title: Guillain-Barré syndrome in northern China. Relationship to Campylobacter jejuni infection and anti-glycolipid antibodies.
abstract: Guillain-Barré syndrome has been considered to be primarily an acute inflammatory demyelinating polyneuropathy (AIDP). Our experience with Guillain-Barré syndrome in northern China differs from the traditional concept. Electrophysiologically and pathologically, most of our patients have motor axonal degeneration with minimal cellular inflammation, which we have termed 'acute motor axonal neuropathy' (AMAN). The current studies were undertaken to characterize prospectively the clinical, electrophysiological, and serological features of Guillain-Barré syndrome, defined clinically, in northern China. In 1991 and 1992, we characterized by electrodiagnostic criteria 129 Chinese patients with Guillain-Barré syndrome. The AMAN form was present in 65% of patients, the AIDP form in 24% and 11% were unclassifiable. For the 38 patients who presented from January to October, 1992, we performed serological assays for antibodies to Campylobacter jejuni and to glycolipids. Of these 38 patients, 55% had AMAN, 32% had AIDP and 13% were unclassifiable. Sixty-six percent of the 38 had serological evidence of recent C. jejuni infection as compared with 16% of village controls (P = 0.001). Seventy-six percent of AMAN patients and 42% of AIDP patients were seropositive. IgG anti-GM1 antibodies were more frequent in Guillain-Barré syndrome patients compared with village controls (42% versus 6%; P < 0.01). However, no statistically significant correlations were found between the pattern of disease, AMAN or AIDP, anti-glycolipid antibodies, or C. jejuni antibodies. Based on electrophysiological criteria, Guillain-Barré syndrome in northern China can be divided into two predominant forms: AIDP and AMAN. The AMAN form is more common and predominates in the yearly summer outbreaks of Guillain-Barré syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
authors.forename: T W
authors.initials: TW
authors.lastname: Ho
authors.forename: B
authors.initials: B
authors.lastname: Mishu
authors.forename: C Y
authors.initials: CY
authors.lastname: Li
authors.forename: C Y
authors.initials: CY
authors.lastname: Gao
authors.forename: D R
authors.initials: DR
authors.lastname: Cornblath
authors.forename: J W
authors.initials: JW
authors.lastname: Griffin
authors.forename: A K
authors.initials: AK
authors.lastname: Asbury
authors.forename: M J
authors.initials: MJ
authors.lastname: Blaser
authors.forename: G M
authors.initials: GM
authors.lastname: McKhann
mesh_terms: D000293:Adolescent; D000328:Adult; D000367:Age Factors; D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood / Q000276:immunology; D000914:Antibodies, Viral / Q000097:blood; D001323:Autoantibodies / Q000097:blood / Q000276:immunology*; D001327:Autoimmune Diseases / Q000453:epidemiology* / Q000209:etiology / Q000276:immunology; D002169:Campylobacter Infections / Q000150:complications / Q000453:epidemiology* / Q000276:immunology; D016123:Campylobacter jejuni / Q000276:immunology; D002648:Child; D002675:Child, Preschool; D002681:China / Q000453:epidemiology; D015897:Comorbidity; D003711:Demyelinating Diseases / Q000453:epidemiology / Q000209:etiology / Q000276:immunology; D004199:Disease Vectors; D005260:Female; D006017:Glycolipids / Q000276:immunology*; D006801:Humans; D007223:Infant; D008297:Male; D008459:Measles virus / Q000276:immunology; D008875:Middle Aged; D016472:Motor Neuron Disease / Q000453:epidemiology / Q000209:etiology / Q000276:immunology; D009431:Neural Conduction; D011129:Polyradiculoneuropathy / Q000145:classification / Q000453:epidemiology* / Q000209:etiology / Q000276:immunology; D011446:Prospective Studies; D012307:Risk Factors; D012621:Seasons
chemical_list: D000907:Antibodies, Bacterial; D000914:Antibodies, Viral; D001323:Autoantibodies; D006017:Glycolipids