In autism, there are minicolumnar abnormalities in the frontal and temporal lobes of the brain.

The minicolumn is a continuing source of research and debate more than half a century after it was identified as a component of brain organization. The minicolumn is a sophisticated local network that contains within it the elements for redundancy and plasticity. Although it is sometimes compared to subcortical nuclei, the design of the minicolumn is a distinctive form of module that has evolved specifically in the neocortex. It unites the horizontal and vertical components of cortex within the same cortical space. Minicolumns are often considered highly repetitive, even clone-like, units. However, they display considerable heterogeneity between areas and species, perhaps even within a given macrocolumn. Despite a growing recognition of the anatomical basis of the cortical minicolumn, as well as its physiological properties, the potential of the minicolumn has not been exploited in fields such as comparative neuroanatomy, abnormalities of the brain and mind, and evolution.

The modular arrangement of the neocortex is based on the cell minicolumn: a self-contained ecosystem of neurons and their afferent, efferent, and interneuronal connections. The authors' preliminary studies indicate that minicolumns in the brains of autistic patients are narrower, with an altered internal organization. More specifically, their minicolumns reveal less peripheral neuropil space and increased spacing among their constituent cells. The peripheral neuropil space of the minicolumn is the conduit, among other things, for inhibitory local circuit projections. A defect in these GABAergic fibers may correlate with the increased prevalence of seizures among autistic patients. This article expands on our initial findings by arguing for the specificity of GABAergic inhibition in the neocortex as being focused around its mini- and macrocolumnar organization. The authors conclude that GABAergic interneurons are vital to proper minicolumnar differentiation and signal processing (e.g., filtering capacity of the neocortex), thus providing a putative correlate to autistic symptomatology.

All subcortical arrangements are primarily nuclear in type. The cortex has been the first part of the brain to evolve a radial and laminar arrangement of cells. The resultant modular arrangement is based on the cell minicolumn: a self-contained ecosystem of connectivity linking afferent, efferent, and inerneuronal connections. Recently, the cell minicolumn has been found to be abnormal in patients with autism. This article relates different aspects of the cell minicolumn and larger-scale neuronal assemblies to potential research techniques and their application to clinical practice.

Gross analyses of large brain areas, as in MRI studies of macroanatomical structures, average subtle alterations in small regions, inadvertently missing significant anomalies. We developed a computerized imaging program to microscopically examine minicolumns and used it to study Nissl-stained slides of normal human, chimpanzee, and rhesus monkey brains in a region of the planum temporale. With this method, we measured the width of cell columns, the peripheral neuropil space, the spacing density of neurons within columns, and the Gray Level index per minicolumn. Only human brain tissue revealed robust asymmetry in two aspects of minicolumn morphology: wider columns and more neuropil space on the left side. This asymmetry was absent in chimpanzee and rhesus monkey brains.