one’s model of the environment must be revised [13]. P300 is thought to be composed of several parts that reflect an information processing cascade when attentional and memory mechanisms are engaged [4]. Since P300 abnormalities in patients with schizophrenia were first found by Roth and Cannon in 1972 [14], many investigations reported that patients with schizophrenia have smaller P300 [15-20]. In studies of ERPs in schizophrenia patients, the oddball paradigm was more useful in studies of the brain in the active rather than the resting state, and demonstrated that amplitude and prolonged latency of the P300 waveform in schizophrenia patients were reduced compared with normal subjects [12, 21-30]. Reduction of P300 amplitude is one of the most replicable biological observations in patients with schizophrenia [31], and P300 amplitude and latency are powerful tools in the study of schizophrenia [32]. The reduced P300 amplitude on EEG in patients with schizophrenia was interpreted as an electrophysiological index relating to thought disorders [32, 33]. The symptom-independent reduction in event-related alpha attenuation in schizophrenia may be useful as an electrophysiological index of the impairment of neural processes distinct from those indexed by symptom-dependent P300 abnormalities [6].
