Institute of Clinical Neurosciences, Royal Prince Alfred Hospital, NSW, Australia.
Muscle Nerve. 2013 Jan;47(1):53-60. doi: 10.1002/mus.23455. Epub 2012 Nov 21.
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.
Excitability of median nerve axons at the wrist was studied in 26 patients.
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.
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.
多发性硬化症可能会累及周围神经。运动兴奋性研究表明，慢 K+电流的上调可能是由于中枢病变导致运动神经元特性改变所致。本研究集中于感觉轴突。
研究了 26 名患者腕部正中神经轴突的兴奋性。
22 名患者可进行感觉记录，唯一的异常是超兴奋性降低。没有证据表明存在膜电位变化或脱髓鞘。免疫调节治疗的患者下降明显。通过改变快 K+通道的门控，可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 K+电流增加一致。
感觉发现与运动发现不同。它们可以用一种体液因子来解释，可能是细胞因子，它可以穿透连接蛋白，并已被证明可以改变 K+通道的门控。
