Cognition-Emotion Dysinteraction in Schizophrenia

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.

Explaining Delusions: Reducing Uncertainty Through Basic and Computational Neuroscience

“…Nevertheless, there do seem to be phenomenological and empirical data linking the broad category of aberrant salience to delusions. 49 There are, of course, complexities. Some rational theories of belief demand that it drives action, that people can only be said to be believers if they act consistently with their beliefs.…”

Aberrant functioning of the putamen links delusions, antipsychotic drug dose, and compromised connectivity in first episode psychosis—Preliminary fMRI findings

“…Based on the previous evidence of striatal fMRI signal aberrance (Romaniuk et al, 2010;Gradin et al, 2011;Anticevic and Corlett, 2012;Morris et al, 2012;Roiser et al, 2013;Rausch et al, 2014) and normalization of striatal functioning during antipsychotic medication (Sarpal et al, 2014), we expected signal correlation to be poorer in the patient group than in the control group, to correlate negatively with delusion scores, and to correlate positively with antipsychotic-equivalent dose.…”

“…Specifically, neuronal salience signaling related to non-salient stimuli may result in subjective need for explanation for the experience of salience, and resulting explanation may be delusional (Anticevic and Corlett, 2012). The putamen has abundant D2Rs and may be a location of the most prominent dopaminergic hyperactivity in psychosis (Howes et al, 2012).…”

“…The aberrant firing of the salienceprocessing neurocircuitry may then relate to the aberrant experience of salience that deviates learning towards formation of delusions (Kapur, 2003;Winton-Brown et al, 2014). In particular, increased salience processing during non-salient stimuli may be involved (Anticevic and Corlett, 2012).…”

FMRI contributions to addressing autobiographical memory impairment in temporal lobe pathology

“…Psychiatric disorders: The case of schizophrenia Schizophrenia has been also associated with impaired AM [144][145][146] in the context of deficits in several cognitive operations (perception, memory) and emotional processing, caused very likely by a more general cognitionemotion disintegration [147] . FMRI examination of AM in schizophrenia revealed an abnormal pattern of activation and correlations with memory performance in the PFC and striatum, respectively [148] .…”