Abstract

To elucidate basic mechanisms underlying neurofeedback we investigated neural mechanisms of training of slow cortical potentials (SCPs) by considering EEG- and fMRI. Additionally, we analyzed the feasibility of a double-blind, placebo-controlled design in NF research based on regulation performance during treatment sessions and self-assessment of the participants. Twenty healthy adults participated in 16 sessions of SCPs training: 9 participants received regular SCP training, 11 participants received sham feedback. At three time points (pre, intermediate, post) fMRI and EEG/ERP-measurements were conducted during a continuous performance test (CPT). Performance-data during the sessions (regulation performance) in the treatment group and the placebo group were analyzed. Analysis of EEG-activity revealed in the SCP group a strong enhancement of the CNV (electrode Cz) at the intermediate assessment, followed by a decrease back to baseline at the post-treatment assessment. In contrast, in the placebo group a continuous but smaller increase of the CNV could be obtained from pre to post assessment. The increase of the CNV in the SCP group at intermediate testing was superior to the enhancement in the placebo group. The changes of the CNV were accompanied by a continuous improvement in the test performance of the CPT from pre to intermediate to post assessment comparable in both groups. The change of the CNV in the SCP group is interpreted as an indicator of neural plasticity and efficiency while an increase of the CNV in the placebo group might reflect learning and improved timing due to the frequent task repetition. In the fMRI analysis evidence was obtained for neuronal plasticity. After regular SCP neurofeedback activation in the posterior parietal cortex decreased from the pre- to the intermediate measurement and increased again in the post measurement, inversely following the U-shaped increase and decrease of the tCNV EEG amplitude in the SCP-trained group. Furthermore, we found a localized increase of activity in the anterior cingulate cortex (ACC). Analyses of the estimation of treatment assignment by the participants indicate feasibility of blinding. Participants could not assess treatment assignment confidently. Participants of the SCP-group improved regulation capability during treatment sessions (in contrast to the participants of the placebo-group), although regulation capability appeared to be instable, presumably due to diminished confidence in the training (SCP- or sham-training). Our results indicate that SCP training in healthy adults might lead to functional changes in neuronal circuits serving cognitive preparation even after a limited number of sessions.

Highlights

  • Local cortical oscillations shape sensory, motor, and cognitive networks and have gained increasing interest in the investigaprocesses (Rothenberger, 2009)

  • NEURONAL PLASTICITY: tCNV, functional magnetic resonance imaging (fMRI), AND PERFORMANCE At the electrophysiological level we found a result somehow contrary to our primary expectations

  • The pre- to intermediate assessment in the SCP group revealed—according to our expectations—a strong increase of the tCNV during the continuous performance test (CPT) in the EEG-lab sessions. This increase in the SCP group significantly exceeded the increase of the tCNV in the placebo group

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Summary

Introduction

Local cortical oscillations shape sensory, motor, and cognitive networks and have gained increasing interest in the investigaprocesses (Rothenberger, 2009) Such changes in neuroelectric tion of mental functioning Distinguishing early (initial, iCNV) and late (terminal, tCNV) components, different cortical and subcortical structures are assumed to be involved. This is indicated by differential source distributions for iCNV and tCNV in previous EEG studies. Using a continuous performance test (CPT) with a long interstimulus-interval (ISI) of 6 s, we found evidence for distinct cortical and subcortical brain regions associated with early and late components of the CNV (Lütcke et al, 2009). The initial CNV was localized mainly in motor and premotor cortical areas and the caudate nucleus

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