The ‘Connectivity’ Link between Autism and Dyslexia
Posted Nov 04 2009 10:01pm
by Emily L. Williams
In an article currently in press in The Journal of Autism and Developmental Disorders, University of Louisville researcher, Dr. Manuel Casanova, provides tantalizing evidence supporting his theory of altered neural connectivity in dyslexia. Casanova proposes that the underlying deficits in dyslexia are due to an increase in long-range connections and a matched decrease of short-range connections. This piggy-backs his earlier research on autism, in which his team reported decreased long-range and increased short-range connectivity in the autistic brain, the opposite as seen in dyslexia.
In a media article in the Louisville Courier-Journal, Casanova stated that this underlying ying-and-yang of autism and dyslexia is a novel theory of relatedness of the two conditions, possibly leading to an explanation of common underlying mechanisms, as well as potentially leading the way to additional treatments for both conditions utilizing Transcranial Magnetic Stimulation (TMS). Already, results from Casanova’s rTMS autism trials have shown promising results in reducing sensory hypersensitivity and general social anxieties, while at the same time retaining those abilities and talents people in the online autistic community have continually expressed concern over losing if treated.
Casanova also promotes the idea that conditions like autism and dyslexia are “differences” and not necessarily “disabilities”. “They just have different cognitive styles,” he says—a stance which those in the pro-Neurodiversity camp have long since supported.
In another article currently in press in the journal, Medical Hypotheses, this author and Casanova have published a more coherent theory briefly exploring the complementary wiring of autism and dyslexia, proposing that the conditions exemplify the extremes of a diverse human bell curve of neural connectivity. The article, rather than labeling them as discrete conditions, suggests that autism and dyslexia are part of the typical diversity of humanity. The bell curve idea, while not new to the study of trait inheritance, is a novel perspective linking autism and dyslexia, a perspective in which studying peoples’ similarities rather that their differences may lead to a greater understanding of diversity and help remove such developmental research from the pathology paradigm of traditional medicine.
Individuals familiar with autism may be aware that dyslexia can also co-occur with autism and therefore may be wondering how the two conditions can be the “same” and “different”. In the new 2009 paper, this concern is addressed, saying that while autism and classic dyslexia are anatomical opposites, the underlying neurobiology of either extreme can cause a disability in reading. Therefore, while classic dyslexia is due to increased long-range/decreased short-range neural connections, the dyslexia associated with autism is due to increases in short-range/decreases in long-range white matter fibers. Since autism and dyslexia are still currently defined by behavioral criteria, this explains how it’s possible to have similar behavioral traits and divergent anatomies.
Casanova plans to continue to research and publish on the idea of the yin-and-yang of conditions like autism and dyslexia. With recent grant funding from the NIH, he also intends to continue exploring the benefits of TMS in improving peoples’ lives while helping them retain the positive aspects of their personalities that make each person a unique part of the human continuum.
Casanova et al. (2009). Increased white matter gyral depth in dyslexia: Implications for corticocortical connectivity. Journal of Autism and Developmental Disorders, in press.
Casanova & Trippe. (2008). Radial cytoarchitecture and patterns of cortical connecitivity in autism. Philosophical Transactions of the Royal Society B, 364 (1522), 1433-1436.
Williams & Casanova. (2009). Autism and dyslexia: A spectrum of cognitive styles as defined by minicolumnar morphometry. Medical Hypotheses, in press.