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Table 3 Summary of articles concerning brain morphophysiological and functional abnormalities

From: The biopsychosocial processes in autism spectrum disorder

Author, date Conclusions Contributions
Levy et al., 2009 [1] AUT is not a monogenic disorder, in many individuals may be the result of a complex amalgam of multiple simultaneous genetic variations, and present morphological and functional brain abnormalities. Highlights the importance of understanding biological markers, patterns of cortical organization and connectivity in advancing the treatment of AUT.
Baron-Cohen et al., 2000 [19] Unlike those with TD in ToM tests, patients with AS or AUT do not show activation of the amygdala when making mentalistic inferences from the eyes. The amygdala may be one of many abnormal neural regions in AUT. Highlights the role of the amygdala in the symptoms of ASD.
Castelli et al., 2002 [20] The physiological cause for the mentalizing dysfunction in AUT can be a bottleneck in the interaction between perceptual processes of higher and lower order. Relates the difficulties in understanding socially relevant movements in AUT to information processing in the visual cortex.
Brunet et al., 2000 [21] Attribution of intentions to others is associated with a complex brain activity involving the right medial prefrontal cortex when a nonverbal task is used. Presents data that validate hypothesis of abnormal brain activation in patients with impaired mentalizing.
Castelli et al., 2000 [22] The regions responsible for processing information about intentions and the ability to make inferences about the mental states of others may have evolved from the ability to make inferences about the actions of other creatures. Suggests evolutionary history for the abilities that make ToM.
Pierce et al., 2001 [23] Compared to typical individuals, autistic "see" faces using different neural systems, unique to each individual. Experiential factors play an important role in the development of the fusiform facial area, related to the processing faces.
Scholz et al., 2009 [24] There are neighboring but distinct regions in the right temporo-parietal junction involved in ToM and orientation of attention. Identifies difficulties in the investigation of brain functions that occupy regions close to each other or overlapping.
Johnson et al., 2007 [25] There is involvement of frontal and parietal attentional networks and sub-cortical excitatory systems in ADHD and a prefrontal cortex dysfunction in children with HFA. Provides detailed evidence of dysfunction in sustained attention in ADHD significantly higher than in HFA.
Kana et al., 2007 [26] The neural circuit linked to inhibition in individuals with ASD is atypically activated and is less synchronized, leaving inhibition to be accomplished by strategic control rather than automatically. Identifies dysfunction in inhibitory cortical level, being disorganized and desynchronized.
Schultz et al., 2000 [27] Individuals with ASD demonstrate during facial discrimination, a pattern of brain activity consistent with strategies based on characteristics or traits more typical of the perception of non-facial objects. Highlights possible dysfunction in processing stimuli related to biological and inanimate objects in ASD.
Dapretto et al., 2006 [28] A dysfunctional mirror neuron system may underlie the social deficits of autism. Substantiates hypothesis of the importance of mirror neurons in the development of social functions.
Jones et al., 2008 [29] The behavior of eye contact is already noticeably compromised in children two years of age with ASD, accompanying the person with autism for life. Subsidizes and highlights the importance of early diagnosis of ASD.