Guillain-Barré syndrome: diagnosis and treatment guidelines

Guillain–Barré syndrome is an acute, rapidly progressive immune-mediated disease of the peripheral nervous system, combining several variants and subtypes with various clinical, pathophysiological and electrophysiological signs. Guillain–Barré syndrome usually develops 1–3 weeks after the viral or bacterial infection, which acts as the trigger triggering autoimmune mechanisms, leading to demyelination and axonal damage. The disease is getting more acute due to the emergence of a new coronavirus infection. Behind the disease’s dipathophysiology there is the activation of cellular and humoral immunity with the production of autoantibodies to specific gangliosides and glycolipids and the formation of circulating immune complexes that attack peripheral nerves and roots (the phenomenon of “molecular mimicry”). The examination of patients requires an integrated approach, including, along with clinical and anamnestic data, the results of laboratory and neurophysiological examination. The treatment of patients with Guillain–Barré syndrome is carried out in an intensive care unit and includes both pathogenetic therapy and nonspecific measures aimed to correct dysfunctions of vital organs, prevent complications and provide symptomatic therapy. Currently, the main direction of pathogenetic therapy of this disease is the use of high-dose intravenous immunotherapy with human normal immunoglobulin preparations or high-volume therapeutic plasmapheresis. Taking into account the absence of data about differences in the effectiveness of these methods, the choice of direction is determined taking into account the contraindications and possible development of adverse events, as well as the capabilities of the medical institution (2 tables, bibliography: 15 refs)