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首页> 外文期刊>Journal of neurology >Entrapment in anti myelin-associated glycoprotein neuropathy.
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Entrapment in anti myelin-associated glycoprotein neuropathy.

机译：陷于抗髓鞘相关糖蛋白神经病。

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摘要

Anti-myelin associated glycoprotein (MAG) neuropathy is a chronic disorder in which IgM antibodies react with Schwann cell glycoproteins, including MAG and peripheral myelin protein 22 (PMP22). Nerve conduction studies show features of axon loss and predominantly distal slowing consistent with demyelination. Because a genetic loss of PMP22 function yields hereditary neuropathy with liability to pressure palsies (HNPP), loss of PMP22 function due to anti- MAG antibodies may result in increased sensitivity to entrapment. We investigated this by performing standardized electrophysiological studies in 16 patients with anti-MAG neuropathy and 16 disease controls with genetically confirmed HNPP. Disproportionate slowing relative to adjacent segments occurred in similar proportions of patients with anti-MAG neuropathy and HNPP, and was of the same magnitude in each group. Affected were the elbow, carpal tunnel and the wrist-hand segments of the median and ulnar nerves. However, in anti-MAG neuropathy as compared to HNPP, absolute values of distal motor latencies and conduction velocities outside entrapment sites were slower and amplitudes were lower. In conclusion, increased sensitivity for entrapment may occur in anti-MAG neuropathy and contribute to part of the nerve damage.
机译：抗髓磷脂相关糖蛋白（MAG）神经病是一种慢性疾病，其中IgM抗体与雪旺细胞糖蛋白（包括MAG和外周髓磷脂蛋白22（PMP22））反应。神经传导研究显示轴突丧失和主要为远端减慢的特征与脱髓鞘相一致。由于PMP22功能的遗传丧失会导致遗传性神经病，并伴有压力性麻痹（HNPP），因此由于抗MAG抗体引起的PMP22功能丧失可能导致对包埋的敏感性增加。我们通过对16例抗MAG神经病患者和16例经遗传学证实的HNPP进行疾病控制的患者进行标准化电生理研究，对此进行了调查。相对于相邻节段，不相称的减慢发生在具有相似比例的抗MAG神经病和HNPP患者中，并且每组的幅度相同。受影响的是肘部，腕管和正中和尺神经的腕部。然而，与HNPP相比，在抗MAG神经病变中，远端运动潜伏期的绝对值和陷于位点外的传导速度较慢，振幅较低。总之，在抗MAG神经病中可能会增加对包埋的敏感性，并导致部分神经损伤。

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