The other related trend is the increase in research on genetic conditions, many of them previously considered to be disorders associated with ID (e.g., Fragile X Syndrome and Williams Syndrome), where increasingly high rates of ASD features and/or diagnoses are reported ( 6, 9). One of these trends is the very large increase in ASD prevalence, accompanied by a strikingly similar decline in ID ( 6– 8) (see Figure 1). A few important trends underscore the importance of reviewing the clinical distinction between ID and ASD. In this review, we focus on the impact of ID on the diagnosis of ASD. Thus, when it comes to discussions of primary/idiopathic versus secondary autism, considering the role of ID in diagnosis and phenotyping is critical. In addition, the rate of genetic abnormality associated with ASD is significantly higher in the presence of comorbid ID ( 4, 5). In fact, genes associated with ASD are often the same genes that are associated with ID ( 2, 3), validating both the phenotypic and genotypic overlap between these conditions. ( 1), where specific genetic etiologies are identified as contributing to the manifestation of ASD. Whereas the rest of this special issue is devoted to specific factors that relate to secondary versus idiopathic autism spectrum disorder (ASD), in this focused review, we discuss a diagnostic concern that cuts across this discussion: When and how should ASD be diagnosed in the presence of intellectual disability (ID) of varying degrees? This discussion is relevant because of the high rate of ID in what is being termed “secondary” or non-idiopathic ASD, similar to what was previously described as “complex” ASD see Miles et al. Especially pertinent to this discussion are findings that a diagnosis of ID in the context of an ASD diagnosis may be one of the strongest indicators that an associated condition or specific etiological factor is present (i.e., secondary autism). Finally, we consider the impact of the blurred diagnostic boundaries between ID and ASD on the study of secondary versus idiopathic ASD. We then consider ways that operationalized criteria may be beneficial for making the clinical distinction between ID with and without ASD. We review the evolution of the autism diagnosis and ASD diagnostic tools to understand how this distinction has been conceptualized previously. We discuss behavioral distinctions between ID and ASD, in light of the diagnostic criterion mandating that ASD should not be diagnosed if symptoms are accounted for by ID or general developmental delay. In this focused review, we consider the impact of ID on the diagnosis of ASD. Thus, regardless of etiology, ASD symptoms may appear across groups of individuals with vastly different profiles of underlying deficits and strengths. A related issue is that, because many of the social communication deficits that define ASD represent a failure to acquire developmentally expected skills, these same deficits would be expected to occur to some extent in all individuals with intellectual disability (ID). The topic of this special issue on secondary versus idiopathic autism allows for discussion of how different groups may come to manifest autism spectrum disorder (ASD) or ASD-like symptoms despite important etiological differences.
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