Specification of Higher Cortical Functions
Patricia S. Goldman-Rakic Yale School of Medicine
One of the dramatic aspects of the behavioral profiles in autism, Turner, and Williams syndromes is that glaring deficits in one cognitive domain coexist with remarkable performance in another. The dissociation of capacity can be striking, as for instance in the capacity of Williams syndrome children to recognize faces and objects in noncanonical views although failing utterly to copy the simplest pictures of ordinary items ( Bellugi, Klima, & Sipple, 1989). Understanding of how cerebral cortex is organized both anatomically and functionally can aid in interpreting the apparent contradictions on behavioral capacity and perhaps shed light on the etiology of disorders by identifying the structures, systems, circuits, and perhaps cell classes involved in a particular condition. Such information would lead to theories of why a particular subset of structures is more vulnerable than others to a genetic or epigenetic event.
A major issue in neurobiology of particular relevance to these developmental disorders is the degree to which specific functions are strictly localized in the central nervous system. The answer to this question has varied widely over this century. Earlier in this century, Lashley ( 1929) was impressed with the lack of specificity of cortical mechanisms because relatively large lesions rarely resulted in lasting behavioral deficits. Although few neuroscientists today would deny localization of function, many still view the cortex as capable of considerable restructuring as a basis for sparing of function after cortical damage. Another school of thought adheres to the more traditional view that the brain is essentially hard-wired and its plasticity limited. Whatever view is held, it is clear that the true degree of neural and behavioral plasticity requires a thoroughgoing analysis of function allocation in the normal brain and the detailed mechanisms underlying the latitude of these