Abstract
Anhedonia constitutes one of the main symptoms of depressive episode. It correlates with suicidality and significantly effects the quality of patient's lives. Available treatments are not sufficient against this group of symptoms. Ketamine is a novel, rapid acting strategy for treatment resistant depression. Here we report the change in symptoms of anhedonia measured by Snaith-Hamilton Pleasure Scale as an effect of eight ketamine infusions as an add-on treatment in 42 patients with treatment resistant depression. We also determined the effect of this change on the severity of depressive symptoms measured by Inventory for Depression Symptomatology-Self Report 30-Item (IDS-SR 30). We have observed statistically significant decrease in the level of anhedonia during ketamine treatment. After adjusting for potential confounders we have found that significant reduction in Snaith-Hamilton Pleasure Scale (SHAPS) after each infusion and 1 week post treatment was observed only among patients who did not use benzodiazepines. The reduction in symptoms of anhedonia mediates the antidepressive effect of ketamine. The results need replication in a larger randomized placebo controlled trial.
Highlights
Anhedonia, the reduction of the ability to experience pleasure, is one of the core symptoms of depression, and approved treatments do not address it sufficiently [1]
Preclinical evidence suggests that glutamate may have a role in anhedonia [15]. These findings suggest that the glutamatergic system and its downstream modulation of dopaminergic activity may be one potential route of the antianhedonic efficacy of ketamine in both unipolar and bipolar treatment resistant depression (TRD)
Pairwise comparisons (Tuckey’s post-hoc tests) show that there was a significant decrease in the Snaith-Hamilton Pleasure Scale (SHAPS) total score from the baseline to each infusion and the post-infusion visit (Figure 1)
Summary
Symptoms of anhedonia turned out to be a robust predictor of a poor outcome of antidepressant treatment in a factor analysis of data from two large studies: Genome-based Therapeutic Drugs for Depression (GENDEP) and Sequenced Treatment Alternatives to Relieve Depression (STAR∗D). This was true irrespective of which antidepressant was used and did not depend on the level of baseline depression [4]. Effective, and rapid-acting antidepressant in unipolar patients [5, 6] and bipolar treatment resistant depression [7]. Studies have indicated that it involves the inhibition of presynaptic and postsynaptic NMDARs in GABAergic interneurons
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