Given converging evidence stemming from studies using functional magnetic resonance (fMRI; e.g., Kiehl et al., 2000), ERP source localization techniques (e.g., Dehaene et al., 1994), combined electrophysiologic, magnetoencephalographic and MRI data (e.g., Miltner et al., 2003), concurrent EEG and fMRI data (e.g., Debener et al., 2005) and intracranial EEG recordings in monkeys (e.g., Emeric et al., 2008), it is widely assumed that the ERN is generated within the anterior cingulate cortex (ACC; for reviews, e.g., van Veen and Carter, 2002, 2006). Because imaging data have documented structural (i.e., reduced volume; Baiano et al., 2007) and functional ACC abnormalities in schizophrenia patients (e.g., Carter et al., 2001; Polli et al., 2008), their reduced ERN amplitudes may originate from an underlying ACC dysfunction (e.g., Mathalon et al., 2002).
