown their unusual characteristics from birth.

The term ‘autism’ wasn’t invented by Kanner; it had been coined thirty years earlier by Eugen Bleuler, born near Zürich, and a contemporary of Kraepelin and Freud. Bleuler used ‘autism’ to describe the self-absorbed, withdrawn characteristics seen in schizophrenia, another label he came up with to replace Kraepelin’s ‘dementia praecox’. Bleuler’s book Dementia Praecox or the Group of Schizophrenias was published in 1911, ten years before Kanner graduated in Berlin and twenty years before Hans Asperger did so in Vienna, so both of them would have been familiar with the word they used to describe the children in their case studies.

Kanner’s syndrome

Kanner based his conclusion that he had identified a previously undiscovered syndrome on 20 “essential common characteristics” shared by the 11 children. Statistically, it’s highly unlikely that 11 children could show 20 common characteristics without having the same syndrome – until you take a closer look at the characteristics. Here’s the list (Kanner gives a short explanation for each of them);

•inability to relate themselves in the ordinary way to people and to situations from the beginning of life
•extreme autistic aloneness
•failure to assume at any time an anticipatory posture preparatory to being picked up
•ability to speak
•excellent rote memory
•personal pronouns are repeated just as heard
•loud noises and moving objects
•monotonously repetitious
•anxiously obsessive desire for sameness
•limitation in the variety of spontaneous activity
•good relation to objects
•masturbatory orgiastic gratification
•relation to people different to that of objects
•good cognitive potentialities
•anxious tenseness
•physically normal
•from highly intelligent families.

What’s interesting about the ‘common’ characteristics is that they are not common to all the children, nor do they all reflect what Kanner describes in his case studies. The second point applies to seven items on the list, which I’ll address in turn.

Ability to speak, excellent rote memory, literalness and personal pronouns are repeated just as heard. Seven of the children had previously been considered deaf or hard of hearing because of their abnormal receptive and/or expressive speech. Three children (Richard, Herbert and Virginia) presented as mute. Richard had once been heard to whisper “good night” and pupils at Virginia’s school claimed she had said ‘chocolate’, ‘marshmallow’, ‘mama’ and ‘baby’ (p.231). There’s no record of Herbert saying anything. Despite speech or language impairments, other children in the group had clear enunciation, sophisticated vocabularies or good sentence structure, and some had specific problems with pronouns. Yet despite this range of differences, Kanner concludes “there is no fundamental difference between the eight speaking children and the three mute children” in terms of “the communicative functions of speech” (p.243).

Food. Six of the children had feeding difficulties as infants (one vomited repeatedly and another was tube-fed). But Kanner interprets these characteristics not as feeding difficulties per se, but in terms of “our patients…anxious to keep the outside world away, indicated this by the refusal of food” and contrasts their behaviour with those of “affect-hungry” children demanding excessive quantities of food when placed in foster-care (p.244).

Failure to assume at any time an anticipatory posture preparatory to being picked up. Kanner notes this in only two specific cases, but says that ‘almost [my emphasis] all the mothers …recalled their astonishment’ at the children’s failure to respond (p.242).

Masturbatory orgiastic gratification. Kanner’s evidence for this is the children’s preoccupation with spinning objects, jumping up and down with glee and rolling and rhythmic movements, despite his records indicating masturbation in only two cases.

Two questions

So, two questions: First, why did Kanner list as “essential common characteristics” characteristics that weren’t common to all the children? Second, why did he interpret some very somatic (bodily) characteristics (feeding, speech, jumping and rolling) in social and sexual terms rather than in terms of feeding, speech and motor movements? The answers, I suggest, lie in the theoretical frameworks that Kanner was using at the time – Kraepelin’s classification of mental disorders, and psychodynamic theory. (Kraepelin’s classification system and the psychodynamic model had both been in use for half a century, so were well-established. Adolf Meyer, who appointed Kanner to his post at Johns Hopkins, had been a keen advocate of both frameworks.)

Why weren’t Kanner’s ‘essential common characteristics’ common to all 11 children?

I mentioned earlier that Kraeplin’s classification system was based on syndromes – patterns of symptoms that tended to co-occur. Two observations about syndromes: First, syndromes are about correlation, not causality. It’s true that symptoms that tend to co-occur are more likely to be causally linked than symptoms that don’t, but all you can deduce from co-occurring symptoms is that the symptoms sometimes co-occur. You can only make deductions about how the symptoms might be causally linked once you know something about what causes them.

Second, although syndromes have consistent core symptoms (if they didn’t they wouldn’t be syndromes), the symptoms shown by individuals tend to vary. So everyone diagnosed with Syndrome Alpha, say, would show the core symptoms A, B and C, but together those people might also show symptoms D to T (making a total of 20 symptoms associated with Syndrome Alpha). Kanner couldn’t tell from a sample of 11 children which symptoms were core ones and which might have appeared by chance. He would no doubt have been interested to hear from clinicians who’d seen cases of any of the symptoms, so he wouldn’t have wanted to miss anything out. Hence he cast his net quite wide. In short, his “essential common characteristics” were characteristics of his proposed syndrome rather than of the individual children.

Why did Kanner interpret somatic abnormalities (feeding, speech and body movements) in social and sexual terms?

I noted in the previous post that psychodynamic theory recognised the link between behaviour and the brain. (Two of the founders of the psychodynamic school, Freud and Jung, had worked with renowned neurologists and Adler had begun his career as an ophthalmologist, so they would have been well aware of the brain-behaviour connection.) Because the brain was involved and the brain is an organ of the body, behavioural drives, like other bodily characteristics, could be inherited. Characteristics were inherited via sexual reproduction, so any characteristics that reduced the chances of sexual reproduction taking place, such as impairments in affect or communication, or atypical sexual behaviour, would be less likely to be passed on to the next generation, would not be ‘normal’ for the species and so could be considered pathological. Psychodynamic theory saw social and sexual behaviour as fundamentally important in normal child development, and impairments in social and sexual drives as being capable of causing problems with feeding, speech and motor control (Kanner cites David Levy and Hilde Bruch, both of whom used a psychodynamic approach, to support his argument). As Kanner says “the outstanding, “pathognomonic”, fundamental disorder is the children’s inability to related themselves in the ordinary way to people and situations…” (p. 242).

Why I see Kanner’s analysis as flawed

I see Kanner’s analysis as flawed because of three assumptions he made. First, that because the individual children’s characteristics overlapped, despite not all the children having all the symptoms, all the children had the same syndrome. Second, that the existence of a syndrome meant that the characteristics of the syndrome must be causally related. Third, the assumption that social and sexual drives are so fundamental that they must be the cause of problems with feeding, speech and motor movements. Although children certainly can refuse to eat or speak because of an underlying issue with affect, knowing what we now know about brain development, it’s highly unlikely that a babe-in-arms would not suckle or that an older child wouldn’t speak for years on end for that reason. Since motor function is implicated in all three behaviours it should at least be considered as a possible cause.

At the time, Kanner’s assumptions weren’t unreasonable, and at the end of his paper, he makes it clear that he’s making assumptions and that there’s uncertainty about how affect could result in the syndrome he proposes. At the time a good deal was known about brain structure and what brain areas controlled what types of behaviour, but brain function was still something of a mystery. In 1943 Karl Lashley was still attempting to find the location of memory, it would be a decade before Crick and Watson unveiled their model of DNA, and two decades before Hubel and Wiesel published their work on cat visual cortex.

In the light of current knowledge about brain function, Kanner’s conclusion that all the children’s unusual behaviors were attributable to an “inability to relate themselves in the ordinary way to people and situations” doesn’t hold water. Despite this, his assumptions have persisted in the diagnostic criteria for autism, and thus in autism research. I suggest the assumption that autism is caused by a fundamental impairment in social interaction has been the main reason why, half a century later, we are still trying to find the causes of autism. In my next post I propose that turning Kanner’s model on its head could break this log-jam.


Kanner, L. (1943). Autistic disturbances of affective contact. Nervous Child, 2, 217-250.
(pdf available on line)

psychiatrists of Europe

"Psychiatrists of Europe! Protect your sanctified diagnoses!" A cartoon by Emil Kraepelin.

Leo Kanner was influenced, I suggest, primarily by two concepts, Kraepelin’s taxonomy of mental disorders and Freudian psychodynamics. But before moving on to Kanner’s landmark paper, I want to take a look at the thinking behind Kraepelin’s classification and Freud’s ideas.

Beliefs about the causes of human behaviour changed a great deal during the 19th century. At the beginning of the 1800s, the long-held idea that human beings had two independent spheres of existence – the spiritual and the physical – was being widely questioned. By the end of the 1800s, another idea was in doubt – this time the separate existence of the mind and the brain. I suggest this challenge came about largely because of two fields of research; the study of brain pathology and Darwin’s work on natural selection.

Brain pathology: the brain-behaviour connection

During the 19th century knowledge about the anatomy and function of the brain increased significantly, mainly because of the study of brain damage. Armed conflict and poor working conditions were commonplace in Europe and the US, so there was no shortage of brain-damaged patients for researchers to observe. Famous case studies were published involving personality changes (Phineas Gage) or specific cognitive impairments (Dejerine’s Monsieur C.). By the end of the century, the link between brain damage – from accidents or stroke – and abnormal behaviour was well established. Finding the cause of abnormal behaviour in people who appeared to have no sign of physical damage proved more challenging.

Kraepelin’s taxonomy

A German psychiatrist called Emil Kraepelin decided to tackle this problem. The chances of finding the causes of somatic disorders (disorders of the body) had improved by applying a simple principle of diagnosis; that the same signs and symptoms in different patients were very likely to have the same cause. If the causes of mental disorders (disorders of the mind) such as delusions, dementia and abnormal behaviour actually originated in an organ of the body, the brain, the same principle of diagnosis could be applied to them. A complication was that the symptoms of different somatic disorders sometimes overlap, so Kraepelin proposed that mental disorders should be identified by their unique pattern of symptoms and by how those patterns changed over time.

From 1887 onwards Kraepelin developed a classification of mental disorders in successive editions of his Textbook of Psychiatry. He concluded that mental disorders could be grouped into two main types; dementia praecox (in which the patient’s condition deteriorated) and manic depressive illness (in which episodes of illness were interspersed by periods of good health). Although classifications of mental disorders have changed a great deal since then, Kraepelin’s system forms the foundation for the Diagnostic and Statistical Manual of Mental Disorders (DSM) and the International Classification of Diseases: Mental and Behavioural Disorders (ICD) used today.

Emil Kraepelin had been born in Neustrelitz, Germany in February 1856. Three months later, 800 km away in what is now Příbor in the Czech Republic, another figure who had a significant influence on the way mental disorders were understood came into the world – Sigmund Freud. (Interestingly, Freud’s parents, like Leo Kanner’s, were Galician Jews.) Eighteen years later, both Freud and Kraepelin were studying medicine – Freud in Vienna and Kraepelin in Leipzig.

The influence of Darwin

When Kraepelin and Freud were three years old, Charles Darwin published his major work On the Origin of Species. What Darwin proposed was that an individual organism’s inherited characteristics determine how well it survives in a given environment. If the organism survives long enough to reproduce, its characteristics will be passed on to its offspring. Over time the characteristics of a particular species will change, the changes reflecting environmental conditions. Given a sufficient length of time completely new species could develop. Darwin’s ideas are an important component of Freud’s concept of psychodynamics.

Freudian psychodynamics

Freud had graduated in 1881 and began work as a neurologist with Theodor Meynert in Vienna. In 1885 he had the opportunity to study under Jean-Martin Charcot, the famous French neurologist. This was a turning point for Freud. Charcot’s use of hypnosis to treat hysteria triggered Freud’s interest in mental disorders and led to his development of psychodynamic theory.

A fundamental concept in psychodynamics is that of instinctive drives such as the desires for food, social interaction and sex, that shape behaviour. With Meynert Freud had studied brain anatomy, and believed that instinctive drives originated in the brain. Like other biological characteristics, drives are passed on to subsequent generations via sexual reproduction. Natural selection acts in favour of drives that increase the likelihood of successful reproduction, resulting over time in species-specific patterns of instinctive behaviour. Freud suggested that the normal development of these patterns can be disrupted by early experiences such as a parent withholding food or affection, or imposing religious or cultural taboos on a child. Because of the importance of sexual reproduction in one generation passing on drives to the next, social and sexual behaviours are a very important part of the psychodynamic framework.

Kraepelin’s taxonomy and Freud’s psychodynamics influenced Leo Kanner partly because of Adolf Meyer, Kanner’s boss at Johns Hopkins Hospital. Meyer, ten years younger than Kraepelin and Freud, had qualified as a neuropathologist in Zurich. Because of problems getting a secure post, he had emigrated to the US in 1892, where he became a highly influential figure, becoming director of the Psychiatric Institute in New York, professor of Psychiatry at Cornell, director of the first inpatient psychiatric unit in the US at Johns Hopkins hospital and president of the American Psychiatric Association. Whilst at John Hopkins he put Kanner in charge of the first academic child psychiatric department and the clinic where Kanner first saw patients with childhood autism.

Reading list

Bentall, R. (2004). Madness Explained: Psychosis and Human Nature, Penguin.

A radical appraisal of the way psychotic illnesses are classified.

Gardner, H. (1977). The Shattered Mind: The Person After Brain Damage, Routledge & Kegan Paul.

A fascinating account of Gardner’s experience working with brain-damaged patients and the history of brain-damage research. And yes, it is the Howard Gardner who wrote Multiple Intelligences.

Again, much of the biographical material came from Wikipedia. For a summary see Hall of Fame.

a postcard from Brody

Postcard from Brody, 1898

In 1924 a young Ukrainian doctor arrived in the USA. His name was Leo Kanner, and in some quarters his name was to become legendary.

Kanner had been born in 1894 into an orthodox Jewish family living near the Ukrainian town of Brody in the Galician region of what was then the Austro-Hungarian empire. 1894 wasn’t a good time to be living in Brody, known then as the ‘Galician Jerusalem’. The assassination of Russian Tsar Alexander II in 1881 triggered a wave of anti-Jewish riots across Russia, the Jews being widely seen as responsible for the assassination despite only one of the assassins being Jewish by birth and the others atheist revolutionaries. The loss of Jewish life during the pogroms of 1881-1884 was significantly less than in the slaughter that took place between 1903 and 1906, but nonetheless from 1881 onwards Brody found itself overwhelmed by waves of Jewish refugees traveling West. Despite this influx, the Jewish proportion of the population of Brody had fallen from 90% in 1869 to 67% by 1910. The town was partially destroyed during the Polish-Soviet war in 1920 and then became an important military base occupied by the Red Army during WWII. After German occupation in 1941, the Jewish population, by then numbering 9,000, was exterminated.

Leo Kanner had managed to stay one jump ahead of catastrophe; he began studying medicine at the University of Berlin in 1913 and finally qualified as a doctor in 1921, his training being interrupted by military service during the First World War. He arrived in the USA in the same year that the Johnson-Reed Act reduced national immigration quotas. Between 1926 and 1929 around 20% of the Galician Jewish population migrated to the US, arriving with an estimated average of $22 each.

Kanner made the most of his new opportunity. After a period at the State Hospital in Yankton County, South Dakota, in 1930 he was appointed to a post at the Johns Hopkins University Hospital, Baltimore, which is where his pioneering work began.


Most of the material in this post is from the Wikipedia entries for Brody and for the History of the Jews in Brody.