Is Autism Monocausal?

A monocausal explanation of Kanner’s syndrome is in the literature for 42 years but got ignored for most of the time. According to it, a single functional termsuffices to characterize the syndrome: “smile blindness.” Smile blindness means that the caretaker’s smile seen by the child has no directly rewarding effect. As a consequence, a certain interactional positive feedback – called reward cycle – cannot build up in the interaction between the children with the caretaker. For an ordinary child, by contrast, the displayed momentary happiness of the parent acts as a strong reward. This “interactional interpretation” of deep autism is not incompatible with the findings of a recent study showing that in a fraction of autistic children, several genes are mutated, one of which is MYO9B which plays a key role in dendritic arborization. 

And a related study focuses instead on MIB1 which encodes an E3 ubiquitin ligase critical for neurogenesis which in turn is regulated by miR-137, a microRNA that regulates neuronal maturation. Such low-level neuro-biochemical observations are hoped to date to be helpful in better understanding the causal mechanism as to why autistic children do lack the faculty of “associating the smile with the reward cycle”. Baron-Cohen et al’s famous diagnosis – “absence of a theory of mind”– is currently attempted to be explained in terms of such an underlying biochemical failure, which approach is no doubt far from misleading.