Sensorimotor integration is abnormal in asymptomatic Parkin mutation carriers

Sensorimotor integration is abnormal in asymptomatic Parkin mutation carriers
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无症状 Parkin 突变携带者感觉运动整合异常

DOI:
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发表时间:
2007
期刊:
影响因子:
9.9
通讯作者:
A. Münchau
A. Münchau
中科院分区:
医学1区
文献类型:
--
作者:
T. Bäumer;P. Pramstaller;H. Siebner;S. Schippling;J. Hagenah;M. Peller;C. Gerloff;C. Klein;A. Münchau

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背景:在帕金森病(PD)患者中,经颅磁刺激(TMS)研究一直表明感觉运动皮质抑制音减少。目前尚不清楚这是与运动症状有关,还是代表了多巴胺能神经元变性的适应性代偿变化。在这里,我们使用数字刺激后短间隔传入抑制(DSAI)和皮质内双脉冲抑制和促进来探讨具有潜在黑质纹状体多巴胺能功能障碍的单个突变Parkin等位基因的临床无症状携带者的皮质内感觉运动兴奋性。方法:对9名杂合子突变携带者和9名健康对照进行研究。对于dSAI测试,将电脉冲施加到右手食指,然后以25、30和40毫秒的刺激间隔(ISI)在左侧运动皮质上施加TMS脉冲。在ISIS为2-15毫秒时测试皮层内双脉冲兴奋性。结果:单突变Parkin等位基因携带者的dSAI在25毫秒的ISI时降低,而成对脉冲TMS正常。结论:感觉运动抑制的相对减少可能是Parkin突变的直接结果,或者是皮质下功能障碍的皮质水平的适应性改变,但不是由运动症状引起的。
Background: In patients with Parkinson disease (PD), transcranial magnetic stimulation (TMS) studies have consistently demonstrated a reduced inhibitory tone in the sensorimotor cortex. It remains unclear whether this is related to motor symptoms or represents adaptive compensatory changes to degeneration of dopaminergic neurons. Here we used short-interval afferent inhibition after digital stimulation (dSAI) and intracortical paired-pulse inhibition and facilitation to probe intracortical sensorimotor excitability in clinically asymptomatic carriers of a single mutant Parkin allele who have a latent nigrostriatal dopaminergic dysfunction. Methods: Nine heterozygous mutation carriers and nine healthy controls were investigated. For dSAI testing, electrical pulses were applied to the right index finger followed by TMS pulses over the left motor cortex at interstimulus intervals (ISI) of 25, 30, and 40 msec. Intracortical paired-pulse excitability was tested at ISIs of 2 to 15 msec. Results: dSAI was reduced at an ISI of 25 msec in carriers of a single mutant Parkin allele, whereas paired-pulse TMS was normal. Conclusion: The relative decrease in sensorimotor inhibition may be a direct consequence of the Parkin mutation or represent adaptive changes at the cortical level in response to a subcortical dysfunction, but is not caused by motor symptoms.