Annals of Indian Academy of Neurology
: 2021  |  Volume : 24  |  Issue : 3  |  Page : 311--312

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

Fu Liong Hiew1, Stefanie Kar Yan Hung2,  
1 Sunway Medical Centre, Bandar Sunway, Selangor, Malaysia
2 Department of Neurology, Kuala Lumpur Hospital, Kuala Lumpur, Malaysia

Correspondence Address:
Dr. Fu Liong Hiew
Consultant Physician and Neurologist, Sunway Medical Centre, No. 5, Jalan Lagoon Selatan, Bandar Sunway, Selangor - 47500

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;24:311-312

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 Jul 31 ];24:311-312
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Full Text

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.


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