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      Enhanced visual processing contributes to matrix reasoning in autism

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          Abstract

          Recent behavioral investigations have revealed that autistics perform more proficiently on Raven's Standard Progressive Matrices (RSPM) than would be predicted by their Wechsler intelligence scores. A widely-used test of fluid reasoning and intelligence, the RSPM assays abilities to flexibly infer rules, manage goal hierarchies, and perform high-level abstractions. The neural substrates for these abilities are known to encompass a large frontoparietal network, with different processing models placing variable emphasis on the specific roles of the prefrontal or posterior regions. We used functional magnetic resonance imaging to explore the neural bases of autistics' RSPM problem solving. Fifteen autistic and eighteen non-autistic participants, matched on age, sex, manual preference and Wechsler IQ, completed 60 self-paced randomly-ordered RSPM items along with a visually similar 60-item pattern matching comparison task. Accuracy and response times did not differ between groups in the pattern matching task. In the RSPM task, autistics performed with similar accuracy, but with shorter response times, compared to their non-autistic controls. In both the entire sample and a subsample of participants additionally matched on RSPM performance to control for potential response time confounds, neural activity was similar in both groups for the pattern matching task. However, for the RSPM task, autistics displayed relatively increased task-related activity in extrastriate areas (BA18), and decreased activity in the lateral prefrontal cortex (BA9) and the medial posterior parietal cortex (BA7). Visual processing mechanisms may therefore play a more prominent role in reasoning in autistics. 2009 Wiley-Liss, Inc.

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          Most cited references95

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          The role of prefrontal cortex in working-memory capacity, executive attention, and general fluid intelligence: An individual-differences perspective

          We provide an "executive-attention" framework for organizing the cognitive neuroscience research on the constructs of working-memory capacity (WMC), general fluid intelligence, and prefrontal cortex (PFC) function. Rather than provide a novel theory of PFC function, we synthesize a wealth of single-cell, brain-imaging, and neuropsychological research through the lens of our theory of normal individual differences in WMC and attention control (Engle, Kane, & Tuholski, 1999; Engle, Tuholski, Laughlin, & Conway, 1999). Our critical review confirms the prevalent view that dorsolateral PFC circuitry is critical to executive-attention functions. Moreover, although the dorsolateral PFC is but one critical structure in a network of anterior and posterior "attention control" areas, it does have a unique executive-attention role in actively maintaining access to stimulus representations and goals in interference-rich contexts. Our review suggests the utility of an executive-attention framework for guiding future research on both PFC function and cognitive control.
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            Cortical activation and synchronization during sentence comprehension in high-functioning autism: evidence of underconnectivity.

            The brain activation of a group of high-functioning autistic participants was measured using functional MRI during sentence comprehension and the results compared with those of a Verbal IQ-matched control group. The groups differed in the distribution of activation in two of the key language areas. The autism group produced reliably more activation than the control group in Wernicke's (left laterosuperior temporal) area and reliably less activation than the control group in Broca's (left inferior frontal gyrus) area. Furthermore, the functional connectivity, i.e. the degree of synchronization or correlation of the time series of the activation, between the various participating cortical areas was consistently lower for the autistic than the control participants. These findings suggest that the neural basis of disordered language in autism entails a lower degree of information integration and synchronization across the large-scale cortical network for language processing. The article presents a theoretical account of the findings, related to neurobiological foundations of underconnectivity in autism.
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              Intellectual ability and cortical development in children and adolescents.

              Children who are adept at any one of the three academic 'R's (reading, writing and arithmetic) tend to be good at the others, and grow into adults who are similarly skilled at diverse intellectually demanding activities. Determining the neuroanatomical correlates of this relatively stable individual trait of general intelligence has proved difficult, particularly in the rapidly developing brains of children and adolescents. Here we demonstrate that the trajectory of change in the thickness of the cerebral cortex, rather than cortical thickness itself, is most closely related to level of intelligence. Using a longitudinal design, we find a marked developmental shift from a predominantly negative correlation between intelligence and cortical thickness in early childhood to a positive correlation in late childhood and beyond. Additionally, level of intelligence is associated with the trajectory of cortical development, primarily in frontal regions implicated in the maturation of intelligent activity. More intelligent children demonstrate a particularly plastic cortex, with an initial accelerated and prolonged phase of cortical increase, which yields to equally vigorous cortical thinning by early adolescence. This study indicates that the neuroanatomical expression of intelligence in children is dynamic.
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                Author and article information

                Journal
                Human Brain Mapping
                Hum. Brain Mapp.
                Wiley
                10659471
                December 2009
                December 2009
                June 15 2009
                : 30
                : 12
                : 4082-4107
                Article
                10.1002/hbm.20831
                2787806
                19530215
                f52259e5-9ac3-4dfd-a373-e2939090ac53
                © 2009

                http://doi.wiley.com/10.1002/tdm_license_1.1

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