Brigita Klimbytė1, Simona Petkutė1, Vytautas Steponavičius1, Vidas Košys2
1Lithuanian University of Health Sciences, Faculty of Medicine, Kaunas, Lithuania
2Lithuanian University of Health Sciences Kaunas Clinics, Department of Family Medicine, Kaunas, Lithuania
Guillain-Barre Syndrome (GBS) is a heterogeneous group of immunocompromised diseases characterized by motor, sensory, and autonomic nerve damage provoked by a preceding infection. Typically, BGS manifests as acute inflammatory demyelinating polyneuropathy. In most cases, the full range of clinical symptoms appear within 4 weeks of the onset of the disease, but some patients develop a lightning-fast course of the disease with severe paralysis and impaired pulmonary ventilation within 1 to 4 days. Guillain-Barré syndrome occurs world-wide with an overall incidence of 1 to 3 cases per 100,000 per year. GBS is thought to result from an immune response to a preceding infection that cross-reacts with peripheral nerve components because of molecular mimicry. The immune response can be directed towards the myelin or the axon of peripheral nerve, resulting in demyelinating and axonal forms of GBS. Clinically manifested as progressive, fairly symmetric ascending paralysis of the extremities, later involving the respiratory, facial, or oculomotor muscles, with slight sensory disturbances and autonomic symptoms. The clinical diagnosis of GBS is supported by cerebrospinal fluid (CSF) and electrodiagnostic studies. The main modalities of therapy for Guillain-Barré syndrome are plasmapheresis and administration of intravenous immune globulin.
Keywords: Guillain-Barre syndrome, demyelinating polyneuropathy.