Table of Contents · 6 sections
Depression (major depressive disorder) is one of the most common mental disorders in the world, affecting over 280 million people. Knowledge of diagnostic criteria, classification, and treatment principles is essential for physicians of any specialty, as up to 50% of patients with depression consult primary care physicians and specialists rather than psychiatrists.
Diagnostic criteria (DSM-5 / ICD-11)
To diagnose a major depressive episode, ≥5 of 9 symptoms must be present for ≥2 weeks, with at least one of the first two being mandatory:
| № | Sign | Mnemonic (SIG E CAPS) |
|---|---|---|
| 1 | Depressed mood (most of the day, nearly every day) | — |
| 2 | Anhedonia (loss of interest and pleasure) | — |
| 3 | Sleep disturbance (insomnia or hypersomnia) | Sleep |
| 4 | Loss of interest in activities | Interest |
| 5 | Feelings of worthlessness or excessive guilt | Guilt |
| 6 | Low energy, fatigue | Energy |
| 7 | Concentration impairment, indecisiveness | Concentration |
| 8 | Appetite/weight changes | Appetite |
| 9 | Psychomotor retardation or agitation | Psychomotor |
| — | Suicidal ideation | Suicidality |
Symptoms must cause clinically significant distress and impairment in social, occupational, or other important areas of functioning.
Classification by severity
| Grade | Criteria | Functioning |
|---|---|---|
| Mild | 5–6 symptoms, minimal intensity | Minor impairment |
| Moderate | 6–7 symptoms, moderate intensity | Noticeable impairment in several areas |
| Severe | Most symptoms, high intensity ± psychotic features | Severe impairment, disability possible |
Pathogenesis: monoamine hypothesis and beyond
- Monoamine hypothesis — deficiency of serotonin (5-HT), norepinephrine (NE), and/or dopamine (DA) in the synaptic cleft. The basis of action for most antidepressants
- Neuroplasticity — ↓ BDNF (brain-derived neurotrophic factor) → atrophy of the hippocampus and prefrontal cortex. Antidepressants increase BDNF
- HPA axis (hypothalamic-pituitary-adrenal axis) — hypercortisolemia in chronic stress → damage to hippocampal neurons
- Neuroinflammation — ↑ proinflammatory cytokines (IL-6, TNF-α, IL-1β) in patients with depression
- Genetics — heritability 30–40%, polygenic
Primary care screening
PHQ-9 (Patient Health Questionnaire-9) — 9 questions, scored 0–3 each:
| Score | Severity | Guidelines |
|---|---|---|
| 0-4 | Minimal / none | Monitoring |
| 5-9 | Mild | Watchful waiting, psychoeducation |
| 10-14 | Moderate | Psychotherapy and/or antidepressant |
| 15-19 | Moderately severe | Antidepressant + psychotherapy |
| 20-27 | Severe | Antidepressant + referral to a psychiatrist |
Treatment
Pharmacotherapy
| Group | Representatives | Mechanism | Features |
|---|---|---|---|
| SSRI | Sertraline, fluoxetine, escitalopram, paroxetine | Serotonin reuptake inhibition | First-line. Side effects: nausea, sexual dysfunction, serotonin syndrome (with MAOIs!) |
| SNRI | Venlafaxine, duloxetine | 5-HT + NE reuptake inhibition | In case of inadequate response to SSRIs, or comorbid pain |
| TCA | Amitriptyline, clomipramine | Non-selective reuptake blockade | Effective but toxic in overdose (cardiotoxicity!). Anticholinergic side effects |
| MAOIs | Phenelzine, tranylcypromine | Monoamine oxidase inhibition | Tyramine crisis (cheese, wine). Do not combine with SSRIs! |
| Atypical | Mirtazapine, bupropion, agomelatine | Diverse mechanisms | Bupropion — no sexual side effects, aids in smoking cessation |
Important: antidepressant effect develops in 2–4 weeks. Treatment continues for ≥6–12 months after remission (relapse prevention).
Psychotherapy
- CBT (cognitive behavioral therapy) is the "gold standard", efficacy proven in mild and moderate depression
- Interpersonal therapy (IPT) — focus on relationships and social roles
- In mild depression, psychotherapy can be the primary treatment (without medication)
Frequently asked questions
How does depression differ from normal sadness?
Normal sadness is a reaction to a specific event, resolves on its own, and does not globally impair functioning. Depression lasts ≥2 weeks, is not tied to a specific cause (or is disproportionate to it), impairs work/study/relationships, is accompanied by neurovegetative symptoms (sleep, appetite, energy), and frequently features feelings of hopelessness and suicidal ideation.
Why don't antidepressants work immediately?
Serotonin reuptake blockade occurs within the first hours, but the clinical effect develops in 2–4 weeks. This is due to the need for adaptive neuroplastic changes: desensitization of 5-HT1A autoreceptors → increased serotonin release; upregulation of BDNF → neurogenesis in the hippocampus; remodeling of synaptic connections.
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