This study aimed to examine alterations in electroencephalography (EEG) phase synchronization in working memory processing in depressed patients. Sixty-four-channel EEG signals were recorded from 33 depressed patients and 32 healthy controls during a visual n-back task. Alterations in functional connections in the patients were investigated using event-related phase coherence in terms of the phase synchronization index (PSI). Compared with the control subjects, the depressed patients showed a lower task-dependent increase in the PSI of delta, theta, and alpha oscillations in a frontoparietal network, but a higher task-dependent increase in the PSI of beta oscillations in the frontoparietal network. Additionally, depressed patients showed a lower task-dependent decrease in the PSI of delta, theta, alpha, and beta oscillations in centro-parieto-occipital sites. Insufficient phase synchronization and desynchronization during working memory processing reflects impairments in cortical inhibition, memory, and attention efficiency in major depression, while the abnormal increase in phase synchronization in beta oscillations in the frontoparietal network may indicate a new cortical circuit concerned with the repair of impaired ability in attention, memory retention, and working memory central executive processing. These findings present a compensatory mechanism for impaired cognitive function in major depression, and advance our understanding of functional aspect of beta oscillations.
This study is to examine changes of functional connectivity in patients with depressive disorder using synchronous brain activity. Event-related potentials (ERPs) were acquired during a visual oddball task in 14 patients with depressive disorder and 19 healthy controls. Electroencephalogram (EEG) recordings were analyzed using event-related phase coherence (ERPCOH) to obtain the functional network. Alteration of the phase synchronization index (PSI) of the functional network was investigated. Patients with depression showed a decreased number of significant electrode pairs in delta phase synchronization, and an increased number of significant electrode pairs in theta, alpha and beta phase synchronization, compared with controls. Patients with depression showed lower target-dependent PSI increment in the frontal-parietal/temporal/occipital electrode pairs in delta-phase synchronization than healthy participants. However, patients with depression showed higher target-dependent PSI increments in theta band in the prefrontal/frontal and frontal-temporal electrode pairs, higher PSI increments in alpha band in the prefrontal pairs and higher increments of beta PSI in the central and right frontal-parietal pairs than controls. It implied that the decrease in delta PSI activity in major depression may indicate impairment of the connection between the frontal and parietal/temporal/occipital regions. The increase in theta, alpha and beta PSI in the frontal/prefrontal sites might reflect the compensatory mechanism to maintain normal cognitive performance. These findings may provide a foundation for a new approach to evaluate the effectiveness of therapeutic strategies for depression.
This study examined the impact of depressive disorders, anxiety disorders and the comorbidity of these disorders on the regional electrophysiological features of brain activity. Sixty-four-channel event-related potentials (ERP) were acquired during a visual oddball task in patients with depressive disorder, patients with anxiety disorders, patients with comorbid depressive and anxiety disorders and healthy subjects. An fMRI-constrained source model was applied to ERP to identify different cortical activities in the patient and control groups. Comorbid patients showed an abnormal frontal-greater-than-parietal P3b topography in the right hemisphere and the highest P3a amplitude at frontal and central sites at the scalp midline. For P3b, depressed patients showed decreased right-lateralized activity in the precentral sulcus (PrCS) and posterior parietal cortex (PPC). Anxious patients demonstrated hyperactive prefrontal cortices (PFC). Comorbid patients presented decreased activity in the cingulate gyrus, right PrCS and right PPC and increased activity in the left PFC and left insular (INS). For P3a, hyperactive left PrCS was found in comorbid patients. Comorbid patients showed both anxiety-related and depression-related activity. A superimposition effect of depression and anxiety was identified with (1) aggravated hypo-function of the right-lateralized dorsal attention and salience networks and (2) complicated anxiety-related hyper-function of the left-lateralized ventral attention and salience networks.
This paper is to study auditory event-related potential P300 in patients with anxiety and depressive disorders using dipole source analysis. Auditory P300 using 2-stimulus oddball paradigm was collected from 35 patients with anxiety disorder, 32 patients with depressive disorder, and 30 healthy controls. P300 dipole sources and peak amplitude of dipole activities were analyzed. The source analysis resulted in a 4-dipole configuration, where temporal dipoles displayed greater P300 amplitude than that of frontal dipoles. In addition, a right-greater-than-left hemispheric asymmetry of dipole magnitude was found in patients with anxiety disorder, whereas a left-greater-than-right hemispheric asymmetry of dipole magnitude was observed in depressed patients. Results indicated that the asymmetry was more prominent over the temporal dipole than that of frontal dipoles in patients. Patients with anxiety disorder may increase their efforts to enhance temporal dipole activity to compensate for a deficit in frontal cortex processing, while depressed patients show dominating reduction of right temporal activity. The opposite nature of results observed with hemispheric asymmetry in depressive and anxiety disorders could serve to be valuable information for psychiatric studies.
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