Barch DM, Ceaser A. Cognition in schizophrenia: core psychological and neural mechanisms. Trends Cogn Sci 16: 27-34

Department of Psychiatry, Washington University in St. Louis, San Luis, Missouri, United States
Trends in Cognitive Sciences (Impact Factor: 21.97). 12/2011; 16(1):27-34. DOI: 10.1016/j.tics.2011.11.015
Source: PubMed


The challenge in understanding cognitive impairment in schizophrenia is that people with this illness have deficits in an array of domains. Here, we briefly review evidence regarding the pattern of deficits within three domains: context processing, working memory and episodic memory. We suggest that there may be a common mechanism driving deficits in these domains - an impairment in the ability to actively represent goal information in working memory to guide behavior, a function we refer to as proactive control. We suggest that such deficits in proactive control reflect impairments in dorsolateral prefrontal cortex, its interactions with other brain regions, such as parietal cortex, thalamus and striatum, and the influence of neurotransmitter systems, such as dopamine, GABA and glutamate.

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    • "Please cite this article as: Baskak, B., et al., Effect of a socıal defeat experıence on prefrontal actıvıty ın schızophrenıa. Psychiatry Research: Neuroimaging (2015), dysfunction in schizophrenia (Goldman-Rakic and Selemon, 1997; Davidson and Heinrichs, 2003; Glahn et al., 2005; Barch and Ceasar, 2012). The PFC is also sensitive to stressful situations, particularly in the social context (Watt et al., 2009; Watt et al., 2014). "
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    ABSTRACT: The social defeat (SD) hypothesis of schizophrenia posits that repeated experiences of SD may lead to sensitization of the mesolimbic dopaminergic system and to precipitation of psychosis. Based on previous definitions adapted to a human experimental paradigm, we prepared a computer simulation of SD to mimic this subjective experience. We measured prefrontal cortex (PFC) activity in subjects with schizophrenia and healthy controls during exposure to a single SD experience with functional near infrared spectroscopy. PFC activity declined in both groups. Compared with the control condition, SD exposure was associated with a broader decline in left ventromedial, right medial and right lateral PFC activity in healthy controls (n=25), and a sharper decline in right ventrolateral PFC activity in subjects with schizophrenia (n=25). The activity in the right ventrolateral PFC, was significantly lower in patients compared with controls. This may be due to a deficiency in emotion regulation or self-control, or it may be related to impaired empathy in schizophrenia. Different patterns of brain activity during the SD experience in subjects with schizophrenia versus healthy controls may provide indirect evidence regarding the SD hypothesis of schizophrenia. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
    07/2015; 233(3). DOI:10.1016/j.pscychresns.2015.07.017
    • "On the other hand, an intriguing finding in psychosis research is that, despite schizophrenia and other psychoses running in families, most affected individuals do not have family history of the illness (Welham et al., 2009). There is now increasing evidence suggesting that cognitive dysfunction is a reliable and stable feature of psychosis (Barch and Ceaser, 2012) and that it predicts psychosocial functioning and functional capacity better than clinical manifestations in schizophrenia patients (Bowie et al., 2008). Moreover, an association between bipolar disorder and cognitive impairment has repeatedly been described even for euthymic patients. "
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    ABSTRACT: Schizophrenia and other psychoses are complex disorders with high rates of cognitive impairment and a considerable degree of genetic and environmental influence on its etiology. Whether cognitive impairment is related to dimensional scores of familial liability is still matter of debate. We conducted a cross-sectional study including 169 patients with psychotic disorders and 26 healthy controls. Attention, memory and executive functions were assessed, and familial loading scores for schizophrenia and mood disorders were calculated. The relationships between familial liability and neuropsychological performance were examined with Spearman׳s correlation coefficients. In addition, patients were classified into three groups by family loading tertiles, and comparisons were performed between the patients in the top and bottom tertiles. Low familial loading scores for schizophrenia showed a significant association with poor executive functioning and delayed visual memory. And these results were also achieved when the subset of psychotic patients in the two extreme tertiles of family loadings of schizophrenia and mood disorders were compared. Low familial liability to schizophrenia seems to be a contributing factor for the severity of cognitive impairment in patients with a broad putative schizophrenia spectrum diagnosis. Copyright © 2015. Published by Elsevier Ireland Ltd.
    04/2015; 227(2-3). DOI:10.1016/j.psychres.2015.03.024
    • "Aberrant salience network activity has been considered to underlie positive symptoms such as delusions and hallucinations due to an inappropriate assignment of salience to stimuli that would normally be considered irrelevant (Menon, 2011; Palaniyappan et al., 2011, 2012). Prefrontal cortex dysfunction is widely supposed to account for negative symptoms (Wolkin et al., 1992) and cognitive deficits (Barch et al., 2012) in schizophrenia, given the similarities to clinical features of patients with frontal lobe lesions. This 'hypofrontality hypothesis' is further supported by a variety of neuroimaging studies that revealed a close link between frontal hypoactivation and negative symptoms (Wolkin et al., 1992; Potkin et al., 2002). "
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    ABSTRACT: Major theories on the neural basis of schizophrenic core symptoms highlight aberrant salience network activity (insula and anterior cingulate cortex), prefrontal hypoactivation, sensory processing deficits as well as an impaired connectivity between temporal and prefrontal cortices. The mismatch negativity is a potential biomarker of schizophrenia and its reduction might be a consequence of each of these mechanisms. In contrast to the previous electroencephalographic studies, functional magnetic resonance imaging may disentangle the involved brain networks at high spatial resolution and determine contributions from localized brain responses and functional connectivity to the schizophrenic impairments. Twenty-four patients and 24 matched control subjects underwent functional magnetic resonance imaging during an optimized auditory mismatch task. Haemodynamic responses and functional connectivity were compared between groups. These data sets further entered a diagnostic classification analysis to assess impairments on the individual patient level. In the control group, mismatch responses were detected in the auditory cortex, prefrontal cortex and the salience network (insula and anterior cingulate cortex). Furthermore, mismatch processing was associated with a deactivation of the visual system and the dorsal attention network indicating a shift of resources from the visual to the auditory domain. The patients exhibited reduced activation in all of the respective systems (right auditory cortex, prefrontal cortex, and the salience network) as well as reduced deactivation of the visual system and the dorsal attention network. Group differences were most prominent in the anterior cingulate cortex and adjacent prefrontal areas. The latter regions also exhibited a reduced functional connectivity with the auditory cortex in the patients. In the classification analysis, haemodynamic responses yielded a maximal accuracy of 83% based on four features; functional connectivity data performed similarly or worse for up to about 10 features. However, connectivity data yielded a better performance when including more than 10 features yielding up to 90% accuracy. Among others, the most discriminating features represented functional connections between the auditory cortex and the anterior cingulate cortex as well as adjacent prefrontal areas. Auditory mismatch impairments incorporate major neural dysfunctions in schizophrenia. Our data suggest synergistic effects of sensory processing deficits, aberrant salience attribution, prefrontal hypoactivation as well as a disrupted connectivity between temporal and prefrontal cortices. These deficits are associated with subsequent disturbances in modality-specific resource allocation. Capturing different schizophrenic core dysfunctions, functional magnetic resonance imaging during this optimized mismatch paradigm reveals processing impairments on the individual patient level, rendering it a potential biomarker of schizophrenia. © The Author (2015). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email:
    Brain 03/2015; DOI:10.1093/brain/awv049 · 9.20 Impact Factor
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