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Fortunately, there have been a number of excellent meta-analytic reviews published over the past decade, integrating the literature comparing test performance among schizophrenia patients and healthy comparison subjects (Dickinson et al. 2005; Heinrichs and Zakzanis 1998; Mesholam-Gately et al. In addition to their own meta-analytic review of individual studies, Dickinson et al. 538) that serves as a summary of meta-analytic reviews (see also Reichenberg and Harvey 2007).
Goldstein 1990a, 2009), and someone well aware of the effects brain damage can have on abstraction ability (Goldstein 1949; Goldstein and Scheerer 1941), emphasized the psychological, not neurobiologic, aspects of what he called the impairment in “abstract attitude” among persons with schizophrenia (Bolles and Goldstein 1938; Goldstein 1939, 1959).
2008), and one that is at least usually (albeit, as discussed below, perhaps not invariably) accompanied by neurocognitive deficits (Dickinson et al. Emil Kraepelin, the first to distinguish schizophrenia () from other forms of serious mental illness, held a strongly neurobiologic conceptualization of this disorder.
As early as 1899 he commented that “From the known clinical and anatomical facts [of dementia praecox] I cannot doubt that we have to do here with a severe and as a rule markedly retrogressive process in the brain cortex” (as translated and cited by May (1931) p. In the 1913 edition of his classic textbook, Kraepelin (1971/1919/1913) discussed possible biological as well as psychosocial causes of dementia praecox, including a number of potential factors which anticipate contemporary neurodevelopmental models of schizophrenia (cf. 2005), such as hereditary predisposition and “injury to the germ” (prenatal injury), as well as commenting on minor facial and other physical anomalies which exist “with striking frequency” among such patients (p. (The latter are currently thought to reflect parallel prenatal aberrations in neurodevelopment (Weinberg et al. 2003); Kraepelin (1971/1919/1913) noted that “If it should be confirmed that the disease attacks by preference the frontal areas of the brain, the central convolutions, and the temporal lobes, this distribution would in a certain measure agree with our present views about the site of the psychic mechanisms which are principally injured by this disease” (p. Kraepelin also characterized dementia praecox as a dysfunction in what would today be labeled “executive functions,” particularly in regard to deficits of “volition” or “will” (see Zec 1995).
Some of his musings about the potential neuropathology underlying schizophrenia appear remarkably contemporary.
For example, he wrote that “There is no doubt that the clinical picture of schizophrenia contains symptoms which may best be understood as expressions of a disturbed function of some apparatus of the brain, particularly of the frontal lobes and the subcortical ganglia...” (Goldstein 1939, p. Yet, his emphasis in describing and explaining cognitive concreteness in schizophrenia remained solidly on the psychological/psychodynamic level. Goldstein (1959) noted his opinion that the abnormal concreteness in schizophrenia “” (italics in original; p. As noted above, the other primary impetus in early and mid-20th century studies of cognitive test performance in schizophrenia was to identify test performance patterns that would reliably discriminate patients with documented brain lesions (“true organicity”) from those with schizophrenia (reviewed in Heaton et al. Commenting on the difficulties in finding useful discriminatory patterns, Watson et al.