Human beings have long dwelled on their paradoxical superiority over other animals. Physically we are weaker and, overall, less adapted to the environment than other species. One might reasonably presume that any human ability that explains our dominance over other animals should reside outside our physical attributes. More specifically, our ability to communicate descriptively and abstractly has steered the search on intelligence/genius to the workings of the brain.
A drawing by Nadia, an autistic girl, when she was only 5 years of age.
Exceptional talents have been reported in a minority of developmentally delayed institutionalized patients. Arguably the incidence may be as high as 10 percent in some series of autistic individuals (Miller, 1999). Recent postmortem studies indicate the presence of a disturbance in the modular elements of the cerebral cortex (so-called minicolumns) of autistic individuals (see my previous blog at https://corticalchauvinism.wordpress.com/2013/01/26/the-cerebral-cortex-and-autism/). Minicolumns appear to be smaller and more numerous in the brains of autistic individuals. Furthermore the surrounding cells that serve to insulate transmission of signals along minicolumns is abnormal. This means that signals are able to cross over to adjacent minicolumns in a cascading fashion.
According to Gustafsson smaller minicolumns predispose autistic patients to a bias in their information processing capacity, favoring the amplification of incoming signals and their discrimination from background noise (Gustafsson, 1997). Variations in the organization of minicolumns and corresponding information processing may therefore underlie some of the outstanding abilities observed in certain autistic individuals.
Several years ago I had the opportunity to examine the brains of 3 distinguished neuroscientists along with a number of age sex-matched neurotypicals from an established brain collection. We used the same computer methods that had been reported in the study of autistic individuals.
The figure illustrates how a computer program is able to identify minicolumns in the cerebral cortex that would otherwise be difficult to discern with the human eye.
The focus of our research was the implementation of a new paradigm in the study of intellectual achievements: variations in the shape and organization of minicolumns. Although none of the reported scientists manifested autistic-like symptomatology, their minicolumnar profiles offered similarities to those previously reported in autism. In effect, the minicolumnar width in our neuroscientists were markedly reduced as compared to the group of controls.
Both comparison and subject cases were derived from the Yakovlev–Haleem collection of the Armed Forces Institute of Pathology (AFIP). Subjects included scientists who died at 58, 84, and 89 years of age. Comparison participants consisted of six subjects aged 44, 50, 71, 72, 86, and 98 years. Although personal history and interviews with those who knew these scientists emphasize their wide range of knowledge (polymaths) and divergent thinking, no claim is presently made regarding their intelligence or creativity. Pathological examination was negative with the exception of degenerative changes consistent with aging in the brains of our oldest scientist and comparison participants. Just as in autistic individuals, computerized image analysis showed significant reductions of minicolumnar width in all areas of the brain examined (Casanova et al., 2002).
Computer modeling suggests the adaptive nature ingrained in having smaller minicolumns. According to these studies, narrower columns favor discrimination. In other words, the information processing system that weighs signal and noise has been tweaked in favor of the signal (Gustafsson, 1997). Focused attention and obsessive preoccupation may lead to rote practice and development of specific talents typically related to superior memory or speed of processing. A minicolumnar phenotype that provides for discrimination and/or focused attention may help explain the savant abilities observed in the intellectually gifted.
The medical literature draws many suggestive links between the intellectually gifted and the mentally marginalized individual. It has been claimed, but not proven, that savant skills are seen in approximately one of every 10 people with autism. Of the known savants with developmental disorders, half have autism. Unsurprisingly, the ‘weak central coherence’ characteristic of autistic perception and cognition allows for unusual and unexpected associations. The resultant ability to manipulate highly organized domain-specific data offers parallels to field independent and divergent thinking that characterizes the originality of autistic thinking and that of the savant. It is this close juxtaposition of signs and symptoms that Andreasen has labeled as ‘living on the edge of chaos’ (2005, p. 31). In this regard we may fittingly conclude that, ‘One of the most important lessons to be learned from the genetic study of many diseases in recent years has been that the paradoxically high frequency of certain conditions is explained by the fact that the important advantages conferred on those who carry the predisposition to these conditions may outweigh the obvious dramatic disadvantages’ (Geschwind as quoted by West, 1997, p. 20).[As an side, I am tempted to disclose that one of the subjects within our study was Norman Geschwind himself]
Andreasen NC. The Creating Brain. NewYork: Dana, 2005.
Casanova MF, Buxhoeveden D, Switala A, Roy E. Minicolumnar pathology in autism. Neurology, 58:428-432, 2002.
Casanova MF, Switala AE, Trippe J, Fitzgerald M. Comparative minicolumnar morphometry of three distinguished scientists. Autism 11(6): 557-569, 2007.
Casanova MF, Trippe J. Radial cytoarchitecture and patterns of cortical connectivity in autism. Proceedings of the Royal Society 364: 1433-1436, 2009. Another useful article of interest in regards to splinter and savant skills and their putative explanation through the organization of the cerebral cortex.
Gustafson L. Inadequate Cortical Feature Maps: A Neural Circuit Theory of Autism, Biological Psychiatry 42: 1138–47, 1997.
Miller LK. The Savant Syndrome: Intellectual Impairment and Exceptional Skill’, Psychological Bulletin 125: 31–46, 1999.
Temple Grandin’s perspective on my article: http://autismdigest.com/brain-cortex-structure-similar-in-brilliant-scientists-and-autism/
West TG. In the Mind’s Eye. Amherst, NY: Prometheus.
Nice discussions on the savant syndrome in autism appear in the following 2 books:
Darold A. Treddert. Islands of Genius: the Bountiful Mind of the Autistic, Acquired, and Sudden Savant. Jessica Kingsley Publishers, 2011.
Lynn Waterhouse. Rethinking Autism: Variation and Complexity. Academic Press, 2012.
Then I wonder what causes autism if not the minicolumnar pathologoy, there would have to be something at a deeper molecular level that causes the autistics symptoms if the scientists did not have them. Also, I don’t believe that autism is one of those diseases that has stayed in the population due to adaptive benefits. It is more likely the main reason autism has stayed in the population is spontaneous mutations. If you’re familiar with Jonathan Sebat’s work, he provides some empirical evidence for this.
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Good comments. I have never said that the minicolumnar abnormalities «cause», rather it is part of the pathology. You have to integrate the findings with abnormalities in cellular migration (heterotopias), cortical malformations (so-called dysplasias). If anything the minicolumnopathy is related to changes in brain volume and corticocortical connectivity. I am hoping to provide an appropriate explanation in the coming months under the heading of a locus minoris resistentia.Best regards.
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Eric Courchesne in an interview now supports your mini-column hypothesis:
ADAM FEINSTEIN: How does your research possibly link up with other brain studies like that on mini-columns by Dr Manuel Casanova in Atlanta, Georgia?
ERIC COURCHESNE: It’s very exciting. What Casanova found was that, in autism, the brain is developing too many mini-columns too rapidly and these are nor really developing maturely. Of course, he is looking at the adult brain. There’s a lot of water that passes under the bridge between 12 months and 30 years of age. So to try to make a direct connection will require a lot more research. But in principle, it fits.
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Thanks for the comment. The interview with Eric seemingly happened many years ago. Eric went on to try and reproduce some of my findings with success (he published a postmortem series on minicolumnarity). As an aside, Adam refers to my being in Atlanta, Georgia when in reality I was working in Augusta, Georgia.
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From a naive rookie: Is it possible that mini-column density is an indirect result – i.e. a case of plasticity, possibly even a self-reinforcing feedback loop – of discrimination, intense thinking/analysis, etc, which may be common to both populations you examined?
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