BRIV_adv
Annals of Indian Academy of Neurology
  Users Online: 3830 Home | About the Journal | InstructionsCurrent Issue | Back IssuesLogin      Print this page Email this page  Small font size Default font size Increase font size

Table of Contents
EDITORIAL COMMENTARY
Year : 2021  |  Volume : 24  |  Issue : 3  |  Page : 311-312
 

SARS-CoV-2 and Guillain-Barre Syndrome (GBS): Insights from ASIA perspectives


1 Sunway Medical Centre, Bandar Sunway, Selangor, Malaysia
2 Department of Neurology, Kuala Lumpur Hospital, Kuala Lumpur, Malaysia

Date of Submission14-Feb-2021
Date of Acceptance15-Feb-2021
Date of Web Publication11-May-2021

Correspondence Address:
Dr. Fu Liong Hiew
Consultant Physician and Neurologist, Sunway Medical Centre, No. 5, Jalan Lagoon Selatan, Bandar Sunway, Selangor - 47500
Malaysia
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/aian.AIAN_133_21

Rights and Permissions

 



How to cite this article:
Hiew FL, Yan Hung SK. SARS-CoV-2 and Guillain-Barre Syndrome (GBS): Insights from ASIA perspectives. Ann Indian Acad Neurol 2021;24:311-2

How to cite this URL:
Hiew FL, Yan Hung SK. SARS-CoV-2 and Guillain-Barre Syndrome (GBS): Insights from ASIA perspectives. Ann Indian Acad Neurol [serial online] 2021 [cited 2021 Sep 21];24:311-2. Available from: https://www.annalsofian.org/text.asp?2021/24/3/311/315861




Guillain-Barré syndrome (GBS) is a heterogeneous disorder with factors related to geography that have a major influence on clinical phenotype, disease severity, electrophysiological subtype, and outcome.[1] During the recent Zika virus epidemic, many expected a sharp rise in the number of GBS cases in Asia, just like what was reported in Latin America.[2],[3] Intriguingly, Asian countries have not seen a similar spike in GBS cases linked to Zika virus even in a region with a high incidence of GBS, suggesting the unique geographical differences.[4],[5] Since the beginning of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic in March 2020 and subsequent reports of cases with neurological manifestations linked to SARS-CoV-2 virus, the number of GBS cases has been in the spotlight and closely monitored across the world.[6],[7]

From European perspectives, the epidemiological or phenotypic clues of SARS-CoV-2 being causative of GBS remains unclear. Despite earlier reported increased incidence of GBS linked to SARS-CoV-2 in many Italian centers, recent evidence from an epidemiological study conducted across the UK has shown otherwise.[8],[9] There is evidence suggesting GBS to be “para-infectious” rather than the typical acute postinfectious immune-mediated polyneuropathy.[6] In addition, a search on the evidence of molecular mimicry between any SARS-CoV2 proteins and human nerve axonal or myelin proteins and glycoproteins showed no significant homology, making molecular mimicry causation less likely although more scientific research is required.[9] Moving on from this, the next important question to explore is whether concurrent SARS-CoV-2 infections with GBS demonstrate different clinical characteristics, severity, and outcome in various parts of the world.

The data presented by Megha D et al.[10] is crucially important and timely for a few reasons. Firstly, despite a major outbreak of SARS-CoV-2 infections started in Asia and the earliest report of GBS with SARS-CoV-2 in these regions, till yet we have a large cohort analysis of GBS associated with SARS-CoV-2 infections. Although the data was not designed to determine the incidence of GBS linked to SARS-CoV-2, the relatively large number of patients provide a good insight into clinical characteristics as well as the overall outcome. Interesting to note is the proportion of GBS subtypes of predominant demyelinating nature (59.5%), higher than expected from an Asian country where acute motor axonal neuropathy is more prevalent.[11] Whether this is the effect of SARS-CoV-2 remains uncertain. Second and important to note was the rates of ICU admission and those requiring ventilation, reaching up to almost 50%. This is consistent with that of the UK cohort, despite demonstrating no significant differences in the pattern of weakness, time to nadir, neurophysiology, CSF findings, or outcome compared to SARS-CoV-2 negative groups.[9] This was likely related to COVID-19 pulmonary involvement, potentially overwhelming the intensive care resources in many less Asian countries if the number of SARS-CoV-2 infections is high. More concerning was that a proportion of patients developed symptoms of SARS-CoV-2 pneumonia 1–2 weeks later with worsening shortness of breath or increasing oxygen requirement. A close observation of this group of patients is needed. Thirdly, we now have better evidence that treatment of GBS linked to COVID-19 infections with intravenous immunoglobulin (IVIg) is safe despite initial concerns of its prothrombotic risk. This has also been shown in the UK cohort.[9]

Till this pandemic is brought under control, we are yet to see the true spectrum of impact from neurological manifestations linked to SARS-CoV-2. Strong epidemiological data is needed to allow us to predict what the virus will do upon rolling out of mass vaccination program and emergence of highly transmissible variants of SARS-CoV-2.



 
   References Top

1.
Doets AY, Verboon C, van den Berg B, Harbo T, Cornblath DR, Willison HJ, et al. IGOS consortium. Regional variation of Guillain-Barré syndrome. Brain 2018;141:2866-77.  Back to cited text no. 1
    
2.
Cao-Lormeau VM, Blake A, Mons S, Lastere S, Roche C, Vanhomwegen J, et al. Guillain-Barré syndrome outbreak associated with Zika virus infection in French polynesia: A casecontrol study. Lancet 2016;387:1531-9.  Back to cited text no. 2
    
3.
Watrin L, Ghawche F, Larre P, Neau JP, Mathis S, Fournier E. Guillain Barré syndrome (42 cases) occurring during a Zika virus outbreak in French polynesia. Medicine (Baltimore) 2016;95:e3257.  Back to cited text no. 3
    
4.
Umapathi T, Kam YW, Ohnmar O, Ng BCJ, Ng Y, Premikha M, et al. The 2016 Singapore Zika virus outbreak did not cause a surge in Guillain-Barré syndrome. J Peripher Nerv Syst 2018;23:197-201.  Back to cited text no. 4
    
5.
GeurtsvanKessel CH, Islam Z, Islam MB, Kamga S, Papri N, van de Vijver DAMC, et al. Zika virus and Guillain-Barré syndrome in Bangladesh. Ann Clin Transl Neurol 2018;5:606-15.  Back to cited text no. 5
    
6.
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. 6
    
7.
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. 7
    
8.
Filosto M, Cotti Piccinelli S, Gazzina S, Foresti C, Frigeni B, Servalli MC, et al. Guillain-Barré syndrome and COVID-19: An observational multicentre study from two Italian hotspot regions. J Neurol Neurosurg Psychiatry 2020;jnnp-2020-324837. doi: 10.1136/jnnp-2020-324837. Online ahead of print.  Back to cited text no. 8
    
9.
Keddie S, Pakpoor J, Mousele C, Pipis M, Machado PM, Foster M, et al. Epidemiological and cohort study finds no association between COVID-19 and Guillain-Barré syndrome. Brain 2020:awaa433.  Back to cited text no. 9
    
10.
MEGHA AT AL AIAN 1303/20.  Back to cited text no. 10
    
11.
Willison HJ, Jacobs BC, van Doorn PA. Guillain-Barré syndrome. Lancet 2016;388:717-27.  Back to cited text no. 11
    




 

Top
Print this article  Email this article

    

 
   Search
 
  
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
    Article in PDF (279 KB)
    Citation Manager
    Access Statistics
    Reader Comments
    Email Alert *
    Add to My List *
* Registration required (free)  


    References

 Article Access Statistics
    Viewed1824    
    Printed54    
    Emailed0    
    PDF Downloaded221    
    Comments [Add]    

Recommend this journal