Original Article
Medication Augmentation after the Failure of SSRIs for Depression
N Engl J Med 2006; 354:1243-1252March 23, 2006
- Abstract
Background
Although clinicians frequently add a second medication to an initial, ineffective antidepressant drug, no randomized controlled trial has compared the efficacy of this approach.
Methods
We randomly assigned 565 adult outpatients who had nonpsychotic major depressive disorder without remission despite a mean of 11.9 weeks of citalopram therapy (mean final dose, 55 mg per day) to receive sustained-release bupropion (at a dose of up to 400 mg per day) as augmentation and 286 to receive buspirone (at a dose of up to 60 mg per day) as augmentation. The primary outcome of remission of symptoms was defined as a score of 7 or less on the 17-item Hamilton Rating Scale for Depression (HRSD-17) at the end of this study; scores were obtained over the telephone by raters blinded to treatment assignment. The 16-item Quick Inventory of Depressive Symptomatology — Self-Report (QIDS-SR-16) was used to determine the secondary outcomes of remission (defined as a score of less than 6 at the end of this study) and response (a reduction in baseline scores of 50 percent or more).
Results
The sustained-release bupropion group and the buspirone group had similar rates of HRSD-17 remission (29.7 percent and 30.1 percent, respectively), QIDS-SR-16 remission (39.0 percent and 32.9 percent), and QIDS-SR-16 response (31.8 percent and 26.9 percent). Sustained-release bupropion, however, was associated with a greater reduction (from baseline to the end of this study) in QIDS-SR-16 scores than was buspirone (25.3 percent vs. 17.1 percent, P<0.04), a lower QIDS-SR-16 score at the end of this study (8.0 vs. 9.1, P<0.02), and a lower dropout rate due to intolerance (12.5 percent vs. 20.6 percent, P<0.009).
Conclusions
Augmentation of citalopram with either sustained-release bupropion or buspirone appears to be useful in actual clinical settings. Augmentation with sustained-release bupropion does have certain advantages, including a greater reduction in the number and severity of symptoms and fewer side effects and adverse events. (ClinicalTrials.gov number, NCT00021528.)
Media in This Article
Figure 1
Time to Remission with Medication.Table 1
Clinical and Demographic Characteristics of Patients.Article Activity
- Article
Numerous studies,1-7 including one by Rush et al.8 reported elsewhere in this issue of the Journal, have shown that major depressive disorder often requires more than one step of treatment to elicit a remission of symptoms. Frequently, a second medication is added to augment the first.4,6 Augmentations of an initial selective serotonin-reuptake inhibitor (SSRI) with sustained-release bupropion, buspirone, mirtazapine, or dopamine agonists (e.g., pramipexole, dextroamphetamine, and methylphenidate) have been evaluated largely in open case series conducted in symptomatic volunteers with few psychiatric or general medical coexisting illnesses.9 No randomized, controlled, prospective trials have directly compared two or more potentially effective second-step augmentation medications, with the exception of a comparison of lithium with thyroid hormone to augment older, tricyclic antidepressants.10,11
From July 2001 through August 2004, we compared the efficacy, safety, and tolerability of augmentation of citalopram (Celexa, Forest Pharmaceuticals), an SSRI, with sustained-release bupropion (Wellbutrin SR, GlaxoSmithKline) or buspirone (Buspar, Bristol-Myers Squibb) as a second step of treatment (level 2) in the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) trial, which is being conducted in primary and psychiatric care settings.4,6 These augmented treatments were compared among patients who did not have a remission or who had an intolerance to citalopram.8,12 Remission of symptoms (rather than response to treatment) was chosen as the primary outcome, because remission is associated with better daily functioning and a better prognosis.
The two commonly used augmentation agents have distinct pharmacologic profiles.4,6 Buspirone, a partial agonist at the postsynaptic 5-hydroxytryptamine1A (5-HT1A) receptor, enhances the activity of SSRIs through the 5HT1A receptors.13 In contrast, sustained-release bupropion appears to produce antidepressant effects by blocking the reuptake of dopamine and norepinephrine. Buspirone is not viewed as an antidepressant monotherapeutic agent, whereas sustained-release bupropion is.1 The evidence of the efficacy of either agent as augmentation for SSRIs rests largely on case reports, case series, and small, inconclusive placebo-controlled studies.5 Augmentation with lithium, a possible second-step addition, was excluded, given its side effects, its toxicity in the case of overdose, and the need for monitoring of blood levels.
Methods
Patient Population and Inclusion and Exclusion Criteria
Procedures related to written informed consent and monitoring have been described elsewhere.4,6,8 All the authors had essential roles in study implementation and supervision, data review, and manuscript development. Medications were supplied to the study at no cost by Bristol-Myers Squibb, Forest Pharmaceuticals, GlaxoSmithKline, King Pharmaceuticals, Organon, Pfizer, and Wyeth-Ayerst Laboratories; otherwise these companies had no role in the study design, data accrual, data analysis, or manuscript preparation.
Study Design
Participants were randomly assigned to receive one of the two augmentation medications (sustained-release bupropion or buspirone)6,12 in a 1:1 ratio, stratified according to the acceptability of treatment and to regional center. Patients who did not have a remission with or who had an intolerance to citalopram alone were eligible for this study, as long as they accepted treatment options that included augmentation with sustained-release bupropion or buspirone. During the trial, the citalopram dose was kept constant (but it could be reduced if side effects occurred). The initial dose of sustained-release bupropion was 200 mg per day during weeks 1 and 2, increasing to 300 mg per day by week 4 and to 400 mg per day (the final dose) during week 6. The starting dose of buspirone was 15 mg per day during week 1, increasing to 30 mg per day during week 2, and then to 45 mg per day during weeks 3 through 5, with a final, maximal dose of 60 mg per day during week 6. Both drugs were taken twice daily.
Protocol Treatment
The aim of augmentation treatment was defined a priori as a remission of symptoms — defined as a score of 5 or less on the 16-item Quick Inventory of Depressive Symptomatology, clinician-rated (QIDS-C-16), which assesses the core symptoms of major depression and on which scores range from 0 to 27, with higher scores indicating greater symptom severity. Clinic visits were recommended at baseline and weeks 2, 4, 6, 9, and 12. Patients with at least a response (defined as a reduction of 50 percent or more in the baseline total QIDS-C-16 score at 12 weeks) and an acceptable level of tolerability could receive treatment for another 2 weeks to determine whether remission would occur with additional time.
Patients could leave the trial before 12 weeks if intolerable side effects occurred, if a remission that was sustained for at least 2 weeks and preferably 4 weeks occurred before 12 weeks (e.g., patients who had a remission by week 4 and remained in remission by week 6 or 9 could move to follow-up), or if substantial symptoms (as determined by a total QIDS-C-16 score of 9 or more) were still present after 9 weeks at maximally tolerated doses. Concomitant treatments were managed as described elsewhere.6,8 Protocol treatment involved the measurement of symptoms and side effects at each clinic visit to ensure the quality of care (measurement-based care).8,14
Clinical Measurements
Information with regard to baseline clinical and demographic characteristics, side effects, and adverse events was collected, as described elsewhere.8 The primary outcome — remission of symptoms — was defined by a score of 7 or less on the 17-item Hamilton Rating Scale for Depression15 (HRSD-17). Scores can range from 0 to 52, with higher scores indicating more severe depression. Scores were obtained by independent, trained, and certified assessors of research outcomes who were unaware of patients' treatment assignments and used telephone-based, structured interviews (in English or Spanish) with participants at entry into and at the end of this study. Secondary outcomes included the rates of response to treatment (defined as a reduction of 50 percent or more from the baseline Quick Inventory of Depressive Symptomatology — Self-Report [QIDS-SR-16] score at the end of this study) and remission (defined as a total score of 5 or less at the end of this study), on the basis of the QIDS-SR-16 scores obtained at each treatment visit (range, 0 to 27).16,17
Statistical Analysis
Summary statistics are presented as described by Rush et al.8 Logistic-regression models were used to compare rates of remission (according to HRSD-17 and QIDS-SR-16 scores) and response (according to QIDS-SR-16 scores), after adjustment for the effect of regional center treatment-acceptability strata,8 and baseline characteristics that were not balanced among the treatment groups. There were seven possible treatment-acceptability strata, which were collapsed into three categories (medication augmentation only, medication or cognitive-therapy augmentation, and other), owing to small numbers of patients in several strata. If final HRSD-17 scores were missing, it was assumed that there was a lack of remission (as defined in the original analysis plan).6 Sensitivity analyses that were performed with the use of two imputation methods yielded results that were consistent with this assumption.8 With the use of data regarding clinic visits, the times to first remission (as determined by a QIDS-SR-16 score of less than 6) and first response (a reduction of 50 percent or more from the baseline QIDS-SR-16 score) were defined as the first observed point. Log-rank tests compared the cumulative proportion of patients without remission and response in the two treatment groups.
All effectiveness and safety analyses were conducted according to the intention-to-treat principle (i.e., the analyses included all patients randomly assigned to each treatment group, regardless of adherence to protocol, actual treatment received, or subsequent withdrawal from assessments, treatment, protocol deviations, or all of these).18
Results
Patients
Overall, 1439 participants enrolled in the second step of treatment (level 2) of the STAR*D trial after intolerance to citalopram developed or they did not have a remission with the use of this agent. The development of the sample of participants is described by Rush et al.8 The final sample included 565 patients randomly assigned to receive augmentation of citalopram with sustained-release bupropion (279 patients) or buspirone (286 patients). Most of the patients who were randomly assigned to receive one of these two augmentation medications (430 of 565, or 76.1 percent) had accepted their assignment to receive only the two augmentation medications; 102 patients (18.0 percent) had accepted their assignment to all three augmentation options (two medications plus cognitive therapy); the remaining 33 patients (5.8 percent) had accepted their assignment to other treatment options that included both medication augmentations.8
Demographic and Clinical Characteristics
Table 1Table 1
Clinical and Demographic Characteristics of Patients. shows the characteristics of the participants. The two groups receiving augmentation with sustained-release bupropion or buspirone did not differ significantly with respect to any of the characteristics, including the rates of concurrent coexisting axis I disorders listed in the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (data not shown), except that those assigned to receive citalopram plus sustained-release bupropion had a shorter overall length of illness (15 years) than did those receiving citalopram plus buspirone (17 years) (P<0.04).Treatment Features
Both augmentation medications were administered in effective doses and were provided for adequate durations of time to detect a benefit. The mean doses at the end of this study were 267.5 mg per day for sustained-release bupropion and 40.9 mg per day for buspirone. Patients receiving citalopram plus sustained-release bupropion had a mean (±SD) of 3.8±1.5 clinic visits (Table 2Table 2
Characteristics of Treatment.), as compared with 3.8±1.7 visits among patients receiving citalopram plus busprione (χ2=0.03, P=0.87). Fourteen percent of those receiving citalopram plus sustained-release bupropion received less than four weeks of treatment, as compared with 21.0 percent of those receiving citalopram plus buspirone (χ2=4.79, P=0.03). The mean duration of treatment at the time of the final dose of the augmentation medication was similar for both groups (7.6 weeks for citalopram plus sustained-release bupropion and 7.1 weeks for citalopram plus buspirone). Those treated with citalopram plus sustained-release bupropion adhered to treatment longer (10.2 weeks) than did those receiving citalopram plus buspirone (9.2 weeks, P=0.01).Symptom Outcomes
On the basis of HRSD-17 scores, remission rates did not differ significantly between the group given citalopram plus bupropion (29.7 percent [83 of 279 patients]) and the group given citalopram plus buspirone (30.1 percent [86 of 286 patients]; χ2=0.01; P=0.93). On the basis of QIDS-SR-16 scores, remission rates (39.0 percent for sustained-release bupropion and 32.9 percent for buspirone, P=0.13) and response rates (31.8 percent for sustained-release bupropion and 26.9 percent for buspirone, P=0.21) were not significantly different (Table 3Table 3
Treatment Outcomes, Side Effects, and Serious Adverse Events.). However, when outcomes were assessed as continuous variables (as is customary in most trials involving the efficacy of antidepressant medication), greater benefit was found with citalopram plus sustained-release bupropion than with citalopram plus buspirone on the basis of percent reductions (from baseline to the end of this study) in QIDS-SR-16 scores (25.3 percent as compared with 17.1 percent, P<0.04). Furthermore, total QIDS-SR-16 scores at the end of this study were significantly lower with citalopram plus sustained-release bupropion treatment than with citalopram plus buspirone (8.0 vs. 9.1, P<0.02). The two groups did not differ significantly with respect to the time to the first QIDS-SR-16 response (log-rank χ2=0.0001, P=0.99) or to first QIDS-SR-16 remission (χ2=0.0024, P=0.96) (Figure 1Figure 1Time to Remission with Medication.). For patients who did have a remission, the mean time to a QIDS-SR-16 remission was 6.3 ±4.8 weeks (median, 5.2) for citalopram plus sustained-release bupropion and 5.4±4.4 weeks (median, 4.1) for citalopram plus buspirone. Similarly, the mean time to a QIDS-SR-16 response among patients who had a response was 6.3 ±4.6 weeks (median, 6.0) for citalopram plus sustained-release bupropion and 6.8±3.9 weeks (median, 4.1) for citalopram plus buspirone.Tolerability and Adverse Events
There were no significant differences between the groups in the maximal frequency, intensity, or burden of side effects (Table 3). Fewer participants taking citalopram plus sustained-release bupropion stopped treatment (i.e., they discontinued the study treatment before four weeks or at or after four weeks, with the reason recorded as due to side effects) because of intolerance than did those taking citalopram plus buspirone (12.5 percent vs. 20.6 percent; χ2=6.86; P<0.001).
The groups did not differ significantly in terms of the number of patients with one or more serious adverse events (3.6 percent for citalopram plus sustained-release bupropion and 4.2 percent for citalopram plus buspirone; χ2=0.14; P=0.71). All together, 24 serious adverse events occurred among 22 patients; of these patients, 3 had at least 1 serious psychiatric adverse event with citalopram plus sustained-release bupropion, whereas 6 had a serious psychiatric adverse event with citalopram plus buspirone. No patient committed suicide during this study. One patient with a preexisting cardiac disease died owing to cardiac arrest.
Discussion
Among patients with depression who did not have a remission during a vigorous trial of up to 14 weeks of citalopram or who could not tolerate such therapy, augmentation with sustained-release bupropion or buspirone was associated with similar remission rates, as reflected by the primary outcome measure of HRSD-17 scores of 29.7 percent for sustained-release bupropion and 30.1 percent for buspirone. Remission rates were slightly higher according to QIDS-SR-16 scores, but these rates were not significantly different (39.0 percent for sustained-release bupropion and 32.9 percent for buspirone). The QIDS-SR-16 remission rates were slightly higher than the HRSD-17 remission rates, because patients for whom there was no HRSD-17 score at the end of this study (139 patients) were judged, according to the a priori study protocol, not to have had a remission; however, 31 of these patients (22.3 percent) had a remission at the end of this study according to the QIDS-SR-16 scores.
A significantly greater reduction from baseline in QIDS-SR-16 symptoms was found among patients receiving augmentation with sustained-release bupropion (25.3 percent) than with buspirone (17.1 percent), and the mean total QIDS-SR-16 scores at the end of this study were significantly lower with sustained-release bupropion (8.0) than with buspirone (9.1). Additional significant differences between the two groups included longer adherence to treatment with sustained-release bupropion (10.2 weeks) than with buspirone (9.2 weeks), lower rates of discontinuation owing to intolerance with sustained-release bupropion (12.5 percent) than with buspirone (20.6 percent), and a lower rate of treatment cessation before four weeks with sustained-release bupropion (14.0 percent) than with buspirone (21.0 percent, P=0.03). These secondary outcomes (which have traditionally been used as primary outcomes in efficacy studies) favored citalopram plus sustained-release bupropion over citalopram plus buspirone. There were no significant differences between the two groups in terms of the duration of treatment at the time of the final dose; overall attrition rates; proportion of serious adverse events; frequency, intensity, and global burden of side effects; or total number of treatment visits. Overall, these findings reveal a consistently more favorable outcome with sustained-release bupropion than with buspirone augmentation of citalopram.
This study might be considered a “real-world” trial of the augmentation of an SSRI — citalopram — with sustained-release bupropion or buspirone after a consistent, well-implemented trial of citalopram has been performed.14 To our knowledge, there have been no randomized, controlled trials involving two or more augmentation medications in representative clinical-practice settings with which to compare our results. Remission rates in our trial were similar to those found in most previous uncontrolled trials of augmentation of SSRIs, which have typically been conducted in research clinics and have involved symptomatic volunteers with nonchronic depression and few general medical and psychiatric coexisting illnesses. Remission rates in our trial should be generalizable to most outpatients with nonpsychotic major depressive disorder who are seen in both primary and psychiatric settings and who have not had adequate benefit with the use of an SSRI alone.
Limitations of the study include the lack of a pill placebo and unblinded delivery of treatment, although the data on the primary outcome measure were collected by evaluators who were unaware of patients' treatment assignments, and the HRSD-17 results were concordant with the QIDS-SR-16 results. Although the use of placebo in the second step of treatment could raise concern and may have limited the generalizability of results if patients with severe or chronic depression declined to participate, the lack of a placebo control does not allow us to exclude spontaneous remission, the nonspecific effects of treatment, or the extended use of citalopram alone as the likely explanation for the present findings.
Factors to be considered when selecting augmentation treatments include efficacy, tolerability, burden of side effects, interactions among drugs, dosing convenience, adherence, and cost. Sustained-release bupropion and buspirone, used to augment therapy with the SSRI citalopram, had similar remission rates on the basis of clinician and self-report ratings, but several important secondary measures favored citalopram plus sustained-release bupropion over citalopram plus buspirone. These findings show that augmentation of SSRIs with either agent will result in symptom remission, with some increased benefits with citalopram plus sustained-release bupropion. These results do raise the question of whether to use augmentation agents (or other treatment combinations) as first-line treatment in an attempt to achieve greater remission rates sooner in more patients than with SSRIs alone.
Supported by a contract (N01MH90003, to the University of Texas Southwestern Medical Center at Dallas) with the National Institute of Mental Health, National Institutes of Health.
The content of this article does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the U.S. government.
Dr. Trivedi reports having received consulting fees from or having served on advisory boards for Bristol-Myers Squibb, Cyberonics, Eli Lilly, Forest Pharmaceuticals, Johnson and Johnson, Pfizer, Sepracor, and Wyeth-Ayerst Laboratories; lecture fees from Bristol-Myers Squibb, Cyberonics, Eli Lilly, Forest Pharmaceuticals, and Wyeth-Ayerst Laboratories; and research support from Bristol-Myers Squibb, Cephalon, Corcept Therapeutics, Eli Lilly, Janssen Pharmaceutica, Pfizer, Predix Pharmaceuticals, and Wyeth-Ayerst Laboratories. Dr. Fava reports having received research support from Abbott Laboratories, Lichtwer Pharma GmbH, and Lorex Pharmaceuticals; lecture fees from Bayer AG, Biovail, BrainCells, Compellis, Cypress Pharmaceuticals, DOV Pharmaceutical, Grünenthal GmbH, Janssen Pharmaceutica, Knoll Pharmaceutical, Lundbeck, Pan American Laboratories, Sepracor, and Somerset Pharmaceuticals; research support and honoraria from Aspect Medical Systems, AstraZeneca, Bristol-Myers Squibb, Cephalon, Eli Lilly, Forest Pharmaceuticals, GlaxoSmithKline, Johnson & Johnson Pharmaceuticals, Novartis, Organon, Pharmavite, Pfizer, Roche, Sanofi–Synthelabo, Solvay Pharmaceuticals, and Wyeth-Ayerst Laboratories. Dr. Thase reports having received consulting fees from AstraZeneca, Bristol-Myers Squibb, Cephalon, Cyberonics, Eli Lilly, Forest Pharmaceuticals, GlaxoSmithKline, Janssen Pharmaceutica, Novartis, Organon, Pfizer, and Wyeth-Ayerst Laboratories; and lecture fees from AstraZeneca, Eli Lilly, GlaxoSmithKline, Organon, and Wyeth-Ayerst Laboratories. Dr. Quitkin reports having received consulting fees from Bristol-Myers Squibb, McKinsey, Sepracor, and Sterne, Kessler, Goldstein, and Fox; and lecture fees from Almirall Prodesfarma (Spain), Eli Lilly, and Pfizer. Dr. Warden reports owning stock in Pfizer and having owned stock in Bristol-Myers Squibb. Dr. Nierenberg reports having received consulting fees from Eli Lilly, Genaissance Pharmaceuticals, GlaxoSmithKline, Innapharma, Sepracor, and Shire; research support from Bristol-Myers Squibb, Cederroth, Cyberonics, Forest Pharmaceuticals, Janssen Pharmaceutica, Lichtwer Pharma, and Pfizer; and research support and honoraria from Eli Lilly, GlaxoSmithKline, and Wyeth-Ayerst Laboratories. Dr. Biggs reports having received consulting fees from Bristol-Myers Squibb, Eli Lilly, GlaxoSmithKline, Merck, and Pfizer. Dr. Rush reports having received consulting fees from or having served on advisory boards for Advanced Neuronetic Systems, Bristol-Myers Squibb, Cyberonics, Eli Lilly, Forest Pharmaceuticals, GlaxoSmithKline, Health Technology Systems, Merck, Neuronetics, Organon, and Wyeth-Ayerst Laboratories; royalties from Guilford Press and Health Technology Systems; lecture fees from Cyberonics, Forest Pharmaceuticals, GlaxoSmithKline, and Merck; and owning stock in Pfizer. No other potential conflict of interest relevant to this article was reported.
This study is dedicated to the memory of Fred Quitkin, M.D., our dear friend and colleague.
We are indebted to Bristol-Myers Squibb, Forest Pharmaceuticals, GlaxoSmithKline, King Pharmaceuticals, Organon, Pfizer, and Wyeth-Ayerst Laboratories for providing medications at no cost for this trial.
Source Information
From the Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas (M.H.T., D.W., M.M.B., K.S.-W., A.J.R.); the Clinical Psychopharmacology Unit, Massachusetts General Hospital, Boston (M.F., A.A.N.); the Epidemiology Data Center, Graduate School of Public Health, University of Pittsburgh (S.R.W., J.F.L.), and the Department of Psychiatry, University of Pittsburgh School of Medicine (M.E.T.) — both in Pittsburgh; the New York State Psychiatric Institute and the Department of Psychiatry, College of Physicians and Surgeons of Columbia University, New York (F.Q.); and the National Institute of Mental Health, Bethesda, Md. (L.R., B.D.L.).
Address reprint requests to Dr. Trivedi at the Mood Disorder Program and Clinic, Department of Psychiatry, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390-9119, or at madhukar.trivedi@utsouthwestern.edu.
The Sequenced Treatment Alternatives to Relieve Depression (STAR*D) trial investigators are listed in the Appendix.
Appendix
The following investigators participated in the STAR*D trial: National Coordinating Center — A.J. Rush, M. Trivedi, D. Warden, M.M. Biggs, K. Shores-Wilson, D. Stegman, M. Kashner; Data Coordinating Center — S. Wisniewski, G.K. Balasubramani, J. Luther, H. Eng; Regional Centers: University of Alabama, Birmingham, and Tuscaloosa Veterans Affairs Medical Center, Tuscaloosa, Ala. — L. Davis, K. Rice, A. Berry, P. Johnson, S. Ambrose, M. Jewell, B. Thomas, E. Waldrop, T. Allen, E. St. John, R. Williams; University of California, Los Angeles — A. Leuchter, I. Lesser, I. Cook, M. Epstein, S. Rosenberg, S. Zeim, L. Sulkowski, J. Iribarren, R. Armstrong, A. Rosales, M. Abrams; University of California, San Diego, La Jolla — S. Zisook, K. Harless, C. Gonzalez, M. Smith, C. Lawrence, J. Palica, M. Rohrs, M. Capous-Desyllas, K. Ganadjian; Northwestern University Medical School, Chicago — W. McKinney, W. Gilmer, C. Kelley, C. Cooler, A. Bauer, J. Fleck, C. Endick; Psychiatric Research Institute, University of Kansas, Wichita — S. Preskorn, D. Hilger, A. Klick-Davis, R. Lusk, J. Elmore, D. Soetaert; Massachusetts General Hospital, Boston — J. Alpert, M. Fava, A. Nierenberg, A. Farabaugh, T. Petersen, W. Merens, P. Cassano, N. Craven, H. Yang, M. Candrian, R. Fraguas; University of Michigan, Ann Arbor — E. Young, S. Marcus, J. Greden, H. Briggs, K. Bullard, A. Kennedy, A. Benway, E. Rickard; New York State Psychiatric Institute and Columbia College of Physicians and Surgeons, New York — F.M. Quitkin, P. McGrath, J.W. Stewart, H. Sackeim, K. Tate-Brown, S. Rees, C. Smith, A. Couraud, J. Lavelle, K. Broderick; University of North Carolina, Chapel Hill — R. Golden, B. Gaynes, J. DeVeaugh-Geiss, A. Ford, S. Barnett, B. Pearson; Laureate Healthcare System, Tulsa, Okla. — J. Mitchell, W. Yates, J. Kuehnert, L. Jernigan, B. Williams, J. Hilton; University of Pittsburgh Medical Center, Pittsburgh — M. Thase, R.H. Howland, E. Friedman, J. Callan, S. Berman, L. Shutt, C. Spotts; Vanderbilt University Medical Center, Nashville — S. Hollon, R. Shelton, M. Lovett, T. Crutcher, T. Patton, J. Hart, R.M Harris-Turner, D. Lilly, B. Sirles, S. Hicks, N. Harris, S. Addington; University of Texas Southwestern Medical Center, Dallas — M. Husain, M. Downing, D. Stegman, E. Shellhorn, B. O'Neal, D. Turner, MacLeod, M. Henson, T. Hawley, S. Gardner; Virginia Commonwealth University, Richmond — S. Kornstein, R. Schneider, S. Belyea, B. Perry, K. Schmitt, T. Goff, K. Lamoree, M. Britton, C. Glassman.
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Citing Articles
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Trina E. Chang, Yonghua Jing, Albert S. Yeung, Susan K. Brenneman, Iftekhar Kalsekar, Tony Hebden, Robert McQuade, Lee Baer, Jonathan L. Kurlander, Angela K. Watkins, Jean A. Siebenaler, Maurizio Fava. (2012) Effect of communicating depression severity on physician prescribing patterns: findings from the Clinical Outcomes in MEasurement-based Treatment (COMET) trial. General Hospital Psychiatry
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F. Martínez-Granados, E. Climent-Grana, E. Pérez-Martínez, J.P. Ordovás-Baines, J. Selva Otaolaurruchi, M.A. Bernabéu Martínez. (2012) Assessing a Therapeutic Exchange Protocol for Second-generation Antidepressants: Clinical Results. Farmacia Hospitalaria (English Edition)
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Ramez Ghanbari, Mostafa El Mansari, Pierre Blier. (2011) Electrophysiological impact of trazodone on the dopamine and norepinephrine systems in the rat brain. European Neuropsychopharmacology
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Thomas C. Baghai, Pierre Blier, David S. Baldwin, Michael Bauer, Guy M. Goodwin, Kostas N. Fountoulakis, Siegfried Kasper, Brian E. Leonard, Ulrik F. Malt, Dan J. Stein, Marcio Versiani, Hans-Jürgen Möller. (2011) Executive summary of the report by the WPA section on pharmacopsychiatry on general and comparative efficacy and effectiveness of antidepressants in the acute treatment of depressive disorders. European Archives of Psychiatry and Clinical Neuroscience
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William M. McDonald, Valerie Durkalski, Edward R. Ball, Paul E. Holtzheimer, Martina Pavlicova, Sarah H. Lisanby, David Avery, Berry S. Anderson, Ziad Nahas, Paul Zarkowski, Harold A. Sackeim, Mark S. George. (2011) Improving the antidepressant efficacy of transcranial magnetic stimulation: maximizing the number of stimulations and treatment location in treatment-resistant depression. Depression and Anxiety 28:11, 973-980
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Fadi T. Maalouf, Mia Atwi, David A. Brent. (2011) Treatment-resistant depression in adolescents: review and updates on clinical management. Depression and Anxiety 28:11, 946-954
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Bradley N. Gaynes, Joel F. Farley, Stacie B. Dusetzina, Alan R. Ellis, Richard A. Hansen, William C. Miller, Til Stürmer. (2011) Does the presence of accompanying symptom clusters differentiate the comparative effectiveness of second-line medication strategies for treating depression?. Depression and Anxiety 28:11, 989-998
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P. Bech, M. Fava, M. H. Trivedi, S. R. Wisniewski, A. J. Rush. (2011) Outcomes on the pharmacopsychometric triangle in bupropion-SR vs. buspirone augmentation of citalopram in the STAR*D trial. Acta Psychiatrica Scandinavicano-no
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Jamie M. Dupuy, Michael J. Ostacher, Jeffrey Huffman, Roy H. Perlis, Andrew A. Nierenberg. (2011) A critical review of pharmacotherapy for major depressive disorder. The International Journal of Neuropsychopharmacology 14:10, 1417-1431
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Richard A. Hansen, Stacie B. Dusetzina, Alan R. Ellis, Til Stürmer, Joel F. Farley, Bradley N. Gaynes. (2011) Risk of adverse events in treatment-resistant depression: propensity-score-matched comparison of antidepressant augment and switch strategies. General Hospital Psychiatry
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Laura J. Thomas, Anna Abel, Nicola Ridgway, Tim Peters, David Kessler, Sandra Hollinghurst, Katrina Turner, Anne Garland, Bill Jerrom, Jill Morrison, Chris Williams, John Campbell, Willem Kuyken, Glyn Lewis, Nicola Wiles. (2011) Cognitive behavioural therapy as an adjunct to pharmacotherapy for treatment resistant depression in primary care: The CoBalT randomised controlled trial protocol. Contemporary Clinical Trials
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Ricardo Moreira. (2011) The Efficacy and Tolerability of Bupropion in the Treatment of Major Depressive Disorder. Clinical Drug Investigation 31, 5-17
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Diogo Azevedo Oliveira Sennfelt, Maria Alice Rodrigues Marques da Silva, Anabela Pereira da Silva Tavares. (2011) Bupropion in the Treatment of Major Depressive Disorder in Real-life Practice. Clinical Drug Investigation 31, 19-24
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Maragatha N. Kuchibhatla, Gerda G. Fillenbaum. (2011) Trajectory Classes of Depression in a Randomized Depression Trial of Heart Failure Patients: A Reanalysis of the SADHART-CHF Trial. The American Journal of Geriatric Pharmacotherapy
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Charlotte L. Allan, Klaus P. Ebmeier. (2011) The Use of ECT and MST in treating depression. International Review of Psychiatry 23:5, 400-412
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David W. Morris, Madhukar H. Trivedi. (2011) Measurement-Based Care for Unipolar Depression. Current Psychiatry Reports
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Gaurav Gulrez, Dinesh Kumar Badyal, Randhir Singh Deswal, Arvind Sharma. (2011) Bupropion as an Augmenting Agent in Patients of Depression with Partial Response. Basic & Clinical Pharmacology & Toxicologyno-no
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F. Martínez-Granados, E. Climent-Grana, E. Pérez-Martínez, J.P. Ordovás-Baines, J. Selva Otaolaurruchi, M.A. Bernabéu Martínez. (2011) Evaluación de un protocolo de intercambio terapéutico de antidepresivos de segunda generación: resultados clínicos. Farmacia Hospitalaria 35:5, 244-253
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Pierre Tran, Phil Skolnick, Pal Czobor, N.Y. Huang, Mark Bradshaw, Anthony McKinney, Maurizio Fava. (2011) Efficacy and tolerability of the novel triple reuptake inhibitor amitifadine in the treatment of patients with major depressive disorder: A randomized, double-blind, placebo-controlled trial. Journal of Psychiatric Research
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Paolo Olgiati, Emanuele Bajo, Marco Bigelli, Diana De Ronchi, Alessandro Serretti. (2011) Should pharmacogenetics be incorporated in major depression treatment? Economic evaluation in high- and middle-income European countries. Progress in Neuro-Psychopharmacology and Biological Psychiatry
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Jolanda Prins, Berend Olivier, S Mechiel Korte. (2011) Triple reuptake inhibitors for treating subtypes of major depressive disorder: the monoamine hypothesis revisited. Expert Opinion on Investigational Drugs 20:8, 1107-1130
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Stuart Eisendrath, Maggie Chartier, Maura McLane. (2011) Adapting Mindfulness-Based Cognitive Therapy for Treatment-Resistant Depression. Cognitive and Behavioral Practice 18:3, 362-370
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Sidney H. Kennedy. (2011) Improving the clinical effectiveness of antidepressant treatment. Journal of Affective Disorders 132, S1-S2
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Daniel M. Blumberger, Benoit H. Mulsant, Paul B. Fitzgerald, Tarek K. Rajji, Arun V. Ravindran, L. Trevor Young, Andrea J. Levinson, Zafiris J. Daskalakis. (2011) A randomized double-blind sham-controlled comparison of unilateral and bilateral repetitive transcranial magnetic stimulation for treatment-resistant major depression. World Journal of Biological Psychiatry1-13
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Michele Fabrazzo, Francesco Perris, Palmiero Monteleone, Giuseppina Esposito, Francesco Catapano, Mario Maj. (2011) Aripiprazole augmentation strategy in clomipramine-resistant depressive patients: An open preliminary study. European Neuropsychopharmacology
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R. H. Perlis, D. V. Iosifescu, V. M. Castro, S. N. Murphy, V. S. Gainer, J. Minnier, T. Cai, S. Goryachev, Q. Zeng, P. J. Gallagher, M. Fava, J. B. Weilburg, S. E. Churchill, I. S. Kohane, J. W. Smoller. (2011) Using electronic medical records to enable large-scale studies in psychiatry: treatment resistant depression as a model. Psychological Medicine1-10
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Sonja Horstmann, Elisabeth B. Binder. (2011) Glucocorticoids as Predictors of Treatment Response in Depression. Harvard Review of Psychiatry 19:3, 125-143
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Philip S. Wang, Alan M. Brookhart, Christine Ulbricht, Sebastian Schneeweiss. 2011. The Pharmacoepidemiology of Psychiatric Medications. , 155-165.
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Albert S. Yeung, Victoria E. Ameral, Sarah E. Chuzi, Maurizio Fava, David Mischoulon. (2011) A pilot study of acupuncture augmentation therapy in antidepressant partial and non-responders with major depressive disorder. Journal of Affective Disorders 130:1-2, 285-289
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F. Andrew Kozel, Kevin A. Johnson, Ziad Nahas, Paul A. Nakonezny, Paul S. Morgan, Berry S. Anderson, Samet Kose, Xingbao Li, Kelvin O. Lim, Madhukar H. Trivedi, Mark S. George. (2011) Fractional Anisotropy Changes After Several Weeks of Daily Left High-Frequency Repetitive Transcranial Magnetic Stimulation of the Prefrontal Cortex to Treat Major Depression. The Journal of ECT 27:1, 5-10
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Henricus G. Ruhé, Geeske van Rooijen, Jan Spijker, Frenk P.M.L. Peeters, Aart H. Schene. (2011) Staging methods for treatment resistant depression. A systematic review. Journal of Affective Disorders
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A. D. Sperber, D. A. Drossman. (2011) Review article: the functional abdominal pain syndrome. Alimentary Pharmacology & Therapeutics 33:5, 514-524
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Jun Chen, Keming Gao, David E Kemp. (2011) Second-generation antipsychotics in major depressive disorder: update and clinical perspective. Current Opinion in Psychiatry 24:1, 10-17
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Andre Russowsky Brunoni, Leandro Valiengo, Alessandra Baccaro, Tamires Araujo Zanao, Janaina Farias de Oliveira, Giselly Pereira Vieira, Viviane Freire Bueno, Alessandra C. Goulart, Paulo Sérgio Boggio, Paulo Andrade Lotufo, Isabela Martins Bensenor, Felipe Fregni. (2011) Sertraline vs. ELectrical Current Therapy for Treating Depression Clinical Trial - SELECT TDCS: Design, rationale and objectives. Contemporary Clinical Trials 32:1, 90-98
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Pierre Blier, Claude Blondeau. (2011) Neurobiological bases and clinical aspects of the use of aripiprazole in treatment-resistant major depressive disorder. Journal of Affective Disorders 128, S3-S10
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Douglas A Drossman. (2011) Abuse, Trauma, and GI Illness: Is There a Link?. The American Journal of Gastroenterology 106:1, 14-25
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Paul R Albert, Brice Le François, Anne M Millar. (2011) Transcriptional dysregulation of 5-HT1A autoreceptors in mental illness. Molecular Brain 4:1, 21
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Martin A. Katzman. (2011) Aripiprazole: A clinical review of its use for the treatment of anxiety disorders and anxiety as a comorbidity in mental illness. Journal of Affective Disorders 128, S11-S20
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K. Ryan Connolly, Michael E. Thase. (2011) If at First You Donʼt Succeed. Drugs 71:1, 43-64
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P. Blomstedt, R. L. Sjöberg, M. Hansson, O. Bodlund, M. I. Hariz. (2011) Deep brain stimulation in the treatment of depression. Acta Psychiatrica Scandinavica 123:1, 4-11
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Toshi A Furukawa, Tatsuo Akechi, Shinji Shimodera, Mitsuhiko Yamada, Kazuhira Miki, Norio Watanabe, Masatoshi Inagaki, Naohiro Yonemoto. (2011) Strategic use of new generation antidepressants for depression: SUN(^_^)D study protocol. Trials 12:1, 116
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Stania A. Dejesus, Vanessa A. Diaz, Wanda C. Gonsalves, Peter J. Carek. (2011) Identification and Treatment of Depression in Minority Populations. The International Journal of Psychiatry in Medicine 42:1, 69-83
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Andrew F. Leuchter, Ian A. Cook, Steven P. Hamilton, Katherine L. Narr, Arthur Toga, Aimee M. Hunter, Kym Faull, Julian Whitelegge, Anne M. Andrews, Joseph Loo, Baldwin Way, Stanley F. Nelson, Steven Horvath, Barry D. Lebowitz. (2010) Biomarkers to Predict Antidepressant Response. Current Psychiatry Reports 12:6, 553-562
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CHAD D. RETHORST, DANIEL M. LANDERS, CRAIG T. NAGOSHI, JULIANNA T. D. ROSS. (2010) Efficacy of Exercise in Reducing Depressive Symptoms across 5-HTTLPR Genotypes. Medicine & Science in Sports & Exercise 42:11, 2141-2147
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Jeff C. Huffman, Jonathan E. Alpert. (2010) An Approach to the Psychopharmacologic Care of Patients: Antidepressants, Antipsychotics, Anxiolytics, Mood Stabilizers, and Natural Remedies. Medical Clinics of North America 94:6, 1141-1160
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Xianchen Liu, Steve Gelwicks, Douglas E. Faries, Stephen L. Able. (2010) Initial duloxetine prescription dose and treatment adherence and persistence in patients with major depressive disorder. International Clinical Psychopharmacology 25:6, 315-322
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Dominique Milea, Florent Guelfucci, Nawal Bent-Ennakhil, Mondher Toumi, Jean-Paul Auray. (2010) Antidepressant monotherapy: A claims database analysis of treatment changes and treatment duration. Clinical Therapeutics 32:12, 2057-2072
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Jonathan S. Comer, Mark Olfson, Ramin Mojtabai. (2010) National Trends in Child and Adolescent Psychotropic Polypharmacy in Office-Based Practice, 1996-2007. Journal of the American Academy of Child & Adolescent Psychiatry 49:10, 1001-1010
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Matthew J. Taylor, Srijan Sen, Zubin Bhagwagar. (2010) Antidepressant Response and the Serotonin Transporter Gene-Linked Polymorphic Region. Biological Psychiatry 68:6, 536-543
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Matthew C. Lucas, Robert J. Weikert, David S. Carter, Hai-Ying Cai, Robert Greenhouse, Pravin S. Iyer, Clara J. Lin, Eun Kyung Lee, Ann Marie Madera, Amy Moore, Kerem Ozboya, Ryan C. Schoenfeld, Sandra Steiner, Yansheng Zhai, Stephen M. Lynch. (2010) Design, synthesis, and biological evaluation of new monoamine reuptake inhibitors with potential therapeutic utility in depression and pain. Bioorganic & Medicinal Chemistry Letters 20:18, 5559-5566
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Georgios Paslakis, Maria Gilles, Michael Deuschle. (2010) Clinically Relevant Pharmacokinetic Interaction Between Venlafaxine and Bupropion. Journal of Clinical Psychopharmacology 30:4, 473-474
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Christian Dolder, Michael Nelson, Andrea Stump. (2010) Pharmacological and Clinical Profile of Newer Antidepressants. Drugs & Aging 27:8, 625-640
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J. Burgdorf, R.A. Kroes, M.C. Beinfeld, J. Panksepp, J.R. Moskal. (2010) Uncovering the molecular basis of positive affect using rough-and-tumble play in rats: a role for insulin-like growth factor I. Neuroscience 168:3, 769-777
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Ricardo W. Binfaré, Michela Mantovani, Josiane Budni, Adair Roberto S. Santos, Ana Lúcia S. Rodrigues. (2010) Involvement of dopamine receptors in the antidepressant-like effect of melatonin in the tail suspension test. European Journal of Pharmacology 638:1-3, 78-83
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Mostafa El Mansari, Bruno P. Guiard, Olga Chernoloz, Ramez Ghanbari, Noam Katz, Pierre Blier. (2010) Relevance of Norepinephrine-Dopamine Interactions in the Treatment of Major Depressive Disorder. CNS Neuroscience & Therapeutics 16:3, e1-e17
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William V Bobo, Richard C Shelton. (2010) Efficacy, safety and tolerability of Symbyax ® for acute-phase management of treatment-resistant depression. Expert Review of Neurotherapeutics 10:5, 651-670
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Harrison G. Pope, Revital Amiaz, Brian P. Brennan, Guy Orr, Mark Weiser, John F. Kelly, Gen Kanayama, Arthur Siegel, James I. Hudson, Stuart N. Seidman. (2010) Parallel-Group Placebo-Controlled Trial of Testosterone Gel in Men With Major Depressive Disorder Displaying an Incomplete Response to Standard Antidepressant Treatment. Journal of Clinical Psychopharmacology 30:2, 126-134
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J. Spijker, W. A. Nolen. (2010) An algorithm for the pharmacological treatment of depression. Acta Psychiatrica Scandinavica 121:3, 180-189
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Gahan J. Pandina, Georges M. Garibaldi, Dennis A. Revicki, Leah Kleinman, Ibrahim Turkoz, Mary J. Kujawa, Ramy A. Mahmoud. (2010) Psychometric evaluation of a Patient-Rated Most Troubling Symptom Scale for Depression: findings from a secondary analysis of a clinical trial. International Clinical Psychopharmacology 25:2, 51-59
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Ciara McCabe, Zevic Mishor, Philip J. Cowen, Catherine J. Harmer. (2010) Diminished Neural Processing of Aversive and Rewarding Stimuli During Selective Serotonin Reuptake Inhibitor Treatment. Biological Psychiatry 67:5, 439-445
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T. Bschor, C. Baethge. (2010) No evidence for switching the antidepressant: systematic review and meta-analysis of RCTs of a common therapeutic strategy. Acta Psychiatrica Scandinavica 121:3, 174-179
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Richard C. Shelton, Olawale Osuntokun, Alexandra N. Heinloth, Sara A. Corya. (2010) Therapeutic Options for Treatment-Resistant Depression. CNS Drugs 24:2, 131-161
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Hans-Jürgen Möller, Wolfgang Maier. (2010) Evidence-based medicine in psychopharmacotherapy: possibilities, problems and limitations. European Archives of Psychiatry and Clinical Neuroscience 260:1, 25-39
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A. F. Leuchter, M. M. Husain, I. A. Cook, M. H. Trivedi, S. R. Wisniewski, W. S. Gilmer, J. F. Luther, M. Fava, A. J. Rush. (2010) Painful physical symptoms and treatment outcome in major depressive disorder: a STAR*D (Sequenced Treatment Alternatives to Relieve Depression) report. Psychological Medicine 40:02, 239
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Jerome Sarris, David J. Kavanagh, Gerard Byrne. (2010) Adjuvant use of nutritional and herbal medicines with antidepressants, mood stabilizers and benzodiazepines. Journal of Psychiatric Research 44:1, 32-41
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Douglas A Drossman. (2009) Beyond Tricyclics: New Ideas for Treating Patients With Painful and Refractory Functional Gastrointestinal Symptoms. The American Journal of Gastroenterology 104:12, 2897-2902
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T. Michael Kashner, Madhukar H. Trivedi, Annie Wicker, Maurizio Fava, Stephen R. Wisniewski, A. John Rush. (2009) The Impact of Nonclinical Factors on Care Use for Patients with Depression: A STAR*D Report. CNS Neuroscience & Therapeutics 15:4, 320-332
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Tracy L. Greer, Madhukar H. Trivedi. (2009) Exercise in the treatment of depression. Current Psychiatry Reports 11:6, 466-472
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A.H. Iyo, N. Kieran, A. Chandran, P.R. Albert, I. Wicks, G. Bissette, M.C. Austin. (2009) Differential regulation of the serotonin 1 A transcriptional modulators five prime repressor element under dual repression-1 and nuclear-deformed epidermal autoregulatory factor by chronic stress. Neuroscience 163:4, 1119-1127
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Ian A. Cook, Aimee M. Hunter, Michelle Abrams, Barbara Siegman, Andrew F. Leuchter. (2009) Midline and right frontal brain function as a physiologic biomarker of remission in major depression. Psychiatry Research: Neuroimaging 174:2, 152-157
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Raymond W. Lam, Sidney H. Kennedy, Sophie Grigoriadis, Roger S. McIntyre, Roumen Milev, Rajamannar Ramasubbu, Sagar V. Parikh, Scott B. Patten, Arun V. Ravindran. (2009) Canadian Network for Mood and Anxiety Treatments (CANMAT) Clinical guidelines for the management of major depressive disorder in adults.. Journal of Affective Disorders 117, S26-S43
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Barbara J. Messinger-Rapport, David R. Thomas, Julie K. Gammack, John E. Morley. (2009) Clinical Update on Nursing Home Medicine: 2009. Journal of the American Medical Directors Association 10:8, 530-553
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T. Michael Kashner, Madhukar H. Trivedi, Annie Wicker, Maurizio Fava, Kathy Shores-Wilson, Stephen R. Wisniewski, A. John Rush. (2009) Release bias in accessing medical records in clinical trials: a STAR*D report. International Journal of Methods in Psychiatric Research 18:3, 147-158
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Andrew F. Leuchter, Ian A. Cook, William S. Gilmer, Lauren B. Marangell, Karl S. Burgoyne, Robert H. Howland, Madhukar H. Trivedi, Sidney Zisook, Rakesh Jain, Maurizio Fava, Dan Iosifescu, Scott Greenwald. (2009) Effectiveness of a quantitative electroencephalographic biomarker for predicting differential response or remission with escitalopram and bupropion in major depressive disorder. Psychiatry Research 169:2, 132-138
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Thorsten Mikoteit, Martin Hatzinger. (2009) Chronische Depression. Zeitschrift für Psychiatrie, Psychologie und Psychotherapie 57:4, 245-251
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Peter Giacobbe, Helen S. Mayberg, Andres M. Lozano. (2009) Treatment resistant depression as a failure of brain homeostatic mechanisms: Implications for deep brain stimulation. Experimental Neurology 219:1, 44-52
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Rachel M. Henke, Alan M. Zaslavsky, Thomas G. McGuire, John Z. Ayanian, Lisa V. Rubenstein. (2009) Clinical Inertia in Depression Treatment. Medical Care 47:9, 959-967
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A. John Rush, Susan E. Siefert. (2009) Clinical issues in considering vagus nerve stimulation for treatment-resistant depression. Experimental Neurology 219:1, 36-43
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Matthew C. Lucas, David S. Carter, Hai-Ying Cai, Eun Kyung Lee, Ryan C. Schoenfeld, Sandra Steiner, Marzia Villa, Robert J. Weikert, Pravin S. Iyer. (2009) Novel, achiral aminoheterocycles as selective monoamine reuptake inhibitors. Bioorganic & Medicinal Chemistry Letters 19:16, 4630-4633
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Michael E. Thase, Aaron M. Koenig. 2009. Outcomes in the Treatment of Major Depressive Disorder. , 22-53.
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Michael Bauer, Andrea Pfennig, Michael Linden, Michael N. Smolka, Peter Neu, Mazda Adli. (2009) Efficacy of an Algorithm-Guided Treatment Compared With Treatment as Usual. Journal of Clinical Psychopharmacology 29:4, 327-333
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Nhu Huynh, Roger S. McIntyre. 2009. Algorithms: STAR*D, Positives, Negatives, and Implications for Clinical Practice. , 117-126.
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John M. Zajecka, Corey Goldstein. 2009. Combining Medications to Achieve Remission. , 54-100.
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Joshua Kantrowitz, Leslie Citrome, Daniel Javitt. (2009) GABAB Receptors, Schizophrenia and Sleep Dysfunction. CNS Drugs PAP,
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Lee A. Dawson, Jeannette M. Watson. (2009) Vilazodone: A 5-HT 1A Receptor Agonist/Serotonin Transporter Inhibitor for the Treatment of Affective Disorders. CNS Neuroscience & Therapeutics 15:2, 107-117
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John J. Boren, Allan M. Leventhal, H. Edmund Pigott. (2009) Just How Effective are Antidepressant Medications? Results of a Major New Study. Journal of Contemporary Psychotherapy 39:2, 93-100
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Madhusudan Grover, Spencer D. Dorn, Stephan R. Weinland, Christine B. Dalton, Bradley N. Gaynes, Douglas A. Drossman. (2009) Atypical Antipsychotic Quetiapine in the Management of Severe Refractory Functional Gastrointestinal Disorders. Digestive Diseases and Sciences 54:6, 1284-1291
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Roy H Perlis, Gonzalo Laje, Jordan W Smoller, Maurizio Fava, A John Rush, Francis J McMahon. (2009) Genetic and Clinical Predictors of Sexual Dysfunction in Citalopram-Treated Depressed Patients. Neuropsychopharmacology 34:7, 1819-1828
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Roy H. Perlis, Bonnie Fijal, David H. Adams, Virginia K. Sutton, Madhukar H. Trivedi, John P. Houston. (2009) Variation in Catechol-O-Methyltransferase Is Associated with Duloxetine Response in a Clinical Trial for Major Depressive Disorder. Biological Psychiatry 65:9, 785-791
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Chad D. Rethorst, Bradley M. Wipfli, Daniel M. Landers. (2009) The Antidepressive Effects of Exercise. Sports Medicine 39:6, 491-511
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Diane Warden, A. John Rush, Stephen R. Wisniewski, Ira M. Lesser, Susan G. Kornstein, G. K. Balasubramani, Michael E. Thase, Sheldon H. Preskorn, Andrew A. Nierenberg, Elizabeth A. Young, Kathy Shores-Wilson, Madhukar H. Trivedi. (2009) What predicts attrition in second step medication treatments for depression?: a STAR*D Report. The International Journal of Neuropsychopharmacology 12:04, 459
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Jonathan Savitz, Irwin Lucki, Wayne C. Drevets. (2009) 5-HT1A receptor function in major depressive disorder. Progress in Neurobiology 88:1, 17-31
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Sheldon H. Preskorn. (2009) Treatment Options for the Patient Who Does Not Respond Well to Initial Antidepressant Therapy. Journal of Psychiatric Practice 15:3, 202-210
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M. Berger, E.L. Brakemeier, C. Klesse, E. Schramm. (2009) Depressive Störungen. Der Nervenarzt 80:5, 540-555
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Madhukar H. Trivedi, Patricia K. Corey-Lisle, Zhenchao Guo, Richard D. Lennox, Andrei Pikalov, Edward Kim. (2009) Remission, response without remission, and nonresponse in major depressive disorder: impact on functioning. International Clinical Psychopharmacology 24:3, 133-138
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Henricus G Ruhé, Jan Booij, Henk C v Weert, Johannes B Reitsma, Eric J F Fransen, Martin C Michel, Aart H Schene. (2009) Evidence Why Paroxetine Dose Escalation is Not Effective in Major Depressive Disorder: A Randomized Controlled Trial With Assessment of Serotonin Transporter Occupancy. Neuropsychopharmacology 34:4, 999-1010
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Dominick Esposito, Peter Wahl, Gregory Daniel, Michael A. Stoto, M. Haim Erder, Thomas W. Croghan. (2009) Results of a retrospective claims database analysis of differences in antidepressant treatment persistence associated with escitalopram and other selective serotonin reuptake inhibitors in the United States. Clinical Therapeutics 31:3, 644-656
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Edward S. Friedman, Michael E. Thase, Stephen R. Wisniewski, Madhukar H. Trivedi, Melanie M. Biggs, Maurizio Fava, Diane Warden, George Niederehe, James F. Luther, A. John Rush. (2009) Cognitive Therapy Augmentation versus CT Switch Treatment: A STAR*D Report. International Journal of Cognitive Therapy 2:1, 66-87
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Saloua Benmansour, Jonathan P Piotrowski, Alfonso V Altamirano, Alan Frazer. (2009) Impact of Ovarian Hormones on the Modulation of the Serotonin Transporter by Fluvoxamine. Neuropsychopharmacology 34:3, 555-564
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Andrew A. Nierenberg, Madhukar H. Trivedi, Bradley N. Gaynes, Jeff Mitchell, Lori L. Davis, Mustafa M. Husain, Stephen R. Wisniewski, Maurizio Fava, Diane Warden, James F. Luther, Adrienne O. van Nieuwenhuizen, David W. Morris, Richard C. Shelton, A. John Rush. (2009) Effectiveness study of venlafaxine-XR combined with aripiprazole for chronic or recurrent major depressive disorder. Australian and New Zealand Journal of Psychiatry 43:10, 956-967
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Mark J. Millan. (2009) Dual- and triple-acting agents for treating core and co-morbid symptoms of major depression: novel concepts, new drugs. Neurotherapeutics 6:1, 53-77
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Philip S Wang, Robert Heinssen, Molly Oliveri, Ann Wagner, Wayne Goodman. (2009) Bridging Bench and Practice: Translational Research for Schizophrenia and Other Psychotic Disorders. Neuropsychopharmacology 34:1, 204-212
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André F Carvalho, Juliana Raulino Machado, João L Cavalcante. (2009) Augmentation strategies for treatment-resistant depression. Current Opinion in Psychiatry 22:1, 7-12
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Madhusudan Grover, Douglas A. Drossman. (2009) Psychopharmacologic and Behavioral Treatments for Functional Gastrointestinal Disorders. Gastrointestinal Endoscopy Clinics of North America 19:1, 151-170
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Sheldon H. Preskorn. (2009) Results of the STAR*D Study: Implications for Clinicians and Drug Developers. Journal of Psychiatric Practice 15:1, 45-49
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Robert H. Howland, A. John Rush, Stephen R. Wisniewski, Madhukar H. Trivedi, Diane Warden, Maurizio Fava, Lori L. Davis, G.K. Balasubramani, Patrick J. McGrath, Susan R. Berman. (2009) Concurrent anxiety and substance use disorders among outpatients with major depression: Clinical features and effect on treatment outcome. Drug and Alcohol Dependence 99:1-3, 248-260
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Sidney H. Kennedy, Henning F. Andersen, Michael E. Thase. (2009) Escitalopram in the treatment of major depressive disorder: A meta-analysis. Current Medical Research and Opinion 25:1, 161-175
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George I. Papakostas, Richard C. Shelton. (2008) Use of atypical antipsychotics for treatment-resistant major depressive disorder. Current Psychiatry Reports 10:6, 481-486
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