key: cord-0991395-djfbuksp
authors: Helbok, Raimund; Beer, Ronny; Löscher, Wolfgang; Boesch, Sylvia; Reindl, Markus; Hornung, Rouven; Schiefecker, Alois Josef; Deisenhammer, Florian; Pfausler, Bettina
title: Guillain‐Barré syndrome in a patient with antibodies against SARS‐COV‐2
date: 2020-06-12
journal: Eur J Neurol
DOI: 10.1111/ene.14388
sha: c38092f86bbc1ccd5e37f9960f89f185eae70b0c
doc_id: 991395
cord_uid: djfbuksp

There are now several reports on neurologic features of SARS‐CoV‐2 infection.(1 2) In a recent study of 214 patients with COVID‐19, 78 (36.4%) patients had neurological manifestations, including headache, dizziness, acute cerebrovascular diseases, and impaired consciousness.(2)

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There are now several reports on neurologic features of SARS-CoV-2 infection. 1 2 In a recent study of 214 patients with COVID-19, 78 (36.4%) patients had neurological manifestations, including headache, dizziness, acute cerebrovascular diseases, and impaired consciousness. 2 3, 4 Here, we report a case of Guillain-Barré syndrome (GBS) with an onset 2 weeks after SARS-CoV-2 infection with highly elevated serum antibodies against SARS-CoV-2, which supports the association between SARS-CoV-2 disease and the

Case: On March 20 th , a 68 years old man developed dry cough, headache, fatigue, myalgia and fever up to 39°C followed by anosmia and ageusia. He was tested for SARS-CoV-2 RNA 10 days after symptom onset, which revealed a negative result and was treated by the primary care physician at home. Premedical history was uneventful and the patient did not take regular medication. On April 1 st , oral methylprednisolone 10mg/d was started for suspected rheumatoid arthritis due to persistent pelvic girdle and muscle pain of the proximal lower extremities, a C-reactive protein of 8.5mg/dL (normal: 0.0-0.5mg/dL), and an elevated erythrocyte sedimentation rate (63mm/1h). On April 3 rd (14 days after onset of pulmonary disease) the patient had recovered from respiratory symptoms, but still complained of severe fatigue and developed symmetric distal tingling in both feet followed by ascending dysesthesias up to the knees and proximal weakness.

The next day he presented at the neurological emergency room with inability to walk. On examination, the patient was alert and fully oriented, afebrile with normal vital signs (oxygen saturation 98% on room air, blood pressure 143/90mmHg, heat rate 85 bpm).

Laboratory examination revealed slightly elevated C-reactive protein (2.3mg/dL, normal: 0.0-0.5mg/dL), fibrinogen level 650mg/dL (normal: 210-400mg/dL), white blood cell count

This article is protected by copyright. All rights reserved 8.1G/L (normal: 4.0-10.0G/L), lactate dehydrogenase 276 U/L (normal: 100-250 U/L) and erythrocyte sedimentation rate 55mm/1h. Neurological examination showed decreased sensation to touch and pinprick in the lower extremities, absent ankle jerk, atactic stance and inability to walk without assistance. Additional truncal dysesthesia prompted spinal cord MRI with unremarkable findings. Lumbar CSF on day 2 after onset of neurological symptoms showed normal cell counts (2/mm³) and protein level (64 mg/dL) and a serum/CSF glucose ratio of 0.83. Due to the history of pulmonary symptoms a chestcomputed tomography was performed and revealed residual ground-glass opacities in both lower lungs suggestive for coronavirus disease 2019 (COVID-19). Based on the neurological presentation GBS was diagnosed, the patient was admitted to the COVID-19 isolation ward and intravenous immunoglobulin therapy (IVIG, 30g) was initiated. His respiratory condition worsened, and the patient required oxygen supplementation (3L/min) followed by pressure support non-invasive ventilation after 36 h. Nerve conduction studies performed on the following day showed F-wave abnormalities in all nerves, delayed distal motor latency in one nerve, reduced distal amplitudes in two and a sural-sparing pattern supporting acute inflammatory demyelinating polyneuropathy subtype of the GBS (table 1) 

This article is protected by copyright. All rights reserved accompanied by respiratory failure the patient underwent elective intubation in a fully conscious state and the initial intravenous immunoglobulin therapy, which was initiated on April 6 th (total dose 30g) was switched to plasma exchange on April 7 th , which was 3 days after symptom onset. In total 4 cycles of plasma exchange were performed. Again, SARS-CoV-2 on PCR assay from bronchoalveolar lavage (BAL) fluid was negative. The patient improved gradually and was transferred to a neuro-rehabilitation facility 4 weeks after symptom onset, where he regained mobility without significant help another 4 weeks later.

To the best of our knowledge, this is the first case of SARS-CoV-2 seropositivity associated with GBS. Given the patient's symptoms of infection, the origin from a highly endemic area of SARS-CoV-2 cases, ground-glass opacities on chest CT-scan on admission, repeatedly negative PCR-SARS-CoV-2 testing in oropharyngeal swabs, CSF and BAL fluid, and the highly positive SARS-CoV-2 antibody testing, we believe that the patient had recovered from COVID-19 with adequate immune response at the onset of GBS. Importantly, respiratory failure was triggered by progressive weakness of in-and expiratory muscles in our patient. Considering the temporal association, we speculate that GBS might have been triggered by humoral immune response against SARS-CoV2 in this patient. Our findings and a recently published cases support the hypothesis that SARS-CoV-2 may trigger GBS as para-/ post-infectious disease as reported by Zika virus. 5, 6 Underling mechanisms for this process may include immune molecular mimicry against nervous system antigens before clinical symptoms of covid-19 are manifested (para-infectious), 3 This article is protected by copyright. All rights reserved 

This article is protected by copyright. All rights reserved 

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