A Neurorobotics Simulation of Autistic Behavior Induced by Unusual Sensory Precision

Recently, applying computational models developed in cognitive science to psychiatric disorders has been recognized as an essential approach for understanding cognitive mechanisms underlying psychiatric symptoms. Autism spectrum disorder is a neurodevelopmental disorder that is hypothesized to affect information processes in the brain involving the estimation of sensory precision (uncertainty), but the mechanism by which observed symptoms are generated from such abnormalities has not been thoroughly investigated. Using a humanoid robot controlled by a neural network using a precision-weighted prediction error minimization mechanism, it is suggested that both increased and decreased sensory precision could induce the behavioral rigidity characterized by resistance to change that is characteristic of autistic behavior. Specifically, decreased sensory precision caused any error signals to be disregarded, leading to invariability of the robot’s intention, while increased sensory precision caused an excessive response to error signals, leading to fluctuations and subsequent fixation of intention. The results may provide a system-level explanation of mechanisms underlying different types of behavioral rigidity in autism spectrum and other psychiatric disorders. In addition, our findings suggest that symptoms caused by decreased and increased sensory precision could be distinguishable by examining the internal experience of patients and neural activity coding prediction error signals in the biological brain

Emergence of sensory attenuation based upon the free-energy principle

The brain attenuates its responses to self-produced exteroceptions (e.g., we cannot tickle ourselves). Is this phenomenon, known as sensory attenuation, enabled innately, or acquired through learning? Here, our simulation study using a multimodal hierarchical recurrent neural network model, based on variational free-energy minimization, shows that a mechanism for sensory attenuation can develop through learning of two distinct types of sensorimotor experience, involving self-produced or externally produced exteroceptions. For each sensorimotor context, a particular free-energy state emerged through interaction between top-down prediction with precision and bottom-up sensory prediction error from each sensory area. The executive area in the network served as an information hub. Consequently, shifts between the two sensorimotor contexts triggered transitions from one free-energy state to another in the network via executive control, which caused shifts between attenuating and amplifying prediction-error-induced responses in the sensory areas. This study situates emergence of sensory attenuation (or self-other distinction) in development of distinct free-energy states in the dynamic hierarchical neural system

Recent Results from LHD Experiment with Emphasis on Relation to Theory from Experimentalist’s View

he Large Helical Device (LHD) has been extending an operational regime of net-current free plasmas towardsthe fusion relevant condition with taking advantage of a net current-free heliotron concept and employing a superconducting coil system. Heating capability has exceeded 10 MW and the central ion and electron temperatureshave reached 7 and 10 keV, respectively. The maximum value of β and pulse length have been extended to 3.2% and 150 s, respectively. Many encouraging physical findings have been obtained. Topics from recent experiments, which should be emphasized from the aspect of theoretical approaches, are reviewed. Those are (1) Prominent features in the inward shifted configuration, i.e., mitigation of an ideal interchange mode in the configuration with magnetic hill, and confinement improvement due to suppression of both anomalous and neoclassical transport, (2) Demonstration ofbifurcation of radial electric field and associated formation of an internal transport barrier, and (3) Dynamics of magnetic islands and clarification of the role of separatrix

不確実な世界における神経発達障害 : 症状の神経ロボットシミュレーション

早大学位記番号:新8830早稲田大

Elucidating multifinal and equifinal pathways to developmental disorders by constructing real-world neurorobotic models

Vigorous research has been conducted to accumulate biological and theoretical knowledge about neurodevelopmental disorders, including molecular, neural, computational, and behavioral characteristics; however, these findings remain fragmentary and do not elucidate integrated mechanisms. An obstacle is the heterogeneity of developmental pathways causing clinical phenotypes. Additionally, in symptom formations, the primary causes and consequences of developmental learning processes are often indistinguishable. Herein, we review developmental neurorobotic experiments tackling problems related to the dynamic and complex properties of neurodevelopmental disorders. Specifically, we focus on neurorobotic models under predictive processing lens for the study of developmental disorders. By constructing neurorobotic models with predictive processing mechanisms of learning, perception, and action, we can simulate formations of integrated causal relationships among neurodynamical, computational, and behavioral characteristics in the robot agents while considering developmental learning processes. This framework has the potential to bind neurobiological hypotheses (excitation-inhibition imbalance and functional disconnection), computational accounts (unusual encoding of uncertainty), and clinical symptoms. Developmental neurorobotic approaches may serve as a complementary research framework for integrating fragmented knowledge and overcoming the heterogeneity of neurodevelopmental disorders

Homogeneous intrinsic neuronal excitability induces overfitting to sensory noise: A robot model of neurodevelopmental disorder

Neurodevelopmental disorders, including autism spectrum disorder, have been intensively investigated at the neural, cognitive, and behavioral levels, but the accumulated knowledge remains fragmented. Here, we propose a mechanistic explanation that unifies the disparate observations via a hierarchical predictive coding and developmental learning framework, which is demonstrated in experiments using a neural network-controlled robot. The results show that, through the developmental learning process, homogeneous intrinsic neuronal excitability at the neural level induced via self-organization changes at the information-processing level, such as hyper sensory precision and overfitting to sensory noise. These changes led to inflexibility, reduced generalization, and motor clumsiness at the behavioral level. These findings might bridge various levels of understandings in autism spectrum and other neurodevelopmental disorders and provide insights into the disease processes underlying observed behaviors and brain activities in individual patients. This study shows the potential of neurorobotics frameworks for modeling how psychiatric disorders arise from dynamic interactions among the brain, body, and uncertain environments

Paradoxical sensory reactivity induced by functional disconnection in a robot model of neurodevelopmental disorder

Hyper- and hyporeactivity to sensory stimuli is a diagnostic feature of autism spectrum disorder and has been reported in many neurodevelopmental disorders. However, the computational mechanisms underlying such paradoxical responses remain unclear. Here, using a robot controlled by a hierarchical recurrent neural network model with predictive processing and a learning mechanism, we simulated how functional disconnection alters the learning process and affects subsequent behavioral reactivity to environmental change. The results show that, through the learning process, functional disconnection between distinct network levels simultaneously lowered the precision of sensory information and higher-level prediction. These changes caused the robot to exhibit sensory-dominated and sensory-ignoring behaviors ascribed to sensory hyperreactivity and hyporeactivity, respectively. Furthermore, local functional disconnection at the sensory processing level similarly induced hyporeactivity due to low sensory precision. These findings suggest a computational explanation for co-existing sensory hyper- and hyporeactivity and insights at various levels of understanding in neurodevelopmental disorders

Neural network modeling of altered facial expression recognition in autism spectrum disorders based on predictive processing framework

Background The mechanism underlying the emergence of emotional categories from visual facial expression information during the developmental process is largely unknown. Therefore, this study proposes a system-level explanation for understanding the facial emotion recognition process and its alteration in autism spectrum disorder (ASD) from the perspective of predictive processing theory. Methods Predictive processing for facial emotion recognition was implemented as a hierarchical recurrent neural network (RNN). The RNNs were trained to predict the dynamic changes of facial expression movies for six basic emotions without explicit emotion labels as a developmental learning process, and were evaluated by the performance of recognizing unseen facial expressions for the test phase. In addition, the causal relationship between the network characteristics assumed in ASD and ASD-like cognition was investigated. Results After the developmental learning process, emotional categories emerged in the natural course of self-organization in higher-level neurons, even though emotional labels were not explicitly instructed. In addition, the network successfully recognized unseen test facial sequences by adjusting higher-level activity through the process of minimizing precision-weighted prediction error. In contrast, the network simulating altered intrinsic neural excitability demonstrated reduced generalization capability and impaired emotional categorization in higher-level neurons. Consistent with previous findings from human behavioral studies, an excessive precision estimation of noisy details underlies this ASD-like cognition. Conclusions These results support the idea that impaired facial emotion recognition in ASD can be explained by altered predictive processing, and provide possible insight for investigating the neurophysiological basis of affective contact