Although most studies indicate that individuals with schizophrenia have smaller ERN amplitudes (Alain, McNeely, He, Christensen, & West, 2002; Bates, Kiehl, Laurens, & Liddle, 2002; Bates, Liddle, Kiehl, & Ngan, 2004; Kim et al., 2006; Morris, Heerey, Gold, & Holroyd, 2007; Morris, Yee, & Nuechterlein, 2006), some evidence suggests that individuals with schizophrenia also have larger CRN amplitudes that are comparable in magnitude to their ERNs (Mathalon et al., 2002; Morris et al., 2006). These findings are similar to what is seen in individuals with prefrontal cortex lesions who have no difference between their ERN and CRN amplitudes (Gehring & Knight, 2000). The similarities between schizophrenia and prefrontal cortex lesion patients are not surprising as deficits in the prefrontal cortex are thought to contribute to the etiology of schizophrenia (Galderisi et al., 2007; Zhou et al., 2007). One difference between these two groups is that PFC lesion patients have normal ERN amplitudes, whereas schizophrenia patients have smaller ERN amplitudes. During errors of commission, schizophrenic patients had a decreased hemodynamic response in the ACC (Carter, MacDonald, Ross, & Stenger, 2001) and
