Overall findings indicate that in addition to dysfunction of parietal regions that are part of the DMN, resting-state disrupted connectivity of the medial temporal cortex with prefrontal areas that are also involved in the DMN or implicated in psychopathological dysfunction may be critical to schizophrenia-like psychosis, especially in individuals with temporal lobe epilepsy. This suggests that DMN dysfunction may be a core neurobiological feature of the disorder. Increase in theta oscillations and in beta phase synchronization appears to represent the underlying neural activity of these deficits. These findings warrant further investigation using larger samples of drug-naïve patients with epilepsy psychosis and eLORETA connectivity method.
