[Electroencephalography in psychiatry--current status and outlook]

The "Psychophysiology Working Group" of AMDP (Arbeitskreis für Methodik und Dokumentation in der Psychiatrie) intends to establish a broad database of EEG data in psychiatry. The purpose is to determine whether the EEG can contribute to the diagnostic classification of psychiatric disorders, the description of the course of the illness and prediction of the therapeutic outcome. Since several studies have shown promising results in recent years, members of the working group have investigated literature and written reviews that are summarized in this contribution. This includes a critical evaluation of the studies cited. We restrict ourselves to schizophrenia, affective disorder and anxiety disorder. Out of more than 3000 available contributions in the world literature, 500 have been evaluated by the group, and around 90 are taken for this summary. The critical review is the basis for future research of the working group and gives the following working hypothese. Under resting EEG conditions anxiety does not show typical deviations from normality. However, EEG recordings under experimentally induced anxiety do show typical changes: in normal persons there is usually an increase in desynchronous fast beta activity (hyperarousal accompanied by cognitive coping), whereas patients with anxiety disorder show hypersynchronized alpha activity, as is usually found in deep relaxation. Thus, hypersynchronized alpha activity might be an expression of a compensatory effort of the system to relax. Anxiolytics induce synchronous 14-18 Hz beta or sub-alpha activity, which may force the system into more rigid patterns (relaxation) and thus could counteract anxiety in normal persons if hyperarousal together with desynchronization is not sufficient. Furthermore, benzodiazepines also show an increase in desynchronous fast beta activity, preferably in the frontocentral areas, which could be useful in chronic anxiety in order to support cognitive efforts. While depressive disorders cause a variety of changes in the awake EEG that can only partly be linked with the clinical picture (neurotic versus endogenous), the sleep EEG shows a decrease in REM latency, and increase in REM density and a decrease in sleep efficiency in patients with depressive symptoms. However, nosological specify is not yet established. Successful antidepressive therapy counteracts these changes. The common feature in the awake EEG is the interaction with vigilance-dependent variables in both directions: stimulation and sedation. Schizophrenia shows different patterns for acute and chronic states. In acute schizophrenia there is a dysrhythmic activity with an increase in beta activity. This is counteracted by neuroleptics, inducing a slowing of frequency and an increase of synchronization. In chronic schizophrenics, there is increased synchronization with low variability of amplitude. In contrast to the treatment in acute schizophrenics, in chronic schizophrenia the therapy response under neuroleptics is indicated by an increase in beta activity and a decrease in synchronization.