A 55-year-old woman was admitted to the hospital with unstable gait followed by four-limb weakness with lower limb predominance. Several days before the onset of neurological symptoms, she developed mild respiratory symptoms, generalized myalgias without fever, and an episode of diarrhea.

On initial examination, she demonstrated moderate weakness mainly affecting the lower limbs (she could stand but was unable to walk), decreased proprioception, distal hypoesthesia, and generalized areflexia. A polymerase chain reaction nasal swab test was positive for severe acute respiratory syndrome–coronavirus 2; respiratory support was not required. Blood tests, cerebrospinal fluid analysis, chest X ray, and cranial computed tomography revealed no abnormalities.

Due to suspected Guillain-Barré syndrome (GBS), electrodiagnostic studies (EDx) were performed on day 9 after admission, and the patient was treated with intravenous immunoglobulin 0.4 g/kg for 5 days.

An initial nerve conduction study (NCS) revealed increased temporal dispersion (158%) and reduced proximal/distal compound muscle action potential (CMAP) size (0.5) in the right median and ulnar nerves with elbow stimulation (normal distal CMAP), reduced tibial conduction velocities bilaterally (29 m/s), and absent tibial and median F waves. Thus, the patient met three criteria for demyelinating polyneuropathy.¹

Electromyographic signals were recorded, using a 38 × 0.45-mm Neuroline concentric needle (Ambu, Ballerup, Denmark), from the right deltoid, extensor digitorum communis, first dorsal interosseous, tensor fascia latae, and vastus lateralis, and bilaterally from the tibialis anterior and gastrocnemius, and then bandpass filtered at 20 Hz to 10 kHz and stored using a KeyPoint.Net 3.22 device (Alpine Biomed, Fountain Valley, California). Spontaneous activity was qualitatively analyzed and motor unit potentials (MUPs) from electromyographic (EMG) signals with 200 ± 50 turns/s were quantitatively analyzed offline using decomposition-based quantitative EMG² and near-fiber EMG (NFEMG),^{3, 4} which together aid in the diagnosis of neuromuscular disorders by quantifying intrinsic motor unit (MU) morphological and electrophysiological properties. A near-fiber MUP (NFM) is created by low-pass double-differentiation filtering a MUP, which, like SFEMG bandpass filtering, emphasizes contributions from fibers close to the needle detection surface (near fibers [NFs]). MUP area represents MU size. NFM duration (the time between the NFM onset and end positions) and NFM dispersion (the time between the first and last detected NF contribution) do not reflect MU size; rather, they reflect MU electrophysiological temporal dispersion (ie, differences in MU axonal branch conduction, neuromuscular junction [NMJ] transmission, and muscle fiber action potential [MFAP] conduction times). NFM segment jitter reflects NFM temporal instabilities, caused by variability in MU axonal branch conduction, NMJ transmission, and MFAP conduction times.

Initially, low-amplitude and -frequency positive sharp waves and fibrillation potentials were recorded bilaterally from the tibialis anterior and gastrocnemius. Recruitment was reduced in all muscles sampled, with a predominance of large-area and irregularly shaped MUPs recorded from early-recruited MUs (more pronounced in distal lower limb muscles). Initial NFEMG measures showed increased dispersion and segment jitter in nearly all lower limb muscles sampled (Figure 1).

Subsequent EDx, performed 5 weeks later, showed improved NCS results. Although the criteria for demyelinating polyneuropathy were still met, significant clinical improvement was seen, as the patient was able to walk with minor assistance.

In addition, MUP area, NFM dispersion, and segment jitter were all reduced Figure 1. Figure 2 shows examples of initial and subsequently recorded MUPs and NFMs.

In GBS, early recruitment of MUs with large MUPs is a consequence of conduction block affecting small-diameter axons.⁵ However, the electrophysiology of MUPs in GBS (ie, quantification of MUP size, temporal dispersion, and stability) is not usually included in the diagnostic protocols for GBS.⁶ Our results could be explained by both a transient impairment of smaller diameter myelinated motor axons (possibly a consequence of conduction block affecting proximal nerve segments, manifesting as early recruitment of large MUs and reduced numbers of small area MUPs) and possible transient electrophysiological impairment of either MU distal axonal branches or their NMJs (manifesting as transient increased NFM dispersion and segment jitter).

Also, axonal degeneration and rapid regeneration of short myelinated segments of intramuscular terminal axonal branches has been associated with immune-mediated subtypes of GBS,⁷ which could explain the early active denervation and rapid motor recovery observed.

These findings support the combined use of EMG and NFEMG in suspected polyneuropathy. Because MUP area reflects MU size while NFM duration, dispersion, and stability reflect MU electrophysiological dispersion and stability, respectively, their combined use can provide valuable information for early diagnosis and management of treatable disorders.

一名 55 岁女性，因步态不稳，四肢无力，下肢为主而入院。在神经系统症状出现前几天，她出现了轻微的呼吸道症状，全身性肌痛，但不发烧，并出现腹泻。

初步检查时，她表现出中度无力，主要影响下肢（她可以站立但无法行走）、本体感觉减退、远端感觉减退和全身反射消失。聚合酶链反应鼻拭子检测对严重急性呼吸系统综合症-冠状病毒 2 呈阳性；不需要呼吸支持。血液检查、脑脊液分析、胸部 X 线检查和颅脑计算机断层扫描未发现异常。

因疑似格林巴利综合征（GBS），入院后第9天进行电诊断检查（EDx），静脉注射免疫球蛋白0.4 g/kg 5天。

最初的神经传导研究 (NCS) 显示，肘部刺激（正常远端 CMAP）时，右侧正中神经和尺神经的时间离散度增加 (158%) 和近端/远端复合肌肉动作电位 (CMAP) 大小降低 (0.5)。双侧传导速度 (29 m/s)，胫骨和正中 F 波缺失。因此，该患者符合脱髓鞘性多发性神经病的三个标准。¹

使用 38 × 0.45 毫米 Neuroline 同心针（Ambu，Ballerup，丹麦）记录肌电图信号，从右侧三角肌、趾伸肌、第一背骨间肌、阔筋膜张肌和股外侧肌，以及双侧胫骨前肌和腓肠肌，然后以 20 Hz 至 10 kHz 带通滤波并使用 KeyPoint.Net 3.22 设备（Alpine Biomed，Fountain Valley，California）存储。对自发活动进行定性分析，并使用基于分解的定量 EMG ²和近纤维 EMG (NFEMG)、^3、4离线定量分析来自肌电图 (EMG) 信号的运动单位电位 (MUP) 200 ± 50 圈/秒通过量化内在运动单位 (MU) 的形态学和电生理学特性，它们共同帮助诊断神经肌肉疾病。近光纤 MUP (NFM) 是通过对 MUP 进行低通双微分滤波创建的，它与 SFEMG 带通滤波一样，强调来自靠近针检测表面的光纤（近光纤 [NFs]）的贡献。MUP 区域代表 MU 大小。NFM 持续时间（NFM 开始和结束位置之间的时间）和 NFM 分散（第一个和最后一个检测到的 NF 贡献之间的时间）不反映 MU 大小；相反，它们反映了 MU 电生理时间离散（即 MU 轴突分支传导、神经肌肉接头 [NMJ] 传输和肌纤维动作电位 [MFAP] 传导时间的差异）。NFM 段抖动反映 NFM 时间不稳定性，

最初，从胫骨前肌和腓肠肌双侧记录低幅度和频率的正尖波和颤动电位。在所有采样的肌肉中，招募都减少了，主要是从早期招募的 MU 中记录到的大面积和不规则形状的 MUP（在远端下肢肌肉中更为明显）。最初的 NFEMG 测量显示几乎所有采样的下肢肌肉中的离散度和节段抖动增加（图 1）。

5 周后进行的后续 EDx 显示 NCS 结果有所改善。尽管仍符合脱髓鞘性多发性神经病的标准，但由于患者能够在轻微帮助下行走，因此观察到了显着的临床改善。

此外，MUP 区域、NFM 色散和段抖动都减少了图 1。图 2 显示了初始和随后记录的 MUP 和 NFM 的示例。

在 GBS 中，具有大 MUP 的 MU 的早期募集是传导阻滞影响小直径轴突的结果。⁵然而，GBS 中 MUP 的电生理学（即 MUP 大小、时间分散和稳定性的量化）通常不包括在 GBS 的诊断协议中。⁶我们的结果可以解释为较小直径有髓运动轴突的瞬时损伤（可能是传导阻滞影响近端神经节段的结果，表现为大 MU 的早期募集和小面积 MUP 的数量减少）和可能的瞬时电生理损伤MU 远端轴突分支或其 NMJ（表现为瞬时增加的 NFM 分散和段抖动）。

此外，肌内末端轴突分支的短有髓段的轴突变性和快速再生与免疫介导的 GBS 亚型有关⁷，这可以解释观察到的早期主动去神经支配和快速运动恢复。

这些发现支持在疑似多发性神经病中联合使用 EMG 和 NFEMG。由于 MUP 面积反映 MU 大小，而 NFM 持续时间、离散度和稳定性分别反映 MU 电生理离散度和稳定性，因此它们的组合使用可为可治疗疾病的早期诊断和管理提供有价值的信息。