Collectively, these findings support previous studies suggesting heritability of frontostriatal structures among individuals with ADHD and suggest disruption in frontostriatal white matter tracts as one possible pathway to the disorder.

O bjects are defined by a multitude of features, such as color, shape, and motion, with each of the features processed by a host of visual areas located in ventral and dorsal regions of the cerebral cortex (1). The mechanism by which the brain integrates such distributed neural information to form a cohesive perception of objects is still unknown. Treisman and Gelade (2), Treisman (3), and others (4, 5) have proposed that the different features of each object are neurally bound together by means of attention to the object's location. Spatial attention is thought to be particularly critical for proper binding whenever there are multiple objects simultaneously present in the scene. It is under such conditions that the relationships between object features are most ambiguous, and hence more prone to conjunction errors (3, 4).Although spatial attention figures prominently in several models of feature binding, there is as yet little neurological evidence to support this location-based hypothesis. The parietal cortex is a likely candidate substrate given that it has been associated with the representation and manipulation of spatial information (6-10). However, the neural evidence to date is equivocal about the role of the parietal cortex in feature binding. Although some neuropsychological studies support the hypothesis that the parietal cortex is involved in feature integration (11-13), others do not (14). In addition, previous functional imaging studies have either shown no evidence for parietal cortex involvement in feature conjunction (15-17) or have produced inconclusive evidence (18-20) because of potential confounds such as task difficulty and͞or eye movements (19,21).To demonstrate that the parietal cortex plays a role in visual feature binding and to buttress the claim that this role is related to spatial attention, three criteria should be fulfilled. First, it is essential to localize the region(s) of the parietal cortex that are involved in spatial attention given that the parietal lobe also has been associated with nonspatial functions (19,(22)(23)(24). Second, the same parietal region(s) should show conjunction-related activation (i.e., more engaged in conditions requiring integration of features compared to conditions requiring only single feature judgments, even after controlling for task difficulty and eye movements). Third, the conjunction-related activation should primarily occur when there are multiple objects simultaneously present in the visual scene; for it is under such conditions that the relationship between objects features is ambiguous (4, 12, 13). In other words, the activation should be specifically observed under conditions in which spatial attention can assist proper feature binding. Here we report evidence from a series of fMRI experiments that specific regions of the right parietal cortex satisfy all three criteria. MethodsSubjects. Subjects were healthy, right-handed individuals, free of any history of neurological or psychiatric problems. All subjects gave written informed consent b...

This study extends findings of fronto-striatal dysfunction to adults with ADHD and highlights the importance of frontostriatal and frontocerebellar circuitry in this disorder, providing evidence of an endophenotype for examining the genetics of ADHD.

Background-Recent studies have suggested that the social and cognitive impairments in autism are associated with neural processing deficits in specific brain regions. However, these studies have primarily focused on neural systems responsible for face processing and social behaviors. Although repetitive, stereotyped behaviors are a hallmark of autism, little is known about the neural mechanisms underlying these behaviors in the disorder.

These results suggest that ADHD is associated with abnormal processing in attentional networks, with specific dysfunction in striatal circuitry. Methylphenidate may act to normalize activity within this network.

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There is now considerable evidence that white matter abnormalities play a role in the neurobiology of autism. Little research has been directed, however, at understanding (a)typical white matter development in autism and how this relates to neurocognitive impairments observed in the disorder. In this study we used probabilistic tractography to identify the cingulum bundle in 21 adolescents and young adults with autism spectrum disorder (ASD), and 21 age- and sex-matched healthy volunteers. We investigated group differences in the relationships between age and fractional anisotropy, a putative measure of white matter integrity, within the cingulum bundle. Moreover, in a preliminary investigation, we examined the relationship between cingulum fractional anisotropy and executive functioning using the Behavior Rating Inventory of Executive Function (BRIEF). The ASD participants demonstrated significantly lower fractional anisotropy within the cingulum bundle compared to the typically developing volunteers. There was a significant group-by-age interaction such that the ASD group did not show the typical age-associated increases in fractional anisotropy observed among healthy individuals. Moreover, lower fractional anisotropy within the cingulum bundle was associated with worse BRIEF behavioral regulation index scores in the ASD group. The current findings implicate a dysregulation in cingulum bundle white matter development occurring in late adolescence and early adulthood in autism spectrum disorder, and suggest that greater disturbances in this trajectory are associated with executive dysfunction in ASD.