LAUSR

the course of hospitalization. Antiganglioside antibodies are principally associated with autoimmune peripheral neuropathies. In these disorders, immune attack is inadvertently directed at peripheral nerve by autoantibodies that target glycan structures borne by glycolipids, particularly gangliosides concentrated in nerve myelin and axons. The most thoroughly studied disorder, in which IgG autoantibodies against gangliosides arise following acute infections, notably C. jejuni enteritis, is the acute paralytic disease, GBS. Two GBS variants, AMAN and Miller Fisher syndrome, are consistently and highly associated antiglycolipid autoantibodies. In AMAN, the primary target is the motor axolemmal membrane4 rather than the myelin sheath, and antiganglioside antibodies are directed to sialylated epitopes on GM1a, GM1b, GD1a, and GalNAc-GD1a.5 In light of our clinical, electromyoneurography, and laboratory findings, it is conceivable that COVID-19, similarly to C. jejuni enteritis, triggers the production of specific subclasses of antiganglioside antibodies causing acute motor neuropathy. It is now widely confirmed that GBS should be considered as neurological complications of COVID-19 infection, but further studies are needed to better define the pathogenesis and therefore the clinical and prognostic characteristics of all possible GBS variants.