A meta-analysis of 41 functional neuroimaging studies of executive function in schizophrenia revealed that both healthy controls and schizophrenia patients activate a similar cortical-subcortical network during executive tasks, including the dorsolateral prefrontal cortex (DLPFC), anterior cingulate cortex (ACC), and ventrolateral PFC. However, schizophrenia patients showed reduced activation in key areas such as the left DLPFC, rostral/dorsal ACC, and left thalamus, while increased activation was observed in midline cortical areas. These findings suggest a general-purpose cognitive control network with critical nodes in the DLPFC and ACC, but with altered activity in schizophrenia patients. The study also found that schizophrenia patients exhibited compensatory hyperactivation in other PFC areas, possibly to offset deficits in the DLPFC and ACC. The results indicate that schizophrenia is associated with impaired executive function, which is linked to dysfunction in the prefrontal cortex. The meta-analysis supports the idea of a unitary dysfunction in a cognitive control network rather than multiple isolated deficits. The study highlights the importance of considering both the distribution and direction of activation changes in understanding schizophrenia's neural basis. The findings have implications for the pathophysiology of cognitive dysfunction in schizophrenia and the development of targeted therapies. The study also notes that the results are not primarily influenced by the N-back task, suggesting a broader pattern of dysfunction. Overall, the meta-analysis provides a comprehensive view of the neural mechanisms underlying executive dysfunction in schizophrenia.A meta-analysis of 41 functional neuroimaging studies of executive function in schizophrenia revealed that both healthy controls and schizophrenia patients activate a similar cortical-subcortical network during executive tasks, including the dorsolateral prefrontal cortex (DLPFC), anterior cingulate cortex (ACC), and ventrolateral PFC. However, schizophrenia patients showed reduced activation in key areas such as the left DLPFC, rostral/dorsal ACC, and left thalamus, while increased activation was observed in midline cortical areas. These findings suggest a general-purpose cognitive control network with critical nodes in the DLPFC and ACC, but with altered activity in schizophrenia patients. The study also found that schizophrenia patients exhibited compensatory hyperactivation in other PFC areas, possibly to offset deficits in the DLPFC and ACC. The results indicate that schizophrenia is associated with impaired executive function, which is linked to dysfunction in the prefrontal cortex. The meta-analysis supports the idea of a unitary dysfunction in a cognitive control network rather than multiple isolated deficits. The study highlights the importance of considering both the distribution and direction of activation changes in understanding schizophrenia's neural basis. The findings have implications for the pathophysiology of cognitive dysfunction in schizophrenia and the development of targeted therapies. The study also notes that the results are not primarily influenced by the N-back task, suggesting a broader pattern of dysfunction. Overall, the meta-analysis provides a comprehensive view of the neural mechanisms underlying executive dysfunction in schizophrenia.