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Different mechanisms underlying changes in excitability of peripheral nerve sensory and motor axons in multiple sclerosis

机译:多发性硬化症周围神经感觉和运动轴突兴奋性改变的不同机制

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Introduction: Subtle involvement of peripheral nerves may occur in multiple sclerosis. Motor excitability studies have suggested upregulation of slow K+ currents, probably secondary to altered motoneuron properties resulting from the central lesion. This study concentrates on sensory axons. Methods: Excitability of median nerve axons at the wrist was studied in 26 patients. Results: Sensory recordings were possible in 22 patients, and reduced superexcitability was the sole abnormality. There was no evidence for changes in membrane potential or demyelination. The decrease was significant in patients taking immunomodulatory therapy. These findings could be reproduced in a computer model by changing the gating of fast K+ channels. Motor axon findings were consistent with previously reported increased slow K+ current. Conclusions: The sensory findings differ from motor findings. They can be explained by a humoral factor, possibly cytokines, which can penetrate the paranode and have been documented to alter the gating of K+ channels.
机译:简介:多发性硬化症可能会发生周围神经的轻微侵犯。运动兴奋性研究表明,缓慢的K +电流上调,这可能是由于中央病变引起的运动神经元特性改变所致。这项研究集中于感觉轴突。方法:研究了26例患者腕部正中神经轴突的兴奋性。结果:22位患者可以进行感官记录,而超兴奋性降低是唯一的异常。没有证据表明膜电位或脱髓鞘发生改变。在接受免疫调节治疗的患者中,这种下降是显着的。通过更改快速K +通道的门控,可以在计算机模型中重现这些发现。运动轴突的发现与先前报道的慢钾电流增加有关。结论:感觉发现与运动发现不同。可以通过体液因子(可能是细胞因子)来解释它们,这些因子可以穿透腹旁淋巴结,并有文献记载可以改变K +通道的门控。

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