Paper
Autism Overflows with Syntheses
Published May 16, 2009 · M. Belmonte, Y. Bonneh, Y. Adini
Neuropsychology Review
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Citations
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Influential Citations
Abstract
Editor: We were surprised to find our case study “Cross-modal extinction in a boy with severely autistic behaviour and high verbal intelligence” (Bonneh et al. 2008) impugned by Professor Waterhouse (2008) as an example of “unsynthesized and hoc theories” cluttering autism research. Our article never purports to constitute a theory in itself, and from its very beginning relates our observations of singlechannel perception to an established theoretical context described in terms of stimulus overselectivity (Lovaas et al. 1979), monotropism (Murray et al. 2005), and impaired attention shifting (Allen and Courchesne 2001). Waterhouse misattributes to us a causal claim that “autism results from monochannel of [sic] winner-takes-all perceptual processing” when in fact all that we claim is that our case results support the existence of such winner-takes-all processing in autism. Our point is not to clutter and to contend with existing theory, but rather to extend such theory to ‘lowfunctioning’ cases in a way that might further the very synthesis to which Waterhouse and we all aspire— hence our unifying theme of perturbed neural interactions (Rubenstein and Merzenich 2003). Though integrative, cooperative autism research has a long way to go still, Waterhouse’s assertion that “the field has not made progress in creating a synthesized, standard predictive causal theory of autism” seems to assume that statements that do not explicitly cite or support each other must necessarily be in conflict and competition. This assumption of irreconcilability is a defeatist fallacy. As Waterhouse herself observes, ideas of weak central coherence (Happe and Frith 2006) and the various takes on abnormal connectivity (Castelli et al. 2002; Just et al. 2004; Neuropsychol Rev (2009) 19:273–274 DOI 10.1007/s11065-009-9099-9
Autism research has a long way to go, but a unified, cooperative approach can advance our understanding of the disorder and its neural mechanisms.
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