Alteration of cortical but not spinal inhibitory circuits in idiopathic scoliosis.

The Journal of Spinal Cord Medicine Pub Date : 2022-03-01 Epub Date: 2020-03-23 DOI:10.1080/10790268.2020.1739893
Václav Boček, Martin Krbec, Peter Vaško, Karel Brabec, Markéta Pavlíková, Ivana Štětkářová
{"title":"Alteration of cortical but not spinal inhibitory circuits in idiopathic scoliosis.","authors":"Václav Boček,&nbsp;Martin Krbec,&nbsp;Peter Vaško,&nbsp;Karel Brabec,&nbsp;Markéta Pavlíková,&nbsp;Ivana Štětkářová","doi":"10.1080/10790268.2020.1739893","DOIUrl":null,"url":null,"abstract":"<p><p><b>Background:</b> The pathogenesis of adolescent idiopathic scoliosis (AIS), including the role of brain and spinal inhibitory circuits, is still poorly elucidated. The aim of this study was to identify which central inhibitory mechanisms are involved in the pathogenesis of AIS.<b>Design:</b> A prospective neurophysiological study, using a battery of neurophysiological tests, such as cutaneous (CuSP) and cortical (CoSP) silent periods, motor evoked potentials (MEP) and paired-pulse transcranial magnetic stimulation (ppTMS).<b>Settings:</b> Neurophysiological laboratory.<b>Participants:</b> Sixteen patients with AIS (14 females, median age 14.4) and healthy controls.<b>Outcome measures:</b> MEPs were obtained after transcranial magnetic stimulation (TMS) and recorded from the abductor pollicis muscle (APB). ppTMS was obtained at interval ratios (ISI) of 1, 2, 3, 6, 10, 15 and 20 ms. The cortical silent period (CoSP) was recorded from the APB. The cutaneous silent period (CuSP) was measured after painful stimuli delivered to the thumb while the subjects maintained voluntary contraction of the intrinsic hand muscles. The data were analyzed and compared with those from healthy subjects.<b>Results:</b> The CoSP duration was significantly prolonged in AIS patients. A significantly higher amplitude of ppTMS for ISI was found in all AIS patients, without remarkable left-right side differences. No significant difference in MEP latency or amplitude nor in the CuSP duration was obtained.<b>Conclusion:</b> Our observation demonstrates evidence of central nervous system involvement in adolescent idiopathic scoliosis (AIS). Lower intracortical inhibition, higher motor cortex excitability, and preserved spinal inhibitory circuits are the main findings of this study. A possible explanation of these changes could be attributed to impaired sensorimotor integration predominantly at the cortical level.</p>","PeriodicalId":501560,"journal":{"name":"The Journal of Spinal Cord Medicine","volume":" ","pages":"186-193"},"PeriodicalIF":0.0000,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10790268.2020.1739893","citationCount":"3","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Journal of Spinal Cord Medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/10790268.2020.1739893","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2020/3/23 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 3

Abstract

Background: The pathogenesis of adolescent idiopathic scoliosis (AIS), including the role of brain and spinal inhibitory circuits, is still poorly elucidated. The aim of this study was to identify which central inhibitory mechanisms are involved in the pathogenesis of AIS.Design: A prospective neurophysiological study, using a battery of neurophysiological tests, such as cutaneous (CuSP) and cortical (CoSP) silent periods, motor evoked potentials (MEP) and paired-pulse transcranial magnetic stimulation (ppTMS).Settings: Neurophysiological laboratory.Participants: Sixteen patients with AIS (14 females, median age 14.4) and healthy controls.Outcome measures: MEPs were obtained after transcranial magnetic stimulation (TMS) and recorded from the abductor pollicis muscle (APB). ppTMS was obtained at interval ratios (ISI) of 1, 2, 3, 6, 10, 15 and 20 ms. The cortical silent period (CoSP) was recorded from the APB. The cutaneous silent period (CuSP) was measured after painful stimuli delivered to the thumb while the subjects maintained voluntary contraction of the intrinsic hand muscles. The data were analyzed and compared with those from healthy subjects.Results: The CoSP duration was significantly prolonged in AIS patients. A significantly higher amplitude of ppTMS for ISI was found in all AIS patients, without remarkable left-right side differences. No significant difference in MEP latency or amplitude nor in the CuSP duration was obtained.Conclusion: Our observation demonstrates evidence of central nervous system involvement in adolescent idiopathic scoliosis (AIS). Lower intracortical inhibition, higher motor cortex excitability, and preserved spinal inhibitory circuits are the main findings of this study. A possible explanation of these changes could be attributed to impaired sensorimotor integration predominantly at the cortical level.

Abstract Image

特发性脊柱侧凸中皮质抑制回路而非脊髓抑制回路的改变。
背景:青少年特发性脊柱侧凸(AIS)的发病机制,包括脑和脊髓抑制回路的作用,仍然知之甚少。本研究的目的是确定哪些中枢抑制机制参与AIS的发病机制。设计:一项前瞻性神经生理学研究,使用一系列神经生理学测试,如皮肤(CuSP)和皮质(CoSP)沉默期、运动诱发电位(MEP)和双脉冲经颅磁刺激(ppTMS)。设置:神经生理实验室。参与者:16名AIS患者(14名女性,中位年龄14.4岁)和健康对照。结果测量:经颅磁刺激(TMS)后获得mep,并记录外展拇外展肌(APB)。分别在间隔比(ISI)为1、2、3、6、10、15和20 ms时获得ppTMS。APB记录皮质沉默期(CoSP)。测量拇指疼痛刺激后的皮肤沉默期(CuSP),同时受试者保持手部固有肌肉的自愿收缩。对这些数据进行分析,并与健康受试者的数据进行比较。结果:AIS患者CoSP持续时间明显延长。在所有AIS患者中,ISI的ppTMS振幅均显著升高,但左右侧无显著差异。MEP潜伏期、振幅和CuSP持续时间均无显著差异。结论:我们的观察证实了青少年特发性脊柱侧凸(AIS)涉及中枢神经系统的证据。较低的皮质内抑制、较高的运动皮质兴奋性和保留的脊髓抑制回路是本研究的主要发现。对这些变化的一种可能解释是主要在皮层水平上感觉运动整合受损。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信