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肘部尺神经病变恢复过程中似乎未发生明显的神经再生。

No Major Nerve Regeneration Seems to Occur during Recovery of Ulnar Neuropathy at the Elbow.

作者信息

Podnar Simon

机构信息

Institute of Clinical Neurophysiology, Division of Neurology, University Medical Center Ljubljana, SI-1525 Ljubljana, Slovenia.

出版信息

J Clin Med. 2023 Jun 7;12(12):3906. doi: 10.3390/jcm12123906.

DOI:10.3390/jcm12123906
PMID:37373601
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10299067/
Abstract

There are three main potential mechanisms of recovery after nerve lesion: (1) resolution of conduction block, (2) collateral reinnervation, and (3) nerve regeneration. Their relative contributions in recovery after focal neuropathies are not well established. In a group of previously reported prospective cohort of patients with ulnar neuropathy at the elbow (UNE), I performed a post-hoc analysis of their clinical and electrodiagnostic findings. I compared amplitudes of the compound muscle action potential (CMAP) and sensory nerve action potential (SNAP) on ulnar nerve stimulation, as well as qualitative concentric needle electromyography (EMG) findings in the abductor digiti minimi muscle on the initial and follow-up examinations several years later. Altogether, 111 UNE patients (114 arms) were studied. During median follow-up period of 880 days (range: 385-1545 days), CMAP amplitude increased ( = 0.02), and conduction block in the elbow segment recovered (from median 17% to 7%; < 0.001). By contrast, SNAP amplitude did not change ( = 0.89). On needle EMG, spontaneous denervation activity diminished ( < 0.001), motor unit potential (MUP) amplitude increased ( < 0.001), and MUP recruitment remained unchanged ( = 0.43). Findings of the present study indicate that nerve function in chronic focal compression/entrapment neuropathies seems to improve mainly due to the resolution of the conduction block and collateral reinnervation. Contribution of nerve regeneration seems to be minor; the majority of axons lost in chronic focal neuropathies probably never recover. Further studies using quantitative methods are needed to validate present findings.

摘要

神经损伤后恢复的主要潜在机制有三种

(1)传导阻滞的解除;(2)侧支神经再支配;(3)神经再生。它们在局灶性神经病变恢复过程中的相对作用尚未明确。在一组先前报道的肘部尺神经病变(UNE)患者的前瞻性队列中,我对他们的临床和电诊断结果进行了事后分析。我比较了尺神经刺激时复合肌肉动作电位(CMAP)和感觉神经动作电位(SNAP)的波幅,以及几年后初次检查和随访检查时小指展肌的定性同心针肌电图(EMG)结果。总共研究了111例UNE患者(114条手臂)。在中位随访期880天(范围:385 - 1545天)内,CMAP波幅增加(P = 0.02),肘部节段的传导阻滞恢复(从中位值17%降至7%;P < 0.001)。相比之下,SNAP波幅没有变化(P = 0.89)。针极EMG显示,自发电活动减少(P < 0.001),运动单位电位(MUP)波幅增加(P < 0.001),而MUP募集情况保持不变(P = 0.43)。本研究结果表明,慢性局灶性压迫/卡压性神经病变中的神经功能改善似乎主要归因于传导阻滞的解除和侧支神经再支配。神经再生的作用似乎较小;慢性局灶性神经病变中丢失的大多数轴突可能无法恢复。需要进一步采用定量方法的研究来验证目前的发现。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e377/10299067/e0fabe473855/jcm-12-03906-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e377/10299067/e2f7a96fb313/jcm-12-03906-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e377/10299067/e0fabe473855/jcm-12-03906-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e377/10299067/e2f7a96fb313/jcm-12-03906-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e377/10299067/e0fabe473855/jcm-12-03906-g002.jpg

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