Etiology and pathogenetic mechanisms
The exact cause of the disease is not fully understood, but genetic factors play a leading role. It is important to understand that it is not the disease itself that is inherited, but only a predisposition to it. In unipolar depression, the ratio of genetic, shared family, and random factors is approximately 46% — 32% — 12%.
The basis of pathogenesis is explained by the monoamine hypothesis. According to this hypothesis, symptoms develop due to a deficiency of noradrenaline and serotonin, or due to changes in the sensitivity of the corresponding receptors. Antidepressants (for example, MAO inhibitors or SSRIs, such as fluoxetine) increase the amount of neurotransmitters in the synaptic cleft, which over time leads to a downregulation of postsynaptic receptors.
In addition to monoamines, other biological mechanisms are involved in the pathogenesis:
- Neuropeptides: Substance P can inhibit the release of serotonin.
- Hormonal background: the role of the hypothalamic-pituitary-adrenal axis has been proven (positive dexamethasone suppression test in 50% of patients). Steroid hormones also influence the development of depressions, which explains the high frequency of the pathology in women (associated with the cycle and menopause).
- Biorhythms: desynchronization of sleep-wake rhythms is observed, associated with the function of the pineal gland and melatonin synthesis. It is not for nothing that sleep deprivation often gives a short-term positive effect, and melatonin receptor agonists (for example, agomelatine) are used in therapy.
- Intracellular signaling: G-proteins play an important role in postsynaptic signal transduction. Lithium preparations alter their expression, preventing affective fluctuations.
Differential diagnosis
Affective disorders are not strictly specific. Depressive symptoms can mask severe somatic pathology or be a manifestation of other psychoses.
Non-psychiatric causes of depression:
- Oncology: depression is particularly often comorbid with pancreatic cancer.
- Endocrine disorders: hypofunction of the thyroid gland, adrenal glands, or parathyroid glands.
- Neurology: strokes, epilepsy, Parkinson's disease, multiple sclerosis, consequences of traumatic brain injury.
- Iatrogenic factors: intake of reserpine, propranolol, glucocorticoids, oral contraceptives.
- Withdrawal syndrome: upon withdrawal of alcohol, cocaine, amphetamines.
- Infections and autoimmune processes: HIV, infectious mononucleosis, systemic lupus erythematosus.
Differences from schizophrenia: In recurrent disorder, the integrity of symptoms is preserved and there are no personality changes characteristic of schizophrenia. If depression develops within the framework of schizophrenia, it is atypical: indifference and abulia (apathy-abulia) come to the fore rather than melancholy. Pseudohallucinations and delusions of control are often added.
Special forms: involutional and reactive depression
In ICD-10, these conditions are not distinguished as separate nosologies, but in the tradition of Russian psychiatry, they are usually considered separately due to differences in prognosis.
- Involutional melancholia (depression):
It begins at the age of 45–55 years. The leading symptom is not retardation, but anxious agitation with hysteriform reactions (wailing, shouting). Nihilistic hypochondriacal delusions are characteristic — Cotard's syndrome (persistent belief in the rotting or destruction of internal organs). The condition is closely associated with organic CNS damage (e.g., atherosclerosis), is difficult to treat, and forms a specific mental defect. A change of scenery often only increases the patient's confusion.
- Reactive depression:
It develops according to the laws of psychogenics in response to severe loss or psychological trauma (divorce, death of a loved one). Somatic manifestations and motor retardation are weakly expressed here, and there are usually no daily mood fluctuations. Recovery occurs as the psychotraumatic situation loses its relevance (on average in 2–3 months).
Prognosis and social consequences
The disease itself does not lead to dementia or pronounced personality changes. However, frequent hospitalizations, separation from work and family lead to serious social consequences. Patients face self-stigma, career obstacles, and may develop a sense of inadequacy.
The prognosis largely depends on the age of onset. If the debut occurs late (after 55–60 years), the phases become longer, and remissions become shorter and of lower quality. With a continuous course of attacks (continua type) and frequent exacerbations, disability registration is possible.
Briefly: answers to topical questions
What does Protopopov's somatic triad include in depressive syndrome?
Protopopov's somatic triad in depressive syndrome includes three characteristic vegetative symptoms caused by peripheral sympathicotonia.
- Tachycardia — an increased heart rate, indicating an active stress response.
- Pupillary dilation (mydriasis) — an increase in the diameter of the pupils.
- Constipation — a disorder of the gastrointestinal tract function and impaired digestion.
These manifestations are often accompanied by dry, pale, and peeling skin, as well as decreased glandular secretion.
What are the clinical variants of depressive syndrome?
Clinical variants of depressive syndrome are classified by etiology and the leading clinical symptom. According to origin, three main groups are distinguished:
- Somatogenic — organic, symptomatic.
- Endogenous — schizophrenic, circular, periodic, involutional.
- Psychogenic — neurotic, reactive, exhaustion.
According to the leading symptom, the following varieties are distinguished:
- Adynamic (apathetic) — predominance of sluggishness, apathy, indifference.
- Agitated (agitatus) — prolonged speech-motor excitement, up to frenzy.
- Anaesthetic (anaesthesia psychica dolorosa) — agonizing numbness, experience of inner emptiness.
- Asthenic — pronounced asthenia, mental and physical exhaustion.
- Retarded — pronounced motor retardation, slowed thinking.
- Ironic — a sorrowful smile combined with bitter irony.
- Masked (larvated) — hidden behind an abundance of somatic complaints.
What changes in sleep architecture are observed in patients with depression?
Patients with depression show sleep changes and biorhythm desynchronization. According to somnography data, more than 2/3 of patients exhibit:
- faster onset of the REM sleep phase;
- increase in the duration of the REM sleep phase.
There is also biorhythm desynchronization, which is confirmed by the positive effect of sleep deprivation. The disorders are associated with the function of the pineal gland and melatonin synthesis.
Class and exam questions
What is the difference between depression in schizophrenia and recurrent depressive disorder?
In schizophrenia, the structure of affect is dominated by apathy and abulia (indifference and lack of will) rather than sadness. Pseudohallucinations and symptoms of psychic automatism are also frequently present.
What is Cotard's syndrome and when does it occur?
This is a nihilistic hypochondriacal delusion in which the patient is sure that their internal organs have rotted or been destroyed. It is the hallmark of involutional melancholia.
Does ICD-10 recognize reactive depression as a distinct disorder?
No, in ICD-10 it is considered simply as a single depressive episode within the F32 category, although in the Russian school it is separated due to the features of its course and prognosis.
How does sleep affect the course of depression?
In depression, biorhythms are disrupted: the REM sleep phase occurs abnormally quickly. Artificial sleep deprivation can briefly improve the patient's condition.
What else to study on this topic
- Ernst Kretschmer's constitutional theory and cycloid temperament.
- Dysthymia and cyclothymia: the boundary between illness and personality disorder.
- Clinical features of hypomanic episodes.
- Safety principles in psychopharmacotherapy of mood disorders.
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