Based on reports of low-frequency (i.e., delta, theta) resting EEG abnormalities related to disorder-specific pathophysiology in schizophrenia, the increase in slow oscillatory activity in the theta range found in this study most likely indicates resting-state cortical dysfunction in SLPE [61]. This activity was topographically distributed over regions in the medial (i.e., posterior cingulate/precuneus) and lateral parietal cortex that are part of the DMN, which is typically activated during rest [19]. Thus, our source-localization finding supports and extends the notion that the parietal lobe plays a crucial role in the pathogenesis of psychosis [20], [62], and that DMN dysfunction may be a core neurobiological feature in both schizophrenia [3], [5] and SLPE. Consistent with this argument, we previously reported abnormal parietal activation closely associated with the delusional state of patients suffering from episodic interictal epileptic psychosis [63]. In addition, Sundram et al [64] in a voxel-based morphometry study noted that extratemporal cortical abnormalities, in particular prominent parietal gray matter deficits occurred in patients with temporal epilepsy with psychosis. This evidence suggests that parietal dysfunction is not exclusive of the classic form
