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Table of Contents
Year : 2021  |  Volume : 9  |  Issue : 4  |  Page : 264-267

Guillain-Barré Syndrome Associated with COVID-19: A Neurochallenge!!

Department of General Medicine, Mallige Medical Centre, Bengaluru, Karnataka, India

Date of Submission20-Jul-2021
Date of Decision06-Sep-2021
Date of Acceptance20-Sep-2021
Date of Web Publication20-Oct-2021

Correspondence Address:
Dr. Dilmo Yeldo
Mallige Medical Centre, 31/32 Crescent Road, Madhava Nagar, Gandhi Nagar, Bengaluru - 560 001, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ajim.ajim_76_21

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent for Coronavirus disease 2019 (COVID-19), originated in Wuhan, China in the fall of 2019 which has soon become a global pandemic engulfing the entire world, presents with a myriad of symptoms from asymptomatic to severe disease with acute respiratory distress syndrome and multiple organ dysfunction and severe inflammatory response. New associations and clinical problems keep appearing with the new virus and here, we are reporting a case of Guillain-Barré syndrome (GBS) presented to us with complaints of progressive proximal muscle weakness and bilateral facial paralysis. The initial nerve conduction study was normal, but clinical examination showed us a picture of acute inflammatory demyelinating polyradiculoneuropathy and the patient was treated with intravenous immunoglobulin to which the patient responded dramatically. Repeat nerve conduction study showed typical features of GBS. Thus, a differential diagnosis of GBS should be kept in mind by all physicians/neurologists who encounter any neurological symptoms (especially muscle weakness) while treating or post-COVID-19 infection.

Keywords: Acute inflammatory demyelinating polyradiculoneuropathy, COVID-19 infection, Guillain-Barré syndrome, intravenous immunoglobulin, nerve conduction study

How to cite this article:
Ravindra T S, Yeldo D, Arjun B S. Guillain-Barré Syndrome Associated with COVID-19: A Neurochallenge!!. APIK J Int Med 2021;9:264-7

How to cite this URL:
Ravindra T S, Yeldo D, Arjun B S. Guillain-Barré Syndrome Associated with COVID-19: A Neurochallenge!!. APIK J Int Med [serial online] 2021 [cited 2022 May 29];9:264-7. Available from: https://www.ajim.in/text.asp?2021/9/4/264/328683

  Introduction Top

The coronavirus disease 2019 (COVID-19) pandemic is a major worldwide health disorder. There is an increasing number of neurological complications recognized with COVID-19 including patients with Guillain-Barré Syndrome (GBS) and its variants. The main clinical, electrophysiological, and cerebrospinal fluid (CSF) features of the patients so far reported proved to be similar to GBS cases related to other infectious diseases. GBS is a neurological autoimmune disease that can deteriorate hastily, thus requiring high clinical suspicion, early identification, and appropriate management. In the past, also in the context of a viral disease outbreak, it has been pointed out that the Zika virus may be a risk factor for GBS. Whether COVID-19 patients are also at high risk of GBS, is largely unknown. Here, we are presenting a case of 63-year-old female who came with complaints of proximal muscle weakness with bifacial paralysis which started about 10 days after the patient tested positive for COVID-19 infection.

  Case Report Top

A 63-year-old female, with no known medical comorbidities, presented to our hospital with a history of numbness of toes of both legs and fingers of the upper limb for 4 days, unable to walk for 3 days and unable to sit for 2 days. The patient attender also noticed slurring of speech and deviation of her lower jaw to the left side for 2 days. She also complaints of back pain for 10 days.

The patient had a history of fever, cough, and cold 18 days back. She had done a COVID-19 RT-PCR test 15 days back which was positive. She was admitted to a local hospital and treated with intravenous (IV) steroids, low molecular weight heparin, antipyretics, and other supportive measures. She was improved with treatment and discharged to home after 5 days.

On examination, vitals were stable.

CNS examination

  • Higher mental functions-normal.
  • Cranial Nerve examination - Bilateral Facial Palsy [Table 1]
  • Motor System Examination - Bilateral hypotonia on all limbs and Proximal muscle weakness of Both Upper limb and both Lower limb [Table 2]
  • Deep Tendon Reflexes - Absent on Both sides [Table 2]
  • Superficial Reflexes - Preserved on both sides except Absent Plantar Reflex [Table 2]
  • Sensory system examination-normal
  • Cortical sensations-normal
  • Coordination and gait was not able to elicited because of weakness
  • Examination of the spine was normal
  • All other system examinations were within the normal limits.
Table 1: Cranial nerve examination

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Table 2: Motor system examinations

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Initial blood investigations showed mild hyponatremia (129 mEq/L) and moderate vitamin D deficiency. COVID-19 RT-PCR was positive (detected low). Magnetic resonance imaging (MRI) lumbar spine with whole spine screening showed diffuse disc disease at multiple levels (C5-6, C6-7, L4-5, and L5-S1), no focal root compression. The initial nerve conduction study on the day of admission showed normal nerve conduction, no abnormalities.

A clinical diagnosis of GBS with bilateral facial nerve palsy was made and the patient was started on IV immunoglobulin (IVIg) (2 g/kg) in divided doses over 5 days. She improved symptomatically after 3 days of starting immunoglobulin and was able to raise her both upper limbs and lower limbs (hip power– 3/5). Repeat nerve conduction study after 5 days showed motor-sensory axonal and demyelinating polyneuropathy (lower limb > upper limb).

At the time of discharge, the patient was able to stand and walk with support. The patient came for review after 2 weeks. At that time, she was walking normally without any support and had regained full muscle power in both upper limbs and lower limbs.

  Discussion Top

COVID-19 infection caused by the SARS-CoV-2 virus is primarily a respiratory infection but has been associated with a variety of neurological symptoms including dizziness, headache, confusion, myalgia, and loss of taste and smell.[1] GBS is an acute generalized polyradiculoneuropathy that is preceded by a symptomatic infection such as campylobacter jejuni, Epstein–Barr virus, influenza, or cytomegalovirus in about two-thirds of cases.[2] GBS associated with COVID-19 is now getting reported, but the strength and mechanism of the association and the clinical and electrodiagnostic patterns remain unclear.


Despite numerous case reports of GBS associated with COVID-19, the prevalence remains unclear, since ascertainment and reporting are uneven. It is also possible that GBS cases may have been incorrectly attributed to critical illness neuromyopathy, or undiagnosed in the setting of severe systemic illness. Most patients reported GBS were over age 50 years and males which ascertains that the incidence of GBS rises with age.[3]


GBS is a postinfectious syndrome which is defined by an onset that is delayed from the acute symptoms of infection and by a mechanism that is distinct from the infection. The postinfectious mechanism of GBS is also supported by the finding of autoantibodies that result from an immune response directed to an epitope of the infectious agent that then cross-reacts with a structurally similar component of the peripheral nerve (molecular mimicry) resulting in delayed immune-mediated damage to the peripheral nerve.[4]

The immune-mediated phenomenon in COVID-associated GBS seems plausible for most patients but another pathophysiological process needs to be thought of in a group of outliers. This group of outliers is constituted by patients in whom the symptoms of GBS either precede or are almost concurrent with the symptoms of COVID-19. In our case, even if the neurological symptoms of GBS has occurred 15 days post the patient got tested positive, COVID-19 RT-PCR at the time of diagnosis of GBS was weakly positive. This leads to confusing and challenging state and a detailed workup is required for understanding the pathophysiology behind GBS associated with COVID-19 infection.


The classification of GBS subtypes and variants is based on the clinical picture and electrophysiological and pathological findings[5]

Common subtypes:

  • Acute inflammatory demyelinating polyradiculoneuropathy
  • Acute motor axonal neuropathy
  • Acute motor-sensory axonal neuropathy.

Rare variants:

  • Miller Fisher syndrome
  • Ataxic variant (acute ataxic neuropathy)
  • Pharyngeal-cervical-brachial variant
  • Multiple cranial neuropathy variant
  • Facial diplegia with paresthesias
  • Paraparetic variant
  • Acute pandysautonomia.

Clinical features and diagnosis

The diagnosis of GBS depends on clinical criteria supported by electrophysiological studies and CSF findings[6]

Features required for diagnosis:

  • Progressive weakness of both legs and arms
  • Areflexia.

Clinical features supportive of diagnosis:

  • Progression over days to 4 weeks
  • Relative symmetry of symptoms and signs
  • Mild sensory symptoms or signs
  • Bifacial palsies
  • Autonomic dysfunction
  • Absence of fever at onset
  • Recovery beginning 2–4 weeks after progression ceases.

Laboratory features supportive of diagnosis:

  • Elevated CSF protein with <10 cells/μL
  • Electrodiagnostic features of nerve conduction slowing or block.

The most common nerve conduction study abnormalities seen in the first 2 weeks of illness are absent H reflexes and absent, delayed, or impersistent F waves, findings that are common in polyneuropathies but not specific for the demyelinating types. Abnormal F waves in the presence of normal conduction velocities and distal latencies are more specific findings since they suggest proximal demyelination.


IVIg (0.4 g/kg body weight daily for 5 days) and plasma exchange (200–250 ml plasma/kg body weight in five sessions) are equally effective treatments for GBS.[7],[8] As IVIg is also easier to administer and generally more widely available than plasma exchange, it is usually the treatment of choice. Besides IVIg and plasma exchange, no other procedures or drugs have been proven effective in the treatment of GBS. Furthermore, plasma exchange followed by IVIg is no more effective than either treatment alone and insufficient evidence is available for the efficacy of add-on treatment with IV methylprednisolone in IVIg-treated patients.[9]

A globally applicable clinical guideline for GBS is especially important as new outbreaks of pathogens like Covid-19 that trigger GBS have become an emerging threat. To generate this globally applicable clinical guideline for GBS, the ten most important steps in the management of GBS, covering diagnosis, treatment, monitoring, prognosis and long-term management, were identified by a group of international experts on GBS [Figure 1].[10]
Figure 1: Approach to the diagnosis and management of Guillain-Barré syndrome. *Frequency of monitoring is dependent on the clinical picture and should be assessed in individual patients. CSF: Cerebrospinal fluid, EGRIS: Erasmus GBS Respiratory Insufficiency Score (Box 3), GBS: Guillain-Barré syndrome, ICU: Intensive care unit, mEGOS: Modified Erasmus GBS outcome score

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  Conclusion Top

GBS is an acute inflammatory polyradiculoneuropathy associated with numerous viral infections. GBS-associated COVID-19 appears to be an uncommon condition with similar clinical and electrodiagnostic patterns to GBS before the pandemic. In the spectrum of neurologic manifestations of COVID-19, GBS should be considered by treating physicians/neurologists in patients with muscle weakness and peripheral nervous system symptoms. Future studies should compare patients with COVID-19-associated GBS to those with contemporaneous non-COVID-19 GBS and determine whether the incidence of GBS is elevated in those with COVID-19.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her 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

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;77:683-90.7  Back to cited text no. 1
Jacobs BC, Rothbarth PH, van der Meché FG, Herbrink P, Schmitz PI, de Klerk MA, et al. The spectrum of antecedent infections in Guillain-Barré syndrome: A case-control study. Neurology 1998;51:1110-5.  Back to cited text no. 2
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. 3
Willison HJ, Jacobs BC, van Doorn PA. Guillain-Barré syndrome. Lancet 2016;388:717-27.  Back to cited text no. 4
Griffin JW, Li CY, Ho TW, Tian M, Gao CY, Xue P, et al. Pathology of the motor-sensory axonal Guillain-Barré syndrome. Ann Neurol 1996;39:17-28.  Back to cited text no. 5
Asbury AK, Cornblath DR. Assessment of current diagnostic criteria for Guillain-Barré syndrome. Ann Neurol 1990;27 Suppl: S21-4.  Back to cited text no. 6
Hughes RAC, Swan AV, van Doorn PA. Intravenous immunoglobulin for Guillain-Barré syndrome. Cochrane Database of Systematic Reviews 2014, Issue 9. Art. No: CD002063. DOI: 10.1002/14651858.CD002063.pub6.  Back to cited text no. 7
Verboon C, van Doorn PA, Jacobs BC. Treatment dilemmas in Guillain-Barré syndrome. J Neurol Neurosurg Psychiatry 2017;88:346-52.  Back to cited text no. 8
van Koningsveld R, Schmitz PI, Meché FG, Visser LH, Meulstee J, van Doorn PA, et al. Effect of methylprednisolone when added to standard treatment with intravenous immunoglobulin for Guillain-Barré syndrome: Randomised trial. Lancet 2004;363:192-6.  Back to cited text no. 9
Leonhard SE, Mandarakas MR, Gondim FA, Bateman K, Ferreira ML, Cornblath DR, et al. Diagnosis and management of Guillain-Barré syndrome in ten steps. Nat Rev Neurol 2019;15:671-83.  Back to cited text no. 10


  [Figure 1]

  [Table 1], [Table 2]


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