Abstract
Guillain-Barre syndrome is an acute inflammatory demyelinating polyradiculoneuropathy of autoimmune etiology, which is characterized by peripheral paralysis and protein-cell dissociation in the cerebrospinal fluid in most cases. The Guillain-Barre syndrome prevalence is 0.6-2.4 cases per 100 thousand population. In Moscow, about 200 people are taken ill with Guillain-Barre syndrome each year. Currently, four main clinical variants of Guillain-Barre syndrome are described: acute inflammatory demyelinating polyradiculoneuropathy, axonal form, acute motor axonal neuropathy, and Miller-Fisher syndrome. Disease development is preceded by contact with the viral or bacterial infections causative agent such as Campylobacter jejuni, Mycoplasma pneumonia, cytomegalovirus, Epstein-Barr virus and influenza virus. Guillain-Barre syndrome pathogenesis is «molecular mimicry» between infectious agents surfaces and the peripheral nerves structures. High titer of antibodies to the GM1, GD1a, GD1b and GQ1b gangliosides is found in patients blood serum. Diagnostic criteria for the Guillain-Barre syndrome diagnosis are the physical examination results, cerebrospinal fluid analysis and electroneuromyographic study. The North American motor deficit severity scale is used to assess the neurological status. This scale allows to evaluate the patient’s condition and movement abilities. Currently plasmapheresis and immunoglobulin G therapy are the main treatment options for patients with Guillain-Barre syndrome. The favorable prognosis in the form of disease clinical manifestations regression reaches 60-80%. Mortality in Guillain-Barre syndrome is 5% in average and may reach 20% in patients on mechanical ventilation. The most common death causes of patients with Guillain-Barre syndrome are respiratory failure, aspiration pneumonia, sepsis, and pulmonary embolism. Early treatment initiation can reduce serious complications risk, including respiratory failure, what ultimately leads to decrease in mortality and patients disablement.
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