The new coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection, has become a pandemic. Here, we report a patient with Guillain‐Barré syndrome (GBS) who had evidence of a coronavirus disease 2019 (COVID‐19) infection, but was otherwise asymptomatic for COVID‐19 except for a low‐grade fever.

A 53‐year‐old previously healthy woman presented with a 3‐day history of dysarthria associated with progressive weakness and numbness of the lower extremities. She had no history of recent infection or vaccination. Vital signs were normal. A neurologic examination revealed mild dysarthria due to jaw weakness and bilateral, predominantly lower limb weakness, with 4−/5 strength in knee and ankle flexor and extensor muscles, and 4−/5 in the left and 4+/5 in right hip flexor muscles by the Medical Research Council (MRC) scale. She could walk only with assistance. There was slight weakness in her hand muscles. Reduced sensation to pinprick was found distally to the upper thighs. Tendon reflexes were absent in the lower extremities. GBS was considered to be the most likely diagnosis.

Biochemical screening (electrolytes, liver and kidney function tests, C‐reactive protein) and HIV test were normal other than mild neutropenia (1.49 cells/μL) and a high monocyte percentage (19.77; normal 4–12) in the complete blood count. Nerve conduction studies (NCS) confirmed a demyelinating pattern with conduction blocks and temporal dispersion in motor nerves (Figure 1A, Table 1). Ulnar and median nerves demonstrated normal minimal F‐wave latencies with decreased persistence (median 55%; ulnar 65%) and increased chronodispersion (median 22.1 ms; ulnar 18.0 ms) (Table 1; Figure 1B). Plasma exchange (five sessions; one every other day) was performed 5 days after the onset of neurologic symptoms.

Magnetic resonance imaging (MRI) of the lumbar and cervical spines revealed asymmetrical thickening and hyperintensity of postganglionic roots supplying the brachial and lumbar plexuses in short‐tau inversion recovery (STIR) sequences (Figure 1C,D). Focal intensities suspicious for COVID‐19 pneumonia were incidentally identified in peripheral areas of lungs on STIR sequence of the brachial plexus MRI (Figure 1E). She had a mild fever (37.5°C) but no cough, dyspnea, anosmia, or ageusia. Chest computed tomography showed bilateral peripheral ground‐glass opacities and consolidations on both lungs (Figure 1F); the patient was placed in isolation. She had mild lymphopenia (1.042/mm³) and high C‐reactive protein level (33.2 mg/L; normal 0–5 mg/L). Nasopharyngeal swab for real‐time polymerase chain reaction (RT‐PCR) SARS‐CoV‐2 was positive. She was treated with hydroxychloroquine and azithromycin. Cerebrospinal fluid (CSF) analysis on day 7 of admission showed a protein level of 32.6 mg/dL with no leucocytes and a CSF test for SARS‐CoV‐2 was negative. Two weeks after the onset of symptoms, the neurologic findings had improved markedly; MRC scores were 4+/5 in lower limb muscle groups, and she was able to walk without assistance.

Neurologic manifestations during the course of COVID‐19 infection have been described.1 Previous reports of GBS and COVID‐19 demonstrated marked respiratory symptoms before or concurrent with the onset of neurologic symptoms.2-4 In contrast, our patient with GBS had evidence of a COVID‐19 infection, but was otherwise asymptomatic for COVID‐19 except for a low‐grade fever.

We speculate that the pathophysiologic mechanism of GBS in COVID‐19 may be para‐infectious rather post‐infectious, likely due to “molecular mimicry” that preferentially affects the nervous system before the respiratory system. Another explanation could be direct viral neuropathogenic effects on the nervous system.5

This possibility that this patient acquired the virus nosocomially cannot be ruled out, because we did not perform microbiologic testing at the time of admission. In the neurology clinic, during the hospitalization period, none of the other patients or staff had symptoms, and none of the contacts had positive PCR results for SARS‐CoV‐2. The initial laboratory test demonstrating a high monocyte percentage might also support an infection before hospital admission.6

The diagnosis of acute‐onset chronic inflammatory demyelinating polyneuropathy (CIDP) cannot be excluded. Nearly 16% of patients with CIDP show an acute onset, and plasma exchange might have prevented progression. Motor weakness with less prominent sensory signs at presentation support the diagnosis of GBS.7

In conclusion, our findings highlight the importance of attention to the subtle clinical findings of COVID‐19 infection in newly diagnosed GBS.

新型冠状病毒，即严重急性呼吸综合征冠状病毒 2 (SARS-CoV-2) 感染，已成为大流行病。在这里，我们报告了一名格林巴利综合征 (GBS) 患者，他有 2019 年冠状病毒病 (COVID-19) 感染的证据，但除低烧外，其他方面没有 COVID-19 症状。

一名 53 岁的既往健康女性因 3 天构音障碍病史就诊，并伴有进行性下肢无力和麻木。她没有近期感染或疫苗接种史。生命体征正常。神经系统检查显示由于下颌无力和双侧（主要是下肢）无力导致轻度构音障碍，膝关节和踝屈伸肌力量为 4-/5，左侧为 4-/5，右侧髋屈肌为 4+/5肌肉研究委员会 (MRC) 量表。她只能在帮助下行走。她的手部肌肉有些虚弱。在大腿上部的远端发现针刺感觉减弱。下肢腱反射消失。GBS被认为是最可能的诊断。

除轻度中性粒细胞减少（1.49 个细胞/μL）和全血细胞计数中单核细胞百分比高（19.77；正常 4-12）外，生化筛查（电解质、肝肾功能检测、C 反应蛋白）和 HIV 检测均正常。神经传导研究 (NCS) 证实了一种脱髓鞘模式，具有传导阻滞和运动神经的时间分散（图 1A，表 1）。尺神经和正中神经表现出正常的最小 F 波潜伏期，持续性降低（中位数 55%；尺神经 65%）和时间离散增加（中位数 22.1 ms；尺神经 18.0 ms）（表 1；图 1B）。在神经系统症状发作后 5 天进行血浆置换（五次；每隔一天一次）。

腰椎和颈椎的磁共振成像 (MRI) 显示在短 tau 反转恢复 (STIR) 序列中供应臂丛和腰丛神经的节后根不对称增厚和高信号 (图 1C,D)。在臂丛 MRI 的 STIR 序列中偶然发现了疑似 COVID-19 肺炎的病灶强度（图 1E）。她有轻微的发烧（37.5°C），但没有咳嗽、呼吸困难、嗅觉丧失或听力丧失。胸部计算机断层扫描显示双侧外周磨玻璃影和双肺实变（图 1F）；该患者被隔离。她有轻度淋巴细胞减少症（1.042/mm ³) 和高 C 反应蛋白水平 (33.2 mg/L; 正常 0–5 mg/L)。鼻咽拭子实时聚合酶链反应 (RT-PCR) SARS-CoV-2 呈阳性。她接受了羟氯喹和阿奇霉素治疗。入院第 7 天的脑脊液 (CSF) 分析显示蛋白质水平为 32.6 mg/dL，没有白细胞，并且 SARS-CoV-2 的 CSF 检测结果为阴性。症状出现两周后，神经系统表现明显改善；下肢肌肉组的 MRC 评分为 4+/5，并且她能够在没有帮助的情况下行走。

已经描述了 COVID-19 感染过程中的神经系统表现。1先前关于 GBS 和 COVID-19 的报告表明，在出现神经系统症状之前或同时出现明显的呼吸道症状。2-4相比之下，我们的 GBS 患者有 COVID-19 感染的证据，但除低烧外，其他方面没有 COVID-19 症状。

我们推测，GBS 在 COVID-19 中的病理生理机制可能是副感染性而非感染后性，这可能是由于“分子拟态”优先影响呼吸系统之前的神经系统。另一种解释可能是病毒对神经系统的直接影响。5

不能排除该患者在医院获得病毒的可能性，因为我们在入院时没有进行微生物检测。在神经内科门诊，住院期间，其他患者或工作人员均无症状，接触者均未出现 SARS-CoV-2 PCR 结果阳性。最初的实验室测试表明单核细胞百分比很高，也可能支持入院前的感染。6

不能排除急性发作性慢性炎症性脱髓鞘性多发性神经病（CIDP）的诊断。近 16% 的 CIDP 患者表现出急性发作，血浆置换可能阻止了进展。表现时感觉体征不明显的运动无力支持 GBS 的诊断。7

总之，我们的研究结果强调了关注新诊断 GBS 中 COVID-19 感染的微妙临床发现的重要性。