Yokota T, Saito Y, Yuki N, Tanaka H
Department of Neurology, Tokyo Medical and Dental University, Japan.
Muscle Nerve. 1996 Jul;19(7):823-8. doi: 10.1002/mus.880190702.
In multifocal motor neuropathy (MMN) the threshold of electrical stimulation showed a persistent, marked increase for the motor nerve which decreased after treatment with intravenous immunoglobulin or oral cyclophosphamide; whereas, the threshold was normal for the sensory nerve. This discrepancy of the thresholds for motor and sensory nerves indicates that the increased threshold for motor nerve is not caused by change in perineural capacitance, such as subperi- and endoneural edema or perineural thickening. Inching studies showed that the site of the elevated motor nerve threshold was closely associated with conduction slowing and block. For the cause of the increased threshold, therefore, we suppose the presence of a factor which interferes with reorganization of the nodal property in the remyelinative process or which directly blocks sodium channels where the blood-nerve barrier is impaired in MMN.
在多灶性运动神经病(MMN)中,电刺激阈值显示运动神经持续、显著升高,静脉注射免疫球蛋白或口服环磷酰胺治疗后降低;而感觉神经阈值正常。运动神经和感觉神经阈值的这种差异表明,运动神经阈值升高并非由神经周电容变化引起,如神经束膜下和神经内膜水肿或神经周增厚。步进研究表明,运动神经阈值升高的部位与传导减慢和阻滞密切相关。因此,对于阈值升高的原因,我们推测存在一种因素,它在再髓鞘化过程中干扰结特性的重组,或直接阻断MMN中血神经屏障受损部位的钠通道。