Guillain-Barré syndrome (GBS), an acute immune-mediated polyneuropathy with diverse degrees of weakness, usually reaches its severity culmination within 4 weeks. It can be subdivided into acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal neuropathy (AMAN), acute motor, and sensory axonal neuropathy (AMSAN) and Miller-Fisher syndrome (MFS), etc. One of the widely accepted mechanisms of GBS is a molecular mimicry hypothesis, which holds that the immune system will be activated in response to infectious antigens that are structurally similar to axonal components or peripheral nerve myelin, causing tissue-specific nerve root and peripheral nerve damage in susceptible individuals.
An antecedent infection, such as a bacterial or viral infection or minor trauma, Zika virus in particular, is often associated with GBS. All of the major GBS specific clinical or electrodiagnostic patterns have been reported in association with COVID-19. However, a distinctive GBS phenotype was not observed among COVID-19 patients, and it remains to be determined whether SARS-CoV-2 is an etiologic agent/trigger for GBS. Interestingly, recent case series have reported a potential association between COVID-19 vaccination and GBS, shedding novel light on the need for vigilance in patients with neurologic symptoms following COVID-19 vaccination and for postvaccination surveillance programs to assess causality of GBS. What is the relevant mechanism of it?
Intravenous immunoglobulin (IVIg) and plasma exchange (PE) are considered as effective GBS immunotherapies. While early IVIg or PE therapy can improve neurological outcomes equally, subsets of patients may respond slowly, partially, or worsen with either treatment. Therefore, it is imperative to understand the pathogenesis of GBS better, identify pathways that can be effectively blocked pharmacologically, and investigate targeted molecular therapies for GBS subtypes and subgroups of patients who are resistant to PE or IVIg, or who are suspected to be poorly treated based on clinical and electrophysiological factors. For instance, the role of blood-nerve barrier deficits in GBS pathogenesis should not be neglected. Pathogenic leukocyte trafficking could be a biologically relevant target.
Here, we raised this Research Topic, focusing on the mechanisms of GBS and the relationship between GBS and COVID-19 and COVID-19 vaccination. In this Research Topic, we welcome all types of articles including Original Research, Review, Mini-Review, Hypothesis and Theory, Perspective, Clinical Tria, and Opinion articles that cover.
Guillain-Barré syndrome (GBS), an acute immune-mediated polyneuropathy with diverse degrees of weakness, usually reaches its severity culmination within 4 weeks. It can be subdivided into acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal neuropathy (AMAN), acute motor, and sensory axonal neuropathy (AMSAN) and Miller-Fisher syndrome (MFS), etc. One of the widely accepted mechanisms of GBS is a molecular mimicry hypothesis, which holds that the immune system will be activated in response to infectious antigens that are structurally similar to axonal components or peripheral nerve myelin, causing tissue-specific nerve root and peripheral nerve damage in susceptible individuals.
An antecedent infection, such as a bacterial or viral infection or minor trauma, Zika virus in particular, is often associated with GBS. All of the major GBS specific clinical or electrodiagnostic patterns have been reported in association with COVID-19. However, a distinctive GBS phenotype was not observed among COVID-19 patients, and it remains to be determined whether SARS-CoV-2 is an etiologic agent/trigger for GBS. Interestingly, recent case series have reported a potential association between COVID-19 vaccination and GBS, shedding novel light on the need for vigilance in patients with neurologic symptoms following COVID-19 vaccination and for postvaccination surveillance programs to assess causality of GBS. What is the relevant mechanism of it?
Intravenous immunoglobulin (IVIg) and plasma exchange (PE) are considered as effective GBS immunotherapies. While early IVIg or PE therapy can improve neurological outcomes equally, subsets of patients may respond slowly, partially, or worsen with either treatment. Therefore, it is imperative to understand the pathogenesis of GBS better, identify pathways that can be effectively blocked pharmacologically, and investigate targeted molecular therapies for GBS subtypes and subgroups of patients who are resistant to PE or IVIg, or who are suspected to be poorly treated based on clinical and electrophysiological factors. For instance, the role of blood-nerve barrier deficits in GBS pathogenesis should not be neglected. Pathogenic leukocyte trafficking could be a biologically relevant target.
Here, we raised this Research Topic, focusing on the mechanisms of GBS and the relationship between GBS and COVID-19 and COVID-19 vaccination. In this Research Topic, we welcome all types of articles including Original Research, Review, Mini-Review, Hypothesis and Theory, Perspective, Clinical Tria, and Opinion articles that cover.
