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近端正中神经病变:62例患者的电诊断及超声检查结果

Proximal median nerve neuropathy: electrodiagnostic and ultrasound findings in 62 patients.

作者信息

Shields Lisa B E, Iyer Vasudeva G, Zhang Yi Ping, Shields Christopher B

机构信息

Norton Neuroscience Institute, Norton Healthcare, Louisville, KY, United States.

Neurodiagnostic Center of Louisville, Louisville, KY, United States.

出版信息

Front Neurol. 2024 Dec 5;15:1468813. doi: 10.3389/fneur.2024.1468813. eCollection 2024.

DOI:10.3389/fneur.2024.1468813
PMID:39703354
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11655337/
Abstract

OBJECTIVES

Proximal median nerve (PMN) neuropathies are caused by lesions proximal to the carpal tunnel, which include the forearm, elbow, upper arm, and brachial plexus. Differentiating between carpal tunnel syndrome and PMN neuropathies is important to guide management and is based on clinical, electrodiagnostic (EDX), and ultrasound (US) findings. This study describes the clinical, EDX, and US features in 62 patients with PMNs.

METHODS

All patients underwent EDX studies, and 52 (83.9%) had a US study. The patients were assigned to one of the following four localization zones of PMN neuropathies based on clinical and EDX criteria: Zone 1: extends from the fascicles in the brachial plexus contributing to the median nerve to the innervation of the pronator teres (PT); Zone 2: distal to the branch to the PT and proximal to the origin of the anterior interosseous nerve (AIN); Zone 3: involves the origin of the AIN; and Zone 4: distal to the origin of the AIN and proximal to the carpal tunnel. The localization was based on the pattern of muscle weakness, topography of EMG abnormalities, and US study findings.

RESULTS

The anatomical locations of the PMN neuropathies based on clinical, EDX, and US findings were as follows: Zone 1 in 38 patients (61.3%), Zone 2 in 6 patients (9.7%), Zone 3 in 7 patients (11.3%), and Zone 4 in 11 patients (17.7%). The most common etiology among all 62 patients was iatrogenic injury (30 [48.4%]), followed by non-iatrogenic trauma (20 [32.2%]). The following EDX findings were noted: prolonged distal motor latency (29 [46.8%]), decreased motor nerve conduction velocity in the forearm (22 [35.5%]), low amplitude or absent compound muscle action potentials (50 [80.6%]), and abnormal or absent sensory nerve action potentials (50 [80.6%]). Of the 52 (83.9%) patients who underwent US studies, a total of 22 (42.3%) patients showed an increased cross-sectional area of the median nerve. A neuroma was observed in 9 patients (17.4%).

CONCLUSION

It is often possible to localize the site of the median nerve involvement and gain insight into the underlying cause based on clinical and EMG findings, but in certain cases, a US study may be necessary to confirm the location.

摘要

目的

正中神经近端(PMN)神经病由腕管近端的病变引起,这些病变包括前臂、肘部、上臂和臂丛神经。区分腕管综合征和PMN神经病对于指导治疗很重要,且基于临床、电诊断(EDX)和超声(US)检查结果。本研究描述了62例PMN患者的临床、EDX和US特征。

方法

所有患者均接受了EDX检查,52例(83.9%)患者接受了US检查。根据临床和EDX标准,将患者分为PMN神经病的以下四个定位区域之一:区域1:从臂丛神经中支配正中神经的束状结构延伸至旋前圆肌(PT)的支配区域;区域2:在PT分支的远端且在前骨间神经(AIN)起始点的近端;区域3:涉及AIN的起始点;区域4:在AIN起始点的远端且在腕管的近端。定位基于肌肉无力的模式、肌电图异常的部位以及US检查结果。

结果

根据临床、EDX和US检查结果,PMN神经病的解剖位置如下:区域1有38例患者(61.3%),区域2有6例患者(9.7%),区域3有7例患者(11.3%),区域4有11例患者(17.7%)。62例患者中最常见的病因是医源性损伤(30例[48.4%]),其次是非医源性创伤(20例[32.2%])。记录到以下EDX检查结果:远端运动潜伏期延长(29例[46.8%]),前臂运动神经传导速度降低(22例[35.5%]),复合肌肉动作电位波幅降低或消失(50例[80.6%]),以及感觉神经动作电位异常或消失(50例[80.6%])。在接受US检查的52例(83.9%)患者中,共有22例(42.3%)患者显示正中神经横截面积增大。9例患者(17.4%)观察到神经瘤。

结论

通常可以根据临床和肌电图检查结果定位正中神经受累部位并深入了解潜在病因,但在某些情况下,可能需要进行US检查以确认位置。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4815/11655337/91436b177b86/fneur-15-1468813-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4815/11655337/947ed256bb1b/fneur-15-1468813-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4815/11655337/ddb3fdc3ba6d/fneur-15-1468813-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4815/11655337/faacb756b4ca/fneur-15-1468813-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4815/11655337/7250d4d7232f/fneur-15-1468813-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4815/11655337/8865f639771d/fneur-15-1468813-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4815/11655337/91436b177b86/fneur-15-1468813-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4815/11655337/947ed256bb1b/fneur-15-1468813-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4815/11655337/ddb3fdc3ba6d/fneur-15-1468813-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4815/11655337/faacb756b4ca/fneur-15-1468813-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4815/11655337/7250d4d7232f/fneur-15-1468813-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4815/11655337/8865f639771d/fneur-15-1468813-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4815/11655337/91436b177b86/fneur-15-1468813-g006.jpg

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