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

Abstract

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.

Post-Error Behavior in Active Cocaine Users: Poor Awareness of Errors in the Presence of Intact Performance Adjustments

“…Furthermore, this sample does show impairment in other ACC-related cognitive functions, such as inhibitory control and error awareness. Although we do not have neuroimaging data from the BAT, it is based on the Go/NoGo format which has previously shown a relationship between post-error slowing and error-related ACC activity , replicating a relationship demonstrated with other cognitive tasks such as the flanker (Gehring et al, 1993) and Stroop tasks (Kerns et al, 2004(Kerns et al, , 2005. Despite this evidence some studies have failed to demonstrate a relationship between error-related ACC activity and post-error slowing (Gehring and Fencsik, 2001), or have associated different neural signatures with post-error slowing, such as the ERP error positivity (Pe) waveform (Hajcak et al, 2003).…”

“…Studies examining the diminished error-related ACC response of older adults have also failed to show that it bears any relationship to posterror slowing (Themanson et al, 2005;West and Moore, 2005), and studies examining drug-related increases (Riba et al, 2005a;Tieges et al, 2004) or decreases (Easdon et al, 2005;Riba et al, 2005b) in the ACC response to errors have also failed to show a relationship to post-error slowing. It is intriguing that those studies examining within-subject relations between ACC activity and post-error slowing have found significant correlations (eg, Kerns et al, 2005, Gehring et al, 1993, whereas the above-mentioned studies using between-group comparisons have not. Between-group comparisons may be influenced by other independent variables that distinguish the groups, for example, anatomical variability, which while not directly related to performance monitoring could potentially mask the ACC/post-error slowing relationship seen at the single-subject level.…”

“…We had predicted, on the basis of previous studies demonstrating a relationship between diminished errorrelated ACC responses and decreased post-error slowing (de Bruijn et al, 2004;Kerns et al, 2005;Ridderinkhof et al, 2002), that cocaine users, who have previously shown this diminished error-related ACC response (Kaufman et al, 2003), would have impaired post-error slowing. Given the intact post-error slowing of the current cocaine-using sample, we must consider whether any significant methodological or sample differences between the current study and those that had formed the hypothesis might account for the unexpected finding.…”

“…Similarly, dysfunctional neural responses to errors in other clinical groups have also shown to relate to their general symptom profile. For example, patients with schizophrenia have diminished levels of ACC activity in response to errors (Kerns et al, 2005;Mathalon et al, 2002), with the level of dysfunction relating to the severity of disorganization symptoms (ie, formal thought disorder, inappropriate affect, and bizarre behavior) (Bates et al, 2002;Berman et al, 1997;Frith and Done, 1989;Liddle et al, 1992). Alzheimer's disease has also been associated with a progressive deterioration in error awareness (Cahn et al, 1997;Neils-Strunjas et al, 1998) and the neural response to errors (Mathalon et al, 2003).…”

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

“…Indeed, there are multiple examples of distinct disorders that are characterized by common pathophysiological mechanisms. For example, anxiety disorders and mood disorders share hyperactive amygdala responses to negatively valenced stimuli [2,3] and schizophrenia and post-traumatic stress disorder are both characterized by prefrontal dysfunction during tasks that require sustained attention [4,5]. Such overlap suggests the utility of examining common patterns of dysregulated brain function and associated phenotypes with the ultimate goal of more accurately linking pathophysiological processes to rationally derived and targeted interventions.…”