Cognitive impairments are a core feature of schizophrenia, and are a royal road to follow in investigating neurobiological impairments as well as models of pathogenesis in this illness. The dominant model of schizophrenia during the past century has been the Kraepelinian concept of a degenerative disease, based on observations of cognitive decline, and captured in the term dementia praecox. However, the view that abnormal neurodevelopment may underlie schizophrenia has been gaining acceptance in recent decades. This idea is not new; the observation of defi cits in social interaction as well as premorbid signs in childhood was noted by Bleuler and Kraepelin (see Malmberg, Lewis, David, & Allebeck, 1998; Marenco & Weinberger, 2001) and Clouston (1891) who observed developmental dysmorphic abnormalities, such as high arched palate, in patients he considered as having “adolescent insanity.” Southard at the Boston Psychopathic Hospital (now the Massachusetts Mental Health Center) observed brain changes in schizophrenia that were attributed to developmental deviations (Casanova, 1995). Bender (1953) and subsequently Fish and Hagin (1972) argued that schizophrenia might refl ect a developmental “encephalopathy.”