Verbatim: About autism severity

This episode of Verbatim finds autism researchers and clinicians wrestling in various ways with the (apparently) elusive concept of autism severity:

Note that in several cases, formal criteria for Autistic Disorder were met but a diagnosis of PDD-NOS or Asperger’s Disorder was given to the family. The reason for this was that the child had previously been given a diagnosis of PDD-NOS or Asperger’s and had continued to improve so that symptoms were fewer or milder than they had been. It was considered to be counterproductive to give the parents a more severe diagnosis when the child had actually shown significant improvement, and in many cases, the symptoms were present but in relatively mild form. (Kelley et al., 2006)

Indeed, in some ways, children with AS [Asperger syndrome] are more severe than those with autism as the discrepancy between their intellectual potential and their actual adaptation in terms of socialization and communication is so very marked; they look so "normal" but their behavior is so "odd." There is also some evidence that adolescents with AS have more symptoms of anxiety and depression than do children with autism (Szatmari et al., 1989), although the mechanism for this finding may only be that they have the ability to communicate their distress more readily. In this context, they have the more severe disorder because they have better communcation skills. It all depends on what dimension of severity one is talking about. (Szatmari, 2000)


References:

Kelley, E., Paul, J.J., Fein, D., & Naigles, L.R. (2006). Residual language deficits in optimal outcome children with a history of autism. Journal of Autism and Developmental Disorders, 36, 807-828.

Szatmari, P. (2000). Perpectives on the classification of Asperger syndrome. In A. Klin, F.R. Volkmar & S.S. Sparrow (Eds.), Asperger Syndrome (pp. 403-417). New York: Guilford.

Szatmari, P., Bartolucci, G., & Bremner, R. (1989). Asperger's syndrome and autism: Comparisons on early history and outcome. Developmental Medicine and Child Neurology, 31, 709-720.

The origins of ABA-based autism interventions

When it comes to behaviour analytic approaches to autism, the paper that started it all, and set the tone for what was to come, was Fuller (1949), the first published report of operant conditioning in a human being.

Fuller opens his paper by noting that classical conditioning had been tested in "normal and subnormal" humans. For example, it had been found that "subnormal" children formed conditioned responses to shock faster than "normal" children. But so far, operant conditioning had only been tested in animals ("infra-humans"). Fuller was given permission--no mention of by whom--to experiment on a person he described as an 18 year old "vegetative idiot" incarcerated in a "feeble-minded institution."

This person, referred to as "S," is reported never to move his trunk or legs, though no reason is given for this. According to Fuller, S had limited movement of his head, shoulders and arms, but couldn't roll over or change his position from where he was left lying on his back all day. S was never given solid food; liquids and semi-solids were "stuffed into his mouth," Fuller reports, while S coughed and choked. While Fuller writes that S never made any sounds, "in the course of the experiment vocalizations were heard."

Fuller's experiment started by depriving S of food for 15 hours. A syringe full of warm milk-sugar solution, which was squirted into the corner of S's mouth, was the reinforcer. A bit of this solution was given to S when he raised his right arm.

Eventually, S was conditioned such that after being deprived of food for five hours, he raised his right arm 19 times in 16 minutes. After this he fell asleep. The next morning, he raised his right arm and opened his mouth simultaneously. And while S had earlier also raised his left arm sometimes, by this point, he only raised his right arm.

Fuller declared success at this point, and then extinguished this response by removing the food reinforcer. The extinction procedure took 70 minutes, at which point S stopped raising his right arm. This completed the experiment.

Fuller wrote about S:

"An interesting feature of this study is the example it affords of phylogenetic overlap. While of normal human parentage, this organism was, behaviorally speaking, considerably lower in the scale than the majority of infra-human organisms used in conditioning experiments--dogs, rats, cats."

The physicians in the institution in which S had been an inmate (this word is used) for a year had reported to Fuller that S had not, in all his 18 years, learned anything at all. Fuller simply accepted this as true, even though he had no relevant information about S's history and minimal information about S's present. This allowed Fuller, and many behaviour analysts to follow, to be very impressed with what Fuller accomplished in conditioning S. After all, Fuller is reported to have trained a vegetative organism to move, a stunning and unprecedented achievement.

Along these lines, here is Fuller's conclusion:

"For years, many psychologists have experimented exclusively with infra-human [subjects], and they have expressed a preference for the simple, less variable behavior of the lower organisms in the laboratory. Perhaps by beginning at the bottom of the human scale the transfer from rat to man can be effected."

Fuller's "classic" paper, a landmark in the history of ABA, resonates with the much later words of Ivar Lovaas and his colleagues, about autistic human beings:

"You see, you start pretty much from scratch when you work with an autistic child. You have a person in the physical sense—they have hair, a nose and a mouth—but they are not people in the psychological sense. One way to look at the job of helping autistic kids is to see it as a matter of constructing a person. You have the raw materials, but you have to build the person." (from an interview with Chance, 1974)

"In any case, what one usually sees when first meeting an autistic child who is 2, 3, or even 10 years of age is a child who has all the external physical characteristics of a normal child—that is, he has hair, and he has eyes and he has a nose, and he may be dressed in a shirt and trousers—but who really has no behaviors that one can single out as distinctively ‘human’. The major job then, for a therapist—whether he's behaviorally oriented or not—would seem to be a very intriguing and significant one, namely, the creation or construction of a truly human behavioral repertoire where none exists." (Lovaas & Newsom, 1976)

"To use another analogy, at the beginning of treatment, the children may be regarded as having close to a tabula rasa. In this sense they can be considered very young persons, as persons with little or no experience, presenting the teacher with the task of building a person where little had existed before." (Lovaas & Smith, 1989)

"Instead, the fascinating part for me was to observe persons with eyes and ears, teeth and toenails, walking around yet presenting few of the behaviors one would call social or human. Now, I had the chance to build language and other social and intellectual behaviors where none had existed, a good test of how much help a learning-based approach could offer." (Lovaas, 1993)

The currently predominant autism advocacy policy position that autistics can't learn, develop, communicate, progress, etc., or become human, except via ABA programs, reminds me of assumptions behaviour analysts have made about the nature of Fuller's S. They just know, like Fuller did, that S had never learned anything at all until Fuller came along. Fuller needed no evidence for this, or any information about S's past. He just knew there were subhumans in human form, including vegetative human organisms who were lower in the scheme of things than rats (and were treated as such). So all he had to do was to never, ever question any of this, and then go out and find one of these vegetative organisms and experiment on him. And so Fuller became famous, just like Dr Lovaas did later for "building" human behaviours in autistic children who he claimed had none at all, for "building" a person where he claimed none existed.


References:

Chance, P. (1974). "After you hit a child, you can't just get up and leave him; you are hooked to that kid": A conversation with O. Ivar Lovaas about self-mutilating children and why their parents make it worse. Psychology Today, 7, 76-84.

Fuller, P. R. (1949). Operant conditioning of a vegetative human organism. American Journal of Psychology, 62, 587-590

Lovaas, O.I. (1993). The development of a treatment-research project for developmentally disabled and autistic children. Journal of Applied Behavior Analysis, 26, 617-30.

Lovaas, O.I., & Newsom, C.D. (1976). Behavior modification with psychotic children. In H. Leiteberg (ed.), Handbook of Behavior Modification and Behavior Therapy. Englewoood Cliffs, NJ: Prentice-Hall.

Lovaas, O.I., & Smith, T. (1989). A comprehensive behavior theory of autistic children: Paradigm for research and treatment. Journal of Behavior Therapy and Experimental Psychiatry, 20, 17-29.

Autism in California: The MIND's new epidemiology

The MIND's recently published autism epidemiology (Hertz-Picciotto & Delwiche, 2009) has been widely publicized (press release is here, typical media story is here), with the upshot that large increases in reported rates of autism are real rather than apparent and should be studied as such.

Bloggers have taken on several aspects of the MIND's new autism epidemiology (here, here, here, here, with more and a summary here) as well as discrepancies between the paper itself and how it has been promoted. I'm going to add just a few more points to consider.

This isn't the MIND's first crack at epidemiology. Their previous highly publicized but unrefereed report, described as "A Comprehensive Pilot Study," was shown, in a refereed paper (Gernsbacher et al., 2005), to suffer from "unwarranted conclusions" about the effect of changes in how autism is diagnosed on reported rates of autism.

So what's new, this time around? Hertz-Picciotto and Delwiche use census data to account for migration into California, so as to generate what they call incidence (rather than prevalence) figures. Also, they've included individuals identified as autistic, for the purpose of receiving services, before age three.

But the basis for the MIND's new epidemiology remains the same: the California DDS data. Turning DDS figures into incidence data doesn't alter the problem that DDS-type administrative numbers should not be used as epidemiology. The pitfalls of using service-based numbers have been explored formally in the literature (e.g., Laidler, 2005; Gernsbacher et al., 2005) and expressed less formally by an NIH official:

"I'll call a kid a zebra if it will get him the educational services I think he needs."

Hertz-Picciotto and Delwiche's inclusion of children identified in service records as autistic before age 3 raises the problem that early diagnosis of autism may be very unstable. In Turner and Stone (2007), only 53% of children diagnosed autistic at an average age of 29 months kept their autism diagnosis at an average age of 53 months. Diagnostic instability was related to earliness of diagnosis (the earlier the diagnosis, the less stable it was) but unrelated to interventions received.

Like Hertz-Picciotto and Delwiche's conclusions about changes in diagnostic criteria (pulled from an unrelated Finnish prevalence study; Kielinen et al., 2000), their conclusions about effect of including other autistic spectrum diagnoses (Asperger's and PDD-NOS, which the authors presume are "milder cases") do not arise from the incidence data they report. Instead, figures were taken from an earlier paper involving a specific (much smaller and narrower) sample of children recruited to study environmental causes of autism (Hertz-Picciotto et al., 2006).

According to Hertz-Picciotto and Delwiche, their study involves children with the specific diagnosis of autism only. The authors refer to "an International Classification of Diseases (ICD) code of 299.0 (autistic disorder)" (except of course this is a DSM-IV, not ICD, code and category), while assuming that children diagnosed with other autistic spectrum diagnoses do not meet ADI-R or ADOS cut-offs for autism or ASD (ADI-R has autism cut-offs only). This, the premise of the authors' analysis re what they presume to be "milder cases," doesn't stand up well to scrutiny.

For example, in Baird et al. (2006), 69% of children with non-autism autistic spectrum diagnoses met autism criteria on the ADI-R. This doesn't count Asperger children, who were lumped in with autistic children, virtually all (98%) meeting ADI-R autism criteria. In work I'm involved in, virtually all Asperger individuals (as virtually all autistics) meet all ADI-R and ADOS cut-offs for autism.

Also, in using the ADOS (which has, more recently, been revised again) and ADI-R, as well as clinical experience, Baird et al. (2006) produced a range of prevalence figures for children aged 9-10, from ~25/10,000 to ~116/10,000. That's a 4.6-fold discrepancy in the same sample at the same time with the same instruments and the same group of diagnosing clinicians.

Maybe there are other ways of exploring whether children receiving DDS autism services in the past are similar to children receiving these services more recently. In their unrefereed 2002 report, the MIND compared subsamples of children born from 1983 to 1985 with children born from 1993 to 1995. In the earlier subsample, 61% were judged to be in the range of intellectual disability, whereas in the later subsample, 27% were--a discrepancy noted by Gernsbacher et al. (2005).

More data about the entire population receiving DDS autism services are available. In a 1999 DDS report, graphed data show that whereas in 1987, ~84% of those receiving DDS autism services were judged to be in the range of intellectual disability, by 1998 that figure was 58%. A further look at DDS quarterly reports shows that by the beginning of 2002, that figure was 42%, and by the end of 2007 it was 33%. Between 1987 and 2007, the proportion of individuals receiving DDS autism services and scoring in the severe and profound ranges of intellectual disability dropped from ~36% to ~6%.

So--there are a few more reasons to question Hertz-Picciotto and Delwiche's conclusions about the effect of differences in how autism is defined and diagnosed. Also, there are many reasons to question the whole enterprise of trotting out DDS numbers yet again and pretending that, with enough distracting decorations stuck on, they in fact are epidemiology. After all, Hertz-Picciotto and Delwiche are denying the existence of older autistics, and they are doing this by using poor quality data dressed up in definitive conclusions. I would be much more cautious than Dr Hertz-Picciotto and her university have been, in going out in public wearing the MIND's new epidemiology.


Reference:

Irva Hertz-Picciotto, Lora Delwiche (2009). The Rise in Autism and the Role of Age at Diagnosis Epidemiology, 20 (1), 84-90 DOI: 10.1097/EDE.0b013e3181902d15

Where are the autism researcher bloggers?

Of course there are bloggers blogging about autism, everywhere, in staggering if not epidemic numbers. But my question is about bloggers who are also autism researchers. Where are they?

Prominent academics, scientists and researchers who blog aren't hard to find, including Nobel and Fields Medal winners, major journal editors, and clumpings together of well-known figures in various areas of research. You can't go far in Science Blogs without colliding with NIH-funded researchers in various non-autism fields.

And there are many bloggers who blog about autism research, including researchers, clinicians and academics in non-autism areas. But I'm looking for autism researchers who blog, about any subject, but particularly about autism research. For my blog-searching purposes, "autism researchers" are those whose main field of research is autism and whose autism-related work has been published in peer-reviewed journals.

Apart from me, there is the postdoctoral fellow Lindsay Oberman, who sporadically blogs at Psychology Today. Back in 2006, New Scientist published a letter I wrote in response to an informal article authored by Dr Oberman. Michael Merzenich has been in the authorship of a few autism-related papers and also has a blog, but he has extensively published in non-autism areas and is not primarily known as an autism researcher.

The Hub blogger and behaviour analyst Interverbal promises to cough up some published research some day, for which I'm impatiently waiting. There are now other behaviour analysts who blog about autism, but those I have located are service providers, rather than researchers.

In the remarkably science-and evidence-free vaccines-cause-autism camp, there's Mark Blaxill, known for calling autism a "silent holocaust." Mr Blaxill has been in the authorship of a few published papers, and is the sole author of a 2004 review in which he beautifully demonstrated--without in the least noticing--that amount of thimerosal in routine childhood vaccinations is totally unrelated to prevalence of autism. Autism Diva was kind enough to give me the space to point out the obvious. Mr Blaxill blogs with his ilk at "Age of Autism," but who would call him an autism researcher?

So where are they, the autism researcher bloggers, and if there really are so few of us, why might this be? There is no shortage of researchers in the area of autism, and autism has been a high profile field for longer than there have been blogs. I've limited my blog reading to English-language blogs, and I've left out individuals who are involved in autism research but who haven't yet published any of this research in the peer-reviewed literature. So maybe my criteria are too limited. But where are--for example--any of the numerous well-known autism researchers I've seen at IMFAR year after year? Why aren't any of them bloggers? Can anyone point me to more autism researcher bloggers?