CLINICAL HANDBOOK OF SCHIZOPHRENIA

92 I. CORE SCIENCE AND BACKGROUND INFORMATIONfunctions (Zec, 1995). For instance, Kraepelin viewed problems in volition or will as centralto this disorder. He also put substantial emphasis on the role of attentional deficits;for instance, he distinguished between “active attention” (aufmerksamkeit), which he assertedis impaired at all stages of the illness, and “passive attention” (auffassung), whichhe described as being mostly impacted in acute stages of the illness.Despite the awareness of cognitive deficits in schizophrenia from its earliest conceptualization,some of the prominent theories of schizophrenia in the United States in themid–20th century were strongly influenced by psychoanalytic and interpersonal theoriesabout the etiology of the illness, the popular (although not universal) notion being thatschizophrenia was a “functional” (as opposed to “organic” or neurological) condition. Aparticularly notorious theory that arose in the 1930s was that of the so-called schizophrenogenicmother. This concept had roots in the writings of several influential figuresin the early to mid–20th century (reviewed in Hartwell, 1996). For instance, Sullivan positedthat personality is shaped by early interpersonal relationships, especially with themother, and that schizophrenia is a result of pathological early relationships. Similarly,Levy concluded that an “overprotective mother” played a major etiological role in herchild’s later development of schizophrenia. It is interesting to note that while Americanpsychiatry was emphasizing psychodynamic and interpersonal models of schizophreniaaround the 1930s, Freud began emphasizing the neurobiological underpinning of thiscondition, and noted that patients with schizophrenia appeared to have a hereditary predispositionto the illness.It would be a mischaracterization to suggest that the biological basis of schizophreniawas not recognized in American psychiatry. Practices, such as fever or seizure induction,as well as brain surgery (e.g., frontal lobotomy) before the introduction ofneuroleptic medications in the 1950s clearly speak to 20th-century recognition of the involvementof the brain in the manifestation of symptoms of schizophrenia. The introductionof neuroleptic medications in 1952, and their increased use thereafter, as well as therise of the dopamine hypothesis, also fostered wider recognition of schizophrenia assomething more than a “functional” disorder. However, full appreciation of the importanceand central role of cognitive deficits in schizophrenia has only emerged on a widespreadbasis within the last few decades, with exponential growth in neuropsychologicalresearch consistent with the wider recognition of the importance of cognitive deficits inschizophrenia. Indeed, harkening back to Kraepelin, some have suggested that schizophrenia,at its core, may be a neurocognitive disorder.THE NATURE OF COGNITIVE DEFICITS IN SCHIZOPHRENIAPatterns and Level of Cognitive ImpairmentThe substantial growth in the empirical literature of neuropsychological deficits inschizophrenia over the past two to three decades has shown that the majority of patientswith schizophrenia have mild-to-moderate neuropsychological deficits. Heinrichs andZakzanis (1998) conducted a meta-analysis of 204 studies of cognition in schizophreniaand concluded that 60–80% of patients with schizophrenia have at least mild neurocognitivedeficits. That figure is consistent with findings from our research group, showingthat about a quarter of patients with schizophrenia continue to function in the “normal”range of neurocognition (Palmer et al., 1997). No single pattern of deficits is unique orcommon to all patients with schizophrenia, but some of the most frequently impairedabilities include attention, working memory, visual and verbal learning, psychomotorspeed, and executive functions.