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Year : 2021  |  Volume : 35  |  Issue : 3  |  Page : 118-121

COVID-19-associated Guillain‒Barre syndrome: Is it parainfectious or postinfectious?

Department of Medicine, Jawaharlal Nehru Institute of Medical Science, Imphal, Manipur, India

Date of Submission21-Jan-2022
Date of Acceptance22-Feb-2022
Date of Web Publication15-Jun-2022

Correspondence Address:
M Ratankumar Singh
Department of Medicine, Jawaharlal Nehru Institute of Medical Science, Imphal, Manipur
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jms.jms_6_22

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COVID -19 since its inception from the month of December 2019 has been associated with myriads of systemic complication apart from the respiratory failure, with Guillain-Barre syndrome (GBS) being one of the prominent neurological complication. More than 220 patients with GBS have been reported thus far. We wish to share 3 cases of GBS associated with COVID 19 admitted in our institute. GBS is one of the most common causes of acute, acquired weakness and is often provoked by a preceding infection, which triggers an immune response, cross-reacts with shared epitopes on peripheral nerve (molecular mimicry). Interestingly one of the cases developed limb weakness concurrently with the respiratory symptoms, probably during the viremic phase; the other 2 cases few weeks after recovering from COVID 19. So, is there a specific association with covid 19 and GBS? If associated, is it Para infectious or Post infectious? Further studies are needed to unravel its association with COVID 19.

Keywords: COVID-19, Guillain‒Barre syndrome

How to cite this article:
Singh AI, Rothangpui, Singh M R, Thangjam R, Shivaranjan C. COVID-19-associated Guillain‒Barre syndrome: Is it parainfectious or postinfectious?. J Med Soc 2021;35:118-21

How to cite this URL:
Singh AI, Rothangpui, Singh M R, Thangjam R, Shivaranjan C. COVID-19-associated Guillain‒Barre syndrome: Is it parainfectious or postinfectious?. J Med Soc [serial online] 2021 [cited 2022 Jul 2];35:118-21. Available from:

  Introduction Top

Talking about COVID has become a tradition for everyone since its discovery in December 2019 in Wuhan, China.[1] We eat, sleep, and dream of COVID nowadays, changing the way we work for a daily living almost 100 years after the great H1N1 epidemic of 1918. As severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) is causing the epidemic with series of unending waves, the body of research around SARS-CoV-2 and the pathophysiology of the disease process and its management expands and evolves every day. Patients with COVID-19 typically present with fever and respiratory symptoms; however, a wide range of other symptoms have been described. While the neurological sequelae of the virus remain poorly understood, there are a growing number of reports of neurological manifestations of COVID-19, where 78 (36.4%) out of 214 patients admitted with COVID-19 had neurological symptoms ranging from anosmia and taste disturbances to cerebrovascular to strokes and seizures.[2]

In addition, there is increasing recognition of a link between COVID-19 and Guillain‒Barré Syndrome (GBS), with published reports following COVID-19 from different corners of the world.[3],[4],[5],[6] To help add to this small but developing body of evidence, here we are describing three cases of GBS in patients infected with COVID-19, after getting relevant full informed consent.

  Case Reports Top

Case 1

A 29-year-old male, chronic smoker, and alcoholic with recently detected diabetes mellitus was referred on August 24, 2021, to our hospital from a local private hospital, with a history of acute-onset progressive ascending paralysis of both upper and lower extremities which started 10 days back. The patient has been quadriplegic 2 days before admission with facial and respiratory muscle weakness causing CO2 narcosis needing ventilatory support.

On physical examination, he was afebrile with blood pressure (BP) 118/80 mmHg, heart rate of 95 beats/min, and maintaining oxygen saturation of 98% on Synchronized Intermittent Mandatory Ventilation, SIM-VC mode (mechanical ventilation). Neurologically he was fully conscious, with motor power showing weakness in all four limbs with a Medical Research Council (MRC) scale of 3/5 in proximal, 4/5 in distal of upper extremities, 2/5 in proximal, 3/5 in distal of lower extremities. Deep tendon reflexes were absent with generalized hypotonia. There was no bowel and bladder involvement.

Potassium level was normal with unremarkable complete hemogram except for the raised erythrocyte sedimentation rate (ESR) of 62 mm/h. HbA1C was 12.35 gm%. COVID-19-RTPCR (Reverse transcription polymerase chain reaction) was negative, however, anti-SARS-CoV-2 – IgG positive (87.01 BAU/ml), and anti-SARS-CoV-2 – IgM were positive (2.35 BAU/ml). He was not vaccinated for COVID 19.

Noncontrast computed tomography of the brain was normal. Cerebrospinal fluid (CSF) analysis showed markedly elevated protein level of 323 mg % with normal cell count of 2 cell/cumm, showing characteristic albumin-cytologic dissociation of GBS. Nerve conduction study could not be done.

Case 2

On September 14, 2021, a 51-year-old female, post-COVID status, presented with weakness of both upper and lower extremities, slurring of speech, and difficulty swallowing for the last 5 days. Weakness is acute in onset, initially involve the distal muscles then gradually progress to involve the proximal muscles. She had no urinary or fecal incontinence. Two weeks prior to hospitalization, she suffered from mild-to-moderate COVID-19, becoming RT-PCR negative 12 days back.

On examination, she was afebrile with BP 120/88 mmHg, heart rate of 86 beats/min, respiratory rate of 18/min, and oxygen saturation of 98% at room air. The muscle strength examination shows weakness in all four limbs, with a Medical Research Council (MRC) scale of 4/5 in proximal as well as distal group of upper extremity muscle and 3/5 in proximal and distal group of muscles of the lower extremities. Deep tendon reflexes were absent in lower extremities and reduced in upper extremities. There is lower motor neuron type bilateral facial nerve palsy. There was no bowel and bladder involvement.

Laboratory examination results are unremarkable except for the raised ESR of 45 mm/1st h. CSF analysis showed characteristic albumin-cytologic dissociation of GBS with raised protein of 121 mg % and normal cell count of 3 cells/mm3.

Magnetic resonance imaging of the brain without contrast was within normal limit. Nerve conduction velocity study showed prolonged latency with reduced amplitude of motor nerve with decreased conduction velocity of sensory nerve, compatible with both axonal and demyelinating neuropathy.

Case 3

On December 10, 2020, a 28-year-old, right-handed female was referred from a District Hospital to our center with 1-week history of progressive limb weakness and foot dysesthesia. On the evening, prior to admission to the district hospital, she noted some difficulty standing in unaided and noticed some tingling sensations in her feet. The next morning, she was unable to stand and her arms felt weak and for which she was taken to the district hospital.

Incidentally, she also reported a 1-week history of fever, cough, myalgia, and headache. On presentation to our institute, she was febrile, had tachycardia (heart rate 110 bpm), and bilateral crepitations on lung auscultation. Her oxygen saturation was 88% on room air with respiratory rate of 28 breaths/min. Limb examination revealed reduced tone with symmetrical weakness of 4/5 on the Medical Research Council (MRC) Power Grading scale in upper and lower limbs. She had diminished triceps reflexes and absent bicep, supinator, knee, and ankle reflexes bilaterally. Pinprick sensation was impaired to the right midfoot and left ankle, with intact cranial nerves.

After 72 h, her lower limb power had reduced to 3/5 proximally and 2/5 distally and all limb reflexes were absent. The overall impression was of a progressive flaccid symmetrical sensory and motor neuropathy.

On investigation, hemogram showed significant thrombocytosis (690 × 109/L) and a raised C-reactive protein (25 mg/L). Renal profile, electrolyte, serum thyroid, and clotting parameters were all within the normal range. Antinuclear antibody, antineutrophil cytoplasmic antibodies, virus screen (HIV, hepatitis B, and hepatitis C) were negative. Her chest X-ray on admission showed mild heterogenous infiltrates in bilateral lower zones. Her SARS-CoV-2 (COVID-19) nasopharyngeal swab RTPCR was positive, became negative for COVID-19 on 7th day of admission in our institute and she was shifted to non-COVID intensive care unit for further management.

CSF analysis revealed high CSF protein (73 mg/dl) with normal glucose and cell count, showing albuminocytologic dissociation. Nerve conduction study was done on day 12 of admissions which revealed reduced conduction velocity and prolonged distal motor latencies in motor and sensory nerves more prominently in the LL.

Intravenous immunoglobulin 0.4g/Kg/day for a period of 5 days was given for all the three described cases. All of them showed remarkable recovery with successful extubation of the first case and were discharged on stable condition.

  Discussion Top

GBS is an autoimmune condition characterized by rapidly progressive limb weakness, often with sensory and cranial nerve deficits and can result in significant morbidity and mortality. The syndrome is typically postinfectious, with two-thirds of adult patients reporting respiratory or gastrointestinal infections in the 6 weeks prior to presentation, which is thought to trigger an immune response which reacts with shared epitopes on peripheral nerve (molecular mimicry) and can affect all myelinated nerves (motor, sensory, cranial, and sympathetic) leading to neuropathy.[7]

A number of well-recognized antecedent infections have been identified in case‒control studies, including bacteria such as Campylobacter jejuni and viruses such as Cytomegalovirus and Epstein‒Barr virus. In the two cases described, the patient developed significant neuropathy few weeks after the development and recovery of COVID symptoms, which raises the possibility of a postinfectious course, similar to classical GBS cases described in association with antecedent respiratory and gastrointestinal infections.[8]

The last case developed limb weakness concurrently with other COVID symptoms suggesting the possibility of parainfectious neuropathy. While parainfectious neuropathies may develop as an unusual hyperimmune response, they could also represent a direct toxic or neuropathic effect from SARS-COV. Similar description is reported with demonstration of SARS-COV RNA in CSF.[9] Hence, further research is needed to differentiate between these two possibilities in COVID-19 patients.

The Italian series reported that 5 (0.42%) out of 1200 patients admitted to their hospitals with COVID-19 presented with GBS, which is disproportionately high for a rare disease that affects 1.6/100,000 person-year (matched for the average age of their cohort).[6],[10] This case series is adding evidence to the increasing recognition that COVID-19 could be an infectious trigger for GBS.

The clinical manifestations of GBS are varied, from mild limb weakness to respiratory muscle involvement requiring mechanical ventilation. Studies have found that the severity of GBS is associated with the causative organism, demonstrated by the higher rates of severe axonal forms following C. jejuni infection.[11] As such, it is important to further look at the link between COVID-19 and GBS to help with diagnosis, prognostication, and institution of early immunological therapy and whether COVID-related GBS is associated with more respiratory and bulbar involvement.

Despite the small sample size, this could represent an interaction between the COVID-19 pneumonitis and GBS increasing the likelihood of needing respiratory support. Alternatively, this may suggest that COVID-19 is a trigger for a more severe and rapidly progressing neuropathy.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Lu H, Stratton CW, Tang YW. Outbreak of pneumonia of unknown etiology in Wuhan, China: The mystery and the miracle. J Med Virol 2020;92:401-2.  Back to cited text no. 1
Mao L, Jin H, Wang M, Hu Y, Chen S, He Q, et al. Neurologic manifestations of hospitalized patients with coronavirus disease 2019 in Wuhan, China. JAMA Neurol 2020;77:683-90.  Back to cited text no. 2
Zhao H, Shen D, Zhou H, Liu J, Chen S. Guillain-Barré syndrome associated with SARS-CoV-2 infection: Causality or coincidence? Lancet Neurol 2020;19:383-4.  Back to cited text no. 3
Sedaghat Z, Karimi N. Guillain Barre syndrome associated with COVID-19 infection: A case report. J Clin Neurosci 2020;76:233-5.  Back to cited text no. 4
Virani A, Rabold E, Hanson T, Haag A, Elrufay R, Cheema T, et al. Guillain-Barré Syndrome associated with SARS-CoV-2 infection. IDCases 2020;20:e00771.  Back to cited text no. 5
Toscano G, Palmerini F, Ravaglia S, Ruiz L, Invernizzi P, Cuzzoni MG, et al. Guillain-Barré syndrome associated with SARS-CoV-2. N Engl J Med 2020;382:2574-6.  Back to cited text no. 6
Doets AY, Verboon C, van den Berg B, Harbo T, Cornblath DR, Willison HJ, et al. Regional variation of Guillain-Barré syndrome. Brain 2018;141:2866-77.  Back to cited text no. 7
Brasil P, Sequeira PC, Freitas AD, Zogbi HE, Calvet GA, de Souza RV, et al. Guillain-Barré syndrome associated with Zika virus infection. Lancet 2016;387:1482.  Back to cited text no. 8
Khan F, Sharma P, Pandey S, Sharma D, Vijayavarman V, Kumar N, et al. COVID-19-associated Guillain-Barre syndrome: Postinfectious alone or neuroinvasive too? J Med Virol 2021;93:6045-9.  Back to cited text no. 9
Sejvar JJ, Baughman AL, Wise M, Morgan OW. Population incidence of Guillain-Barré syndrome: A systematic review and meta-analysis. Neuroepidemiology 2011;36:123-33.  Back to cited text no. 10
Willison HJ, Jacobs BC, van Doorn PA. Guillain-Barré syndrome. Lancet 2016;388:717-27.  Back to cited text no. 11


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