PDF(Pubmed)
Abstract：
BACKGROUND: Ischemic stroke may trigger neuroplastic changes via proliferation, migration towards the lesion, and differentiation of neuroprogenitor cells into mature neurons. Repetitive Transcranial Magnetic Stimulation (rTMS) may promote brain plasticity. This study aimed to assess rTMS\'s effect on post-stroke endogenous neuroplasticity by dosing plasma miRs 17~92, Netrin-1, Sema3A, and BDNF.
METHODS: In this case-controlled study, we randomized 19 ischemic stroke patients within five days from symptoms onset (T0) to neuronavigated-rTMS or sham stimulation. Stimulation was applied on the stroke hemisphere daily between the 7th and 14th day from stroke onset. Blood samples were collected at T0, before the first rTMS section (T7), and at the end of the last rTMS session (T14). Five healthy controls were also enrolled in this study.
RESULTS: Of 19 patients, 10 received rTMS and 9 sham stimulation. Compared with the sham group, in the rTMS group, plasma levels of miRs17~92 and Ntn-1 significantly increased whereas Sema3A levels tended to decrease. In multivariate linear regression analyses, rTMS was independently related to Ntn-1 and miR-25 levels at T14.
CONCLUSIONS: We found an association between rTMS and neurogenesis/axonogenesis biomarker enhancement. Our preliminary data suggest that rTMS may positively interfere with natural endogenous plasticity phenomena of the post-ischemic human brain.
METHODS: In this case-controlled study, we randomized 19 ischemic stroke patients within five days from symptoms onset (T0) to neuronavigated-rTMS or sham stimulation. Stimulation was applied on the stroke hemisphere daily between the 7th and 14th day from stroke onset. Blood samples were collected at T0, before the first rTMS section (T7), and at the end of the last rTMS session (T14). Five healthy controls were also enrolled in this study.
RESULTS: Of 19 patients, 10 received rTMS and 9 sham stimulation. Compared with the sham group, in the rTMS group, plasma levels of miRs17~92 and Ntn-1 significantly increased whereas Sema3A levels tended to decrease. In multivariate linear regression analyses, rTMS was independently related to Ntn-1 and miR-25 levels at T14.
CONCLUSIONS: We found an association between rTMS and neurogenesis/axonogenesis biomarker enhancement. Our preliminary data suggest that rTMS may positively interfere with natural endogenous plasticity phenomena of the post-ischemic human brain.
摘要：
背景：缺血性卒中可能通过增殖引发神经可塑性改变，向病变迁移，和神经祖细胞分化为成熟神经元。重复经颅磁刺激(rTMS)可促进脑可塑性。本研究旨在通过给药血浆miRs17~92、Netrin-1、Sema3A、BDNF。
方法：在本病例对照研究中，我们将19例缺血性卒中患者从症状发作(T0)至神经导航性rTMS或假刺激5天内随机分组.在中风发作的第7天至第14天之间每天对中风半球施加刺激。在第一个rTMS切片（T7）之前，在T0收集血样，并且在最后的rTMS会话结束时(T14)。5名健康对照也被纳入本研究。
结果：在19例患者中，10接受rTMS和9假刺激。与假手术组相比，在rTMS组中，血浆miRs17〜92和Ntn-1水平显着增加，而Sema3A水平趋于降低。在多元线性回归分析中，在T14时，rTMS与Ntn-1和miR-25水平独立相关。
结论：我们发现rTMS与神经发生/轴突发生生物标志物增强之间存在关联。我们的初步数据表明，rTMS可能会积极干扰缺血后人脑的自然内源性可塑性现象。
方法：在本病例对照研究中，我们将19例缺血性卒中患者从症状发作(T0)至神经导航性rTMS或假刺激5天内随机分组.在中风发作的第7天至第14天之间每天对中风半球施加刺激。在第一个rTMS切片（T7）之前，在T0收集血样，并且在最后的rTMS会话结束时(T14)。5名健康对照也被纳入本研究。
结果：在19例患者中，10接受rTMS和9假刺激。与假手术组相比，在rTMS组中，血浆miRs17〜92和Ntn-1水平显着增加，而Sema3A水平趋于降低。在多元线性回归分析中，在T14时，rTMS与Ntn-1和miR-25水平独立相关。
结论：我们发现rTMS与神经发生/轴突发生生物标志物增强之间存在关联。我们的初步数据表明，rTMS可能会积极干扰缺血后人脑的自然内源性可塑性现象。
