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肢体截肢后皮质兴奋性变化中的NMDA介导机制。

NMDA-mediated mechanisms in cortical excitability changes after limb amputation.

作者信息

Schwenkreis P, Maier C, Pleger B, Mansourian N, Dertwinkel R, Malin J-P, Tegenthoff M, Zenz M

机构信息

Department of Neurology, Ruhr-University Bochum, BG-Kliniken Bergmannsheil, Buerkle-de-la-Camp-Platz 1, D-44789 Bochum, Germany.

出版信息

Acta Neurol Scand. 2003 Sep;108(3):179-84. doi: 10.1034/j.1600-0404.2003.00114.x.

Abstract

OBJECTIVES

The aim of our study was to determine the role of N-methyl-d-aspartate (NMDA)-mediated mechanisms in cortical excitability changes after limb amputation, and their possible relationship to phantom pain.

MATERIALS AND METHODS

Sixteen upper limb amputees who were suffering from chronic phantom pain received the NMDA-antagonist memantine or placebo for 3 weeks. Intracortical inhibition (ICI) and intracortical facilitation (ICF) were determined at baseline and on day 21 using transcranial magnetic stimulation. Simultaneously, phantom pain intensity was assessed.

RESULTS

Memantine reduced ICF and enhanced ICI to roughly the same extent as seen in healthy subjects in a previous study. These changes were not correlated to the reduction of phantom pain.

CONCLUSION

We therefore conclude that NMDA-mediated mechanisms influence changes of ICI and ICF occurring after limb amputation. However, our results suggest that these cortical excitability changes and phantom pain are independent of each other.

摘要

目的

我们研究的目的是确定N-甲基-D-天冬氨酸(NMDA)介导的机制在肢体截肢后皮质兴奋性变化中的作用,以及它们与幻肢痛的可能关系。

材料与方法

16名患有慢性幻肢痛的上肢截肢者接受了NMDA拮抗剂美金刚或安慰剂治疗3周。在基线和第21天使用经颅磁刺激测定皮质内抑制(ICI)和皮质内易化(ICF)。同时,评估幻肢痛强度。

结果

美金刚降低ICF并增强ICI,其程度与先前研究中健康受试者所见大致相同。这些变化与幻肢痛的减轻无关。

结论

因此,我们得出结论,NMDA介导的机制影响肢体截肢后发生的ICI和ICF变化。然而,我们的结果表明,这些皮质兴奋性变化和幻肢痛是相互独立的。

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