A great deal of brain research has been focused on uncovering the causes of autism – a disease of the brain striking very early on in life that often leaves children severely mentally disabled. As a result, theories of the cause of autism have been rapidly evolving. I am particularly interested in the theory that autism involves impaired cortical connectivity. This could impair the ability to integrate incoming sensory information with sensory expectations, which may be a key operation at the heart of both sensory processing and motor control. For some time now, there have been theories that autism involves problems in short-range cortical connectivity – e.g., problems with dendrite pruning. Tomorrow at Sensorimotor Journal Club, Kasra Khatibi will present a report on a study that found impaired long-range cortical connectivity in autism:
Just, M. A., Cherkassky, V. L., Keller, T. A., Kana, R. K., & Minshew, N. J. (2007). Functional and anatomical cortical underconnectivity in autism: Evidence from an fmri study of an executive function task and corpus callosum morphometry. Cerebral Cortex, 17(4), 951-961. (link to pdf of article)
The brain activation of a group of high-functioning autistic participants was measured using functional magnetic resonance imaging during the performance of a Tower of London task, in comparison with a control group matched with respect to intelligent quotient, age, and gender. The 2 groups generally activated the same cortical areas to similar degrees. However, there were 3 indications of underconnectivity in the group with autism. First, the degree of synchronization (i.e., the functional connectivity or the correlation of the time series of the activation) between the frontal and parietal areas of activation was lower for the autistic than the control participants. Second, relevant parts of the corpus callosum, through which many of the bilaterally activated cortical areas communicate, were smaller in cross-sectional area in the autistic participants. Third, within the autism group but not within the control group, the size of the genu of the corpus callosum was correlated with frontal-parietal functional connectivity. These findings suggest that the neural basis of altered cognition in autism entails a lower degree of integration of information across certain cortical areas resulting from reduced intracortical connectivity. The results add support to a new theory of cortical underconnectivity in autism, which posits a deficit in integration of information at the neural and cognitive levels.