Christopher I. Moore

D Murray

DP Kennedy

E Courchesne

F Castelli

F Happé

G Allen

Helen J. Simon

JLR Rubenstein

John F. Houde

MA Just

Matthew K. Belmonte

Michael M. Merzenich

MK Belmonte

Natacha A. Akshoomoff

OI Lovaas

Portia E. Iversen

T Wilson

Tal Kenet

Waterhouse, L

Y Takarae

Yael Adini

Yoram S. Bonneh

YS Bonneh

English

Belmonte, MK

Bonneh, YS

Adini, Y

Iversen, PE

Akshoomoff, NA

Kenet, T

Moore, CI

Simon, HJ

Houde, JF

Merzenich, MM

Nottingham Trent Institutional Repository (IRep)

AUTISM OVERFLOWS WITH SYNTHESES  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 Lynn 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 single-channel 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 & Courchesne 2001).  Professor 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 'low-functioning' cases in a way that might further the very synthesis to which Professor Waterhouse and we all aspire-- hence our unifying theme of perturbed neural interactions (Rubenstein & Merzenich 2003).  Though integrative, cooperative autism research has a long way to go still, Professor 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 Professor Waterhouse herself observes, ideas of weak central coherence (Happé & Frith 2006) and the various takes on abnormal connectivity (Castelli et al. 2002; Just et al. 2004; Courchesne & Pierce 2005a; Takarae et al. 2007; Wilson et al. 2007) offer great potential for synthesis.  So do reports of complementary anatomical (Courchesne & Pierce 2005b) and physiological (Kennedy & Courchesne 2008) abnormalities.  We ought perhaps to have noted explicitly the consistency of our cross-modal results with this emerging, integrated theory of perturbed neural information processing.  The synthetic potential remains, though, even when authors themselves might not take note of it, or worse, when they try to set themselves apart by seizing on rhetorical rather than data-driven distinctions.  We do not accept that autism is as simple as a collection of single-variable relationships that remain segregated through all levels of function from genes and environment to behaviour.  The true picture is likely much more tangled, converging from multiple causes and diverging into multiple endophenotypes but traversing a common core of abnormal neural information processing (Belmonte et al. 2004b).  This computational abnormality can arise from various, even complementary perturbations of physical connectivity (Belmonte et al. 2004a); the fact that not all individual cases of autism share the same genetic or environmental antecedents or the same epiphenomena (e.g. early white-matter hypertrophy) need not, therefore, imply any similar lack of unity at a core level.  Studies of informative single cases can be important hypothesis-generating steps towards including the under-studied and under-served 'low-functioning' population in the basic research that leads to informed and empirically well founded therapies.  Matthew K. BELMONTE Department of Human Development, Cornell University, Ithaca, NY, USA Yoram S. BONNEH Center for Brain and Behavior Research, University of Haifa, Haifa, Israel Yael ADINI Rehovot, Israel Portia E. IVERSEN Autism Speaks, Los Angeles, CA, USA Natacha A. AKSHOOMOFF Department of Psychiatry, School of Medicine, University of California, San Diego, CA, USA Tal KENET Department of Neurology, Massachusetts General Hospital, Boston, MA, USA Christopher I. MOORE Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA Helen J. SIMON Smith-Kettlewell Eye Research Institute, San Francisco, CA, USA John F. HOUDE Department of Otolaryngology, University of California, San Francisco, CA, USA Michael M. MERZENICH Keck Center for Integrative Neuroscience, University of California, San Francisco, CA, USA  References  Allen, G., & Courchesne, E. (2001). Attention function and dysfunction in autism. Frontiers in Bioscience, 6, D105-D119. Belmonte, M.K., Allen, G., Beckel-Mitchener, A., Boulanger, L.M., Carper, R.A., & Webb, S.J. (2004a). Autism and abnormal development of brain connectivity. Journal of Neuroscience, 24, 9228-9231. Belmonte, M.K., Cook, E.H. Jr., Anderson, G.M., Rubenstein, J.L.R., Greenough, W.T., Beckel-Mitchener, A., Courchesne, E., Boulanger, L.M., Powell, S.B., Levitt, P.R., Perry, E.K., Jiang, Y., DeLorey, T.M., & Tierney, E. (2004b). Autism as a disorder of neural information processing: directions for research and targets for therapy. Molecular Psychiatry, 9, 646-663. Unabridged edition at http://www.cureautismnow.org/conferences/summitmeetings/ Bonneh, Y.S., Belmonte, M.K., Pei, F., Iversen, P.E., Kenet, T., Akshoomoff, N.A., Adini, Y., Simon, H.J., Moore, C.I., Houde, J.F., & Merzenich, M.M. (2008). Cross-modal extinction in a boy with severely autistic behaviour and high verbal intelligence. Cognitive Neuropsychology, 25, 635-652. Castelli, F., Frith, C., Happé, F., & Frith, U. (2002). Autism, Asperger syndrome and brain mechanisms for the attribution of mental states to animated shapes. Brain, 125, 1839-1849. Courchesne, E., & Pierce, K. (2005a). Why the frontal cortex in autism might be talking only to itself: local over-connectivity but long-distance disconnection. Current Opinion in Neurobiology, 15, 225-230. Courchesne, E., & Pierce, K. (2005b). Brain overgrowth in autism during a critical time in development: implications for frontal pyramidal neuron and interneuron development and connectivity. International Journal of Developmental Neuroscience, 23, 153-170. Happé, F. & Frith, U. (2006). The weak coherence account: detail-focused cognitive style in autism spectrum disorders. Journal of Autism and Developmental Disorders, 36, 5-25. Just, M.A., Cherkassky, V.L., Keller, T.A., & Minshew, N.J. (2004). Cortical activation and synchronization during sentence comprehension in high-functioning autism: evidence of underconnectivity. Brain, 127, 1811-1821. Kennedy, D.P., & Courchesne, E. (2008). The intrinsic functional organization of the brain is altered in autism. NeuroImage, 39, 1877-1885. Lovaas, O.I., Koegel, R.L., & Schreibman, L. (1979). Stimulus overselectivity in autism: a review of research. Psychological Bulletin, 86, 1236-1254. Murray, D., Lesser, M., & Lawson, W. (2005). Attention, monotropism and the diagnostic criteria for autism. Autism, 9, 139-156. Rubenstein, J.L.R., & Merzenich, M.M. (2003). Model of autism: increased ratio of excitation/inhibition in key neural systems. Genes, Brain and Behavior, 2, 255-267.  Takarae, Y., Minshew, N.J., Luna, B., & Sweeney, J.A. (2007). Atypical involvement of frontostriatal systems during sensorimotor control in autism. Psychiatry Research, 156, 117-127. Waterhouse, L. (2008). Autism overflows: increasing prevalence and proliferating theories. Neuropsychology Review, 18, 273-286. Wilson, T., Rojas, D.C., Reite, M.L., Teale, P., & Rogers, S.J. (2007). Children and adolescents with autism exhibit reduced MEG steady-state gamma responses. Biological Psychiatry, 62, 192-197. 

Attention, monotropism and the diagnostic criteria for autism.

Atypical involvement of frontostriatal systems during sensorimotor control in autism.

Autism overflows: increasing prevalence and proliferating theories.

Children and adolescents with autism exhibit reduced MEG steady-state gamma responses.

Model of autism: increased ratio of excitation/inhibition in key neural systems.

Autism overflows with syntheses

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