A decade ago, the neuropathology of schizophrenia was an aging tortoise being overtaken by the young hare of molecular genetics. The smart money was on positional cloning finding the schizophrenia gene(s), after which the pathobiology of the disorder would finally be revealed. The race, however, has taken a different turn. The hare is no longer sure what race it is in, nor where the finishing line is.¹ Meanwhile, the tortoise has found a new turn of speed, aided by the stiffening breeze of MRI evidence for structural abnormalities,² new techniques, and better methodologies.³ Although no findings akin to a diagnostic lesion have been identified, there is an increasingly convergent body of data that cytoarchitectural alterations in the cerebral cortex accompany the disorder.⁴ By cytoarchitectural is meant aspects of neuronal structure and distribution, such as perikaryal size, shape, density and laminar position, as well as differences at the level of the . . . [Full text of this article]