Schizophrenia as a social brain disorder In recent decades there has

Schizophrenia as a social brain disorder in recent

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Schizophrenia as a social brain disorder In recent decades there has accumulated a significant evidence base from a range of research methodologies supporting the notion of social brain dysfunction in schizophrenia. Neuropsychological, functional and structural imaging and clinical approaches all confirm the centrality of social brain dysfunction in a syndrome that we might term: ‘natural kind schizophrenia.’ In other words, when social brain dysfunction is taken as the core diagnostic and pathological phenomenon, there exists a clinical entity that is empirically amenable to study as a ‘bounded and objectively real natural kind.’ A summary of this evidence is presented in Table 2. Table 2: Evidence for social brain dysfunction in schizophrenia Methodology Major Findings Key References Ethological observations Problems with interpersonal nonverbal behaviours (e.g. poor eye contact, little eyebrow movement, few upper face movements, low scores on pro-social behaviour, gesture and displacement activities.) Pitman et al 1987 Krause et al 1989 Troisi 1999 Troisi et al 1998 Brüne 2003 Neuropsycholo gy Impairment of social cognition and theory of mind ability (e.g. eye gaze and facial affect recognition deficits, general emotion recognition deficits, impaired mentalization and ‘mind-reading’ ability with social perception and attributional errors.) Frith 1994 Corcoran et al 1995 Doody et al 1998 Sarfati et al 1999 Pickup & Frith 2001 Leonhard & Corrigan 2001 Brüne 2003 Pinkham et al 2003 14
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Functional Imaging Social cognition activation paradigms show functional abnormalities in a network comprising the dorsolateral-prefrontal, orbitofrontal paracingulate and inferior parietal cortices, the superior temporal and lateral fusiform gyri and the amygdala. This has been termed ‘functional dysconnectivity’ in schizophrenia. Friston et al 1991 Frith et al 1995 Friston & Frith 1995 Fletcher et al 1999 Russell et al 2000 Streit et al 2001 Honey et al 2002 Pinkham et al 2003 Lee et al 2004 Amodio & Frith 2006 Structural Imaging MRI and diffusion tensor DT-MRI show structural abnormalities of the same prefrontal, temporal and parietal association areas listed above as well as disruption of white matter fascicule connecting these regions – so-called ‘structural dysconnectivity.’ Lawrie & Abukmeil 1998 Buchsbaum et al 1998 Gur et al 2000 Szeszko et al 2000 Wright et al 2000 Sigmundsson et al 2001 Agartz et al 2001 Kubicki et al 2002 Burns et al 2003 Clinical evidence ‘Negative symptoms’ incorporate many aspects of social cognition and behaviour, correlate with structural and functional deficits in prefrontal and limbic structures and predict poor course and outcome in schizophrenia. Tamminga et al 1992 Ross & Pearlson 1996 Kirkpatrick 1997 Gur et al 2000 Sanfilipo et al 2000 Sigmundsson et al 2001 Couture et al 2006 Resolving the ‘schizophrenia problem’ – in evolutionary terms The ‘schizophrenia problem’ can be described in terms of the failure of a century’s observations and research to converge on a ‘natural kind’ that is empirically valid and meaningful as a biological phenomenon. I have argued that this frustrating lack of cohesion and agreement and the resultant confusion and controversy aroused by the concept is in part a result of the 15
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