Evidence from previous studies has suggested that the inter-individual differences in human brain-wave patterns (EEG) are predominantly determined by genetic factors. In particular, the within-pair EEG concordance of monozygotic (mz) twins was found to be typically as high as r = 0.81 across channels and frequency bands, thus being comparable to that between repeated assessments on the same individual with typically r = 0.83. Yet our investigations into mz twins discordant and concordant for schizophrenia yielded a significantly reduced within-pair EEG concordance for both, the pairs discordant for schizophrenia and the pairs concordant for schizophrenia. For the within-pair correlation of the global EEG parameter "total power 0-32 Hz", for example, we found a value of r = 0.772 for the healthy twins which is typical of normal mz twins, a reduced value of r = 0.513 for the twins discordant for schizophrenia, and an extremely low correlation of r = 0.210 for the twins concordant for schizophrenia . This marked reduction of within-pair concordance was with 0.488/0.189 [2-5 Hz], 0.484/0.388 [5-8 Hz], 0.642/0.507 [8-12 Hz] and 0.147/0.544 [12-16 Hz] equally true for all power-related EEG parameters in the pairs concordant for schizophrenia. The pairs discordant for schizophrenia displayed a reduction of within-pair concordance for the EEG parameters "centroid" and "symmetry" which measure the power-frequency distribution of frequency bands: 0.258/0.123 [2-5 Hz], 0.294/0.317 [5-8 Hz] and 0.411/0.560 [8-12 Hz]. ANOVAs with "channel", "co-twin" and "affection status" as main effects, "channel"*"co-twin" and "channel"*"affection status" as crossed effect, and "proband" as nested effect within channels, supported the above results. Specifically, the total EEG power [0-32 Hz] was virtually identical in the healthy co-twins (p > 0.8402), but different between affected and unaffected subjects (p < 0.0001). A multivariate discriminant function of EEG parameters distinguished reproducibly between affected and unaffected subjects at an overall performance of >75% correctly classified subjects, while the severity of illness, as derived from EEG-differences between affected and unaffected subjects, was closely related to the severity of illness as provided by psychopathology syndrome scores. Consequently, EEG anomalies associated with schizophrenia and manifested differently in the mz co-twins concordant for schizophrenia are likely the effect of nongenetic, pathologic processes that evolved independently in the co-twins’ genetically identical brains once the illness began to progress. The existence of such nongenetic processes would suggest a modification of the standard phenotype-to-genotype search strategies of molecular-genetic studies that aim to link the schizophrenia phenotype to genetic vulnerability factors.