The Minicolumnopathy of Autism

Abstract

The organization of the cerebral cortex is centered around a modular construct. The smallest module capable of information processing is the minicolumn. Recent studies on minicolumnar morphometry using either pyramidal cell arrays or the gray level index (GLI) suggest distinct abnormalities of this structure in several psychiatric conditions including schizophrenia, dyslexia, and autism. More specifically, minicolumns in autism as compared to controls seem thinner and more numerous. An increased number of minicolumns indicates the supernumerary division of periventricular germinal cells. A reduction in size of pyramidal cell somas within affected minicolumns suggests a bias towards shorter corticocortical connectivity. Compartmentalization of the minicolumn indicates that the majority of the deficit is found within the peripheral neuropil space. This compartment includes, among other things, many of the inhibitory elements of the cerebral cortex and provides the so-called “shower curtain of inhibition” to the minicolumn. Laminae studies indicate that in autism the peripheral neuropil defect extends the width of the cerebral cortex. A possible explanation to the above described minicolumnar abnormalities is the heterochronic division of germinal cells. Neuroblasts generated from heterochronic divisions of germinal cells can give rise to heterotopias and dysplastic cortical lesions. Once the radially migrating neuroblasts (future pyramidal cells) reach the cortex they develop asynchronously from tangentially dividing neuronal elements (interneurons). The resultant excitatory/inhibitory imbalance may provide for seizures and sensorimotor abnormalities