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Journal Information
Vol. 35. Issue 6.
Pages 412-415 (July - August 2020)
Vol. 35. Issue 6.
Pages 412-415 (July - August 2020)
Letter to the Editor
DOI: 10.1016/j.nrleng.2020.06.002
Open Access
Guillain-Barré syndrome associated with SARS-CoV-2 infection. Comments after 16 published cases
Síndrome de Guillain-Barré tras infección por SARS-CoV-2. Comentarios tras la publicación de 16 nuevos casos
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C. Guijarro-Castroa,b,c,
Corresponding author
crisxqgui@gmail.com

Corresponding author.
, M. Rosón-Gonzáleza, A. Abreua, A. García-Arratibela,d, M. Ochoa-Mulasa,d
a Servicio de Neurología, CINAC Puerta del Sur, Móstoles, Madrid, Spain
b Coordinadora del Grupo de Estudio de Humanidades e Historia de la Neurología de la SEN, Spain
c Facultad de Medicina, UEM, Madrid, Spain
d Facultad de Medicina, CEU, Madrid, Spain
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Tables (2)
Table 1. Motor and sensory nerve conduction findings.
Table 2. Patient profiles.
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Dear Editor:

It was with great interest that we read the article by Velayos-Galán et al.1 We would like to report a similar case of Guillain-Barré syndrome (GBS) that manifested after bilateral pneumonia due to SARS-CoV-2 infection, and analyse the data published on this entity.

On 4 May 2020, a 70-year-old man presented subacute weakness in all 4 limbs, which worsened over the following 5 days. Three weeks earlier, he had presented bilateral pneumonia due to SARS-CoV-2 infection: a chest CT scan showed ground-glass opacities in both lungs, and PCR results were positive for SARS-CoV-2 in nasopharyngeal and oropharyngeal swabs. The patient was treated with oxygen therapy, hydroxychloroquine, azithromycin, ceftriaxone, and dexamethasone. The patient had no relevant medical history. His body temperature was 36.5°C and baseline oxygen saturation was 99%. Pulmonary auscultation revealed no alterations. A neurological examination revealed asymmetrical weakness (Medical Research Council grade 4/5 in the right hand; 4+/5 in the left hand; 4/5 in the left leg, and 3+/5 in the right leg) and areflexia in the legs and feet. Two days after admission, symptoms worsened. Muscle strength was 4/5 in the arms and hands and 3/5 in the legs and feet. Light touch and pin prick distal sensitivity was decreased in distal regions.

Laboratory analysis at admission revealed lymphocytopaenia (0.52 × 103 cells/L; normal range: 1.1-3.2 × 103 cells/L) and thrombocytopaenia (113 × 103 cells/L; normal range: 125-300 × 103 cells/L). CSF analysis showed normal cell count (0 × 103 cells/L; normal range: 0-8 × 103 cells/L) and a slightly increased protein level (49 mg/dL; normal range: 8-43 mg/dL). Nerve conduction studies performed on day 6 revealed delayed distal latencies and absence of F waves in the early phase, in the context of mixed-type (axonal and demyelinating) acute motor polyneuropathy of moderate and symmetrical intensity in all 4 limbs, with associated axonal sensory involvement, loss of motor units, and signs of neurogenic involvement of the muscles analysed without acute denervation (Table 1). The patient was diagnosed with GBS and started treatment on high-dose intravenous immunoglobulins (0.4 g/kg/day for 5 days) 8 hours after admission; symptoms improved on day 3 of treatment.

Table 1.

Motor and sensory nerve conduction findings.

Motor nerve conduction study  Distal latency (ms)Amplitude (mV)Conduction velocity (m/s)F-wave latency (ms)
    (at +10 days)    (at +10 days)    (at +10 days)    (at +10 days) 
Left median nerve  5.2  7.8  2.7  37.1  38.9     
Right median nerve  5.6  7.8  4.4  2.9  45.2  40.4     
Right ulnar nerve  4.7  7.7  3.2  0.86  44.8  43.6     
Left peroneal nerve  4.8  5.8  2.5  2.3  34.7  34.5     
Right peroneal nerve  4.5  6.7  3.2  1.6  31.1  35.8     
Left tibial nerve  5.7  5.4  1.6  1.4  35.7  37.9  67.9  69.8 
Right tibial nerve  6.2  6.9  1.1  1.3  34.2  37.1  69.8  68.1 
Sensory nerve conduction study  Amplitude (μV)Conduction velocity (m/s)
    (at +10 days)    (at +10 days) 
Left median nerve    2.4    46.9 
Right median nerve  4.4  6.2  47.3  49.7 
Right ulnar nerve  8.3  Absent  50  Absent 
Left sural nerve  4.2  2.9  46.5  45.1 
Right sural nerve  4.6  3.9  48.5  48.5 

Upon discharge, 14 days after admission, he only presented mild weakness in the interosseous muscles of the hands (4+/5) and dorsiflexor muscles of both feet (4+/5), as well as generalised areflexia. The PCR results for SARS-CoV-2 at discharge were negative.

To our knowledge, 3 cases of concomitant GBS and SARS-CoV-2 infection with parainfectious profiles1–3 and 13 cases of GBS subsequent to SARS-CoV-2 infection4–12 have been reported to date (Table 2). The favourable progression of most of the patients who presented GBS after the infection is noteworthy.

Table 2.

Patient profiles.

Patient  Symptom onset  Symptoms  CSF  EMG  Treatment  Progress  Authors 
43-year-old man  Respiratory infection and diarrhoea 10 days before  Progressive tetraparesis, distal sensory alteration. Bilateral facial palsy, dysphagia.  Not reported  Demyelinating polyradiculoneuritis  Ig for 5 days.  Favourable  Velayos-Galán et al.1 
          Dolquine®, lopinavir, ritonavir.     
          Corticosteroids     
70-year-old woman  14 days before onset of respiratory symptoms (fever and cough)  Hand and foot paraesthesia. Gait alterations. Respiratory failure  Albuminocytologic dissociation. PCR for SARS-CoV-2 not available  Demyelinating, sensorimotor polyradiculoneuritis  Ig 0.4 g/kg/day for 5 days  Respiratory failure, no subsequent progression is specified.  Alberti et al.2 
61-year-old woman  8 days before respiratory symptoms (dry cough and fever)  Weakness and fatigue  Albuminocytologic dissociation.  Demyelinating neuropathy  Arbidol, lopinavir, ritonavir  Favourable; full recovery  Zhao et al.3 
      PCR not conducted         
54-year-old woman  15 days before onset of anosmia and ageusia  Proximal symmetric paraparesis, sensory alterations in the limbs. Dysphagia  Albuminocytologic dissociation. PCR test not available  Demyelinating polyneuropathy  Ig 0.4 g/kg/day for 5 days  Initial exacerbation. Almost complete recovery  Scheidl et al.5 
70-year-old woman  3 days after respiratory symptoms (dry cough)  Quadriplegia and sensory alterations  Albuminocytologic dissociation.  Sensorimotor axonal neuropathy  Ig 2 g/kg for 5 days  No improvement after treatment  Otmani et al.6 
      Negative PCR results    Dolquine®·     
          Azithromycin     
70-year-old man  10 days after acute respiratory syndrome  Paraparesis, distal allodynia, difficulties in bladder voiding, and constipation  Albuminocytologic dissociation. Negative PCR results  Demyelinating, sensorimotor polyneuropathy  Ig 0.4 g/kg/day for 5 days  Rapid recovery  Coen et al.7 
71-year-old man  7 days after onset of fever  Paraesthesia at limb extremities followed by flaccid tetraparesis. Moderate dyspnoea and low back pain  High protein levels and mild pleocytosis. Negative PCR results  Acute sensory and motor polyradiculoneuritis with predominant demyelinating features  Ig 0.4 g/kg/day for 5 days, ritonavir + lopinavir, hydroxychloroquine  Respiratory failure, death  Alberti et al.2 
76-year-old woman  8 days after onset of respiratory symptoms (fever and cough)  Low back pain radiating to both thighs, predominantly proximal progressive tetraparesis, distal-onset paraesthesia  Not performed  Not performed  None administered due to fast progression  Dysphagia, dyspnoea requiring mechanical ventilation, followed by death  Marta-Enguita et al.8 
54-year-old man  10 days after dry cough and fever. 2 days after diarrhoea.  Hypoaesthesia and weakness in the lower limbs  Not conducted due to typical symptoms  Not conducted due to typical symptoms  Ig 0.4 g/kg/day for 5 days. Hydroxychloroquine  Progressive improvement  Virani et al.9 
64-year-old man  11 days after onset of fever and cough  Distal paraesthesia in feet and hands followed by flaccid tetraparesis  Albuminocytologic dissociation  Demyelinating polyneuropathy  Ig 0.4 g/kg/day  Respiratory failure requiring mechanical ventilation  Camdessanche et al.10 
65-year-old man  15 days after respiratory symptoms (cough, fever, and dyspnoea)  Acute ascending quadriparesis progressing to bilateral facial paresis and quadriplegia  Patient did not consent to the procedure  Axonal sensorimotor polyneuropathy  Hydroxychloroquine, lopinavir + ritonavir, azithromycin.  Unknown  Sedaghat et al.11 
          Ig 0.4 g/kg/day for 5 days     
Unknown  7 days after onset of fever, cough, and ageusia  Flaccid tetraparesis, facial diplegia. Paraesthesia in the upper limbs. Respiratory failure  Albuminocytologic dissociation. Negative PCR results  Unknown  2 cycles of Ig 0.4 g/kg/day for 5 days  Persistent weakness of the lower limbs, paraplegia, and dysphagia  Toscano et al.12 
Unknown  10 days after onset of fever and pharyngitis  Facial diplegia. Paraesthesia in the lower limbs and ataxia  Albuminocytologic dissociation. Negative PCR results  Unknown  Ig 0.4 g/kg/day for 5 days  Improved ataxia and facial diplegia  Toscano et al.12 
Unknown  10 days after onset of fever and cough  Flaccid tetraparesis and facial weakness. Respiratory failure  Albuminocytologic dissociation. Negative PCR results  Unknown  2 cycles of Ig 0.4 g/kg/day for 5 days  Progression to flaccid quadriplegia and respiratory failure  Toscano et al.12 
Unknown  5 days after onset of cough and hyposmia  Flaccid tetraparesis and ataxia  Normal. Negative PCR results  Unknown  Ig 0.4 g/kg/day for 5 days  Mildly improved tetraparesis, inability to stand at 1 month  Toscano et al.12 
Unknown  7 days after onset of cough, ageusia, and anosmia  Flaccid quadriplegia. Facial weakness. Respiratory failure  Slightly elevated protein level. Negative PCR results  Unknown  Ig 0.4 g/kg/day for 5 days and plasmapheresis  Unknown  Toscano et al.12 

CSF: cerebrospinal fluid; EMG: electromyography; Ig: immunoglobulins; PCR: polymerase chain reaction.

In our patient, the gradual progression of neurological symptoms resembles that observed with postinfectious aetiologies. Therefore, we suspect an association between acute polyneuropathy and SARS-CoV-2 infection. This association is supported by the fact that the patient observed home isolation for 21 days before neurological symptom onset, as well as the negative results for antiganglioside antibodies. However, the postinfectious onset, acute clinical course, and typical neurophysiological findings of GBS (mixed-type polyneuropathy of motor and sensory fibres), together with the absence of history of autoimmune, neoplastic, or neurological disease, suggest postinfectious aetiology. A significant limitation is the lack of availability of SARS-CoV-2 serology tests and CSF PCR tests at our centre.

While our case is suggestive of a possible association between GBS and SARS-CoV-2 infection, further case reports with epidemiological data are needed to demonstrate a causal relationship. This case also underscores the need to consider possible neurological symptoms of SARS-CoV-2 infection.

The authors agree that there is a need for careful observation of neurological complications of SARS-CoV-2 infection.

The Spanish Society of Neurology is currently conducting a national observational study on neurological presentations and manifestations of COVID-19.

References
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A. Velayos-Galán, P.D.S. Saucedo, F.P. Postigo, E. Botia-Paniagua.
Síndrome de Guillain-Barré asociado a infección por SARS-CoV-2.
Neurologia., (2020),
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P. Alberti, S. Beretta, M. Piatti, M. Karantzoulis, M.L. Piatti, P. Santoro, et al.
Guillain-Barré syndrome related to COVID-19 infection.
Neurol Neuroimmunol Neuroinflamm., 7 (2020), pp. e741
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H. Zhao, D. Shen, H. Zhou, J. Liu, S. Chen.
Guillain-Barré syndrome associated with SARS-CoV-2 infection: causality or coincidence?.
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M. Padroni, V. Mastrangelo, G.M. Asioli, L. Pavolucci, S. Abu-Rumeileh, M. Grazia Piscaglia, et al.
Guillain-Barré syndrome following COVID-19: new infection, old complication?.
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E. Scheidl, D. Diez Canseco, A. Hadji-Naumov, B. Bereznai.
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H. Otmani, B. Moutawakil, M. Rafai, N. Benna, C. Kettani, M. Soussi, et al.
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[7]
M. Coen, G. Grégoire Jeanson, A. Culebras Almeida, A. Hübers, F. Florian Stierlin, I. Najjar, et al.
Guillain-Barré syndrome as a complication of SARS-CoV-2 infection.
[8]
I. Marta-Enguita, I. Rubio-Baines, I. Gastón-Zubimendi.
Fatal Guillain-Barre syndrome after infection with SARS-CoV-2.
[9]
A. Virani, E. Rabold, T. Hanson, A. Haag, R. Elrufay, T. Cheema, M. Balaan, N. Bhanot.
Guillain-Barré syndrome associated with SARS-CoV-2 infection.
IDCases., 20 (2020), pp. e00771
[10]
J.P. Camdessanche, J. Morel, B. Pozzetto, S. Paul, Y. Tholance, E. Botelho-Nevers, et al.
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Z. Sedaghat, N. Karimi.
Guillain Barre syndrome associated with COVID-19 infection: a case report.
[12]
G. Toscano, F. Palmerini, S. Ravaglia, L. Ruiz, P. Invernizzi, M. Giovanna Cuzzoni, et al.
Guillain–Barré syndrome associated with SARS-CoV-2.

Please cite this article as: Guijarro-Castro C, Rosón-González M, Abreu A, García-Arratibel A, Ochoa-Mulas M. Síndrome de Guillain-Barré tras infección por SARS-CoV-2. Comentarios tras la publicación de 16 nuevos casos. Neurología. 2020;35:412–415.

Copyright © 2020. Sociedad Española de Neurología
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