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 Bleuler used ‘autism’ to describe the self-absorbed, withdrawn characteristics seen in schizophrenia, another label he came up with to replace Kraepelin’s ‘dementia praecox’.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.