AUTHOR=Anticevic Alan , Corlett Philip R. TITLE=Cognition-Emotion Dysinteraction in Schizophrenia JOURNAL=Frontiers in Psychology VOLUME=3 YEAR=2012 URL=https://www.frontiersin.org/journals/psychology/articles/10.3389/fpsyg.2012.00392 DOI=10.3389/fpsyg.2012.00392 ISSN=1664-1078 ABSTRACT=

Evolving theories of schizophrenia emphasize a “disconnection” in distributed fronto-striatal-limbic neural systems, which may give rise to breakdowns in cognition and emotional function. We discuss these diverse domains of function from the perspective of disrupted neural circuits involved in “cold” cognitive vs. “hot” affective operations and the interplay between these processes. We focus on three research areas that highlight cognition-emotion dysinteractions in schizophrenia: First, we discuss the role of cognitive deficits in the “maintenance” of emotional information. We review recent evidence suggesting that motivational abnormalities in schizophrenia may in part arise due to a disrupted ability to “maintain” affective information over time. Here, dysfunction in a prototypical “cold” cognitive operation may result in “affective” deficits in schizophrenia. Second, we discuss abnormalities in the detection and ascription of salience, manifest as excessive processing of non-emotional stimuli and inappropriate distractibility. We review emerging evidence suggesting deficits in some, but not other, specific emotional processes in schizophrenia – namely an intact ability to perceive emotion “in-the-moment” but poor prospective valuation of stimuli and heightened reactivity to stimuli that ought to be filtered. Third, we discuss abnormalities in learning mechanisms that may give rise to delusions, the fixed, false, and often emotionally charged beliefs that accompany psychosis. We highlight the role of affect in aberrant belief formation, mostly ignored by current theoretical models. Together, we attempt to provide a consilient overview for how breakdowns in neural systems underlying affect and cognition in psychosis interact across symptom domains. We conclude with a brief treatment of the neurobiology of schizophrenia and the need to close our explanatory gap between cellular-level hypotheses and complex behavioral symptoms observed in this illness.