There's a paper I just read, that said, in part:
Enhanced Perceptual Functioning in Autism wrote:
There are currently two major sources of heterogeneity in primary PDDs, i.e. individuals presenting with an autistic phenotype unrelated to toher diagnosable conditions and/or gross neurological abnormalities. The first distinction, currently labelled the Asperger vs. autism distinction, opposes individuals with a precocious use of speech, unremarkable visuo-spatial abilities, and frequent motor clumsiness, to individuals with superior visuo-spatial abilities and late or absent use of expressive speech. Within the latter autistic group, a secondary source of variability opposes the individuals who use oral language to those who don't. Use of overt speech has to be distinguished from a high vs. low functioning distinction, considering the high IQs (measured by, e.g., PPVT or Raven's Progressive Matrices) of certain "mute" autistics, and their frequent ability to read and to communicate via text. The other distinction is that some members of the autistic group develop considerable expertise in certain materials and are labelled "autistic savants".
There are no available convincing data that autism with vs. without overt peaks of ability, with vs. without overt speech, or overall autism vs. Asperger syndrome, differs at a genetic level. Even language abilities cannot be used to distinguish autism from Asperger syndrome, as written language experts are as representative of autism as oral language experts are representative of Asperger's. Although attractive, the endophenotype explanation of differences within autistic cognitive profiles produced conflicting findings (Nurmi et al., 2003; Ma et al., 2005). Also, the search for anomalies in the genes implicated in dysphasia in available autistic samples was unsuccessful (Gauthier et al., 2003; MRC, 2001; Tager-Flusberg, Joseph, & Folstein, 2001; Volkmar, Lord; Bailey, Schultz & Klin, 2004). The sole phenotypic distinction which is currently supported by data is that which separates primary (Pavone et al., 2004) or "essential" (Miles et al., 2005) autism, which is characterized by higher IQ, high heritability, low epilepsy rate, and absence of brain macroscopic abnormalities, vs. secondary (or "complex") autism, with higher incidence of mental retardation, epilepsy and brain abnormalities, and lower heritability.
In the absence of specific genetic subtyping, the explanation of PDD subtypes by a post-natal overspecialization processes have to be also considered, inasmuch as savant syndrome provides an autistic model for the subtyping of PDD. The heterogeneity of the autistic phenotype at older ages would result from an overspecialization to a certain perceptual material inherent to the developmental course of autism. Autistic subtypes with and without a visuo-spatial peak, autism with or without overt speech, and even the autism vs. Asperger distinction may be at least partially produced by differences in objects of expertise, in opportunity or lack thereof to enact perceptual specialization and expertise, and by the related "stoppage rule" associated with this specialization when it is allowed the means to develop. A precocious (Asperger), late (autistic with competent speech), or either slight or futile (autistic with sparse speech) investment in oral language as a perceptually defined material of interest should play a major role in eventual phenotypic heterogeneity. Conversely, the nature of the apparent neglect for "unchosen" domains may be identical for savant syndrome, autism and possibly Asperger syndrome. Although this hypothesis may appear unconventional and speculative, we contend that importing a model within PDD to explain PDD is less risky than the common use of importing brain-injured models of non-autistic individuals to account for an autistic difference. For example, use of frontally injured, typically developing patients to construct the executive deficit hypothesis is based on superficial analogies (Pennington & Ozonoff, 1996) and on a "residual normalcy" (Thomas & Karmiloff-Smith, 2002) assumption. Similarly, the use of typically developing temporally injured patients has produced dead-end models, like our "agnosia" hypothesis of autism (Mottron et al., 1997).
That's from "Enhanced Perceptual Functioning in Autism: An Update, and Eight Principles of Autistic Perception" by Laurent Mottron, Michelle Dawson, Isabelle Soulières, Benedict Hubrt, and Jake Burack.
My interpretation of this (and of the rest of the paper, in this regard) is that the way some people look at autism, as analogous to adult brain damage to previously NT people, is probably not accurate. The differences between different "subtypes" of autism may have more to do with what kind of perceptual specialization a person develops, than some intrinsic, original, essential difference in the brain structures between the different autism subtypes.
And also, that comparing autistic children, to brain-damaged adults, is a flawed analogy but one that neurologists have been making for a long time. (I read the paper they referenced on that too, and it's all about how there's kind of an assumption that "neurodevelopmental disorders" and adult brain damage are similar kinds of things, just because some of the results may look similar, and that people who've always been neurologically atypical are described in terms of "damaged" and "intact" functions. One of the counterexamples they gave was that people with Williams Syndrome supposedly had "intact" facial recognition, i.e. the same way normal people do it, just with other skills missing around it. It turned out that people with Williams syndrome used huge portions of their brains, rather than the typical small specialized area, to recognize faces. So they were questioning whether you could just claim that in someone who's always been neuro-atypical, there were sort of "damaged" island-areas and then "intact" other-areas and that kind of thing.)
(There's a lot more to this paper than this, but I thought that part was relevant to threads like this one.)
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"In my world it's a place of patterns and feel. In my world it's a haven for what is real. It's my world, nobody can steal it, but people like me, we live in the shadows." -Donna Williams
24 Nov 2005, 6:53 am
