Causes of deep depressive disorder. Depression Mechanisms

The etiology of deep depressive disorder is unclear. Life events (such as job loss, change of residence) and intellectual stress are associated with an increased risk of depressive disorder, but the exact causes are unclear. With this disorder, neurochemical changes in the central nervous system can occur in response to stress. There is evidence that deep depression has a genetic component, although this is not as obvious as for schizophrenia. However, when studying twins, the concordant levels are similar. The genetic factor of depression is thought to be 50%.

The alleged neurohormonal and neurochemical causes of depression have received some confirmation. The hypothalamic-pituitary-adrenal (GGN) system, which controls the hormonal homeostasis of the body, is involved in the process to a greater extent. It was noted that depressed patients have a higher cortisol concentration curve and that cortisol is not suppressed by dexamethasone in 50% of them. Stable feedback mechanisms suggest that the cortisol receptors in the hippocampus of depressed subjects are pathological. Nonspecific pathology has also been detected in the responses of thyroid hormone and growth hormone.

The neurochemical theory of depression involving biogenic amines , NE, 5-HT and dopamine. The initial hypothesis suggested that depression was due to functional deficiency of the amine transmitter (e.g., NE, dopamine, 5-HT), in part because tricyclic antidepressants and monoamine oxidase inhibitors (MAOIs) facilitated neurotransmission in the aminergic nervous systems and were effective. It is also known that drugs that deplete amine stores (such as reserpine) can cause depression.

An increased number of 5-HT receptors in the brains of people who committed suicide was attributed to a low concentration of 5-HT, while low levels of 5-HT metabolites were found in studies of cerebrospinal fluid (CSF) in patients with depression. Animal studies have shown that all effective antidepressants reduce the sensitivity of (3-adrenergic receptors and 5-HT2A receptors to agonists. Delayed response to treatment coincides with the time taken to regulate these receptors. Therefore, it is possible that receptors for biogenic amines rather than their levels are related to depression.

The dopaminergic system can also be involved in the etiology of the disease: a decrease in the central concentration of dopamine can lead to depression, and drugs that increase the central dopamine concentration can reduce depression.

Other systems that may be involved in the onset of depression may be the GABA system and the neuropeptide system, especially vasopressin and endogenous opiates. Secondary reseller systems can play a key role in the effectiveness of certain treatments.

The cardinal symptoms of depression are usually divided into emotionally-cognitive and biological. To be diagnosed with a deep depressive disorder, the symptoms must be constant for at least 2 weeks. Emotionally cognitive symptoms may include sadness, suffering, decreased enjoyment of life, feelings of hopelessness or guilt, slow speech, meaningless conversation and suicidal ideology. Symptoms change during the day, but are more pronounced in the morning: low tone and fatigue, apathy and poor concentration, changes in appetite (usually decreased, with loss of body weight), drowsiness, early morning awakening (the patient wakes up very early in the morning and cannot fall asleep), low libido and daily mood swings. Deep depressive disorders are classified as psychotic depression if they are accompanied by delusions and hallucinations. The latter are usually negative in content.

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