Lívia Hartmann de Souza

Interpersonal psychotherapy as add-on for treatment-resistant depression: A pragmatic randomized controlled trial

BACKGROUND Treatment-resistant depression (TRD) is an extremely prevalent clinical condition. Although Interpersonal Psychotherapy (IPT) is an established treatment for uncomplicated depression, its effectiveness has never before been studied in patients with TRD in real-world settings. We investigate IPT as an adjunct strategy to treatment as usual (TAU) for TRD patients in a pragmatic, randomized, controlled trial. METHODS A total of 40 adult patients with TRD (satisfying the criteria for major depressive disorder despite adequate antidepressant treatment) were recruited from a tertiary care facility for this pragmatic trial and blinded to the evaluator. Patients were randomized to one of two treatment conditions: (1) TAU - pharmacotherapy freely chosen by the clinician (n=23) and (2) TAU+IPT (n=17). Assessments were performed at weeks 8, 12, 19 and 24. Changes in the estimated means of the Hamilton Depression Rating Scale score were the primary outcome measure. Secondary outcomes included patient-rated scales and quality of life scales. We used a linear mixed model to compare changes over time between the two groups. RESULTS Both treatments lead to improvements in depressive symptoms from baseline to week 24 with no significant between group differences in either primary: TAU (mean difference: 4.57; CI95%: 0.59-8.55; d=0.73) vs. IPT+TAU (mean difference: 5.86, CI95%: 1.50-10.22; d=0.93) or secondary outcomes. LIMITATIONS Our relatively small sample limits our ability to detect differences between treatments. CONCLUSIONS Both treatments lead to equal improvements in depressive symptoms. We found no evidence to support adding IPT to pharmacotherapy in patients with TRD. TRIAL REGISTRATION ClinicalTrials.gov-NCT01896349.

Childhood trauma and dimensions of depression: a specific association with the cognitive domain.

Objective: To investigate associations between a history of childhood trauma and dimensions of depression in a sample of clinically depressed patients. Methods: A sample of 217 patients from a mood-disorder outpatient unit was investigated with the Beck Depression Inventory, the Hamilton Depression Rating Scale, the CORE Assessment of Psychomotor Change, and the Childhood Trauma Questionnaire. A previous latent model identifying six depressive dimensions was used for analysis. Path analysis and Multiple Indicators Multiple Causes (MIMIC) models were used to investigate associations between general childhood trauma and childhood maltreatment modalities (emotional, sexual, and physical abuse; emotional and physical neglect) with dimensions of depression (sexual, cognition, insomnia, appetite, non-interactiveness/retardation, and agitation). Results: The overall childhood trauma index was uniquely associated with cognitive aspects of depression, but not with any other depressive dimension. An investigation of childhood maltreatment modalities revealed that emotional abuse was consistently associated with depression severity in the cognitive dimension. Conclusion: Childhood trauma, and specifically emotional abuse, could be significant risk factors for the subsequent development of cognitive symptoms of major depression. These influences might be specific to this depressive dimension and not found in any other dimension, which might have conceptual and therapeutic implications for clinicians and researchers alike.

Illness severity and biomarkers in depression: Using a unidimensional rating scale to examine BDNF

BACKGROUND Numerous studies have reported reduced peripheral brain-derived neurotrophic factor (BDNF) in major depression (MD). However, most of these studies used multidimensional depression rating scales, and failed to identify a relationship between BDNF levels and depression severity. Unidimensional scales are a more valid measure of syndrome severity. In these scales, items are ordered in increasing severity, so that as scores increase, syndrome severity increases; thus, each item adds unique information, and items can be totaled to a meaningful sum. The current study used the HAM-D6, a unidimensional measure of depression, to examine if it could identify a correlation between serum BDNF and depression severity. METHODS Serum BDNF levels and symptom severity were assessed in 163 depressed patients, including those with both unipolar (84.0%) and bipolar (16.0%) depression. The evaluation of depression severity included the total HAM-D17 and 3 subscales, including the HAM-D6. RESULTS On average, patients presented moderate to severe depression (HAM-D17=21.2±5.5). Overall BDNF levels were 60.4±22.6ng/mL. The correlation between serum BDNF and depression severity was modest and not different when assessed by the HAM-D6 subscale or the HAM-D17 as a whole (z=0.951; p=0.341), despite being statistically significant for the HAM-D6 (r=-0.185; p=0.019; 95% CI: -0.335 to -0.033), but not for the entire HAM-D17 (r=-0.127; p=0.108; 95% CI: -0.272 to 0.027). CONCLUSION We could not identify a strong relationship between serum BDNF levels and depression severity using the HAM-D6. This is in concordance with results of previous studies that reported no correlation between these variables, and indicates that the properties of the clinical measures used cannot explain the results these studies.