Alterations of EEG gamma activity in schizophrenia have been reported during sensory and cognitive tasks, but it remains unclear whether changes are present in resting state. Our aim was to examine whether changes occur in resting state, and to delineate those brain regions where gamma activity is altered. Furthermore, we wanted to identify the associations between changes in gamma activity and psychopathological characteristics. We studied gamma activity (30-48 Hz) in 60 patients with schizophrenia and 76 healthy controls. EEGs were acquired in resting state with closed eyes using a high-density, 256-channel EEG-system. The two groups were compared in absolute power measures in the gamma frequency range. Compared to controls, in patients with schizophrenia the absolute power was significantly elevated (false discovery rate corrected p < 0.05). The alterations clustered into fronto-central and posterior brain regions, and were positively associated with the severity of psychopathology, measured by the PANSS. Changes in gamma activity can lead to disturbed coordination of large-scale brain networks. Thus, the increased gamma activity in certain brain regions that we found may result in disturbances in temporal coordination of task-free/resting-state networks in schizophrenia. Positive association of increased gamma power with psychopathology suggests that altered gamma activity provides a contribution to symptom presentation.

Adult attention-deficit/hyperactivity disorder (aADHD) has recently been better recognized and treated in many European countries. In spite of this development, aADHD still features as a "hidden" comorbidity, often not diagnosed even in patients under psychiatric treatment for other psychiatric disorders. The aim of this study was to establish the prevalence rates of unrecognized aADHD in academic centers providing regular psychiatric services in the Czech Republic and Hungary. In a population of psychiatric in-and outpatients, Adult ADHD Self-Report Scale was administered. All positively and about half of the negatively screened subjects were clinically interviewed and the DSM diagnosis of ADHD was determined based on the symptom list and Conners' Adult ADHD Rating Scale. The estimated point prevalence rate of unrecognized comorbid aADHD among psychiatric in-and out patients was 6.99% (95% lower CI: 5.11, 95% upper CI 8.86) according to the DSM-IV-TR criteria and 9.27% (95% lower CI: 7.13, 95% upper CI 11.40) according to the DSM-5 criteria. Current suicide risk was significantly associated with the presence of undiagnosed aADHD; however, life time suicide attempts, depression, dysthymia, alcohol and substance dependence, anxiety and stress related disorders were not. Further educational efforts are needed to improve the recognition and treatment of aADHD in adults

Gamma activity is reduced in adult ADHD, and the reduction has a predominantly right centroparietal distribution. Our findings are consistent with childhood ADHD literature with respect to diminished posterior gamma activity in patients, which may reflect altered dorsal attention network functions. Gamma abnormalities might provide a link between neurophysiological functioning and neuropsychological deficiencies, thereby offering an opportunity to investigate the neurobiological mechanisms that underlie the clinical symptoms of ADHD.

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Deficits in error-processing are postulated in core symptoms of ADHD. Our goal was to investigate the neurophysiological basis of abnormal error-processing and adaptive adjustments in ADHD, and examine whether error-related alterations extend beyond traditional Regions of Interest (ROIs), particularly to those involved in adaptive adjustments, such as the Salience Network system. We obtained event-related potentials (ERPs) during a Go/NoGo task from 22 adult-ADHD patients and 29 matched healthy controls using a high-density 256-electrode array. Error-related ERPs with error-negativity (ERN) and error-positivity (Pe) served as probes of error-processing. In ADHD patients both ERN and Pe were significantly reduced, and the reduction was associated with core psychopathological symptoms. The ERP-attenuation was prominent not only at traditional ROI-electrodes but across many other brain areas, with a distinctive subset of group-differences and symptom-correlations manifested at temporo-parietal sites, with right-lateralization. Source-localization uncovered two neural-sources for the error-related ERPs: one in the cingulate cortex near midline, which was present in both groups; and one in the right insular cortex, which was present only in the control group. The neural patterns of impairments may be the result of coexisting deficits in the dorsal midline error-processing brain network involved in "error-processing proper" and the right-lateralized temporo-parietal salience network involved in the evaluation of significance of the error-signals. Our source-localization findings potentially identify a missing link between the previously reported structural change, i.e., reduced insular volume, and the well-established behavioral deficits in ADHD.