
Neuroplasticity induction using transcranial magnetic stimulation
Author(s) -
М Е Черненко
Publication year - 2019
Publication title -
psihìatrìâ, nevrologìâ ta medična psihologìâ
Language(s) - English
Resource type - Journals
eISSN - 2411-166X
pISSN - 2312-5675
DOI - 10.26565/2312-5675-2019-12-07
Subject(s) - transcranial magnetic stimulation , neuroscience , neuroplasticity , psychology , long term potentiation , neurotrophin , synaptic plasticity , stimulation , medicine , receptor
In this article, we have displayed the results of an analysis of modern scientific data on the induction of neuroplasticity using transcranial magnetic stimulation. We presented the multilevel neuroplastic effects of electromagnetic fields caused by transcranial magnetic stimulation (TMS). The authors of the article determined that transcranial magnetic stimulation uses variable magnetic fields to non-invasively stimulate neurons in the brain. The basis of this method is the modulation of neuroplasticity mechanisms with the subsequent reorganization of neural networks. Repeated TMS (rTMS), which is widely used in neurology, affects neurotransmitters and synaptic plasticity, glial cells and the prevention of neuronal death. The neurotrophic effects of rTMS on dendritic growth, as well as growth and neurotrophic factors, are described. An important aspect of the action of TMS is its effect on neuroprotective mechanisms. A neuroimaging study of patients with Parkinson's disease showed that rTMS increased the concentration of endogenous dopamine in the ipsilateral striatum. After rTMS exposure, the number of β-adrenergic receptors in the frontal and cingulate cortex decreases, but the number of NMDA receptors in the ventromedial thalamus, amygdala, and parietal cortex increases. These processes ultimately lead to the induction of prolonged potentiation. In response to rTMS, neuronal excitability changes due to a shift in ion balance around a population of stimulated neurons; this shift manifests itself as altered synaptic plasticity. Combinations of rTMS treatment and pharmacotherapy (e.g., small doses of memantine) may block the alleviating effect during prolonged potentiation. Studies using models of transient ischemic attack and prolonged ischemia have shown that rTMS protects neurons from death and alters the blood flow and metabolism in the brain. It has been demonstrated that TMS has a proven ability to modulate the internal activity of the brain in a frequency-dependent manner, generate contralateral responses, provide, along with the neuromodulating and neurostimulating effect, affect the brain as a global dynamic system.