Background: The difficulty in timely evaluating patient response to antidepressants has brought great challenge to the treatment of major depressive disorder (MDD). Some studies found that the electroencephalogram (EEG) microstates might be a reliable marker to evaluate patient response to treatment. The present study aims to evaluate the relationship between EEG microstate parameters and MDD symptoms before and after treatment to identify predictive biological markers for patient response.Methods: Thirty drug-naïve MDD patients (20 females and 10 males) were enrolled in this study. All the patients received effective dosages of selective serotonin reuptake inhibitors, and EEG recordings were collected at baseline and 2 weeks of treatment. Brain activities during the eyes-closed state were recorded using 64-channel electroencephalography, and the patients' microstates were clustered into four maps according to their topography (labeled A, B, C, and D). The differences of EEG microstates before and after treatment were compared using paired t-test. Spearman correlation coefficients were calculated to identify the relationships between the improvement of depression and anxiety symptoms and microstate parameters.Results: The mean duration (69.67 ± 10.33 vs. 64.00 ± 7.70, p < 0.001) and occurrence (4.06 ± 0.69, vs. 3.69 ± 0.70, p = 0.002) of microstate B decreased significantly after treatment. The proportion of microstate B also decreased (27.53 ± 5.81, vs. 23.23 ± 4.61, p < 0.001), while the occurrence of microstate A increased after treatment. A significant negative correlation was found between the change of score of Hamilton Rating Scale for Anxiety and the increase of the occurrence of microstate A (r = −0.431, p < 0.05) after 2 weeks of treatment. The reduction of the duration of microstate B was found to be predictive of patient response to antidepressants after 3 months.Conclusion: This study explored the relationship between changes of EEG microstates and patient response to antidepressants. Depression symptoms might be associated with the duration of microstate B and anxiety symptoms related to the occurrence of microstate A. Therefore, the duration of microstate B and the occurrence of microstate A are potential biological markers for MDD patients' early response and further clinical outcomes.
Background: Major depressive disorder (MDD) is associated with a wide range of cognitive deficits. However, it remains unclear whether there will be a major cognitive deficit independently caused by depression at acute episodes of MDD. Method: A comprehensive neurocognitive test battery was used to assess the executive function, processing speed, attention, and memory in 162 MDD patients and 142 healthy controls (HCs). A multivariate analysis of variance, hierarchical regression analyses and general linear regression analyses were used to explore the possible major cognitive deficits and their predictor variables. Results: MDD patients showed extensive impairment in all four cognitive domains. Impairment of executive function and processing speed were found to persist even with other cognitive domains and clinical variables being accounted for. Executive function and processing speed were further predicted by total disease duration and depression severity, respectively. Conclusions: Executive function and processing speed may be two distinct major deficits at acute episodes of MDD. Furthermore, the executive function is likely originated from the cumulative effect of disease duration and processing speed is possibly derived from the temporary effect of current depressive episode.
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