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Mechanisms of Internalization in Schizophrenia: The Roles of Salience Dysregulation and Cognitive Dysmetria

Mechanisms of Internalization in Schizophrenia: The Roles of Salience Dysregulation and Cognitive Dysmetria

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An essay for the 2012 Undergraduate Awards (International Programme) Competition by Erin Ramsperger. Originally submitted for PSY371: Thinking and Reasoning at University of Toronto, with lecturer John Vervaeke in the category of Psychology
An essay for the 2012 Undergraduate Awards (International Programme) Competition by Erin Ramsperger. Originally submitted for PSY371: Thinking and Reasoning at University of Toronto, with lecturer John Vervaeke in the category of Psychology

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Published by: Undergraduate Awards on Aug 31, 2012
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Mechanisms of Internalization in Schizophrenia:The Roles of Salience Dysregulation and Cognitive Dysmetria
The positive symptoms of schizophrenia (hallucinations and delusions) are unique to theschizophrenic disorders, and are a particularly debilitating symptom of psychopathology (APA,2000). Salience dysregulation theory attempts to explain the presence of hallucinations anddelusions through the notion of augmented incentive salience, wherein irregular dopamineneurotransmission results in otherwise neutral or innocuous stimuli becoming salient (Berridge& Robinson, 1998; Kapur, 2003, 2004). The result is the perception of images and associationsthat do not exist (Kapur, 2003,2004). Alternatively, cognitive dysmetria theory conceptualizesschizophrenia in terms of cerebellar-cerebrum disconnectivity resulting in mis-processing of incoming information. The disconnectivity results in an inability to distinguish between internaland external sources of information, causing hallucinations and delusions (Andreasen, Nopoulos,O’Leary, Miller, Wassink, & Flaum, 1999; Andreasen & Pierson, 2008). Problematically, neither salience dysregulation theory nor cognitive dysmetria theory is capable of accounting for thedependent relationship between salience attribution and information processing. A framework  built on the basis of the wake-sleep algorithm for unsupervised learning in neural networks(Hinton, Dayan, Frey, & Neal, 1995) is proposed to facilitate the synthesis of saliencedysregulation theory and cognitive dysmetria theory to provide a causal explanation of theneurocognitive mechanisms underlying the positive symptoms of schizophrenia.
Schizophrenia is a disorder characterized by a combination of symptoms includingcognitive impairment (e.g. impaired working memory and executive functioning), negativesymptoms (the withdrawal of particular behaviour, e.g. apathy and anhedonia), and positive
symptoms (the presence of atypical behaviour, i.e. delusions and hallucinations, otherwise“psychosis“) (American Psychiatric Association, 2000; Mueser & McGurk, 2004). Psychoticsymptoms are sufficient, but not necessary for the DSM-IV diagnosis of schizophrenia. That is,not every individual diagnosed with schizophrenia suffers from psychosis, but every individualwho suffers from psychosis qualifies for a diagnosis of schizophrenia (American PsychiatricAssociation, 2000). The heterogeneity within the disorder has resulted in a diverse body of literature addressing various aspects of schizophrenia. With the goal of narrowing the theoreticalscope of this paper, the emphasis of analysis will be placed on the positive symptoms of schizophrenia due to their particularly debilitating effect on functioning, and their uniqueassociation with the schizophrenic disorders.
Current Theories of Psychosis
In recent years, two prominent theories of the development of psychosis in schizophreniahave been posited - the “salience dysregulation” theory of schizophrenia (Kapur, 2003, 2004),and the “cognitive dysmetria” theory of schizophrenia (Andreasen, Nopoulos, O’Leary, Miller,Wassink, & Flaum, 1999; Andreasen & Pierson, 2008). The salience dysregulation theory of schizophrenia is largely concerned with the role of dopamine in the modulation of salienceattribution. The cognitive dysmetria theory of schizophrenia is concerned with disconnectivity between the cerebellum and various cortical areas, and the resulting cognitive impairments.Although these theories have produced independent bodies of empirical literature (e.g. Holt etal., 2006; Howes et al., 2009; McGowan, Lawrence, Sales, Quested & Grasby, 2004 versusLoeber, Cintron, & Yurgelun-Todd, 2001; Okugawa, Nobuhara, Sugimoto & Kinoshita, 2005) itappears that a convergence of the theories might facilitate the construction of a more cohesiveimage of the development of psychosis in schizophrenia. Whereas cognitive dysmetria theoryfocuses on the ways in which incoming information is processed, salience dysregulation theory
addresses the ways in which external information is selectively attended. Combined, saliencedysregulation and cognitive dysmetria have the potential to explain the whole process of theselective attention to information, and the ways in which the selected information is processed toinfluence perception.Briefly, Hinton, Dayan, Frey and Neal’s (1995) wake-sleep algorithm for unsupervisedlearning in neural networks (as interpreted through Vervaeke, Lillicrap and Richards (2009)model of internalization and Ito’s (2008) theory of internal models in the cerebellum) is analgorithm for machine learning consisting of two distinct phases. In the wake phase, the neuralnetwork engages with the external environment and actively attends to selected patterns of information. In the sleep phase, the neural network disengages from the external environmentand engages in internal communication with other modules within the network in order to process the selected patterns of information. Through the application of the wake-sleep algorithmthis paper will argue that salience dysregulation influences psychosis at the “wake” level of internalization, while cognitive dysmetria influences psychosis at the “sleep” level of internalization, ultimately establishing a plausible overarching theory of psychosis linked to thecognitive machinery for internalization.
Salience Dysregulation and Schizophrenia
The salience dysregulation theory of schizophrenia is rooted in the role of dopamine inthe attribution of incentive salience (e.g. Berridge & Robinson, 1998; Spanagel, & Weiss, 1999;Ungless, 2004). In contrast to basic hedonia hypotheses of dopamine, in which dopamineneurotransmission increases as a function of pleasant responses to appetitive stimuli, theincentive salience hypothesis of dopamine suggests that dopamine mediates the attribution of salience to external stimuli, regardless of hedonic response (Berridge, 2007). Essentially, rather than functioning as an indicator of “liking” of a particular stimulus, dopamine tags stimuli as

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