Table of Contents:
Introduction: Major depression is one of the most common and serious psychiatric disorders with far-reaching consequences for the person concerned, the social environment and society. The aim of this EEG-study is the demonstration of an impairment of executive functions (especially inhibition) on the behavioral and the electrophysiological level of unipolar depressives using a modified Go/Nogo-task. In depressive patients deficits in executive functions and electrophysiological changes have been reported. With neuroimaging (fMRI) it could be shown that depressives have a dysfunctional activation of a neural network related to the ACC and PFC and parts of this neural network are activated by paradigms that require executive functions. Because of the inconsistency of previous study results, our intention was to prove the inhibitory deficit by means of behavioral data and ERPs and hereby draw conclusions about a dysfunctional activation of the frontocingulate network.
Materials and Methods: 25 unipolar depressive patients and 25 healthy controls participated in the study (age, gender and education matched). The patients were partially remitted and received a combined psycho- and pharmacotherapy. To examine inhibition we used a modified Go/Nogo-task (with compatible and incompatible stimulus-response-mapping), while EEG was recorded.
Results: Behavioral data showed that more errors were made during the inhibition condition and that subjects responded more quickly when Nogo stimuli (incompatible) were shown. At elektrophysiological level (ERP amplitude) a Go/Nogo-effect and a "compatibility" effect were detected, and for the P3 a Go/Nogo X Compatibility interaction. Regarding the P3 latency a compatibility X group-interaction was found. Depressvie patients showed an extension of the P3 latency under incompatible conditions, most likely due to a delayed incompatible Go-P3.
Discussion: Depressive patients differed from healthy controls in the delayed incompatible (Go) P3 latency. This stimulus relies on response inhibition. Its delay suggests that the evaluative process of inhibition is delayed in depression. It can be concluded, that the activation of neural networks belonging to ACC and PFC under incompatible stimulus-response conditions, particularly in the context of inhibition processes, are delayed in depressive patients. A further question is whether the dysfunctional inhibition affects clinical symptoms, such as an increased tendency to reminate.