Abstract:
Transcranial direct current stimulation (tDCS) and cognitive control trainings (CCT) have emerged as promising tools to ameliorate the treatment of major depression disorder (MDD) by means of targeting hypoactivation of the dorsolateral prefrontal cortex (dlPFC) and the associated impaired cognitive control (CC). Based on the dependency of excitability changes by tDCS on current network activity, a combination of tDCS and CCT has been put forward. Research so far suggests synergistic efficacy of such a combination, however further evaluation as well as investigation of optimal stimulation intensity is still pending. Moreover, despite findings of beneficial effects of CCTs, neural mechanisms underlying them is still scarce. Thus, the goals of this doctoral research are (a) to investigate the effects of a tDCS enhanced CCT on MDD, (b) to expand knowledge about optimal stimulation intensity and (c) to examine neural mechanisms underlying the effectiveness of a CCT. These research questions were addressed in three studies. In study I feedback-locked event-related potentials (ERPs) were derived from healthy subjects during the paced auditory serial addition task (PASAT), an effective CCT for MDD. Larger neural activation after negative feedback in all three processing stages (feedback related negativity, P300, late positive potential) indicates an increased resource allocation towards negative content. Moreover, processing stage dependent associations of ERPs and PASAT performance indicate early distraction and late resource allocation by increased neural activation after negative feedback. In Study II we investigated the antidepressant effect of a tDCS-augmented PASAT training for MDD and compared two stimulation intensities (1 vs. 2 mA) with sham tDCS. Depression scores significantly decreased over the course of the training. However, no additional effect of tDCS augmentation was found neither for high- nor low- intensity tDCS directly after the training. A non-significant medium effect sized tendency towards a larger reduction of MDD scores at the three months follow-up in the 1mA group might reflect preliminary indications of beneficial long-term effects of low-intensity tDCS. In Study III signatures, identified in study I were utilized to investigate underlying neural mechanisms of PASAT performance in MDD patients. A larger neural activation after negative than positive feedback only in late feedback processing stages found in study III is in accordance with time frames of typical findings about attentional negativity biases in MDD. However, the lack of associations of valence-specific ERPs with PASAT performance and MDD scores indicates that by the signatures found in study I only limited knowledge about neural mechanisms underlying efficacy of PASAT training for MDD can be gained.
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