ABSTRACT
Despite over a century of painstaking work, the pathophysiological substrate of schizophrenia remains poorly elucidated. The lack of progress in our understanding the neurobiological basis of this illness is partly related to uncertainty in its clinical boundaries; the question of what precisely constitutes schizophrenia has been a matter of debate, and different theorists have varied about its “core” disturbance. In the early twentieth century, Emil Kraepelin believed that the unifying aspects of this illness are its chronicity and declining course (Tandon et al. 2009). Eugene Bleuler (1911) argued that the central feature of this illness is the “splitting “of mental functions, which leads to a tetrad of symptoms, including disturbance of association, disturbance of affect, autism (social withdrawal) and ambivalence. Kurt Schneider (1959), who considered the fundamental disturbance in schizophrenia to be one of ego boundaries, proposed a set of “first rank” symptoms, such as passivity phenomena, representing self–other boundary diffusion. The World Health Organization International Classification of Diseases (ICD; www.who.int/classifications/icd/en) and the American Psychiatric Association Diagnostic and Statistical Manual of Mental Disorders (DSM; www.psychiatry.org/practice/dsm) used a combination of these cross-sectional and longitudinal clinical features to create a definition of schizophrenia for widespread use in clinical practice.
