refrigerator mothers

You could be forgiven for assuming that the ‘refrigerator mothers’ theory for the cause of autism has been consigned to the wastebasket of history. That might be true for children with a formal diagnosis of autistic disorder, but parents are still often under suspicion if their children have autistic characteristics but no diagnosis, or indeed any unusual behavioural characteristics but no diagnosis. Bruno Bettelheim is often credited with inventing the term ‘refrigerator mothers’, but Leo Kanner appears to have come up with the refrigerator analogy first.

Leo Kanner

Leo Kanner

In the comment section at the end of his 1943 paper, Kanner weighs up the evidence for the possible causes of autistic behaviour. The children have schizophrenic characteristics, but their condition differs from schizophrenia because it’s been present from birth – suggesting a biological origin. On the other hand “in the whole group, there are very few really warmhearted fathers and mothers” (p. 250), suggesting that development could have been disturbed by parental behaviour. In the end, Kanner concludes “The children’s aloneness from the beginning of life makes it difficult to attribute the whole picture exclusively to the type of the early parental relations with our patients. We must, then assume that these children have come into the world with innate inability to form the usual, biologically provided affective contact with people, just as other children come into the world with innate physical or intellectual handcaps [sic]” (p. 250).

But Kanner later changes his mind. In 1949 he describes his patients as in refrigerators which did not defrost.* In his 1956 paper with Leon Eisenberg he contrasts the low incidence of psychosis and neurosis in the children’s relatives (a sample of around 1000) with the much higher incidence in families of children with schizophrenia and concludes “Thus, if one limits his search for genetic factors to overt psychotic and neurotic episodes in family members, the results would appear to be negative” (p.8). After some discussion of parental characteristics, he decides; “The emotional frigidity in the typical autistic family suggests a dynamic experiential factor in the genesis of the disorder in the child” (p.8) and “These children were, in general, conceived less out of a positive desire than out an acceptance of childbearing as part of the marital contract” (p.10). But less than a decade later, when Bernard Rimland, in his book Infantile Autism: The Syndrome and Its Implications for a Neural Theory of Behaviour suggested that autism might have its origins in the brainstem, Kanner wrote the foreword. And in 1969, Kanner told the first annual meeting of the then National Society for Autistic children “I herewith especially acquit you people as parents” (Feinstein, 2010).

The discussion in the 1956 paper sheds light on what initially appears to be wavering on Kanner’s part about the cause of autism – now he’s blaming biology, now he’s blaming the parents. Kanner wasn’t so much undecided as aware that both factors could be involved. He goes into some detail about the interaction of biological and environmental factors in producing autistic characteristics and describes early infantile autism as ‘a total psychobiological disorder’ – in other words, it isn’t a case of its cause being either genetic or parental. As Michael Rutter observed; “What we have to differentiate is evidence of a broader phenotype. Kanner switched back and forward, which is a mark of his integrity” (Feinstein 2010).

Bruno Bettelheim

Bruno Bettelheim

For Bruno Bettelheim there was no uncertainty about the cause of autism. At first glance, Kanner and Bettelheim appear to have a good deal in common. They were both born into Jewish families in central Europe around the beginning of the 20th century. Both had their studies interrupted; Kanner by military service, Bettelheim by the death of his father. Both fled to the USA as ethnic refugees, both married and raised families there, and both became successful, respected figures in the field of child development. There the resemblance ends.

Bettelheim was born into a well-to-do Viennese family in 1903. As a teenager, he was fascinated by psychoanalysis and read all he could about it. He enrolled as a student of philosophy and history of art at the University of Vienna, but postponed his studies when his father died from syphilis and he had to take over the family lumber business. In 1930 Bruno married his first wife, Gina, who worked at a Montessori nursery. The couple took in a young American child, Patsy, whose mother had sent her to Vienna for therapy with Editha Sterba, a member of the Vienna Psychoanalytic Institute. Bruno was in therapy with Editha’s husband Richard for a while, and his connections with Patsy, the nursery and the Sterbas were to prove a turning point in his career.

Eventually, he was able to resume his studies and was awarded a doctorate in February 1938. Within a month, German troops had entered Austria and Gina had left for the USA with Patsy. Bruno remained in Vienna with his mother and sister. In June, he was arrested, jailed and then taken to Dachau. In September he was moved to Buchenwald and released the following April in an amnesty to mark Hitler’s 50th birthday. Patsy’s mother, Agnes, had managed to arrange a visa for him, and Bruno was reunited with Gina in the USA in May 1939. By then it was obvious that their marriage was over – both had had affairs – and Bruno settled down with Trude, a former girlfriend. His experience with psychoanalysis and child development also got him a job in the education department at the University of Chicago, which led to his appointment as director of the university’s Orthogenic School in 1944, where he was to remain until the early 1970s.

Most of these biographical details are from Richard Pollak’s fascinating biography of Bettelheim The Creation of Dr B. Pollak is aware that his account might be seen as biased. His younger brother, Stephen, had attended the Orthogenic School until his death in an accident whilst on holiday. Bettelheim’s disdain for the boys’ parents and his claim that Stephen had committed suicide despite Richard witnessing Stephen’s fall from a hayloft, and Bettelheim’s suicide in 1990, were what prompted Pollak to research Bettelheim’s life. Although Bettelheim probably had the children’s best interests at heart and certainly changed the Orthogenic School for the better, reactions to him were mixed to say the least. Comments from school staff, parents, children and his students are peppered with reports of admiration, intimidation and humiliation. There’s little doubt that he beat the children and there are some stories of sexual contact, although these accounts, if true, need to be set in context; corporal punishment was common at the time and the psychoanalytic theory embraced by Bettelheim saw sexual expression as natural. Some people hated him, but others felt that Bettelheim’s methods, even if frowned upon, were well-intentioned.

Refrigerator mothers

Probably more widespread harm was caused by Bettelheim’s view of parents, especially mothers. Bettelheim disapproved of children at his school going home for visits and viewed mothers as cold, uncaring and responsible for their children’s behavioural problems. Bettelheim set out his ideas in a series of books including The Empty Fortress: Infantile Autism and the Birth of the Self. Despite the popularity and influence of this book, it’s not clear how much experience of autistic children Bettelheim actually had. He claimed that two autistic children had lived at his home, although Patsy appears to have been the only one, and she wasn’t diagnosed as autistic. Visitors to the Orthogenic School commented on the fact that the children appeared to be normal, if troubled, kids. Bettelheim admitted only children with no physical or intellectual impairment, thus ruling out more severely autistic children. And the success of his techniques was called into question too. In the 1980s a study showed that during Bettelheim’s period as director Orthogenic School, of 220 children entering the school, only 13 were admitted with a diagnosis of autism (Bettelheim diagnosed many children himself) and not all the children had made the progress he claimed.

Aside from contrasts in their life experience, with regard to their contribution to autism research I want to highlight two key differences between Kanner and Bettelheim; the way they used evidence and their level of relevant expertise.

Use of evidence

Kanner had a medical background, derived testable hypotheses from the best theory available at the time, and wasn’t afraid to change his conclusions if the evidence dictated. Bettelheim had trained in philosophy and appears to have made up his mind in advance about the cause of autism and then selected evidence to support his theory. Pollak refers to an essay Bettelheim wrote about the philosophers who shaped his thinking as a student. Significantly, the philosophers – Lessing, Lange and Vaihinger – all saw historical truth as a construct of the mind. Vaihinger argued in his book The Philosophy of “As If” that even though fictions should not be mistaken for true propositions, they can work As If true (Pollak, 1997; p.15). Bettelheim seems to have put Vaihinger’s ideas into practice; in a cv compiled in 1942 he exaggerated his credentials and frequently reported events in a way which conflicted with the recollection of other witnesses.

Level of relevant expertise

Kanner was aware that his theories about the cause of autistic characteristics were limited by the biological knowledge available at the time. Nonetheless, he clearly understood the complexity of child development and was careful to rule out a number of possible causes for autism before arriving at his conclusions. Without doubt, Bettelheim was also knowledgeable, about psychoanalysis and theories of child development that is; the reference section in The Empty Fortress is extensive. But he appears to have had little knowledge about biology and his explanations for the children’s behaviour are in terms of psychoanalytic concepts only. Indeed, he was actively opposed to biological theories for the causes of autism, attacking Kanner and Rimland in The Empty Fortress and telling Thomas Kemper that his brain studies must indicate a different kind of autism (Feinstein, 2010).

Bettelheim’s influence

What puzzles me is how Bettelheim’s book could become so influential amongst professionals with medical training, long after research into genetics and brain function had shown that psychoanalytic and psychodynamic theories of child development were lacking. Bettelheim was preoccupied by psychoanalytic symbolism. He saw the children’s interest in balls, balloons, light fittings and automobile headlamps as symbolic of their relationship with the breast. Their words had deep symbolic meaning – ‘breakfast’ meant ‘break breast’, ‘Connecticut’ meant ‘connect-I-cut’ and even an interest in the weather on the part of a non-verbal child symbolized her fear that she might be devoured (‘weather’ meant ‘we/eat/her’). This should have been enough to suggest that his theory might not have a solid grounding. Bettelheim’s use of symbolism extended to his lectures, resulting in the (in)famous knitting/masturbation story. Bettelheim is reported to have said to a female student, knitting during one of his lectures; “Don’t you realize your knitting is nothing but a sublimated form of masturbation? You’re sitting in front of the entire class masturbating.” The student is alleged to have replied; “Dr Bettelheim, when I knit, I knit! And when I masturbate, I masturbate!”

Despite the lack of evidence for his theories they were very influential. The Empty Fortress was the first book on autism translated into Spanish, Bettelheim’s lectures were shown on French national tv, in the 1980s most of the books on autism in Danish libraries were by Bettelheim, and it wasn’t until 1998 that the International Association for Child and Adolescent Psychiatry and Allied Professions decided that “parents have absolutely no responsibility for their children’s autism” (Feinstein 2010). As Judy Barron, the parent of an autistic child, observed when she read The Empty Fortress, “I wasn’t a scientific reader and I certainly wasn’t a researcher; I was a twenty-four-year-old mother; but I just didn’t see any evidence to support his pronouncements” (Pollak, 1997, p. 275).

The use of evidence and levels of expertise; two factors that I plan to explore further in the next post.


Bettelheim, B. (1967). The Empty Fortress: Infantile Autism and the Birth of the Self. The Free Press.
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.
Feinstein, A (2010). A History of Autism. Wiley Blackwell.
Kanner, L. (1943). Autistic disturbances of affective contact. Nervous Child, 2, 217-250.
*Kanner L (1949). Problems of nosology and psychodynamics in early childhood autism. American Journal of Orthopsychiatry, 19, 416–26.
Pollak, Richard (1997). The Creation of Dr B, Simon & Schuster

*Paper behind paywall – the citation is from various sources.

image of Bettelheim: Ottofroehlich under Creative Commons licence

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.

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.

research notes: Leo Kanner

Human beings cannot be purely objective; we all bring cognitive and emotional biases to the data we encounter. The point of the scientific method is to compensate for those biases as much as possible. But even the way we use the scientific method can be skewed by our worldview. For obvious reasons it’s difficult to make allowances for the biases of people living in our own time and our culture – we will be subject to similar biases ourselves. But I’ve found it useful to look into the background of researchers from other times and other cultures – it’s easy to assume they saw the world in the way we do, when that’s very unlikely.

So my first post is about Leo Kanner’s social and economic background. In the second, I plan to explore the theoretical framework he would have been using. It could be that what was happening in Kanner’s homeland might have nothing to do with his autism hypothesis, but it does shed some light on what he might have experienced before becoming a pioneering psychiatrist.