title: Immunoglobulin improves a model of acute motor axonal neuropathy by preventing axonal degeneration.
abstract: BACKGROUND
  The action mechanism of IV immunoglobulin (IVIg) for Guillain-Barré syndrome has yet to be clarified.
  
  
  OBJECTIVE
  To evaluate clinical, histologic, and immunologic effects in a disease model of acute motor axonal neuropathy (AMAN) treated by IVIg.
  
  
  METHODS
  Rabbits were sensitized with gangliosides including GM1 and divided randomly into two groups at disease onset. One group received IV homologous gamma-globulin (400 mg/kg/day) for 5 days (n = 15), and the other received saline (n = 15). Disease severity was scored (0 to 13 points) daily. Sixty days after onset, anti-GM1 antibodies were tested by ELISA, and the number of degenerative axons was counted in spinal anterior roots.
  
  
  RESULTS
  Between both groups at onset, there was no difference in any characteristics including clinical score. The IVIg group had faster recovery than the saline group (p = 0.03). The percentage of rabbits that improved by a score of < or =4 was higher in the IVIg (53%) than in the saline (13%) group 60 days after onset (p = 0.03). Anti-GM1 IgG titers 60 days after onset did not differ between the groups. The anterior roots of rabbits surviving 60 days after onset showed lower frequency of axonal degeneration in the IVIg-treated (n = 11; mean 4.5%) than in the saline-treated (n = 8; mean 11.1%) rabbits (p = 0.01).
  
  
  CONCLUSIONS
  The therapeutic efficacy of IVIg in an AMAN model was confirmed. IVIg may not affect the production or catabolism of anti-GM1 IgG, but it may prevent axonal degeneration of motor nerves.
authors.affiliation: Department of Neurology, Dokkyo University School of Medicine, Tochigi, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Nishimoto
authors.forename: M
authors.initials: M
authors.lastname: Koga
authors.forename: M
authors.initials: M
authors.lastname: Kamijo
authors.forename: K
authors.initials: K
authors.lastname: Hirata
authors.forename: N
authors.initials: N
authors.lastname: Yuki
mesh_terms: D000818:Animals; D001369:Axons / Q000473:pathology*; D004195:Disease Models, Animal; D020275:Guillain-Barre Syndrome / Q000473:pathology / Q000628:therapy*; D016756:Immunoglobulins, Intravenous / Q000627:therapeutic use*; D008297:Male; D016472:Motor Neuron Disease / Q000473:pathology / Q000628:therapy*; D009410:Nerve Degeneration / Q000517:prevention & control*; D011817:Rabbits; D012720:Severity of Illness Index
chemical_list: D016756:Immunoglobulins, Intravenous