Adaptive Cognitive Control in Schizophrenia: Neural Correlates of Error- and Conflict- Processing Beyond the Anterior Cingulate Cortex

Date of Award

Winter 12-15-2012

Author's School

Graduate School of Arts and Sciences

Author's Department

Biology & Biomedical Sciences (Neurosciences)

Degree Name

Doctor of Philosophy (PhD)

Degree Type



Schizophrenia (SCZ) is one of the most debilitating neuropsychiatric disorders. Cognitive dysfunction has been identified as a core feature of this illness. This dissertation presents an integrative approach to examine the neural and behavioral correlates of adaptive cognitive control in healthy controls and individuals with SCZ. We first examined functional dissociations between error- and conflict- processing in an extended cingulo-opercular and cerebellar network previously shown to demonstrate robust error-related activity. Our results evidenced functional subregions within the dorsal anterior cingulate cortex; with portions responding to error situated more ventrally and anteriorly compared to more dorsal/posterior regions responding also to conflict. This dorsal/ventral distinction is to some extent present in other brain regions, including the parietal lobe and cerebellum. The brain activation patterns for error compared to conflict suggest that multiple mechanisms of control are engaged in the detection of increasing cognitive demands and adjust behavioral responses accordingly. Second, we examined group differences in behavioral performance and brain activation related to error- and conflict- processing at a network level between individuals with SCZ and healthy controls. Further, we examined the relationship between the different components of this extended cingulo-opercular and cerebellar network in terms of their timing relationship to one another (i.e. functional connectivity). Our results indicate that error- and conflict-processing are surprisingly intact in individuals with SCZ. However, the integration of key cognitive control regions, including the anterior prefrontal cortex, inferior parietal lobule, thalamus and cerebellum is affected in individuals with SCZ. Our findings provide further evidence in support neurobiological theories of SCZ that explain its behavioral manifestations as a functional dysconnection syndrome.


English (en)

Chair and Committee

Deanna M Barch

Committee Members

Todd S Braver, Denise Head, Tamara Hershey, Jose Mathews, Steven E Petersen


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