ABSTRACT
This chapter examines evidence for a disorder of the intrinsic motive processes of the purposeful self in autism spectrum disorder, which leads to weakening of shared experience in early childhood. Changed motor and affective regulations that identify autism are traced to faults in neurogenesis in the core brainstem systems of the fetus. These fundamental systems have evolved to serve the development of sensory guidance for motor activity and affective regulation of projects of thought and action, including communication of intentions and feelings with other human selves.
Affective neuroscience describes subcortical organs in mammals that are responsible for the coherence of a primary conscious self-as-agent, with emotions that communicate feelings for selective sociability with other individuals. In humans, this affective consciousness is adapted as the foundation for active engagement of an infant with a world of objects and people by expressions under the control of shared rhythms of an “intrinsic motive pulse.” We give primary importance to the disorder in autism of the accuracy of timing in this resonant central nervous system, responsible for coordination of movement with companions. We relate this understanding of the disorder to problems in the monitoring of prospective regulation of actions of the conscious self by a body-related affective valence, which affects the arousal of personal satisfaction of purposes or anxiety at their failure, and engagement in affectionate or antagonistic relations. This leads to evaluation of participation in movements with shared feelings for therapy and teaching to help the socioemotional development and learning of children with autism, as well as provide advice for lifetime care.
In autism, the essential embodiment of early childhood experience for growth of knowledge, skill, and collaborative social understanding appears weakened by a sensorimotor deficit in motivation and its affective control. This has lifelong developmental consequences, affecting the intersubjective responses of family, and then cooperative attentions of companions and teachers in the community. Miscoordination of movements leads to frustration, distress, and anxiety, creating social withdrawal and avoidance, or overcompensations expressed as increased arousal and hyperactivity. Indeed, we propose that disabilities in cognitive intelligence and language are secondary to weakness in the prospective control of movements with affective appraisal of anticipated experiences.
We identify the origin of these symptoms in disorders of brainstem mechanisms that develop in the late embryo stage and that are essential for motor and affective regulations, as well as autonomic processing. In particular, data indicate an anatomical and functional disruption of the inferior olive, associated with control of motor timing by the cerebellum, and abnormal development of the neighboring nucleus ambiguus, involved in expressions of social engagement and speech. These nuclei appear to be critical components of the core neuropsychological system that develops abnormally to produce the varied autistic spectrum disorders.
We draw attention to the limitations of research methods in neuroscience and psychology that seek to identify a primary cognitive, information processing, and neocortically mediated disorder by testing the response of the individual in artificial situations. New research using microkinesic descriptive methods clarifies motor deficits that characterize autism. Furthermore, extensive imaging of brain activities supports a philosophical psychology of embodiment that elucidates how confusion in unconscious prospective control of actions from fetal stages impairs the child’s developing subjective agency. Finally, we offer information on movement-based therapies that can help to facilitate learning, self-regulation, and pleasure in social interaction for individuals with autism spectrum disorder.
