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Review
. 2023 Jan 6:15:1091402.
doi: 10.3389/fnmol.2022.1091402. eCollection 2022.

The mechanism and effect of repetitive transcranial magnetic stimulation for post-stroke pain

Long-Jin Pan  1   2 , Hui-Qi Zhu  1   2 , Xin-An Zhang  1 , Xue-Qiang Wang  2   3
Affiliations
Review

The mechanism and effect of repetitive transcranial magnetic stimulation for post-stroke pain

Long-Jin Pan et al. Front Mol Neurosci. .

Abstract

Post-stroke pain (PSP) is a common complication after stroke and affects patients' quality of life. Currently, drug therapy and non-invasive brain stimulation are common treatments for PSP. Given the poor efficacy of drug therapy and various side effects, non-invasive brain stimulation, such as repetitive transcranial magnetic stimulation (rTMS), has been accepted by many patients and attracted the attention of many researchers because of its non-invasive and painless nature. This article reviews the therapeutic effect of rTMS on PSP and discusses the possible mechanisms. In general, rTMS has a good therapeutic effect on PSP. Possible mechanisms of its analgesia include altering cortical excitability and synaptic plasticity, modulating the release of related neurotransmitters, and affecting the structural and functional connectivity of brain regions involved in pain processing and modulation. At present, studies on the mechanism of rTMS in the treatment of PSP are lacking, so we hope this review can provide a theoretical basis for future mechanism studies.

Keywords: mechanisms; pain; rTMS; review; stroke; therapy.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
The mechanisms of rTMS in the treatment of PSP. Schematic illustration of the underlying mechanism of rTMS in the treatment of PSP. rTMS modulates the abnormal excitability of the cerebral cortex by modulating the pain network, improving interhemispheric inhibition, and increasing the number of GABA receptors, BDNF expression, and the number of NMDA receptors to alter brain plasticity, ultimately relieving PSP. VPL, ventral posterolateral nucleus; S1, primary somatosensory cortex; S2, secondary somatosensory cortex; MD, mediodorsal nucleus; IHI, interhemispheric inhibition; ICI, intracortical inhibition; GABA receptor, gamma-aminobutyric acid receptor; BDNF, brain-derived neurotrophic factor; NMDA receptor, N-methyl-D-aspartate receptor; LTP, long-term potentiation.
See this image and copyright information in PMC

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