ABSTRACT
Guillain-Barré syndrome (GBS) is a rare immune-mediated acute polyradiculo-neuropathy that typically develops after a previous gastrointestinal or respiratory infection. This narrative overview aims to summarise and discuss current knowledge and previous evidence regarding triggers and pathophysiology of GBS. A systematic search of the literature was carried out using suitable search terms. The most common subtypes of GBS are acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). The most common triggers of GBS, in three quarters of cases, are previous infections. The most common infectious agents that cause GBS include Campylobacter jejuni (C. jejuni), Mycoplasma pneumoniae, and cytomegalovirus. C. jejuni is responsible for about a third of GBS cases. GBS due to C. jejuni is usually more severe than that due to other causes. Clinical presentation of GBS is highly dependent on the structure of pathogenic lipo-oligosaccharides (LOS) that trigger the innate immune system via Toll-like-receptor (TLR)-4 signalling. AIDP is due to demyelination, whereas in AMAN, structures of the axolemma are affected in the nodal or inter-nodal space. In conclusion, GBS is a neuro-immunological disorder caused by autoantibodies against components of the myelin sheath or axolemma. Molecular mimicry between surface structures of pathogens and components of myelin or the axon is one scenario that may explain the pathophysiology of GBS.
Subject(s)
Campylobacter jejuni , Guillain-Barre Syndrome , Humans , Amantadine , Autoantibodies , Axons/pathology , Guillain-Barre Syndrome/etiologyABSTRACT
Guillain-Barre Syndrome (GBS) has been repeatedly reported as a neurological complication of COVID-19 (post-COVID GBS [PCG]). Whether the introduction of SARS-CoV-2 vaccines reduced the prevalence of PCG is unknown. This narrative review aimed to compare the number of published PCG cases between the second half of 2020 (no vaccination available) with those of the first half of 2021 (vaccination available). A total of 124 articles reported 300 patients with PCG between January 2020 and June 2021. The ages ranged from 7 to 94y. There was male dominance. The latency between the onset of COVID-19 and the onset of PCG ranged from -10 to 90d Acute, inflammatory, demyelinating polyneuropathy was diagnosed in 171 patients, acute, motor axonal neuropathy in 24, and acute, motor, and sensory axonal neuropathy in 16 patients. Regarding treatment, 241 patients received immunoglobulins, 28 patients' plasmaphereses, and 7 patients' steroids. Artificial ventilation was required in 59 patients. Full recovery was achieved in 42 cases, partial recovery in 163 cases, and 17 patients died. The number of published PCG patients fell from 192 in the second half of 2020 to 75 patients in the first half of 2021. It is concluded that the prevalence of PCG has decreased since the introduction of SARS-CoV-2 vaccines. SARS-CoV-2 vaccinations have a positive effect on the prevalence of PCG.
Subject(s)
COVID-19 , Guillain-Barre Syndrome , COVID-19 Vaccines , Humans , Male , Prevalence , SARS-CoV-2ABSTRACT
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ABSTRACT
Finsterer J, Scorza FA. Neuro-COVID Requires Comprehensive Work-up. Indian J Crit Care Med 2021;25(8):956-957.
Subject(s)
COVID-19 , Guillain-Barre Syndrome , Guillain-Barre Syndrome/complications , Humans , SARS-CoV-2ABSTRACT
Guillain-Barre syndrome (GBS) following a SARS-CoV-2 vaccination has been repeatedly observed but GBS following a SARS-CoV-2 infection in a vaccinated patient has not been reported. A 69yo female developed paresthesias of both lower and upper limbs which were followed by progressive muscle weakness. The history was positive for a mild SARS-CoV-2 infection 15 days earlier. COVID-19 occurred despite a first dose of a vector-based SARS-CoV-2 vaccine, 40 days prior to onset of GBS. Since CSF investigations and nerve conduction studies were indicative of GBS, subtype acute, inflammatory, demyelinating polyneuropathy (AIDP), immunoglobulins (30 g/d) were started. After two weeks complete recovery was achieved. In conclusion, SARS-CoV-2 infections may develop despite full vaccination and may be complicated by GBS. Since no other trigger of GBS could be identified, a causal relation between the SARS-CoV-2 infection and GBS was suspected.