Several years ago I corresponded with a parent (let’s call him Jim) who was interested in our findings of disturbed cortical organization in the brains of autistic individuals. The cerebral cortex is made of repeating circuits, called minicolumns, that depending on how they are connected provide for the emergence of higher functions like judgment, face recognition, and language. In our research we had discovered that these units were more numerous and malformed in autistic individuals. The finding made sense to Jim, but he still had some qualms about the same. He had consulted about them with a member of the MIND institute who stated categorically that minicolumns did not exist and the findings were therefore invalid.
It is interesting that I have given numerous lectures, including plenary presentations, and this concern or criticism has never been brought to my attention. I am presently editing a book on minicolumns to be published by Springer. The book is based on a conference that I chaired and among 15 invited speakers, 3 were members of the National Academy of Sciences. At present the validity of the minicolumnar construct can’t be denied and has been validated by numerous investigators using a variety of techniques. There are now numerous articles from the anthropological literature that attest as to how changes in this structure account for some of the evolutionary gains of our species. I think the most important work in this regard has been done by Oleg Favorov and more recently still by Ioan Opris. Among other things there is now direct proof that the emergence of working memory stems directly from the function of minicolumns. Working memory refers to the property of the brain by which it can transiently hold on to information in order to manipulate the same. It is essential for our ability to imitate, communicate via gestures or empathize with others.
The turn around in thinking about minicolumns is a throwback to Schopenhauer’s pessimistic view about human nature. Schoenhauer claimed that certain findings, important ones, will be denied vehemently at first but, later on, when they are proven correct, the same critics will claim that the findings were well known all along. Just to say that criticisms change and shift rather than get corrected. The overall result is almost like trying to hit a moving target. Researchers have their own pet ideas and rarely read anything from the medical literature that may contradict the same. A Google search as to “what is the cause of autism” brought me close to 55 million hits. One example, high on the list of possibilities, is how the immune system attacks the brain “thus” causing autism. We have to stretch our own credibility to accept for granted this supposition. There are many missing steps between an autoimmune reaction and “thus” causing autism.
I think that the proliferation of causative theories for autism is based on the fact that different authors have not been forced to explain observed and corroborated findings when discussing their ideas. Among some credible information is the fact that the brains of autistic individuals experience growth during early postnatal years that far surpasses that of neurotypicals. Microscopically there is ample evidence of migratory disturbances (of primitive neurons) and focal cortical malformations. Evidence from neuroimaging and electrophysiology attest to disturbances in the connectivity of the cerebral cortex. These findings serve to explain the presence of seizures and sensory abnormalities in autism. They have also suggested the possibility of medical interventions (e.g., rTMS). How would an autoimmune disorder explain the previous findings? Maybe it could, but thus far proposing authors have not even attempted to do so.
I would say that before authors propose any theories on causation that they should try to explain how their ideas explain (or are related) to observed abnormalities.
I just published a review article in the journal Brain entitled: Prefrontal cortical minicolumn: from executive control to disrupted cognitive processing (doi:10.1093/brain/awt359). The same is a rather technical explanation as to how minicolumns are involved in higher cognitive functions, and how their function is disturbed in pathological states. Anyone interested in obtaining a copy can email me directly at email@example.com