|Year : 2021 | Volume
| 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
|Date of Submission||14-Feb-2021|
|Date of Acceptance||15-Feb-2021|
|Date of Web Publication||11-May-2021|
Dr. Fu Liong Hiew
Consultant Physician and Neurologist, Sunway Medical Centre, No. 5, Jalan Lagoon Selatan, Bandar Sunway, Selangor - 47500
Source of Support: None, Conflict of Interest: None
|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
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. 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., 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., 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.,
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., There is evidence suggesting GBS to be “para-infectious” rather than the typical acute postinfectious immune-mediated polyneuropathy. 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. 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. 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. 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. 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.
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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