Abstract
Previous models or hypotheses of autism spectral disorder (ASD) failed to take into full consideration the chronological and causal developmental trajectory, leading to the emergence of diverse phenotypes through a complex interaction between individual etiologies and environmental factors. Those phenotypes include persistent deficits in social communication and social interaction (criteria A in DSM-5), and restricted, repetitive patterns of behavior, interests, or activities (criteria B in DSM-5). In this article, we proposed a domain-general model that can explain criteria in DSM-5 based on the assumption that the same etiological mechanism would trigger the various phenotypes observed in different individuals with ASD. In the model, we assumed the following joint causes as the etiology of autism: (1) Hypoplasia of the pons in the brainstem, occurring immediately following neural tube closure; and (2) Deficiency in the GABA (γ-aminobutyric acid) developmental switch during the perinatal period. Microstructural abnormalities of the pons directly affect both the structural and functional development of the brain areas strongly connected to it, especially amygdala. The impairment of GABA switch could not only lead to the deterioration of inhibitory processing in the neural network, but could also cause abnormal cytoarchitecture. We introduced a perspective that atypical development in both brain structure and function can give full explanation of diverse phenotypes and pathogenetic mechanism of ASD. Finally, we discussed about neural mechanisms underlying the phenotypic characteristics of ASD that are not described in DSM-5 but should be considered as important foundation: sleep, global precedence, categorical perception, intelligence, interoception and motor control.
Highlights
Autism spectrum disorders (ASDs) are neurodevelopmental conditions that are diagnosed on the basis of the following two criteria: A. persistent deficits in social communication and interactions and B. restricted, repetitive patterns of behavior, interests, and activities (American Psychiatric Association, 2013; Table 1)
Theory of Atypical Emotion-Related Self-Regulation, Executive Attention, and Self-Control Caused by Brainstem Deficit Here, we focus on the latter theory based on the possible effect of early brainstem functioning on the regulation of emotions, inhibitory control and social cognitive impairment, observed in developmental disorders, including autism spectral disorder (ASD)
Asada et al (2016) have reported that a decrease in personal space has been observed in ASD adults. These results suggest that the amygdala plays an important role in triggering a strong emotional response when personal space is invaded, and that it is important for adjusting interpersonal distance
Summary
Autism spectrum disorders (ASDs) are neurodevelopmental conditions that are diagnosed on the basis of the following two criteria: A. persistent deficits in social communication and interactions and B. restricted, repetitive patterns of behavior, interests, and activities (American Psychiatric Association, 2013; Table 1). Ameis and Catani (2015) reported alterations in the uncinate fasciculus and the frontal and temporal thalamic projections in autistic brains based on their meta-analysis of 72 DTI studies of white matter Because these areas are involved in the ‘‘Yakovlev’’ circuit, they considered these alterations to be neural substrates of socio-emotional dysfunction in ASD. Hyperconnectivity Observed in Young Children with Autism Uddin et al (2011) investigated functional connectivity in children with ASD aged 7–12 years and found hyperconnectivity within the salience network (SN), including the ACC, superior frontal gyrus, thalamus and insular cortex They showed that children with ASD could be discriminated from TD children with high classification accuracy by multivariate pattern analysis of gray matter volume of the regions within the DMN. It has been reported that visual hypersensitivity could be explained in part by the hyperactivation of the sympathetic nervous system, yet it is strongly correlated with the activation of AIC (Nieuwenhuis et al, 2005; Ridderinkhof et al, 2009)
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