Decreased Conflict- and Error-Related Activity in the Anterior Cingulate Cortex in Subjects With Schizophrenia

Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania, United States
American Journal of Psychiatry (Impact Factor: 12.3). 11/2005; 162(10):1833-9. DOI: 10.1176/appi.ajp.162.10.1833
Source: PubMed


People with schizophrenia have exhibited reduced functional activity in the anterior cingulate cortex during the performance of many types of cognitive tasks and during the commission of errors. According to conflict theory, the anterior cingulate cortex is involved in the monitoring of response conflict, acting as a signal for a need for greater cognitive control. This study examined whether impaired conflict monitoring in people with schizophrenia could underlie reduced anterior cingulate activity during both correct task performance and error-related activity.
Functional activity in the anterior cingulate of 13 schizophrenia patients and 13 healthy comparison subjects was investigated by using event-related fMRI and a Stroop task that allowed simultaneous examination of activity during both conflict (incongruent trials) and error (commission of error trials).
In the presence of comparable reaction time measures for conflict as well as comparable error rates, the schizophrenia subjects showed both decreased conflict- and error-related activity in the same region of the anterior cingulate cortex. Moreover, those with schizophrenia did not exhibit significant post-conflict or post-error behavioral adjustments.
Concurrently reduced conflict- and error-related activity in the anterior cingulate cortex along with reduced trial-to-trial adjustments in performance has not previously been reported in schizophrenia. The current results suggest that impaired conflict monitoring by the anterior cingulate cortex might play an important role in contributing to cognitive control deficits in patients with schizophrenia.

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    • "Reduced ERN amplitude has also been reported in individuals with high clinical (Laurens et al., 2010; Perez et al., 2011) and genetic (Simmonite et al., 2012) risk for schizophrenia, indicating a possible trait marker for vulnerability to psychosis. Post-error reaction time slowing has been found in some studies (Alain et al., 2002; Kerns et al., 2005), but not all (Bates et al., 2002; Mathalon et al., 2002; Morris et al., 2006). "
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    ABSTRACT: Objective: Previous research suggests that deficits in error monitoring contribute to psychosis and poor functioning. Consistent with the NIMH Research Domain Criteria initiative, this study examined electrophysiological brain activity, appraisal of self-performance, and personality traits related to psychosis during error monitoring in individuals with and without a history of psychosis across disorders. Methods: Error-related negativity (ERN), correct response negativity (CRN), error positivity (Pe), and correct response positivity (Pc) were recorded in 14 individuals with a history of psychosis (PSY) and 12 individuals with no history of psychosis (CTR) during a flanker task. Participants continuously rated their performance and completed the Schizotypal Personality Questionnaire-Brief Revised (SPQ-BR). Results: Compared with CTR, PSY exhibited reduced ERN and Pe amplitudes and was also less accurate at evaluating their performance. Group differences were specific to error trials. Across all participants, smaller Pe amplitudes were associated with greater scores on the SPQ-BR Cognitive-Perceptual factor and less accuracy in subjective identification of errors. Conclusions: Individuals with a history of psychosis, regardless of diagnosis, demonstrated abnormal neural activity and imprecise confidence in response during error monitoring. Significance: Results suggest that disruptions in neural circuitry may underlie specific clinical symptoms across diagnostic categories.
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    • "Structural magnetic resonance imaging (MRI) and neuropathological findings demonstrate gray matter reductions of the ACC in patients with psychosis, occurring already prior to its onset and, eventually, progressing with illness duration (Fornito et al., 2009). In functional MRI (fMRI) studies, patients with schizophrenia showed reduced conflict-(Snitz et al., 2005) as well as errorrelated activity in the ACC (see Melcher et al., 2008, for a review; Carter et al., 2001; Alain et al., 2002; Kerns et al., 2005), which may normalize upon administration of antipsychotic medications (Snitz et al., 2005; Adams and David, 2007). Studies reported hypo-activation in patients only for the rostral division of the ACC during Stroop (Carter et al., 1997), Go/NoGo (Laurens et al., 2003), oddball (Liddle et al., 2006), or emotion recognition tasks (Habel et al., 2010). "
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    ABSTRACT: Cognitive functioning is impaired in patients with schizophrenia, leading to significant disabilities in everyday functioning. Its improvement is an important treatment target. Neurofeedback (NF) seems a promising method to address the neural dysfunctions underlying those cognitive impairments. The anterior cingulate cortex (ACC), a central hub for cognitive processing, is one of the brain regions known to be dysfunctional in schizophrenia. Here we conducted NF training based on real-time functional magnetic resonance imaging (fMRI) in patients with schizophrenia to enable them to control their ACC activity. Training was performed over 3 days in a group of 11 patients with schizophrenia and 11 healthy controls. Social feedback was provided in accordance with the evoked activity in the selected region of interest (ROI). Neural and cognitive strategies were examined off-line. Both groups learned to control the activity of their ACC but used different neural strategies: patients activated the dorsal and healthy controls the rostral subdivision. Patients mainly used imagination of music to elicit activity and the control group imagination of sports. In a stepwise regression analysis, the difference in neural control did not result from the differences in cognitive strategies but from diagnosis alone. Based on social reinforcers, patients with schizophrenia can learn to regulate localized brain activity. However, cognitive strategies and neural network location differ from healthy controls. These data emphasize that for therapeutic interventions in patients with schizophrenia compensatory strategies may emerge. Specific cognitive skills or specific dysfunctional networks should be addressed to train impaired skills. Social NF based on fMRI may be one method to accomplish precise learning targets.
    Frontiers in Behavioral Neuroscience 06/2015; 9:169. DOI:10.3389/fnbeh.2015.00169 · 3.27 Impact Factor
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    • "Additionally, they are again consistent with the relationship between schizotypy in healthy subjects and the schizophrenia continuum. Consistently, previous studies have indicated that patients with schizophrenia have abnormal prefrontal activity and worse behavioral performance during attentional processing (Weiss et al., 2003; Honey et al., 2005; Kerns et al., 2005; Laurens et al., 2005; MacDonald et al., 2005; Gur et al., 2007). Furthermore, evidence of abnormal prefrontal activity has been reported during cognitive processing in patients with schizophrenia carrying the rs1076560 T allele (Bertolino et al., 2009a,b, 2010; Blasi et al., 2010). "
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    ABSTRACT: "Schizotypy" is a latent organization of personality related to the genetic risk for schizophrenia. Some evidence suggests that schizophrenia and schizotypy share some biological features, including a link to dopaminergic D2 receptor signaling. A polymorphism in the D2 gene (DRD2 rs1076560, guanine > thymine (G > T)) has been associated with the D2 short/long isoform expression ratio, as well as striatal dopamine signaling and prefrontal cortical activity during different cognitive operations, which are measures that are altered in patients with schizophrenia. Our aim is to determine the association of schizotypy scores with the DRD2 rs1076560 genotype in healthy individuals and their interaction with prefrontal activity during attention and D2 striatal signaling. A total of 83 healthy subjects were genotyped for DRD2 rs1076560 and completed the Schizotypal Personality Questionnaire (SPQ). Twenty-six participants underwent SPECT with [(123)I]IBZM D2 receptor radiotracer, while 68 performed an attentional control task during fMRI. We found that rs1076560 GT subjects had greater SPQ scores than GG individuals. Moreover, the interaction between schizotypy and the GT genotype predicted prefrontal activity and related attentional behavior, as well as striatal binding of IBZM. No interaction was found in GG individuals. These results suggest that rs1076560 GT healthy individuals are prone to higher levels of schizotypy, and that the interaction between rs1076560 and schizotypy scores modulates phenotypes related to the pathophysiology of schizophrenia, such as prefrontal activity and striatal dopamine signaling. These results provide systems-level qualitative evidence for mapping the construct of schizotypy in healthy individuals onto the schizophrenia continuum.
    Frontiers in Behavioral Neuroscience 07/2014; 8(235):eCollection2014. DOI:10.3389/fnbeh.2014.00235 · 3.27 Impact Factor
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