Introduction

In Kanner’s (1943) original description of infantile autism, he conjectured that the disorder was based in an “innate inability to form the usual, biologically provided affective contact with people” (1943, p. 250). He regarded the disorder as inborn, rooted in the constitution of the mind, rather than learned or acquired through experience. Kanner later abandoned this biological perspective in favor of one that emphasized the role of environmental factors, and in particular he implicated emotionally cold and unavailable parents as an important causal influence (Kanner, 1949). This “psychogenic” viewpoint was embraced by psychiatry and went largely unchallenged for many years. However, factions in psychiatry (e.g. Van Krevelen, 1958) and psychology (e.g. Rimland, 1964) began to voice strong opposition to this theory, arguing instead that the disorder resulted from profound central nervous system dysfunction of unknown origin.

The biological perspective subsequently gained support from observations that children with what is now termed autistic disorder (AD) had a raised prevalence of certain minor physical anomalies (Walker, 1977; see Ozgen et al. (2010) for a recent review) and were more likely to demonstrate positive findings on neurologic examinations. Schain and Yannet (1960), for example, reported a high frequency of seizure disorder in their cohort of 50 children with autistic disorder attending a residential school for children with mental retardation. As pediatric neurologists, they highlighted the role of limbic dysfunction in epileptogenesis and speculated that AD may be based in limbic system damage or maldevelopment. In support of this assertion, they disclosed the results from a single autopsy case whose “only neuropathologic findings consisted of dropping out of cells in the hippocampal formation” (p. 565).