Interview: Treating emotions in depression:clinical experience

Pedro Antônio SCHMIDT DO
CNRG, Porto Alegre, BRAZIL

Treating emotions in depression: clinical experience

Interview with P. A. Schmidt do Prado- Lima, Brazil

Targeting emotions in the treatment of major depressive disorder is not a new idea. Since tricyclic antidepressants were first used, psychiatrists have been trying to fully understand the differences in the profiles between the various drugs, not only in terms of side effects, but also in terms of therapeutic effects. For example, is there a difference between imipramine and clomipramine? Is one or the other more apt to protect against suicidal behavior? Is one or the other more apt to provoke this behavior in some patients? Is one or the other more likely to be effective in cases of panic disorder or obsessive- compulsive disorder? Is one or the other better at diminishing impulsivity? I believe such differences exist and think that we must use this knowledge, often easy to recognize in clinical practice, but difficult to demonstrate in clinical trials.

Medicographia. 2013;35:334-336 (see French abstract on page 336)

Are positive and negative emotions connected during major depressive disorder?

For such a complex question, there is no single, simple answer. However, from one point of view, I think that two different scenarios may occur in relation to emotions during major depressive disorder, and both of them could be present to some extent in the same patient at the same time. Firstly, there is a predominance of negative emotions over positive ones. It is this scenario, the expression of negative emotions, which is most frequently recognized in depression. Even memory is affected by this valence, allowing depressive people to remember negative events in their lives perfectly, while other memories are difficult for them to recall.1 Secondly, patients may experience blunted emotions. This is not a new idea, for example, this incapacity to feel is rated in item 8 of the Montgomery-Asberg Depression Rating Scale (MADRS).2 For patients that experience this flattening of emotions during depression, selective serotonin reuptake inhibitors (SSRIs) may often maintain or even increase this “neutrality,” although improving other aspects of depressive syndrome. In this sense, negative and positive emotions could be connected in depressive patients.

What is the clinical advantage of targeting emotions in depression?

This question could be approached in two ways: based on use of psychotherapy (mainly cognitive behavioral therapy) or based on use of medications. Regarding use of medications, we must first take into account that different drugs act in different ways; we need to take advantage of this to improve the treatment response. In general, though these differences between drugs are not evidenced by clinical trials, we must not deny their existence because we do not as yet have the means of identifying them in standard psychopharmacological clinical trials. It is usually difficult to clinically recognize and develop a consensus about subtle profile differences among drugs within the same class.

The most popular class of antidepressants is the selective serotonin reuptake inhibitors (SSRIs). We often observe patients that respond partially to these medications, while maintaining symptoms of emotional blunting. Addition of a dopaminergic medication in the treatment regimen could improve the response. Looking at this effect, it seems that we have medications that prompt people to be more phlegmatic, “British” (for example, SSRIs), and medications that allow people to be more exuberant in expressing emotions, more “Italian” (for example, bupropion). Taking this into consideration, we can help patients that seek more intensity in their feelings, for example, those complaining that they are incapable of crying in appropriate situations, which is very common.

What does the emergence of positive feeling tell us about the recovery process?

We have to recognize that antidepressant treatment is different from some endocrinological ones. In hypothyroidism, the use of thyroid hormone regularizes thyroid function so that it is as if the disorder were not present. Likewise, patients and even doctors often imagine that antidepressant treatment can regularize the level of brain amines to ideal levels and thus return the brain to the predepressive state. Unfortunately, that is not the case. The medication changes the patient’s emotions and behavior to such an extent that some claim antidepressants can even change the “personality” of the patient. So, the treatment must take these changes into account.

For example, we can diminish impulsivity (and emotion) using SSRIs. Indeed, for some patients this could be beneficial, but for others absolutely not. In general, an antidepressant treatment must not only remove the suffering, the guilt, and the sadness, but also restore the capacity to feel pleasure, happiness, and interest. Merely substituting absence of feelings for the suffering is not a good strategy for the patients; it is only good for the scores in scales.

Are positive and negative emotions equally blunted after a major depressive disorder?

Some patients can have a partial recovery after depression, treated or not. If they were treated, this partial response could be related to the medication used, as explained above.

One of the symptoms that may persist is blunted positive and/ or negative emotion. At first glance, this could be viewed as an advantage for the patient, as a lack of emotion is better than suffering, but over time treatment must deal with this partial response. By contrast, ignoring this symptom (if it is a partial response) or side effect (if it is due to the antidepressant used) changes the patient’s perspectives, options, behavior, and attitude.

Why is treatment based on targeting emotions not popular in major depressive disorder?

Our clinical practice must be scientifically oriented. That is the reason that we have adopted evidence-based medicine and why we expend so much effort and so many resources to find evidence to justify one or another clinical decision. The problem is that we must recognize that we are not able to investigate and establish the evidence for all clinical aspects. For example, guidelines in general do not take into account comorbidities, which are very frequent in psychiatry. In regards to major depressive disorders, only now are we beginning to identify the evidence for treating clinical subtypes and the differences in the therapeutic effect of different antidepressants. It is important to remember that twenty years ago even the differences between tricyclic antidepressants and SSRIs were not recognized, although now they appear obvious. Recently, the advent of new antidepressants with different mechanisms of action has stirred up interest in whether or not those different drugs produce different therapeutic effects.3 _

1. Murphy FC, Sahakian BJ, O’Carroll RE. Cognitive impairment in depression: psychological models and clinical issues. In: Ebert D, Ebmeier KP, eds. New Models for Depression. Basel: Karger;1998. Adv Biol Psychiatry; vol 19:1-19.
2. Montgomery SA, Asberg M. A new depression scale designed to be sensitive to change. Br J Psychiatry. 1979;134:382-389.
3. Millan MJ. Multi-target strategies for the improved treatment of depressive states: conceptual foundations and neuronal substrates, drug discovery and therapeutic application. Pharmacol Ther. 2006;110:135-370.

Keywords: antidepressants; blunted emotions; major depressive disorder; negative emotions; positive emotions