Abstract
Autism spectrum disorder (ASD) is a challenging neurodevelopmental disorder with symptoms in social, language, sensory, motor, cognitive, emotional, repetitive behavior, and self-sufficient living domains. The important research question examined is the elucidation of the pathogenic neurocircuitry that underlies ASD symptomatology in all its richness and heterogeneity. The presented model builds on earlier social brain research, and hypothesizes that four social brain regions largely drive ASD symptomatology: amygdala, orbitofrontal cortex (OFC), temporoparietal cortex (TPC), and insula. The amygdala’s contributions to ASD largely derive from its major involvement in fine-grained intangible knowledge representations and high-level guidance of gaze. In addition, disrupted brain regions can drive disturbance of strongly interconnected brain regions to produce further symptoms. These and related effects are proposed to underlie abnormalities of the visual cortex, inferior frontal gyrus (IFG), caudate nucleus, and hippocampus as well as associated symptoms. The model is supported by neuroimaging, neuropsychological, neuroanatomical, cellular, physiological, and behavioral evidence. Collectively, the model proposes a novel, parsimonious, and empirically testable account of the pathogenic neurocircuitry of ASD, an extensive account of its symptomatology, a novel physiological biomarker with potential for earlier diagnosis, and novel experiments to further elucidate the mechanisms of brain abnormalities and symptomatology in ASD.
Highlights
Autism spectrum disorder (ASD) is a familiar neurodevelopmental disorder, with a complex and heterogeneous symptomatology that normally persists throughout life
orbitofrontal cortex (OFC), temporoparietal cortex (TPC), and insula, are disrupted in ASD and supporting evidence is summarized; these constitute addressed: widespread ASD symptoms can be explained as direct effects of disrupted social brain the proposed common pathogenic mechanism of ASD
inferior frontal gyrus (IFG) dysfunctions likely participate in the ASD symptoms of impaired expressive behaviors and gestures [58], the frequent impairment of syntax reported in verbal individuals [9], and the difficulties in goal-directed and planning aspects of cognition [168]
Summary
Autism spectrum disorder (ASD) is a familiar neurodevelopmental disorder, with a complex and heterogeneous symptomatology that normally persists throughout life. Many symptoms are hypothesized to flow directly from the four social brain regions’ disruptions, and are consistent with those brain regions’ known processing This information is set out, and is intended to comply with the framework of the research domain criteria (RDoC), in that the disordered neurocircuitry level of analysis is related to disturbed features, behaviors, cognitions, and other symptom domains [54,55,56]. Substantive explanations are offered for extensive ASD symptoms and features including: disordered visual scanpaths, apparent social disinterest, indiscriminate visual and auditory processing, abnormal sensory sensitivities, preference for concrete-level cognition, impaired conceptual processing, rote learning, inflexible repetitive routines, aspects of poor self-care and impaired daily living skills, stress, dysphoric emotions, stereotypies, and self-injurious behaviors (SIBs). The model should facilitate the development of interventions that are based on pathogenic mechanisms
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