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Controversy seems to follow autism like the tail on a kite. From the earliest descriptions of autism, clinicians questioned whether this disorder was an independent entity. For instance, in 1959, Bender1 highlighted the imprecision of the term because many distinctly different etiological pathways could converge in the same disorder and concluded that autism was neither an etiological nor clinical entity. In contrast, in 1952 Van Krevelen’s skepticism about the existence of autism was reversed when he encountered his first patient who was “as much like those described by Kanner as one raindrop is like another.”2 Others argued whether autism was psychogenic or hardwired in biology and suggested that factors as diverse as mothering3 or the reticular formation4 could be the common etiologic denominator. More recently, controversy continues and is reflected in changes in diagnostic criteria and the increasing recognition of heterogeneity that incorporates the word “spectrum” into the diagnosis. With each new prevalence estimate that suggests inexplicable and substantial increases in the number of children diagnosed with the disorder,5 the urgency to better understand causation is amplified.
King BH. Promising Forecast for Autism Spectrum Disorders. JAMA. 2015;313(15):1518–1519. doi:10.1001/jama.2015.2628
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