In recent years, the study of depression in various neurological disorders has become relevant, for example, in epilepsy, migraine, after a stroke and traumatic brain injury, in Alzheimer’s disease and other diseases. Scientific and practical data are accumulating on the neurobiological and neuropsychological factors of depression, organic factors contributing to the development of depression. There was a decrease in the hippocampus and the neural network of the fronto-limbic region in depression, which is confirmed by neuroimaging data and postmortem studies, which indicate damage to the nerve fibers between the hippocampus and the preforontal area of the cerebral cortex. From a neurobiological point of view, a number of mediators play a role in the pathogenesis of depression. These are serotonin, norepinephrine , dopamine, gamma- aminobutyric acid.
A decrease in the number of 5-HT1A serotonin antagonist receptors correlates with the degree of epileptogenic activity of the cerebral cortex. At receipt of 5-HT in the synaptic gap is its inactivation and moving back through the conveyor 5-HTT. Genetic abnormalities of 5-HTT affect the activity of limbic structures, which are associated with the development of depression, suicidal behavior, and schizophrenia. In depression, dysfunctions of the norepinephrine system were found. Prolonged stress reduces the density of alpha-2A receptors, especially in the hippocampus and amygdala.
Data on the role of dopamine are not entirely clear, but it has been established that dopaminergic neurons located from the ventral tegmental area to the prefrontal region of the cerebral cortex, striatum, and anterior cingulate gyrus, affect the pathogenesis and clinic of depression. At this point in time, the following neurobiological theories of depression exist:
- Monoaminergic ;
- Disorders in the hypothalamic-pituitary-adrenal axis;
- Neuroimmune theory.
According to the neuroimmune theory, cytokines play an important role in the genesis of depression. They are potential therapeutic modulators of mood disorders.
Disorders of a depressive nature are observed in 26% of women and 12% of men with migraines. In this regard, it becomes clear why propranolol and amitriptyline are equally effective in both migraine and depression. Serotonin reuptake inhibitors and SNRIS drugs ( venlafaxine ) are less effective for migraine . Depression occurs more often in stroke patients with a frequency of 30-50%. But in such a situation, there is also a two-way influence: with depression, the risk of stroke increases, and with impaired cerebral circulation, depression occurs. Antidepressants reduce the risk of death in stroke patients. One third of people with epilepsy have dysthymia and depression. In depression, there is a resistance of the convulsive syndrome to traditional antiepileptic treatment. Movement disorders ( Huntington’s , Parkinson’s) also cause depression. With Pakinson’s disease , it is observed – in 50% of patients, with Gentinkton’s disease – 40%. However, there is very little research on the treatment of depression for movement disorders. The literature only describes that SSRI inhibitors are less effective in movement disorders than nortriptyline . In diseases of movement, dopaminergic structures are damaged , therefore, the drug venlafaxine is more effective than drugs of the SSRI group, and less toxic than tricyclic and tetracyclic antidepressants. With multiple sclerosis, depression occurs in 35% of patients.
In the clinic of Professor V.L. Just a minute in Moscow, you can undergo examination and treatment of depression and related diseases.