Guillain-Barre´ syndrome (GBS) is an acute inflammatory demyelinating polyneuropathy most commonly characterized by rapidly progressive, essentially symmetric weakness and areflexia. This study examined clinical symptoms of clinical variants of GBS through a cerebrospinal fluid (CSF) study, nerve conduction (NCV) study, treatment, and prognosis. There were 16 children with GBS who visited our hospital from January 2011 to December 2013. Guillen-Barre´-like syndromes with transient synovitis were noted in three children. Clinical variants of GBS with acute demyelinating encephalomyelitis were observed in one child. Previous infections were noted in 16 children with Guillen-Barre´-like syndrome. There were ascending infections in 16 cases. Fifteen children showed symmetric infections, and one showed asymmetric infection. In NCV, slow waves were noted in two cases. We treated using intravenous immunoglobulin (IVIG) in four cases, IVIG with steroid in two, cases and supportive care in 10 (62.5%) cases. Five children treated with IVIG and 10 with supportive care management were completely improved.Our study suggests that supportive care is effective as a treatment for clinical variants of GBS. Further study is necessary for more patients.

Guillain-Barré syndrome (GBS) is the most common cause of acute flaccid paralysis and autoimmune polyradiculoneuropathy. Campylobacter jejuni is the most commonly identified infectious trigger for GBS. A sialic-acid containing lipopolysaccharide (LPS) of Campylobacter is thought to be involved in the triggering of GBS. The galE (UDPgalactoset- epimerase) gene of Campylobacter spp. is involved in the synthesis of LPS. In this study, we detected the galE gene in Campylobacter spp. responsible for triggering the onset of GBS. The PCR assay detected the presence of the gene in 14 of the 25 (56%) Campylobacter isolates from domestic chicken, 20 of the 28 (71.4%) Campylobacter isolates from imported chicken and 50 of the 51 (98%) Campylobacter isolates from human clinical samples. Also, the specific 497-bp region of galE sequence in Campylobacters responsible for triggering the onset of GBS was amplified from GBS patient. These results could provide evidence of the first GBS-related C. jejuni infection in Korea.