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 Bleuler used ‘autism’ to describe the self-absorbed, withdrawn characteristics seen in schizophrenia, another label he came up with to replace Kraepelin’s ‘dementia praecox’.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