PMC:7309518 / 2237-3445 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7309518","sourcedb":"PMC","sourceid":"7309518","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7309518","text":"ata indicate that COVID-19 can trigger not only GBS but other autoimmune neurological diseases necessitating vigilance for early diagnosis and therapy initiation. Although COVID-19 infection, like most other viruses, can potentially worsen patients with pre-existing autoimmunity, there is no evidence that patients with autoimmune neurological diseases stable on common immunotherapies are facing increased risks of infection.\n\nGuillain-Barré syndromes (GBSs) comprise a spectrum of polyneuropathies characterized by acute (within 1–4 weeks) ascending motor weakness, mild or moderate sensory abnormalities, occasional cranial nerve involvement, and muscle or radicular pain. According to the degree of involvement of the motor or sensory nerves, myelin sheath, axon, or cranial nerve predominance, the most common subtypes are the acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal neuropathy (AMAN), and the Miller Fisher syndrome (MFS) characterized by acute ophthalmoplegia, gait ataxia, and areflexia.1 GBS is one of the prototypic viral-triggered autoimmune neurologic diseases as approximately 70% of the patients have a preceding by 1–3 weeks, flu-like, viral illness.1–3 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