ABSTRACT
As a behavioral neurologist who has, for research purposes, taken the approach exemplified by this volume, it is appropriate for me to share the thinking that propelled such a choice. Embarking upon research into the mechanisms underlying learning disabilities, those “high-prevalence, low-severity” entities that exist in a gray zone between mental retardation and normalcy (and between syndrome and symptom), my neurological training motivated an attempt to reduce heterogeneity in the population to be studied. At which end of the selection process could such a reduction in heterogeneity be accomplished, given all the variables involved in the psychological and educational testing for learning disabilities? The decision was facilitated by the solicitation by certain groups with neurogenetic disorders to look into their learning disabilities. With this pragmatic push, it appeared logical to reduce heterogeneity in the learning-disabled population by sampling neurogenetic syndromes and thus proceeding from gene to brain to cognitive architecture to manifest learning disability. Turner syndrome (see relevant chapters in this volume) was an early example; a series of studies on the syndrome were pioneers in starting from biology and moving through neuropsychology into psychoeducational territory (Alexander & Money, 1966; Money, 1973; Shaffer, 1962). With the advances in imaging brain anatomy among the living with magnetic resonance imaging, it became possible to plan studies in which directly visualized brain architecture could be inserted in the causal chain.
