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How should primary care doctors select which antidepressants to administer?
Gerald Gartlehner1, Kylie Thaler, Seth Hill
1Department of Evidence-based Medicine and Clinical Epidemiology, Danube University, Karl Dorrek-Strasse 30, 3500, Krems, Austria. gerald.gartlehner@donau-uni.ac.at
Second-generation antidepressants show similar efficacy for major depressive disorder, but evidence is limited for dysthymia and subsyndromal depression regarding benefits and serious adverse events.
Area of Science:
- Pharmacology
- Psychiatry
- Clinical Medicine
Background:
- Second-generation antidepressants are options for depressive disorders.
- Major depressive disorder, subsyndromal depression, and dysthymia are treatable conditions.
Purpose of the Study:
- To summarize evidence on the comparative benefits and harms of second-generation antidepressants.
- To guide clinicians in selecting antidepressants for depressive disorders.
Main Methods:
- Systematic reviews of available evidence.
- Analysis of comparative efficacy, administration, costs, and adverse events.
Main Results:
- Similar efficacy for major depressive disorder across second-generation antidepressants.
- Limited evidence on benefits for dysthymia and subsyndromal depression.
- Unclear comparative risks for serious adverse events like suicidality and serotonin syndrome.
Conclusions:
- Choice of second-generation antidepressant for major depressive disorder may depend on factors other than efficacy.
- Further research is needed to clarify benefits and risks for dysthymia and subsyndromal depression.
- Clinicians require more guidance on comparative harms of these antidepressants.
Related Concept Videos
Antidepressant Drugs: Overview
Antidepressant Drugs: MAOIs and Other Agents
Antidepressant Drugs: Tricyclics, SSRIs, and SNRIs
Drug Therapy
Antianxiety Medications
Psychosis: Goals of Pharmacotherapy
Anxiolytic Drugs: Overview
Primary Types of Anxiolytic Drugs
1. Benzodiazepines:
Benzodiazepines bind to the GABA-A receptor in the brain, enhancing GABA's interaction. This action reduces neurotransmission, effectively blocking anxiety-associated limbic circuitry.
