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Saturday, May 17, 2008
Champagne Terrace/Bordeaux (Novotel London West)
9:30 AM
Background:
Autism has become understood as a spectrum of signs and symptoms varying in severity and number across individuals. As autistic spectrum disorders (ASDs) have become more broadly-defined and widely-recognized, there is support for viewing etiologies as heterogeneous—resulting in many ‘autisms’: These can be characterized in terms of genotypic, phenotypic, neuroanatomical, and neurochemical differences (e.g., Geschwind, IMFAR, 2007). Concurrently, the need to help ASD-identified individuals has increased exponentially with treatments including pharmacological, behavioral, developmental, and educational approaches. Among clinicians and clinical researchers involved in treatment, there is increasing understanding that this heterogeneity means that treatment is not one-size-fits-all, though there is little agreement on a conceptual framework for aligning symptoms/ profiles/ subtypes with specific treatment approaches.
Objectives:
The approach taken here is that ASDs can be re-conceptualized as related autism-specific learning disabilities (ALDs) and autism-specific learning styles (ALSs).
Methods:
Symptoms of ASDs can be operationally understood, then deconstructed by viewing them as arising from a matrix of specific disabilities cross-tabulated by preserved abilities. Each ALD can be characterized as the product of specific defects in perception, processing, retention or expression of some perceptual, affective or cognitive stimuli. Then, preserved abilities form naturally-arising compensations depending on ALDs, resulting in self-accommodations wherein stronger capacities are deployed when specific neuropathology blocks expression of typical function (Siegel, 2003, 2005, 2007).
Results:
Using this model, targeted clinical treatments can be selected accordingly, and characterized as taught accommodations that optimize efficiency of self-accommodation processes.
Conclusions:
The ALD/ALS model has two important applications: 1) It breaks symptoms of ASDs into what are essentially, readily observed endophenotypes (e.g., low affiliative drive) which should be more useful in characterization of homologues within pedigrees than diagnosis alone, and 2) precisely specifies learning defects so they can be addressed with more targeted intervention strategies (e.g., pivotal response strategies to leverage low affiliative drive).
Autism has become understood as a spectrum of signs and symptoms varying in severity and number across individuals. As autistic spectrum disorders (ASDs) have become more broadly-defined and widely-recognized, there is support for viewing etiologies as heterogeneous—resulting in many ‘autisms’: These can be characterized in terms of genotypic, phenotypic, neuroanatomical, and neurochemical differences (e.g., Geschwind, IMFAR, 2007). Concurrently, the need to help ASD-identified individuals has increased exponentially with treatments including pharmacological, behavioral, developmental, and educational approaches. Among clinicians and clinical researchers involved in treatment, there is increasing understanding that this heterogeneity means that treatment is not one-size-fits-all, though there is little agreement on a conceptual framework for aligning symptoms/ profiles/ subtypes with specific treatment approaches.
Objectives:
The approach taken here is that ASDs can be re-conceptualized as related autism-specific learning disabilities (ALDs) and autism-specific learning styles (ALSs).
Methods:
Symptoms of ASDs can be operationally understood, then deconstructed by viewing them as arising from a matrix of specific disabilities cross-tabulated by preserved abilities. Each ALD can be characterized as the product of specific defects in perception, processing, retention or expression of some perceptual, affective or cognitive stimuli. Then, preserved abilities form naturally-arising compensations depending on ALDs, resulting in self-accommodations wherein stronger capacities are deployed when specific neuropathology blocks expression of typical function (Siegel, 2003, 2005, 2007).
Results:
Using this model, targeted clinical treatments can be selected accordingly, and characterized as taught accommodations that optimize efficiency of self-accommodation processes.
Conclusions:
The ALD/ALS model has two important applications: 1) It breaks symptoms of ASDs into what are essentially, readily observed endophenotypes (e.g., low affiliative drive) which should be more useful in characterization of homologues within pedigrees than diagnosis alone, and 2) precisely specifies learning defects so they can be addressed with more targeted intervention strategies (e.g., pivotal response strategies to leverage low affiliative drive).