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      Dissociation in performance of children with ADHD and high-functioning autism on a task of sustained attention

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          Abstract

          Attention deficit hyperactivity disorder (ADHD) and autism are two neurodevelopmental disorders associated with prominent executive dysfunction, which may be underpinned by disruption within fronto-striatal and fronto-parietal circuits. We probed executive function in these disorders using a sustained attention task with a validated brain-behaviour basis. Twenty-three children with ADHD, 21 children with high-functioning autism (HFA) and 18 control children were tested on the Sustained Attention to Response Task (SART). In a fixed sequence version of the task, children were required to withhold their response to a predictably occurring no-go target (3) in a 1–9 digit sequence; in the random version the sequence was unpredictable. The ADHD group showed clear deficits in response inhibition and sustained attention, through higher errors of commission and omission on both SART versions. The HFA group showed no sustained attention deficits, through a normal number of omission errors on both SART versions. The HFA group showed dissociation in response inhibition performance, as indexed by commission errors. On the Fixed SART, a normal number of errors was made, however when the stimuli were randomised, the HFA group made as many commission errors as the ADHD group. Greater slow-frequency variability in response time and a slowing in mean response time by the ADHD group suggested impaired arousal processes. The ADHD group showed greater fast-frequency variability in response time, indicative of impaired top-down control, relative to the HFA and control groups. These data imply involvement of fronto-parietal attentional networks and sub-cortical arousal systems in the pathology of ADHD and prefrontal cortex dysfunction in children with HFA.

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          Molecular genetics of attention-deficit/hyperactivity disorder.

          Results of behavioral genetic and molecular genetic studies have converged to suggest that both genetic and nongenetic factors contribute to the development of attention-deficit/hyperactivity disorder (ADHD). We review this literature, with a particular emphasis on molecular genetic studies. Family, twin, and adoption studies provide compelling evidence that genes play a strong role in mediating susceptibility to ADHD. This fact is most clearly seen in the 20 extant twin studies, which estimate the heritability of ADHD to be .76. Molecular genetic studies suggest that the genetic architecture of ADHD is complex. The few genome-wide scans conducted thus far are not conclusive. In contrast, the many candidate gene studies of ADHD have produced substantial evidence implicating several genes in the etiology of the disorder. For the eight genes for which the same variant has been studied in three or more case-control or family-based studies, seven show statistically significant evidence of association with ADHD on the basis of the pooled odds ratio across studies: DRD4, DRD5, DAT, DBH, 5-HTT, HTR1B, and SNAP-25.
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            Primate anterior cingulate cortex: where motor control, drive and cognition interface.

            T. Paus (2001)
            Controversy surrounds the function of the anterior cingulate cortex. Recent discussions about its role in behavioural control have centred on three main issues: its involvement in motor control, its proposed role in cognition and its relationship with the arousal/drive state of the organism. I argue that the overlap of these three domains is key to distinguishing the anterior cingulate cortex from other frontal regions, placing it in a unique position to translate intentions to actions.
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              Unusual brain growth patterns in early life in patients with autistic disorder: an MRI study.

              To quantify developmental abnormalities in cerebral and cerebellar volume in autism. The authors studied 60 autistic and 52 normal boys (age, 2 to 16 years) using MRI. Thirty autistic boys were diagnosed and scanned when 5 years or older. The other 30 were scanned when 2 through 4 years of age and then diagnosed with autism at least 2.5 years later, at an age when the diagnosis of autism is more reliable. Neonatal head circumferences from clinical records were available for 14 of 15 autistic 2- to 5-year-olds and, on average, were normal (35.1 +/- 1.3 cm versus clinical norms: 34.6 +/- 1.6 cm), indicative of normal overall brain volume at birth; one measure was above the 95th percentile. By ages 2 to 4 years, 90% of autistic boys had a brain volume larger than normal average, and 37% met criteria for developmental macrencephaly. Autistic 2- to 3-year-olds had more cerebral (18%) and cerebellar (39%) white matter, and more cerebral cortical gray matter (12%) than normal, whereas older autistic children and adolescents did not have such enlarged gray and white matter volumes. In the cerebellum, autistic boys had less gray matter, smaller ratio of gray to white matter, and smaller vermis lobules VI-VII than normal controls. Abnormal regulation of brain growth in autism results in early overgrowth followed by abnormally slowed growth. Hyperplasia was present in cerebral gray matter and cerebral and cerebellar white matter in early life in patients with autism.
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                Author and article information

                Journal
                Neuropsychologia
                Neuropsychologia
                Pergamon Press
                0028-3932
                1873-3514
                2007
                2007
                : 45
                : 10
                : 2234-2245
                Affiliations
                [a ]School of Psychology and Trinity College Institute of Neuroscience, Trinity College Dublin, Dublin 2, Ireland
                [b ]School of Medicine and Health Sciences and Trinity College Institute of Neuroscience, Trinity College Dublin, Dublin 2, Ireland
                [c ]Cognitive Neurophysiology Laboratory, Nathan S. Kline Institute, Orangeburg, NY 10962, United States
                [d ]Howard Florey Institute and Centre for Neuroscience, University of Melbourne, Australia
                [e ]Academic Child Psychiatry Unit, Department of Pediatrics, University of Melbourne, Australia
                [f ]Department of Psychology, Monash University, Australia
                [g ]Cognitive Neuroscience Laboratory, School of Psychology and Queensland Brain Institute, University of Queensland, Brisbane, Australia
                Author notes
                [* ]Corresponding author at: School of Psychology and Trinity College Institute of Neuroscience, Trinity College Dublin, Dublin 2, Ireland. Tel.: +353 1 896 8403; fax: +353 1 671 2006. johnsoka@ 123456tcd.ie
                Article
                NSY2560
                10.1016/j.neuropsychologia.2007.02.019
                2000292
                17433378
                d50aff7d-a486-4b8d-bf6a-a27643bb43fa
                © 2007 Elsevier Ltd.

                This document may be redistributed and reused, subject to certain conditions.

                History
                : 18 August 2006
                : 13 February 2007
                : 19 February 2007
                Categories
                Article

                Neurology
                response inhibition,response time,arousal,executive function,fast fourier transform,variability

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