Objective: In numerous studies that have addressed transcranial direct current stimulation (tDCS) devices, participants visit the hospital regularly and undergo stimulation directed by health professionals. This method has the advantage of being able to deliver accurate stimuli in a controlled environment, but it does not adopt the merits of tDCS portability and applicability. Thus, it may be necessary to investigate how self-administered tDCS treatment at home affects depression-related symptoms. Methods: In this randomized, single-blinded clinical trial, 58 patients with major depressive disorder were assigned to active and sham tDCS stimulation groups, and treatment responses were evaluated biweekly over six weeks. Both active and sham tDCS treatment group were treated with escitalopram. All participants were instructed the protocol and usage of at-home tDCS device, and self-administered tDCS treatment at their home. Results: The beck-depression inventory score decreased significantly as treatment progressed, and the degree of symptom improvement was significantly higher in the active group than in the sham tDCS group. There were no significant differences between the two groups in other indices, including the Hamilton Depression Scale. Conclusion These results suggest that patient-administered tDCS treatment might be effective in improving subjective symptoms of depression.

Objective: Although the effects and safety of transcranial direct current stimulation (tDCS) treatment in depressive patients are largely investigated, whether the self-administration of tDCS treatment at patient’s home is comparable to clinic-based treatment is still unknown. Methods: In this single-arm, multi-center clinical trial, 61 patients with mild to moderate major depressive disorder were enrolled. tDCS treatment was delivered at the patient’s home once a day, 5 to 7 times a week for 6 weeks, and each session lasted for 30 minutes. The primary outcome was a total Beck-Depression Inventory-II score, and no concurrent antidepressants were used. Results: The remission rates in both Full-Analysis (FA) (n = 61) and Per-Protocol (PP) (n = 43) groups were statistically significant (FA: 57.4% [0.44−0.70], PP: 62.8% [0.47−0.77]; percent [95% confidence interval]). The degree of depression-related symptoms was also significantly improved in 2, 4, and 6 weeks after the treatment when compared with baseline. There was no significant association between treatment compliance and remission rate in both FA and PP groups. Conclusion These results suggest that acute treatment of patient-administered tDCS might be effective in improving the subjective feeling of depressive symptoms in mild to moderate major depressive disorder patients.

Objective: To investigate the association between genetic polymorphisms of brain-derived neurotrophic factor (BDNF) or serotonin transporter gene-linked polymorphic region (5-HTTLPR) and tinnitus, and the mediating effects of psychological distress on this association. Methods: Eighty-six patients experiencing tinnitus and 252 controls were recruited. The Tinnitus Handicap Inventory was used to assess the severity of tinnitus and the Beck Depression Inventory-II (BDI-II), Beck Anxiety Inventory-II (BAI-II), and the Korean version of the Brief Encounter Psychosocial Instrument (BEPSI-K) were used to assess psychological distress. We compared the association of BDNF rs6265 (Val66Met) and 5-HTTLPR variants in the two groups. The mediating effects of BDI-II, BAI-II, and BEPSI-K were examined using multiple regression analysis and validated by the Sobel test and bootstrapping. Results: No significant differences were found between the groups regarding BDNF Val66Met and 5-HTTLPR, but the 5-HTTLPR variants trended toward association. Depressive symptoms appeared to act as a mediator on the relationship within the 5-HTTLPR s/s genotype and the severity of tinnitus. Conclusion Our findings provide a speculative idea on the association between the serotonergic system and tinnitus and suggest that depressive symptoms act as a mediator in tinnitus. Therefore, screening for depressive symptoms in patients with tinnitus is essential and intervention for depressive symptoms may help alleviate the severity of tinnitus.

Objective: To investigate the association between genetic polymorphisms of brain-derived neurotrophic factor (BDNF) or serotonin transporter gene-linked polymorphic region (5-HTTLPR) and tinnitus, and the mediating effects of psychological distress on this association. Methods: Eighty-six patients experiencing tinnitus and 252 controls were recruited. The Tinnitus Handicap Inventory was used to assess the severity of tinnitus and the Beck Depression Inventory-II (BDI-II), Beck Anxiety Inventory-II (BAI-II), and the Korean version of the Brief Encounter Psychosocial Instrument (BEPSI-K) were used to assess psychological distress. We compared the association of BDNF rs6265 (Val66Met) and 5-HTTLPR variants in the two groups. The mediating effects of BDI-II, BAI-II, and BEPSI-K were examined using multiple regression analysis and validated by the Sobel test and bootstrapping. Results: No significant differences were found between the groups regarding BDNF Val66Met and 5-HTTLPR, but the 5-HTTLPR variants trended toward association. Depressive symptoms appeared to act as a mediator on the relationship within the 5-HTTLPR s/s genotype and the severity of tinnitus. Conclusion Our findings provide a speculative idea on the association between the serotonergic system and tinnitus and suggest that depressive symptoms act as a mediator in tinnitus. Therefore, screening for depressive symptoms in patients with tinnitus is essential and intervention for depressive symptoms may help alleviate the severity of tinnitus.