title: Patterns and serial changes in electrodiagnostic abnormalities of axonal Guillain-Barré syndrome.
abstract: BACKGROUND
  In Guillain-Barré syndrome (GBS), anti-ganglioside antibodies are strongly associated with the acute motor axonal neuropathy (AMAN) form, but there are also cases of the demyelinating form of GBS (acute inflammatory demyelinating polyneuropathy [AIDP]) with anti-ganglioside antibodies.
  
  
  OBJECTIVE
  To elucidate the patterns and sequential changes in electrodiagnostic abnormalities of anti-ganglioside-positive GBS.
  
  
  METHODS
  Detailed serial electrodiagnostic findings were reviewed for 51 patients with GBS. Anti-ganglioside antibodies were measured by ELISA.
  
  
  RESULTS
  Antibodies to GM1, GM1b, GD1a, or GalNAc-GD1a were present in 25 patients. Of these, 12 (48%) showed the AMAN pattern, 5 (20%) the AIDP pattern, and 3 (12%) isolated F-wave absence in the first examination. All five patients with the AIDP pattern showed prolonged distal latencies, but three eventually showed the AMAN pattern or rapid normalization. The remaining two still had similarly prolonged distal latencies in weeks 4 to 6, but the serial changes were distinct from those in the anti-ganglioside-negative AIDP patients who showed progressive increases in distal latencies over 2 months after onset.
  
  
  CONCLUSIONS
  Besides the simple axonal degeneration pattern, patients with anti-ganglioside-positive Guillain-Barre syndrome can show transient conduction slowing/block in the distal or proximal nerve segments, mimicking demyelination, but anti-ganglioside antibodies do not appear to be associated with acute inflammatory demyelinating polyneuropathy.
authors.affiliation: Department of Neurology, Chiba University Graduate School of Medicine, Japan. hiragaa@mail3.alpha-net.ne.jp
authors.forename: A
authors.initials: A
authors.lastname: Hiraga
authors.forename: S
authors.initials: S
authors.lastname: Kuwabara
authors.forename: K
authors.initials: K
authors.lastname: Ogawara
authors.forename: S
authors.initials: S
authors.lastname: Misawa
authors.forename: T
authors.initials: T
authors.lastname: Kanesaka
authors.forename: M
authors.initials: M
authors.lastname: Koga
authors.forename: N
authors.initials: N
authors.lastname: Yuki
authors.forename: T
authors.initials: T
authors.lastname: Hattori
authors.forename: M
authors.initials: M
authors.lastname: Mori
mesh_terms: D000328:Adult; D001323:Autoantibodies / Q000276:immunology*; D001369:Axons / Q000276:immunology / Q000473:pathology*; D018450:Disease Progression; D004568:Electrodiagnosis; D005260:Female; D005677:G(M1) Ganglioside / Q000031:analogs & derivatives / Q000276:immunology; D005732:Gangliosides / Q000276:immunology*; D020275:Guillain-Barre Syndrome / Q000175:diagnosis* / Q000276:immunology / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009431:Neural Conduction / Q000276:immunology*; D010525:Peripheral Nerves / Q000276:immunology / Q000473:pathology / Q000503:physiopathology*; D011237:Predictive Value of Tests
chemical_list: D001323:Autoantibodies; D005732:Gangliosides; C064020:ganglioside GD1alpha; D005677:G(M1) Ganglioside; C029624:ganglioside M1b