Antidepressant Medication Treatment Research Articles

Treatment Differences in Primary and Specialty Settings in Veterans with Major Depression.

The Veterans Health Administration (VHA) supports the nation's largest primary care-mental health integration (PC-MHI) collaborative care model to increase treatment of mild to moderate common mental disorders in primary care (PC) and refer more severe-complex cases to specialty mental health (SMH) settings. It is unclear how this treatment assignment works in practice. Patients (n = 2610) who sought incident episode VHA treatment for depression completed a baseline self-report questionnaire about depression severity-complexity. Administrative data were used to determine settings and types of treatment during the next 30 days. Thirty-four percent (34.2%) of depressed patients received treatment in PC settings, 65.8% in SMH settings. PC patients had less severe and fewer comorbid depressive episodes. Patients with lowest severity and/or complexity were most likely to receive PC antidepressant medication treatment; those with highest severity and/or complexity were most likely to receive combined treatment in SMH settings. Assignment of patients across settings and types of treatment was stronger than found in previous civilian studies but less pronounced than expected (cross-validated AUC = 0.50-0.68). By expanding access to evidence-based treatments, VHA's PC-MHI increases consistency of treatment assignment. Reasons for assignment being less pronounced than expected and implications for treatment response will require continued study.

EEG biomarker informed prescription of antidepressants in MDD: a feasibility trial

Using pre-treatment biomarkers to guide patients to the preferred antidepressant medication treatment could be a promising approach to enhance its current modest response and remission rates. This open-label prospective study assessed the feasibility of using such pre-treatment biomarkers, by using previously identified EEG features (paroxysmal activity; alpha peak frequency; frontal alpha asymmetry) to inform the clinician in selecting among three different antidepressants (ADs; escitalopram, sertraline, venlafaxine) as compared to Treatment As Usual (TAU). EEG data were obtained from 195 outpatients with major depressive disorder prior to eight weeks of AD treatment. Primary outcome measure was the percentage change between before and after treatment on the Beck Depression Inventory-II (BDI-II). We compared TAU and EEG-informed prescription through AN(C)OVAs. Recruitment started with patients receiving TAU to establish baseline effectiveness, after which we recruited patients receiving EEG-informed prescription. 108 patients received EEG-informed prescription and 87 patients received TAU. Clinicians and patients were satisfied with the protocol. Overall, 70 (65%) of the EEG-informed clinicians followed recommendations (compared to 52 (60%) following prescriptions in the TAU group), establishing feasibility. We here confirm that treatment allocation informed by EEG variables previously reported in correlational studies, was feasible.

Glycaemic trajectory and predictors of suboptimal glycaemic control in people with type 2 diabetes.

We aimed to describe the glycaemic trajectory and define characteristics associated with suboptimal glycaemic control in the type 2 diabetes clinic. Higher glycosylated haemoglobin (HbA1c) at 1 year was associated with higher baseline HbA1c, concurrent anti-depressant or antipsychotic medication, higher bodyweight and low treatment adherence. These characteristics may help identify patients unlikely to attain HbA1c treatment targets and be better served by a different model of care.

Preliminary Evidence That Cortical Amyloid Burden Predicts Poor Response to Antidepressant Medication Treatment in Cognitively Intact Individuals With Late-Life Depression

Amyloid accumulation, the pathological hallmark of Alzheimer's disease, may predispose some older adults to depression and cognitive decline. Deposition of amyloid also occurs prior to the development of cognitive decline. It is unclear whether amyloid influences antidepressant outcomes in cognitively intact depressed elders. A pharmacoimaging trial utilizing florbetapir (18F) PET scanning followed by 2 sequential 8-week antidepressant medication trials. Twenty-seven depressed elders who were cognitively intact on screening. After screening, diagnostic testing, assessment of depression severity and neuropsychological assessment, participants completed florbetapir (18F) PET scanning. They were then randomized to receive escitalopram or placebo for 8 weeks in a double-blinded two-to-one allocation rate. Individuals who did not respond to initial treatment transitioned to a second open-label trial of bupropion for another 8 weeks. Compared with 22 amyloid-negative participants, 5 amyloid-positive participants exhibited significantly less change in depression severity and a lower likelihood of remission. In the initial blinded trial, 4 of 5 amyloid-positive participants were nonremitters (80%), while only 18% (4 of 22) of amyloid-negative participants did not remit (p = 0.017; Fisher's Exact test). In separate models adjusting for key covariates, both positive amyloid status (t = 3.07, 21 df, p = 0.003) and higher cortical amyloid binding by standard uptake value ratio (t = 2.62, 21 df, p = 0.010) were associated with less improvement in depression severity. Similar findings were observed when examining change in depression status across both antidepressant trials. In this preliminary study, amyloid status predicted poor antidepressant response to sequential antidepressant treatment. Alternative treatment approaches may be needed for amyloid-positive depressed elders.

Do people living in disadvantaged circumstances receive different mental health treatments than those from less disadvantaged backgrounds?

BackgroundSocio-economic status (SES) has been linked to treatment outcomes for mental health problems, whilst little to no literature has explored the effects of SES on access to both medication and psychological therapy. The aim of this study was to explore whether access to mental health treatments differed by SES.MethodsThe North West Coast Household Health Survey (HHS) collected data from residents aged 18+ from across 20 disadvantaged and 8 less disadvantaged neighbourhoods in 2015, and from 20 disadvantaged neighbourhoods in 2018. Logistic regression was used to explore the effects of SES on access to treatment (medication, psychological therapy) for people who had experienced mental health problems in the past 12 months.ResultsOf 6860 participants, 2932 reported experiencing mental health problems in the past 12 months. People from more disadvantaged backgrounds experienced greater rates of anxiety and depression. Anti-depressant and anti-psychotic medication treatment was significantly more common in residents with lower SES, as well as counselling. Regression analysis showed that residents from more disadvantaged neighbourhoods who reported mental distress were more likely to receive medication.ConclusionsThis appears to be the first study showing higher levels of treatment with medication and psychological therapy in people from disadvantaged backgrounds. Future research needs to address the underlying factors associated with increased mental health treatment uptake in people from lower socio-economic backgrounds.

Effect of repetitive transcranial magnetic stimulation (rTMS) treatment of major depressive disorder (MDD) on cognitive control

BackgroundMajor Depressive Disorder (MDD) is commonly accompanied by cognitive control dysfunction that may persist after remission of clinical symptoms with antidepressant medication treatment. Repetitive Transcranial Magnetic Stimulation (rTMS) is an effective treatment alternative for medication-resistant MDD. In this study, we investigated whether rTMS treatment had a beneficial effect not only on depressive symptoms, but on also cognitive control dysfunction. Methods77 subjects with MDD received a 30-session treatment course of 10 Hz rTMS administered at the left dorsolateral prefrontal cortex (DLPFC). Treatment efficacy was assessed using the Inventory of Depressive Symptomatology Self-Rated (IDS-SR) before and after treatment, with clinical response defined as 50% or greater decrease in the IDS-SR score at treatment 30. Cognitive control function was assessed before and after treatment using the Stroop word-color interference task. We examined changes in Stroop accuracy and reaction time for congruent and incongruent trials, as well as in relation to changes in depressive symptoms. ResultsPerformance accuracy improved particularly for the rTMS responders in the incongruent condition, with older subjects benefitting most from the rTMS treatment. Improvement in reaction times was positively associated with clinical improvement, especially in the incongruent condition. LimitationsWe used a single cognitive task in a naturalistic setting without control for individual rTMS treatment parameters or concomitant medication. ConclusionsOverall, these results indicate that rTMS treatment for MDD has beneficial effects on psychomotor speed and cognitive control. Future studies should extend these findings to larger patient populations and other cognitive domains.

Prevention of Recurrence After Recovery From a Major Depressive Episode With Antidepressant Medication Alone or in Combination With Cognitive Behavioral Therapy

Antidepressant medication (ADM) maintenance treatment is associated with the prevention of depressive recurrence in patients with major depressive disorder (MDD), but whether cognitive behavioral therapy (CBT) treatment is associated with recurrence prevention remains unclear. To determine the effects of combining CBT with ADM on the prevention of depressive recurrence when ADMs are withdrawn or maintained after recovery in patients with MDD. A total of 292 adult outpatients with chronic or recurrent MDD who participated in the second phase of a 2-phase trial. Participants had recovered in the first phase of the trial receiving ADM, either alone or in combination with CBT. The trial was conducted in research clinics in 3 university medical centers in the United States. Patients in phase 2 were randomized to receive maintenance of or withdrawal from ADM and were followed up for 3 years. The first and last patients entered phase 2 in August 2003 and October 2009, respectively. The last patient completed phase 2 in August 2012. Data were analyzed from December 2013 to December 2018. Maintenance of or withdrawal from treatment with ADM. Recurrence of an MDD episode using longitudinal interval follow-up evaluations; sustained recovery across both phases. A total of 292 participants (171 women, 121 men; mean [SD] age 45.1 [12.9] years) were included in analyses of depressive recurrence. Maintenance ADM yielded lower rates of recurrence compared with ADM withdrawal regardless of whether patients had achieved recovery in phase 1 with ADM alone (48.5% vs 74.8%; z = -3.16; P = .002; number needed to treat [NNT], 2.8; 95% CI, 1.8-7.0) or ADM plus CBT (48.5% vs 76.7%; z = -3.49; P < .001; NNT, 2.7; 95% CI, 1.9-5.9). Sustained recovery rates differed as a function of phase 2 condition, with maintenance ADM superior to ADM withdrawal (z = 2.90; P = .004; OR, 2.54; 95% CI, 1.37-4.84; NNT, 2.3; 95% CI, 1.5-6.4). Phase 1 condition was not associated with differential rates of sustained recovery (ADM alone vs ADM plus CBT; z = 0.22; P = .83; OR, 1.08; 95% CI, 0.52-2.11; NNT, 26.0; 95% CI, number needed to harm 3.2 to NNT 2.8), nor was there a significant interaction of phase 1 condition and phase 2 condition (z = 0.30; P = .77; OR, 1.14; 95% CI, 0.49-2.88). Maintenance ADM treatment, but not previous exposure to CBT, was associated with reduced rates of depressive recurrence. In previous studies, when CBT has been provided without ADM, CBT has shown a preventive effect on depressive relapse. Whether CBT also has a preventive effect on depressive recurrence, or if adding ADM interferes with any such preventive effect, remains unclear. ClinicalTrial.gov identifier: NCT00057577.

Short- and Long-Term Antidepressant Clinical Trials for Major Depressive Disorder in Youth: Findings and Concerns.

The diagnosis of major depressive disorder (MDD) in U.S. youth is increasing as is the rate of antidepressant medication (ADM) treatment for the disorder. Fluoxetine and escitalopram are FDA approved for the short term and maintenance treatment of MDD in youth. Placebo-controlled short-term ADM trials represent the basis for Food and Drug Administration (FDA) approval. Meta-analyses in 2007 and 2016 revealed that short-term ADM treatment of youth diagnosed with MDD resulted in no meaningful benefit for children and only marginal benefit for adolescents. Placebo substitution trials of ADM short-term responders represent the basis for FDA approval of ADM maintenance treatment. These ADM placebo substitution maintenance trials for youth with MDD are characterized by high dropout rates, a rapid withdrawal that often can follow the switch to placebo, and relapse rates that are not dissimilar from those in the natural course of the disorder. Without the evidence from problematic ADM placebo substitution trials, there is no acceptable support for the inclusion of ADM in maintenance treatment for MDD in youth.

Borderline personality disorder and depressive disorder.

Borderline personality disorder (BPD) is frequently accompanied by low mood, the features of which may satisfy the diagnostic criteria for major depressive disorder (MDD). Treatment of depressive symptoms in the absence of BPD-appropriate treatment is less effective and may cause iatrogenic harm. This paper briefly reviews the co-occurrence of BPD and depressive disorder and suggests ways of differentiating these disorders and optimising treatment within the Australian Mental Health context. Depressive symptoms are present in the majority of people with BPD. To address the difficulty differentiating clinically distinct MDD from depressive symptoms that are integral to BPD psychopathology, it is suggested that depressive symptoms arising from a primary diagnosis of BPD (i) may exhibit transience and be stress reactive, (ii) lack a robust clinical response to antidepressant medication and/or electroconvulsive treatment and (iii) are responsive to BPD-appropriate psychotherapy.

EXERCISE AS AN AUGMENTATION TO PHARMACOTHERAPY FOR DEPRESSION IN OLDER AND YOUNGER ADULTS: A FEASIBILITY TRIAL EXPLORING BIOLOGICAL MECHANISMS

Introduction Exercise interventions for depression that also examine biological mechanisms are rare and none have included both younger and older adults with Major Depression. Our pilot intervention study tested the feasibility of conducting a physical exercise intervention as augmentation to pharmacotherapy for depression in younger and older adults while also exploring possible neural mechanisms underlying the antidepressant effects of exercise. Methods Fifteen sedentary younger (20-39 years) and older adults (60-79 years) meeting criteria for a Major Depressive Episode were randomized to receive a 12-week medication regimen of venlafaxine XR or venlafaxine XR plus physical exercise. The exercise intervention involved supervised moderate-intensity aerobic exercise sessions three times per week for 12 weeks. The primary aim was to develop the infrastructure for conducting an exercise intervention in adults with Major Depression while also collecting brain imaging measures to better understand mechanisms. The Montgomery Asberg Depression Rating Scale (MADRS) was used to assess change in depressive symptoms, the VO2submaximal test was used to assess change in cardiorespiratory fitness, and 7T structural MR imaging was used to assess change in regional brain morphology (i.e., cortical thickness) relevant to depression. Data analysis was conducted using repeated measures ANOVA and paired-samples and independent samples t-tests. Results Our results demonstrated feasibility of conducting a physical exercise intervention combined with pharmacotherapy trial in depressed younger and older adults. Ten younger adults and five older adults were randomized to receive treatment and 11 participants completed the study. There was 0% attrition and a 91% attendance rate (i.e., 33/36 sessions) among participants engaged in the exercise intervention. Although efficacy of the intervention was unable to be tested, trends suggested that the addition of physical exercise to medication treatment for depression may lead to rapid and stable decline in depressive symptoms and exercise-related improvements in cardiorespiratory fitness may be linked to an increase in cortical thickness in regions sensitive to depression (i.e., orbitofrontal cortex, anterior cingulate cortex, parahippocampal gyrus). Further, sensitivity analyses suggested that treatment-related increases in cortical thickness in the right medial orbitofrontal cortex and right rostral anterior cingulate cortex were associated with improved performance on measures of verbal learning and memory (p Conclusions This pilot clinical trial involving physical exercise as an augmentation to antidepressant medication treatment enabled this interdisciplinary research team to develop the infrastructure for conducting an exercise intervention for depression in late-life and early adulthood while also examining biological mechanisms. Recruitment challenges were overcome, and intervention adherence was exceptional. Trending associations between exercise-related improvements in fitness and changes in cortical thickness are promising avenues for future large-scale studies to explore. This research was funded by This project was supported by the Advanced Center for Intervention and Services Research (ACISR). PDF: http://submissions.mirasmart.com/Verify/AAGP2019/Original/AAGP2019-000336/AAGP2019-000336_Fig1.pdf PDF: http://submissions.mirasmart.com/Verify/AAGP2019/Original/AAGP2019-000336/AAGP2019-000336_Fig2.pdf

Psychological therapies for treatment-resistant depression in adults.

Psychological therapies for treatment-resistant depression in adults.

Cross-sectional networks of depressive symptoms before and after antidepressant medication treatment

PurposeRecent reviews have questioned the efficacy of selective serotonin reuptake inhibitors (SSRIs) above placebo response, and their working mechanisms remain unclear. New approaches to understanding the effects of SSRIs are necessary to enhance their efficacy. The aim of this study was to explore the possibilities of using cross-sectional network analysis to increase our understanding of symptom connectivity before and after SSRI treatment.MethodsIn two randomized controlled trials (total N = 178), we estimated Gaussian graphical models among 20 symptoms of the Beck Depression Inventory-II before and after 8 weeks of treatment with the SSRI paroxetine. Networks were compared on connectivity, community structure, predictability (proportion explained variance), and strength centrality (i.e., connectedness to other symptoms in the network).ResultsSymptom severity for all individual BDI-II symptoms significantly decreased over 8 weeks of SSRI treatment, whereas interconnectivity and predictability of the symptoms significantly increased. At baseline, three communities were detected; five communities were detected at week 8.ConclusionsFindings suggest the effects of SSRIs can be studied using the network approach. The increased connectivity, predictability, and communities at week 8 may be explained by the decrease in depressive symptoms rather than specific effects of SSRIs. Future studies with larger samples and placebo controls are needed to offer insight into the effects of SSRIs.Trial RegistrationThe trials described in this manuscript were funded by the NIMH.Pennsylvania/Vanderbilt study:5 R10 MH55877 (https://projectreporter.nih.gov/project_info_description.cfm?aid=6186633&icde=28344168&ddparam=&ddvalue=&ddsub=&cr=1&csb=default&cs=ASC&MMOpt=).Washington study:R01 MH55502 (https://projectreporter.nih.gov/project_info_description.cfm?aid=2034618&icde=28344217&ddparam=&ddvalue=&ddsub=&cr=5&csb=default&cs=ASC).

EEG gamma synchronization is associated with response to paroxetine treatment

BackgroundResistance to medication is a significant problem in psychiatric practice, and effective methods for predicting response are needed to optimize treatment efficacy and limit morbidity. Gamma oscillations are considered as an index of the brain's general cognitive activity; however, the role of gamma oscillations in disease has not been studied sufficiently. AimThis study aimed to determine if gamma power during rest can be used to predict response to anti-depressant medication treatment. MethodHamilton Depression Rating Scale (HDRS) score and resting state gamma power was measured in 18 medication-free patients during an episode of major depression. After 6 weeks of paroxetine monotherapy HDRS was administered again. ResultsBaseline gamma power at frontal, central and temporal electrodes before treatment was significantly related to post-treatment change in HDRS scores. ConclusionThe results indicate that gamma oscillations could be considered a marker of response to paroxetine treatment in patients with major depression.

PLACEBO-CONTROLLED TRIAL OF DONEPEZIL FOLLOWING ANTIDEPRESSANT TREATMENT IN PATIENTS WITH COMORBID DEPRESSION AND COGNITIVE IMPAIRMENT

In patients with comorbid depression and cognitive impairment, antidepressants are commonly used but the utility of cholinesterase inhibitors (CheI) as cognitive enhancers is not established. Eighty elderly (55–95 years old) depressed, cognitively impaired (DEP-CI) patients participated in the DOTCODE study at two sites: Columbia and Duke University Medical Centers. 40 of 79 patients who received antidepressant medication in the initial phase met criteria for amnestic mild cognitive impairment (MCI). After 16 weeks of open-label antidepressant treatment with antidepressants, primarily citalopram or venlafaxine, 61 patients were randomized to receive 62 weeks of the CheI donepezil 5–10 mg daily or placebo in a randomized, double-blind trial. Linear mixed effects models with random subject-specific intercepts were used to model ADAS-Cog13 and Selective Reminding Test (SRT) Total Immediate Recall over the course of the study. All models include baseline value of the outcome, age, study site, treatment, visit week, and the interaction between treatment and visit week (and interaction terms to test for moderators). In the first 16 weeks, depression improved in most patients and 39 of 61 randomized patients (64%) met responder criteria. In the 61 randomized patients, donepezil did not differ from placebo in change in the co-primary measures of ADAS-Cog13 (F=0.18, p=0.83) and SRT total recall (F=0.06, p=0.9). Four patients were diagnosed with probable Alzheimer's disease by end-trial. Apolipoprotein E e4 allele and MRI hippocampal volume were unrelated to differences in outcomes between donepezil and placebo. Periventricular hyperintensities (PVH) did not distinguish changes in cognition on donepezil from placebo on ADAS-Cog13 (F1,39 = 0.14, p = 0.71) but did on SRT total recall (F1,39 = 4.23, p = 0.04); less PVH was associated with greater improvement with donepezil on SRT total recall. In patients with comorbid depression and cognitive impairment, the addition of donepezil following antidepressant medication treatment did not improve cognition compared to placebo, though donepezil treatment was associated with better cognition in patients with less cerebrovascular disease. The findings add to those from studies in mild cognitive impairment without depression that have not demonstrated superiority for CheI over placebo in improving cognition.

Meta-analyses of comparative efficacy of antidepressant medications on peripheral BDNF concentration in patients with depression

BackgroundBrain derived neurotrophic factor (BDNF) is one of the most important regulatory proteins in the pathophysiology of major depressive disorder (MDD). Increasing numbers of studies have reported the relationship between serum/plasma BDNF and antidepressants (ADs). However, the potential effects of several classes of antidepressants on BDNF concentrations are not well known. Hence, our meta-analyses aims to review the effects of differential antidepressant drugs on peripheral BDNF levels in MDD and make some recommendations for future research.MethodsElectronic databases including PubMed, EMBASE, the Cochrane Library, Web of Science, and PsycINFO were searched from 1980 to June 2016. The change in BDNF levels were compared between baseline and post-antidepressants treatment by use of the standardized mean difference (SMD) with 95% confidence intervals (CIs). All statistical tests were two-sided.ResultsWe identified 20 eligible trials of antidepressants treatments for BDNF in MDD. The overall effect size for all drug classes showed that BDNF levels were elevated following a course of antidepressants use. For between-study heterogeneity by stratification analyses, we detect that length of treatment and blood samples are significant effect modifiers for BDNF levels during antidepressants treatment. While both SSRIs and SNRIs could increase the BDNF levels after a period of antidepressant medication treatment, sertraline was superior to other three drugs (venlafaxine, paroxetine or escitalopram) in the early increase of BDNF concentrations with SMD 0.53(95% CI = 0.13–0.93; P = 0.009).ConclusionsThere is some evidence that treatment of antidepressants appears to be effective in the increase of peripheral BDNF levels. More robust evidence indicates that different types of antidepressants appear to induce differential effects on the BDNF levels. Since sertraline makes a particular effect on BDNF concentration within a short amount of time, there is potential value in exploring its relationship with BDNF and its pharmacological mechanism concerning peripheral blood BDNF. Further confirmatory trials are required for both observations.

Antidepressant Medication Treatment and Risk of Death.

Although previous studies have assessed whether depression is a mortality risk factor, few have examined whether antidepressant medications (ADMs) influence mortality risk. We estimated hazards of 1-year all-cause mortality associated with ADMs, with use occurring within 90 days of depression diagnosis among 720 821 patients who received treatment in a Veterans Health Administration facility during fiscal year 2006. We addressed treatment selection biases using conventional Cox regression, propensity-stratified Cox regression (propensity score), and 2 forms of marginal structural models. Models accounted for multiple potential clinical and demographic confounders, and sensitivity analyses compared findings by antidepressant class. Antidepressant medication use compared with no use was associated with significantly lower hazards of 1-year mortality risk in Cox (hazard ratio [HR], 0.93; 95% confidence interval [CI], 0.90-0.97) and propensity score estimates (HR, 0.94; 95% CI, 0.91-0.98), whereas marginal structural model-based estimates showed no difference in mortality risk when the exposure was specified as "as-treated" in every 90-day intervals of the 1-year follow-up (HR, 0.91; 95% CI, 0.66-1.26) but showed increased risk when specified as "intent-to-treat" (HR, 1.07; 95% CI, 1.02-1.13). Among patients treated with ADMs belonging to a single class in the first 90 days, there were no significant differences in 1-year all-cause mortality risks. When accounting for clinical and demographic characteristics and treatment selection bias, ADM use was associated with no excess harm.

Reconfiguration of hub-level community structure in depressions: A follow-up study via diffusion tensor imaging

BackgroundThe role of abnormal communications among large-scale brain networks have been given increasing attentions in the pathophysiology of major depressive disorder (MDD). However, few studies have investigated the effect of antidepressant medication treatment on the information communication of structural brain networks, especially converged from the individual analysis. MethodsNineteen unipolar MDD patients completed two diffusion tensor imaging (DTI) scans before and after 8-week treatment with selective serotonin reuptake inhibitor. DTI data of 37 matched healthy controls were acquired. We focused on a hub-level community structure network, and investigated whether it had differences on the whole structure and which regions drove these differences in terms of modular affiliation and hub role shift. Data were analyzed by the novel permutation network framework, which appraised the topological consistency of hubs and reserved an individual information. ResultsCompared to the pre-treatment state, post-treatment patients exhibited increasing number of modular members in the modules that included the right medial superior frontal gyrus (SFGmed) or the thalamus. Moreover, the result suggested a hub role shift of the left insula from a provincial-hub before treatment to a connector-hub after treatment. Additionally, reduced inter-module degree in the right SFGmed was positively correlated with the reduced sum score of 17-item Hamilton depression rating scale at the follow-up. ConclusionsAntidepressant medication treatment might be associated with modular reconfigurations of hubs within the fronto-limbic circuit. Moreover, increased inter-module connections of the left insula might improve its integration ability, promoting the remission of MDD. The correlation results of the right SFGmed suggested it might be a valuable indicator for treatment response.

Baseline Psychological Treatment Reduces the Effect of Coaching in a Randomised Trial of a Depression Self-Care Intervention

To explore the effects of baseline psychological and antidepressant medication treatment in a trial of lay telephone coaching in a low-intensity, supported depression self-care intervention. A single blind, individually randomised, pragmatic trial was conducted among primary care adults with chronic physical conditions and comorbid depressive symptoms. Eligible subjects were randomised to receive a depression self-care toolkit with (intervention group) or without (control group) telephone coaching provided by trained lay coaches. For this brief communication, a secondary analysis of the trial data focused on the effects of baseline psychological and antidepressant treatments on mental health outcomes (Patient Health Questionnaire 9 [PHQ-9], SF-12 Mental Component Summary [MCS], Generalized Anxiety Disorder 7 [GAD-7]) and satisfaction with the intervention. In total, 223 patients were randomised, and 165 (74.0%) completed both 3- and 6-month follow-ups. There were 2 significant interactions of baseline treatment and study group for 6-month mental health outcomes. A significant benefit of coaching on 6-month PHQ-9 was seen only among participants who were not receiving baseline psychological treatment. A smaller interaction was found for baseline antidepressant medications and 6-month mental health. There was a significant main effect for baseline psychological treatment and lower 6-month satisfaction. Depressed patients receiving baseline psychological treatment may not benefit from lay coaching offered as part of a low-intensity depression self-care intervention.

Effective Treatments of Late-Life Depression in Long-Term Care Facilities

Purpose: The purpose of this study was to identify effective treatment to manage the depression of older residents. Methods: Using Klein and Bloom’s criteria, we analyzed the number of subjects, designs and methodologies, residential types, intervention types and duration of treatment, standardized measures, and findings. Data searches were conducted to classify empirical studies and to review empirical literature published from 2007 to 2014. A systematic research synthesis of 25 articles was conducted to investigate how various treatments affected depression among older residents. Results: The results show that antidepressant medication treatment appears less efficacious in treating less severe depression. Discussion: These findings reveal that minor depression should be treated initially with a nonpharmacologic intervention to avoid unnecessary medication risks. The findings further suggest the need for more comprehensive analyses of longitudinal research and the need for more studies that examine the combination of medication and psychotherapy for depressed older adults.

Salience Network Functional Connectivity Predicts Placebo Effects in Major Depression

BackgroundRecent neuroimaging studies have demonstrated resting-state functional connectivity (rsFC) abnormalities among intrinsic brain networks in major depressive disorder (MDD); however, their role as predictors of treatment response has not yet been explored. Here, we investigate whether network-based rsFC predicts antidepressant and placebo effects in MDD. MethodsWe performed a randomized controlled trial of two week-long, identical placebos (described either as having active fast-acting, antidepressant effects or as inactive) followed by a 10-week open-label antidepressant medication treatment. Twenty-nine participants underwent an rsFC functional magnetic resonance imaging scan at the completion of each placebo condition. Networks were isolated from resting-state blood oxygen level-dependent signal fluctuations using independent component analysis. Baseline and placebo-induced changes in rsFC within the default mode, salience, and executive networks were examined for associations with placebo and antidepressant treatment response. ResultsIncreased baseline rsFC in the rostral anterior cingulate within the salience network, a region classically implicated in the formation of placebo analgesia and the prediction of treatment response in MDD, was associated with greater response to 1 week of active placebo and 10 weeks of antidepressant treatment. Machine learning further demonstrated that increased salience network rsFC, mainly within the rostral anterior cingulate, significantly predicts individual responses to placebo administration. ConclusionsThese data demonstrate that baseline rsFC within the salience network is linked to clinical placebo responses. This information could be employed to identify patients who would benefit from lower doses of antidepressant medication or nonpharmacologic approaches or to develop biomarkers of placebo effects in clinical trials.