Autism Biomedical Information Network



What is autism? A biomedical perspective...


Overview

The "social force vector"
Evolutionary biology of autism
The mind has a modular design
The language subsystem
The mini-module of socially-motivated learning
The theory of "theory of mind"
Autism as a neurodevelopmental disorder
Genetic and nongenetic factors

The "social force vector"

My own view is that autism is the absence, or profound diminution of the intensity, of the innate biological drive to "connect" with other human beings. Researchers in cognitive neuroscience might refer to this as an impaired affiliative drive. For most of us, our daily lives are dominated by our social nature. It is as if there is an irresistible magnetic force that naturally draws people together. This primal "force of nature" is like a vector pointing from one person to another, tending to draw them irresistably together. The word, vector, is a term used in physics that denotes direction and magnitude of force. In the sense I am using it, it is usually a force of mutual attraction between two people. It is reinforced by the feeling of taking pleasure in the company of another person in all its mutuality. However, we know from daily experience that even among "typical" people, that this social attractive-force vector varies in intensity. We all know people who are very "social, " gregarious, and like to be around people. However, we also know people who prefer to be alone and have rather solitary lives. They may be exceedingly awkward in social situations and have anxiety to the point of social phobia. Autism may be at the extreme end of this continuum.

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Evolutionary biology of autism

Sadly, the "social force vector" is the piece that's missing in autism. It is not a trivial piece. It has firm roots in the deep structure of the mind and it has become embedded in our basic nature as a consequence of some 5 million years of evolution (see abstract of my paper in the Proceedings of the 1996 Annual Conference of the Autism Society of America, Milwaukee). Highly nuanced social processing was essential for the survival of early human societies that depended on cooperative group living. At least in part this was probably a way to recruit other persons in the task of child-rearing in view of the relatively long period of helplessness and dependency of human infants. This also served the ends of avoidance of conflict, social control within the group, and negotiating trade and territorial limits with other groups. High-level communication was also necessary to organize hunting and foraging expeditions to promote survival of the clan. It was also essential for the purpose of preserving and transmitting experience-based knowledge and traditions (wisdom) to succeeding generations. And, of course, language is important for gossip (as engagingly discussed by Robin Dunbar in "Grooming, Gossip, and the Evolution of Language," Harvard University Press, 1996).

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The mind has a modular design

If the mind has a modular design, as is believed by some (refer to the writings of John Tooby and Leda Cosmides; their term is "neural automata"), then the many modules concerned with social cognition are profoundly impaired in autism. After all, persons with other types of developmental disability are socially-capable if not always socially-competent (for example, Down's syndrome). They want to be around their family and friends. The modules that subserve social cognition are so basic to human nature, that their absence means, at least to me, a profound neurobiological ":amputation." I don't mean an actual grossly evident neurological lesion. The modules for social cognition are not in any one place but map topologically to many brain regions, although it is likely that certain structures in the temporal lobe play a key role (the amygdala, among others). Obviously the structural changes in the brain would be subtle, as is evident from Margaret Bauman's neuropathologic studies.

Arrayed around the core of a diminished biological urge to "connect" with other human beings, are other impaired social cognition modules. Language is the most obvious. After all, language is the quintessential tool for communication and building relationships. Other modules include socially-motivated learning, socially-defined behavioral self-regulation, abstract metarepresentational thinking about other peoples minds (theory of mind), the ability to observe and then imitate typical human behavior, and the ability to sequence movement in ways that emulate typical body movements. These all flow out of and, in fact, are intrinsic to the complex neurobiology of social cognition.

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The language subsystem

An integral component of the social cognition system is the language subsystem which is markedly impaired in autism. Competency in language is uniquely basic to human nature and to the imperative of building and maintaining cooperative relationships that, in evolutionary terms, favored survival of the clan. The ability to generate subtly nuanced affect-loaded expressive language is severely impaired in autism. Also, on the input side, there is a marked impairment of the ability to decode verbal and nonverbal social signals as cues for behavioral self-regulation (or "co-regulation," to use the term of Lynn Waterhouse). It is as if the person with autism does not have a "social rules look-up table" to guide him or her through social situations.

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The mini-module of socially-motivated learning

We all know how difficult it is to "teach" children with autism. This flies in the face of the powerful drive by even-young infants to mimic and reproduce behaviors modelled by those around them and to seek the positive reinforcement of approval from their caretakers. There is probably a mini-module for learning by imitation which is reinforced by praise, love, and affection. This is yet another component of the social cognition system that is impaired in autism.

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The theory of "theory of mind"

Although I will have more to say about this at a later time, it is believed that persons with autism are unaware of the mental life of other persons (see "Mindblindness" by Simon Baron-Cohen, MIT Press, 1995). They are oblivious to the language of "mentalese" in others, i.e., thoughts, feelings, abstractions and imaginings that are at the core of the "interior life" of another person. This may be thought of as an impairment in perspective-taking. i.e., an inability to imagine what it is like to be "in someone else's shoes" or to adopt the point of view of another person. A person with autism may be unaware of the personal distress signals in other persons and also be unable to generate an empathic behavioral response. An everyday example of "mindblindness" is the scenario when a teacher in a classroom says something to the entire class. The child with autism believes that the teacher is speaking only to him or her.

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Autism as a neurodevelopmental disorder

This view considers autism a neurodevelopmental disorder, present but undetectable at birth, arising during fetal life as critical stages of neuronal cell differentiation and migration unfold in a pre-programmed sequence. Certain neural cell clusters become task-specialized for different aspects of social cognition. Some of these clusters (or convergence zones) tie mini-modules together so that a coherent internal image of a discrete social cognition event collocates in the mind-brain (for example the smile of recognition by an infant of his mother). In this view, autism arises as a consequence of the failure to develop the full complement of "hard wiring" or neuronal circuitry (or a specialized subset of neurotransmitter receptors) that ties all these pieces together. The end result is that a pleasure-based biological imperative to connect with other human beings in the fullest sense of mutuality of love, warmth, and caring is severely affected in autism. (I will have a commentary later on the child with autism who is apparently "normal" at birth but appears to regress later, sometimes attributed to a coincidence, such as a recent immunization).

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Genetic and nongenetic factors

It is clear from the existence of families with more than one child with autism that there is a strong genetic influence. Currently there are a number of gene-mapping studies in progress which have yielded suggestive data but definitive results are not yet available. However, it appears that the mechanism of inheritance is complex and may involve several genes. Possible gene defects might include effects on the production of nerve cell growth factors or "guide wire" substances that direct nerve cell migration.

Although most instances of autism appear to be sporadic and "idiopathic," a minority of cases may be associated with single-gene disorders (for example, tuberous sclerosis or PKU) or may be a consequence of maternal viral illness early in pregnancy affecting the fetal brain during a critical stage of neurodevelopment.

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Commentary by Ronald J. Kallen, M.D., ©1999
This page last updated on 2/8/99