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Abstract
Guillain - Barre syndrome is an acute inflammatory demyelinating polyradiculoneuropathy of autoimmune etiology, characterized by peripheral paralysis and, in most cases, protein-cell secretion in the cerebrospinal fluid. The incidence of Guillain-Barre syndrome is 0.6-2.4 cases per 100,000 population. The development of the disease is preceded by contact with a viral or bacterial infection of the body, for example, Campylobacter jejuni, Mycoplasma pneumoniae, cytomegalovirus, Epstein-Barr virus and influenza virus. The pathogenesis of Guillain-Barre syndrome is based on the "molecular mimicry" between infectious agents on its surface and the structures of the peripheral nerves. High titers of antibodies to GM1, GD1a, GD1b and GQ1b gangliosides are detected in the serum of patients. Diagnostic criteria for the diagnosis of Guillain-Barre syndrome are examination data, analysis of cerebrospinal fluid and electroneuromyographic study. Plasmapheresis and immunoglobulin G therapy are currently the mainstays of treatment for patients with Guillain-Barré syndrome. The favorable prognosis in terms of regression of clinical manifestations of the disease reaches 60-80%.