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Repetitive transcranial magnetic stimulation restores altered functional connectivity of central poststroke pain model monkeys
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Title: | Repetitive transcranial magnetic stimulation restores altered functional connectivity of central poststroke pain model monkeys |
Authors: | Kadono, Yoshinori Browse this author | Koguchi, Keigo Browse this author | Okada, Ken-ichi Browse this author | Hosomi, Koichi Browse this author | Hiraishi, Motoki Browse this author | Ueguchi, Takashi Browse this author | Kida, Ikuhiro Browse this author | Shah, Adnan Browse this author | Liu, Guoxiang Browse this author | Saitoh, Youichi Browse this author |
Issue Date: | 17-Mar-2021 |
Publisher: | Nature Research |
Journal Title: | Scientific reports |
Volume: | 11 |
Start Page: | 6126 |
Publisher DOI: | 10.1038/s41598-021-85409-w |
Abstract: | Central poststroke pain (CPSP) develops after a stroke around the somatosensory pathway. CPSP is hypothesized to be caused by maladaptive reorganization between various brain regions. The treatment for CPSP has not been established; however, repetitive transcranial magnetic stimulation (rTMS) to the primary motor cortex has a clinical effect. To verify the functional reorganization hypothesis for CPSP development and rTMS therapeutic mechanism, we longitudinally pursued the structural and functional changes of the brain by using two male CPSP model monkeys (Macaca fuscata) developed by unilateral hemorrhage in the ventral posterolateral nucleus of the thalamus. Application of rTMS to the ipsilesional primary motor cortex relieved the induced pain of the model monkeys. A tractography analysis revealed a decrease in the structural connectivity in the ipsilesional thalamocortical tract, and rTMS had no effect on the structural connectivity. A region of interest analysis using resting-state functional magnetic resonance imaging revealed inappropriately strengthened functional connectivity between the ipsilesional mediodorsal nucleus of the thalamus and the amygdala, which are regions associated with emotion and memory, suggesting that this may be the cause of CPSP development. Moreover, rTMS normalizes this strengthened connectivity, which may be a possible therapeutic mechanism of rTMS for CPSP. |
Rights: | https://creativecommons.org/licenses/by/4.0/ |
Type: | article |
URI: | http://hdl.handle.net/2115/81236 |
Appears in Collections: | 医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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