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Background Major depressive disorder (MDD) is often comorbid with anxiety disorders or symptoms. Brain hyperactivity, frontal alpha asymmetry (FAA), and parietal alpha asymmetry (PAA) have been considered as trait markers in patients with MDD. This study investigated the electroencephalogram (EEG) patterns among patients with MDD comorbid with anxiety symptoms. Methods One hundred and thirty-five patients with MDD comorbid with anxiety (MDD group) and 135 healthy controls (HC group) were analyzed. The Beck Depression Inventory-II (BDI–II) and Beck Anxiety Inventory (BAI) were completed, and 19 EEG channels were measured during the resting state, depressive recall and recovery tasks, and happiness recall and recovery tasks. FAA and PAA were computed by log (F4 alpha)–log (F3 alpha) and log (P4 alpha)–log (P3 alpha). Results The FAA and PAA indices between the two groups showed no significant differences; however, compared with the HC group, the MDD group had lower total delta and theta values, and higher total beta, low beta, and high beta values in the resting state. The total beta value positively correlated with the BDI–II and BAI scores in the MDD group. Limitations Most patients had anxious MDD and taking prescriptions, antidepressants or benzodiazepine may affect EEG patterns. Conclusion Compared with HCs, patients with MDD comorbid with anxiety had a higher beta activity in the entire brain region, supporting the role of brain hyperactivity, instead of FAA or PAA, as a trait marker in these patients. A neurofeedback protocol could be developed in future based on the brain hyperactivity findings.

Heart rate variability biofeedback (HRV-BF) has been confirmed to increase heart rate variability (HRV) and cardiac outflows by baroreflex in healthy populations and clinical patients. Autogenic training (AT) is common used in the psychological intervention. This study integrates a single-session of HRV-BF and AT into a high-technology mobile application (app), and examines the effects on HRV indices, breathing rates, and subjective relaxation scores. Healthy college students were recruited and assigned to the single-session HRV-BF group or AT group. Participants in the HRV-BF group received HRV-BF combined with paced breathing training, which gradually stepped down their breathing rates from 12, to 8, to 6 breaths/per min; and received feedback of HRV indices from the app. Participants in the AT group received autogenic training and feedback of heart rate from the app. A chest belt Zephyr BioHarness was connected through Bluetooth to a Zenfone5 mobile phone, it collected the signals of interbeat intervals and breathing rates at pre-training, mid-training, and post-training stages. The Kubios HRV software was used to analyze HRV indices. The results reveal higher HRV indices and lower breathing rates during mid-training and post-training in the HRV-BF group compared to the AT group. There were higher high-frequency of HRV at post-training than pre-training in the AT group. Participants of both groups increased their subjective relaxation scores after training. The HRV-BF protocol increased cardiac outflows by baroreflex and decreased breathing rates, and the AT protocol increased high-frequency of HRV. These high-technology wearable devices combined with psychological interventions will apply to various populations in the future.

Background Alpha-asymmetry neurofeedback (ALAY) was applied to patients with major depressive disorder (MDD) based on the theory of frontal alpha asymmetry. Neurophysiological studies have found a higher high-beta activity of electroencephalography (EEG) at the posterior cortex among patients with comorbid MDD and anxiety symptoms. The present study examined the effects of ALAY and high-beta down-training (Beta) neurofeedback in symptoms of depression and anxiety and EEG parameters. Method Eighty-seven patients with comorbid MDD and anxiety symptoms were allocated to the ALAY, Beta, or control groups. Both neurofeedback groups received ten-session neurofeedback. All participants completed the Beck Depression Inventory II (BDI-II), Beck Anxiety Inventory (BAI), and five minutes resting EEG recording at pre-test and post-test. EEG raw signals were transformed into an A1 score [log (F4 alpha) - log (F3 alpha)], P3 and P4 high-beta power. Results BDI-II and BAI scores decreased at post-test in both ALAY and Beta groups, but no significant difference between the two groups. No significant interaction effect in A1 score at pre-test and post-test between the ALAY, Beta, and control groups. The P3 high-beta was significantly decreased in the Beta group, an increase in the control group, and no change in the ALAY group at post-test compared to the pre-test. Conclusions Both neurofeedback groups decreased symptoms of depression and anxiety. The Beta group was more effective in decreasing high-beta power at the parietal cortex compared to other groups. This non-invasive psychological intervention can be used in the future for patients with comorbid MDD and anxiety symptoms.

Introduction: Alpha asymmetry of the left and right frontal hemisphere is a potential biomarker for major depressive disorder (MDD). Neurofeedback (NFB) is a clinical intervention program for regulating brain activity and decreasing alpha asymmetry. The purpose of this study was to explore the efficacy of NFB among patients with MDD. Methods: Fourteen patients with MDD were randomly assigned to a NFB group that received neurofeedback training 1 hr weekly for 6 weeks and to a control group that was treated without training. A 5-min resting baseline of electroencephalogram (EEG) was recorded at F3 (left) and F4 (right) before and after NFB, and the alpha power was analyzed as an asymmetry index (A1). Results: The A1 of the control group decreased from pre- to post-interventions while the A1 of the NFB group increased from pre- to post-interventions. Anxiety and depression scores of the responder group decreased from pre- to post-interventions, while the scores of the non-responder group increased from pre-to post-interventions. Conclusion: Patients who respond to the NFBtraining showed a decrease in anxiety and depression scores compared to those who do not. This study indicated that NFB could improve left frontal hypoarousal or right frontal hyperarousal among patients with MDD.

Characteristics of the distressed (Type D) personality include negative affectivity (NA) and social inhibition (SI), which are associated with an increased risk of major adverse cardiac events and mortality among patients with coronary artery disease (CAD). The aims of this study were to examine: (1) the correlation of NA and SI with psychological characteristics, heart rate variability (HRV) indices, and lipids profiles and (2) the differences in psychological characteristics, HRV indices, and lipid profiles between patients with CAD with Type D personality and those with non-Type D personality. A cross-sectional study was conducted on 168 patients with CAD. The Taiwanese 14-item Type D Scale, Chinese Hostility Inventory-Short Form, Beck Depression Inventory-II, Beck Anxiety Inventory, and Anger Rumination Scale were administered to all of the participants. The raw signals of electrocardiograms were recorded over a 5-min baseline resting period and then transformed to HRV indices representing short-term cardiac autonomic activations. Lipid profiles were acquired from patients’ medical records. NA was positively correlated with hostility, depression, anxiety, and anger rumination. With respect to pathophysiological mechanisms for CAD with Type D personality, NA was negatively correlated with standard deviation of all normal-to-normal intervals (SDNN) and total power of HRV and positively correlated with total cholesterol. SI was positively correlated with suppressive hostility behavior and anger rumination; however, SI was not significantly correlated with expressive hostility behavior, or HRV indices and lipid profiles. Pathophysiological mechanisms leading to higher rates of adverse outcomes in CAD in individuals with Type D personalities may involve cardiac autonomic imbalance and lipid dysregulation.