Restoration of motor inhibition through an abnormal premotor-motor connection in dystonia.

Restoration of motor inhibition through an abnormal premotor-motor connection in dystonia.
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DOI:
10.1002/mds.22814
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发表时间:
2010-04-30
期刊:
影响因子:
8.6
通讯作者:
Chen, Rou-Shayn
Chen, Rou-Shayn
中科院分区:
医学1区
文献类型:
--
作者:
Huang, Ying-Zu;Rothwell, John C.;Lu, Chin-Song;Wang, JiunJie;Chen, Rou-Shayn

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为了阐明使用背侧运动前皮质(PMD)rTMS治疗肌张力障碍的理论基础,我们研究了健康受试者和一组局灶性手前肌张力障碍和DYT1基因携带者的运动系统对rTMS应用于PMD的抑制形式的反应。采用300和600脉冲(cTBS300和cTBS600)的连续theta Burst经颅磁刺激(CTBS)治疗PMD,通过测量初级运动皮质(M1)单脉冲经颅磁刺激(TMS)诱发的MEP波幅、M1区皮质内短间隔抑制/促进(SICI/ICF)、第三时相脊髓相互抑制(RI)和书写测试来量化其后遗症。此外,在DYT1基因携带者中,通过单独的实验研究了cTBS300超过M1和PMD对MEP的影响。在健康受试者中,超过PMD的cTBS300和cTBS600抑制MEP 30min或更长时间,cTBS600降低SICI和RI。相反,与PMD相比,两种形式的CTBS对MEP都没有显著影响,而cTBS600增加了SICI和RI的有效性,并改善了作家痉挛患者的写作。NMDYT1对cTBS300的反应较左侧PMD正常。我们认为,肌张力障碍患者PMD-M1相互作用的减少可能是由于PMD-M1连接的兴奋性降低所致。因此,运动前rTMS的可能治疗作用可能涉及PMD对SICI和RI的间接影响,本研究表明,CTBS可以使这两种影响正常化。
To clarify the rationale for using rTMS of dorsal premotor cortex (PMd) to treat dystonia, we examined how the motor system reacts to an inhibitory form of rTMS applied to the PMd in healthy subjects and in a group of patients with focal hand dystonia and DYT1 gene carriers. Continuous theta burst transcranial magnetic stimulation (cTBS) with 300 and 600 pulses (cTBS300 and cTBS600) was applied to PMd and its after-effects were quantified by measuring the amplitude of MEPs evoked by single pulse transcranial magnetic stimulation (TMS) over the primary motor cortex (M1), short interval intracortical inhibition/facilitation (SICI/ICF) within M1, the third phase of spinal reciprocal inhibition (RI) and writing tests. In addition, in DYT1 gene carriers, the effects of cTBS300 over M1 and PMd on MEPs were studied in separate experiments. In healthy subjects cTBS300 and cTBS600 over PMd suppressed MEPs for 30min or more and cTBS600 decreased SICI and RI. In contrast, neither form of cTBS over PMd had any significant effect on MEPs, while cTBS600 increased effectiveness of SICI and RI and improved writing in patients with writer's cramp. NMDYT1 had a normal response to cTBS300 over left PMd. We suggest that the reduced PMd to M1 interaction in dystonic patients is likely to be due to reduced excitability of PMd-M1 connections. The possible therapeutic effects of premotor rTMS may therefore involve indirect effects of PMd on SICI and RI, which this study has shown can be normalised by cTBS.
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