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Background: Ketamine and esketamine have both shown significant antidepressant effects in treatment-resistant depression (TRD), and conflicting evidence suggests that induced dissociation by these drugs can be a clinical predictor of esketamine/ketamine's efficacy., Methods: This study is a secondary analysis from a bi-center, randomized, controlled trial. Participants were randomly assigned 1:1 to receive an IV infusion of esketamine (.25 mg/kg) or racemic ketamine (.50 mg/kg) over 40 minutes. Dissociative symptoms were assessed using the Clinician-Administered Dissociative State Scale (CADSS) 40 minutes following the beginning of the infusion. The variation in depression scores was measured with the Montgomery-Asberg Depression Rating Scale (MADRS), which was administered before the intervention as a baseline measure and 24 hrs, 72 hrs, and 7 days following infusion., Results: Sixty-one patients were included in the analysis. Examining CADSS scores of 15 or below, for every 1-point increment in the CADSS score, there was a mean change of -0.5 (SD = 0.25; p-value 0.04) of predicted MADRS score from baseline to 24 hrs. The results for 72 hrs and 7 days following infusion were not significant. Limitations: This study was not designed to assess the relationship between ketamine or esketamine-induced dissociation and antidepressant effects as the main outcome, therefore confounding variables for this relationship were not controlled., Conclusion: We suggest a positive relationship between dissociation intensity, measured by CADSS, and antidepressant effect 24 hours after ketamine and esketamine infusion for a CADSS score of up to 15 points., Competing Interests: ALTL reports grants and personal fees from Janssen Pharmaceutical, personal fees from Daiichi Sankyo, Cristalia Produtos Químicos e Farmacêuticos, Libbs, Pfizer, Myralis Farma, Aché Laboratórios, Hypera Pharma, and Sanofi-Aventis, grants from Eli Lilly, H. Lundbeck A/S, Servier Laboratories, Hoffman-La Roche, Forum Pharmaceuticals and from the following public funding programs CNPq and FAPESP. LCQ reports consulting fees from Allergan, Abbott, Cristalia, Janssen Pharmaceutical, and Lundbeck and research fees from Janssen Pharmaceutica and Fundação Baiana de Infectologia. No other conflicts of interest declared concerning the publication of this article.

Objectives: Evidence suggests that ketamine's influence on brain-derived neurotrophic factor (BDNF) might be involved in its mechanism of rapid antidepressant action. We aimed to evaluate the differential impact of ketamine and esketamine on serum BDNF levels and its association with response patterns in treatment-resistant depression (TRD)., Methods: Participants (n = 53) are from a randomized, double-blind clinical trial comparing the efficacy of single-dose ketamine (0.5mg/kg, n = 27) and esketamine (0.25mg/kg, n = 26) in TRD. Depression severity was assessed before and 24 hours, 72 hours, and 7 days after the intervention, using the Montgomery-Åsberg Depression Rating Scale (MADRS). Blood samples were collected before infusion, 24 hours, and 7 days afterwards., Results: There were no significant changes in BDNF levels at post-infusion evaluation points, and no difference in BDNF levels comparing ketamine and esketamine. Both drugs exhibited similar therapeutic effect. There was no association between BDNF levels and response to treatment or severity of depressive symptoms., Conclusion: There was no significant treatment impact on BDNF serum levels - neither with ketamine nor esketamine - despite therapeutic response. These results suggest that ketamine or esketamine intervention for TRD has no impact on BDNF levels measured at 24 hours and 7 days after the infusion., Competing Interests: Acioly L. T. Lacerda reports grants and personal fees from Janssen Pharmaceutical; personal fees from DaiichiSankyo, Cristália, Libbs, Pfizer, Myralis-Farma, Aché Laboratórios, Hypera-Pharma, and Sanofi-Aventis; grants from Eli-Lilly, Lundbeck, Servier-Laboratories, Hoffman-La-Roche, and Forum-Pharmaceuticals. Lucas C. Quarantini reports consulting fees from Allergan, Abbot, Janssen-Pharmaceutical and Lundbeck, and research fees from Janssen-Pharmaceutical. No other conflicts of interest declared concerning the publication of this article.

Introduction: Anhedonia is defined as the reduced ability to feel pleasure and is a core symptom of various psychiatric disorders such as depression and schizophrenia. The Snaith-Hamilton Pleasure Scale (SHAPS) was developed to assess the presence of anhedonia. The objective of this study was to assess the psychometric properties of the Brazilian Portuguese version of the SHAPS., Methods: In this study, the SHAPS (14 items) was translated into Brazilian Portuguese and validated using data obtained from 228 subjects within a clinical sample. Psychometric properties were assessed using item response theory (logistic models) and classical test theory (Cronbach's alpha). We checked for external validity using a non-parametric correlation with an independent scale: Hospital Anxiety and Depression Scale - Depression subscale (HAD-D)., Results: The SHAPS presented good internal consistency, with a Cronbach's α coefficient of 0.759 and adequacy to an IRT 1 parameter logistic (Rasch) model. The SHAPS presented significant correlation with the external measure HAD-D, with Spearman's ρ = 0.249 (S = 1368914; p < 0.001)., Conclusion: These results suggest that the Brazilian Portuguese version of the SHAPS is a reliable and valid instrument to assess hedonic tone.