Background:
Dyfunctions of prefrontal neuronal circuits contribute to the pathophysiology of depression.
Previous studies showed increased functional MRI (Greicius et al. 2007) and EEG connectivity
in patients with depression (Fingelkurts et al. 2007; Leuchter et al. 2012). In this
study we investigated a large sample of patients with major depression (n = 228) and
gender- and age-matched healthy subjects (n = 215) using resting state EEG and eLORETA
in terms of spectrotemporal dynamics and brain connectivity.
Methods:
Spectrotemporal dynamics during resting state with closed eyes were analyzed in sensor
and source space to examine functional EEG connectivity alterations between groups.
Quantitative measures of delta (δ), theta (θ), alpha (α), beta (β) and gamma (γ) power (µV2), hemispheric asymmetry, coherence, phase and eLORETA (current density, connectivity)
analyses were calculated from artifact-free EEG recordings.
Results:
EEG δ power was increased in all brain regions in the group of patients with a focus
in frontal regions. We also found increased frontal θ and α power. Further analyses
revealed significant hemispheric differences between the groups. There were increased
δ, θ, α, and β asymmetries in the left hemisphere between fronto-frontal, -central,
-parietal and -occipital regions. We also found increased coherence differences in
the δ, θ and α bands for fronto-frontal, -central, -temporal, -occipital, parieto-temporal,
and occipto-temporal electrodes for both hemispheres. Decreased coherence was found
between fronto-temporal, left fronto-frontal, and centro-parietal electrodes. In addition
there were changes in phase differences in the δ, θ, α-bands between patients and
healthy subjects. Differences in source current density (eLORETA) were found for the
δ, θ, α-band in the subgenual and the rostral anterior cingulate cortex with increased
current density in the patients.
Conclusion:
The main finding of the present study was an increase in cortical slow-wave activity
in sensor and source space in patients with depression revealing marked differences
in prefrontal cortical networks. Functional δ, θ and α-connectivity (coherence and
phase) were altered with a predominance in the left hemisphere. Dysfunctions of the
anterior cingulate cortex, together with alterations in functional connectivity may
contribute to the pathophysiology of major depression.