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【正文】 20xx). In contrast, individuals with ASD show impairments in executive processes and in synthesizing plex sensory input to arrive at a “big picture” understanding of their environment, likely contributing to the classical deficits in social munication and reciprocal social interactions. While dysfunctional reciprocal interactions are the core behavioral manifestations of ASD, clinical heterogeneity as well as enhanced cognitive functioning in particular domains should be accounted for in any plete etiologic and neurodevelopmental account of ASDs. A prehensive model, explaining all core deficits of ASD and accounting for the broader autism phenotype, is not fully developed. Yet, an emerging hypothesis, based on multidimensional research spanning genes to behavior, posits that deficits in reciprocal social behavior may result from dysfunctional longrange connections between brain regions that are highly evolved in humans (Just et al., 20xx。 Courchesne amp。 Pierce, 20xx。 Geschwind amp。 Levitt, 20xx。 Mundy et al., 20xx). From 重慶郵電大學(xué)本科畢業(yè)設(shè)計(jì)（論文） 23 a developmental perspective, this model suggests that disruption in the initial architecture and connectivity of local circuits constrains the experience dependent changes that normally allow for the reanization of connections, to create stable longrange connections during development. This “developmental disconnection” model also provides an explanation for the preservation or enhancement of certain cognitive functions, such as enhanced visual and auditory discrimination. This enhanced function could be the result of increased local work connectivity stemming from both faulty initial circuitry and inefficient longrange connectivity. For example, disconnection of dorsolateral prefrontal and anterior cingulate cortex from sensory association areas – necessary for joint attention early in infancy –may lead to a cascade of events preventing the development of language and typical social behavior (Mundy et al., 20xx). The failure to establish normative connections between these regions may simultaneously allow for increased connectivity within sensory association cortices, leading to enhanced sensory discrimination and increased attention to detail. While this model serves as an initial framework for understanding autistic symptomatology it is clear that much more work needs to be done to bridge the gaps between different levels of autism research. Task Based fMRI and Functional Connectivity Studies Functional MRI (fMRI) studies of highfunctioning individuals with ASD have consistently reported hypoactivation in brain regions involved in a variety of tasks that tap into social cognition (see Pelphrey and Carter, 20xx, for review). Abnormal activity has been reported in specialized regions such as the amygdala (. Dalton et al., 20xx), fusiform gyrus (., Schultz et al., 20xx), inferior frontal gyrus (., Dapretto et al., 20xx) and medial prefrontal cortex (., Castelli et al., 20xx). Individuals with autism also fail to show normal deactivation patterns in works such as the default mode work (DMN。 Kennedy et al., 20xx。 Di Martino et al.,20xx), which is implicated in social cognitive and theory of mind processes (Raichle et al., 20xx。 AndrewsHanna et al., 20xx). This array of findings in different brain regions highlights the need for characterization of ASD as a disorder involving the interactions of multiple brain systems, as ASD is not likely to be understood in terms of disruption in a single brain region or system. Multiple neuroimaging studies of autism have examined functional connectivity (.,correlated activity) between different brain regions in ASD, finding functional underconnectivity between brain regions during the performance of a variety of different cognitive tasks, including language processing (Just et al., 20xx), emotion processing (Kleinhans et al., 20xx), working memory (Koshino et al., 20xx。 Kana et al., 20xx), motor function (Mostofsky et al., 20xx), or visuospatial processing (Villalobos et al., 20xx). Just et al. (20xx) suggested that widespread underconnectivity could be related to all higherlevel cognitive deficits observed in autism. However, other studies have characterized ASD as a disorder of “altered” or 重慶郵電大學(xué)本科畢業(yè)設(shè)計(jì)（論文） 24 “abberant” connectivity, given findings of overconnectivity within thalamocortical (Mizuno et al., 20xx) and striatocortical circuits (Turner et al., 20xx。 Di Martino et al., 20xx) suggesting a more plex pattern. These findings support work dysfunction, yet highlight the need to examine connectivity within and between different systems. Intrinsic Functional Connectivity Functional brain imaging studies have demonstrated that, even in the absence of an overt cognitive task, there exist synchronized low frequency spontaneous fluctuations in neuronal activity across different brain works (Biswal et al., 1995。 see Fox and Raichle, 20xx, for review). These works undergo increasing integration (. increasing longrange within work connectivity) and segregation (. reduced connectivity between works) across typical development (TD。 Fair et al., 20xxa, 20xx, 20xx。 Kelly et al., 20xx。 Supekar et al., 20xx。 Stevens et al., 20xx。 Dosenbach et al., 20xx). Recent studies characterizing intrinsic fluctuations in ASD have consistently found that taskindependent (., intrinsic) functional connectivity, including interhemispheric (Anderson et al., 20xx。 Dinstein et al., 20xx) and DMN connectivity is reduced in ASD (Cherkassky et al., 20xx。 Kennedy, 20xx。 Weng et al., 20xx。 Assaf et al., 20xx). Thus evidence suggests that intrinsic connectivity works in autism show an altered pattern of connectivity that may reflect an “immature” development of these works. Structural Connectivity Diffusion tensor imaging (DTI) measures the a