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Sci Rep. 2015 Nov 24;5:17138. doi: 10.1038/srep17138.

Source analysis of P3a and P3b components to investigate interaction of depression and anxiety in attentional systems.

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Laboratory of Neural Engineering, Shenzhen University, Shenzhen, China, 518060.
Department of Psychological and Brain Sciences, University of California, Santa Barbara, Santa Barbara, CA, 93106, USA.
Shenzhen Kangning Hospital, Shenzhen, China, 518020.
The first Affiliated Hospital of Shenzhen University, Shenzhen, China, 518035.
Department of Orthopaedics and Traumatology, The University of Hong Kong, Pokfulam, Hong Kong.


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.

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