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发作性运动诱发性运动障碍中的胼胝体传导

Transcallosal conduction in paroxysmal kinesigenic dyskinesia.

作者信息

Kasikci Tayfun, Bek Semai, Koc Guray, Yucel Mehmet, Kutukcu Yasar, Odabasi Zeki

机构信息

a Gulhane Medical Faculty , Ankara , Turkey.

出版信息

Somatosens Mot Res. 2017 Dec;34(4):235-241. doi: 10.1080/08990220.2017.1421158. Epub 2018 Jan 15.

DOI:10.1080/08990220.2017.1421158
PMID:29334840
Abstract

OBJECTIVES

Detecting whether a possible disequilibrium between the excitatory and inhibitory interhemispheric interactions in paroxysmal kinesigenic dyskinesia (PKD) exists.

METHODS

This study assessed measures of motor threshold, motor evoked potential latency, the cortical silent period, the ipsilateral silent period and the transcallosal conduction time (TCT) in PKD patients. Data were compared between the clinically affected hemisphere (aH) and the fellow hemisphere (fH).

RESULTS

The transcallosal conduction time from the aH to the fH was 11.8 ms (range = 2.3-20.7) and 13.6 ms (range = 2.8-67.7) from the fH to the aH. The difference in TCT in the affected side was significant (p = .019).

CONCLUSION

The findings demonstrated that, although inhibitory interneurons act normally and symmetrically between the motor cortices and transcallosal inhibition was normal and symmetrical between both sides, the onset of transcallosal inhibition was asymmetrical. The affected hemisphere's inhibition toward the unaffected hemisphere is faster compared to the inhibition provided by the fellow hemisphere. These results are consistent with an inhibitory deficit in the level of interhemispheric interactions.

SIGNIFICANCE

This study revealed a defect in inhibition of the motor axis could be responsible in the pathological mechanisms of kinesigenic dyskinesia.

摘要

目的

检测发作性运动诱发性运动障碍(PKD)患者兴奋性和抑制性半球间相互作用是否存在失衡。

方法

本研究评估了PKD患者的运动阈值、运动诱发电位潜伏期、皮质静息期、同侧静息期和胼胝体传导时间(TCT)。对临床受累半球(aH)和对侧半球(fH)的数据进行了比较。

结果

从aH到fH的胼胝体传导时间为11.8毫秒(范围=2.3 - 20.7),从fH到aH的胼胝体传导时间为13.6毫秒(范围=2.8 - 67.7)。患侧TCT的差异具有统计学意义(p = 0.019)。

结论

研究结果表明,虽然抑制性中间神经元在运动皮质之间正常且对称地发挥作用,胼胝体间抑制在两侧也正常且对称,但胼胝体间抑制的起始是不对称的。与对侧半球提供的抑制相比,受累半球对未受累半球的抑制更快。这些结果与半球间相互作用水平的抑制缺陷一致。

意义

本研究揭示运动轴抑制缺陷可能是运动诱发性运动障碍病理机制的原因。

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